OCCUPATIONAL HEALTH
AND THE SERVICE MEMBER

The Coat of Arms
1818
Medical Department of the Army

A 1976 etching by Vassil Ekimov of an
original color print that appeared in
The Military Surgeon, Vol XLI, No 2, 1917

Textbooks of Military Medicine

Published by the

Office of The Surgeon General
Borden Institute
US Army Medical Department Center and School
Health Readiness Center of Excellence
Fort Sam Houston, Texas

Edward A. Lindeke
Colonel (Retired), MS, US Army
Director, Borden Institute

The TMM Series

Published Textbooks

Medical Consequences of Nuclear Warfare (1989)

Conventional Warfare: Ballistic, Blast, and Burn Injuries (1991)

Occupational Health: The Soldier and the Industrial Base (1993)

Military Dermatology (1994)

Military Psychiatry: Preparing in Peace for War (1994)

Anesthesia and Perioperative Care of the Combat Casualty (1995)

War Psychiatry (1995)

Medical Aspects of Chemical and Biological Warfare (1997)

Rehabilitation of the Injured Soldier, Volume 1 (1998)

Rehabilitation of the Injured Soldier, Volume 2 (1999)

Medical Aspects of Harsh Environments, Volume 1 (2002)

Medical Aspects of Harsh Environments, Volume 2 (2002)

Ophthalmic Care of the Combat Casualty (2003)

Military Medical Ethics, Volume 1 (2003)

Military Medical Ethics, Volume 2 (2003)

Military Preventive Medicine, Volume 1 (2003)

Military Preventive Medicine, Volume 2 (2005)

Recruit Medicine (2006)

Medical Aspects of Biological Warfare (2007)

Medical Aspects of Chemical Warfare (2008)

Care of the Combat Amputee (2009)

Combat and Operational Behavioral Health (2011)

Military Quantitative Physiology: Problems and Concepts in Military Operational Medicine (2012)

Medical Consequences of Radiological and Nuclear Weapons (2013)

Forensic and Ethical Issues in Military Behavioral Health (2014)

Combat Anesthesia: The First 24 Hours (2015)

Otolaryngology/Head and Neck Surgery Combat Casualty Care in Operation Iraqi Freedom and Operation Enduring Freedom (2015)

Medical Aspects of Biological Warfare (2018)

Military Veterinary Services (2019)

Occupational Health and the Service Member (2019)

“Waiting out the dust storm”: Sgt. 1st Class Lance Amsden, platoon sergeant for the 1st Platoon, Company C, 1st Battalion, 501st Infantry Regiment, 4th Brigade Combat Team (Airborne), 25th Infantry Division, watches as CH-47 Chinook helicopters circle above during a dust storm at Forward Operating Base Kushamond, Afghanistan, July 17, 2009, during preparation for an air assault mission.

Taken July 2009 by Army Photographer Pfc Andrya Hill.

OCCUPATIONAL HEALTH
AND THE SERVICE MEMBER

Senior Editor

TIMOTHY M. MALLON, MD, MPH
Colonel (Retired), Medical Corps, US Army
Adjunct Assistant Professor
Department of Preventive Medicine & Biostatistics
Uniformed Services University of the Health Sciences

Office of The Surgeon General
Borden Institute
US Army Medical Department Center and School
Health Readiness Center of Excellence
Fort Sam Houston, Texas

2019

Editorial Staff:

Joan Redding
Senior Production Editor

Aiesha Harvy
Volume Editor

Douglas Wise
Senior Layout Editor

Venetia Valiga
Illustrator

Richard Dredden
Layout Editor

This volume was prepared for military medical educational use. The focus of the information is to foster discussion that may form the basis of doctrine and policy. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

Dosage Selection:

The authors and publisher have made every effort to ensure the accuracy of dosages cited herein. However, it is the responsibility of every practitioner to consult appropriate information sources to ascertain correct dosages for each clinical situation, especially for new or unfamiliar drugs and procedures. The authors, editors, publisher, and the Department of Defense cannot be held responsible for any errors found in this book.

Use of Trade or Brand Names:

Use of trade or brand names in this publication is for illustrative purposes only and does not imply endorsement by the Department of Defense.

Neutral Language:

Unless this publication states otherwise, masculine nouns and pronouns do not refer exclusively to men.

CERTAIN PARTS OF THIS PUBLICATION PERTAIN TO COPYRIGHT RESTRICTIONS. ALL RIGHTS RESERVED.

NO COPYRIGHTED PARTS OF THIS PUBLICATION MAY BE REPRODUCED OR TRANSMITTED IN ANY FORM OR BY ANY MEANS, ELECTRONIC OR MECHANICAL (INCLUDING PHOTOCOPY, RECORDING, OR ANY INFORMATION STORAGE AND RETRIEVAL SYSTEM), WITHOUT PERMISSION IN WRITING FROM THE PUBLISHER OR COPYRIGHT OWNER.

Published by the Office of The Surgeon General

Borden Institute

US Army Medical Department Center and School

Health Readiness Center of Excellence

Fort Sam Houston, Texas

Library of Congress Cataloging-in-Publication Data

Names: Mallon, Timothy M., editor. | US Army Medical Department Center and School, issuing body.

Title: Occupational health and the service member / senior editor, Timothy M. Mallon.

Description: Fort Sam Houston, Texas : Office of The Surgeon General, Borden Institute, US Army Medical Department Center and School, Health Readiness Center of Excellence, 2019. | Series: Textbooks of military medicine | Includes bibliographical references and index.

Identifiers: LCCN 2018057259 (print) | LCCN 2018059263 (ebook) | ISBN 9780160949647 (ebook) | ISBN 9780160949838 (ebook) | ISBN 9780160949845 (ebook) | ISBN 9780160949616 (print)

Subjects: | MESH: Occupational Health | Occupational Exposure | Accidents, Occupational | Military Personnel

Classification: LCC RC967 (ebook) | LCC RC967 (print) | NLM WA 400 | DDC 613.6/2--dc23

LC record available at https://lccn.loc.gov/2018057259

PRINTED IN THE UNITED STATES OF AMERICA

26, 25, 24, 23, 22, 21, 20, 19      5 4 3 2 1

Contents

Copyright

Contributors

Foreword by The Surgeon General

Preface

1.   The Tri-Service Industrial Base
P. K. Underwood

2.   US Air Force Occupational and Environmental Health Program
Patrick F. Whitney and Jon R. Jacobson

3.   Safety and Occupational Health Progams for the US Navy and US Marine Corps
Pamela L. Krahl, Deborah Bohlman, Lynn E. Cook, Anne McDonough, and Richard J. Thomas

4.   The Evolution of Occupational Medicine Practice in the US Navy
Pamela L. Krahl, Brian Riley, and Richard J. Thomas

5.   US Army Occupational Health Programs and Services
Timothy M. Mallon, M. Debra Parker, Jennylynn Balmer, David P. Deeter, and Janet M. Ruff

6.   History of Army Occupational Health, 1991–2015
Jack M. Heller, Timothy M. Mallon, Coleen P. Baird, Deanna K. Harkins, Mahmut Atabay, John P. Cuellar, and Joel C. Gaydos

7.   Army Occupational Health Program Management
Timothy M. Mallon

8.   Agency Medical Evaluations
Gregory J. Martin, Wendy E. Miklos, Jerald Cook, and J. C. Phillip Spottswood

9.   Federal Workers’ Compensation Programs
Cameron J. L. Nelson, Sheryl A. Bedno, and Timothy M. Mallon

10.   Medical Surveillance
Timothy M. Mallon, Cameron J.L. Nelson, David P. Deeter, and Janet M. Ruff

11.   Health Hazards to Healthcare Workers
Melissa A. McDiarmid, Kevin P. Michaels, Marlene Sanchez, Gary E. Herr, Michael J. Testa, Daniel J. Caldwell, and Timothy M. Mallon

12.   Army Hearing Program
Doug W. Ohlin, Sharon L. Beamer, and Marjorie Grantham

13.   Respiratory Protection
Timothy M. Mallon, Cameron J. L. Nelson, Tifani Gleason, Brandon Gardner, Gregory J. Martin, and John P. Barrett

14.   Industrial Hygiene Program Management
Sandra Parker-Monk and John W. Yasalonis

15.   Ergonomics
John Pentikis and Jay Clasing

16.   Aerospace Medicine
Alfred C. Emmel, Raymond R. Batz, and John J. Venezia

17.   Military Diving Operations
Michael G. Zakaroff, Ryan W. Snow, Richard D. Vann, and James Vorosmarti

18.   Physiology and Medical Aspects of Diving
Ryan W. Snow, Michael G. Zakaroff, James Vorosmarti, Jr, and Richard D. Vann

19.   Undersea Medicine
Grace Landers

20.   Hazardous Substances in the Workplace
Papiya Ray and Cameron J. L. Nelsons

21.   Occupational and Environmental Lead
Carol I. Tobias, Richard L. Lachiver, and Han Q. Bui

22.   Ionizing Radiation
Carlos E. Corredor, Scott Goodison, Douglas Barrickman, David Alberth, Mark W. Bower, Craig Jones, Michael W. Mueller, Harris Edge, and Samuel G. Dunston

23.   Nonionizing Radiation
Bryan D. Kobe, Kieran T. Lerch, Ernest C. Brumage, John J. Defrank, Penelope K. Galoff, Charles W. Hicks Jr, and David H. Sliney

24.   Carbon Monoxide
Steven R. Smith, John W. Downs, Thomas D. Louwers, Gregory J. Martin, Timothy B. Weyandt, and Charles David Ridgeley, Jr

25.   Beryllium
Dale Harman, Nicole S. Chavis, and Timothy M. Mallon

26.   Shipboard Medicine
Terrance Riley, Timothy J. Bergan, Robert N. Uniskiewicz, and Louis Kroot

27.   Deployment Surveillance
Raúl Alexander Mirza, Elisabeth M. Hesse, and Coleen Bair

28.   Explosives and Propellants
Timothy M. Mallon, Peter G. Matos, W. Scott Monks, Raul A. Mirza, and Donald T. Bodeau

29.   Biological Monitoring
Timothy M. Mallon, Richard P. Phipps, Juilee Thakar, Collyn Woeller, Dean P. Jones, Douglas I. Walker, Karan Uppal, Mark Utell, and Thomas Thatcher

30.   Cold Stress
Andy Chern and David W. Degroot

Abbreviations and Acronyms

Index

Contributors

DAVID ALBERTH, MS

Formerly, Health Physicist, Master Consultant, Health Physics Program, Army Institute of Public Health, US Army Public Health Command, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010; Deceased

MAHMUT ATABAY, MS

Second Lieutenant, US Army; Medical Services Corps, Health Physics Operations Officer, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

COLEEN P. BAIRD, MD, MPH

Division Chief, Department of Environmental Medicine, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

JENNYLYNN BALMER, RN, MPA

Occupational Health Nurse Consultant, Occupational and Environmental Health Portfolio, Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010

JOHN P. BARRETT, MD, MPH

Colonel, Medical Corps, US Army; Deputy Chief, Epidemiology Division, Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814

DOUGLAS BARRICKMAN, BS

Major (Retired), Medical Service Corps, US Army; Radiation Safety Officer, Augusta VA Medical Center, Department of Veterans Affairs, Augusta, Georgia 30904

RAYMOND R. BATZ, DO, MPH

Captain, Medical Corps, US Navy; Force Surgeon, III Marine Expeditionary Force, PSC 559 Box 6853, FPO AP 96377, Okinawa, Japan

SHARON L. BEAMER, AuD, CCC-A

Program Analyst, Navy Bureau of Medicine and Surgery, 7700 Arlington Boulevard, Falls Church, Virginia 22042

SHERYL A. BEDNO, MD, MPH

Lieutenant Colonel, Medical Corps, US Army; Chief, Preventive Medicine Service, Womack Medical Center, Fort Bragg, North Carolina 28310

TIMOTHY J. BERGAN, DO, MPH

Lieutenant Commander, Medical Corps, US Navy; Force Medical Officer, Military Sealift Command, Medical Department (Code: N13X), Bldg SP-64, 471 C Street, Norfolk, Virginia 23511-2419

DONALD T. BODEAU, MD, MPH

Department of Occupational Medicine, Midelfort Clinic, 733 West Clairemont Avenue, Eau Claire, Wisconsin 54701

DEBORAH BOHLMAN, RN

Regional Nurse Consultant, Naval Health Clinic, 695 Kinkaid Road, Annapolis, Maryland 21402-5050

MARK W. BOWER, PhD

Colonel (Retired), Medical Service Corps, US Army; Command Radiation Safety Officer, Regional Health Command-Pacific, Madigan Army Medical Center, 9040 Jackson Avenue, Tacoma, Washington 98431

ERNEST C. BRUMAGE, MS

Physicist, Occupational health Sciences Directorate, Nonionizing Radiation Division, US Army Public Health Center, Aberdeen Proving Ground,Maryland 21010-5403

HAN Q. BUI, MD, MPH

Commander, Medical Corps, US Navy; Chief, Occupational and Environmental Medicine, Naval Health Clinic Quantico, 3259 Catilin Avenue, Quantico, Virginia 22134

DANIEL J. CALDWELL, PhD, MHS

Lieutenant Colonel, US Army; Chief, Exposure Assessment Section, Occupational Health Research Detachment, Wright Patterson Air Force Base, Ohio 45433-7400; formerly, Chief Medical Systems Safety and Health Branch, Industrial Hygiene Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

JAMES CAVINESS, MD, MS

Occupational Medicine Physician, Branch Health Clinic China Lake, Department of Occupational Health, 1 Administration Circle, Building 1403, China Lake, California 93555

NICOLE S. CHAVIS, MPH

Research Associate, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

ANDY CHERN, MD, MPH

Captain, Medical Corps, US Army; Associate Program Director and Assistant Professor, Occupational & Environmental Medicine Residency Program, Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

JAY CLASING, PhD

Lieutenant Colonel, Medical Specialist Corps; Manager, Industrial Hygiene Field Services Division, US Army Public Health Center, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010-5403

JERALD COOK, MD, MS

Lieutenant Commander, Medical Corps, US Navy; Occupational Health Department Head, Robert E. Bush Naval Hospital, 1145 Sturgis Road, Twenty-nine Palms, California 92278

LYNN E. COOK, AuD

Occupational Audiologist, Naval Health Clinic, 695 Kinkaid Road, Annapolis, Maryland 21402-5050

CARLOS E. CORREDOR, MSNE

Major (Retired), Medical Service Corps, US Army; Health Physicist, Health Physics Program, Army Institute of Public Health, US Army Public Health Command, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010

JOHN P. CUELLAR, MS

Colonel, US Army, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

DAVID P. DEETER, MD, MPH

Lieutenant Colonel (P), US Army; Director, Occupational and Environmental Health, and Director, Occupational Medicine Residency Program, US Army Environmental Health Agency, Edgewood Area, Aberdeen Proving Ground, Maryland 21010-5422; formerly, Occupational Health Consultant to the Surgeon General

JOHN J. DeFRANK

Chief, Nonionizing Radiation Division, Occupational Health Sciences Directorate US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

DAVID W. DEGROOT, PhD

Major, Medical Service Corps, US Army; Deputy Chief, Department of Clinical Investigation, Tripler Army Medical Center, Honolulu, Hawaii 96859

JOHN W. DOWNS, MD

Major, Medical Corps, US Army; Chief, Department of Preventive Medicine, Blanchfield Army Community Hospital, Fort Campbell, Kentucky 42223

SAMUEL G. DUNSTON, MS

Major (Retired), US Army; Nuclear Medical Science Officer, Laser/Microwave Division; formerly, Chief, Medical Health Physics Branch, US Army, Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

HARRIS EDGE

Chief, Industrial Health Physics Branch, Health Physics Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

ALFRED C. EMMEL, MD, MPH

Colonel (Retired), US Air Force; Attending Physician, Emergency Medicine and Occupational Medicine, Presbyterian Hospital, 1100 Central Avenue, SE, Albuquerque, New Mexico 87106

PENELOPE K. GALOFF

Physical Scientist, Laser Branch, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

BRANDON GARDNER, DO, MPH

Major, Medical Corps, US Army; Chief, Occupational Medicine Branch, US Army Medical Department Center and School, 3599 Winfield Scott Road, Fort Sam Houston, Texas 78234

JOEL C. GAYDOS, MD, MPH

Colonel (Retired), US Army, Occupational Medicine Physician, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

SCOTT GOODISON, BS

Radiation Safety Officer, Army Institute of Public Health, US Army Public Health Command, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010

MARJORIE GRANTHAM, PhD

Colonel (Retired), US Army; Technical Science Writer, Ho-Chunk Technical Solutions, Austin, Texas 78723

DEANNA K. HARKINS, MD, MPH

Medical Officer, Department of Environmental Medicine, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

DALE HARMAN, MD, MPH

Captain (Retired), Medical Corps, US Navy; Occupational and Environmental Medicine Physician, Independent Contractor, Portsmouth, New Hampshire 03870

JACK M. HELLER, PhD

Environmental Scientist, Department of Environmental Medicine, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

GARY E. HERR, MS, MPH

Major, US Army; Chief, Environmental Health and Industrial Hygiene, Preventive Medicine Services, William Beaumont Army Medical Center, El Paso, Texas 79920

ELISABETH M. HESSE, MD, MTM&H

Major, Medical Corps, US Army; Division Chief, Disease Epidemiology Division, US Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010-5403

CHARLES W. HICKS JR

Physical Scientist, Laser Branch, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

JON R. JACOBSON, DO, MPH

Colonel, US Air Force; Air Force Chief of Occupational Medicine; Occupational Medicine Consultant to the Air Force Surgeon General, Defense Health Headquarters, 7700 Arlington Blvd, Falls Church, Virginia 22042

CRAIG JONES, BS

Health Physicist, Health Physics Program, Army Institute of Public Health, US Army Public Health Command, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010

DEAN P. JONES, PhD

Professor, Clinical Biomarkers Laboratory, Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University, Atlanta, Georgia 30322

BRYAN D. KOBE

Electronics Engineer, Occupational Health Sciences Directorate, Nonionizing Radiation Division, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

PAMELA L. KRAHL, MD, MPH

Captain, Medical Corps, US Navy; Occupational and Environmental Medicine Residency Program Director, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814-4799

LOUIS KROOT, MD

Commander (Retired), Medical Corps, US Navy; Surface Medical Department Officer; currently, Department of Emergency Medicine, University of Kentucky Chandler Medical School, Lexington, Kentucky 40536-0298

RICHARD L. LACHIVER, MD, MPH

Formerly; Medical Director, Occupational Health Service of York Hospital, York, Pennsylvania; Major, US Army; Program Manager for Occupational Medicine and Residency Training Director, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland

GRACE LANDERS, MD

Lieutenant, Medical Corps, US Navy; Naval Medical Center Portsmouth; Resident, Emergency Medicine, 620 John Paul Jones Circle, Portsmouth, Virginia 23708

KIERAN T. LERCH, MS

Physicist, Occupational Health Sciences Directorate, Nonionizing Radiation Division, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

THOMAS D. LOUWERS, MD, MPH

Lieutenant Commander, US Navy; Physician, Department of Occupational Medicine, Naval Hospital Bremerton, Bremerton, Washington 98337

TIMOTHY M. MALLON, MD, MPH

Colonel (Retired), Medical Corps, US Army; Adjunct Assistant Professor, Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

GREGORY J. MARTIN, MD, MPH

Colonel, Medical Corps, US Army; Chief, Occupational Medicine, Madigan Army Medical Center, 9925 5th Street,Building 9025, Tacoma, Washington 984319

PETER G. MATOS, MD, MPH

Formerly, Major, US Army; Command Surgeon, US Army Joint Munitions Command, Rock Island Arsenal, Illinois 61259-5000

MELISSA A. McDIARMID, MD, MPH

Professor of Medicine, Epidemiology and Public Health; Director, Division of Occupational & Environmental Medicine, University of Maryland School of Medicine, 11 South Paca Street, Suite 200, Baltimore, Maryland 21201

ANNE McDONOUGH, MD, MPH

Lieutenant Commander, Medical Corps, US Navy (Undersea Medical Officer/Diving Medical Officer); Department Head, Occupational Medicine Department, US Naval Hospital, PSC 827 Box 281, FPO AE 09617, Naples, Italy

KEVIN P. MICHAELS, MD, MPH

Colonel (Retired), US Army; Medical Director, Providence Hospital, Department of Occupational Health, 5100 Rangeline Service N, Mobile, Alabama 36619

WENDY E. MIKLOS, MD, MPH

Lieutenant Colonel, Medical Corps, US Army; Chief, Department of Preventive Medicine, US Army Medical Activity/Fort Carson, Department of Preventive Medicine, MCXE-PMD, 1650 Cochrane Circle, Fort Carson, Colorado 80913

RAÚL ALEXANDER MIRZA, DO, MPH

Major, Medical Corps, US Army; Division Chief, Occupational Medicine Division, US Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010-5403

W. SCOTT MONKS, PA-C, MPAS

Army Public Health Center, Directorate of Clinical Public Health & Epidemiology, Division of Occupational Medicine, Aberdeen Proving Ground, Maryland 21010

MICHAEL W. MUELLER, MPH

Lieutenant Colonel, US Army; Health Services Command Radiation Protection Staff Officer, Fort Sam Houston, Texas 78234

CAMERON J. L. NELSON, MD, MPH

Commander, Medical Corps, US Navy; Chief of Occupational Medicine, Naval Hospital Bremerton, 1 Boone Road, Bremerton, Washington 98312

DOUG W. OHLIN, PhD

Formerly, Chief, Hearing Conservation Program, US Army Center for Health Promotion and Preventive Medicine, Aberdeen Proving Ground, Maryland 21010; Deceased

M. DEBRA PARKER, JD, MSN

Colonel (Retired), US Air Force; formerly, Senior Occupational Health Nurse Consultant, Occupational and Environmental Health Portfolio, Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010

SANDRA PARKER-MONK, CIH

Program Manager, Occupational Health Sciences, Army Public Health Center, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010

JOHN PENTIKIS, PhD

Ergonomist, US Army Public Health Center, 8977 Sibert Road, Aberdeen Proving Ground, Maryland 21010-5403

RICHARD P. PHIPPS, PhD

Professor, Departments of Medicine and Environmental Medicine, University of Rochester Medical Center, Rochester, New York 14618

PAPIYA RAY, MD, MPH

Occupational Medicine Consultant Physician, Federal Occupational Health, 7700 Wisconsin Avenue, Suite 7201, Bethesda, Maryland 20857

CHARLES DAVID RIDGELEY, JR, MD

Lieutenant Colonel, US Army; Occupational Medicine Physician, Occupational and Environmental Medicine Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

BRIAN RILEY, DO, MPH

Commander, Medical Corps, US Navy; Occupational Medicine Department Head, Naval Branch Health Clinic, 881 USS James Madison Road, Kings Bay, Georgia 31547

TERRANCE RILEY, MD

Formerly, Captain (Retired), Medical Corps, US Navy; Professor of Neurology, Department of Neurology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030; Deceased

JANET M. RUFF, RN, MPH

Senior Occupational Health Nurse Consultant (Retired), Occupational and Environmental Medicine Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

MARLENE SANCHEZ, MD, MPH

Commander, US Navy; Director of Public Health, Department of Occupational Medicine, Naval Health Clinic Hawaii, 480 Central Avenue, Building 1750, Joint Base Pearl Harbor-Hickam, Hawaii 96860-4908

DAVID H. SLINEY, PhD

Chief, Laser Branch, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

STEVEN R. SMITH, MD, MPH

Colonel (Retired), Medical Corps, US Army; formerly, Chief, Occupational Medicine, Department of Preventive Medicine, Madigan Army Medical Center, Joint Base Lewis-McChord, Washington 98433

RYAN W. SNOW, MD

Lieutenant, Medical Corps, US Navy; Diving Medical Officer, Explosive Ordnance Disposal Mobile Unit Five, Santa Rita, Guam

J.C. PHILLIP SPOTTSWOOD, JD, MPH

Medical Policy and Program Specialist, Hiring Policy, US Office of Personnel Management, 1900 E Street, NW, Room 6500, Washington, DC 20415

MICHAEL J. TESTA, MS

Major, US Army; Chief, Healthcare Hazards Division, US Army Public Health Center, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010-5403

JUILEE THAKAR, PhD

Professor, Departments of Microbiology & Immunology and Biostatistics & Computational Biology, University of Rochester Medical Center, Rochester, New York 14618

THOMAS THATCHER, PhD

Research Associate Professor, Department of Medicine/Pulmonary and Critical Care, University of Rochester Medical Center, Rochester, New York 14618

RICHARD J. THOMAS, MD, MPH

Captain (Retired), Medical Corps, US Navy; Associate Professor, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814-4799

CAROL I. TOBIAS, MBA, BSN

Nurse Consultant, US Army Center for Public Health (Provisional), 1570 Wise Road, Building 1570, Aberdeen Proving Ground, Maryland 21010

P. K. UNDERWOOD, MD, MPH, MHA

Colonel (Retired), US Army; Army Materiel Command, Command Surgeon, Redstone Arsenal, Alabama 35898

ROBERT N. UNISKIEWICZ, MD, MPH

Lieutenant Commander, Medical Corps, US Navy; Occupational Medicine Department Head, Naval Medical Center Portsmouth, 620 John Paul Jones Circle, Portsmouth, Virginia 23708

KARAN UPPAL, PhD

Assistant Professor, Clinical Biomarkers Laboratory, Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University, Atlanta, Georgia 30322

MARK UTELL, MD

Professor, Departments of Medicine and Environmental Medicine, University of Rochester Medical Center, Rochester, New York 14618

RICHARD D. VANN, PhD

Captain, US Navy Reserve (Retired); Divers Alert Network, Center for Hyperbaric Medicine and Environmental Physiology, Box 3823, Duke University Medical Center, Durham, North Carolina 27710

JOHN J. VENEZIA, DO, MPH

Major, Medical Corps, US Army; Associate Program Director, Department of Occupational Medicine, US Army School of Aviation Medicine, 340 Hulse Road, Naval Air Station, Pensacola, Florida 32508

JAMES VOROSMARTI, JR, MD

Captain, Medical Corps, US Navy (Retired); Consultant in Occupational, Environmental, and Undersea Medicine, 16 Orchard Way South, Rockville, Maryland 20854

DOUGLAS I. WALKER, PhD

Assistant Professor, Clinical Biomarkers Laboratory, Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University, Atlanta, Georgia 30322

TIMOTHY B. WEYANDT, MD, MPH

Director, Occupational Health Program, Pennsylvania State University, University Park, Pennsylvania 16802; Lieutenant Colonel, US Army (Retired); formerly, Medical Advisor for Clinical, Occupational, and Environmental Health; US Army Biomedical Research and Development Laboratory, Fort Detrick, Maryland

PATRICK F. WHITNEY, MD, MSPH

Lieutenant Colonel (Retired), Medical Corps; US Air Force; formerly, Commander, 7th Aerospace Medicine Squadron; Occupational Medicine Consultant to the Air Force Surgeon General

COLLYN WOELLER, PhD

Professor, Department of Environmental Medicine, University of Rochester Medical Center, Rochester, New York 14618

JOHN W. YASALONIS, CIH

Formerly, Lieutenant Colonel, US Army; Industrial Hygiene Consultant to The US Army Surgeon General, Headquarters, Department of the Army, 5109 Leesburg Pike, Falls Church, Virginia

MICHAEL G. ZAKAROFF, MD

Lieutenant, Medical Corps, US Navy; Diving Medical Officer, Mobile Diving and Salvage Unit One, Pearl Harbor, Hawaii 96818

Foreword

The first Textbook of Military Medicine on occupational health for the Soldier and workers in the military industrial base was published in 1993. It described the development of occupational and environmental health and occupational medicine in the Army from 1775 until 1990. This follow-on volume covers 1990 to 2015, a period during which the United States was involved in prolonged warfare. In these operations, deployed Soldiers encountered multiple potentially harmful environmental exposures and reported postdeployment adverse health effects they often related to these exposures. The exposures included impressively large sandstorms; emissions from burning oil wells in Kuwait; chemical agents released during the destruction of chemical weapons caches; hexavalent chromium from a damaged industrial site; sulfur gases from a large, prolonged sulfur mine fire; and emissions from the destruction of all types of waste in large burn pits over many years. The absence of timely, reliable exposure data that could be directly linked to the Soldiers exposed, and the absence of defined symptom complexes that could be used to diagnose postdeployment illnesses, led to anxiety and frustration for the service members affected and those caring for them.

In response, Veterans’ groups and Congress called for the Department of Defense (DoD) to document potentially harmful exposures related to deployment, and to identify the adverse health outcomes that might result. Registries were initiated to record and archive exposures of concern and Veterans’ maladies, and the Army was required to identify and evaluate Soldiers previously exposed to chemical warfare agents during deployment. Epidemiologic resources to study deployment-related illnesses included considerable amounts of area sampling data from deployed areas, archived predeployment and postdeployment health questionnaires, administrative health encounter data in the Defense Medical Surveillance System (DMSS), and sera stored in the DoD Serum Repository (DoDSR). Efforts were made to secure deployment-related data in large databases, such as the Defense Occupational and Environmental Health Readiness System, for future reference and study, to use the DMSS for deployment-related epidemiologic studies, and to investigate the possible use of the DoDSR predeployment and postdeployment specimens to identify and study deployment-related exposures.

The National Research Council of the National Academy of Sciences recommended that the DoD significantly improve its capability to identify exposures and perform exposure assessments. In response, the DoD undertook an effort to explore alternatives to environmental and breathing zone sampling with the use of wearable sensors, and to assess the use of biomarkers to identify exposures in the deployed environment using DoDSR sera. The rapidly evolving field of biomarker technology showed promise in determining the internal doses after environmental exposures and identifying biomarkers of effect.

This volume documents the services’ support for workers in the military industrial base, which remains a critical mission that cannot be neglected. It also archives information on exposures of concern among deployed service members, documenting the development of data repositories and registries as well as studies done with this data. Additionally, it identifies innovations in exposure identification and assessment for future efforts. This volume should be useful to practitioners of Military Medicine and those involved in military occupational and environmental health research, so that avoidable exposures among service members and civilian staff can be avoided, and adverse health effects stemming from military service can be treated with the best available knowledge and procedures.

Lieutenant General Nadja Y. West, MD
The Surgeon General
US Army

Washington, DC
March 2019

Preface

Decades have passed since doctors Llewellyn J. Legters and Craig H. Llewellyn of the Uniformed Services University of the Health Sciences, in Bethesda, Maryland, taught that military medicine was occupational medicine because its practice encompasses the treatment and prevention of injuries and diseases related to work in military occupations and military operational environments. Over the last quarter century, health-related events associated with war and other deployments have served to support the Legters-Llewellyn concept. A variety of exposures with the potential to cause harm to our Service Members are described in this volume, as are the problems encountered in identifying and defining these exposures, and performing exposure assessments in military operational environments. Unfortunately, timely, informed medical evaluations of those exposed has not commonly occurred. The authors hope that familiarity with the contents of this volume will instill in military medical providers the importance of taking an occupational history and seeking consultation when an unusual event is suspected or a possible exposure-related clinical case is encountered.

Support for uniformed members is only one side of military occupational medicine. The other side is support for the military industrial base, which provides the warfighters with the equipment and supplies needed to complete their missions. Some of our depots and arsenals are similar to civilian industrial sites, but many are unique in the operations they conduct. The importance of their sustained operations in supporting our military forces cannot be overstated. Any breakdown in productivity in the military industrial base means a breakdown in the supply chain to those facing our enemies. Equally important is the need for flexibility in the base so that production may be increased to meet the needs of the warfighters. All of this underscores the requirement for a healthy, fit workforce. This volume contains essential information for the healthcare teams supporting the industrial base workforce.

This volume of the Textbooks of Military Medicine, published in hardcopy and electronic formats, will be a valuable reference for providers who need to address unique hazards on military installations and during deployments, as well as the occupational hazards in our military industrial base. I hope readers find it a useful update to the first textbook dedicated to the practice of occupational medicine in the Army, which was published in 1993. The US Navy and Air Force occupational health programs have been included in this update. Additionally, the content has been significantly expanded to cover a wide range of topics, including beryllium, aerospace medicine, undersea medicine, diving and the physiology of divining, ergonomics, ionizing and non-ionizing radiation, respiratory protection, workers’ compensation programs, deployment surveillance, and biomonitoring.

This book became a reality due to the commitment and hard work of many people, the encouragement of my wife, Ilona Mallon, the administrative and editorial assistance of Ms. Nicole S. Chavis, and Johanna L. Gribble and mentorship of Colonel (Retired) Joel C. Gaydos

Timothy M. Mallon, MD, MPH
Adjunct Assistant Professor
Department of Preventive Medicine and Biostatistics
Uniformed Services University

Bethesda, Maryland
April 2018

Chapter 1

THE TRI-SERVICE INDUSTRIAL BASE

P. K. UNDERWOOD, MD, MPH, MHA*

INTRODUCTION

THE US ARMY MATERIEL COMMAND

Research, Development and Engineering Command

Tank-Automotive and Armaments Command Life Cycle Management Command

US Army Aviation and Missile Life Cycle Management Command

US Army Communications-Electronics Command

US Army Joint Munitions Command

US Army Contracting Command

US Army Sustainment Command

US Army Military Surface Deployment and Distribution Command

US Army Security Assistance Command

US Army Chemical Materials Agency

Logistics Support Activity

Army Materiel Systems Analysis Activity

QUALITY OF THE WORK ENVIRONMENT

SUMMARY

*Colonel (Retired), US Army; Army Materiel Command, Command Surgeon, Redstone Arsenal, Alabama 35898

INTRODUCTION

The Army Materiel Command (AMC) is the industrial base for the Armed Services. Its motto is, “If a Soldier shoots it, drives it, flies it, wears it, communicates with it, or eats it—AMC provides it.” The AMC song, “The Arsenal for the Brave,” perfectly captures its raison d’être:

On the front lines to victory

We are the Army for the free

Equipping Soldiers every day

We are the arsenal for the brave

Committed to serving our country with pride

Leading the way to win the fight

Providing equipment to protect and defend

We’re the Army Materiel Command!

Because AMC is the industrial base for the joint military effort, one could reasonably substitute “service members” for “soldiers” in the song. AMC exists to support the war fight with any and all of the materiel required to prosecute a war, respond to a humanitarian crisis, provide disaster relief, and support friendly foreign militaries.

From an occupational health perspective, AMC’s equity lies in its workforce. Its civilian workers are exposed to unique hazards. Occupational health services became necessary for the civilian workforce during World War II, when workers needed protection from the unique hazards that stemmed from the manufacture and use of modern weapons. Since the terrorist attacks of September 11th, the workforce has endured a frenetic increase in the amount and diversity of materiel requirements for a nation at war in two geographic areas of operation. Understandably, the amount and degree of work-related illness and exposure to hazards in such an environment has also increased. For example, work hours have been extended to fulfill demands. New, potentially more caustic agents have been developed, such as insensitive high explosives. In addition, members of the civilian workforce who deployed to theater in support of logistical needs have all the attendant consequences of experiencing a deployment, such as physical and emotional stress. The civilian workforce at AMC is clearly part of the large Army “family” and is not immune to the stresses and strains of involvement in the war effort. This is particularly evident in the increase in number of civilian suicides.

In terms of assessing and reporting on the health of the AMC, the AMC surgeon plays a vital role. The surgeon acts as the eyes and ears of the commander when it comes to the occupational health of the command. According to AMC Regulation 10-2, the surgeon has the following mission and functions.

Mission: The mission of the Office of the Surgeon is to provide policy and guidance to AMC and subordinate elements on all health-related matters.

Functions: The functions of the Office of the Surgeon are to:

1. Serve as the single point of contact (POC) for medical policy, training, and technical medical guidance to ensure compliance with medical doctrine and practices.

2. Coordinate medical care, occupational health, preventive medicine, radiological health, and environmental health matters with the Army Office of The Surgeon General (OTSG) and the Army Medical Command (MEDCOM) to ensure legal and regulatory compliance, consistency with established medical practices, and improvement of medical support to AMC.

3. Integrate occupational health policies and procedures into all aspects of industrial and other workplace operations to promote a healthy and fit workforce and to minimize illness and injury losses incurred by military and civilian workers.

4. Minimize risk to Soldiers and civilians who use fielded equipment and support materiel developers by conducting and coordinating toxicity clearances and Health Hazard Assessments for all materiel acquisition.

5. Monitor and support medical aspects of the Chemical Surety Program (CSP) for AMC.

6. Enhance deployment medical readiness by establishing and implementing effective predeployment preventive medicine guidelines and training for all deployable civilian personnel.

7. Provide management/internal control over the Army Radiation Safety regulation.[1]

One example of recent efforts by the command surgeon staff is the authorship of a new AMC command policy memorandum on completion of the Post Deployment Health Reassessment (PDHRA) process for deployed civilians.[2] Other examples of broad-based initiatives by the command surgeon staff include the Hearing Conservation Program across the AMC industrial base,[3] as well as an effort to close indoor smoking rooms (which are still allowed at Rock Island Arsenal as an exception to Executive Order 13058, published in 1997, which protects federal employees and the public from exposure to tobacco smoke in the federal workplace[4]).

Under the direction of the MEDCOM commander, the Army Medical Department (AMEDD) resources and staffs occupational health clinics that provide occupational health services for the AMC workforce employed by government-owned, government-operated plants (GOGOs).

THE US ARMY MATERIEL COMMAND

The AMC celebrated 50 years of service in 2012, having been activated on May 8, 1962, and becoming fully operational on August 1, 1962.[5] Its first commander, Lieutenant General Frank S. Besson Jr, chose the name “Army Materiel Command” for its simplicity and clarity. Its mission was to manage the life cycle of materiel from the initial concept through research and development, procurement, production, supply, distribution and maintenance, and, ultimately, disposal. Initially established at what is now the Ronald Reagan Washington National Airport, AMC headquarters has had several homes. From the environs of the airport, it moved to Alexandria, Virginia, and then to Fort Belvoir, Virginia. As a result of a Defense Base Closure and Realignment Commission recommendation to the president in 2005, it has been located at Redstone Arsenal in Alabama since 2011.[6] The basic structure of AMC changed in 1986 with the passage of the Goldwater-Nichols Department of Defense (DoD) Reorganization Act. Essentially, AMC was removed from command oversight of acquisition when the Army created the Assistant Secretary of the Army for Research, Development, and Acquisition, with a military deputy.

The current mission of AMC is to develop, deliver, and sustain materiel to ensure a dominant joint force for the United States and its allies. Its vision is to provide America’s service members with the decisive edge. Since the terrorist attacks of September 11th, AMC has supported troops in both Iraq and Afghanistan by resetting and repairing equipment in a timely manner and providing contracting services when needed. In short, virtually anything a service member needs is provided by AMC. The core competencies of AMC are to equip, sustain, integrate, and enable: as the premier provider of materiel readiness, AMC “provides.” As of September 30, 2013, there were 67,938 employees across the AMC enterprise, 96% of whom are civilian and 4% military.[7] They are assigned to duty locations in 42 states and 29 countries. The vast majority of permanent civilian positions (66%) are professional, technical, or administrative. Of these positions, 41% require acquisition certification. Fifty-nine percent of white collar personnel have a bachelor’s degree, master’s degree, or PhD. Of the civilian workforce, 10.1% are retired military.

Industrial activities are organized in three different configurations:

1. GOGOs. These plants are owned and operated by AMC and staffed with federal employees. Sierra Army Depot (AD), Deseret Chemical Depot (CD), Tooele AD, Pueblo CD, McAlester Army Ammunition Plant (AAP), Red River AD, Corpus Christi AD, Pine Bluff Arsenal, Anniston AD, Blue Grass AD, Tobyhanna AD, Watervliet Arsenal, Letterkenny AD, and Crane Army Ammunition Activity are all GOGOs. In addition, there are two port facilities (Military Ocean Terminal-Concord and Military Ocean Terminal-Sunny Point) that are also GOGOs.

2. Government-owned, contractor-operated plants (GOCOs). These plants are owned by AMC but operated by a contractor who independently employs the workers. Hawthorne AD, Lake City AAP, Iowa AAP, Milan AAP, Joint Systems Manufacturing Center, Scranton AAP, Radford AAP, and Holston AAP are all GOCOs.

3. Contractor-owned, contractor-operated operations (COCOs). These plants are owned and operated by private-sector manufacturers. AMC purchases their products.

The responsibility for provision of occupational health services depends on the ownership and operation of the plant. AMEDD provides occupational health services only at GOGOs.

To convey the depth and breadth of AMC’s responsibilities, as well as its occupational health needs, a brief synopsis of its major subordinate commands, activities, and respective missions is provided below.

Research, Development and Engineering Command

The Research, Development and Engineering Command (RDECOM) headquarters is based at Aberdeen Proving Ground, Maryland. Its mission is to develop technology solutions for service members to maintain the decisive edge on the battlefield. It has seven subordinate centers under its command.

1. The US Army Research Laboratory is the Army’s executive agent for development, execution, and transfer of extramural basic science research. This type of research provides service members with enhancements in protection, lethality, networks, and sensors. This workforce makes up the largest source of world-class integrated research and analysis in the Army.

2. The Aviation and Missile Research, Development, and Engineering Center conducts research and exploratory and advanced development for aviation and missile weapons systems.

3. The US Army Armament Research, Development and Engineering Center advances armaments technology and engineering innovation for more than 90% of the Army’s lethality, focusing on advanced weapons, ammunition, and fire control systems.

4. The US Army Communications-Electronics Research, Development and Engineering Center supplies advanced command, control, communications, computers, intelligence, surveillance, and reconnaissance (C4ISR) capabilities.

5. The US Army Edgewood Chemical Biological Center is the technical organization responsible for non-medical chemical and biological defense. It is the only “all hazard” laboratory in the United States capable of dealing with items that are potentially contaminated with chemical, biological, or radiological material.

6. The US Army Natick Soldier Research, Development and Engineering Center treats the soldier as a combat system. It is charged with developing and using innovations in science and technology to improve and maximize survivability, sustainability, mobility, combat effectiveness, and field quality of life. Its core competencies include joint service combat feeding, modeling and simulation of aerial delivery, clothing and protective equipment, specialized shelters for command and control and threat environments, soldier and small-unit technology maturation and demonstration, and human systems integration sciences, which makes use of applied behavioral and cognitive sciences.

7. The US Army Tank Automotive Research, Development and Engineering Center develops, integrates, and sustains technology solutions for all manned and unmanned DoD ground systems and combat support systems, collectively known as the Ground System Enterprise. Geographically located at Detroit Arsenal, it is at the center of the automotive industry and its collateral intellectual property expertise.

Tank-Automotive and Armaments Command Life Cycle Management Command

Headquartered in Warren, Michigan, the Life Cycle Command’s mission is to develop, acquire, field, and sustain soldier and ground systems. It has six subordinate centers.

1. Anniston Army Depot, founded in 1940 and located in Anniston, Alabama, repairs, overhauls, modifies, and upgrades combat vehicles (except the Bradley and Multiple Launch Rocket Systems), artillery systems, bridging systems, small arms, and secondary components.

2. Rock Island Arsenal Joint Manufacturing and Technology Center is located in Rock Island, Illinois. It claims the honor of having built the first American manufactured tank. Its mission is to provide products and services through developing and manufacturing, integration, testing, and logistics. Its many capabilities range from having a full-purpose foundry, fabrication and welding of metals, heat treating, machining, painting, and engineering. In its possession are two of only thirteen existing seven-axis machining centers in the world, along with 200 computer-controlled machines and more than 950 conventional machines.

3. Red River Army Depot, founded in 1941 and located in Texarkana, Texas, conducts ground combat and tactical system sustainment maintenance operations. It is engaged in the remanufacturing and recapitalization of tactical wheeled vehicles; production of M1 road wheels; and the repair and overhaul of electronic systems, heavy tanks, and artillery. It is the designated center of industrial and technical excellence (CITE) for Bradley Fighting Vehicles, the Multiple Launch Rocket System, rubber products, and tactical wheeled vehicles—including the Heavy Expanded Mobility Tactical Truck, the High Mobility Multipurpose Wheeled Vehicle, the Armored Security Vehicle, the Heavy Equipment Transporter, the High Mobility Artillery Rocket System, multiple configurations of trailers, and the Small Emplacement Excavator vehicle. Additionally, it has the technical resources to design, fabricate, and manufacture a wide variety of items, ranging from specialty parts to unique prototype weapons systems and vehicles.

4. Sierra Army Depot, founded in 1942, is located in Herlong, California. It is the CITE for all petroleum and water distribution systems. It is home to the Army’s three largest operational project systems: the Inland Petroleum Distribution System, Water Support Systems, and Force Provider. It serves as an expeditionary logistics center, providing the full range of logistics support through long-term storage, maintenance, care of supplies in storage, equipment reset, and container management. Its mission includes equipment reset, new assembly and kitting operations, training support, maintenance of medical readiness stock, and redistribution of Class II and IX items. It has established an end-of-first-life-cycle center for excess combat vehicles. It has also been designated the Army’s consolidation and distribution center for the Clothing Management Office, which supports brigade-level organizational clothing and individual equipment reset operations.

5. Watervliet Arsenal, located in Watervliet, New York, is the nation’s oldest continuously active arsenal, having been founded in 1813 in support of the War of 1812. It is the principal manufacturer of large-caliber weapons. It provides manufacturing, engineering, procurement, and quality assurance for cannons, mortars, and associated materiel. It partners with all of the acquisition community to design and build prototypes of the latest and next-generation weapons.

6. The US Army Natick Soldier Research, Development and Engineering Center (described above), which is also a part of RDECOM.

US Army Aviation and Missile Life Cycle Management Command

The US Army Aviation and Missile Life Cycle Management Command (AMCOM) is headquartered at Redstone Arsenal. Its mission is to unite all organizations that design, acquire, integrate, field, and sustain Army aviation, missile, and unmanned aircraft weapons systems. AMCOM is a member of the Aviation and Missile Materiel Enterprise, whose other members include the Aviation and Missile Research, Development and Engineering Center, the Army Contracting Command-Redstone, the Program Executive Officer (PEO) Aviation, and the PEO Missiles and Space. AMCOM supports six of the Army’s 16 major warfighting systems. It has two Army depots—Corpus Christi and Letterkenny—that provide depot-level support to aviation and missile systems.

US Army Communications-Electronics Command

The US Army Communications-Electronics Command is located at Aberdeen Proving Ground. It is the “one-stop shop” for life cycle support of communications-electronics systems and equipment carried by soldiers. Its mission is to develop, acquire, provide, and sustain C4ISR and battle command capabilities for the joint combat service member. In addition to its headquarters, it has four subordinate organizations.

1. Tobyhanna Army Depot, founded in 1953, is located in Tobyhanna, Pennsylvania. It provides maintenance, manufacturing, integration, and fielded repair to C4ISR systems worldwide. The Army has designated Tobyhanna Army Depot as the CITE for C4ISR, avionics, and missile guidance and control. It also provides maintenance, fabrication, and system integration for the Army, Navy, and Air Force C4ISR systems.

2. The Central Technical Support Facility is located at Fort Hood, Texas. It is the test, integration, and certification testing facility for the Army LandWarNet/Battle command systems.

3. The Logistics and Readiness Center is located at Aberdeen Proving Ground. It provides global logistics support for C4ISR systems and equipment.

4. The Software Engineering Center is located at Aberdeen Proving Ground. It provides life cycle software solutions on the battlefield to ensure that service members are fed, housed, moved, and supplied.

US Army Joint Munitions Command

The Joint Munitions Command (JMC) headquarters is at Rock Island Arsenal. Its mission is to manage production, storage, issue, and demilitarization of conventional ammunition for all US military services. Through a process called centralized ammunition management, JMC supplies combat units with the right munitions at the right time and the right place. In addition to a training and explosives safety center at the Defense Ammunition Center in McAlester, Oklahoma, JMC has oversight of 10 ammunition plants and four Army depots and arsenals.

Ammunition Plants

1. The Anniston Defense Munitions Center is located in Anniston, Alabama. Its mission is to provide receipt, storage, shipment, maintenance, inspection, demilitarization, and recycling of ammunition and missiles.

2. The Crane Army Ammunition Activity, founded in 1941, is located in Crane, Indiana. As a strategic mobility platform, its mission is to receive, store, ship, produce, renovate, and demilitarize conventional ammunition, missiles, and related components. It is also deemed a munitions center of excellence; as such, it produces mortar and artillery illumination and infrared items. It is a major producer of large-caliber Navy gun ammunition and has capabilities for missile warhead pressing, depleted uranium remanufacture, and C4 extrusion, as well as loading and renovating munitions and bombs, insensitive munitions, and actuating devices. Demilitarization capabilities include steam-out and water-jet processes, high-pressure washout, permitted open burn/open detonation, contained detonation, and white phosphorus conversion. Tools, dyes, fixtures, gauges, production equipment, and components are fabricated in its machining center.

3. Holston Army Ammunition Plant, founded in 1942, is located in Kingsport, Tennessee. Its mission is to manufacture secondary detonating explosives, including Research Department Explosive, an explosive nitroamine; High Melting Explosive, a relatively insensitive nitroamine high explosive; triaminotrinitrobenzene, a powerful, extremely insensitive aromatic explosive; 3-nitro-l, 2, 4-triazol-5-one, an insensitive munition; and all of their related formulations. Research and development focus on next-generation energetic materials, covering synthesis, formulation, development of analytical methods, and explosive performance testing.

4. Iowa Army Ammunition Plant, founded in 1941, is a GOCO facility operated by American Ordinance LLC in Middletown, Iowa. Its mission is to produce and deliver large-caliber ammunition for the DoD. Production capabilities include the M795, M107, M927, Hawk, Stinger, Stryker Reactive Armor Tile, Expeditionary Fire Support System, Modular Artillery Charge System, and the entire family of 120-mm tank ammunition.

5. Lake City Army Ammunition Plant, founded in 1941, is located in Independence, Missouri. It operates the independent North Atlantic Treaty Organization test center for small arms ballistics. Operated by Orbital ATK (Dulles, VA), an American aerospace manufacturer and defense industry company, the plant is a GOCO facility. Its mission is to provide ammunition to train, maintain, and sustain combat operations by ordering bulk metals, chemicals, and propellants and fabricating them into complete 5.56-mm, 7.62-mm, and .50-caliber ammunition. Additionally, it loads, assembles, and packs 20-mm ammunition.

6. Letterkenny Munitions Center, founded in 1941, is located in Chambersburg, Pennsylvania, and is a tenant activity on Letterkenny Army Depot. It is a strategic mobility platform that provides munitions and missile support. It performs surveillance, receipt, storage, issue, testing, and minor repair for the Army Tactical Missile System and Guided Multiple Launch Rocket System missiles, as well as the High-Speed Anti-Radiation Missile and Joint Air-to-Surface Stand-Off Missile (primarily used in the Air Force) and the Sidewinder, Sparrow, Advanced Medium Range Air-to-Air Missile, and Penguin missiles (primarily used in the Navy).

7. McAlester Army Ammunition Plant, founded in 1943, is located in McAlester, Oklahoma. Its mission is to produce and store a variety of munitions. It is a large-scale producer of bombs and stores one-third of all munitions stock for the DoD. It has capability to renovate bombs, rockets, projectiles, mortars, small arms, propelling charges, and shipping containers. In addition, it fabricates wood and metal pallets, maintains and repairs mobile railroad track, and disassembles missiles. It operates a chemical and explosive laboratory and two digital x-ray facilities. It is also the centralized ammunition management agency for the southwest region, which encompasses seven states and Puerto Rico, including 33 Army installations.

8. Milan Army Ammunition Plant, founded in 1941, is located in Milan, Tennessee. Its mission is to provide joint munitions by loading, assembling, and packing medium- to large-caliber ammunition (40-mm, M918/M385, and M430/M433). It manufactures the M74 grenade and loads it into the Army Tactical Missile System Warhead. It receives and ships containerized cargo. It also has ability for high-explosive artillery/mortar melt pour; assembly and packaging of 105-mm, 155-mm, 60-mm, and 81-mm ammunition; extrusion of C4 plastic explosives, C4 used for mine-clearing line charges (M58A4/N68A2), and M112/M183 demolition charges; and assembly of reactive armor tiles for the Bradley Fighting Vehicle.

9. Radford Army Ammunition Plant, founded in 1940, is located in Radford, Virginia. Its mission is to manufacture propellants and explosives for field artillery, air defense, tank, missile, aircraft, and weapons systems for the DoD. The plant operates chemical, metrology, and ballistics labs. It also is the sole producer of nitrocellulose and solventless propellant for various rocket motors in the continental United States.

10. Scranton Army Ammunition Plant, founded in 1951, is located in Scranton, Pennsylvania. Largely unaltered since its construction in 1908 as a steam locomotive erecting and repair facility for the Delaware, Lackawanna & Western Railroad, the plant is on the National Register of Historic Places as part of the Steamtown Historic District. The Army acquired it in 1951 and converted it to produce metal parts. It is now a GOCO facility operated by General Dynamics (Falls Church, VA). Its mission is to manufacture and deliver large-caliber steel projectiles for artillery, mortar, and Navy projectile metal parts. It manufactures 105-mm to 155-mm diameter projectiles, including the 105-mm MK64-2; the 120-mm M929, M930, M931, M933, M934 HE, and M983; and the 155-mm M107, M110, and M795.

Depots and Arsenals

1. Blue Grass Army Depot, founded in 1941, is located in Richmond, Kentucky. It is a strategic mobility platform whose mission is to provide conventional munitions, missiles, nonstandard ammunition, and chemical defense equipment logistical support.

2. Hawthorne Army Depot, founded in 1930, is located in Hawthorne, Nevada. Its mission is to provide for receipt, storage, rewarehousing, preservation and packaging, surveillance, renovation, demilitarization/disposal, and issue of conventional ammunition. With 7,685,000 square feet of storage, it is the premier demilitarization facility for conventional ammunition. It also serves as the storage site for the nation’s stockpile of elemental mercury.

3. Pine Bluff Arsenal, founded in 1941, is located in Pine Bluff, Arkansas. Its mission is to produce ammunition and perform chemical/biological defense production and repair, depot storage and surveillance, and homeland security. It has been designated as the CITE for chemical and biological defense equipment. The arsenal has white phosphorus canister fill capability and supplies smoke munitions. It develops unique pyrotechnic mixing technologies, including facilities for red phosphorus mixing, extrusion, and pressing, and 40-mm colored smoke grenade production. It rebuilds and recertifies protective gas masks for the Army and the Defensive Chemical Test Equipment Services for the manufacture of several large filters and the M291 decontamination kit.

4. Tooele Army Depot, founded in 1943, is located in Tooele, Utah. As a major power projection platform, its mission is to receive, store, issue, demilitarize, renovate, and test conventional ammunition. It also designs, manufactures, fields, and maintains ammunition-peculiar equipment.

US Army Contracting Command

The Army Contracting Command, with headquarters is at Redstone Arsenal, acquires equipment, supplies, and services for combat missions. It has two subordinate commands: (1) the Expeditionary Contracting Command for locations outside the continental United States and (2) the Mission and Installation Contracting Command, headquartered at Fort Sam Houston and comprised of six major contracting centers within the United States (Aberdeen Proving Ground, New Jersey, Orlando, Redstone, Rock Island, and Warren).

US Army Sustainment Command

The Army Sustainment Command is headquartered in Rock Island Arsenal. Its mission is to organize, train, and sustain a deployable force and integrate materiel and services for service members. In essence, it ensures that troops have the right equipment at the right time to accomplish their missions. The Army’s field-level maintenance and supply capabilities, as well as seven field support brigades and the Logistics Civil Augmentation Program Support Unit, are under the Sustainment Command’s command and control.

US Army Military Surface Deployment and Distribution Command

The Army Military Surface Deployment and Distribution Command is headquartered at Scott Air Force Base in Illinois. Its mission is to provide expeditionary and sustained end-to-end deployment and distribution. In essence, it plans and executes the surface delivery of equipment and supplies. It is the Army service component command of the US Transportation Command and a major subordinate command of the AMC. It operates 24 ports throughout the continental United States and abroad, averaging about 20 million square feet of deployment and redeployment cargo movements (roughly equating to 314 vessel operations) each year. It has a total of five transportation brigades under its command, in addition to a transportation engineering agency at Scott Air Force Base.

US Army Security Assistance Command

The Army Security Assistance Command is headquartered at Redstone Arsenal. Its mission is to manage security assistance programs and foreign military sales for the Army. From pre-letter of request through development, execution, and closure, USASAC is responsible for the life cycle management of foreign military sales cases, managing about 4,600 cases a year, valued at more than $134 billion. It is also responsible for financial policy and security assistance information management, as well as providing policy, procedure, and guidance for the Army security assistance community.

US Army Chemical Materials Activity

The Army Chemical Materials Activity is headquartered in the Edgewood area of Aberdeen Proving Ground. Its mission is to enhance national security by storing and ultimately eliminating US chemical warfare materiel (CWM), in addition to supporting CWM responses. There are only two sites remaining where CWM is stockpiled: Blue Grass Chemical Activity (mustard and nerve agent) and Pueblo Chemical Depot (mustard agent), both of which will have their stockpiles destroyed through the auspices of the Assembled Chemical Weapons Alternatives, a US Army element. The stockpiles of CWM at Anniston, Pine Bluff, Deseret, and Umatilla have all been effectively destroyed. The Army Chemical Materials Activity also responds to non-stockpiled CWM, such as World War II munitions, when it is discovered. For example, there are currently 17 known dumping sites on Redstone Arsenal where chemical weapons were buried following World War II, when it was standard practice to drain, burn, or bury surplus munitions.[8] The Army Chemical Materials Activity works with the treaty mission as the Army’s executive agent and partners with the Chemical Stockpile Emergency Preparedness Program.

The Logistics Support Activity

The Logistics Support Activity is headquartered at Redstone Arsenal. It is the home of the Logistics Information Warehouse, the Army’s official storehouse for collecting, storing, organizing, and delivering logistics data. Its mission is to provide timely and integrated life cycle logistics information, knowledge, and expertise in support of service members around the world to meet full-spectrum operational requirements.

Army Materiel Systems Analysis Activity

The Army Materiel Systems Analysis Activity has a worldwide presence, including a forward support cell located at AMC headquarters at Redstone Arsenal. Its mission is to conduct analyses across the materiel life cycle to inform critical decisions for current and future service member needs.

QUALITY OF THE WORK ENVIRONMENT

AMC’s qualtiy of the work environment (QWE) initiative supports efforts to improve the work environment. The 32nd vice chief of staff of the US Army, General Peter Chiarelli, began the QWE program after he visited Lake City Army Ammunition Plant and decided that working conditions at the plant, though within acceptable regulations and standards, could be improved. The existing standards were inadequate to ensure that the civilian, contractor, and military workforce had a “comfortable and quality” place to work. Because no standards for comfort and quality existed, developing QWE standards was critical not only for documentation and correction of findings, but also for long-term integration into Army daily business processes. To accomplish these goals, cross-functional teams of subject matter experts in facilities engineering and fire safety, as well as life safety, industrial hygiene, ergonomics, occupational health, and safety, conducted assessments across 23 organic industrial base sites. To assess the sites, the teams developed initial QWE criteria based on existing industry standards and created new benchmarks. Following the assessments, each site was provided an individualized report, including a synopsis of programmatic findings for industrial hygiene, safety, ergonomics, occupational health, fire protection, life safety, facilities engineering, criteria findings, and feedback from employee surveys.

From a strategic perspective, major occupational health challenges for the civilian workforce remain. Several common findings from the QWE assessments illustrate these challenges. For example, there are problems with the Defense Occupational and Environmental Health Readiness System-Industrial Hygiene (DOEHRS-IH), the mandated Army computer software program that automates and archives industrial health program data. DOEHRS-IH contains exposure-based occupational healthcare information and creates a longitudinal exposure record. However, it also depends on data being entered into the program, which is a laborious, time-consuming process. Industrial hygienists must not only conduct surveys, but also enter all the data into DOEHRS-IH. QWE assessments revealed that although surveys were being conducted, in many cases data were not being entered into the database because of staffing issues.

Another issue brought to light by the QWE assessments was the chronic underfunding of maintenance and repairs to industrial facilities; most of the buildings are over 70 years old. Even though AMC owns approximately 15% of the Army’s inventory of plants, it receives less than 3% of military construction funding. The Army needs to develop a funding strategy through the Program Objective Memorandum process to replace these facilities. The initial cost estimate for all sites is $3.5 billion over 20 years. In the interim, AMC has already sought funding to make some facility improvements through several modalities, including the Army Working Capital Fund, contractor investment, and the capital investment; sustainment, restoration, and modernization; operation and maintenance; and production-based support programs.

AMC partners with the Army Public Health Center to develop a path forward to address QWE issues at MEDCOM occupational health clinics that support AMC sites, particularly to identify improvements to the industrial hygiene, ergonomic, and occupational health portions of the QWE assessments. AMC will continue to pursue funding in accordance with the Army Organic Industrial Base Strategic Plan, 2012–2022, to ensure that depots and arsenals will remain modernized and capable of sustaining their core depot and critical manufacturing capabilities.[9]

SUMMARY

In its inherent mission to supply all classes of materiel, AMC is the Army’s wellspring, enabling the Army to conduct kinetic, humanitarian, and disaster relief operations alike. Since the beginning of Operation Enduring Freedom in Afghanistan in 2001, the operational tempo has been high across AMC’s industrial base in support of two wars in two locations. During this time AMC personnel have processed and handled well over 3.5 million pieces of equipment. As the war in Iraq came to an end, AMC was fully engaged with retrograde movement of materiel out of that theater. As of this writing, the war in Afghanistan is still being prosecuted. According to diplomatic decisions between the United States and Afghanistan, US forces returned home in December 2014, leaving behind a cadre of advisors. There is an ongoing reduction in workload from wartime highs, as redeployment from Afghanistan continues. There will be uncertainty in the overall requirements placed on AMC’s industrial base with the end of combat operations in Afghanistan, and a reshaping initiative for the strength of the Army, as well as other US armed services.

During any interwar period, what is certain is the vital importance of maintaining the skills of the workforce and the ability to readily ramp up production capability when the next conflict inevitably occurs. It is vital that resources be available to ensure that AMC maintains its place as the premier logistical platform for the US armed forces, and that it sustains the prepositioned stock of materiel and equipment in various areas around the globe. This is important not only for kinetic operations, but also for logistical support of humanitarian efforts and disaster relief operations. As General Omar Bradley once said, “Amateurs talk strategy. Professionals talk logistics.” Just as the military services rely on the materiel support provided by the AMC, the AMC rests on the backbone of its workforce, and its workforce must be healthy to perform at maximum capacity. Occupational health plays a key role in keeping the workforce healthy and resolving issues in the work environment that could adversely impact the health of its workers. These are all the building blocks for success in fighting wars and securing peace.

REFERENCES

1.   Organization and Functions: Headquarters, US Army Materiel Command (HQAMC). Redstone Arsenal, AL: AMC; October 14, 2008. AMC Regulation 10-2.

2.   US Army Materiel Command. Completion of the Post-Deployment Health Reassessment (PDHRA) by Department of Army Civilians (DACs) Who Deploy in Support of the US Army Materiel Command (AMC). Redstone Arsenal, AL: AMC; April 10, 2013. AMC Command Policy Memorandum 690-11.

3.   Headquarters, Department of the Army. Army Hearing Program. Washington, DC: HQDA; February 1, 2008. Special Text No. 4-02.501.

4.   Clinton WJ. Protecting Federal Employees and the Public From Exposure to Tobacco Smoke in the Federal Workplace. Washington, DC: The White House; August 8, 1997: Section 2, Exceptions. Executive Order 13058.

5.   US Army Materiel Command Historical Office. AMC 50th Anniversary, 1962–2012. Redstone Arsenal, AL: AMCHO; 2013: 9.

6.   Defense Base Closure and Realignment Commission website. Final deliberations and decisions. August 23, 2005. http://www.brac.gov/Deliberations.aspx. Accessed September 2, 2016.

7.   US Army Materiel Command. Sustaining the Strength of the Nation. 2013–2014 ed. Tampa, FL: Faircount Media Group; 2013.

8.   Gore L. Army begins long process of cleaning up post-WW II chemical weapons buried at Redstone Arsenal. May 6, 2013. AL.com. http://blog.al.com/breaking/2013/05/army_begins_long_process_of_cl.html. Accessed September 2, 2016.

9.   US Army. Army Organic Industrial Base Strategic Plan, 2012–2022. https://www.army.mil/e2/c/downloads/276549.pdf. Accessed September 2, 2016.

Chapter 2

US AIR FORCE OCCUPATIONAL AND ENVIRONMENTAL HEALTH PROGRAM

PATRICK F. WHITNEY, MD, MSPH,* and JON R. JACOBSON, DO, MPH†

INTRODUCTION

PROGRAM OVERVIEW

ROLES AND RESPONSIBILITIES

Headquarters Level

Major Commands

Installation Level

Supervisor

Employee

PLANNING

EXECUTION

MANAGEMENT REVIEW

EMERGING DEVELOPMENTS IN AIR FORCE OCCUPATIONAL MEDICINE

SUMMARY

*Lieutenant Colonel (Retired), Medical Corps; US Air Force; formerly, Commander, 7th Aerospace Medicine Squadron; Occupational Medicine Consultant to the Air Force Surgeon General

†Colonel, US Air Force; Air Force Chief of Occupational Medicine; Occupational Medicine Consultant to the Air Force Surgeon General, Defense Health Headquarters, 7700 Arlington Blvd, Falls Church, Virginia 22042

INTRODUCTION

This chapter provides an overview of the US Air Force occupational and environmental health (OEH) program’s structure and function. The Air Force OEH program protects the health of airmen and civilian employees, ensures the readiness of personnel, and enhances combat and operational capabilities.[1] The Air Force OEH program assesses and manages health risks through the application of OEH risk-reduction strategies. OEH program personnel participate in life cycle acquisition, sustainment, weapons systems, munitions, and materiel systems development to ensure that health threats are identified and appropriately managed.[1]

PROGRAM OVERVIEW

The secretary of the Air Force for environment, safety, and occupational health (ESOH) directs the OEH program, which is mandated by the Occupational Safety and Health Administration (OSHA) Act of 1970,[2] Executive Order 12196,[3] 29 CFR 1960,[4] Department of Defense (DoD) instruction (DoDI) 6055.01,[5] and DoDI 6055.05.[6] The OSHA and DoD regulations are implemented by Air Force policy directives (AFPDs) 90-8[7] and 91-2[8] and Air Force instructions (AFIs) 48-145[1] and 91-202,[9] which require that airmen and employees be provided a place of employment free of hazards that cause injury or illness, and that OEH hazards be identified, evaluated, and controlled in order to enhance mission capabilities and protect personnel.

Aerospace medicine and OEH personnel must work closely with bioenvironmental engineering (BE) and public health (PH) personnel to ensure hazards are adequately identified, control measures are put in place, and health surveillance is conducted to ensure controls are working adequately.[1] OEH personnel review new and existing weapon system modifications as part of the acquisition process to ensure that health threats are eliminated and systems designs do not pose a threat. If problems with the design are detected, concerns must be communicated to the team leader so that corrections can be made to minimize health risks.[1] OEH providers must also educate workers on avoiding health risks related to workplace hazards to reduce the incidence of workplace injuries and illnesses.[1] Commanders, civilian leaders, and supervisors must take the lead in supporting OEH control efforts by enforcing regulations and ensuring compliance with safety and health guidelines.[1] However, all airmen and civilian employees share responsibility to actively participate in the process to help ensure the success of the organization’s OEH program.

The Air Force has adopted the use of a management information system (MIS) designed to standardize data entry and enhance data management and health outcomes reporting.[1] With a defined set of roles and responsibilities, the MIS facilitates OEH quality improvement by providing access to program execution data and program management reviews. The Air Force OEH MIS approach involves a “plan-do-check-act” process (Figure 2-1) as a tool for managers to assess program effectiveness as a measure of program quality. The plan-do-check-act cycle goals are to improve quality through improving operations, mission effectiveness, health and safety, and workforce availability while reducing OEH health hazards, risks, costs, and lost work time. The Defense Occupational and Environmental Health Readiness System (DOEHRS) is a key component of the Air Force OEH MIS. DOEHRS is used to capture and archive OEH exposure, enabling the Air Force to meet the long-term recordkeeping requirements.[1]

Installation leadership must be engaged in the risk management process (Figure 2-2) to ensure OEH risks are identified and resources are committed to eliminate the OEH threats. The comprehensive risk assessment process involves identifying hazards, assessing risks, evaluating control options, implementing control measures, and evaluating the control efforts.[1] Air Force aerospace and occupational medicine personnel make significant contributions to organizational risk management by identifying health hazards, characterizing the level of health risk, determining necessary control measures, communicating the risk to affected personnel and their managers, and ensuring medical surveillance is conducted to identify adverse health outcomes.

ROLES AND RESPONSIBILITIES

Headquarters Level

The assistant secretary of the Air Force for installations, environment, and logistics develops policy and provides oversight for the entire Air Force ESOH program.[1] He or she is the designated agency safety and health officer who represents the Air Force when dealing with the Office of the Secretary of Defense, other federal agencies, and Congress. He or she chairs the Headquarters Air Force ESOH council and conducts headquarters-level reviews of the OEH program in accordance with AFI 90-801.[10]

Figure 2-1. US Air Force occupational and environmental health (OEH) management information system process tool.
Reproduced from: US Department of the Air Force. Occupational and Environmental Health Program. Washington, DC: DAF; July 22, 2014. AF Instruction 48-145: Figure 1.1; p 7.

The Air Force surgeon general provides strategic direction and reports on the status of the program annually. The Air Force Medical Support Agency (AFMSA) Aerospace Operations Division supports the Air Force surgeon general by planning, programing, budgeting, and distributing funds to conduct environmental health surveillance and OEH risk assessments, developing medical policy, and overseeing OEH program execution.[1] This includes working with acquisition program managers to ensure new procurements get reviewed and undergo ESOH evaluation as required by AFI 63-101,[11] as well as reviewing OEH risk reduction efforts to ensure that resources are prioritized appropriately and submitted for inclusion in the appropriate budget and funding request. Additionally, AFMSA monitors performance measures to assess OEH program effectiveness.

Major Commands

Major command (MAJCOM) surgeons serve as medical advisors to commanders and are responsible for establishing OEH medical support priorities. They support geographically separated units with military medical treatment facilities in their area of responsibility. MAJCOM surgeons oversee mission execution by supporting OEH hazard identification, control, mitigation, and elimination.[1] The MAJCOM surgeon monitors OEH program performance across all bases within the command. He or she distributes information on new policies and legislation and works to resolve OEH programmatic issues with the AFMSA.[1]

Installation Level

Installation commanders are responsible for ensuring that all military and civilian employees are provided a safe and healthful worksite. The installation commander directs the installation ESOH council, which is a senior leadership group, and oversees the execution of the ESOH program on the installation per AFPD 90-8.[7]

Each Air Force installation also has an OEH working group that includes representatives from the BE, PH, and flight and operational medicine (FOM) as principal members (the working group is also referred to as “Team Aerospace”). Representatives from the installation safety department also frequently attend. Workplace supervisors are invited to attend when their workplace requirements are under review. The OEH working group is charged with assigning medical surveillance exam requirements based on worksite hazard assessments per DoDI 6055.05M,[12] National Fire Protection Association Guide 1582,[13] AFI 48-145,[1] AFI 44-102,[14] and AFI 48-123.[15] The OEH working group alerts supervisors to OEH-related training requirements and tracks OEH performance measures to assess program effectiveness. The OEH working group participates in a collaborative process to assess, plan, and advocate for OEH services needed to meet an ill or injured worker’s health needs and coordinate care in order to minimize delays in diagnosis, treatment, and return to work.[1] The OEH working group additionally tracks injury and illness trends and medical surveillance completion rates, which are reported to the installation ESOH council.

Figure 2-2. US Air Force occupational and environmental health (OEH) risk management process.
ACGIH: American Conference of Governmental Industrial Hygienists
DoD: Department of Defense
OEHWG: OEH working group
OSHA: Occupational Safety and Health Administration
Reproduced from: US Department of the Air Force. Occupational and Environmental Health Program. Washington, DC: DAF; July 22, 2014. AF Instruction 48-145: Figure 1.2, p 8.

Team Aerospace: Bioenvironmental Engineering

BE personnel perform typical industrial hygiene functions and assist the local commander and supervisors by integrating OEH input into resource management decisions. BE staff evaluate the adequacy of existing administrative and engineering controls and personal protective equipment use to protect against OEH hazards.[1] They assess the need for and recommend OEH hazard controls for new work processes or changes to existing systems.

BE staff conduct investigations of new operations and proposed changes to existing equipment and facilities to identify and reduce potential OEH hazards. They perform health risk assessments for sites containing hazardous chemicals and low-level radioactive materials that threaten Air Force communities. Once the risk assessment is complete, a risk categorization is assigned to each workplace, as detailed in Table 2-1, and the complete list is provided to members of the OEH working group.[1] BE staff utilize the health risk assessment data to design sampling strategies to quantify the risk of exposure to the hazards and communicate health and safety risks to commanders and affected individuals.[1] Similarly exposed military and civilian employees are grouped into the same risk category using the “similar exposure group” concept.[1]

BE staff also identify and assess environmental exposure pathways on military installations and in deployed locations and ensure personnel who are potentially exposed are included in population medical surveillance for the specific hazards of concern. They support limited-scope medical treatment facilities and medical aid stations as well as geographically separated units. This support may include overseeing activities and performing in-depth OEH site assessments, including exposure sampling, in accordance with AF Tactics, Techniques, and Procedures 3-2.82, Occupational and Environmental Health Site Assessment.[16]

Annually, BE personnel prepare an area of responsibility consolidated conceptual site model, which identifies a prioritized list of surveillance activities[1] that need to be completed in the year ahead, and present the results to the OEH working group. BE personnel also use DOEHRS to capture incident response and deployment-specific OEH exposure data in accordance with policy.[1] They provide technical consultation and expertise on OEH hazards, training, regulatory requirements, and workplace-specific OEH exposure data.

Team Aerospace: Public Health

PH personnel provide input on OEH medical surveillance exams, training, and risk communication efforts. PH staff coordinates with supervisors to maximize surveillance examination completion rates and minimize the impact on the mission while surveillance examinations are performed. Staff conducts OEH surveillance and epidemiological analysis of the surveillance data, examining trends in injuries and illnesses. This analysis includes injuries and illnesses related to hearing loss, exposure incidents, and clinic visits by type, job, workplace, and health outcomes, including pregnancies among military and civilian employees.

TABLE 2-1

WORKPLACE CATEGORIZATION AND REQUIRED ROUTINE ASSESSMENT FREQUENCY

Workplace Priority

Considerations

Required Assessment Frequency (Months)

High

Hazards poorly defined or poorly controlled; work environment or processes unstable

Inherent OEH risk present with medium to high hazard potential

Routine OSHA expanded standard requirements (eg, 29 CFR 1910.1026, Chromium VI)

Requirement for special purpose occupational exams, other than audiograms

Potential for significant OEH regulatory noncompliance

Every 12

Medium

Hazards well defined and controlled; work environment and processes stable

Inherent OEH risk present with relatively low hazard potential

Minimal potential for hazards to go out of control or create significant risk

Requirement for annual audiograms

Potential for OEH regulatory noncompliance

Every 30

Low

No hazards; work environment and processes stable

Nonexistent or negligible sources of OEH risk present

Full OEH regulatory compliance

Locally determined

OEH: occupational and environmental health

OSHA: Occupational Safety and Health Administration

PH personnel educate supervisors and workers about communicable and chronic disease risk and the potential for adverse health outcomes. They conduct routine annual shop visits, along with BE staff, to all workplaces that have a high risk of exposure to hazards that may cause adverse health outcomes. PH staff conduct population health surveillance to detect OEH illnesses and ensure any cases are reported and promptly investigated and documented. Staff also monitor and track OEH illnesses and injuries and investigate their causes, ensuring internal and external consistency in the quality of the data collected. OEH illness and injury data is presented to installation’s ESOH council.

PH personnel also manage the installation reproductive hazards and fetal protection program. All pregnant workers are interviewed, and potential OEH threats and health risks in the workplace are documented. PH staff also serve as consultants to workplace supervisors and employees regarding the scheduling and delivery of OEH-specific training, making training materials available and offering training assistance.

Team Aerospace: Flight and Operational Medicine

A FOM representative is the chair of the OEH working group. FOM personnel conduct medical surveillance exams, ensuring exams are followed through to completion, as well as a number of other examinations such as preplacement, termination, return-to-work, and disability evaluations, as well as initial and periodic flying physicals. The medical surveillance examination completion rates are tracked, as are cancellation rates, both of which get reported to the OEH working group per AFI 48-101.[17] FOM staff also deliver work-related injury and illness care for those who fly and civilian employees. Other military members get their OEH services through their primary care provider; however, FOM providers review any work, fitness, or deployment restrictions resulting from this care. FOM staff are also involved in workplace evaluations, conducting annual shop visits to those worksites assessed as high-risk by BE personnel.[1]

Supervisor

The workplace supervisor is responsible for ensuring workers a safe and healthy work environment that complies with all OEH program requirements. Supervisors support installation-level and organizational-level objectives and targets and implement corrective actions for identified OEH discrepancies. They appoint a unit health monitor to support coordination of medical surveillance exam requirements and notify unit personnel of due and overdue medical surveillance exam requirements.

Workplace supervisors must ensure that all OEH hazards are identified and abated to the maximum extent possible. They are responsible for implementing required OEH hazard controls and making sure the controls are functioning correctly. Supervisors must ensure all workers comply with OEH requirements including the proper use of personal protective equipment. Supervisors must make personal protective equipment available for personnel to use when required, ensure it is used correctly in the workplace, and ensure personnel are properly instructed on the proper care and cleaning of their personal protective equipment. Supervisors must also see that employees have received training on workplace-specific OEH hazards, and that the training is documented in accordance with AFI 91-301.[18]

Supervisors must also ensure that the preplacement health assessments are completed for all employees before they begin working in hazardous areas. Supervisors must notify PH staff when military and civilian employees are separating or retiring so a termination examination can be conducted. Supervisors must also notify installation safety, PH, and BE staff promptly when an employee sustains a work-related injury or illness and when someone becomes pregnant.

Employee

Employees are responsible for understanding the work processes and hazards associated with the job. This includes knowing about OEH risks and planned strategies to control the threat, including use, maintenance, and storage of personal protective equipment. Employees must actively participate in workplace health hazard identification and health risk assessments and agree to wear hazard monitoring equipment. Employees must notify their supervisor if they are advised they have been occupationally exposed above safe levels, or if they have developed work-related health conditions.

PLANNING

OEH personnel use the planning process to identify and prioritize OEH hazards, program deficiencies, and opportunities for improvement. The goal of planning is to establish program objectives, identify risk reduction opportunities, and ensure OEH program improvement. AFMSA Aerospace Operations Division establishes and communicates OEH program priorities to major commands, including specific objectives, and develops procedures for:

- establishment or review of legal and other requirements;

- objectives and targets;

- communications and data gathering;

- assessments;

- management reviews; and

- reports.

Figure 2-3. Critical elements of the Air Force occupational and environmental health program.
AFI: Air Force instruction
AFMAN: Air Force manual
AFPD: Air Force policy directive
DoD: Department of Defense
DoDI: DoD instruction
Reproduced from: US Department of the Air Force. Occupational and Environmental Health Program. Washington, DC: DAF; July 22, 2014. AF Instruction 48-145: Figure 3.1, p 26.

The Headquarters Air Force ESOH council annually reviews and approves OEH program priorities, objectives, and targets, which are then communicated down to installation-level OEH staffs. The installation commander, as director of the installation ESOH council, reviews and approves installation-specific OEH program priorities, objectives, and targets. The most critical elements of the Air Force OEH program are contained in Air Force 90-series and 48-series publications, as illustrated in Figure 2-3. MAJCOM and installation-level supplements to these documents are published as needed to address organization-specific needs.

EXECUTION

Central to the execution of the Air Force OEH program is exposure assessment, which is used to identify and characterize OEH hazards associated with worksite operations, determine the effectiveness of exposure controls, and collect and archive exposure data.[1] The Air Force exposure assessment process incorporates eight elements of the DoD industrial hygiene exposure assessment,[6] as illustrated in Figure 2-4. The assessment is conducted to identify and determine the extent of workplace hazards that exist during mission execution. Air Force Manual 48-146[19] and School of Aerospace Medicine technical guides provide detailed information on conducting an assessment [1] (see Table 2-1 for the recommended frequency of these assessments). The timetable may be adjusted by the OEH working group based on recommendations from BE staff regarding the need to identify, assess, and control specific hazards.[1]

Figure 2-4. Air Force occupational and environmental health exposure assessment model.
DoD: Department of Defense
IH: industrial hygiene
SEG: similar exposure group
Reproduced from: US Department of the Air Force. Occupational and Environmental Health Program. Washington, DC: DAF; July 22, 2014. AF Instruction 48-145: Figure 4.1, p 28.

As previously mentioned, BE personnel annually provide the OEH working group a planned schedule for conducting worksite assessments. The schedule sets off a cascade of events that include shop visit scheduling and data gathering, as well as reviewing and analyzing data from the previous year. For each worksite, these events are completed in the month before the worksite is discussed during the OEH working group meeting (usually a monthly meeting). During the meeting, the reviewed worksite’s medical surveillance exam requirements are determined and plans made to address any trends noted. Following the meeting, medical surveillance exams for the employees of that worksite are scheduled. This cyclical flow is repeated throughout the year for each worksite and is described in detail in Air Force Manual 48-146.[19]

FOM providers perform OEH clinical surveillance to detect breakdowns in exposure controls and biomarkers related to exposure, ideally at or before the time clinical disease develops. Generally, installations have developed individual risk assessments and clinical surveillance guidelines; however, emphasis is shifting toward the use of headquarters-developed assessments that will standardize the process and provide for greater confidence in hazard characterizations. Medical surveillance data for exposures will become more uniform as the capability to broadly assess and analyze OEH risks improves.

Team Aerospace supports Air Force mission objectives by keeping personnel healthy and at work through injury and illness prevention efforts that target high risk processes and operations. An effective monitoring and assessment program can identify significant deviations from baseline OEH program performance. This may alert senior leaders that the OEH program needs improvement. Installation commanders must track operational performance using established and accepted Air Force OEH metrics. Installation commanders may develop and use unique objectives and targets to assess program success, incorporating monitoring, measurements, assessments, audits, incident investigations, and corrective actions.

MANAGEMENT REVIEW

Program management reviews allow leaders at all levels to critically evaluate OEH program performance and implement improvements. Senior leaders at all levels provide appropriate direction for correcting deficiencies, which may include investment, policy changes, and adjustments to goals and objectives. Performance measures are reviewed by the ESOH council for appropriateness and adjusted as necessary to drive performance toward established OEH program objectives and targets.

The effectiveness of the Air Force OEH program is assessed at the headquarters level, MAJCOM level, and installation level based on input from the installation ESOH council, which identifies unmet needs and prioritizes requirements for funding that will optimize mission performance and minimize risk and cost. This collaborative process of assessment, planning, facilitation, and advocacy for options and services protects the health and welfare of airmen and civilian employees. The collaborative process facilitates communication and coordination of care, which minimizes delays in diagnosis, treatment, and return to work.

Program management reviews are done to critically evaluate OEH program performance and help to identify needed improvements annually.[1] Headquarters Air Force personnel, MAJCOM personnel, and the installation ESOH council members participate in these reviews. The program management review evaluates:

- effectiveness of the OEH program,

- whether OEH objectives and targets were met,

- success of risk-reduction efforts,

- changes in OEH program requirements,

- any needed improvements,

- whether root cause analyses are done when indicated, and

- whether corrective actions were taken to improve the program.

Senior leaders are critical to the management review process because they can direct personnel and financial resources to ensure identified deficiencies are corrected, needed policy changes are put in place, and the OEH program action plan is prioritized appropriately.[1] OEH program performance targets at all levels get reviewed and are adjusted to drive performance toward established OEH program goals and objectives. The review is documented in ESOH council minutes to meet regulatory requirements.[1]

EMERGING DEVELOPMENTS IN AIR FORCE OCCUPATIONAL MEDICINE

Recognizing that much OEH work is completed within primary care clinics, the Air Force has begun a multiyear restructuring with the end goal of creating an independent clinic known as the base operational medicine clinic (BOMC). The BOMC will be a centralized location for all OEH clinical services needed for an installation. It will be staffed by individuals who have been specifically trained in the principles of occupational medicine. This will enable both flight and primary care providers to focus on traditional medical care functions, while BOMC providers develop streamlined, standardized workflows to improve the quality and reliability of the exams.

The Air Force is also exploring ideas to improve the central component of the OEH program—the exposure assessment. Total Exposure Health (TEH) is an initiative to expand the scope of exposure assessment from just the workplace or deployed setting to the environment and lifestyle. The development and utilization of advanced exposure collection sensors and devices such as wearables and smart devices, and the use of advanced informatics technologies such as exposomics, epigenetics, genomics, and bioinformatics are instrumental in TEH development. Such precision health is expected to extend readiness and performance, reduce illness and injury, and encourage healthy lifestyle choices, which are the ultimate goals of the Air Force OEH program.

SUMMARY

The Air Force OEH program establishes guidance for installations to protect the health of airmen and civilian employees to maximize combat and operational capabilities. Utilizing the Air Force OEH MIS standardizes data entry, management, and reporting. A key component of future data mining efforts, the MIS relies on systems such as DOEHRS to provide exposure information and link to health records so that personnel can be related to health outcomes. Health risk assessments provide commanders and other decision-makers information on workplace risks as well as the means to control these hazards and evaluate the efficacy of mitigation measures. Medical surveillance can be targeted to people working in areas where the level of exposure exceeds safe levels. Responsibility to keep the workplace safe involves active participation from all Air Force personnel. Specific roles are outlined by federal regulations and Air Force and DoD instructions, but safety is everyone’s responsibility. From the Air Force surgeon general to the worker on the production line, anyone can make a significant difference in keeping the workplace a healthy and safe environment.

REFERENCES

1.   US Department of the Air Force. Occupational and Environmental Health Program. Washington, DC: DAF; July 22, 2014. AF Instruction 48-145. http://static.e-publishing.af.mil/production/1/af_sg/publication/afi48-145/afi48-145.pdf. Accessed August 16, 2017.

2.   The Occupational Safety and Health Act of 1970. Pub L No. 91-596, with amendments. December 29, 1970. http://www.osha.gov/publications/osh-act-reprint-3-09-04.pdf. Accessed October 12, 2016.

3.   Executive Order 12196. Occupational safety and health programs for federal employees. October 1, 1980. https://www.archives.gov/federal-register/codification/executive-order/12196.html. Accessed October 12, 2016.

4.   29 CFR, Part 1960. https://www.osha.gov/pls/oshaweb/owasrch.search_form?p_doc_type=STANDARDS&p_toc_level=1&p_keyvalue=1960. Accessed October 12, 2016.

5.   US Department of Defense. DoD Safety and Occupational Health (SOH) Program. Washington, DC: DoD; October 14, 2014. DoD Instruction 6055.01. http://dtic.mil/whs/directives/corres/pdf/605501p.pdf. Accessed December 28, 2016.

6.   US Department of Defense. Occupational and Environmental Health Program. Washington, DC: DoD; November 11, 2008. DoD Instruction 6055.05. http://www.dtic.mil/whs/directives/corres/pdf/605505p.pdf. Accessed October 12, 2016.

7.   US Department of the Air Force. Environment, Safety, and Occupational Health (ESOH) Management and Risk Management. Washington, DC: DAF; September 1, 2004. AF Policy Directive 90-8.

8.   US Department of the Air Force. Safety Programs. Washington, DC: DAF; May 1, 2017. AF Policy Directive 91-2.

9.   US Department of the Air Force. The US Air Force Mishap Prevention Program. Washington, DC: DAF; June 24, 2015. AF Instruction 91-202.

10.   US Department of the Air Force. Environment, Safety, and Occupational Health Councils. Washington, DC: DAF; March 25, 2005. AF Instruction 90-801.

11.   US Department of the Air Force. Integrated Life Cycle Management. Washington, DC: DAF; March 7, 2013. AF Instruction 63-101.

12.   US Department of Defense. Occupational Medical Examination and Surveillance Manual. Washington, DC: DoD; September 16, 2008. DoD Instruction 6055.05M.

13.   National Fire Protection Association. Standard on Comprehensive Occupational Medical Program for Fire Departments. Quincy, MA: NFPA; 2013. NFPA Guide 1582. http://www.nfpa.org/codes-and-standards/all-codes-and-standards/list-of-codes-and-standards?mode=code&code=1582. Accessed August 15, 2017.

14.   US Department of the Air Force. Medical Care Management. Washington, DC: DAF; March 17, 2015. AF Instruction 44-102.

15.   US Department of the Air Force. Medical Examination and Standards. Washington, DC: DAF; September 24, 2009. AF Instruction 48-123.

16.   US Navy, Air Force, and Army. Occupational and Environmental Health Site Assessment. Washington, DC: DN, DAF, DA; April 2012. AF Tactics, Techniques, and Procedures 3-2.82.

17.   US Department of the Air Force. Aerospace Medicine Operations. Washington, DC: DAF; October 19, 2011. AF Instruction 48-101.

18.   US Department of the Air Force. Air Force Occupational and Environmental Safety, Fire Protection, and Health (AFOSH) Program. Washington, DC: DAF; June 1, 1996. AF Instruction 91-301.

19.   US Department of the Air Force. Occupational and Environmental Health Program Management. Washington, DC: DAF; December 5, 2012. AF Manual 48-146.

Chapter 3

SAFETY AND OCCUPATIONAL HEALTH PROGRAMS FOR THE US NAVY AND US MARINE CORPS

PAMELA L. KRAHL, MD, MPH*; DEBORAH BOHLMAN, RN†; LYNN E. COOK, AuD‡; ANNE McDONOUGH, MD, MPH§; and RICHARD J. THOMAS, MD, MPH¥

INTRODUCTION

ORGANIZATION OF DEPARTMENT OF THE NAVY AND NAVY MEDICINE

A BRIEF HISTORY OF NAVY PREVENTIVE MEDICINE AND OCCUPATIONAL HEALTH AT THE DECK PLATE AND IN THE FIELD

CURRENT STRATEGIC-LEVEL SAFETY AND OCCUPATIONAL HEALTH RESPONSIBILITIES

LAWS, REGULATIONS, AND GUIDANCE

ORGANIZATION AND STAFFING OF MARINE CORPS SAFETY AND OCCUPATIONAL HEALTH PROGRAMS TODAY AND NAVY MEDICINE’S ROLE

ORGANIZATION AND STAFFING OF NAVY SAFETY AND OCCUPATIONAL HEALTH PROGRAMS TODAY AND NAVY MEDICINE’S ROLE

Safety

Industrial Hygiene

Occupational and Environmental Medicine

Audiology

Consultative Support and Oversight

EXAMPLES OF SAFETY AND OCCUPATIONAL HEALTH PROGRAM COMPONENTS AND RESOURCES

Navy and Marine Corps Public Health Center Technical Manuals

Medical Surveillance and Certification Exams and the Medical Matrix

Hearing Conservation Program

Worksite Visits

Program Self-Assessment and Process Improvement

SUMMARY

*Captain, Medical Corps, US Navy; Occupational and Environmental Medicine Residency Program Director, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814-4799

†Regional Nurse Consultant, Naval Health Clinic, 695 Kinkaid Road, Annapolis, Maryland 21402-5050

‡Occupational Audiologist, Naval Health Clinic, 695 Kinkaid Road, Annapolis, Maryland 21402-5050

§Lieutenant Commander, Medical Corps, US Navy (Undersea Medical Officer/Diving Medical Officer); Department Head, Occupational Medicine Department, US Naval Hospital, PSC 827 Box 281, FPO AE 09617, Naples, Italy

¥Captain (Retired), Medical Corps, US Navy; Associate Professor, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814-4799

INTRODUCTION

The primary mission of the Department of the Navy (DoN) safety and occupational health (SOH) program is to provide US Navy (USN) and US Marine Corps (USMC) active duty personnel and civilian employees a safe and healthy workplace. The Navy SOH program and Marine Corps safety program comprise the DoN SOH program for all military and civil service personnel, although uniquely military operations require flexibility in implementation of medical surveillance requirements for operational forces. The programs include medical surveillance of personnel in military-unique environments, foreign nationals under status of forces agreements, and contract workers with occupational and environmental medicine (OEM) services in their contacts. This chapter provides an overview of the scope and organization of Navy SOH programs and the role of Navy medicine support of these programs in the USN and USMC. More complete details can be found in the Navy Occupational and Environmental Medicine Field Operations Manual.[1]

ORGANIZATION OF THE DEPARTMENT OF THE NAVY AND NAVY MEDICINE

The DoN differs from other military departments in that it consists of two distinct military services (the USN and the USMC) that jointly report to the civilian secretary of the Navy. DoN has several principal components: the operating forces of the USN (referred to as the “Fleet”) and the USMC (referred to as the “Fleet Marine Force”), the USN and USMC reserve components, and, in time of war, the US Coast Guard (currently a component of the US Department of Homeland Security); the shore establishment, which provides support to the operating forces; and executive offices known as the Navy Department (Figure 3-1).

The Navy Bureau of Medicine and Surgery (BUMED) is a shore establishment command reporting directly to the chief of naval operations (CNO) as the echelon one commander (ie, BUMED is an echelon two command). The surgeon general of the Navy, a three-star flag officer, serves as chief of the BUMED, and in this role provides oversight on direct and indirect systems providing health services to all USN personnel, USMC personnel (in conjunction with the medical officer of the Marine Corps, a Navy rear admiral Medical Department officer), and other beneficiaries.[2],[3] The Navy surgeon general has direct authority over shore-based medical assets (which are under two echelon three regional commands, Navy Medicine East and Navy Medicine West). The Navy and Marine Corps Public Health Center (NMCPHC) falls under Navy Medicine East as an echelon four command. The regional commanders direct the military medical treatment facilities (MTFs), which range in size from large tertiary care medical centers to small ambulatory care clinics.[3] Navy Medicine East is headquartered in Portsmouth, Virginia, and the headquarters for Navy Medicine West is in San Diego, California. Exhibits 3-1 and 3-2 list the MTFs in each region.

The role of the regional commands is to support the MTFs in the delivery of world-class healthcare to active duty personnel, their dependents, retirees, and other beneficiaries. Regional experts determine proper staffing, as well as the equitable distribution of fiscal resources. The regional commands serve as a conduit to funnel information down from BUMED and a channel to raise concerns up from the MTFs to the attention of BUMED.[3]

The MTFs provide medical care, including OEM, audiology, and industrial hygiene services, to employees of the shore establishment as well as to the operating forces when in port, as needed. The Navy currently has two tertiary care medical centers: Naval Medical Center (NMC) Portsmouth on the Atlantic coast and NMC San Diego on the Pacific coast. Both facilities offer the full range of specialty care, including both inpatient and outpatient services. In 2011, as directed by the 2005 Base Realignment and Closure Commission, the National Naval Medical Center was merged with Walter Reed Army Medical Center to form the joint Walter Reed National Military Medical Center (WRNMMC) in Bethesda, Maryland, reporting to the newly created Defense Health Agency. WRNMMC remains a world-class tertiary care medical center, serving uniformed and civilian beneficiaries from all services.[4]

Figure 3-1. Department of the Navy organization. The US Navy was founded on October 13, 1775, and the Department of the Navy was established on April 30, 1798. There are three principal components: (1) the Navy Department, consisting of executive offices mostly in Washington, DC; (2) the operating forces, including the Marine Corps, the reserve components, and, in time of war, the US Coast Guard (in peacetime, the Coast Guard is a component of the Department of Homeland Security); and (3) the shore establishment. The dashed line marked “Support” indicates the cooperative relationship of the Navy-Marine Corps team, in which each of the operating forces supports the other.
Adapted from: http://www.navy.mil/navydata/organization/org-over.asp.

EXHIBIT 3-1

NAVAL MEDICAL TREATMENT FACILITIES IN NAVY MEDICINE EAST AREA OF RESPONSIBILITY

- Naval Medical Center Portsmouth, Portsmouth, Virginia

- Naval Hospital Beaufort, Beaufort, South Carolina

- Naval Hospital Camp Lejeune, Camp Lejeune, North Carolina

- US Naval Hospital Guantanamo Bay, Guantanamo Bay, Cuba

- Naval Hospital Jacksonville, Jacksonville, Florida

- US Naval Hospital Naples, Naples, Italy

- Naval Hospital Pensacola, Pensacola, Florida

- US Naval Hospital Rota, Rota, Cádiz, Spain

- US Naval Hospital Sigonella, Sigonella, Italy

- Captain James A. Lovell Federal Health Care Center, Great Lakes, Illinois

- Naval Health Clinic Annapolis, Annapolis, Maryland

- Naval Health Clinic Charleston, North Charleston, South Carolina

- Naval Health Clinic Cherry Point, Cherry Point, North Carolina

- Naval Health Clinic Corpus Christi, Corpus Christi, Texas

- Naval Health Clinic New England, Newport, Rhode Island

- Naval Health Clinic Patuxent River, Patuxent River, Maryland

- Naval Health Clinic Quantico, Quantico, Virginia

- 2nd Dental Battalion, Camp Lejeune, North Carolina

The Navy’s community hospitals are staffed by dedicated professionals and support staff who understand the unique needs of military members and their families throughout the world. In addition, more than 100 Naval health clinics and smaller branch health clinics are located on or near Navy bases worldwide.[5] These ambulatory clinics provide primary care, along with limited specialty care, and refer patients to the larger hospitals and medical centers or to the Tricare network when inpatient or additional specialty care is needed.

EXHIBIT 3-2

NAVAL MILITARY TREATMENT FACILITIES IN NAVY MEDICINE WEST AREA OF RESPONSIBILITY

- Naval Medical Center, San Diego, California

- Naval Hospital Bremerton, Bremerton, Washington

- Naval Hospital Camp Pendleton, Camp Pendleton, California

- Naval Health Clinic, Lemoore, California

- Naval Hospital Oak Harbor, Oak Harbor, Washington

- Naval Hospital Twenty-nine Palms, Twenty-nine Palms, California

- US Naval Hospital Guam, Agana Heights, Guam

- US Naval Hospital Okinawa, Okinawa, Japan

- US Naval Hospital Yokosuka, Yokosuka, Japan

- Naval Health Clinic Hawaii, Pearl Harbor, Hawaii

- 1st Dental Battalion, Camp Pendleton, California

- 3rd Dental Battalion, Okinawa, Japan

Front-line medical support of the operating forces is provided by Navy medical personnel assigned to units of USN and USMC operating forces, as well as by field activities of the NMCPHC (Figures 3-2 through 3-5).

A BRIEF HISTORY OF NAVY PREVENTIVE MEDICINE AND OCCUPATIONAL HEALTH AT THE DECK PLATE AND IN THE FIELD

Before World War II, USN Medical Department personnel serving on Navy ships and at shore stations with the US Marines carried out preventive medicine programs based on service guidance from BUMED.[6] By 1942, in the South Pacific area of operations, disease nonbattle injuries due to malaria and other infectious diseases accounted for greater losses than combat injuries.[7],[8] In response, the US Army and Navy developed disease control teams comprised of malariologists, entomologists, and parasitologists working with Navy corpsmen to provide direct support to US and allied forces in theater at the unit level.[7],[9] For example, detachments of the Malaria and Epidemic Control Organization, known as epidemiology units, evaluated areas with high rates of preventable illnesses such as malaria among deployed troops, decreasing the incidence of communicable diseases in these areas throughout the remainder of the war.[7],[8] Of the 122 epidemiology units existing at the conclusion of World War II, all but six were disbanded by 1949. The six remaining units were renamed epidemic disease control units, and were tasked with providing technical assistance to commands to prevent epidemic disease conditions.[6]

During the Korean War, a renewed focus on preventive medicine became necessary.[9] The Navy organized two shipboard mobile units to provide preventive medicine in forward areas. Known as fleet epidemic disease control units (FEDCUs), these teams studied and controlled communicable diseases among both United Nations forces and prisoners of war. Due to difficulty in mobilizing the FEDCUs, the units evolved from shipboard to air-transported teams. In 1952 their mission was changed to “preventing or controlling health problems of naval importance due to biological, physical, chemical or other causes.”[6] In March 1953, the units were redesignated as USN preventive medicine units (PMUs). In 1957, the PMUs were assigned more specialized and technical services: four PMUs were assigned to provide direct fleet support and two were designated as disease vector control centers (DVCCs), located in Jacksonville, Florida, and Alameda, California.[9] In 1971, the PMUs became Navy environmental and preventive medicine units (NEPMUs), with expanded fleet support services in industrial hygiene and occupational health.[5] At the same time, the DVCCs were redesignated as disease vector ecology control centers (DVECCs).[9]

Figure 3-2. USS Constitution’s 1812 Marine Guard fire vintage Springfield flintlock muskets during the “Constitution Day Cruise” while the ship is underway. Boston, Massachusetts, June 23, 2006. US Navy photo by Airman Nick Lyman.
Reproduced from: http://www.navy.mil/view_image.asp?id=36221.

Figure 3-3. “The US Marine Corps War Memorial. The Marine Corps War Memorial stands as a symbol of this grateful Nation’s esteem for the honored dead of the US Marine Corps. While the statue depicts one of the most iconic photos of World War II, the memorial is dedicated to all Marines who have given their lives in the defense of the United States, since 1775.” Located in Arlington, Virginia, the statue depicts five Marines and a Navy corpsman raising a visible flag on February 23, 1945, during the battle on the Japanese island of Iwo Jima. This memorial represents the honor, courage, and commitment of the US Marines and the Navy Medical Department personnel, who provide worldwide support to the Marine Corps. US Navy photo.
Reproduced from: http://www.navy.mil/management/photodb/photos/040709-N-0295M-001.jpg.

Figure 3-4. The US Navy and Marine Corps project the influence of the United States by having ready naval forces worldwide at sea at all times. US Navy photo by Photographer’s Mate 2nd Class Daniel J. McLain.
Reproduced from: http://www.navy.mil/management/photodb/photos/150415-N-SF984-096.JPG.

In the early 20th century, Navy medicine also provided groundbreaking occupational medicine support to military aviation and submariners. In 1923 a Naval medical officer assigned to the Boston Navy Yard attended 1 year of occupational health training at Harvard University. This was a landmark in military occupational medicine.[10] A specific division of industrial medicine was first set up at BUMED in 1941, and in the first 2 years more than 50 Naval medical officers completed post-medical degree certification programs in industrial hygiene (Figure 3-6).[11] By 1947, the Navy Medical Service Corps had been formed. The Medical Service Corps now has commissioned officer SOH specialists such as audiologists, entomologists, environmental health specialists, and industrial hygienists, among 11 allied health disciplines.[12]

Figure 3-5. Organization of the Navy Medical Department.
Data source: Navy Bureau of Medicine and Surgery. Chief, Bureau of Medicine and Surgery Organization. Falls Church, VA: Department of the Navy; December 22, 2016. BUMEDINST 5450.165C. http://www.med.navy.mil/directives/ExternalDirectives/5450.165C.pdf. Accessed October 12, 2017.

Figure 3-6. An industrial hygiene officer assigned to Navy Environmental and Preventative Medicine Unit Six (NEPMU-6) tests an air sample for contaminants. US Navy photo by Journalist 2nd Class Ryan C. McGinley.
Reproduced from: http://www.navy.mil/management/photodb/photos/060207-N-3019M-003.jpg.

The birth of a comprehensive Navy occupational health program occurred at a Naval Bureau of Weapons facility in Crane, Indiana, in 1964.[13] The need for a comprehensive occupational health program for Navy line and medical commands had become apparent, and the senior medical officer at this facility was tasked with providing consultative support for all Naval weapons facilities worldwide. The concept of establishing a single Navy consultative center for occupational health soon gained support. Through a series of organizational consolidations and relocations, the center moved from Crane, Indiana, to Cincinnati, Ohio, and then to Norfolk, Virginia. By 1978, the Navy Environmental Health Center (NEHC) had evolved into the focal point for the development of BUMED occupational health program consultation and guidance. The move closer to the large concentration of Fleet and the Fleet Marine Force personnel and commands in Tidewater, Virginia, reflected NEHC’s increasing worldwide responsibilities, including the Navy SOH inspection program, analytic laboratory services, radiation health program support, hazardous materials identification, asbestos hazard control, and hearing conservation programs.[13]

Figure 3-7. Commander Richard Maiello, an industrial hygienist attached to the Forward Deployed Preventive Medicine Unit Seven (FDPMU-7), conducts training on the Chemical Volatile Organic Compound Unit, which is used to screen soil, water, and air for the detection of toxic materials such as chemical, biological, and radiological agents. US Navy photo by Photographer’s Mate 2nd Class Steven P. Smith.
Reproduced from: http://www.navy.mil/view_image.asp?id=36275

NEHC assumed command and control of the four NEPMUs and the two DVECCs in March 1981, further expanding its mission to include preventive medicine.[6],[13] The scope of NEPMU services likewise had expanded from epidemiology and infectious disease control to include industrial hygiene, consolidated industrial hygiene laboratories, environmental health, and deployable multidisciplinary teams, referred to as forward deployable preventive medicine units (FDPMUs; Figure 3-7). FDPMUs were based on the success of prototypes fielded in 1990–1991, during the Persian Gulf War. The current locations of the four NEPMUs are Rota, Spain; Norfolk, Virginia; San Diego, California; and Pearl Harbor, Hawaii. The Navy Entomology Center of Excellence (NECE) is located in Jacksonville, Florida. Both the FDPMUs and the NECE deploying units served with distinction while providing forward support in both the Iraq and Afghanistan conflicts.

With increasing recognition of the need for USN/USMC-wide guidance on wellness, preventive behavioral health, and physical fitness, these programs were consolidated at NEHC in the 1990s. NEHC moved to its current location on the grounds of the Naval Medical Center, Portsmouth, Virginia, in 2002, and was renamed the NMCPHC in 2007 to reflect the worldwide need and focus of SOH and preventive medicine programs for both the USN and USMC.[13]

CURRENT STRATEGIC-LEVEL SAFETY AND OCCUPATIONAL HEALTH RESPONSIBILITIES

The assistant secretary of the Navy for energy, installations, and environment is the designated agency SOH officer for the DoN. Implementation of SOH programs is delegated to the deputy assistant secretary of the Navy for safety. The overarching principles of aggressive and comprehensive leadership involvement, personal responsibility on and off duty, worksite analysis, operational risk management, medical surveillance, certification, and training are emphasized as part of the secretary of the Navy implementation policy.[14] A commitment to safety and occupational health for every individual throughout the DoN chain of command is considered the foundation of safe and healthful working conditions. The DoN SOH program’s organizational structure and chain of command reflects the complexity and wide range of USN and USMC missions.

Echelon one commanders (the CNO and the commandant of the Marine Corps [CMC]) issue SOH policy, guidance, and standards that meet or exceed the requirements of Department of Defense instructions (DODIs) pertaining to SOH, including DODI 6055.1, DoD Safety and Occupational Health (SOH) Program,[15] and DODI 6055.05, Occupational and Environmental Health (OEH).[16] Naval SOH subject matter expertise is provided to both the CMC and CNO by the commander of the Naval Safety Center in Norfolk, Virginia, who also serves as the CNO’s special assistant for safety matters and is responsible for program sponsorship of occupational health Navy-wide.[14],[17] Additionally, the Navy surgeon general serves as the principal advisor to the CNO on the provision of centralized, coordinated policy, guidance, and professional advice on health service programs for DoN, including occupational health services (the medical officer of the Marine Corps, a one-star Navy medical flag officer, is the principal health services policy advisor to the CMC, as described previously).[3]

For SOH matters of mutual interest, policy is issued jointly by the USN and USMC to ensure uniformity (eg, Mishap Investigation, Reporting and Record Keeping, which is both Chief of Naval Operations Instruction [OPNAVINST] 5102.1 and Marine Corps Order [MCO] P5102.1).[18] For SOH program requirements unique to the mission of the two services, the services issue service-specific policies.[14]

The Naval Safety Center commander is the SOH program sponsor. While primarily responsible to the CNO and secretary of the Navy for compliance with DODI 6055.1[15] and 6055.05,[16] both ashore and afloat, certain areas of SOH policy are governed by specialty components. A complete listing of specialty subject matter responsibility is found in Appendix 2A of the Navy Safety and Occupational Health Program Manual,[17] and examples are listed in Exhibit 3-3.

Echelon two commands each create and maintain SOH instructions for guidance to their subordinate commands. These instructions “shall emphasize known significant occupational health problems”[17] through their respective design, engineering, maintenance, supply, facilities and training cycles. In the Navy, the accountability and inspection process is split between the Naval inspector general, for shore-based commands, and the Board of Inspection and Survey, for forces afloat. The Naval Safety Center commander and BUMED are further tasked with providing subject matter expertise to all other USN and USMC echelon two commands in the areas of safety and health, respectively.

EXHIBIT 3-3

CHIEF OF NAVAL OPERATIONS STAFF RESPONSIBILITIES FOR OPERATIONAL UNIT SAFETY POLICY

Staff Code

Area of Responsibility

N85

Expeditionary warfare: parachute, diving, and air drop safety, assigned ships and small craft.

N86

Surface warfare: assigned surface ships.

N87

Submarine warfare: submarines, assigned surface ships, deep submergence systems, and diving.

N09F

Naval aviation safety (aircraft-specific policies are at lower level). The Commander, Naval Air Forces, is responsible for safety of assigned ships (ie, aircraft carriers).

N00N

Nuclear propulsion program safety: reactor and associated Naval nuclear propulsion plants and radioactivity.

N09F

Shore safety.

N41

Conventional explosive safety.

N46

Nuclear explosive safety.

LAWS, REGULATIONS, AND GUIDANCE

Executive Order 12196 approves alternate SOH standards for the Department of Defense (DoD) based on performance of military and uniquely military duties.[19] Overarching guidance and standards for the DoN SOH programs are provided by three DoN directive series, OPNAVINST 5100.23 for USN forces ashore,[17] OPNAVINST 5100.19 for forces afloat,[20] and MCO 5100.19 for USMC forces.[21] Additional Navy instructions provide amplifying guidance for specific programs (eg, the Navy Radiation Health Protection Manual).[22] When DoN standards are not in conformance with the most recent Occupational Safety and Health Administration (OSHA) standards, the current OSHA standards are used as interim guidance until new DoN standards can be developed and issued. Other nationally recognized sources of SOH guidance, such as the American Conference of Governmental Industrial Hygienists and the American National Standards Institute, are also considered when evaluating workplaces. The Office of Personnel Management sets medical qualification requirements for federal civilian employees in certain positions, and other federal agencies, such as the Department of Transportation, may specify physical examination requirements and standards for personnel performing specific transportation duties.

ORGANIZATION AND STAFFING OF MARINE CORPS SAFETY AND OCCUPATIONAL HEALTH PROGRAMS TODAY AND NAVY MEDICINE’S ROLE

USMC commands apply Public Law 91-596, the Occupational Safety and Health Act of 1970,[23] to all non–military-unique work environments per MCO 5100.29B.[24] A variety of published USMC orders provide procedures for safety and occupational health officials and supervisory personnel (Exhibit 3-4). SOH training is integrated into programs and technical and tactical publications, with occupational medicine, industrial hygiene, and allied health professional support provided by Navy medical personnel assigned to both BUMED and operational units. Functionally, BUMED supports USMC SOH programs with the same process as Navy operational and shore commands. Occupational health medical specialists, technicians, nurses, and physicians are billeted primarily to fixed shore-based Navy medical clinics.

BUMED provides medical officers from all specialty backgrounds to meet the primary care and occupational health medical requirements at the unit level. Navy Medical Department industrial hygiene officers (IHOs) are assigned to various billets in the Fleet Marine Force to provide both safety and industrial hygiene program management and consultation services.

NMCPHC is the USN and USMC center for public health support, including epidemiology, exposure monitoring, and illness and injury tracking. Through its echelon four NEMPUs, NMCPHC provides health risk assessments and field operation support. As previously described, NMCPHC provides deployable public health specialty support through FDPMUs, consisting of the four NEPMUs and one NECE mobile unit.[13],[25],[26]

ORGANIZATION AND STAFFING OF NAVY SAFETY AND OCCUPATIONAL HEALTH PROGRAMS TODAY AND NAVY MEDICINE’S ROLE

The responsibility for conducting an integrated and aggressive SOH plan throughout the Navy is delegated to the level of commanding officers and officers in charge both at sea and ashore. They are responsible for ensuring the SOH program is robust and functioning at all levels of their command. Daily SOH operation and functions within Navy commands are facilitated by the three SOH specialized professional components: safety professionals, industrial hygienists, and occupational medicine providers.

Safety

Each Navy command assigns a safety officer accountable directly to the commanding officer for managing safety programs in compliance with the applicable shore or afloat instructions. Full-time safety professionals are required for every unit with more than 400 personnel. Smaller commands may assign the role as a collateral duty, or one full-time safety professional may provide services to two or more smaller commands. The OPNAVINST 5100.23 series[17] provides guidance on appropriate safety staff size for larger commands, and for shared safety professionals.

Safety functions are subdivided into two categories: mission safety and base operating support (BOS) safety. In 2003, Navy Installations Command was established as an echelon two command tasked and funded for providing BOS, including certain safety programs ashore such as traffic safety, recreation and off-duty safety, radiation safety, and explosives safety. BOS functions are those considered to be common to the host installation or the base. Installation safety professionals manage these programs with input and support from tenant command safety professionals, who coordinate the program within their units. Line commands are supported by occupational medicine professionals through the establishment of periodic safety council meetings.

EXHIBIT 3-4

US MARINE CORPS OCCUPATIONAL SAFETY AND HEALTH PROGRAM ORDERS AND OTHER APPLICABLE DIRECTIVES

Marine Corps Orders Series

- P5100.8, Marine Corps Ground Occupational Safety and Health Program

- 5100.29, Marine Corps Safety Program

- 3500.27, Marine Corps Operational Risk Management Program

- M5100.19, Marine Corps Traffic Safety Program

- P5102.1, Marine Corps Mishap Reporting Program

- 5100.30, Marine Corps Off-Duty and Recreation Safety Program

- 1553.3, Marine Corps Training Management

- 6200.1, Marine Corps Heat Injury Prevention Program

- 6260.1, Marine Corps Hearing Conservation Program

- P8020.10, Marine Corps Ammunition Management and Explosives Safety Policy Manual

- 5104.1, Navy Laser Hazard Control Program

- 5104.2, Marine Corps Radio Frequency Electromagnetic Field Personnel Protection Program

- 5104.3, Marine Corps Radiation Safety Program

- P11000.11, Marine Corps Fire Prevention

- 5100.32, Marine Corps Safety Awards Program

- P3570.1, Policies and Procedures for Firing Ammunition for Training, Target Practice, and Combat

- 5040.6, Marine Corps Inspections

Other Applicable Directives and Manuals

- Executive Order Executive Order 12196, 45 FR 12769, 3 CFR, Occupational safety and health programs for federal employees (1980)

- The Occupational Safety and Health Act of 1970 (Pub L 91-596, with amendments), Section 19, Federal Agency Safety Programs and Responsibilities

- Navy Safety and Occupational Health Program Manual (OPNAVINST 5100.23G)

___________________

Data source: Department of the Navy, US Marine Corps. Marine Corps commander’s guide to safety.
http://www.imef.marines.mil/Portals/68/Docs/IMEF/Safety/Marine%20Corps%20Commander’s%20Guide%20to%20Safety%20(2).pdf. Accessed October 11, 2017.

Mission safety relates specifically to the mission performed by the command. Echelon two commands receive separate funding for ensuring the safety of the unique and integral mission functions of their command. Mission safety examples for shore commands include Joint Commission compliance (BUMED), military construction and environmental clean-up (Naval Facilities Command), or ship maintenance work (Naval Sea Systems Command).

Based on this structure, Navy medicine regions and larger MTFs have full-time safety professionals whose primary focus is mission safety for BUMED commands. However, OEM and industrial hygiene specialists must work with safety professionals in all areas of the DoN to achieve the goal of providing a safe and healthy workplace for all DoN personnel.

Echelon two commands must inspect subordinate commands at least every 36 months, and supervisors and designated safety officials must inspect workspaces at least annually to ensure compliance with SOH policies.

Industrial Hygiene

Uniformed IHOs are Navy Medical Service Corps officers who are assigned to both USN and USMC line commands (ashore and afloat), as well as BUMED activities. Navy IHO billets afloat are primarily on larger ships such as aircraft carriers or large amphibious ships. Navy IHOs at operational units are often assigned as the command safety officer, and provide industrial hygiene services to their operational command (Figure 3-8). Industrial hygiene services ashore are provided by the MTFs, predominantly by civil service industrial hygienists who support installations, tenant commands, facilities, shipyards, ranges, flight lines, and operational units and ships in port within the MTF’s area of responsibility.[10] OPNAVINST 5100.23G[17] uses a formula based on the employee population and hazards of an area to estimate the number of industrial hygienists necessary to provide the required support.

Occupational and Environmental Medicine

Occupational healthcare for active duty service members ashore varies by location, provided either through a dedicated occupational health clinic or by a primary care provider. While at sea or deployed, most USN and USMC active duty service members receive occupational healthcare from primary care providers. Occupational health services rendered by the primary care provider include management of work-related illnesses and injuries, individual medical readiness, predeployment and postdeployment assessments and care, documentation of exposure monitoring, and limited duty determinations (Figure 3-9). Approximately 50 Medical Corps billets across the Navy are designated for physicians trained in OEM.[1] These billets are concentrated at MTFs supporting shore commands that perform shipbuilding or maintenance, at tertiary care medical centers, at BUMED Headquarters, and at NMCPHC. BUMED clinics rely heavily on civil service physicians trained or experienced in OEM, but are also staffed by general medical officers, primary care physicians, nurse practitioners, and physician assistants.

Occupational medicine specialty care providers at MTFs focus primarily on providing care to DoN civil service and contract workers. Occupational medicine care for active duty members assigned to shore duty is generally limited to specialty examinations for surveillance of specific work exposures. Occupational health clinics may also provide travel medicine, preventive medicine, and deployment or overseas duty screenings for civil service workers and active duty personnel. A few clinics also provide acute care for minor work-related injuries for civil service and eligible contractors. Occupational health program management responsibility lies with a civilian clinic nurse manager. The clinic nurse trains and oversees civilian occupational health technicians and general duty corps staff within the clinic and reports clinical operations and metrics to the echelon three Navy medicine region.

Figure 3-8. Puget Sound, October 26, 2006. Lt Cmdr Paul Treadway, Industrial Hygiene Officer and Assistant Safety Officer of the Nimitz-class aircraft carrier USS Abraham Lincoln (CVN 72), uses a sound level meter to demonstrate the high decibel levels on Lincoln’s flag bridge as spaces are being rehabilitated. Treadway and other ship and shipyard safety personnel conduct daily safety walkthroughs throughout the ship to ensure sailors and workers are wearing proper personal protective equipment to protect against industrial hazards such as high noise levels. Lincoln is currently in dry dock at Puget Sound Naval Shipyard undergoing rehabilitation and maintenance as part of a dry dock planned incremental availability period. US Navy photo by Mass Communication Specialist Seaman James R. Evans (released). Navy photo ID: 061026-N-7981E-019.
Reproduced from: http://www.navy.mil/view_image.asp?id=40336.

USN and USMC occupational health services for active duty personnel while deployed or assigned to a ship are provided by the assigned unit (“platform”) primary care provider. Major hazard-specific elements of shipboard and deployed SOH prevention programs include asbestos management, heat stress management, hazardous material control and management, hearing and sight conservation, respiratory protection, electrical safety, radiation safety, gas-free engineering, lead control, tag-out (a procedure used to prevent injury while servicing equipment or machinery), and personal protective equipment.[20] Enrollment in medical surveillance programs is based primarily on the industrial hygiene survey. On submarines and small surface ships, the primary care provider is often an independent duty corpsman or medical department representative (a corpsman), while larger ships have general medical officers (post-internship physicians) and senior medical officers (usually post-residency physicians), as well as other specialists. Aircraft carrier senior medical officers must have completed a residency in aerospace medicine. The OPNAVINST 5100.19 series[20] provides detailed guidance for SOH programs aboard Navy vessels.

Figure 3-9. Civilian and Navy active duty members play and important role in the safety and occupational health programs serving the US Navy and Marine Corps. Portsmouth, Virginia, June 5, 2014. Tarnisha Brown, a Navy Medicine audio technician working aboard a hearing conservation bus at Norfolk Naval Shipyard, and Hospital Corpsman 3rd Class James Champion, from Tuscaloosa, Alabama, demonstrates the proper use of hearing protection to sailors assigned to the aircraft carrier Dwight D. Eisenhower (CVN 69). Dwight D. Eisenhower is undergoing a scheduled docking planned incremental availability at Norfolk Naval Shipyard. US Navy photo by Mass Communication Specialist Seaman Wesley J. Breedlove (released). Navy photo ID: 40605-N-SR567-054.
Reproduced from: http://www.navy.mil/view_image.asp?id=177253.

Audiology

Active duty and civil service audiologists serve worldwide at Navy MTFs, providing local and regional services for clinical consultations and programmatic requirements (eg, all US Marines require annual audiograms while on active duty because many personnel are exposed to high noise environments; Figure 3-10). Clinical audiology services such as diagnosis and rehabilitation of auditory and balance problems are offered at most Navy MTFs. In addition, many centers employ audiologists designated as either part-time or full-time occupational audiologists, specializing in hearing conservation program management as well as the determination of auditory fitness for duty. Currently, approximately 54 Navy audiologists specialize exclusively in occupational audiology; about half are active duty Navy Medical Service Corps officers and the others are DoN civil service personnel. They are located at medical centers, hospitals, and a few health clinics. Occupational audiologists serve at the NEPMUs in Norfolk and San Diego, one audiologist serves at the NMCPHC, and a uniformed audiology action officer is on the staff at BUMED. Audiologists also serve as regional subject matter experts (SMEs) and consultants at the two Navy regional medical commands, as described below.

Consultative Support and Oversight

In addition to the larger clinical care components at shore facilities, Navy medicine provides medical support, including OEM and industrial hygiene, for both services (see Figure 3-5). Both military and civil service safety and occupational health professionals serve on the DoN, CNO, and CMC staffs as well as at BUMED to develop policy for SOH and OEM programs.

Regional consultants support the SOH mission by providing technical assistance and oversight to the MTFs. These teams consist of four members including an occupational audiologist, an industrial hygienist, an occupational health nurse, and a safety specialist. All team members are experienced experts in their field, well versed in DOD, USN, and USMC instructions, guidelines, and directives that apply to their particular programs. These SMEs are available to answer policy questions and interpret guidelines, as well as to bring concerns from the field to BUMED when guidelines are ambiguous, outdated, or unclear.

Figure 3-10. The extremely close proximity to jet noise and the conflicting requirement to be in constant communication with a pilot attempting to land on an aircraft carrier at sea puts a Navy or Marine Corps landing signal officer at continuing risk of noise-induced hearing loss. Pacific Ocean, August 6, 2003. Landing Signal Officer Brian Felloney helps guide the pilot of an F/A-18F Super Hornet assigned to the “Diamondbacks” of Strike Fighter Squadron One Zero Two (VFA-102) to land on the flight deck aboard USS John C. Stennis (CVN 74). Stennis is at sea conducting training exercises in the southern California operating area. US Navy photo by Photographer’s Mate 2nd Class Jayme Pastoric (released). Navy photo ID: 030806-N-9769P-015.
Reproduced from: http://www.navy.mil/management/photodb/photos/030806-N-9769P-015.jpg.

Regional SOH experts also provide advice, technical reviews, and representation on working groups, as requested by BUMED or a higher authority. They encourage interdepartmental and intradepartmental communication, collaboration, and cooperation among all professional SOH disciplines. They are responsible for ensuring that required SOH training occurs, that effective mishap and incident reporting is accomplished, and that required medical surveillance and follow-up is performed in a timely fashion, using the appropriate reporting and management systems, including the Web-Enabled Safety System (WESS) and the Enterprise Safety Applications Management System (ESAMS).

The regional SOH team oversees implementation of these programs at the MTFs, providing both informal and formal program review. Team members provide three types of visits:

1. Assist visits. Commands may request an assist visit for specific training, to review an entire program, to review part of a particular program, or even to review a single process. The SME’s resulting report is seen only by the commanding officer of the requesting command unless the command chooses to forward the report to the region.

2. Oversight visits. Regional SMEs are not required by any regulation to perform oversight visits, but may choose to do them periodically depending on available resources. A variety of tools such as checklists may be used to review compliance with SOH programs. A report of the findings is provided to the site’s commanding officer.

3. Safety and occupational health management evaluations. The BUMED instruction (BUMEDINST) 5100.13 series[27] requires formal compliance inspections via SOH management evaluations. All SOH programs must undergo formal review every 3 years. Regional staff attempt to schedule SOH management evaluations at a reasonable time before an impending BUMED Medical Inspector General Inspection and Joint Commission Survey, in order to allow commands time to fix any discrepancies identified. Formal checklists are used to review program compliance; a formal report is sent from the region to BUMED, with a copy sent to the commanding officer of the inspected command.

EXAMPLES OF SAFETY AND OCCUPATIONAL HEALTH PROGRAM COMPONENTS AND RESOURCES

Navy and Marine Corps Public Health Center Technical Manuals

NMCPHC publishes an extensive series of technical manuals such as the Navy Occupational Medicine Field Operations Manual.[1] An implementation guide for professionals establishing a comprehensive OEM practice, this manual includes information on OEM practice including program elements, trend analysis, worksite visits, preplacement exams, medical surveillance, job certification, fitness-for-duty exams, treatment of work-related illnesses and injuries, health promotion, travel medicine, consultation to management and employees, risk communication, occupational safety and health education and training, employee counseling and referral to employee assistance programs, occupational health clinic staffing, and program assessment.[1] Other technical manuals focus on specific topics including hearing conservation, reproductive and developmental hazards, prevention of heat and cold stress injuries, and bloodborne pathogen exposure control.

Medical Surveillance and Certification Exams and the Medical Matrix

A core function of Navy OEM is performing medical surveillance and certification exams. Medical surveillance is performed to identify unexpectedly high levels of exposure or exposure-related health effects in time to protect the worker or the worker population. Certification exams are done to determine whether an employee is fit to perform the duties of the job. The NMCPHC OEM department publishes the Medical Surveillance Procedures Manual and Medical Matrix[28] as the authoritative guide for occupational medical surveillance and certification programs for the Navy. The Medical Matrix Validation Committee was tasked in March 1988 with designing a Navy program for hazard-based medical surveillance by developing a standard examination protocol presented in a useable format. Since the original manual was published in January 1989, the committee has continued to review existing programs and write new programs as needed for stressors that may lead to chronic health effects. The medical matrix is divided into four sections: chemical stressors, physical stressors, mixed exposures, and specialty (or certification) exams. Each stressor program consists of the following information: medical history questions (personal and occupational), recommended laboratory and ancillary tests, areas of physical exam focus, program-specific special requirements, and a program description including references.

Hearing Conservation Program

Federal hospital services for veterans were consolidated after the First World War into the Veterans Bureau. Auditory injury, including both tinnitus and hearing loss, has been the most prevalent compensated disability from the advent of the Veterans Administration (VA) in World War II through today.[29],[30] Even when considered independently, tinnitus and hearing loss are the two most prevalent compensated VA disabilities, according to the Department of Veterans Affairs Annual Benefits Report for fiscal year 2013, not only for new recipients, but also overall for all veterans, with a combined compensation cost of approximately $1.4 billion annually. The VA also buys over 600,000 hearing aids every year, representing nearly one-quarter of all US sales.[30]

Tinnitus and hearing loss are the top two disabilities during times of peace and war, indicating that noise is a problem not only in combat, but also in training and maintenance operations. Naval shipyards, ports, flight lines, surface ships, and submarines are full of noise-hazardous machines and operations that are loud enough to cause permanent hearing loss. Efforts to minimize noise exposure through engineering and administrative controls are not always feasible, either for economic or technological reasons, and the Navy is left with a workforce that must work in areas and perform operations that may be hazardous to their hearing health.

Hearing conservation is, by far, the Navy’s largest medical surveillance program. While the program is typically managed by occupational audiologists who are usually located at the larger medical centers and hospitals, an effective hearing conservation program requires cooperation and teamwork from a number of related disciplines. Noise levels are measured by industrial hygienists. While abatement efforts remain the primary goal, it is not always feasible to engineer out noise, or to rotate schedules to minimize cumulative exposures. Employees who are exposed to hazardous levels of workplace noise are enrolled into the hearing conservation program, in which their hearing levels are monitored at least annually. When early changes are seen, follow-up care is provided to determine the nature and type of loss, as well as appropriate case management. Noise-exposed individuals are fit with hearing protective devices that are appropriate for their work environment, and trained in their care and use. Annual training also covers the hazards of noise exposure, the nature of the hearing conservation program, and on- and off-duty practices that may minimize the possibility of hearing loss. Occupational health, audiology, industrial hygiene, and safety personnel all work in conjunction with worksite supervisors and noise-exposed employees to prevent the development of occupational hearing loss (see Figures 3-9 and 3-10). Early intervention and appropriate case management are key to preventing further hearing loss for the identified workers and their coworkers with similar noise exposures.

Figure 3-11. The ocean maritime environment causes corrosion on ships that require constant attention. In this photograph active duty sailors involved in hull maintenance operations face ergonomic, noise, vibration, particulate, and fall hazards in their daily work. Portsmouth, Virginia, April 6, 2015. Hull Maintenance Technician 2nd Class A. Lightfoot, right, and Hull Technician Fireman R. Beaver perform maintenance and upkeep above the bridge of the aircraft carrier USS Harry S. Truman (CVN 75). Harry S. Truman is undergoing a condensed incremental availability period at Norfolk Naval Shipyard while training and acquiring certifications required for its upcoming deployment scheduled for later this year. US Navy photo by Mass Communication Specialist Seaman M. Gillan (released). Navy photo ID: 150406-N-MU551-134.
Reproduced from: http://www.navy.mil/view_image.asp?id=194427.

Figure 3-12. Navy industrial processes such as a shipyard overhaul of ships and submarines require active engagement of all members of the Navy safety and occupational health team to ensure a safe and healthy workplace. Bremerton, Washington, June 30, 2014. The guided-missile submarine USS Ohio (SSGN 726) arrives at Puget Sound Naval Shipyard and Intermediate Maintenance Facility for a scheduled major maintenance period. The shipyard and maintenance facility is one of four public shipyards that play a major role in maintaining America’s fleet and providing wartime surge capability to keep the nation’s ships ready for combat. US Navy photo by Jason Kaye (released). Navy photo ID: 140630-N-IZ282-005.
Reproduced from: http://www.navy.mil/local/PSNS/.

Audiometric data is collected via the Defense Occupational and Environmental Health Readiness System–Hearing Conservation module, which includes a DoD-wide data repository for all noise-exposed individuals. Computerization of the database facilitates management of this comprehensive program, allowing program managers to track important metrics such as compliance with annual audiometric testing and rates of abnormal exams indicating hearing loss, which facilitates early and focused intervention as well as optimal use of limited resources.

The Navy’s hearing conservation program is guided by not only the OSHA law (29 CFR 1910.95),[31] but also by the relevant DoD and Navy instructions described previously.[15]–[17],[20] In addition, the NMCPHC publishes a technical manual of program procedures,[28] and BUMED issues best practice guidelines.[32]

Figure 3-13. US Marine tactical and ground support vehicles are painted with a chemical agent resistance coating that contains isocyanate paint. Corrosion control involves washing vehicles such as depicted here and special corrosion control teams that paint vehicles periodically in spray booths and in temporary work locations to control corrosion as it occurs. Operations like this may require an industrial hygiene evaluation and monitoring, audiometric field testing, and respiratory protection. Twenty-nine Palms, California. A 3rd Light Armored Reconnaissance Battalion Marine cleans off excess dirt from a light-armored vehicle equipped with a new anti-tank weapons system at the 3rd LAR ramp prior to operational testing on range 500 aboard the Combat Center, February 10, 2015. 3rd LAR has been training alongside 1st Tank Battalion and 1st LAR during operational testing of the new system. Official Marine Corps photo by Lance Cpl Medina Ayala-Lo (released).
Reproduced from: http://media.dma.mil/2015/Mar/02/2001019041/-1/-1/0/150210-M-RO214-648.JPG

Worksite Visits

Worksite visits are a valuable tool for occupational medicine providers to ascertain firsthand information to assist supervisors with decreasing injuries and illnesses in their employees. Currently, BUMED requires all occupational medicine providers to complete 12 worksite visits each year. Ideally, the visits are partnered with safety or industrial hygiene, and they should focus on areas where employees are enrolled in medical surveillance programs. If injury or illness patterns are noted, the associated worksites may also be visited. During the worksite visit, the provider observes employees doing their job, including if and how any personal protective equipment is worn, and if safeguards are being used appropriately (Figures 3-11 to 3-13).

Program Self-Assessment and Process Improvement

NMCPHC also promulgates the Occupational Medicine Program Assessment (OMPA) as a self-assessment tool to assist both regional and local inspectors and local participants in evaluating the programs under their cognizance. The OMPA is a comprehensive overview of medical surveillance programs in place at an MTF. The OMPA also records clinic staffing, access, no-show rates, and completion of worksite visits. These assessments are completed annually for each MTF, with the results submitted via the regions to BUMED. For MTFs with subordinate branch health clinics, the occupational medicine program manager from the parent command collates and validates the OMPA submission prior to submission to BUMED via the region. Certain reviews are mandatory, such as medical recordkeeping, medical surveillance exams, certification exams, staffing, and hearing conservation. However, each occupational medicine program has different medical surveillance programs in place based on the hazards in the supported commands. The recurring process creates a living report. Each quarter, three to four programs are reviewed for compliance using the Occupational Health Program Evaluation Guide (OHPEG)[33] to guide record reviews.

The OHPEG is a tool designed to assist Navy OEM physicians and OHNs with performing a standardized assessment of quality and effectiveness of medical surveillance and certification programs. The OHPEG highlights many, but not all, of the programs defined by the medical matrix. Based on referenced regulatory requirements, the OHPEG is used to identify elements to be verified during program and medical record reviews. The OHPEG is formatted as a series of program self-assessment forms and medical record review forms. For example, the Asbestos Medical Surveillance Program section of the OHPEG consolidates the references of the pertinent regulatory requirements. OHPEG assessments are one component of the larger OMPA.

SUMMARY

This chapter has described the Navy Medical Department contributions to USN and USMC SOH programs. The many mutual overlapping missions of the USN and USMC require a flexibility of organization and use of resources to provide the optimal SOH program to protect the safety and health of the many people who contribute to the worldwide mission of the DoN. The topic of federal workers’ compensation programs and how they apply to USN and USMC civil service employees will be addressed in Chapter 9 of this volume.

REFERENCES

1.   Navy Environmental Health Center. Navy Occupational and Environmental Medicine Field Operations Manual. Portsmouth, VA: NEHC; April 2017. NMCPHC TM 6260.9A. http://www.med.navy.mil/sites/nmcphc/Documents/oem/OEM_FOM_05-April-2017.pdf. Accessed September 21, 2017.

2.   Chief, Bureau of Medicine and Surgery. Offices of the Surgeon General and Chief, Bureau of Medicine and Surgery Organization. Washington, DC: Department of the Navy; June 15, 2011. BUMEDINST 5450.165B CH-2. http://www.med.navy.mil/directives/ExternalDirectives/5450.165B%20With%20Changes.pdf. Accessed August 25, 2016.

3.   Chief, Bureau of Medicine and Surgery. Bureau of Medicine and Surgery Organizational Manual. Washington, DC: Department of the Navy; October 22, 2010. BUMEDINST 5430.8A.

4.   Walter Reed National Military Medical Center Website. About us: celebrating two proud histories. https://www.wrnmmc.capmed.mil/About%20Us/SitePages/History.aspx. Accessed September 21, 2017.

5.   Navy Bureau of Medicine and Surgery website. Navy Medicine around the globe. http://www.med.navy.mil/SiteInfo/Pages/default.aspx. Accessed August 25, 2016.

6.   Navy Environmental and Preventive Medicine Unit Five website. NEPMU Five command history. http://www.med.navy.mil/sites/nepmu5/Pages/history.aspx. Accessed August 25, 2016.

7.   US Army Medical Department. Medical Department, US Army, Preventive Medicine in World War II, Volume VI: Communicable Diseases, Malaria, Part VIII, New Hebrides, Solomon Islands, Saint Matthias Group and Ryukyu Islands. Washington, DC: Department of the Army, Office of the Surgeon General; 1963. http://history.amedd.army.mil/booksdocs/wwii/Malaria/default.html. Accessed September 21, 2017.

8.   US Navy Medical Department. History of the Medical Department of the United States Navy in World War II. The Solomons Campaign. http://www.ibiblio.org/hyperwar/USN/USN-Medical/I/USN-Medical-2.html#Solomons. Accessed August 25, 2016.

9.   Peterson RV, Wooster MT, Need JT, Hoffman E. History of Navy entomology, 1941–2011. http://www.med.navy.mil/sites/nmcphc/Documents/nece/history-of-navy-entomology.pdf. August 25, 2016.

10.   Gillooly PF, ed. History of Navy Industrial hygienists, monograph prepared for the 50th anniversary of the formation of the Navy Medical Service Corps (unpublished document, 1997). Navy Department, Bureau of Medicine and Surgery, Washington, DC.

11.   Stephenson CS, Burton OL. Industrial hygiene program of the US Navy. Am J Public Health. 1943;33(4):319–323.

12.   Navy Medical Service Corps website. Navy medicine history showcase. http://www.med.navy.mil/bumed/nmhistory/Pages/Showcase.aspx. Accessed October 12, 2017.

13.   Navy and Marine Corps Public Health Center website. Our history. http://www.med.navy.mil/sites/nmcphc/about-us/Pages/our-history.aspx. Accessed August 25, 2016.

14.   Secretary of the Navy. Department of the Navy Policy for Safety, Mishap Prevention, Occupational Health and Fire Protection Programs. Washington, DC: Department of the Navy; October 26, 2005. SECNAVINST 5100.10J.

15.   Department of Defense. DoD Safety and Occupational Health (SOH) Program. Washington, DC: DoD; October 14, 2014. DoD Instruction 6055.01 http://dtic.mil/whs/directives/corres/pdf/605501p.pdf. Accessed August 25, 2016.

16.   Department of Defense. Occupational and Environmental Health (OEH). Washington, DC: DoD; November 11, 2008. DoD Instruction 6055.05. http://www.dtic.mil/whs/directives/corres/pdf/605505p.pdf. Accessed August 25, 2016.

17.   US Navy, Chief of Naval Operations. Navy Safety and Occupational Health Program Manual. Washington, DC: Department of the Navy; December 30, 2005. OPNAVINST 5100.23G.

18.   Department of the Navy and Headquarters, US Marine Corps. Navy and Marine Corps Mishap and Safety Investigation, Reporting, and Record Keeping Manual. Washington, DC: Department of the Navy; January 7, 2005. OPNAVINST 5102.1D/MCO P5102.1B.

19.   Executive Order 12196, 45 FR 12769, 3 CFR. Occupational safety and health programs for federal employees. October 1, 1980.

20.   US Navy, Chief of Naval Operations. Navy Safety and Occupational Health Program Manual for Forces Afloat. Washington, DC; Department of the Navy; May 30, 2007. OPNAVINST 5100.19E.

21.   Commandant of the Marine Corps. Marine Corps Occupational Safety and Health Policy. Washington, DC: Headquarters, UCMC; May 15, 2006. Marine Corps Order (MCO) 5100.8. http://www.marines.mil/News/Publications/MCPEL/Electronic-Library-Display/Article/899091/mco-51008/. Accessed October 12, 2017.

22.   Navy Bureau of Medicine and Surgery. Navy Radiation Health Protection Manual. Washington, DC: BUMED; February 2011. NAVMED P-5055. http://www.med.navy.mil/directives/Pub/5055%20(Feb%202011).pdf. Accessed August 25, 2016.

23.   The Occupational Safety and Health Act of 1970. Pub L 91-596, with amendments. December 29, 1970.

24.   Commandant of the Marine Corps. Marine Corps Safety Program. Washington, DC: Headquarters, UCMC; July 28, 2011. Marine Corps Order (MCO) 5100.29B. http://www.marines.mil/Portals/59/Publications/MCO%205100.29B.pdf. Accessed September 21, 2017.

25.   Navy and Marine Corps Public Health Center website. Forward deployable preventive medicine unit (FDPMU). http://www.med.navy.mil/sites/nmcphc/expeditionary-platforms/fdpmus/Pages/default.aspx. Accessed August 25, 2016.

26.   Navy Bureau of Medicine and Surgery. Mission and Functions of Navy and Marine Corps Public Health Center and Its Subordinate Commands. Washington, DC: Department of the Navy; October 16, 2008. BUMEDINST 5450.157B. http://www.med.navy.mil/sites/nmcphc/Documents/policy-and-instruction/Governance-and-National-Health-Initiatives/BUMEDINST_5450_157B.pdf. Accessed August 25, 2016.

27.   Navy Bureau of Medicine and Surgery. Bureau of Medicine and Surgery Safety and Occupational Health Program. Washington, DC: BUMED; June 2015. BUMEDINST 5100.19F. http://www.med.navy.mil/directives/ExternalDirectives/5100.13F.pdf. Accessed September 21, 2017

28.   Navy and Marine Corps Public Health Center. Medical Surveillance Procedures Manual and Medical Matrix. 11th ed. Portsmouth, VA: NMCPHC; July 2011. Technical Manual NMCPCH-TM OM 6260.

29.   Navy and Marine Corps Public Health Center. Navy Medical Department Hearing Conservation Program Procedures. Portsmouth, VA: NMCPHC; September 2009. Technical Manual NMCPHC-TM 6260.51.99-2.

30.   Department of Veterans Affairs. Fiscal year 2013 Annual Benefits Report. http://www.benefits.va.gov/REPORTS/abr/ABR_FY_13.asp. Accessed August 25, 2016.

31.   29 CFR, Part 1910.95. Occupational noise exposure.

32.   Navy and Marine Corps Public Health Center. Best Practice Guidelines for Hearing Conservation Program Management. Portsmouth, VA: NMCPHC; March 2007. http://www.med.navy.mil/sites/nmcphc/Documents/oem/best-practices-hcp.pdf. Accessed August 25, 2016.

33.   Navy and Marine Corps Public Health Center. Occupational Health Program Evaluation Guide (OHPEG). Portsmouth, VA: NMCPHC; August 2009. http://www.med.navy.mil/sites/nmcphc/Documents/policy-and-instruction/oem-occupational-health-program-evaluation-guidance.pdf. Accessed August 25, 2016.

Chapter 4

THE EVOLUTION OF OCCUPATIONAL MEDICINE PRACTICE IN THE US NAVY

PAMELA L. KRAHL, MD, MPH*; BRIAN RILEY, DO, MPH†; and RICHARD J. THOMAS, MD, MPH‡

INTRODUCTION

THE COLONIAL NAVY: BASIC CARE FOR SAILORS AND MARINES

Preventive Care

Pre-Employment Physicals

THE NEW US NAVY AND FOUNDATIONS OF NAVY OCCUPATIONAL MEDICINE

Dr Edward Cutbush: A Medical Pioneer in the New Navy

The Screening of Recruits

Steam-Powered Ships: More Capable and More Dangerous

THE NAVY IN THE 20TH CENTURY: INCREASING HAZARDS

The Advent of Navy Flight Medicine and Dive Medicine

Care for Occupational Injuries and Illnesses in Civilian Employees

World War I: Need for Occupational Health Programs Is Recognized

World War II: Comprehensive Navy Occupational Health Programs

The Navy and Marine Corps Public Health Center

NAVY OCCUPATIONAL AND ENVIRONMENTAL MEDICINE TODAY

SUMMARY

*Captain, Medical Corps, US Navy; National Capital Consortium Occupational and Environmental Medicine Residency Program Director, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20817

†Commander, Medical Corps, US Navy; Occupational Medicine Department Head, Naval Branch Health Clinic, 881 USS James Madison Road, Kings Bay, Georgia 31547

‡Captain (Retired), Medical Corps, US Navy; Associate Professor, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20817

That men are exposed to particular diseases from the occupations which they follow, is a fact well known; but to remedy this evil, is a matter of some difficulty.

…

SAILORS may also be numbered amongst the laborious. They undergo great hardships from change of climate, the violence of weather, hard labour, bad provisions &c. Sailors are of so great importance both to the trade and safety of this kingdom, that too much pains can never be bestowed in pointing out the means of preserving their lives.[1]

—William Buchan, 1785

INTRODUCTION

Dr. William Buchan (1729–1805) was a Scottish physician who practiced in England and Scotland. His medical textbook, Domestic Medicine,[1] was widely republished in North America during the period of the American Revolution and the formation of the new United States of America. Buchan clearly understood and succinctly described the occupational challenges of those who man ships.[1] The evolution of occupational medicine practice in the US Navy is inextricably linked to the service’s history of medical support. This chapter will describe the history of medical support to the US Navy and how today’s practice of occupational and environmental medicine in the Navy evolved from these early foundations.

THE COLONIAL NAVY: BASIC CARE FOR SAILORS AND MARINES

The American colonies emerged in the maritime tradition of the British Royal Navy and the strong tradition of civilian sailors of the United Kingdom. The first civilian shipyard to build warships in North America opened in 1690, when HMS Falkland was constructed for the British Royal Navy. This shipyard was located in the Piscataqua River Estuary between New Hampshire and Maine, near the current location of the US Naval Shipyard in Portsmouth.2,3 Early medical care of sailors in the colonial Navy mirrored that of the British Royal Navy. The underpinnings of what would become naval occupational medicine were first documented in 1617 by the “father of marine medicine,” John Woodall (1569–1643), when he wrote about his experiences at sea and the impact of the seafaring life on the health of the men.[4]

Prior to the Revolutionary War, a medical contingent of a surgeon, surgeon’s mate, or both, was employed onboard due to the length of voyages between the various colonies in the new world and for voyages across the Atlantic Ocean.[2] Congress established the colonial Navy in October 1775, and the Marines one month later, in November 1775.5,6 The naval forces of the insurrection against King George III and his British government consisted of three types of vessels: privateers authorized by letters from the Continental Congress, civilian merchant ships converted into warships, and ships commissioned by the colonies (such as the Board of War of the State of Massachusetts Bay) or by the Continental Congress.[7]

The eventual US Navy Medical Department began with a small number of surgeons, assistant surgeons, and surgeon’s mates who were either hired by local advertisement or reassigned from Army units (possibly seeking better working conditions than the care of the sick and injured in the field). John Adams of Massachusetts, a signer of the Declaration of Independence and second president of the United States, played a role in adopting regulations from the British Royal Navy for the organization of US Navy ships. These regulations were published as “Rules for the Regulation of the Navy of the United Colonies of North-America” on November 28, 1775.[8] Article 11 specifically called for the assignment of a surgeon’s mate, and Article 16 delineated that a “convenient place shall be set aside for sick or hurt men … when the surgeon shall advise.”[8] In Naval and Maritime Medicine During the American Revolution,[2] Dr. Maurice Bear Gordon describes the meager training of the men who fulfilled these roles, only a fraction of whom had formal medical education in either North America or England. In 1775 Dr. John Jones of New York published the first American surgery text, a pamphlet titled “Plain, Concise, Practical Remarks on the Treatment of Wounds and Fractures,”[9] which was widely used in the war by surgeons of the Continental Army and Navy.[2]

Gordon summarized the diaries of four physicians who served as ship surgeons during the American Revolutionary War.[2] One of them, Dr. Ezra Green of Massachusetts, served in both the Continental Army and Navy. His extensive diaries chronicle his time serving as surgeon on the Ranger, an 18-gun Continental Navy sloop commanded by Captain John Paul Jones. Gordon speculates that Greene was personally appointed by Jones, who “had authority from the Continental Congress to appoint his officers, both commissioned and warrant.”[2] Historical records of the names of 136 men who served as surgeons in the American Navy[2] overlaps somewhat with a list published in an 1876 monograph by J.M. Toner[10] of “nearly twelve hundred” physicians who served in the Medical Department of the Continental Army.

Preventive Care

The primary duties of the surgeon and his staff were to provide the crew with daily sick-call and the emergent care of wounds that resulted from the inherent dangers of life at sea, in port, or from combat. Sailing ships required large crews to keep the ship sailing, and although preventive medicine and occupational medicine were not practiced by name in the Navy at that time, their underlying principles were a critical part of the mission of the surgeon and his staff. As an example, scurvy was a major health threat for the crews of these sailing ships. Dr James Lind determined that the use of lemon juice could control scurvy in sailors in his Treatise of the Scurvy in 1753. But perhaps because he was “an undistinguished physician in the eyes of his contemporaries, the naval medical service being on the lowest rung of the professional ladder,”[11] it was not until nearly 50 years later that Sir Gilbert Blane succeeded in convincing the Royal Navy to adopt the policy of regular administration of lemon or lime juice.[2] Perseverance in advocating for preventive measures remains a fundamental characteristic of preventive medicine practice, including in the Navy.

Pre-Employment Physicals

A historical antecedent to the 20th century occupational medicine concept of pre-employment physicals can be found as early as 1783 in the instructions of the Maryland commissioners of ships. The parameters for successfully enlisting into this component of the fledgling American Navy included being able bodied and without any abnormalities of the limbs; in good health without hernias or other visible infirmities; taller than 5 feet, 4 inches; and between the ages of 16 and 50 years.[2] No surviving documents describe whether examinations for these qualifications were regularly performed or document what percentages of potential sailors were disqualified.

THE NEW US NAVY AND FOUNDATIONS OF NAVY OCCUPATIONAL MEDICINE

According to the Naval History and Heritage Center website:

Over the course of the War of Independence, the Continental Navy sent to sea more than fifty armed vessels of various types. The navy’s squadrons and cruisers seized enemy supplies and carried correspondence and diplomats to Europe, returning with needed munitions. They took nearly 200 British vessels as prizes, some off the British Isles themselves, contributing to the demoralization of the enemy and forcing the British to divert warships to protect convoys and trade routes. In addition, the navy provoked diplomatic crises that helped bring France into the war against Great Britain.[12]

But following the Revolutionary War, the humble experiment of a Continental Navy to support and defend the American colonies came to a close with the sale of Alliance, the Continental Navy’s last vessel, in 1785.[13]

The US Navy was reborn 5 years after the formation of the United States in 1789, when the Congress of the United States commissioned six new frigates, of which only three were completed and manned.[14] From the beginning, these vessels were authorized to have a medical department. The Naval Armament Act of 1797 authorized the completion of three additional frigates: the United States, the Constitution (Figure 4-1), and the Constellation, and also specified the guidelines for compensation if a sailor or marine was wounded or disabled while serving in the line of duty.

Figure 4-1. The USS Constitution, launched October 21, 1797, and authorized by the Naval Act of 1794, was one of the three original frigates of the US Navy and is today the oldest commissioned warship afloat. Boston Harbor, MA, August 29, 2014.
Reproduced from: http://www.navy.mil/management/photodb/photos/140829-N-XP344-282.JPG.

Thus, by the 1790s the following basic tenets of military public health were in place:

- medical personnel assigned to defined roles in the operational and support forces, and recognized as important to the mission and welfare of the fighting forces;

- pre-employment screening;

- treatment of illness and injury at the worksite for sailors and marines (though not for civilian workers);

- methodologies to study the risk factors for morbidity and mortality;

- prevention of disease and injury; and

- compensation for sailors or marines injured on the job and no longer able to work (again, not for civilian workers).

The life and practice of a Naval surgeon in the early 19th century was illuminated in 1979 by a fortuitous discovery at the USS Constitution Museum, located at the former Charlestown Naval Yard (now called the Boston Historical Park). Dr J. Worth Estes of Boston University discovered the medical records that Dr Peter St. Medard penned during his cruise aboard the frigate New York from 1802 to 1803. St. Medard’s meticulous records provide an unparalleled view of the injuries, illness, and care of sailors during this era.[13] After his cruise on the New York, St. Medard attained a position as a surgeon at the Charlestown Navy Yard.

The Navy Yard was opened in Charlestown, Massachusetts, after Secretary of the Navy Benjamin Stoddert purchased tracts of land in six cities for shipyards in 1801. During the War of 1812, the Charlestown Navy Yard completed the Navy’s first ship-of-the-line, the 74-gun Independence.[15] A surgeon and surgeon’s mate were assigned to each yard for the care of sailors assigned to the ships “in ordinary,” referring to ships that were taken out of service during periods of relative inactivity and maintained by a skeleton crew and civilian yard workers. The surgeon was responsible for care of the sailors and marines assigned to the yard, as well as “any workman who was injured or taken sick in the yard.”[14] Thus, by 1804, the additional element of onsite treatment of illness and injury for civilian workers was added to the US Navy’s occupational health program.

Doctor Edward Cutbush: A Medical Pioneer in the New Navy

Surgeon Edward Cutbush (1772–1843) embodied the Naval surgeon’s dual responsibilities to maintain the combat strength of the ship and the individual health of the crew during his 30-year naval career, which spanned from 1799 to 1829.[16] Cutbush graduated from what is now the University of Pennsylvania in Philadelphia as a medical doctor at age 22. Two formative experiences in his early medical training in the 1790s influenced his later career. The first was his care for wounded soldiers, both French and British, who were brought to Philadelphia after a sea battle off the coast of Delaware, which was facilitated by his fluency in French as well as English. The second was his arduous work among the quarantined patients and staff of the Pennsylvania Hospital in the center of Philadelphia during a yellow fever outbreak. This service brought him commendation from the City of Philadelphia.[17]

Cutbush subsequently served with the Pennsylvania militia, including a brief tour as surgeon general during the Whiskey Rebellion of 1794.[10] He began his naval career by applying in writing to the secretary of the Navy for a position, and he was appointed in 1799. He served aboard the frigate United States as a surgeon and quickly convinced the captain to vaccinate the crew against smallpox using Edward Jenner’s method.[18]

In 1804 Cutbush sailed on the frigate President and was sent ashore in Italy to establish the first overseas US Naval hospital for care of sick and injured sailors of the US Navy Mediterranean Squadron who were too ill or injured to remain at sea. Using ingenuity and resourcefulness, he established this hospital in the city of Siracusa on the island of Sicily.

Cutbush returned to duty at the Philadelphia Naval Shipyard in 1807. Based on his experiences with both the Army and Navy, Cutbush and his former teacher, Dr Benjamin Rush of the University of Pennsylvania (a signer of the Declaration of Independence in 1776 and a founder of the Pennsylvania Hospital), published one of the first American treatises on the medical care of military personnel: Observations on the Means of Preserving the Health of Soldiers and Sailors; and on the Duties of the Medical Department of the Army and Navy: with Remarks on Hospitals and their Internal Arrangement.[19]

In 1813, Cutbush left the Philadelphia Naval Shipyard for duty in Washington, DC. There he served as advisor to the secretary of the Navy on medical matters while simultaneously serving as the senior medical officer of the Washington Navy Yard. Cutbush was among a group of senior surgeons who developed a formal training program for new Naval surgeons and surgeon’s mates in Philadelphia and established a board of medical examiners. He also was involved with the precursors of the Smithsonian Institution and George Washington University School of Medicine, and after over 30 years of service to his country, was instrumental in the formation of the Geneva Medical College, now known as the State University of New York Upstate School of Medicine.

By the time of his retirement in 1829 at age 57, Edward Cutbush’s career exemplified many of the qualities of a successful US Navy occupational medicine physician even today:

- strong academic credentials;

- the ability to serve in precarious medical conditions, including being quarantined among the sick;

- service to the fleet on operating ships and to the civilian personnel who maintained ships in shipyards;

- the ability to develop new solutions for challenges as they emerge, such as the first overseas US Naval hospital and the formation of the board of medical examiners;

- publishing medical findings to advance the discipline of military medicine;

- serving as a senior medical officer at an installation;

- advising the senior line leadership of the Navy; and

- teaching new Navy personnel as well as maintaining an academic association with civilian colleagues.

The Screening of Recruits

G.R.B. Horner, MD, a graduate of the University of Pennsylvania School of Medicine, thoroughly described the duties and resultant diseases and injuries of seamen in 1854. Horner devoted a chapter of his book to the process of examination of young men who wished to join the US Navy and Marine Corps in a variety of positions including, “seaman of any grade, marines, warrant and commissioned officers.”[20] At the time of Horner’s description of the diseases and injuries of sailors, though, the majority of Navy ships were still powered by sail. In the 1874 Report of the Navy Surgeon General, Surgeon James Kleghorn (1838–1909) described the ongoing difficulties of screening suitable candidates for the fleet and the Marines. The dire work conditions of a receiving ship (Figure 4-2), with cramped spaces and poor lighting, did not make the difficult task of discerning who was “the deceptive recruit” any easier, in the words of Kleghorn.[21]

Hospital care for Navy and Merchant Marine sailors and marines began with the Seaman’s Sickness and Disability Act of 1798. These naval personnel had funds deducted from their pay (starting at 20 cents per month) to support this care.[2] The manning and organization of ship’s medical departments changed little between 1798 and the formation of Navy Bureau of Medicine and Surgery (BUMED) in 1842.[22] A professional Medical Corps for the US Navy with uniformed officers would emerge in 1871, followed by the Hospital Corps (1898), Nurse Corps (1908), Dental Corps (1912), and Medical Service Corps (1947).

Figure 4-2. Spar deck of USS Independence while it was in use as a receiving ship in the early 1900s at Mare Island Navy Yard, California. Note hammocks stowed atop the bulwark, light guns installed in some of the gun ports, and the large wooden roof.
Photo courtesy of Naval History and Heritage Command, catalog no. 52636. Donation of Rear Admiral Ammen Farenholt, Medical Corps, US Navy.

Steam-Powered Ships: More Capable and More Dangerous

The development of steam-powered ships is considered the greatest technological advance in the history of the Navy.[23] Visionaries such as Commodore Matthew Perry pushed for the development of steam-powered ships, which advanced from small prototypes developed as early as the War of 1812 to later large side-wheelers. The USS Princeton was commissioned in 1843 as the first propeller-driven, steam-powered warship and carried the largest naval gun in the world, the “Peacemaker.” During a demonstration of the “Peacemaker” for dignitaries including President John Tyler on February 28, 1844, the gun exploded, killing six people, including Secretary of the Navy Thomas Gilmer, Secretary of State Abel Upshur, and Captain Beverly Kennon, the chief of the Bureau of Construction and Repair (Figure 4-3). Investigation of the disaster led to the development of new techniques for constructing stronger, more structurally sound cannons.[24]

This event was a fitting start to this new era of steam-powered ships, which placed sailors in harm’s way due to a multitude of new hazards such as heat, noise, fuel fires, and moving equipment. Although the March 1862 battle between the ironclads USS Monitor and CSS Virginia (converted from the former USS Merrimac that had been scuttled in Portsmouth, VA) tactically came to a draw, the damage and sinking of adjacent Union sailing ships by the CSS Virginia in Hampton Roads, Virginia, signaled the eventual end of the era of sailing warships in the US Navy. Over the remainder of the 19th century, the fleet would shift to steam power, with the majority being steam powered by the late 1880s.[25]

THE NAVY IN THE 20TH CENTURY: INCREASING HAZARDS

After the Civil War, interest in maintaining a standing Navy decreased, and in 1877 the strength of the US Navy reached a low point of 8,609 men, only 21 percent of the Civil War peak of 43,787 in 1864. Influenced by the writings of Albert Thayer Mahan and others, the country began to realize the need for the United States and its Navy to have the ability to project sea power as a military force in defense of national interests and maritime trade anywhere in the world. The first steam-powered cruisers were launched in the 1880s, and the first dreadnaughts (battleships), USS Texas and USS Maine, joined the fleet in 1895.[25]

Figure 4-3. “Awful Explosion of the ‘Peace-Maker’ on board the U.S. Steam Frigate Princeton, on Wednesday, 28th Feby. 1844.” Lithograph published by N. Currier, New York, 1844. It depicts the explosion of a heavy gun on board USS Princeton, in the Potomac River, which killed or mortally wounded seven and injured about twenty people. Some of those present are identified below the image, including (from left): Mr. Wilkins; Mr. Perrine; Lieutenant Hunt; Representative Virgil Maxcy of Maryland; Secretary of State Abel P. Upshur; Captain Beverly Kennon, chief of the Bureau of Construction, Equipment and Repair; Thomas Gilmer, secretary of the Navy; Captain Robert F. Stockton; sailors; Senator Phelps and Senator Thomas Hart Benton. Maxcy, Upshur, Kennon and Gilmer were among those killed. Stockton and Benton were among the injured.
Courtesy of the US Navy Art Collection, Washington, DC; US Naval History and Heritage Command photograph, catalog no. NH 58906-KN.

England sparked a naval arms race with its launch of the “world’s most powerful battleship,” the HMS Dreadnaught, in 1906.[26] The United States, along with Germany, Japan, and other countries, responded by building increasingly larger and more heavily armed warships, starting with the USS Michigan on May 26, 1908.[27] Other advances followed quickly, and these changes further shaped the Navy Medical Department.

The study of the diseases of workers related to naval shipbuilding and duty onboard ships at sea became more scientific with the publication of annual reports of the Navy surgeon general beginning in 1907. The same year, the first numbered volume of the Bulletin of the Naval Medical Department appeared, described as “relating to hygiene, tropical and preventive medicine, pathology, laboratory suggestions, advanced therapeutics, surgery, medical department organization for battle, new methods of treatment, and all other matters of more or less professional interest and importance under the conditions peculiar to the service and pertaining to the physical welfare of the naval personnel.”[28] By the time the third volume was published in 1909, Navy medical officers in the fleet and at shore stations made regular contributions regarding treatment and preventive strategies for occupational injuries and illnesses. For example, hearing loss in boiler tenders and gunners’ mates was an “accepted way of life”[29] prior to a 1909 study of early hearing protection efforts such as the Elliot hearing protector, Plasticine flexible inserts in the US Navy, and Antiphon (a German invention) flexible inserts in the British Royal Navy.[30]

The Advent of Navy Flight Medicine and Dive Medicine

The advent of military aviation and the submarine force required military medical professionals to develop new medical research technology and treatment regimens for both preventive and curative aspects of these specific fields of military medicine. BUMED Circular Letter 125221 defined the first physical requirements for prospective naval aviators.[31] In July 1922, eight US Navy medical officers reported to flight training at Naval Air Station Pensacola, and four had already completed the flight surgeon’s course at the US Army Technical School of Aviation Medicine at Mitchell Field, Long Island, New York, in November 1921. The eight officers were subsequently designated the US Navy’s first flight surgeons. Qualifications for flight surgeons were formalized on November 14, 1924, that required completion of the 3-month Army course, as well as 3 months of “satisfactory service with a Naval Aviation unit before designation.”[32] The interservice agreement with the Army for providing aviation medicine training ended on January 18, 1927, with the establishment of the Aviation Section of the Naval Medical School in Washington, DC. Flight surgeons have served continuously since then (Figure 4-4).

Although professional diving is documented as early as the 5th century BCE, the 18th and 19th centuries brought experiments with new forms of diving bells and submersible vehicles in Europe and the United States.[33] The physiology of extreme atmospheres in relation to both caisson disease in workers building supports for bridges and the medical experiences of submariners led to manuscripts written by Navy medical officers starting in 1916.[34] The first US Navy diving school opened in 1915, and the Navy’s famous Experimental Diving Unit was established in 1927. US Navy helium-oxygen diving experiments began in the l930s, and the mixed gas was first used extensively in the rescue of 33 sailors trapped on the stricken submarine USS Squalus and its subsequent salvage from a depth of 243 feet in 1939 (Figure 4-5).[35]

Figure 4-4. Flight surgeon and two hospital corpsmen (white caps and jerseys with red crosses) at their flight station in the starboard catwalk, amidships, on a training escort carrier, during World War II. They stand ready with medical kits, stretcher, blankets and other emergency gear.
Photo courtesy of the National Archives and Records Administration, catalog no. 80-G-K-2618.

Care for Occupational Injuries and Illnesses in Civilian Employees

Prior to the current federal and state workers’ compensation laws, injured employees who needed a doctor’s care had only a slim possibility of winning a civil tort action in court. But a century before these laws, sailors, marines, and civilian workers assigned to ships out of service (“in ordinary”) or to naval shipyards received medical care for immediate injuries from medical officers.[14] Based on a European model, the first workers’ compensation law for federal employees was passed in 1882. This law provided compensation for employees or survivors of members of the US Life Saving Service (now called the US Coast Guard) who were disabled or killed in the line of duty.[36] Workers’ compensation legislation for civilian employees at the state level began in Wisconsin in 1911.[37] Two important federal acts followed and are the basis of the modern system for care of occupational injuries for civil service and non-appropriated fund workers: the Federal Employees’ Compensation Act of September 7, 1916 (5 USC 81), and the Longshore and Harbor Workers’ Compensation Act of 1927 (33 USC 901–950). The US Navy’s occupational health policies paralleled these advances in legislation, and by 1914, the Manual for the Medical Department of the United States Navy clearly delineated several additional facets of occupational medicine: initial and periodic physical examinations related to Navy yard service, compensation for injury, prevention of eye injuries, and medical standards for acceptance or rejection of applicants.[38]

Figure 4-5. McCann rescue chamber in the water alongside the USS Falcon (ASR-2) during the rescue of 33 men still alive and trapped in the sunken submarine Squalus, off the New Hampshire coast, circa May 24–25, 1939. The submarine sank when the main induction valve in the engine room stuck in the open position, flooding the after compartments when it submerged.
Photo courtesy of the National Museum of the US Navy, US Naval History and Heritage Command Photograph Collection.

World War I: The Need for Occupational Health Programs Is Recognized

With the United States’ entry into World War I in April 1917, mass-production of cargo and transport ships became an immediate priority. The federal government formed the Emergency Fleet Corporation to build these ships. The largest shipyard in the world at that time was Hog Island, near Philadelphia, which launched a ship every 5 1/2 days at the peak of production. Many of Hog Island’s 30,000 workers had no previous factory experience.[39]

Initial safety and occupational health services in these shipyards were directed to the care of civilian workers’ injuries and the abatement of the numerous safety hazards causing them. These rudimentary programs aimed to keep the workforce on the job, but were largely ineffective and considered to be an impairment to the war effort. By 1917 the amount of lost-time injuries and associated costs prompted the federal workers’ compensation program administrator to request inspections of several Navy shipyards.[29]

As the war wound down, the need for robust occupational medicine programs for the civilian workforce became clear, and these comprehensive programs were beginning to take shape. Starting in 1917, safety engineers were assigned to the shipyards, with full-time medical officers following in 1922. Under the leadership of Dr Robert Jones, the preventive medicine division at BUMED incorporated occupational health practices, recommending job-specific pre-employment physical examinations and periodic examinations based on occupational exposures such as asbestos, silica, and lead. For instance, a 1922 issue of the United States Naval Bulletin contained an article called “Occupational Hazards and Diagnostic Signs: A Guide to Impairments to Be Looked for in Hazardous Occupations.”[40] In 1923, Lieutenant Linwood Smith, a physician from the Boston Naval Shipyard clinic, completed a postgraduate program at the Harvard School of Public Health, becoming the Navy’s first formally trained physician in occupational health.[41]

At the Philadelphia Naval Shipyard in 1925, Dr Ernest Brown conducted a pioneering survey of lead poisoning in welders that included clinical assessment, evaluation of work practices, environmental sampling, and the development of hazard control strategies such as changes in work practice and adaptation of respiratory protective equipment. Brown would go on to present “Industrial Hygiene and the Navy in National Defense”[42] at the fifth annual meeting of the Air Hygiene Foundation of America in New York in 1940. This work describes the organization and functions of the New York Navy Yard’s medical department. Consisting of ten medical officers, five dental officers, one nurse, forty-five enlisted men, and two civilian clerks, the department’s chief activities were pre-employment, periodic, and retirement physical examinations, with special emphasis on crane operators, engine men (hoisting and portable), and locomotive engineers; the diagnosis, treatment, and disposition of industrial injuries and occupational diseases; the administration of compensation cases; and industrial hygiene and plant sanitation. Duties are described for the industrial medical officer and the safety engineer, including guidance on conducting industrial hygiene surveys and reporting industrial accidents and illnesses. Brown also named thirteen occupational hazards found in US Navy yards, including silica, lead, metal fumes, and asbestos.

World War II: Comprehensive Navy Occupational Health Programs

The lessons learned about how to mass-produce ships during World War I set the stage for shipbuilding in advance of World War II. At the time of the attack on Pearl Harbor in 1941, eight naval shipyards were hurriedly building America’s “two-ocean Navy.”[43] Eighteen new shipyards were later added just to mass-produce cargo ships (known as “Liberty” ships), and the number of American shipyard workers increased exponentially from 168,000 in 1940 to 1,772,000 by November 1943. The high turnover rate of the workforce meant that the total number of workers exposed to the shipyard environment was even higher. As the intensity of the war effort exploded, the inexperienced and untrained new laborers faced demanding production rates in the shipyards. They worked in an often dangerous environment while performing unfamiliar industrial processes, such as electric arc welding, with potentially harmful health effects.[44]

The Navy’s small team of occupational medicine physicians had diligently evaluated both military operational and civilian working environments between World War I and World War II. But the need to dedicate additional resources for occupational health programs to support the war effort was clear, and the secretary of the Navy allocated 1% of the payroll toward developing and expanding occupational medicine services at the shipyards.[43] Rear Admiral Charles Stephenson, in charge of preventive medicine at BUMED, developed a comprehensive strategy for occupational health services, complete with marketing posters. These occupational health services were based on the framework described by Brown in 1940, which included pre-employment examinations, injury care, medical surveillance of known occupational health hazards, and industrial hygiene field surveys.[29] Safety and medical departments were established at each shipyard, with the medical department led by a medical officer reporting directly to the shipyard commander. The first industrial hygiene offices were established within these shipyard medical departments, and filled with newly commissioned officers, the US Navy’s first industrial hygienists. These officers were fresh from courses at the Harvard and Columbia schools of public health, where they trained alongside Navy medical officers completing occupational medicine master’s degree programs.29,43

Medical officers provided health examinations and concentrated efforts on the treatment of numerous eye, hand, foot, and head injuries; illnesses such as silicosis, lead poisoning, and metal fume fever; and effects of other known toxic hazards such as carbon monoxide, chromium, mercury, cyanide, and solvents. Less attention was paid to noise and asbestos exposure until the late 1950s. Although asbestosis was a known occupational hazard, studies conducted in the shipyards at that time erroneously concluded that asbestos was relatively safe.29,43

The end of World War II signaled the beginning of the “nuclear age,” and with it new types of specialists joined the occupational health team: radiation health officers and radiation specialist officers. Originally, their primary duties were to provide radiation safety and biology support to the nuclear weapons testing program, but these duties soon expanded as the Navy developed radiation control practices for nuclear powered ships, conducted radiobiology research, and expanded clinical applications of radioisotopes and radiography. Corpsmen received new training in ionizing radiation when assigned to duties onboard nuclear submarines and as nuclear medicine technicians, and physicians attended a new nuclear medicine course. Since 1946, Navy personnel occupationally exposed to ionizing radiation have been monitored to ensure recommended exposure limits are not exceeded. Additionally, radiation physical exams have been required in some form since 1951.[45]

In the early to mid-1950s, toxicology also garnered additional interest from BUMED. Two shipboard explosions, on the USS Leyte Gulf and the USS Bennington, were linked to hydraulic fluids that were both explosive and flammable. But the search for a safer hydraulic fluid led to unanswered questions about toxicity of the proposed substitutes. Around that time, initial trials of the USS Nautilus, the first nuclear-powered submarine, showed that the scrubbers in its atmospheric control plant contaminated the air with monoethanolamine, which threatened to limit the duration of submerged operations. However, little information about the health effects of continuous exposure to air contaminants over long periods of time existed on which to make decisions. Inquiry into these two issues led BUMED to begin planning for an operational toxicology and health engineering unit in early 1957. In January 1959, the secretary of the Navy formally established the US Navy Toxicology Unit to rapidly conduct toxicologic investigations and research in response to fleet requirements.[46]

The Navy and Marine Corps Public Health Center

Recognizing the need for occupational health programs encompassing all fleet readiness and training ordnance field activities, in 1964 the Navy Bureau of Weapons directed the senior medical officer at Naval Ammunition Depot Crane, Indiana, to coordinate efforts at all Naval ammunition depots and Naval stations and established the Naval Ordnance Systems Command Environmental Health Center. By 1971, this function was consolidated under BUMED as the Navy Industrial Environmental Health Center (NIEHC). This command was described in a 1976 edition of Environmental Research:

This organization is located in Cincinnati, Ohio, and is being developed as a prime coordinator for occupational and environmental health programs. This center is staffed with occupational health physicians, industrial hygienists, chemists, engineers, and a nurse. This group provides field support and consultative services to Regional Medical Officers and other Commands on request. Their services include in-depth and specialized industrial hygiene and occupational health evaluations and analyses. They have an additional mission to ensure the wide dissemination of pertinent information on occupational and environmental health having Navy significance. NIEHC provides assistance to BUMED in education and training. NIEHC also serves as the third-year residence training for Navy occupational health physicians.[43]

The requirement for an integrated computer system to assist the Navy with compliance with the Occupational Safety and Health Act of 1970 was identified January 29-30, 1979, during a conference on Navy occupational health in Seattle, Washington:

The conference objectives were to consider organizational factors in the implementation of Navy occupational health programs, to address issues of cost effectiveness in Navy occupational health programs, and to facilitate the development of a meaningful research program in this area. Participants included operations and line managers, safety experts, industrial hygienists, epidemiologists, behavioral researchers, and physicians. Individual perspectives, viewpoints, and goals were diverse and often contradictory. The threads that bound the participants together were a deep commitment to improved occupational health care in the Navy and a clear conviction that the current occupational health program faces serious difficulties. The conference demonstrated the wealth of available expertise that can be brought to bear immediately on the Navy’s current occupational health problems. It also pinpointed several areas that require extensive research and development. Among the major areas in the latter group were epidemiological studies to identify additional hazardous agents in the work environment, development of environmental monitoring techniques, the design of training and reward systems that will increase compliance with sound occupational health practices, and the design of future work environments to minimize occupational health risks.[47]

BUMED subsequently tasked the Naval Health Research Center to develop this new, computerized occupational health monitoring system. After a review of commercially available systems failed to identify one that would meet the Navy’s requirements, a prototype system was developed and installed in June 1981 at Naval Aviation Depot North Island. This system was known as the Navy Occupational Health Information Management System (NOHIMS). An enhanced version, NOHIMS Version 2.0, added numerous occupational safety functions, as well as additional environmental and medical functions, and was rolled out in 1987.[48]

The primary objectives of the NOHIMS project were to provide comprehensive workplace monitoring and medical surveillance, and also to make this data available for trend analyses, epidemiologic studies, and program compliance monitoring.[49] Although NOHIMS was a short-lived project, its enduring legacy is the Navy’s Medical Surveillance Procedures Manual, known as the “Medical Matrix.” In support of NOHIMS, the Medical Matrix Committee was established and developed the first Medical Matrix, which continues to provide guidance for all personnel conducting medical surveillance and certifications in the US Navy and Marine Corps.

NAVY OCCUPATIONAL AND ENVIRONMENTAL MEDICINE TODAY

Today, about 40 active duty and 40 civilian occupational medicine physicians are assigned around the world, providing medical surveillance and certification exams, treatment of work-related illnesses and injuries, and other occupational health services to active duty sailors and marines and civilian Navy and Marine Corps employees. They work hand in hand with industrial hygienists, occupational health nurses and technicians, environmental health officers, safety professionals, audiologists, and line leaders and management to maintain the readiness of the Navy and Marine Corps civilian workforces, and provide consultative support in the medical surveillance and certification of active duty sailors and marines. The Navy and Marine Corps Public Health Center provides consultation and manages execution of multiple occupational and environmental health programs relevant to today’s practice, including asbestos medical surveillance, hearing conservation, radioactive material permitting, radiation dosimetry, blood-borne pathogen exposure, respiratory protection, Federal Employees’ Compensation Act case management, drug screening, health hazard assessment, and risk communication, as well as continued updates of the Medical Surveillance Procedures Manual (Medical Matrix).[50]

Areas of increasing focus for the occupational medicine community today are environmental health and disaster preparedness and emergency management. The future of Navy occupational and environmental medicine lies in the further development of the electronic medical record and information systems to better support the coordinated efforts of the occupational and environmental health team, as well as advancements in trend analyses and epidemiologic studies. As in 1979 and throughout the history of Navy medicine, the occupational medicine community continues to demonstrate a deep commitment to improved occupational healthcare in the Navy.

SUMMARY

Navy occupational medicine practice has evolved to support sailors, marines, and civilian employee from the US Navy’s sailing origins through the development of steam-powered ships, Naval aviation, submarines, and nuclear power. With these technological advances, occupational medicine practice has become increasingly comprehensive, scientific, and interdisciplinary. Despite these changes, the key mission of Navy occupational medicine remains unchanged: to support the readiness of the US Navy and US Marine Corps by preventing occupational illnesses and injuries in the workforce.

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32.   Grossnick RA, Armstrong WJ. United States Naval Aviation, 1910-1995. Washington, DC: Naval Historical Center, Department of the Navy; 1997.

33.   US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; April 15, 2008.

34.   McDowell R. Diseases incident to submarine duty. US Nav Med Bull. 1917;11:44–45.

35.   Phillips JL. The Bends: Compressed Air in the History of Science, Diving, and Engineering. New Haven, CT: Yale University Press; 1998.

36.   Szymendera S. Reviewing Workers’ Compensation for Federal Employees. Washington, DC: Congressional Research Service. May 12, 2011. http://edworkforce.house.gov/uploadedfiles/05.12.11_szymendera.pdf

37.   Wisconsin Department of Workforce Development. Timeline history: Wisconsin Industrial Commission. http://dwd.wisconsin.gov/dwd/dwdhistory/year_pages/wis_indstrl_comm.htm. September 9, 2016.

38.   US Navy Department Bureau of Medicine and Surgery. Manual for the Medical Department of the United States Navy. Washington, DC: Government Printing Office; 1914.

39.   Smithsonian Institution, National Museum of American History. On the water: answering the call, 1917–1945, building ships for victory. http://americanhistory.si.edu/onthewater/exhibition/6_2.html. Accessed September 9, 2016.

40.   Dublin LI, Leiboff P. Occupation Hazards and Diagnostic Signs: A Guide to Impairments to Be Looked for in Hazardous Occupations. Washington, DC: US Bureau of Labor Statistics, 1922. Bulletin 306.

41.   Gillooly PF, ed. History of Navy industrial hygienists. [unpublished monograph prepared for 50th anniversary of the formation of the Navy Medical Service Corps, Navy Department, Bureau of Medicine and Surgery, Washington, DC, 1997].

42.   Brown E. Industrial hygiene and the Navy in national defense. War Med. 1941(1):3–14.

43.   Lawton GM, Snyder PJ. Occupational health programs in United States naval shipyards. Environ Res. 1976;11(2):162–165. doi:10.1016/0013-9351(76)90071-2.

44.   Rieke FE. Lead intoxication in shipbuilding and shipscrapping, 1941 to 1968. Arch Environ Health. 1969;19(4):521–539. doi:10.1080/00039896.1969.10666879.

45.   George J, Yacovissi R, Thompson R. History of radiation health officers and radiation medical specialists of the Medical Service Corps, US Navy, 1947–2003. May 23, 2003. http://www.slideshare.net/brucelee55/30-may-1996doc. Accessed September 9, 2016.

46.   Review of the U.S. Naval Medical Research Institute’s Toxicology Program. Washington, DC: National Academies Press; 1994.

47.   Drexler JA Jr, Jones AP, Gunderson EKE, eds. Problems and Strategies of Implementing Navy Occupational Health and Safety Programs. Seattle, WA: Battelle Human Affairs Research Centers; San Diego, CA: Naval Health Research Center; 1979.

48.   Pugh WM, Beck DD. Preliminary Specifications for a Navy Occupational Health Information Monitoring System (NOHIMS). San Diego, CA: Naval Health Research Center; 1981. Report no. 21-36. http://oai.dtic.mil/oai/oai?verb=getRecord&metadataPrefix=html&identifier=ADA112661. Accessed September 9, 2016.

49.   Hermansen LA, Pugh WM. An Overview of the Navy Occupational Health Information Management System (NOHIMS). San Diego, CA: Naval Health Research Center; 1988. Report no. 88-14. http://oai.dtic.mil/oai/oai?verb=getRecord&metadataPrefix=html&identifier=ADa198163. Accessed September 9, 2016.

50.   Navy and Marine Corps Public Health Center. Our history. http://www.med.navy.mil/sites/nmcphc/about-us/Pages/our-history.aspx. Accessed September 9, 2016.

Chapter 5

US ARMY OCCUPATIONAL HEALTH PROGRAMS AND SERVICES

TIMOTHY M. MALLON, MD, MPH*; M. DEBRA PARKER, JD, MSN†; JENNYLYNN BALMER, RN, MPA‡; DAVID P. DEETER, MD, MPH¥; and JANET M. RUFF, RN, MPH§

INTRODUCTION

LAWS, REGULATIONS, AND GUIDANCE

Public Law 79-658

The Occupational Safety and Health Act

Federal Employees’ Compensation Program

Regulations and Guidance Applicable to Occupational Health

Occupational Health Business Plan

Marketing

Occupational Health Program Evaluation

ORGANIZATION OF THE ARMY’S OCCUPATIONAL HEALTH PROGRAM

Medical Center or Medical Activity Occupational Health Clinic

Army Health Clinic Occupational Health Program

Occupational Health Program Staffing

MEDICAL RECORDS MANAGEMENT

OCCUPATIONAL HEALTH PROGRAMS AND SERVICES

Medical Surveillance

Administrative Medical Examinations

Fitness-for-Duty and Disability Retirement Examinations

Worksite Evaluations

Health Hazard Education

Monitoring Absences Due to Illness

Immunizations

Epidemiological Investigations of Occupational Illnesses and Injuries

Health Promotion

Emergency Treatment of Illnesses and Injuries

SUMMARY

*Colonel (Retired), US Army; Adjunct Assistant Professor, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

†Colonel (Retired), US Air Force; formerly, Senior Occupational Health Nurse Consultant, Occupational and Environmental Health Portfolio, Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010

‡Occupational Health Nurse Consultant, Occupational and Environmental Health Portfolio, Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010

¥Lieutenant Colonel (P), US Army; Director, Occupational and Environmental Health, and Director, Occupational Medicine Residency Program, US Army Environmental Health Agency, Edgewood Area, Aberdeen Proving Ground, Maryland 21010-5422; formerly, Occupational Health Consultant to the Surgeon General

§Senior Occupational Health Nurse Consultant (Retired), Occupational and Environmental Medicine Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

INTRODUCTION

This chapter is being published as an update to Chapter 3, US Army Health Programs and Services, in the previous edition of this textbook.[1] Much of the chapter has been revised to reflect the new policies and programs that affect the occupational health program at the installation level. The references have been updated as well.

This chapter describes the Army Occupational Health Program (OHP), which promotes health and protects civilian and military personnel from workplace hazards. The OHP’s mission is to protect the health of the worker through prevention of injuries and illnesses; to ensure the organization complies with federal, state, and local laws; and lastly to keep workers’ compensation medical and disability costs as low as possible through prevention of workplace injuries and management of injured workers’ cases to ensure their timely return to work while minimizing long-term disability. For OHP to be effective, the senior leadership in the organization must actively support the program. The OHP manager must coordinate and communicate directly and frequently with other members of the safety and occupational health team, both internal and external to the organization and Army, to develop and maintain a successful program.

Soldiers frequently perform work separate from their combat duties, during which they encounter hazardous exposures similar to civilian exposures. In this context, the military must address the potentially harmful effects of soldiers’ work and work conditions, just as these are addressed for civilian employees in the federal government and private-sector workforce. The challenge for military occupational health is to work with commanders to ensure that soldier exposures are evaluated, that health risks are identified and prevented if possible, and that outcomes are documented in the soldier’s medical record.

Department of the Army (DA) civilian employees are eligible to be seen in the occupational health clinic for job-related health services including work-related immunizations, work-related injury and illness care, health promotion and wellness education, preplacement and post-hire physical examinations, periodic physicals, and disability retirement physicals. Civilian employees can be seen in the emergency room for emergency care and for minor non-occupational illnesses in Army Medical Department facilities. In deployed settings, federal civilian employees are eligible to use the military medical treatment facility (MTF) for work-related injuries and illnesses and emergency care.

In 1974, the Health Services Command stood up and took command and control of all installation clinics, nursing offices, and occupational health clinics. The responsibilities for managing civilian employee healthcare were assigned to Army preventive medicine services. In 1994, the Army Medical Department reorganized under the Army surgeon general, and the US Army Medical Command (MEDCOM) was formed. Under MEDCOM, there are currently four regional health commands (RHCs), two in the United States (Eastern and Central) and two outside the United States (Europe and Pacific). The Pacific RHC also encompasses Alaska, Hawaii, and Washington state. The four RHCs have command and control over the MTFs in their respective regions.

LAWS, REGULATIONS, AND GUIDANCE

Several laws and regulations protect the health and promote the effectiveness of all federal employees—military and civilian. The guidance provided is intended to serve as the professional minimum criteria for program performance to help occupational health providers and managers implement the OHP and self-assess their programs’ performance.

Public Law 79-658

The first law that authorized access to care for federal civilian employees was Public Law 79-658.[2] This law authorized federal agencies to establish health service programs to promote and maintain the physical and mental fitness of their employees, but it limited health services to the following:

- on-the-job illness and injury treatment,

- emergency dental care,

- physical examinations for employment, and

- health promotion services.

The Occupational Safety and Health Act

Public Law 91-596, the Occupational Safety and Health Act (OSHA),[3] requires that all employers provide a safe and healthy working environment for their employees. Executive Order 12196[4] requires that all federal agencies comply with the law. OSHA issued regulations under 29 CFR 1960,[5] Basic Program Elements for Federal Employee Occupational Safety and Health Programs, that require federal agencies to establish an occupational safety and health program. OSHA regulations under 29 CFR 1910[6] provide the legal requirements for medical surveillance regarding lead, noise, asbestos, and a number of other hazards. Another important OSHA regulation, 29 CFR 1904, Recording and Reporting Occupational Injuries and Illnesses,[7] establishes recordkeeping requirements for agencies. These are often difficult to meet, particularly the requirement for keeping records for 30 years past employment.

Federal Employees’ Compensation Program

The Federal Employees’ Compensation Act (FECA)[8] was passed in 1916. FECA provides medical and disability benefits to employees who have an injury or illness at work (see Chapter 9, Federal Workers’ Compensation Programs, for more detail). The law also includes death benefits for anyone who dies as a result of a work-related injury or illness. The Department of Labor’s Office of Federal Workers’ Compensation Programs administers FECA benefits, and its regulations are published in 20 CFR.[9] The Office of Workers’ Compensation Programs, through its Division of Federal Employees’ Compensation, has issued guidelines on filing FECA claims for employees and supervisors.10,11 Claims by non-appropriated fund employees who are injured on the job are managed by the Division of Longshoremen’s and Harbor Workers’ Compensation,[12] which handles workers’ compensation claims for employees paid with non-tax dollars. Department of Defense (DoD) regulations for FECA claims processing and program management are followed at the installation level.[13]

Regulations and Guidance Applicable to Occupational Health

DoD instructions direct implementation of the occupational safety and health program for military and civilian DoD employees. Guidance is defined in DoD Instruction (DoDI) 6055.01, DoD Safety and Occupational Health Program[14]; DoDI 6055.5, Occupational and Environmental Health[15]; and DoDI 6055.05-M, Occupational Medical Examinations and Surveillance Manual.[16] Army Regulation (AR) 40-5[17] and DA Pamphlet (PAM) 40-11,[18] both called Preventive Medicine, provide service-specific implementing instructions for healthcare providers regarding the preventive medicine program, including occupational medicine.

To ensure effective management of the OHP, staff must develop and maintain administrative documents. A good administrative structure is critical to providing effective occupational health services and managing the program. In addition to the laws and regulations that have already been discussed, other Army directives include (a) an installation occupational health regulation, (b) an OHP document, (c) standard operating procedures (SOPs), and (d) medical directives for occupational health nurses.

Installation Occupational Health Regulation

The installation occupational health regulation defines policy and guidance as it applies to a particular installation. This regulation should discuss the scope of the mission, including who is eligible for services within the occupational health clinic. It should spell out the responsibilities of occupational health, industrial hygiene, and safety staff; supervisors; and employees, both military and civilian. The regulation should be staffed through all the organizations listed above to ensure support for the regulation and make sure all stakeholders have visibility of the applicable requirements. Once the occupational health regulation is published, it must be kept current through annual or biennial reviews and updates. The occupational health provider and the occupational health nurse must contribute to any installation directive that involves occupational health, from its initial development through the staffing stages.

Program Document

Commanders of medical centers (MEDCENs) and Medical Department activities (MEDDACs) must take responsibility for the OHP document, which details the available occupational health services for the supported units. The program document should include performance goals for each program element, target dates for the accomplishment of each objective, and the methods planned to achieve the objective. The OHP status report (OHPSR) is the tool used to collect program performance data for each element of the OHP, and this data is collected from each installation for an annual performance assessment of the Army OHP. The OHP document should be part of the preventive medicine program document for the installation. The OHP manager and staff should review the document annually. The installation and MTF mission, priorities, and resources should drive the goals and objectives of the OHP document.

Frequently, the manager of the occupational health clinic will be called upon to (a) defend the program against reductions in the budget, personnel, and space; (b) justify requests for more resources; and (c) assure the commander that the clinic is contributing to accomplishment of the installation’s mission. An up-to-date, meaningful program document, representing both a plan for the future and a report on past performance, will be invaluable in these situations. The success of the OHP depends on having a well-developed program document and business plan, as well as highly motivated and resourceful occupational health staff who skillfully execute the mission. The quality of the program depends on a commitment to excellence and caring and compassionate providers who will ensure the health and wellbeing of the soldiers and civilian employees assigned to the installation. Further, the OHP manager must be able to convey information about the program’s quality to the senior installation and medical leadership using objective metrics of performance.

Standard Operating Procedures

The occupational health clinic benefits from having well-written SOPs that give detailed step-by-step operating instructions for accomplishing program-specific clinical tasks. The SOP, which is internal to the occupational health clinic, is designed to inform physicians, nurses, nurse practitioners, and physician assistants about routine procedures that standardize practice throughout the clinic. It serves as a training tool so that everyone is familiar with the scope and depth of practice expected for clinical encounters. The SOP is designed to help new providers quickly learn how things are done in the clinic, as well as providing continuity during staff and leadership changes. SOPs are valuable only when they are utilized, and they should be updated annually or more frequently if program elements change due to new OSHA, National Institute for Occupational Safety and Health, or Centers for Disease Control and Prevention guidance.

Medical Directives

The occupational medicine physician or primary care physician supporting the OHP manager can write medical directives that serve as written orders to the occupational health nurse for administering treatment. The directives are very specific, usually covering one type of encounter that details the extent of the history, physical exam, and treatment the nurse is authorized to perform. Medical emergencies do arise when the occupational medicine physician is not available, and the medical directives afford the occupational health nurse an opportunity to provide medical care during these incidents. Further, the medical directives permit occupational health nurses to perform medical screening and surveillance examination elements (blood draws, immunizations, etc) that do not require the presence of a physician.

Medical directives should be tailored to the scope of occupational health services provided at the installation and the competencies of the individual occupational health nursing staff. The directives should be prepared collaboratively by the physician, the occupational health nurse manager, and chief nurse of the MTF. The physician must ensure that the services provided are within the scope of the nursing license for the state and that the nurses are competent to provide the services before signing the directives. All parties who participate in the development of the medical directives should co-sign the final version. The medical directives should be reviewed annually by the occupational medicine physician and the occupational health nurse. It should be signed and dated after each review.

Occupational Health Business Plan

The OHP manager should develop a business plan that includes an assessment of the requirements needed to maintain worker health given the hazards at the worksite. The business plan should:

- state program mission and responsibilities,

- identify individuals and organizations covered by the program,

- determine the requirements of both individuals and organizations,

- ensure the OHP is capable of meeting mission requirements with existing resources,

- identify unmet needs for local OHP requirements,

- determine what additional activities and resources are needed to fulfill OHP requirements, and

- identify ways to obtain needed resources internal and external to the organization, including personnel, financing, supplies, and equipment.

Marketing

The marketing of occupational health services on the installation is necessary to provide visibility for the OHP and to make stakeholders aware of the potential benefits of using available services. It will also aid in predicting what future services will be needed by both management and employees. Through marketing, the OHP can reach out to identify customers’ needs and then develop a service that satisfies these needs consistent with the business plan. To satisfy the customers’ needs, the OHP manager must invest time and effort to understand:

- customers’ level of satisfaction with existing services,

- whether customers have any unmet needs for services,

- the best methods to provide these services,

- whether OHP resources allow for providing these services,

- the timeline for when the additional services may be provided, and

- who the bill payer will be for the additional services.

Marketing is a continuous, systematic process with formal and informal targets of opportunity. Visibility of the OHP can be increased through networking at professional organizations and participating in community activities and regular committees with safety and occupational health professionals. Most importantly, the OPH is marketed by demonstrating and documenting cost effectiveness and customer satisfaction, and communicating to all stakeholders that the OHP is an important and value-added service. OHP staff should take advantage of social media and use brochures that can be distributed to the human resources office, safety personnel, installation headquarters, and the commissary.

Occupational Health Program Evaluation

All federal agencies are required to collect occupational injury and illness data and record it in the OSHA 300 Log of Federal Occupational Injuries and Illnesses.[7] The installation’s safety officer usually has the primary responsibility for collecting data and maintaining the log. The safety officer must coordinate with occupational health staff and the installation compensation specialist to ensure that the data are complete. The safety office should report all of the following in the log:

- occupational illnesses,

- job-related injuries that resulted in death or disability,

- job-related injuries that caused employees to lose time at work (other than the day on which the injury occurred), and

- job-related injuries that require medical care.

A review of the OSHA log is one indicator of the effectiveness of the occupational health and safety programs.

AR 40-5[17] and DA PAM 40-11[18] require OHP managers to perform an annual OHP self-assessment and submit an annual OHPSR for their program to the OHP manager at the US Army Public Health Center (USAPHC). These documents also require an external program assessment every 3 years performed by the RHC, MEDCOM, or USAPHC. The use of annual self-assessments and triennial external evaluations offer standardized processes to evaluate the effectiveness of OHPs, identify strengths and significant problem areas, and set priorities for improvement.

ORGANIZATION OF THE ARMY’S OCCUPATIONAL HEALTH PROGRAM

The Army operates more than 80 occupational health clinics around the world. OHP needs vary from installation to installation, so the program’s structure and scope vary by location. Army occupational health clinics either work directly for MEDCOM, or they work for and support the Army Material Command (AMCOM).

When working under a MEDCEN or MEDDAC, an occupational health clinic is part of the preventive medicine service. When the clinic works on an installation supported by AMCOM, Training and Doctrine Command (TRADOC), or Forces Command (FORSCOM), it is part of an Army health clinic. MEDCOM Organization and Functions Regulation 10-1[19] prescribes the organization and functions of clinics under MEDCOM command. AR 40-1, Composition, Mission, and Functions of the Army Medical Department,[20] describes the operations of Army health clinics and occupational health clinics that are not under MEDCOM command and control. AR 40-5[17] provides additional guidance for the management of OHPs in both situations. AR 40-400, Patient Administration,[21] and AR 40-3, Medical, Dental, and Veterinary Care,[22] specify who has access to occupational health services and under what circumstances the occupational health clinic may provide care.

Medical Center or Medical Activity Occupational Health Clinic

When occupational health is part of the preventive medicine service, the chief of preventive medicine oversees and supervises the chief of occupational health. The OHP manager is responsible for the day-to-day operation of the administrative and clinical aspects of occupational health. The MEDCEN or MEDDAC supports the OHP by providing laboratory and radiology services required for medical surveillance examinations and treatment of work-related injury and illnesses.

The occupational health clinic is usually staffed by an occupational health nurse, an occupational health technician, a records clerk, and an administrative staff member, depending on the size of the population served and the occupational health services provided. There is a clinical provider who may be a physician, physician assistant, or nurse practitioner. The provider or the occupational health nurse serves as the OHP manager. In the absence of an occupational medicine physician, the chief of preventive medicine often provides clinical support for the OHP if resources do not permit hiring a provider. At some locations, the occupational health clinic may be part of family medicine and primary care. In this case, a provider from the family medicine clinic may provide the clinical support for the OHP.

Army Health Clinic Occupational Health Program

AMCOM, TRADOC, and FORSCOM installations have an employee health clinic that is part of the Army health clinic on the installation. The Army health clinic is under the control of the local installation commander, yet the medical mission for occupational health is directly overseen by the preventive medicine service or department of primary care and family medicine at the supporting regional MEDCEN or MEDDAC. Army health clinic staff usually include one or two providers (either military or civilian), several civilian nurses, and other administrative and support personnel. A provider is usually appointed as the officer-in-charge of the clinic. The Army health clinic usually has in-house laboratory and radiology capability, or employees are sent off base for these services. The mission of the Army health clinic includes providing clinical care to both civilian employees and active duty military personnel on base, as well as family members and retirees.

Patients who require referral to a specialist may be sent to the supporting MEDDAC or MEDCEN, but only after prior coordination with the specialty clinic. Alternatively, patients may be referred to a local specialist. However, such a referral must be approved by the deputy commander for clinical services at the supporting MEDDAC or MEDCEN before an appointment is scheduled. Often financial arrangements for referral of civilian employees to see specialists for work ability determinations must be coordinated in advance through resource management at the MTF and the USAPHC, particularly for compliance with AR 190-56, The Army Civilian Police and Security Guard Program.[23]

The staffing and support of Army health clinics by MEDCOM has historically been a challenge, causing problems for installation commanders who want the best care available for personnel on the installation. Army health clinic staffing dramatically improved when MEDCOM and DoD approved the budget plan for 2010 to 2014, which provided $50 million for Army occupational health and industrial hygiene programs over the 5-year period. The OHP manager must coordinate with the USAPHC if personnel or resources are deemed insufficient to execute the mission.

An Army health clinic OHP manager—either the occupational medicine physician, nurse practitioner, physician assistant, or senior occupational health nurse—should be designated in writing. In clinics without an occupational medicine physician or other provider, one of the primary clinic providers should be assigned the responsibility of providing clinical support for the OHP.

Occupational Health Program Staffing

The size and type of the staff of an occupational health section depend on the population to be served, type of installation, range of occupational health services provided, and availability of resources. All OHPs require at least one full-time civilian occupational health nurse, either a full-time or part-time provider, and clerical support. The OHP can request USAPHC staff assistance to run the Automated Staffing Assessment Model for Preventive Medicine24,25 to document shortfalls in staffing and to request additional staffing. This model, developed by the MEDCOM Manpower Division, is a multivariate model that determines staffing requirements for preventive and occupational medicine. The model inputs include workload, population served, impacts on productivity, cost savings and cost avoidance, and established best practices for preventive and occupational medicine.

Credentialing and Privileging

Credentialing is how an MTF determines what procedures may be performed or which conditions may be treated by each healthcare professional. Credentialing for each provider is based on relevant education, training, experience, and each state’s licensing board and the scope of practice permitted by the licensing board. Credentialing may be defined as the process of assessing and validating the qualifications of a licensed professional to provide health services. Per the Joint Commission,[26] each facility should have professional criteria as the basis for granting initial or renewed/revised clinical privileges. These criteria must pertain to, at a minimum, evidence of current licensure, relevant training and/or experience, current competency, and health status.

Privileging is the process MTFs use to determine the specific procedures and treatments that each licensed independent healthcare professional may perform. The provider credentials packet includes the requirements to begin the privileging process and is based upon AR 40-68, Quality Assurance Administration.[27] Once professional and technical personnel are assigned to the clinic, each individual is responsible for maintaining current licensure and certification according to legal and professional requirements.

Occupational Health Providers

The occupational health provider may be a military or civilian physician, physician assistant, or nurse practitioner. The qualifications of a civilian physician and military physician may vary somewhat. The MEDCEN or MEDDAC credentialing committee must approve the occupational health provider’s clinical privileges as an occupational health physician, physician assistant, or nurse practitioner. Civilian occupational medicine physicians or other civilian providers must meet the minimum qualifications of the Office of Personnel Management (OPM)[28] to be selected for the position. In addition, training or prior experience in the field of occupational health is needed. The occupational health provider can be assigned as a part-time or full-time member of the occupational health clinic staff, based on staffing requirements. Part-time support is seldom adequate because these providers also have clinical duties in the primary care clinic, which limits time spent on occupational health duties.

Occupational Health Nurses

The Army employs civilian occupational health nurses, who are usually registered nurses, to work in the occupational health clinic. These nurses must meet the minimum OPM qualifications and hold a current state license to practice nursing. MEDCEN or MEDDAC clinical privileges are not required for occupational health nurses who practice within the scope of nursing practice for their state license. Occupational health nurses may seek additional training beyond a bachelor’s degree by earning a master’s degree in occupational health nursing. This additional training is often thought necessary to become a certified occupational health nurse. The master’s-level coursework usually includes management principles; industrial toxicology; the cause, prevention, control, and treatment of occupational injuries and illnesses; principles of industrial hygiene and epidemiology; concepts and practices of job-related medical surveillance; and legal and regulatory aspects of occupational health. A course in biostatistics is also helpful for the occupational health nurse manager who is performing health surveillance on specific worker populations.

Industrial Hygienists

The industrial hygienist assists the occupational health clinic staff by providing information on industrial hygiene program efforts to support and maintain a safe and healthful workplace, as mandated by OSHA,[3] DoDIs,14–16 ARs,[17] and DA PAM 40-503, Industrial Hygiene.[29] The industrial hygienist should provide the clinic with copies of worksite visit reports that identify and quantify occupational health hazards. These reports should also recommend appropriate medical surveillance enrollment when the action level specified in OSHA regulation is half the permissible exposure level (PEL), or when the American Council of Governmental and Industrial Hygienists (ACGIH) threshold limit value (TLV) is exceeded. When workplace chemical exposures exceed the OSHA PEL or ACGIH TLV, the industrial hygienist, in conjunction with the site supervisor and safety manager, conducts an investigation to identify the source of the exposure, characterize the degree of exposure, and write a summary report that documents for those workers involved the chemicals involved, the exposure levels encountered, and duration of exposures. The industrial hygienist also provides the clinic results of air sampling, wipe sampling, or noise dosimetry surveys. He or she reviews plans and blueprints for modifications to and construction of new worksite facilities or operations to ensure adequate planning for heating, ventilation, and air-conditioning systems, making sure the ventilation planned for workplace hazards will protect worker health and safety. The industrial hygienist also collaborates with occupational health, safety, and human resources to provide employee health education, and participates on the installation safety and occupational health and FECA working groups.

Safety Personnel

Safety personnel collaborate with occupational health and industrial hygiene staff to ensure that civilian employees and soldiers follow safe work practices, use appropriate personal protective equipment, and report work-related injuries and illnesses. Occupational health providers and staff should be aware of the numerous Army safety regulations and pamphlets, including AR 385-10,[30] DA PAM 385-1,[31] and DA PAM 385-10,[32] to ensure occupational health coordination of efforts and participation as appropriate in safety and OHP activities. Coordination on worksite visits, the FECA program, and injury and illness reporting and investigation of accidents are but a few of the many issues that require occupational health providers and safety staff to work together.

Supervisors

Supervisors must ensure that personnel comply with all safety and occupational health requirements, such as attendance at medical surveillance and screening exams, training, use of personal protective equipment, safe work practices, and respirator fit testing. Supervisors also play a large role supporting the FECA program when they review the circumstances surrounding an employee’s claim for compensation benefits for a work-related injury. The supervisor must sign the claim form attesting to the facts as presented by the civilian employee, or check that the claim should be controverted if the facts in the case are different than what was reported.

Employees

Employees must follow safe and healthful work practices, use personal protective equipment when required, and make note of and report suspected unsafe or hazardous work situations to their supervisor. Employees must also comply with the requirements of the OHP and participate in medical surveillance programs when required by OPM[33] and ARs.[17] Employees should report any work-related injury to their supervisor at the time of occurrence or no more than 72 hours later, and report to the occupational health clinic in compliance with the installation commander’s “clinic-first” policy. This will ensure the circumstances related to the injury are documented in the employee’s medical record in the occupational health clinic and help to ensure timely completion of claim forms that will initiate continuation of pay and medical benefits.

MEDICAL RECORDS MANAGEMENT

The civilian employee medical record (CEMR) contains all records pertaining to occupational health physical examinations, workers’ compensation records, and administrative reports. The purpose of the CEMR is to document the medical history of the patient and medical care provided for injuries and illnesses. The CEMR records in chronological order any work-related changes in health status, comprehensive health histories, workplace exposure records based on sampling conducted by industrial hygiene staff, a healthcare professional’s written medical opinions regarding workplace examinations and whether the employee developed injuries or illnesses related to the job, and a record or all medical conditions, medications, and treatment for all work-related conditions.

OPM owns the CEMR and delegates its custody to the MTF commander. The chief of the MTF’s Patient Administration Division acts on behalf of the commander in matters that involve medical records. Periodically, the chief of the Patient Administration Division or their representative inspects the employee health records to ensure compliance with AR 40-66 recordkeeping requirements[34] and make sure medical encounters are properly coded using ICD-10.[35] Upon request, the patient administration division will provide training on coding rules and guidelines for all providers.

The CEMR and active duty treatment record should be maintained separately and each record marked appropriately to facilitate identification. If the civilian employee has dual status as a National Guard member or Reservist, or they retired from the active duty military, then the service member’s outpatient treatment record should not be consolidated into the CEMR. It is strongly recommended that the OHP manager ask civilian employees who hold dual status to sign both the Privacy Act[36] and the Health Insurance Portability and Accountability Act (HIPAA)[37] notice giving informed consent that information in their health record may be utilized and included in the medical history section of the occupational health record. This will prevent problems later if questions of work ability arise when HIPAA may limit access to the information in the military treatment record unless an informed consent was signed by the employee.

OPM’s Guide to Personnel Recordkeeping[38] and AR 40-66[34] direct how the CEMR should be maintained, and all entries into the CEMR must be made. The Report of Medical History (DD Form 2807-1) is used to obtain a health history from all civilian employees and to initiate a medical record upon employment. Once the medical record is initiated, the form should be kept in the Service Member Treatment Record (DA Form 3444) or in the CEMR folder (SF 66-D). DA and DoD forms are the only approved forms for use in the medical record. The MTF commander may approve the use of any forms that were developed locally. Office of Workers’ Compensation forms related to medical treatment (CA-1, CA 15, CA-16, and CA 17) may also be maintained in the medical record. The CEMR should be sent to the civilian personnel office of the gaining unit when the employee transfers to another agency, or sent to the National Records Center when the employee retires.

Small radiographs (8.5 × 11″ or smaller) should be placed in the CEMR and retired or forwarded to the gaining unit. However, larger chest radiographs (larger than 8.5 × 11″) should be maintained at the MTF for 30 years beyond the termination of employment. The CEMR must have a copy of the written radiologist’s findings, the last known location of the radiograph, and how the plain film can be obtained. If the employee is transferring to another federal agency, the large films must be forwarded to the gaining agencies’ supporting occupational health clinic.

Like any other medical record, the CEMR must be maintained in accordance with the Privacy Act[36] and HIPAA.[37] Both OSHA and National Institute for Occupational Safety and Health personnel must be given access to the CEMR when they are investigating workplace exposures to toxic materials or harmful physical agents such as radiation and noise.

OCCUPATIONAL HEALTH PROGRAMS AND SERVICES

OHPs provide medical, dental, and veterinary personnel with clinical preventive and occupational health services. Occupational health staff conduct work-related medical surveillance and perform various administrative medical examinations, as well as educating employees about health hazards in the workplace. The occupational health clinic conducts medical screening of civilian employees who have been absent from work, and also provides immunizations for at-risk employees to prevent workplace infections. Clinic staff also conduct worksite visits to evaluate the workplace for hazardous conditions. Occupational health providers may conduct epidemiological studies of workplace injuries or illnesses to target at-risk workers with countermeasures to reduce injuries and illnesses. Finally, employees can be seen in the occupational health clinic for emergency treatment of work-related illnesses and injuries and non–work-related minor illnesses and injuries.

Medical Surveillance

Job-related medical surveillance consists of systematically and periodically collecting and analyzing health data on groups of employees for the purpose of early detection of an increased risk or actual presence of job-related health effects. Medical surveillance is prospective and ongoing in nature. Designing a medical surveillance program requires identification of employees with a potential exposure to job-related hazards. Medical surveillance is covered in detail in Chapter 10 of this book.

Administrative Medical Examinations

Managers need to know whether employees are able to perform the essential duties of their job safely, without undue risk to themselves or others, in order to make employment decisions. Administrative medical examinations will determine if the employee can perform the job safely and efficiently. The occupational health provider’s role is to assess whether any medical or psychological conditions exist, and if so, determine whether the condition is stable and whether the individual’s ability to perform the essential functions of the job is impacted by the condition. OPM has established medical standards and physical requirements for only a limited number of jobs (refer to Chapter 8, Agency Medical Evaluations, for a more in-depth discussion of OPM’s existing regulations and requirements for employee medical examinations).

The occupational health clinic performs a variety of administrative physical examinations that include preplacement/post-hire physical examinations, periodic medical examinations, fitness-for-duty examinations, and retirement disability examinations. The occupational health provider performs the preplacement/post-offer physical examination to assess the employee’s abilities to do the job, and also to establish a baseline medical assessment against which future assessments regarding workplace exposure can be compared. OPM mandates medical examinations for civilian employees only when the job has physical standards, the workplace involves hazardous exposures, or the employing agency requires a physical.

The Civilian Personnel Office usually forwards the job description and the OF 178, Certificate of Medical Examination, or DA Form 3437, Non-Appropriated Funds Certificate of Medical Examination, to occupational health clinic staff for completion by the examining provider. The OF 178 lists the specific job’s physical requirements and the environmental factors that the employee will encounter on the job. Though not required by OPM, applicants for positions with duties that are sedentary or moderately active should complete a DD Form 2801-1, Report of Medical History, and take advantage of baseline screening, such as for blood pressure, vision, and hearing.

Periodic administrative examinations are performed to evaluate an employee’s continuing ability to perform the job. OPM requires personnel in only a few positions to undergo periodic medical examinations. It is considered a standard of practice for occupational health providers to perform periodic examinations on selected groups of employees who have OPM medical examination requirements. The frequency of the periodic examination is specified in the appropriate AR: AR 190-56, The Civilian Police and Army Security Guard Program,[23] requires periodic examinations for police and security; AR 600-55, The Army Driver and Equipment Operator Standardization Program (Selection, Training, Testing, and Licensing),[39] requires periodic examinations for drivers of commercial vehicles; and AR 50-6, Nuclear and Chemical Weapons and Materiel, Chemical Surety,[40] and the corresponding DA PAM require periodic physicals for employees in the chemical surety program. OSHA regulations also provide guidance regarding medical surveillance examinations for specific workplace exposures, particularly carcinogens, and the National Fire Protection Association Standard 1582[41] provides guidance for firefighter examinations.

Fitness-for-Duty and Disability Retirement Examinations

Per 5 CFR 339, OPM allows agencies to direct an employee in writing to undergo a medical examination provided there is sufficient reason to believe they are unable to perform the essential duties of the position due to physical or mental impairment.[33] The agency must inform the employee in writing of the reasons for the examination and notify them of their right to have a physician submit needed medical documentation to address work ability. Further, the agency must pay for medical examinations employees are directed to undergo.

Supervisors may request a fitness-for-duty examination for an employee by asking the human resources office to direct the employee to undergo the exam. Human resources staff will then issue the employee a letter directing them to report to the occupational health clinic for the exam at a specified time. The occupational health clinician will complete the examination and note in writing the employee’s capability to meet the physical or medical requirements of a position. The agency may also offer a psychiatric evaluation to help establish the employee’s work ability. An employee who submits a request for medical accommodation under the Americans With Disabilities Act,[42] as amended, or the Family and Medical Leave Act[43] must submit supporting medical documentation.

Worksite Evaluations

Occupational health staff conduct worksite evaluations annually and when operations change. These evaluations can be performed independently or with safety and industrial hygiene staff. Occupational health clinic staff should conduct worksite visits because it allows the provider to gain an understanding of organization work practices and hazards, and how well the employees comply with requirements to use personal protective equipment. During the visits, staff should encourage employees to take full advantage of the services offered by the occupational health clinic, including health promotion and health hazard training.

Health Hazard Education

OSHA mandates that employees receive training on workplace hazards in 29 CFR 1910.1200, Hazard Communication.[44] Supervisors are primarily responsible for ensuring that employees get mandated training and that the training meets OSHA requirements. The safety and occupational health team has a role in ensuring the training is a success. Occupational health providers train employees about the signs and symptoms of exposure, what medical surveillance is done to identify worker exposure, and what potential health outcomes might occur as a result of workplace exposures. In addition, the provider should indicate when emergency treatment is needed for an acute exposure and identify what clothing and equipment is needed to protect against the hazard. Occupational health clinic staff may provide job-related health education individually during job-related health evaluations, or train groups of employees who are exposed to the same hazards. Documentation of the education is required in the CEMR.

The occupational health clinic can also provide health promotion and wellness classes to assist employees in achieving optimal health. This education is usually given when the employee receives healthcare or approaches clinic staff with questions or problems. Providers may supplement the health education provided in the clinic by making educational pamphlets available to employees or publishing health information in the installation newspaper for dissemination to the workforce.

Monitoring Absences Due to Illness

The occupational health provider can help keep employees healthy, which minimizes lost work time and helps supervisors maintain productivity. This will also reduce the burden on supervisors and the Civilian Personnel Office in terms of tracking work absences. Illness absence monitoring ensures that employees are well enough to perform the job safely; however, the identification and control of abuse of leave benefits is a supervisory and Civilian Personnel Office responsibility.

The installation occupational health regulation should include processes for monitoring absences due to illness that involve evaluating and treating employees who become ill or are injured during duty hours, or referring them to their treating provider. This will ensure the appropriate disposition of ill employees, permit the occupational health clinic staff to provide health education, increase awareness of health problems, and increase the staff’s ability to detect sentinel health events.

Employees who treat patients and those who handle food must report to clinic staff for evaluation after any illness or injury. Generally, if other employees are out for 3 days, they should also be asked to be evaluated at the clinic. Occupational health providers should determine the appropriate duration of work absences, and they must decide whether civilian employees can return to work safely after a work absence due to illness and ensure they are well enough to work. If employees cannot perform their full duties, they may be able to return to work with limitations or work elsewhere for a limited period of time. An evaluation after a work absence due to a job-related illness is essential to document the accident particulars and note the work ability of the employee.

Injured workers should also report to the occupational health clinic so that a medical evaluation can be performed to assess their work ability. These evaluations may require only a review of medical reports, or they may call for a directed physical examination. The occupational health physician should request specialty consultation when indicated.

Immunizations

Research laboratories using certain biological warfare agents and clinical laboratories using live bacteria and viruses that require biosafety level 2 or higher protection pose a potential health risk for their employees. Some of these hazards are also found in hospitals, medical and dental clinics, and animal-care facilities. Employees who travel to certain foreign countries may also be at increased risk.

Army immunization guidance is published in AR 40-562, Immunizations and Chemoprophylaxis.[45] The immunization program provides appropriate immunizations for healthcare personnel who are at risk. AR 40-562 mandates that military and civilian healthcare providers who are at risk for blood-borne pathogen exposure be immunized against hepatitis B.45(p12) The occupational health clinic also offers rubella, tetanus, and influenza immunizations for medical and dental personnel; rabies prophylaxis for veterinary staff and animal handlers; and special vaccinations for staff in research medical laboratories. The occupational health clinic screens high-risk dental, medical, and veterinary personnel for active tuberculosis as well.

Clinic staff also provide immunizations to civilian personnel against illnesses such as influenza to prevent communicable disease outbreaks and reduce work time lost to illness. Staff must assess whether the available immunization is sufficient to effectively control the threat. The Advisory Committee on Immunization Practices provides guidance for healthcare providers, published on the Centers for Disease Control and Prevention website.[46]

Epidemiological Investigations of Occupational Illnesses and Injuries

Occupational health clinic providers should conduct an epidemiological investigation when an occupational illnesses or a cluster of occupational injuries in the same worksite occurs. For example, five lower back strain cases in a short period of time at the same location should prompt an investigation into the cause.

Any factors at the worksite that may have contributed to the condition are the subject of the epidemiological investigation. The scope of the investigation should extend beyond individual cases to include all those at risk of illness or injury. The investigation should include members of safety, industrial hygiene, and preventive medicine services, as well as supervisors and human resources staff.

An epidemiological investigation can be a simple investigation of exposure at the worksite, or it can be a detailed assessment that includes sample collection and analysis of suspected agents, medical examinations, test results and diagnosis, and a literature review. The occupational health team may also contact the USAPHC for assistance with the epidemiological investigation through command channels.

Health Promotion

The Army Health Promotion Program is designed to promote and maintain the health and well-being of both military and civilian personnel. Health promotion and wellness programs have improved employee morale and reduced absenteeism and presenteeism (being at work without being productive). Army installations must establish a wellness council that meets the requirements of AR 600-63, Army Health Promotion.[47] All employees are encouraged to participate in fitness and exercise programs. However, ARs permit only employees in jobs with physical fitness requirements, such as police and firefighters, to be granted regular time off to participate in fitness training. Other employees may receive only a one-time grant of no more than 3 hours of administrative time per week, for 6 to 8 weeks, to participate in command-sponsored physical fitness programs. Occupational health providers may provide medical examinations to clear employees for participation in the physical fitness program.

Emergency Treatment of Illnesses and Injuries

Civilian employees are eligible for diagnosis and treatment of occupational injuries and illnesses in the occupational health clinic21,22; they may sometimes be seen for non-occupational illnesses and injuries as well. Civilians may be seen in the emergency room for emergent, non–work-related conditions to prevent the loss of life or limb, or to relieve suffering until they can be seen by their private physician. Some civilian contractors may be seen for work-related and non–work-related conditions if specified by the terms of their contract. This is usually permitted only in locations where civilian treatment facilities are not available, such as a deployed setting or other remote location. Finally, civilian employees may be seen in the occupational health clinic for non-occupational injuries or illnesses of a minor nature for first aid or palliative care that would enable the employee to complete the work shift before they see their physician. Civilian employees may also ask to be seen for minor treatments such as suture removal or for blood pressure monitoring, which will be supported if space is available and the occupational health clinician supports it to minimize lost work time.

SUMMARY

The OHP Army mission is to promote health and to provide job-related, occupational healthcare services for civilian employees and active duty service members, including the operation of 80 occupational health clinics worldwide. This chapter has reviewed the basic structure and program guidance for the OHP. OHP staffing, resources, and programs were reviewed to give providers an awareness of the scope and complexity of the program. The pertinent OSHA, DoD, and Army regulations were reviewed in a comprehensive fashion to show how the regulations and policy guidance apply in the occupational health setting.

The occupational health clinic provides core occupational health services, including job-related medical surveillance, administrative medical examinations, health hazard education, monitoring of absences due to illness, immunizations, health promotion, and treatment of work-related injuries and illnesses. The ARs relating to the provision of occupational health services provide guidance on who has access to occupational health services. The occupational health provider must be aware of military personnel who have workplace hazards and may require periodic medical surveillance like their civilian counterparts. In such cases, the occupational health clinician must include these personnel in periodic medical surveillance because their primary care providers may be unfamiliar with the workplace hazards.

REFERENCES

1.   Deeter DP, Ruff JM. US Army health programs and services. In: Deeter DP, Gaydos JC, eds. Occupational Health: The Soldier and the Industrial Base. Textbook of Military Medicine series. Washington, DC: Department of the Army, Office of The Surgeon, General, Borden Institute; 1993: Chap 3.

2.   Health Services Program. Pub L No. 79-658, 5 USC 7901.

3.   The Occupational Safety and Health Act of 1970. Pub L No. 91-596, December 29, 1970, as amended through January 1, 2004.

4.   Executive Order 12196. Occupational safety and health programs for federal employees. October 1, 1980. https://www.archives.gov/federal-register/codification/executive-order/12196.html. Accessed October 12, 2016.

5.   29 CFR, Part 1960. Basic program elements for federal employees’ occupational safety and health programs and related matters. https://www.osha.gov/pls/oshaweb/owasrch.search_form?p_doc_type=STANDARDS&p_toc_level=1&p_keyvalue=1960. Accessed October 12, 2016.

6.   29 CFR, Part 1910. Occupational safety and health standards. https://www.osha.gov/pls/oshaweb/owasrch.search_form?p_doc_type=STANDARDS&p_toc_level=1&p_keyvalue=1910. Accessed October 12, 2016.

7.   29 CFR, Part 1904. Recording and reporting occupational injuries and illness. https://www.osha.gov/pls/oshaweb/owasrch.search_form?p_doc_type=STANDARDS&p_toc_level=1&p_keyvalue=1904. Accessed October 12, 2016.

8.   Federal Employees’ Compensation Act. Pub L No. 93-416. http://www.dol.gov/owcp/dfec/regs/statutes/feca.htm. Accessed August 28, 2016.

9.   20 CFR, Part 10. Claims for compensation under the Federal Employees’ Compensation Act, as amended. https://www.law.cornell.edu/cfr/text/20/part-10. Accessed October 12, 2016.

10.   US Department of Labor, Office of Workers’ Compensation Programs. Questions and Answers About Federal Employees’ Compensation Act (FECA). Washington, DC: DoL; 2002. Publication CA-550. http://www.dol.gov/owcp/dfec/regs/compliance/DFECFolio/q-and-a.pdf. Accessed October 8, 2016.

11.   US Department of Labor, Office of Workers’ Compensation Programs. Injury Compensation for Federal Employees. Washington, DC: DoL; 2009. Publication CA-810. http://www.dol.gov/owcp/dfec/regs/compliance/DFECfolio/CA-810.pdf. Accessed October 8, 2016.

12.   US Department of Labor, Office of Workers’ Compensation Programs. Procedures manual website. http://www.dol.gov/owcp/procedure-manual.htm. Accessed October 8, 2016.

13.   US Department of Defense. DoD Civilian Personnel Management System: Injury Compensation. Washington, DC: DoD; 2009. DoD Instruction 1400.25: Subchap 810. http://www.dtic.mil/whs/directives/corres/pdf/1400.25-V810.pdf. Accessed October 8, 2016.

14.   US Department of Defense. DoD Safety and Occupational Health (SOH) Program. Washington, DC: DoD; 2014. DoD Instruction 6055.01. http://dtic.mil/whs/directives/corres/pdf/605501p.pdf. Accessed December 2, 2016.

15.   US Department of Defense. Occupational and Environmental Health (OEH). Washington, DC: DoD; 2008. DoD Instruction 6055.05. http://www.dtic.mil/whs/directives/corres/pdf/605505p.pdf. Accessed October 12, 2016.

16.   US Department of Defense. Occupational Medical Examination and Surveillance Manual. Washington, DC: DoD; 2008. DoD Instruction 6055.05M.

17.   US Department of the Army. Preventive Medicine. Washington, DC: DA; 2007. Army Regulation 40-5.

18.   US Department of the Army. Preventive Medicine. Washington, DC: DA; 2005. DA Pamphlet 40-11.

19.   US Army Medical Command. Organization and Functions. Joint Base San Antonio, TX: MEDCOM; 2013. MEDCOM Regulation 10-1.

20.   US Department of the Army. Composition, Mission, and Functions of the Army Medical Department. Washington, DC: DA; 2013. Army Regulation 40-1.

21.   US Department of the Army. Patient Administration. Washington, DC: DA; 2010. Army Regulation 40-400.

22.   US Department of the Army. Medical, Dental, and Veterinary Care. Washington, DC: DA; 2013. Army Regulation 40-3.

23.   US Department of the Army. The Army Civilian Police and Security Guard Program. Washington, DC: DA; 2013. Army Regulation 190-56.

24.   Hodson MJ, Eaton JL, Mallon TM. Staffing and quality metrics in occupational health clinics. Paper presented at: American Occupational Health Conference; March 25, 2011; Washington, DC.

25.   Thomsen KN. Health Promotion and Wellness Staffing Methods [graduate management project]. Ft Sam Houston, TX: US Army-Baylor Program in Health Care Administration; 1999. http://www.dtic.mil/dtic/tr/fulltext/u2/a420874.pdf. Accessed August 16, 2017.

26.   Joint Commission. Ambulatory Care Program: The Who, What, When, and Wheres of Credentialing and Privileging. Oak Brook, IL: Joint Commission; 2016. https://www.jointcommission.org/assets/1/18/AHC_who_what_credentialing_booklet.pdf. Accessed August 16, 2017.

27.   US Department of the Army. Quality Assurance Administration. Washington, DC: DA; 2009. Army Regulation 40-68.

28.   US Office of Personnel Management. Handbook of Occupational Groups and Families. Washington, DC: OPM; 2009.

29.   US Department of the Army. The Army Industrial Hygiene Program. Washington DC: DA; 2013. Army Pamphlet 40-503.

30.   US Department of the Army. The Army Safety Program. Washington DC: DA; 2010. Army Regulation 385-10.

31.   US Department of the Army. Small Unit Safety Officer / Noncommissioned Officer Guide. Washington DC: DA; 2013. Army Pamphlet 385-1.

32.   US Department of the Army. The Army Safety Program. Washington DC: DA; 2010. Army Pamphlet 385–10.

33.   5 CFR, Part 339. Medical qualifications and determinations, as amended. https://www.gpo.gov/fdsys/pkg/CFR-2011-title5-vol1/xml/CFR-2011-title5-vol1-part339.xml. Accessed October 12, 2016.

34.   US Department of the Army. Medical Record Administration and Health Care Documents. Washington, DC: DA; 2008. Army Regulation 40-66.

35.   Centers for Medicare and Medicaid Services. ICD-10-CM/PCS frequently asked questions. https://www.cms.gov/Medicare/Coding/ICD10/Frequently-Asked-Questions.html. Accessed August 16, 2017.

36.   Privacy Act of 1974. 5 USC. § 552a. https://www.justice.gov/opcl/privacy-act-1974. Accessed October 12, 2016.

37.   Health Insurance Portability and Accountability Act of 1996 (HIPAA). Pub Law No. 104-191, August 21, 1996, as amended August 14, 2002.

38.   US Office of Personnel Management. The Guide to Personnel Recordkeeping. Washington, DC: OPM; 2011. https://www.opm.gov/policy-data-oversight/data-analysis-documentation/personnel-documentation/personnel-recordkeeping/recguide2011.pdf. Accessed August 17, 2017.

39.   US Department of the Army. The Army Driver and Operator Standardization Program (Selection, Training, Testing, and Licensing). Washington, DC: DA; 2007. Army Regulation 600-55.

40.   US Department of the Army. Nuclear and Chemical Weapons and Materiel, Chemical Surety. Washington, DC: DA; 2008. Army Regulation 50–6.

41.   National Fire Protection Association. NFPA 1582: Standard on Comprehensive Occupational Medical Program for Fire Departments. Quincy, MA: NFPA; 2013. http://www.nfpa.org/codes-and-standards/all-codes-and-standards/list-of-codes-and-standards?mode=code&code=1582. Accessed October 12, 2016.

42.   Americans with Disabilities Act of 1990, as amended. Pub L No. 101-336. http://library.clerk.house.gov/reference-files/PPL_101_336_AmericansWithDisabilities.pdf. Accessed September 30, 2016.

43.   Family and Medical Leave Act (FMLA) of 1993. Pub L No. 103-3. https://www.dol.gov/whd/regs/statutes/fmla.htm. Accessed August 9, 2017.

44.   29 CFR, Part 1910.1200. Hazard communication. https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=standards&p_id=10099. Accessed August 12, 2017.

45.   US Department of the Army. Immunizations and Chemoprophylaxis. Washington, DC: DA; 2006. Army Regulation 40-562.

46.   Centers for Disease Control and Prevention, National Center for Immunization and Respiratory Diseases. Advisory Committee on Immunization Practices (ACIP) website. https://www.cdc.gov/vaccines/acip/. Accessed October 12, 2016.

47.   US Department of the Army. Army Health Promotion. Washington, DC: DA; 2007, 2010. Army Regulation 600-63.

Chapter 6

HISTORY OF ARMY OCCUPATIONAL HEALTH, 1991–2015

JACK M. HELLER, PhD*; TIMOTHY M. MALLON, MD, MPH†; COLEEN P. BAIRD, MD, MPH‡; DEANNA K. HARKINS, MD, MPH§; MAHMUT ATABAY, MS¥; JOHN P. CUELLAR, MS¶; and JOEL C. GAYDOS, MD, MPH**

INTRODUCTION

PERSIAN GULF WAR (1990–1991)

BOSNIA, HERZEGOVINA, AND KOSOVO (1995–1999)

OPERATION IRAQI FREEDOM AND OPERATION ENDURING FREEDOM (2001–2015)

OCCUPATIONAL AND ENVIRONMENTAL HEALTH INFORMATICS

SUMMARY

*Environmental Scientist, Department of Environmental Medicine, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

†Colonel (Retired), US Army, Adjunct Assistant Professor, Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814

‡Division Chief, Department of Environmental Medicine, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

§Medical Officer, Department of Environmental Medicine, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

¥Second Lieutenant, US Army; Medical Services Corps, Health Physics Operations Officer, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

¶Colonel, US Army, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

**Colonel (Retired), US Army, Occupational Medicine Physician, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

INTRODUCTION

The Vietnam War (1956–1975) became associated with exposure to the defoliant Agent Orange through the persistence of health complaints with no identified syndrome or specific cause and resulting debates about the appropriateness of compensation for affected veterans.1–3 Consequently, practitioners of military preventive medicine worked to identify ways to prevent future similar problems, including improving capabilities for the early recognition and thorough assessment of potentially harmful exposures to hazardous materials. The Persian Gulf War (1990–1991) was short, but exposures to potentially hazardous materials such as plumes from burning oil wells occurred, and long-term health effects among deployed service members again became a national concern.[4] Later, when US peacekeeping forces entered the former Yugoslavia in 1995, quick identification and characterization of potentially hazardous materials enabled commanders to take appropriate action to avoid or minimize exposures.[5] Unfortunately, the protracted Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF), beginning in 2001, produced many exposures. Again there were concerns about long-term health effects and complaints of illnesses, many of which could not be linked to defined exposures or characterized by a recognized symptom complex.[6] The concerns about deployment-related exposures and health effects are documented in multiple reports from the Institute of Medicine, at least three medical journal special editions, and a monograph.7–12

A primary focus of military medicine is taking care of military members while they are training and performing their global missions, with emphasis on the prevention of illnesses and injuries. Therefore, military medicine is the practice of occupational and environmental medicine in support of the critical workforce that is responsible for protecting and defending the country.[13] This chapter identifies and summarizes the challenges that faced military occupational and environmental medicine physicians, environmental health scientists, and others in the military occupational health and preventive medicine communities in dealing with environmental exposures and novel or poorly defined medical problems in deployed US service members since the beginning of the Persian Gulf War.

PERSIAN GULF WAR (1990–1991)

After the Persian Gulf War, over 200,000 veterans claimed they had developed Gulf War illness (GWI), an illness that correlated with their exposures, while deployed.[14] The medical community struggled to identify a medical explanation for the variable and nonspecific constellation of symptoms, sometimes referred to as “mystery illness” and more popularly “Gulf War Syndrome,” experienced by these veterans.

The anxiety associated with concerns about health and related costs that followed the use of Agent Orange in Vietnam have been staggering.2,3 However, it was not until the Persian Gulf War that leaders in the US Department of Defense (DoD) recognized the need to address environmental exposures in service members with the objective of preventing these and any related adverse health outcomes.4,5 Previously, DoD was primarily concerned with arthropod-borne infectious diseases and microbial contamination of food and water that could quickly produce large numbers of casualties, significantly reducing the fighting strength and jeopardizing the success of the military mission. DoD planners considered potential chemical warfare agent use and burning oil well fires, but other concerns were identified only after the conflict ended.

The Persian Gulf War consisted of a build-up phase (Operation Desert Shield, August 2, 1990–January 17, 1991) and a combat phase, Operation Desert Storm (January 17, 1991–February 28, 1991).[1] During the Persian Gulf War, Iraqi forces set fire to more than 750 oil wells that burned between February 2, 1991, and October 29, 1991, significantly decreasing the air quality over much of the country of Kuwait (Figures 6-1 and 6-2).[4] The symptoms included some combination of chronic headache, chronic shortness of breath and breathing difficulties, widespread pain, memory and concentration problems, persistent fatigue, gastrointestinal problems, skin abnormalities, and mood disturbances. Most of the symptoms did not fit the diagnostic criteria for established medical or psychiatric conditions.6,15 The Persian Gulf War was unusual in that returning veterans reported these kinds of symptoms in much larger numbers than were reported in previous wars.16–19

Figure 6-1. Burning oil wells seen at night from Camp Freedom, Kuwait, May 1991.
Photograph courtesy of Jack M. Heller, PhD, US Army Center for Health Promotion and Preventive Medicine.

Figure 6-2. Formation of a composite “super plume” over the Ahmadi Oil Fields, Kuwait, May 1991.
Photograph courtesy of Jack M. Heller, PhD, US Army Center for Health Promotion and Preventive Medicine.

On December 5, 1991, Public Law 102-190, National Defense Authorization Act for Fiscal Years 1992 and 1993 (10 USC 1086),[20] was passed, requiring the secretary of defense to establish and maintain a record of service members exposed to the combustion products from the burning oil wells (Figure 6-3). Section 734 of this law and Section 704 of Public Law 102-585, Veterans Health Care Act of 1992 (38 USC 101)[21] required development of a means to define DoD service members’ exposures to oil well fire emissions.4,22 These legislative actions represented a prompt response by the US Congress to address service member exposures and related potential health consequences.

Following the 1991 legislation, DoD preventive medicine personnel conducted required deployment occupational and environmental health (OEH) surveillance for most major conflicts, exercises, and humanitarian and peacekeeping operations. Over 25,000 air, water, soil, and other types of samples were collected worldwide by deployed military members, civilian employees, and contractors in preventive medicine, engineering, and civil affairs. A key question that consistently faced military preventive medicine personnel was how to effectively use the results generated by environmental sampling. They realized that the emphasis had to be placed on prevention. Simply describing an event after a potentially harmful exposure had occurred could not be the primary objective.

Figure 6-3. Burning oil wells emitting different-colored smoke, indicating different combustion products, Ahmadi Oil Fields, Kuwait, May 1991.
Photograph courtesy of Jack M. Heller, PhD, U S Army Center for Health Promotion and Preventive Medicine.

Kuwaiti Oil Well Fires

“The Kuwaiti oil well fires were a result of the scorched earth policy of Iraqi military forces retreating from Kuwait after conquering the country because they were being driven out by Coalition military forces.”[4] “The Gulf War Oil Spill, regarded as the worst oil spill in history, was also caused by the Iraqi forces when they opened valves at the Sea Island Oil Terminal, dumping oil from several tankers into the Persian Gulf.”[4] The Kuwaiti oil fires burned for almost a year, exposing American and other allied forces to the products of combustion from the burning oil. Some military personnel complained of respiratory and other symptoms that became part of what came to be called GWI.

DoD and allied personnel exposed to the burning and gushing oil wells were concerned about potential health effects.[4] The US Environmental Protection Agency (EPA), the Kuwait Environmental Protection Department, French and Norwegian teams, and groups from other countries conducted environmental monitoring and reported that pollutants from the oil wells were not at levels that would cause severe short-term health problems.[4] However, the data were inadequate to evaluate the potential for long-term health effects. Concern persisted, so the US Army Office of the Surgeon General, at the direction of the assistant secretary of defense for health affairs, chaired a triservice medical working group to evaluate potential health effects of the oil smoke. Medical personnel from each US military service and representatives from the US Department of Veterans Affairs (VA), Office of the Assistant Secretary of Defense for Health Affairs, and Office of the Deputy Assistant Secretary of Defense for the Environment, Safety, and Occupational Health formed the working group.

In support of this effort, a team from the US Army Environmental Hygiene Agency (USAEHA), Aberdeen Proving Ground, Maryland, was sent on May 1, 1991, to collect samples and monitor health effects in US forces in southwest Asia, and to prepare a health risk assessment (HRA). The HRA considered health risks from multiple sources such as oil fire smoke; industrial pollution (which was difficult to separate from oil fire smoke contaminants); natural background pollution (eg, heavy metals); and radioactivity, both naturally occurring (in association with oil bearing strata) and resulting from the military use of depleted uranium (DU).

An HRA is the determination of a quantitative or qualitative estimate of health risk related to a well-defined situation and a recognized threat. The steps include the evaluation of health risks, utilization of a dose-response approach to predict health risk, and quantification of exposures to use in risk estimation. This methodology was developed for use in evaluating contaminated environmental sites in the United States prior to cleanup. The original goal of an HRA was to identify a level of risk that was acceptable as a target for remediation, not to identify a level above which health effects will develop. Numerous uncertainties are associated with this methodology, such as the ability to assess only the hazards that are identified and measured, the recognition that concentrations of hazards vary over time and location, the inability to consider the effect of mixtures in the assessment, and the frequent lack of toxicological or epidemiological studies addressing the specific exposure concentration and duration without extrapolation.

Overall, the Kuwaiti oil well fire response consisted of three parts: (1) an environmental monitoring effort, with subsequent HRA; (2) an industrial hygiene (IH) sampling study; and (3) a biological surveillance initiative (BSI).4,23 The BSI was a unique component that measured health parameters in a unit before they deployed, while they were deployed, and upon their return. The BSI is not a typical component of an HRA, since the HRA is generally used to support risk-related decisions made prior to initiating cleanup at a site.

A troop unit exposure model was needed to support the HRA because data were collected at fewer than 10 fixed sites in the theater of operations while troops operated throughout the entire theater, and sampling did not start until 2 months after the fires started. Because actual sampling data did not exist for many points in space and time, the model was used to determine service members’ probable exposure levels to oil fire emissions. The exposure levels were used to generate health risk assessments in accordance with Public Laws 102-190 and 102-585.20,21 The delay in sampling occurred because, even though a USAEHA monitoring team was prepared for deployment in December 1990, the team’s priority for travel into the theater was so low that monitoring efforts did not commence until May 5, 1991.[4]

The large-scale environmental monitoring study conducted by a USAEHA team characterized the concentration of pollutants. The study was complicated because the periods and locations of exposure were extremely variable for the 550,000 US personnel who occupied sites across 880,000 square miles in Kuwait, Saudi Arabia, and Iraq. The USAEHA monitoring effort ended on December 3, 1991. When monitoring began, 558 oil wells were burning. Over 5,000 environmental study samples were collected before all fires were extinguished on November 6, 1991. Sampling was continued from November 6 to December 3, 1991, to collect background pollutant levels. The Army set up permanent ambient air monitoring stations at four sites in Saudi Arabia and six sites in Kuwait where US troops were stationed. Two sampling sites in Kuwait were shut down almost immediately because of logistical problems. National Oceanic and Atmospheric Administration scientists performed modeling to help estimate pollutant concentrations across the battle space where troops were located.

Soil samples and air monitoring data collected by USAEHA in the study were used to calculate exposure point concentrations. Exposure point concentrations for both air and soil were calculated by assessing the concentrations of all contaminants present at the time and location of collection to determine service members’ exposure levels and risk by the air and soil pathways. Risk assessments were done at the seven permanent sites and at the Ahmadi Hospital site in Kuwait, which was adjacent to the burning Ahmadi Oil Field.

In 1994, USAEHA became the central part of a new organization, the US Army Center for Health Promotion and Preventive Medicine (CHPPM). In response to Public Laws 102-190 and 102-585, CHPPM developed a database and public website that included an exposure model.20,21 Persian Gulf War veterans could go to the website and determine if they were at risk for health effects from their exposures in the Gulf, and they could request a copy of the information.4,20–22 Individual exposures were modeled for specific locations and depended upon an individual knowing where he or she had been and for how long.

The risk estimated included risk of cancer, which addressed the risk associated with exposure to each carcinogenic hazard using a linear, non-threshold model most applicable to radiation. Noncancer risk was evaluated by comparing air concentrations to what was considered a threshold safe daily exposure (above which health effects may occur). The result was expressed as a numeric index based on a value of one. One means the acceptable daily dose is equivalent to the average daily exposure; a number larger than one means the dose was higher; and a fraction of one means the dose was lower. Daily risks were not added, so this methodology did not reflect changes with longer duration exposures.

This method involved a great deal of uncertainty. Given the methodology employed and the fact that it was not expected to be well understood by the general public, it is unknown whether requesters of exposure information were reassured or became more concerned after obtaining their personal exposure profile.

Separate from the environmental monitoring effort, IH air sampling was done from May 3, 1991, to June 17, 1991, in Kuwait and Saudi Arabia. Personal, breathing zone air samples were obtained for people working outdoors and, to assess what was considered a worst-case exposure, similar samples were collected on workers in the oil fields next to Kuwait City. The results of the IH air sampling were compared to Occupational Safety and Health Administration (OSHA) standards to permit an assessment of health risk.

The BSI was conducted to simultaneously evaluate acute findings for those exposed and to assess long-term health risks in a cohort of US soldiers.[23] USAEHA occupational and environmental physicians looked for a military unit that might be suitable for the BSI. A US Army unit, the 11th Armored Cavalry Regiment, was selected for the surveillance project. It was stationed in Germany and scheduled to deploy to Kuwait and then return to Germany.[23] A team from USAEHA and other agencies conducted the BSI. Service members from the 11th Armored Cavalry Regiment were given questionnaires and had blood and urine collected for analysis between June 1 and October 14, 1991.23–26 Analytes studied included heavy metals, sister chromatid exchanges, blood volatile organic compounds, and deoxyribonucleic acid adducts. Data and specimens were collected prior to, during, and after deployment to Kuwait.[23] The participating service members were also screened at this time for breathing problems and other self-reported symptoms.[23] The BSI data from the exposed unit did not identify significant health consequences from oil fire exposures.23–26 A lesson learned from this initiative was that some bio-monitoring tests are not useful if the results have no prognostic significance. Also, at that time many biomarkers of exposures had no reference ranges outside of occupational groups and were difficult to interpret.

The predictive results from the HRA (which were generated from environmental data) found no expected significant health consequences from oil fire exposure to exposed troops. In the years that followed, epidemiological studies were conducted utilizing available healthcare data on units identified as exposed to the oil well fires. Unfortunately, since electronic records were limited to hospitalizations, the health outcomes assessed were limited to those conditions requiring hospitalization and did not reflect the relative rate of any more common, less serious conditions.

Public Law 102-190 both required the development of a way to determine the exposures to substances from the oil well fires, and required the secretary of defense to establish and maintain a record of each service member’s exposure to the combustion products of the burning oil wells.[20] Section 734 of this law included a requirement to determine the exposure levels of air contaminants resulting from the oil well fires in both military and civilian personnel who deployed to the Persian Gulf War.[20] The record also had to document the length of time exposed, the circumstances surrounding the exposure, and the location of the exposure. The task of developing a permanent record, in the form of a registry, to characterize and document the exposures of Persian Gulf War veterans was assigned to CHPPM.[4]

The US Armed Services Center for Unit Records Research (CURR) was responsible for determining the locations of all troops on a daily basis from February to November 1991. CHPPM worked with CURR and obtained a copy of the CURR Troop Movement Database for this period. The database was constructed by studying all Persian Gulf War records, including unit logbooks and situation reports that contained daily unit location data by latitude and longitude. CURR provided over 5 million records to develop the database. The Defense Manpower Data Center (DMDC) then created the Persian Gulf War Registry of military personnel, which tracked individuals assigned to the units in the CURR database. The database also included the date individuals entered and left the theater of operations, which was necessary to determine the length of time people were potentially exposed.[4]

The National Oceanic and Atmospheric Administration Air Resources Laboratory assisted CHPPM in the exposure modeling effort by providing output from its Hybrid Single-Particle Lagrangian Integrated Trajectories model to help determine the exposure of each service member. To determine the level of exposure and where the oil fire plume impacted service members, CHPPM analyzed this model in combination with Advanced Very High Resolution Radiometer satellite images.[4] The model predicted concentrations of each contaminant at the breathing zone (2 m) for 40,000 points (15 km grid spacing) in the area affected. The CHPPM team then calculated each service member’s exposure level on a daily basis. Finally, CHPPM used standard EPA risk assessment methods to determine health risk using the modeled exposure data and toxicity factors including reference dose, concentration, and cancer slope factor.[4] Cancer slope factors are used to estimate the risk of cancer associated with exposure to a carcinogenic substance. A slope factor is an upper bound estimate on the increased cancer risk from a lifetime exposure to an agent by ingestion or inhalation.

The Kuwaiti oil well fire exposure assessment considered multiple variables. The oil fire combustion products exposures of interest included suspected carcinogens, noncarcinogenic compounds, and particulate matter. The number of days exposed was factored into the risk assessment model, and the exposure levels were compared to EPA standards to determine risk to individual service members.

The risk of cancer from the oil well fires was added to the risk of getting cancer from other sources, which may include smoking, diet, solar rays, and other environmental and occupational exposures. The excess cancer risk likely attributable to oil fire combustibles was calculated using EPA toxicity factors (cancer slope factor) and includes all cancer-causing compounds in the oil well fire smoke emissions, as well as other cancer risk factors, to determine the total excess cancer risk.

To assess the risk for noncarcinogenic compounds in oil well fire smoke, CHPPM compared the air concentration to an EPA toxicity reference concentration that equates to the amount of a chemical in the air a person could be exposed to for their entire lifetime without causing any adverse health effects. These levels were set to protect sensitive individuals such as the elderly and young children. An additive model was used to assess the impact of multiple, simultaneous noncarcinogenic chemical exposures in the air from the oil well fire smoke. The output was used to obtain a hazard index for the total exposure, which was compared to EPA’s established noncarcinogenic compounds. As long as the hazard indices for the individual noncarcinogenic chemicals total less than 1, no adverse effects are expected.

The total particles in the oil well fire smoke were measured as total suspended particulates. The EPA National Ambient Air Quality Standards mandated by the Clean Air Act of 1970 (Public Law 101-549, Section 812, 1990 Amendments[27]) for total suspended particulates at the time was 75 μg/m^3 of air (annual standard) and 260 μg/m^3 of air (daily standard). CHPPM used 1986 total suspended particulates daily standards because the data were available and the troops were exposed for less than a year (so the annual standard was not appropriate).[4]

The development of the exposure registry for the Kuwaiti oil well fires consumed considerable resources and involved many US government agencies. The response addressed the mandates of Congress, but the quality of the assessment has never been evaluated.

Depleted Uranium

DU is used in munitions and military or civilian equipment because of its high density and relative availability. DU has multiple uses including helicopter rotor counter balances, radiation shielding, components of munitions, and armor on military vehicles.[28] DU is a potential health hazard because uranium is a toxic metal and it is weakly radioactive. Uranium can affect the normal functioning of the kidney, brain, liver, and heart. The impact of DU munitions and combustion of DU-containing materials can generate aerosols that may contaminate wide areas. Some DU aerosols can be inhaled.28,29

Natural uranium (NU) is one of the most common elements on Earth and can be found in rocks, soil, rivers, and oceans. NU is radioactive and is one of the main elements that contributes to terrestrial radioactivity. It is a mixture of different isotopes: uranium-238, uranium-235, and uranium-234. Uranium-238 is the most common isotope, comprising about 99% of the mass of NU.

DU contains the same three isotopes as NU; however, the proportions are different. In DU, much of the uranium-234 and uranium-235 has been removed, and as a consequence, DU is 40% less radioactive than NU. DU arises as a byproduct during the enrichment process of NU to make fuel for nuclear reactors. During the enrichment process the composition of uranium is changed by separating the uranium-234 and uranium-235 from the uranium-238.[29] In short, the more radioactive components are removed from the element and the less radioactive uranium-238 remains, hence the name DU.

DU is widely known for its use as a large-caliber, antiarmor munition penetrator. During the Persian Gulf War, when DU-containing munitions were first used, a number of soldiers raised health concerns. They were exposed to DU aerosols when in vehicles struck by DU munitions. Other soldiers presumed they were exposed when their battlefield duties required them to enter vehicles hit by DU munitions or to be in areas containing DU residues. Responding to the DU health concerns of Persian Gulf War veterans, the VA and DoD initiated a medical follow-up program for exposed individuals and a research program to assess the health risks associated with DU. Supporting this effort were the US Army, Battelle Memorial Institute, Pacific Northwest National Laboratory, and the Lovelace Respiratory Research Institute. These organizations collaborated to create the Capstone Depleted Uranium Aerosol Characterization and Risk Assessment, which was sponsored by the Office of the Special Assistant for Gulf War Illnesses (OSAGWI) and the US Army. An outgrowth from OSAGWI was the publication of Depleted Uranium Aerosol Doses and Risks: Summary of US Assessments (the Capstone Report).[30]

The authors of the Capstone Report intended to provide rigorous, peer-reviewed scientific estimates of the health risks to military personnel from DU aerosol exposure, primarily those soldiers exposed “to DU aerosols inside perforated armored vehicles.”[30] Information on exposures to military personnel near perforated or burning ammunition was also included.[30] The Capstone Report included both exposure assessments and health risk assessments, with the goal of developing accurate data for health risk assessors to use in evaluating soldiers exposed to DU as a result of being in or around a vehicle perforated by a DU munition.[30]

The exposure assessment portion of the Capstone study involved a series of field tests on vehicles struck by DU penetrators. It was conducted in four phases and focused on the concentration and characteristics of aerosols and residues generated inside the vehicles at the time of impact, during settling, after settling had occurred, and in the residues found outside the vehicles. During Phase I and Phase II of the field testing, Bradley fighting vehicles and ballistic hull and turret versions of Abrams tanks without DU armor were used to simulate the battlefield conditions of the Persian Gulf War. Phase III and Phase IV were designed to simulate future conflicts. In these later phases, Abrams tanks with DU armor were used as targets.

The human HRA portion of the Capstone study “used internationally recognized models to estimate the radiological dose and chemical concentrations in the body and translate these values into estimates of risk.”[30] Radiation health risks were evaluated based on radiation doses and risks to individual organs and tissues rather than estimates of whole-body or effective doses. The primary organ of interest with respect to health effects of uranium exposure is the kidney.[31] Because of the concern for adverse effects on the kidneys, the authors of the Capstone Report developed a system to quantify chemical risks based on the concentration of uranium in the kidney.[30] The Capstone Report concluded, “the chemical and radiological doses and risks to human health in inhaling DU aerosols in a perforated vehicle are relatively low when compared to many other combat risks.”[30] The Capstone Report provided quantitative estimates of risk for various exposure scenarios. For example, among the mostly highly exposed populations, the median lifetime fatal cancer risks ranged from 0.005% to 0.45%.[30]

The National Academy of Science’s Committee on Toxicology (NAS-COT) reviewed the Capstone Report and found “the methods and results of the Capstone exposure assessment to be appropriate and well done” and “the Capstone exposure results are reasonable and appropriate for human health-risk analysis of DU.”[32] However, the NAS-COT report also recommended future assessments. The NAS-COT review of the Capstone Report found the study’s approach to assessing cancer risks to be “appropriate because it allows for the lack of uniformity in dose distribution among organs.”[32] With respect to the chemical risks to the kidney, the NAS-COT review recommended that the authors of the Capstone Report review the accuracy of data presented to support its values for the concentration of uranium in the kidneys associated with minimal or no detectable health effects, and that the Army avoid giving the appearance that these uranium concentration values are precise demarcations of the potential for adverse health effects.[32] The authors reviewed the interpretations in the Capstone Report and “identified some apparently conflicting results that might have led to the NAS-COT’s uncertainties.”[33] The authors concluded that their original analyses were correct but recognized that the human data used to develop the risk model were not as robust as desired, adding to the overall uncertainty of the results.[34] To ensure wide dissemination of the results of the Capstone study, the entire March 2009 issue of Health Physics, The Radiation Safety Journal, was dedicated to publishing the results.[34]

DU’s potential for causing adverse health effects derives from both its radiological and chemical properties. However, the chemical toxicity of DU is the principal health concern and the radiological hazards are generally of less concern, because both NU and DU are only weakly radioactive.[32] Uranium is distributed mainly in the bones, liver, and kidneys once it is taken into the body. The bones form a long-term repository for uranium with a half-life of 70 to 200 days.[32] Most of the remaining uranium in the body has a half-life of about 7 to 14 days.[32] Because uranium can accumulate in the kidneys, these organs are of main concern when evaluating human health risks. Kidney damage has been seen in humans and animals after ingestion or inhalation of uranium into the body.[32] However, among soldiers with embedded fragments containing DU, kidney damage has not been seen thus far.[31] It is possible that for more insoluble forms of DU, the radiation dose to the lungs could become the major concern.[35] In summary, the Agency for Toxic Substances and Disease Registry, Atlanta, Georgia, reported that “no other health effects, other than kidney damage, have been found in humans after inhaling or ingesting uranium or in soldiers with uranium metal fragments in their bodies.”[31]

The DoD addressed service members’ concerns about potential exposure to DU through a variety of DoD and service-level policies and directives. The Deployment Health Clinical Center established a website for service members and healthcare providers seeking information regarding DU exposures. This website lists policies, directives, clinical guidance, and fact sheets on DU.[36] The DoD has arranged with the University of Maryland and the Baltimore VA office to maintain a medical screening program to track service members who may have been exposed to DU. A service member who reports DU exposure and requests follow up for DU exposure may be referred to the VA. The VA maintains a registry of service members with embedded DU fragments and others with confirmed exposure to DU, and it has followed these service members since 1993 to identify the long-term health outcomes of exposure.[36]

Overall, the risks associated with exposure to DU on the battlefield are comparable to other battlefield risks. DU garnered considerable attention because it is a radioactive heavy metal, and the health of military personnel is of paramount concern to the DoD. DU and its residues are neither “innocuous nor are they a ‘deadly poison,’” and although risks of exposure are predicted to be low, these risks should be discussed with affected personnel and their family members.[30]

The Institute of Medicine continued to study the potential for health effects in service members potentially exposed to DU long after the Persian Gulf War, and the VA biennial health surveillance program for veterans with DU exposures continues follow-up of this group.37–41 A 2008 Institute of Medicine report included information from the VA that indicated veterans with embedded fragments continue to have elevated urine DU concentrations. However, since the study began in 1993, the VA has found minimal effects on proximal tubule function, cytotoxicity, or pulmonary function.[41]

Chemical Weapons and the Khamisiyah Storage Facility

Chemical agent exposures, both from directed enemy threats and from the destruction of enemy storage sites, were concerns during the Persian Gulf War. US troops were frequently ordered to don their gas masks and protective suits because of chemical warfare agent detections by Czech, French, and American forces.42,43 The nerve agents tabun (GA), sarin (GB), and cyclosarin (GF) and the blister agents sulfur-mustard and lewisite were detected by Coalition forces.[42] Fortunately, no large-scale Iraqi employment of chemical weapons occurred during the war. There were no service members seen for severe chemical injuries, nor were there any fatalities that resulted from nerve agent exposure.[42] The tactical situation on the battlefield prevented Iraqi forces from using their chemical weapons: the speed of the Coalition advance and the effectiveness of the strategic bombing campaign in disrupting Iraq’s military command-and-control system made it difficult for commanders to select targets for chemical attacks. In addition, the prevailing winds shifted to the southeast toward the Iraqi lines at the start of the war.[42] The London Sunday Times reported that “Iraqi military communications indicated that Iraqi President Saddam Hussein had authorized commanders to use chemical weapons at their discretion as soon as Coalition forces began their ground offensive.”[44] A British signals officer who monitored the Iraqi command net “heard the release order to front-line commanders to use chemical weapons against Rhino [coalition] force if they crossed the border.”42,44

Although chemical weapons were not broadly used, US units discovered chemical munitions in Iraqi bunkers during and after the ground war and noted these discoveries in their unit logs. Troops reported acute symptoms of toxic chemical exposure and sought treatment in troop medical clinics. The incidents were described in intelligence reports, operations logs, and command chronologies on DoD websites.42,43,45

Storage areas that posed a potential risk to US service members included four Iraqi chemical weapons sites, the major one being Khamisiyah because of the possibility of a large number of troops having been exposed there. The sites are as follows:

- Muhammadiyat housed bombs containing mustard and nerve agents GB and GF. Exposures may have occurred during aerial bombing.

- The Al Muthanna bunker contained GB. Exposures may have occurred during aerial bombing.

- Ukhaydir housed artillery shells containing mustard. Exposures may have occurred during aerial bombing.

- Khamisiyah contained rockets with GB, GF, and mustard agent. US forces destroyed the weapons cache by demolition.[46]

On March 4, 1991, a total of 37 large ammunition bunkers were destroyed, and Iraq confirmed that Bunker 73 at the Khamisiyah Ammunition Supply Point contained 2,160 rockets filled with chemical warfare agents. On March 10, 1991, another 40 ammunition bunkers and 45 warehouses were destroyed. Soldiers also destroyed approximately 1,250 rockets outside the Khamisiyah Ammunition Supply Point, which the United Nations Special Commission later confirmed contained chemical warfare agents. The demolition operations at Khamisiyah continued through April 1991. The were no reports of chemical warfare agents in the inventories conducted before the bunkers were destroyed, but that may be due to mislabeling or poor recognition of the markings on the munitions. Throughout the US occupation of Khamisiyah, no medical encounters were reported for soldiers seeking treatment for chemical warfare agent exposures.

After the end of the Persian Gulf War and after soldiers of the US Army’s XVIII Airborne Corps destroyed munitions there, US Army units occupied an area in southeastern Iraq that encompassed Khamisiyah. In September 1996 the secretary of the Army directed the department of the Army inspector general to conduct an inquiry to determine the facts surrounding the demolition of ammunition at Bunker 73 at the Khamisiyah Ammunition Storage Facility in March 1991.[47] The inspector general’s findings led the intelligence community to conclude that chemical munitions were present when the facility was destroyed. They concluded that 2,160 rockets filled with GB and GF were present at Khamisiyah, and that 1,400 of these rockets were destroyed in Bunker 73 and an adjacent pit area. Furthermore, 6,000 mustard-filled shells were present at Khamisiyah, and about 2,000 of them were destroyed in Bunker 73. Approximately 430 soldiers participated in the destruction of the facility. The Central Intelligence Agency (CIA) and Defense Intelligence Agency estimates were that chemical munitions destroyed at Khamisiyah may have exposed 100,000 soldiers to low levels of GB (greater than the general population background level of 0.01296 mg-min/m^3, but below the health effects level of 1 mg-min/m^3).[48]

The analysis of the Khamisiyah bunker site, where US forces may have been exposed to chemical agents when they detonated the bunker contents in March 1991, used the troop exposure assessment model to analyze chemical agent release data provided by DoD and other US government agencies. CHPPM provided support for modeling, mapping, and merging the results of the different dispersion and meteorological models, and identifying exposure standards for agents. Its personnel contributed to outreach efforts, including town hall meetings. Additionally, CHPPM staff identified the service members who may have been exposed to chemical agents following the detonation and collaborated with DoD and other government organizations on epidemiological studies of these troops.49–52 CHPPM scientists also determined chemical agent exposures for US forces at three other sites: Al Muthanna,[53] Muhammadiyat,[54] and Ukhaydir.[55]

The initial work of the OSAGWI examined the US military operations at Khamisiyah. On February 21, 1997, OSAGWI published its first report on Khamisiyah.[56] The events were described and the units involved were identified. OSAGWI contacted thousands of service members as part of the effort to do computer modeling of exposures to determine the size and path of the hazard area downwind from the demolition activities. DoD sent 100,000 notification letters to inform individuals of their exposure to chemical warfare agents. The model used computer simulations, based on the best available science, to predict individual exposures. The letters alerted individuals to the exposure but did not address the potential for long-term health effects. The VA did not accept these letters as proof of exposure when veterans submitted claims for compensation.

The OSAGWI computer model was refined by adding improved meteorological data, obtaining better estimates of the quantities released based on CIA estimates, using deposition and decay factors, and taking the toxicity of sarin and cyclosarin into account. Further, the DoD destroyed munitions similar to those found at Khamisiyah using chemicals with similar physical properties to sarin to better predict the downwind dispersion of chemical agents released. These open field demolition tests on 122-mm rockets, conducted in May 1997 at Dugway Proving Ground, Utah, were used to help determine how chemical warfare agent in Iraq’s rockets might have been released by the demolitions at Khamisiyah. Although the fundamental modeling methodology had not changed between 1997 and 2000, modifications were made to obtain improved modeling output, including the revision of the meteorological models, updating the CIA estimate of how much chemical warfare agent was released, and the addition of deposition and decay to the models.46,57 The final model was run in January 2000, and the redefined hazard area included an additional 752 veterans who were potentially exposed to low levels of nerve agent.

In the revised 2000 model, CHPPM incorporated better toxicity data on cyclosarin that was not available in 1997. CHPPM noted that the quantity of sarin was three times that of cyclosarin, but the toxicity of cyclosarin was almost three times that of sarin. Cyclosarin is less volatile than sarin, so it evaporated more slowly. With this refined toxicity data, the revised model produced more precise hazard-area estimates.

CHPPM scientists also recommended that the final January 2000 model use a general population limit based on short-term exposures because the release occurred over a 4-day period. The general population limit represents the limit below which any member of the general population could be exposed over a lifetime without experiencing any adverse health effects. The general population limit was modified with the addition of uncertainty factors and adjustments for the average person, making it more representative of military personnel and less representative of more sensitive seniors and children.

The CURR contributed to the exposure estimates by developing a database beginning in 1993 that contained daily company-level unit geographic locations for the Persian Gulf War Theater. This effort was based on experience gained by developing the Agent Orange Exposure Database after the Vietnam War. For the Persian Gulf War Troop Movement Database, the CURR gathered all the unit history data archives such as log reports, after action reports, and other pertinent information. This amounted to over 5 million pieces of paper from which over 800,000 unit grid coordinates were created.

Beginning in April 1997, Army division and battalion operations officers performed data gap fills at the CURR to provide unit movement records as completely as possible. The CURR finished these efforts in 1999, but continued to work with personnel from other units to improve and update the database. With the CURR Troop Movement Database, CHPPM scientists could identify daily company-level unit identification code (UIC) locations and associate them with potential individual service member exposures in the identified units based on the DMDC Persian Gulf War Registry.

CHPPM combined data from CURR’s Troop Movement Database of 855,000 unit locations with information from DMDC on which troops were assigned to those units to determine which were exposed to chemical agents. The 2000 model produced graphic representations of the projected hazard area with associated levels of exposure for service members from March 10 to 13, 1991. CHPPM scientists overlaid data on US troop unit locations on the graphic representation of the projected hazard area to create a plot that shows the exposed troop units.

The methodology used to locate troops possibly exposed to a particular environmental agent, at a designated time and place, included the following:

- A geographic information system operational base map for the region of interest was prepared with the political boundaries included.

- Troop units were geo-referenced by UIC for the particular time frame in question (eg, March 10–13, 1991) by using the CURR troop unit movement database. For the above assessment, the CURR troop unit movement database used was from November 2000.

- The particular geographic area of interest (Figure 6-4) and the exposure area (derived from meteorological and dispersion modeling) was geo-referenced with the troop units. Using geographic information system techniques, the exposure area was generated by combining modeled outputs from the Defense Threat Reduction Agency, the Naval Surface Warfare Center, and the CIA.

- Using geographic information system techniques, company-level units within the potential hazard area were identified. These units were then sent to OSAGWI, which queried the DMDC Desert Shield/Desert Storm Personnel File (containing 696,693 records) to determine which individuals were in the identified units. The database not only had the last UIC the individual was assigned to, but also contained UIC lists for six distinct time frames for active duty personnel and two additional time frames for reserve units.

Incidents of reported exposures to chemical weapons in the Persian Gulf War were assessed by the OSAGWI from its initial assessment in 1997, to 2002. Summary reports were placed on the website.[45] The investigators reaffirmed earlier findings that chemical warfare agents were present at Khamisiyah and US soldiers destroyed many, but not all, chemical agent weapons in the Khamisiyah pit and Bunker 73.[46]

United Nations Special Commission inspectors also verified the presence of chemical agent rockets in the Khamisiyah pit in October 1991, and the OSAGWI investigation, supported by DoD agencies and the intelligence community, confirmed that US units damaged or destroyed some 2,000 rockets on March 10, 1991. The investigators concluded that demolition of rockets in the pit exposed US units to low levels of chemical warfare agents. However, they were less certain that the destruction of Bunker 73 exposed US service members to chemical agents. Units in the area were a safe distance from the site, and the demolition was thought to have completely destroyed Bunker 73. Additionally, they believed that rains after the event dissipated the chemicals and that prevailing winds blew the chemicals away from US forces. In 1999, the CIA estimated that the amount of agent released was only 5% of that estimated in 1996, further supporting the conclusion that veterans were not likely exposed to chemical warfare agents. The investigators found no evidence that any soldiers at Khamisiyah reported symptoms consistent with exposure to a chemical warfare agent.45,46

Figure 6-4. The Defense Manpower Data Center Troop Identification base map shows unit locations in the area of interest. The modeled potential hazard area overlay depicted on Day 1 (March 10, 1991) following the destruction of chemical agent munitions at the Khamisiyah ammunition storage facility shows that numerous units were within the potential hazard area. Map courtesy of Jacqueline Howard, US Army Public Health Center.

OSAGWI also concurrently investigated other incidents of reported exposures to chemical agents among US forces in 1990–1991 at sites other than Khamisiyah. Anecdotal reports, documentary and physical evidence, and reports of interviews with eyewitnesses and key personnel were analyzed. Investigators looked for evidence that chemical warfare agents were present at the sites and rated each one using a five-point scale ranging from “definitely” to “definitely not,” with intermediate assessments of “exposures likely,” “unlikely,” or “indeterminate.” All incidents were determined to be in either the “definitely not” or “unlikely” category.45,46

Jet Propellants JP-5 and JP-8

The major jet fuels used by military aircraft of the United States and its North Atlantic Treaty Organization (NATO) allies include jet propellant–5 (JP-5) and jet propellant–8 (JP-8). The US Navy chose JP-5 as its primary jet fuel because it is safer to use on ships with its higher flash point and lower volatility, and it provides better Navy jet performance.58,59 JP-8 was adopted by the US Army and Air Force for all aircraft, ground vehicles, and heating and lighting devices.[60] Both JP-5 and JP-8 are refined from crude petroleum.[61] Both fuels are colorless liquids that smell like kerosene, the primary ingredient, and both often contain additive ingredients that permit specialized use. They are liquid at room temperature, but they do vaporize and are considered flammable. The US and NATO effort to adopt a common jet fuel began in the 1980s and finally succeeded in 2000, taking over 20 years to complete because jet engines, vehicle engines, heaters, and other military equipment had to be converted for JP-8 use.[62]

Military service members are exposed to jet propellants in the occupational setting when they work with transporting and storing JP-5 and JP-8, or during refueling operations. Also, environmental exposures occur when cold engine starts of aircraft are conducted. In the occupational setting, maintenance mechanics are required to enter military aircraft fuel cells to look for damage and structural cracks, and often the fuel is not completely removed before their entry. Many service members are exposed when they fill tent heaters and when they perform maintenance on military vehicles (cleaning and degreasing parts) using JP-8.63,64 The routes of entry of JP-8 into the body include inhalation, dermal absorption, and ingestion. Environmental contamination of ground water occurs from spillage or underground storage tank leaks, and may lead to people drinking water containing JP-8. Military fuel handlers are at risk of breathing in vapors of JP-8 when they refuel aircraft and vehicles.

Often maintenance personnel work without the protective coveralls specially made to resist penetration by the fuels. This leads to dermal absorption from coveralls that are soiled and saturated with JP-8. The US Air Force developed a specially designed set of coveralls for its fuel handlers and maintenance personnel that is both nonsparking and resists penetration by JP-8. In addition to coveralls, workers are required to wear impermeable gloves and boots. Because of the low vapor pressure, a respirator is not usually required in most applications.[65]

Carbon monoxide is one of the byproducts of incomplete combustion of JP-5 and JP-8.[61] This represents the most significant health hazard associated with JP-5 and JP-8 and has resulted in more deaths among service members than any other health effect related to these two fuels. Animal studies show that JP-5 and JP-8 are distributed to organs including the brain, lungs, liver, spleen, and kidneys. However, toxicological studies have not well documented the absorption, distribution, metabolism, and excretion of these fuels in humans.

Many of the toxicological properties of JP-5 and JP-8 are dependent upon the refining process and the source of crude oil used in production.[61] Health effects are dependent on the dose of exposure, duration of exposure, route of entry, and sex and age of the affected individual. Many of the health effects related to these fuels can be predicted based on the toxicological properties of kerosene. Case studies involving children who drank kerosene report that they experience vomiting, diarrhea, stomach cramps, drowsiness, restlessness, irritability, and loss of consciousness. In some cases, children who drank large amounts of kerosene developed convulsions followed by coma and death. If kerosene enters the lungs, children experience coughing, pneumonia, and difficulty breathing.[61] As predicted, inhalation of large amounts of JP-8 vapors causes difficulty breathing as well.[61]

The central nervous system effects of exposure to JP-8 or JP-5 vapors include headache, lightheadedness, anorexia, poor coordination, and difficulty concentrating.61,66 Dermal exposure to JP-8 may cause itchy, red skin and occasional blisters. Toxicological studies in animals show that repeated skin exposure to JP-8 causes skin cancer in mice.[64] Studies also found that JP-8 is genotoxic because it induces unscheduled deoxyribonucleic acid synthesis.[65] Metabolic degradation products of JP-5 and JP-8 include benzene, toluene, and xylene, which can be detected in blood and urine.[61] Naphthalene has been suggested as a biomarker of exposure to jet fuel.[67] The International Agency for Research on Cancer classified JP-5 and JP-8 as probable carcinogens but noted that more information is needed for humans.[68]

The Department of Transportation classified JP-5 and JP-8 as hazardous materials that pose a risk to health, safety, and property when moved. OSHA has regulated exposure to these fuels in the workplace.[69] The permissible exposure limit for JP-8 is 400 mg/m^3.[69] The military exposure guideline for exposure to JP-8 is similar to the OSHA standard. One toxicological study of JP-8 in humans noted immune suppression following moderate to high exposures in a long-term study.[70] Many people are exposed to JP-5 and JP-8 at work, and long-term studies are needed to examine the health effects of chronic exposure to these jet fuels.[71]

Gulf War Illness in Summary

The DoD began a long-term research effort in 2006 to understand the causes of GWI and to better characterize the medical condition. Despite several hundreds of millions of dollars being spent on research, a medical explanation for what caused GWI is still not available, nor is there a single diagnosis for the condition. The search for possible causes never ended.6,7,9,14,24

Persian Gulf War veterans questioned possible links between their symptoms and the hazardous substances they encountered while deployed. Some of the exposures causing concern included the following:

- The greatest concern among service members was the smoke generated by oil wells burning in Kuwait for much of 1991.[4]

- Deployers were worried by the chemical agent alarm warnings and nerve agent exposures resulting from the destruction of chemical agent storage facilities in Iraq.

- Some mistrusted the pyridostigmine bromide pills they were given to protect against the acute effects of nerve agents.1,6

- All military personnel who deployed to the Gulf were given anthrax and smallpox vaccines, and many were anxious about side effects.

- Service members were exposed to pesticides and given insect repellants to protect against diseases transmitted by biting insects.

- The military used DU in ammunition fired from tanks and armored vehicles, as well as in the armor of many vehicles.

Personal breathing zone samples were not collected on service members who deployed to the Gulf. As a result, investigators who were trying to determine the cause of GWI were hampered by the lack of available data. Epidemiologic studies that relied on veterans’ self-reported exposures during deployment suffered from recall bias, but some studies still noted poor health outcomes.72,73 Some studies pointed to a limited number of significant risk factors for GWI.74–76 Other studies found many exposures to be highly correlated, suggesting that confounding errors were present in the studies that evaluated associations between exposure and GWI.77–79

In 2008, a congressional federal advisory panel reviewed the scientific literature on the health of Persian Gulf War veterans.[80] The federal advisory panel report noted limitations in the epidemiologic studies in that they failed to assess risk factors for GWI using appropriate analytic methods for complex Persian Gulf War exposures. The panel recommended that studies of GWI include risk factors that are relevant to the outcomes of interest and that analytic methods take into account confounding due to concurrent exposures.[80]

Few studies of GWI provided insights into its causes or the distribution in Persian Gulf War veterans. Further, some studies noted differences in the distribution of disease based on deployment location in theater.18,81 GWI was more prevalent in veterans who deployed to Iraq or Kuwait, where all battles took place, compared to veterans who went elsewhere.

Studies of GWI that controlled for confounding factors due to multiple exposures75–78 found that few exposures were significantly associated with GWI. Only the use of pyridostigmine bromide pills and pesticide exposures were consistently identified risk factors for GWI.74,75,77,78,80 During the Persian Gulf War, US military personnel were poorly informed about pesticide use.[79] Service members tended to overuse pesticides to control swarming and biting insects because they were concerned about sand flies and the diseases they carried.[79] The studies considered the interactions possible between permethrin, used to treat uniforms, and DEET (N,N-diethyl-meta-toluamide), which was applied to the skin to repel insects.

Epidemiologic studies of Persian Gulf War veterans suggested that significant results needed to be adjusted for multiple comparisons and that findings may be due to chance alone. The research community developed several GWI case definitions, including criteria from the Centers for Disease Control and Prevention and a Kansas study.16,18 When the Centers for Disease Control criteria for developing a case definition were applied, the results were consistently in the same direction (positive or negative) but were considerably weaker compared to the Kansas GWI criteria.16,18 GWI is likely a set of conditions that have overlapping symptoms, which makes detecting cases difficult. The etiology of GWI is complex, and many deployment-related exposures probably contributed to the development of the constellation of symptoms known as GWI.[80]

BOSNIA, HERZEGOVINA, AND KOSOVO (1995–1999)

In the mid-1990s, the US military deployed troops to the former Yugoslavia to provide security and promote stability among groups engaged in what was to become a decade-long series of brutal ethnic conflicts.[5] With the long-term health concerns from Vietnam and the Persian Gulf War fresh in their minds, leaders in the DoD and the military services looked for ways to avoid or mitigate potentially harmful deployment exposures, including improving field sampling to identify harmful agents, improving risk assessment processes, and improving policies and doctrine.[5]

Operations Joint Endeavor, Joint Guard, and Joint Forge

The Dayton Accords, the framework for peace in Bosnia and Herzegovina, was signed on December 14, 1995.[5] That same month, about 20,000 US forces arrived in Bosnia as part of NATO’s Operation Joint Endeavor. US Army–Europe became concerned about potential exposures among US forces and tasked CHPPM to assess ambient air quality at Lukavac Base and Tuzla Air Base.[5] Personnel at Lukavac Base were near a coal storage area with operating coal-fired boilers and were exposed to airborne soot and other air pollutants from burning coal and fugitive emissions (Figure 6-5). Similar conditions existed at Tuzla Air Base, where coal-fired boilers provided electricity and heat. Beginning in February 1996, CHPPM scientists conducted air and soil sampling to document the conditions.[5]

Environmental surveillance for Operation Joint Endeavor, Joint Guard, and Joint Forge (Operation Joint Endeavor transitioned to Operation Joint Guard on December 20, 1996; Operation Joint Guard transitioned to Operation Joint Forge on June 20, 1998) was the most comprehensive surveillance effort for any deployed US force to date. It involved a coordinated approach between military tactical and support organizations. The surveillance plan initiated by the 30th Medical Brigade, which provided theater medical support for Europe, became a template for future joint medical surveillance systems as envisioned in DoD Directive 6490.2, Joint Medical Surveillance, August 30, 1997. The surveillance work was done by the US Army 520th Theater Army Medical Laboratory, CHPPM, and CHPPM satellite organizations in Europe and the United States. Samples were collected from all US base camps in Bosnia and from several other international forces camps in Bosnia, Croatia, and Hungary (Figure 6-6). In excess of 2,300 environmental samples were collected and analyzed for over 120,000 different analytes. The environmental media sampled included air, water, and soil. Sampling parameters included volatile organic compounds, semi-volatile organic compounds, metals, pesticides, herbicides, radiation, and particulate matter.

Figure 6-5. Emissions from coal-fired power plants impacted air quality where US forces were located, Bosnia, 1999. Photograph courtesy of Brad Hutchens, US Army Public Health Center.

When samples were analyzed, it was sometimes difficult to determine the significance of the pollutant level relative to a potential health effect. Reference standards did exist, such as the National Ambient Air Quality Standards for criteria pollutants (certain pollutants known to be hazardous to human health), occupational exposure limits, and some comparative values for other chemicals for the general population. However, it was determined that workplace standards were inappropriate for individuals whose exposure might be constant, as opposed to those exposed during an 8-hour workday. Also, the applicability of general population standards for deployed military forces was questioned. There were no comparable standards for some chemicals, so in order to provide context and determine the significance of a finding, the measured level was compared to typical levels in urban and rural environments in the United States. While this did not guarantee that the pollutant level had no associated health effect, it did reflect the fact that US air is not pristine, and is not routinely monitored for many hazards, apart from the National Ambient Air Quality Standards.

Air Sampling Summary

Various compounds were detected in the ambient air of base camps. These results were compared to US environmental standards and guidelines such as the National Ambient Air Quality Standards that address the criteria pollutants (particulate matter, carbon monoxide, ozone, oxides of sulfur, oxides of nitrogen, and lead) and EPA Region 3 risk-based concentrations.[82] These standards and the EPA guidelines are based on lifetime exposures for the entire US population, including sensitive individuals such as young children, those with asthma, and the elderly.

Figure 6-6. The map shows environmental sampling locations for Operation Joint Forge, Bosnia, Herzegovina, and Kosovo, June 20, 1998–December 2, 2004. The photos in the graphic are of Camp Bedrock and Ugljevic, Bosnia, August 1996. Graphic courtesy of Brad Hutchens, US Army Public Health Center.

Particulate matter levels were occasionally elevated up to 2 to 3 times above EPA standards in air samples collected from the base camps. Most of the other compounds detected during the monitoring did not exceed published guidelines. Those compounds that did exceed the standards and guidelines (such as volatile organics, which are not criteria pollutants) were detected at concentrations similar to those present in typical urban areas within the United States. These levels were not expected to pose significant health risks to US forces because the deployed service members were primarily healthy young adults and the duration of their exposures was short.

Water Sampling Summary

US forces primarily used bottled water for consumption and restricted the use of local water to sanitary activities such as showers, laundry, and dishwashing. All water supplies intended for US forces were sampled and analyzed prior to use. Analytical results were compared to health-based standards and guidance such as the EPA primary and secondary maximum contaminant levels (MCLs) established December 16, 1974, under Public Law 93-523, the Safe Drinking Water Act of 1974 (↱42 USC § 300f),[83] and EPA health advisories when an MCL did not exist. The EPA initiated the nonregulatory Health Advisory Program in 1978 to provide information on pollutants that can affect drinking water but were not regulated under the Safe Drinking Water Act. Primary MCLs apply to contaminants that can pose a health threat, while secondary MCLs apply to parameters that may affect the aesthetic quality of water. Overall, very few sources contained compounds at concentrations greater than the primary MCLs. A few sources were contaminated with the pesticide dibromochloropropane in excess of the MCL. The levels detected were not expected to pose a significant health risk to US forces due to the consumption of bottled water. Occasionally, secondary contaminants such as iron and manganese exceeded the secondary MCLs, but no adverse health effects were expected.

Soil Sampling Summary

Various compounds were detected in the surface soils of the base camps. These were compared to the EPA Region 3 risk-based concentrations for soils in industrial settings.[82] The only compounds detected that exceeded these guidelines were total petroleum hydrocarbons from fuel spills at several of the camps and semivolatile organic compounds from coal combustion. These compounds were not of great concern because exposure to the soil could be avoided or mitigated. The observed radiological concentrations in the soil samples from various base camps fell within the expected ranges for naturally occurring radiological materials when compared to the typical concentrations as outlined by the United Nations Special Commission on the Effects of Atomic Radiation Report.[84] With the exception of cesium-137, other anthropogenic or manmade radioisotopes (eg, cobalt-60 and americium-241) were not detected in any samples. The cesium-137 concentrations were slightly elevated when compared to soil samples collected from Hungary and may have been attributable to the fallout from the 1986 Chernobyl Nuclear Power Plant accident.

Pesticide Wipe Sampling Summary

Pesticide residues were detected, such as malathion, chlorpyrifos, malaoxon, and gamma-hexachlorocyclohexane (also known as lindane) in wipe samples collected throughout troop living areas. Several of the pesticides detected were not commonly used in indoor applications. Their presence in the living areas may have been the result of improperly cleaned pesticide application equipment or improperly cleaned shoes and clothing being brought into the living area. Lindane presented the most concern due to its persistence and toxicity. Lindane dust was previously a component in military unit field sanitation team supplies; however, at the time of the surveillance it was not approved for this use. It is possible that unit-level field sanitation team supplies were contaminated from earlier lindane use. Fortunately, the levels detected were low and not considered to pose a threat to US personnel.

Operation Joint Guardian

CHPPM scientists and others in the DoD studied the environmental surveillance events of Operation Desert Storm, Operation Joint Endeavor, Operation Joint Guard, and Operation Joint Forge and took action to further improve their response for future operations. In June 1999, when US forces entered Kosovo as part of the NATO-led Kosovo forces in Operation Joint Guardian,[5] improvements in the tools for planning and conducting environmental health assessments and surveillance contributed to a well-constructed and well-executed environmental surveillance plan. This plan facilitated identification, documentation, and effective communication of environmental health risks to commanders, who could then take action to avoid or mitigate the risks. Preliminary threat assessments included identification of all known industrial facilities at a location, with a consideration of safe zones surrounding these facilities in the event of a catastrophic event. All pertinent data, reports, and assessments were archived for future use in systems that would eventually become the Military Exposure Surveillance Library (MESL) and the Defense Occupational and Environmental Health Readiness System Industrial Hygiene (DOEHRS-IH) Environmental Health module. In addition, to address the health risk to military personnel while deployed, CHPPM initiated a project to establish military-specific exposure levels for use in the interpretation of sampling results. The resulting Military Exposure Guidelines were based on existing limits with some modifications, such as addressing duration where an 8-hour daily occupational limit would be divided by three to reflect the 24-hour exposure in a deployed setting. These were eventually developed for air, water, and soil at varying military health effect levels (eg, severe, significant, and minimal).

The environmental surveillance activities in the former Yugoslavia reflected the culmination of years of effort by the DoD and the military services to prevent adverse health effects associated with environmental exposures among service members after the 1991 Persian Gulf War. In several instances, the results of monitoring were used by commanders in decision-making. For example, a medical facility was moved due to its proximity to an incinerator, and a lead smelter was closed due to high levels of lead measured in the air. The development of DoD and military service environmental surveillance doctrine led to improved equipment and sampling methods as well as more and better training, and these efforts were credited for the successful environmental surveillance efforts in the former Yugoslavia in the 1990s.[5]

OPERATION IRAQI FREEDOM AND OPERATION ENDURING FREEDOM (2001–2015)

On September 11, 2001, terrorist attacks were launched against the World Trade Center (WTC) in New York City and the Pentagon in Washington, DC. The attacks were attributed to the Islamic terrorist group al-Qaeda, which operated out of Afghanistan under the protection of the Taliban regime. On October 7, 2001, the US initiated Operation Enduring Freedom–Afghanistan (OEF-A) to destroy al-Qaeda’s safe base of operations in Afghanistan and end the Taliban’s protection of al-Qaeda. OEF also included antiterrorism operations on a smaller scale in other areas of the world, such as the Philippines (OEF-P) and the Horn of Africa (OEF-HOA). On March 7, 2003, the United States began military operations against Iraq (OIF) because the administration of President George W. Bush claimed Iraq possessed and manufactured weapons of mass destruction and supported terrorist groups, including al-Qaeda. On September 1, 2010, OIF was renamed Operation New Dawn (OND). On December 15, 2011, the United States ended its military mission in Iraq, and on December 28, 2014, the US combat mission in Afghanistan was terminated.

US Army Medical Department OEH personnel provided support on a small scale to US Army Reserve and National Guard troops who responded to the WTC attack. On a much larger scale, they provided immediate and follow-up support for the Pentagon attack. They also assisted with the response to terrorist attacks using anthrax spores sent in the US mail. The very long Second Gulf War produced even more challenging occupational and environmental exposures in deployed forces than was observed in the Persian Gulf War.6,85

9/11 Attacks on the World Trade Center and Pentagon

The 9/11 attacks consisted of four coordinated suicide attacks on major landmarks in the United States. Nineteen al-Qaeda terrorists hijacked four fully fueled passenger airliners from airports on the US east coast and flew the airplanes toward their intended targets. Two planes hit the WTC; American Airlines Flight 11 crashed into the North Tower, and United Airlines Flight 175 hit the South Tower. Both towers collapsed within 2 hours of the attack. Debris and fires resulting from the fall of the two towers destroyed the other building in the WTC complex and significantly damaged ten surrounding buildings. The hijackers flew a third plane, American Airlines Flight 77, into the west side of the Pentagon, causing a partial collapse of that wing of the building. Passengers on the fourth plane were successful in battling the terrorists and caused United Airlines Flight 93 to crash into a field near Shanksville, Pennsylvania, before it reached its intended target in Washington, DC. The attacks killed 2,996 people and caused many billions of dollars in property damage.[86]

In October 2001, following the attack on the WTC, CHPPM was tasked to identify Department of the Army military and civilian personnel who had supported the rescue and relief efforts. CHPPM was also tasked to document potential exposures and activities performed by these people, determine their subjective current health status, identify perceived injuries or illnesses related to their participation, and offer them an opportunity to have their concerns addressed. A total of 256 WTC rescue and relief participants from the US Army Corps of Engineers and the New Jersey Army National Guard were identified and, beginning in January 2002, asked to complete a survey; 162 (63%) responded, most of whom were in the Army Reserve or National Guard. Respondents identified exposures to dust (87%), chemicals (67%), and smoke (44%); 26% requested medical consultation and were contacted by a CHPPM physician.

The Pentagon attack caused structural, fire, and water damage. Various DoD response teams were dispatched to the Pentagon immediately to determine the levels of hazardous contaminants present in all media in and around the Pentagon, recommend mitigation of any hazards that posed a health threat to occupants and personnel conducting response operations, and measure and assess the health impact of contaminants present from the aircraft and building fire and damage. Response teams included a Special Medical Augmentation and Response Team–Preventive Medicine (SMART-PM) from CHPPM and other personnel from the Pentagon Office of Safety and Health and the Uniformed Services University of the Health Sciences (in Bethesda, Maryland) Department of Preventive Medicine and Biometrics.

The mission of the advance party SMART-PM was to assess initial, acute occupational health hazards for personnel occupying the Pentagon and to recommend actions to assess chronic health risks. The advance team used direct reading instruments to measure volatile organic compounds; aldehydes; dusts; carbon monoxide; hydrogen sulfide; oxygen content; radiological hazards (alpha, beta, and gamma radiation); and combustible gases. The mission of the SMART-PM then transitioned to a systematic evaluation of damaged Pentagon corridors and work areas. The team was assigned to determine if personnel were at risk in their work areas from health hazards and contaminants following the attack and the resulting building fire in a structure approximately 60 years old.

A comprehensive sampling plan was developed, with recommendations from subject matter experts outside the DoD, to determine if levels of contamination in and around the Pentagon were safe for workers to resume normal operations with respect to long-term health risks associated with ongoing exposure. Sampling was conducted throughout the building, moving from the most contaminated areas near the crash site to the least contaminated areas of the building. Samples were collected from areas of personnel concentration. These included common areas such as corridors and intersections, and private areas, such as offices and conference rooms. Samples were collected on all floors including the basement, courtyard (Figure 6-7), and Child Development Center. Samples were collected to assess the health consequences of particulate and chemical emissions from fires and impact damage caused by the aircraft crash.

A wide variety of contaminants and products of incomplete combustion could have accumulated in the building because of the burning aircraft, fuel, and materials contained in the Pentagon. Therefore, numerous sampling methods were used to collect the contaminants. Samples were collected to identify and measure metals, volatile organic compounds, polyaromatic hydrocarbons, dioxins, furans, silica, and asbestos. Air samples were collected to assess the inhalation route of exposure, and wipe samples were collected to assess surface contamination and the risk from dermal exposure and incidental ingestion. In particular, wipe samples were analyzed for dioxins on the recommendation of outside consultants. In addition, water samples were obtained to determine if the drinking water system was contaminated. Occupational samples were also collected to assess exposures to personnel working inside and outside the Pentagon. Samples collected at the Pentagon by CHPPM, US Navy, and US Air Force personnel were analyzed at CHPPM and at certified contract laboratories.

A total of 3,273 precleanup samples, including those tested by direct reading instruments, were collected at the Pentagon. An additional 443 postcleanup wipe samples were also collected. Of the precleanup samples, only 14 asbestos and 41 lead wipe samples exceeded American Conference of Governmental Industrial Hygienists or National Institute for Occupational Safety and Health standards. While dioxin was detected frequently in the precleanup wipe samples, particularly near areas of fire, there was no standard available to determine associated health risks. A decision was made to clean and resample areas with high levels so that they could be deemed clean for comparison purposes. Apart from dioxin, only seven asbestos and one lead wipe sample were above health-based standards after cleanup. Conclusions drawn from the sample results were as follows:

- the only samples that exceeded health-based criteria were one lead wipe sample and seven asbestos wipe samples;

- dermal and incidental routes of exposure presented the greater, although still small, risk compared to the inhalation (air) route;

- contamination was concentrated in the area of the incident (corridors 5 and 6) and on the upper floors (4 and 5), because smoke and contamination tended to rise; and

- sampling data supported the conclusion that the health risks from all sampled parameters in the Pentagon, including lead and asbestos, both before and after cleanup, were minimal if any.

Figure 6-7. Environmental sampling conducted in the courtyard at the Pentagon after September 11, 2001.
Photograph courtesy of US Army Public Health Center.

Anthrax Attacks

Later in September 2001, letters containing Bacillus anthracis were mailed to media organizations and US senators.87,88 The first anthrax letters were mailed from Trenton, New Jersey, with a postmark dated September 18, 2001.[87] Letters addressed to Senators Tom Daschle of South Dakota and Patrick Leahy of Vermont were mailed from the same post office on October 9, 2001.[87] The government mail service was immediately shut down when a staffer in Senator Daschle’s office opened the letter on October 15, 2001. Senator Leahy’s letter was later found unopened in an impounded mail bag by State Department workers in Sterling, Virginia.[88]

At least 22 people contracted anthrax and five died.[87] A worker at American Media, Inc, in Boca Raton, Florida, died as a result of his anthrax exposure. The EPA found anthrax spores wherever the mail was distributed in the building, requiring extensive cleanup and decontamination of the buildings.[89] The cleanup and decontamination of the US Postal Service Brentwood Processing and Distribution Center, which served the Washington, DC, area, took 26 months and cost $100 million.

The CHPPM commander dispatched an industrial hygiene SMART-PM to help clean up the Senate Hart Office Building. The Capitol Incident Management Team determined the extent of contamination and developed a remediation plan. The SMART-PM provided consultation to the Defense Advanced Research Projects Agency and the Capitol Incident Management Team regarding the sampling plan and how to remediate the building.

US Army mail handling facilities downstream from the Brentwood Processing and Distribution Center tested positive for anthrax at both federal and non-federal locations. Army mail facilities not originally impacted had to prepare for possible anthrax attacks by evaluating their mail handling procedures and testing their facilities. CHPPM prepared guidance for how to do the risk assessment in mail and nonmail handling facilities, such as offices and break rooms, on Army installations. The goal was to help installations systematically evaluate mail handling facilities to identify vulnerabilities and develop remediation measures if necessary. The Centers for Disease Control and Prevention and the US Army Medical Research Institute for Infectious Diseases helped develop this technical guidance.

A biological contamination response plan consists of a site safety and health plan to protect the responders, and a sampling plan to characterize the extent of contamination. The response plan included instructions for packaging, labeling, and transporting samples; a risk communications strategy; and decontamination procedures. Only industrial hygienists and environmental and preventive medicine professionals with the required training and experience were permitted to carry out the plan. All installation stakeholders were invited to participate to ensure the success of the mission.

CHPPM developed Technical Guide 316, Microbial Risk Assessment for Aerosolized Microorganisms, published in August 2009,[90] which details the procedures to assess aerosolized microbial hazards and characterize risk as a result of environmental, occupational (eg, a laboratory accident), or intentional (eg, terrorist) exposures. Technical Guide 316’s Supplement A1 and C1 through C791–98 were designed to provide exposure guidelines for managing non-weapons-grade Bacillus anthracis incidents. The technical guide was intended to initiate collaboration among subject matter experts to develop peer-reviewed exposure guidelines for aerosolized B anthracis and other bio-aerosols. However, the effort was hampered by the lack of dose-response information on these biological hazards. The supplements discussed issues of pretreatment with medication or vaccination, whether isolation or other administrative controls were needed, what should be used to disinfect or eliminate exposure, and how the space should be cleared for reentry.90–98

Qarmat Ali Water Treatment Plant Chromium Exposures

In March 2003, the Army contracted with Kellogg Brown and Root to restore the infrastructure of the Rumallah oil fields in Basra, Iraq, including restoration of the Qarmat Ali Water Treatment Plant (QA WTP), which treated water for industrial (nonpotable) use.[99] During the summer of 2003, US Army National Guard soldiers were assigned to escort and guard DoD civilian and Kellogg Brown and Root contract workers. From April through September 2003, US Army National Guard troops from four states served on a rotating basis at QA WTP. The worksite had been damaged during military action and vandalized before the restoration began. Containers holding a water treatment chemical containing sodium dichromate had been ruptured, and the powdered chemical contaminated the site. Sodium dichromate, a corrosion inhibitor that contains hexavalent chromium (Cr VI), was found on the ground as a visible powder and detected in the air (Figure 6-8). Eventually, contractors cleaned the area and covered the contaminated sites with asphalt and gravel.

Figure 6-8. Yellow sodium dichromate, a source of hexavalent chromium, on the ground after bags of the chemical were opened at the Qarmat Ali Water Treatment Plant, Iraq, April–September 2003.
Photograph courtesy of US Army Public Health Center.

Cr VI can cause acute and long-term health effects, including lung cancer if inhaled at high enough levels.99,100 The inhalation of dust containing Cr VI at the QA WTP was considered a potential health risk.[99] Cr VI can irritate the eyes, nose, sinuses, lungs, and skin. Symptoms of nasal irritation include a runny or itchy nose, sneezing, nosebleeds, nasal ulcers, and a perforated nasal septum. Asthma, skin irritation, and skin ulcers have also been associated with exposure to Cr VI.[99] Lung cancer can develop from breathing high concentrations of Cr VI over months to years. Cr VI has been labeled a human carcinogen by the EPA.

In September 2003, CHPPM was asked to assess the QA WTP site risks and potential health risk to soldiers and Department of the Army civilians.99,100 The SMART-PM conducted an environmental exposure assessment and medical evaluations of the soldiers there at the time. This evaluation took place in September and October 2003, approximately 1 month after the QA WTP grounds were cleaned and any chemical on the ground was covered by asphalt and gravel to prevent exposure.

Personnel providing security at the time of the health assessments (137 soldiers) were medically evaluated with a history, physical examination, and other testing (described below). The assessment was modeled after the medical surveillance examination used for workers routinely exposed to Cr VI in their occupation, with the addition of other tests. The self-reported average exposure at QA WTP was 18.5 8-hour working days. This exposure, compared to the months and years of occupational exposure cases in which long-term adverse health findings to Cr VI have been documented, was relatively short. Approximately one-fourth of the individuals complained of irritation to the eyes, nose, throat, and lungs. Physical findings were also consistent with mild irritation or inflammation, but only marginally in those who had complained of symptoms, and did not correlate with time spent on the site. There were no nasal perforations or skin findings consistent with “chrome holes,” which are associated with Cr VI exposure. All of the self-reported symptoms and physical findings were nonspecific and could have been related to the desert environment and austere living conditions.

Blood and urine tests uncovered only mild, nonspecific abnormalities, possibly related to dehydration, protein and creatine food supplement use, or preexisting conditions. Abnormal findings were uncommon and only slightly outside the normal ranges. All chest x-rays were normal. One-third of the pulmonary function tests (PFTs) had mild abnormalities, but no baseline tests were available for comparison. The PFT abnormalities were related to inadequate patient effort (making the test indeterminate), mild airway obstruction related to smoking or preexisting asthma, and changes possibly due to the general high particulate matter in and around the base camps. No individuals with abnormal test results reported symptoms, except for those with a history of mild asthma, who generally only noted symptoms related to exertion.

Whole-blood tests for Cr levels were performed as a marker of exposure because whole-blood testing identifies Cr outside red blood cells as well as the Cr taken into red blood cells, which is where Cr VI is likely to reside. Sixty percent of Cr VI that does not enter red blood cells is excreted within 8 hours, but Cr VI stays in red blood cells for their 120-day life span and thus gives some indication of Cr VI exposure during the past 3 to 4 months. Additionally, serum Cr levels reflect mostly trivalent Cr, which is usually not toxic, reflects dietary intake, and would not be an accurate measure of Cr VI levels.

The whole-blood test was selected because remediation had taken place and serum Cr would not be related to exposure prior to remediation. The results for Cr were below analytical detection limits, so there was not a significant systemic uptake of Cr VI. However, low levels of Cr exposure still could have caused or contributed to the symptoms reported by soldiers at the time of their medical evaluations. The whole-blood tests were done at the Armed Forces Institute of Pathology in Washington, DC. Although the choice of test was appropriate, few reference ranges were available for comparison of results. Given the cost and complexity, whole-blood Cr levels are rarely performed, particularly in those not occupationally exposed.

The resulting assessment, including a complete medical evaluation and whole-blood Cr testing of the personnel present at the site, concluded that the site hazards were being mitigated by the contractor; the soldiers and civilians evaluated who were serving at the site during the summer of 2003 did not show any specific findings associated with overexposure to Cr VI; and the site hazards did not create an elevated risk of future adverse health effects for those who had served there. The medical team concluded that exposure levels were so low that long-term health effects were unlikely. The soldiers and civilians evaluated were given fact sheets that discussed the results and their meaning. They were directed to follow up with their primary care provider if they had any examination findings or medical test results outside the normal range. Soldiers were also encouraged to note any concerns on their postdeployment health assessment. The medical team report also noted that both physical signs and self-reported symptoms related to the eyes, nose, throat, and lungs were nonspecific; they may have been associated with the desert environment and harsh living conditions. Long-term adverse health effects, such as cancer, were not expected from the estimated average service on site of 18.5 days (with a range from 2 to 720 hours).

Since 2003, this incident has continued to receive media and other attention, which has continued to raise health concerns. The conclusions of the SMART-PM were validated by the Defense Health Board in November 2008.[99] Overall, the medical response to the QA WTP incident was exemplary according to the Defense Health Board. Based on reevaluations and the Defense Health Board review, CHPPM scientists considered it unlikely that any current symptoms or long-term health problems were likely to be related to this short-term exposure. CHPPM scientists acknowledged, however, that there were uncertainties relating to the possible exposure levels prior to the September–October 2003 environmental and clinical assessments.

In 2008, contractor employees filed a lawsuit alleging exposure to toxic chemicals while working on the site. Due to concerns from Army National Guard units from Oregon, West Virginia, Indiana, and South Carolina, and others who were present for some period at the Qarmat Ali facility prior to the SMART-PM assessment, the DoD and VA encouraged those who had served at Qarmat Ali to participate in a medical surveillance program in 2010. The Army and VA established similar but separate Qarmat Ali medical surveillance programs for active duty service members, US Army Corps of Engineer civilians who were present on the site, and veterans who may have been exposed to Cr VI at Qarmat Ali. While the DoD and VA did not expect to find serious illnesses, it was prudent to monitor the health of those who may have been exposed.

The first VA surveillance examinations were conducted in 2011. The veterans enrolled in the program received a complete physical examination with emphasis on the ears, nose, throat, lungs, and skin, and a chest x-ray and PFT. Of the 808 veterans eligible for the examination, 124 participated.[100] There are a limited number of medical diagnoses that may be consistent with previous exposure to Cr VI. These include cancer of the nasal passages, lung cancer, chronic dermatitis, perforated nasal septum, scarring of nasal passages, and occupational asthma. For this participant group, the mean number of reported days of exposure was 21, and 78 individuals provided a history of respiratory symptoms at the time of exposure. Skin symptoms at the time were reported by 38 individuals. No abnormalities specific to Cr VI exposure (eg, nasal septal perforation) were identified.

For the initial DoD follow-up surveillance examination, 74 individuals were identified for follow-up, of which 9 were ineligible and 3 were not located. Thus, 62 were invited to participate. Ten declined, and the remaining 52 were evaluated, for a participation rate of 82% of those eligible. The time on site reported by these individuals was a median of 12 hours. The majority of individuals were not concerned about the exposure, and only two were concerned about cancer. There were no nasal septal perforations noted on examination, and although a number of skin findings were reported, none were consistent with “chrome holes.” There were no chest films suspicious for lung cancer. Spirometry, the measurement of the air capacity of the lungs, was an optional procedure, so not all participants had it performed. Of the 44 that did, there were only 3 with mild obstruction, none with moderate or severe obstruction, 6 with mild restriction, 2 with moderate restriction, and none with severe restriction. Two participants reported an onset of asthma, which they associated with onsite work at Qarmat Ali. In one case, a former smoker attributed asthma to “deployment in Iraq” rather than specifically to time spent at Qarmat Ali. This person reported spending approximately 16 hours on site. A second individual, who was never a smoker, reported spending up to 120 hours on site and reported that the asthma symptoms began in May 2003. Other respiratory disorders noted from history, physical exam, or laboratory studies included chronic bronchitis, possible interstitial lung disease, and possible chronic obstructive pulmonary disease. Reported cancer diagnoses included squamous cell cancer of the tongue, liposarcoma, prostate cancer, melanoma, and basal and squamous cell carcinomas. Sinusitis was reported by 12 or 14 participants (depending upon the question answered) representing a prevalence of 23% to 27%, which was somewhat higher than published prevalence rates of 14% to 16%.

The Army included a follow-up survey; 34 individuals returned the questionnaires, for a response rate of 67%. Most individuals participated because, although they considered themselves healthy, they wanted to be examined to ensure that they had no related issues or they wanted to ensure the sodium dichromate exposure was documented in their medical record. On a scale from 1 to 5, individuals reported an average knowledge of Cr-related health effects of 2.29, which rose to 3.67 (more knowledgeable) after the evaluation. The average level of concern about specific potential health effects related to Cr was typically around 2.0, but rose to almost 3 after the evaluation. This may reflect more specific concerns after the evaluation. Providers were trained in risk communication prior to participating in the evaluations, and the evaluations were limited to four locations to facilitate consistent risk messaging.

Additional follow-up examinations were planned to occur every 5 years, beginning in 2017, but the exams will no longer include chest x-rays, which are not a very sensitive tool to screen for lung cancer. Instead, the evaluations will include low-dose computed tomography scans when appropriate. Soldier and US Army Corps of Engineer evaluation results were provided to the individual to share with their medical provider and are stored in DOEHRS. Veterans’ examination results are part of the VA Gulf War Registry. Veterans were advised of their right to file a disability claim for any problem that they thought was related to Cr exposure at the QA WTF. Any veteran with abnormal exam findings was referred to a specialist for further evaluation. Civilians were advised to file a claim under the Federal Employees Compensation Act.

Al Tuwaitha Nuclear Complex

Al Tuwaitha Nuclear Research Center in Iraq was contaminated due to military operations in the Persian Gulf War in 1991.[101] The site was bombed during OIF and looted by civilians in 2003. The looting worsened the contamination, which caused great concern on the part of nearby residents, the Iraqi government, and the international community. During the 2003 looting, residents from nearby towns carried barrels from the site into the villages of Ishtar and Al Riyadh, less than 3 km away. Significant dispersion of the radioactive material occurred when the barrels containing yellowcake, a uranium oxide powder, were washed out and the contents scattered near the storage facility and along the roads to Ishtar and Al Riyadh. The barrels were then used to store food and household items.

A team from Texas Tech University, in Lubbock, Texas, conducted sampling at the site and determined the extent of contamination. They determined how the radioactive materials were disbursed and what the sources of contamination were, and assessed the risk to cleanup crews at the site and in the nearby village.[101]

The Al Tuwaitha site had radioactive waste generated from fuel reprocessing. This was determined from the mixture of cesium-137, uranium, cobalt-60, strontium-90, americium-241, and barium-133 that was found on site. Samples collected at the site also showed there was no enriched uranium present.[101] Approximately 6% of the samples collected at the site had elevated levels of radionuclides that required cleanup, removal, and disposal to meet US guidelines. Building surveys indicated there was a substantial amount of material in several buildings, which Iraqi teams had to remove before they could dismantle the most contaminated buildings. Iraq needed a functional radiation analysis facility and a trained technical staff to begin the cleanup, so Iraqi teams attended the required training in Vienna and began to develop proper radio-analytical capabilities.

Efforts to reconstruct the Iraq science and technology sector continue, but these efforts depend on active involvement and collaboration of the international scientific community. Cleanup was estimated to take 15 years.[101]

Ash Shuaiba Port

In support of the Persian Gulf War, Operation Vigilant Warrior (October 8 to December 15, 1994), and OIF, US forces utilized a portion of the Shuaiba Port Industrial Area in Kuwait as a sea port of debarkation/embarkation (SPOD/E). The SPOD/E provided a portal to transport heavy equipment in and out of the theater of operations. The Shuaiba Port Industrial Area contained petroleum refineries, a cement plant, a fertilizer plant, a chlorine plant, and other petrochemical industries (Figure 6-9). Beginning in March 2002, a mobile ambient air monitoring station monitored five of the six EPA criteria pollutants at the SPOD/E. The pollutants monitored comprised particulate matter less than 10 μm in diameter, carbon monoxide (CO), sulfur dioxide (SO_2), nitrogen oxides (NOX), and ozone (O_3). From January 2003 through approximately July 2005, a life support area, known as Camp Spearhead, provided living accommodations for US service members supporting the mission of the SPOD/E (Figure 6-10). The life support area closed in summer 2005, after which service members primarily working at the SPOD/E were housed at other sites, such as Camp Arifjan and the Kuwait Naval Base, largely due to the concerns identified by environmental monitoring.

Figure 6-9. Flares and smoke from petrochemical plants near the life support area, Ash Shuaiba Port, Kuwait.
Photograph courtesy of US Army Public Health Center.

Figure 6-10. Air sampling for particulate matter at Ash Shuaiba Port, Kuwait, August 1999.
Photograph courtesy of Brad Hutchens, US Army Public Health Center.

Several environmental incidents occurred at the port. These included SO_2 emissions from a nearby petroleum refinery on April 2, 2004. At approximately 9:45 am, service members reported strong sulfur odors and a few complained of headaches and nausea. Noticeable and atypical smoky plumes were emanating from the refinery north of Camp Spearhead. The health, safety, and environment contractor for the camp used a handheld sensor to measure concentrations of sulfur and instructed outdoor and non-mission-critical personnel to seek temporary refuge inside air-conditioned structures. Handheld sensor measurements showed maximum concentrations of 8 ppm (20.94 mg/m^3) to 10 ppm (26.18 mg/m^3). At this site, a mobile ambient air monitoring station trailer was located to provide near-continuous measurement for the criteria pollutants (the mobile ambient air monitoring station reported a maximum concentration of about 6 ppm [15.17 mg/m^3] during the Mishraq sulfur fire episode). For reference, the OSHA permissible exposures level is 5 ppm (above this level nearly all individuals will experience irritation). People with asthma may be sensitive to levels as low as 3 ppm. SPOD/E leadership and safety personnel contacted the Kuwait Port Authority safety office to report the emissions and asked them to cease the operations causing the emissions. By 11:40 am, the emissions were no longer affecting the camp, and the SPOD/E leadership and safety personnel announced the all-clear status so personnel could return to normal duties.

Service members at the site also sporadically reported strong smells of other industrial emissions, such as hydrogen sulfide, chlorine, and ammonia, associated with symptoms such as headaches, throat and eye irritation, and nausea. Monitoring devices measuring concentrations of those chemicals showed, except for ammonia, levels below the Military Exposure Guidelines. Reports of these types of incidents were infrequent, and information regarding medical assessments and number of service members affected was seldom recorded. Based on the limited information, possible exposures to events such as these appeared to be localized and short in duration.

Another example of this type of incident was reported in February 2006. Service members reported headaches and throat irritation from what was thought to be exposure to ammonia or unspecified volatile organic compounds. Limited monitoring capabilities reported concentrations of ammonia ranging from 8 ppm (5.8 mg/m^3) to 20 ppm (14.4 mg/m^3). These levels are above the odor threshold but below the level associated with health effects. Information on the number of personnel experiencing symptoms and extent of the symptoms was scant.

Similar to most areas in southwest Asia, the site also experienced periodic dust storms. Data for the period from August 2005 to March 2006 showed a maximum 24-hour concentration of 1,300 μg/m^3 for particulate matter less than 10 μm in diameter, which was likely the result of a dust storm. Data from the same reporting period showed an average concentration of 210 μg/m^3 for particulate matter less than 10 μm in diameter In contrast, the EPA’s acceptable 24-hour level for PM 10 (inhalable particulate matter with diameters that are generally 10 μm and smaller) is 150 μg/m^3. CHPPM teams conducted routine and incident-specific environmental monitoring activities at Shuaiba Port while US forces lived and worked at the port. In addition to successful efforts to relocate the life support area away from the industrial area, frequent town hall meetings were held to communicate findings and their significance to service members on site. At various times, particularly when new units arrived and others left, concerns would resurface, so regular risk communication was encouraged. Industrial hygiene assets evaluated the sites and conducted limited personal sampling (actual individual exposure levels, measured in a person’s breathing zone) on those performing guard duties. Individuals were notified of their results, and all results were entered into medical records.

Mishraq Sulfur Mine Fire and Firefighting Operations

The Mishraq State Sulfur Mine in northern Iraq was set on fire on June 24, 2003 (Figure 6-11). The fire burned for 3 weeks and released 100 times more SO_2 than the Mount Saint Helen’s volcanic eruption in 1980. The satellite photos show that the smoke plume varied in direction and distance, and the plume was visible for miles.[102] The fire released 42 million pounds of SO_2 per day, and the plume contained particulate matter, SO_2, and hydrogen sulfide (H_2S).[102] These gases normally cause nose, throat, and eye irritation but can also burn the skin and cause severe airway obstruction, hypoxemia, pulmonary edema, and even death at high concentrations. At levels over 5 ppm, most individuals begin to experience irritation; those with asthma react at lower levels. The National Institute for Occupational Safety and Health immediately dangerous to life or health values for SO_2 and H_2S are both 100 ppm.[103]

The sulfur-fire plume extended 25 km to the south and was thought to be the cause of widespread reports of odors and mucous membrane irritation. SO_2 and H_2S were detected near Qayyarah Airfield West, where the 101st Airborne Division was located. The smoke plume also reached Mosul, approximately 50 km to the north, as seen on satellite imagery. Approximately 3,000 personnel from the 101st were within a 50-km radius of the fire. Field environmental air sampling data collected by an Army preventive medicine detachment confirmed that SO_2 concentrations were very high and above safe levels. The concentrations of SO_2 measured in the air were expected to cause health effects that ranged from mild to moderate irritation, coughing, and choking. It is likely that exposure levels varied by distance from the mine, time exposed, and activities performed during exposure. However, it was not possible to determine an individual’s actual dose of exposure because no sampling data were available, and individual location and activities were not recorded.[102]

Figure 6-11. US forces patroling the perimeter of the Mishraq sulfur mine fire, Iraq, July 2003.
Photograph courtesy of US Army Public Health Center.

Among the personnel within the 50-km radius were 191 firefighters and support elements from the 52nd Engineer Battalion, 326th Engineer Battalion, and 887th Engineer Battalion. This group represented the majority of personnel involved in firefighting and was considered the most exposed to sulfur dioxide. The personal protective equipment used by firefighters was inadequate for the high levels of SO_2 and H_2S encountered. At these high concentrations, the respiratory protective mask filters need to be changed frequently, but not enough filters were available to permit changing the canisters at the required frequency.[104] Some firefighters on site experienced irritation, minor burns, and blood-tinged nasal discharges, but the medical staff on site recorded no serious health consequences. Medical personnel on site evaluated those with symptoms and conducted a PFT on each of them. Troops providing security for the firefighting operations were likely significantly exposed to the SO_2 as well. Other troops were also likely exposed; there was a 20% increase in sick call visits at Qayyarah Airfield West during the fire, and there was one reported case of an exacerbation of asthma.

It is likely the mixture of H_2S and SO_2 produced a more severe irritation than would be anticipated with an exposure to one of the gases alone. At very high concentrations of SO_2, permanent lung injury may result. Long-term exposure to levels of SO_2 over 5 ppm have caused permanent pulmonary impairment apparently due to repeated episodes of bronchoconstriction. People with asthma and other sensitive individuals who are exposed to relatively low concentrations can experience a decrease in lung function and bronchial constriction.

Preventive medicine personnel at Ft Campbell, Kentucky, who had deployed with the 101st Airborne Division, believed that thousands of returning troops were exposed to the plume at Qayyarah Airfield West.[105] CHPPM became aware of the pulmonary function testing at Ft Campbell in 2004, reviewed the postdeployment health assessments, and noted numerous concerns regarding exposure to sulfur fire smoke.[104] Soldiers with immediate health concerns were medically evaluated and offered a screening PFT. Soldiers with symptoms and an abnormal PFT were referred to Vanderbilt University Medical Center in Nashville, Tennessee, for further evaluation. At that time there were no clear indications of sulfur-fire exposure related health problems in the redeployed troops, although many of them were still in the evaluation process.

In 2007, CHPPM physicians visited Vanderbilt to review the work that had been done and obtain the medical records of the soldiers referred from Ft Campbell. Individuals who complained of dyspnea on exertion sufficient to impair their physical training performance had been referred to the Vanderbilt specialist, and many underwent open lung biopsy and received a diagnosis of constrictive bronchiolitis (CB).[105] CB, an inflammatory disease process that occurs in the terminal bronchioles of the lungs, is irreversible and is hard to treat. It has been seen in individuals with prior inhalation exposures. Individuals with CB can experience symptoms of shortness of breath with exertion. The chest x-ray and PFT may be normal. These findings are similar to those in patients who have asthma or chronic obstructive pulmonary disease. The literature supports the conclusion that small-airway disease can be difficult to diagnose with routine tests, which is why the small airways or bronchioles are often referred to as the silent zone of the lung. However, in a population offered voluntary PFTs, without the benefit of baselines, some will ultimately be referred for either abnormal test results or symptoms. Predictive values from an appropriate reference population are important. Additionally, in the absence of a baseline test, results may be read as normal but actually represent a decline for that individual.

From among the group referred to Vanderbilt, those individuals who complained of dyspnea without a known etiology were evaluated with a protocol that had a low threshold for biopsy. The results from their screening tests were variable, and deviations from normal were categorized as “minimal.” The pool of those referred for dyspnea on exertion did not uniformly have a history of exposure to the sulfur fire, yet CB was frequently diagnosed. As of July 2007, 49 people had undergone an open lung biopsy, and all of the biopsy samples were abnormal. Thirty-eight were diagnosed with CB. Eleven did not have CB but were diagnosed with sarcoidosis, respiratory bronchiolitis interstitial lung disease, hypersensitivity pneumonitis, respiratory bronchiolitis, or another condition. After December 2009, CB was diagnosed in nine more soldiers in the study group. The CB case series was published in 2011.6,85,105,106

The case series represented a unique population that was the product of a potential exposure, a screening program, and a referral process that led to specific diagnostic interventions, possibly with some surveillance bias. The majority of those with a history of potential exposure to the sulfur fire complained of symptoms at the time of the fire, which is compatible with an exposure. Since SO_2 is water soluble, and water soluble compounds react with moist tissues of the eyes, nose, and throat, the most likely presentation for an individual who is at risk of long-term pulmonary damage is significant upper airway damage. Some individuals are very susceptible to the presence of SO_2 and react to concentrations that elicit a milder response in most people. This hyperreactive response occurs the first time the individual is exposed and is not a sensitization. It is important to consider whether a history of an acute upper respiratory response at the time of the fire identified individuals at risk for long-term respiratory sequelae. It is clear that a significant portion of individuals who react acutely to short, high-level exposures (and even to some short, relatively low exposures) to irritants can develop a variety of long-term respiratory outcomes. It is not clear what minimum magnitude of acute response is required to produce long-term adverse outcomes. It is also not clear if the magnitude of the acute response can be used definitively to identify individuals at increased risks for long-term sequelae.

When individuals from the 101st Airborne Division redeployed to Ft Campbell, the screening process was voluntary. Individuals could be symptomatic and screened, symptomatic and not screened, asymptomatic and screened, or asymptomatic and not screened, without regard to exposure potential. Therefore, it was not possible to correctly identify the true population at risk and ensure that they were screened. Of those who ultimately received a diagnosis of CB, approximately a third did not have a clear history of exposure to the sulfur fire. It appeared that with time, more individuals were offered biopsy based on the growing case series and a desire to establish a diagnosis and document potentially disqualifying medical conditions.

The outcome of CB appears to be relatively rare (< 1%, based on the presumed exposed population), although it is difficult to sort out the degree of exposure by location and thus estimate a true incidence. The outcome is also rare in this age group, and serious, with many diagnoses ultimately resulting in an inability to perform military duties. Given that some individuals with a CB diagnosis were not deployed to northern Iraq during this time frame, it is difficult to develop a unifying theory as to potential exposure and outcome.

Apart from the clinical assessment, the original roster of 191 firefighters and support personnel who fought the Mishraq fire was provided to the US Army Public Health Command (USAPHC, which was formed from CHPPM in 2010) for archival purposes (there were no significant adverse health outcomes identified in this group). There was little overlap between this group and those seen on referral to Vanderbilt, indicating that the individuals seeking care at Vanderbilt were not part of the group thought to be most exposed.

In addition to the firefighters and support staff, USAPHC evaluated the entire group of 6,000 troops who were within 50 km of the Mishraq State Sulfur Plant during the fire. This was a cohort of potentially exposed personnel, since no personal sampling was conducted. The predeployment health outcomes for this group were compared with their postdeployment health outcomes. In addition, two control groups were constructed: a similar size group deployed to the same location after the fire, and a group deployed at the same time as the fire but at different locations. Based on completed predeployment and postdeployment health assessment questionnaires, a substantial proportion of all troops returning from OIF and OEF reported medical problems, respiratory symptoms, health concerns, and air pollution concerns associated with their deployments. Those exposed to the Mishraq sulfur fire were more likely to have reported these problems and concerns compared to unexposed personnel.

Based on clinical encounter data in the Defense Medical Surveillance System, returning veterans of OIF and OEF were at increased risk of requiring clinical assessment or care of chronic and ill-defined respiratory conditions compared to their predeployment conditions.[107] This observation was the same across the population groups analyzed in relation to the Mishraq sulfur fire, although not always with statistical significance. The postdeployment increase in respiratory-related healthcare encounters among firefighters who were in the immediate vicinity of the fire did not differ significantly from the increase among unexposed personnel. Troops who deployed to Camp Q-West, not far from where the sulfur fire had burned, but well after the fire had been extinguished, were more likely than sulfur-fire exposed personnel to have an initial postdeployment respiratory disease medical encounter.

These findings provided one of the first indications that there may be some increase in postdeployment encounters for respiratory conditions apart from a specific exposure of concern such as the sulfur fire. This indication was supported in subsequent studies. The above exploratory analysis did not show a definite link between sulfur-fire exposure in Iraq and either chronic or recurring respiratory diseases. However, the results do not rule out the possibility of such an association. Apart from the possible net effects of the sulfur fire on specific subpopulations, it is significant that a sample of all returning OIF and OEF veterans experienced more respiratory problems after their deployment, compared to before deployment.

Due to the lack of information on prognosis over time with CB, discussion among the pulmonary medical community resulted in a recommendation that those diagnosed with CB be evaluated on a periodic basis. The cluster of cases of CB described above and a cluster of 18 cases of acute eosinophilic pneumonia in US service members deployed in or near Iraq during 2003 to 2004 continue to spur professional discussion regarding possible causative or contributing exposures, as well as finalizing appropriate screening and diagnostic criteria.85,105,106,108 Recommendations of the Defense Health Board sulfur fire report included long-term follow-up of the cohort in the military health system, establishment of a registry, consideration of standardized medical evaluations of troops presenting with dyspnea on exertion, and baseline PFTs on all service members given the inhalation hazards encountered in deployed settings. These recommendations have not yet been initiated.[109] Education of healthcare providers, including military, civilian, and VA physicians, was recommended to raise awareness about health effects associated with sulfur-fire exposures. These topics were the subject of joint VA-DoD symposium on airborne hazards related to deployment, professional publications, the Defense Health Board review, and a monograph.12,109–111

Iraq Chemical Warfare Agent Exposure Review

On October 14, 2014, the New York Times published an article entitled “The Secret Casualties of Iraq’s Abandoned Chemical Weapons.”[112] CJ Chivers reported that “from 2004 to 2011, American and American-trained Iraqi troops repeatedly encountered, and on at least six occasions were wounded by, chemical weapons remaining from years earlier in Saddam Hussein’s rule.”[112] Contact with the chemical warfare agents (CWAs) occurred during destruction of what were believed to be conventional weapons caches. The chemical weapons found dated to 1991 or before. The service members conducting these operations, their leaders, and the medical personnel who examined those exposed and injured were not prepared to deal with what they encountered.[112] The author noted that the above events underscored intelligence failures, failure to prepare combat personnel to deal with the aged weapons, and failure to prepare medical personnel for the exposures and injuries that would occur.[112] In addition, existing Army policy mandated lifetime follow-up for all service members with CWA exposure, but this was not being done.113,114

Following the New York Times report, the Army acknowledged its failures and said it would identify and follow those exposed.[115] The under secretary of the Army apologized for the military’s treatment of exposed service members and promised medical support for those with persistent health effects.[115] A formal process for doing this was initiated by the under secretary of defense (personnel and readiness), who designated the Army as the lead agent to develop and implement a process to identify and evaluate current and former service members who were exposed to CWAs in Iraq during OIF (March 20, 2003, to August 31, 2010) or OND (September 1, 2010, to December 18, 2011). He also directed the Army to develop and publish CWA exposure implementation guidance for the services to execute.6,116,117 CWAs were defined as toxic chemicals used in warfare (eg, incorporated into a munition or device specifically designed to cause injury or death). These agents included sarin, soman, tabun, VX, sulfur mustards, lewisite, nitrogen mustard, saxitoxin, ricin, toxic industrial chemicals used as CWA (eg, chlorine and ammonia), and unknown substances.[117]

The implementation plan had four initial goals and one added later:

1. To identify, contact, and evaluate service members and veterans for potential symptomatic CWA exposure.

2. To offer and provide service members and veterans who had a likely or confirmed symptomatic CWA exposure a medical examination.

3. To document the results of these efforts in the DOEHRS and the individual Service Treatment Record and ensure the VA was informed of the findings.

4. To consider appropriate recognition, such as the Purple Heart award, for service members and veterans with injuries resulting from likely or confirmed CWA exposure.

5. To identify the medically and scientifically appropriate level of follow-up for affected service members and veterans, develop the appropriate policy documents, and then implement this follow-up across the services.

Service members and veterans with potential exposures were grouped into four cohorts to facilitate management of the project. Cohort 1 included individuals identified by name in media reports such as the New York Times article as having been potentially exposed. Cohort 2 designees were assigned to the units of Cohort 1 group members at the time of Cohort 1’s reported exposures. Cohort 3 included those potentially exposed based upon a review of DoD operational reports on CWA exposures in Iraq during OIF or OND and reports on deployment health (eg, Post Deployment Health Assessment and Post Deployment Health Reassessment questionnaires). Cohort 4 individuals self-identified as having been potentially exposed to CWAs while deployed to Iraq in support of OIF or OND using the Office of the Deputy Assistant Secretary of Defense for Force Health Protection and Readiness telephone hotline.112,115–118

Electronic service medical records for members of all four cohorts were obtained and electronically searched for any mention of CWA exposure using a very broad list of search terms. Service members and veterans in Cohorts 1 and 4 who could be contacted and consented to be interviewed received a standardized, structured interview with a knowledgeable occupational and environmental medicine clinician. Individuals in Cohorts 2 and 3 were offered a structured interview only if the service medical records screening revealed any of the key words that might be associated with an exposure. If the medical provider conducting the interview determined that the service member or veteran experienced a likely or confirmed symptomatic CWA exposure, a medical examination at the Walter Reed National Military Medical Center in Bethesda, Maryland, was recommended. Even when the interviewing clinician concluded there was no evidence of a likely or confirmed symptomatic CWA exposure, if the service member or veteran requested a medical examination, one was provided at Walter Reed National Military Medical Center. Service members and veterans were fully informed at relevant points in the process that participation in the program was entirely voluntary and that if they opted out, they could opt back in at any time. A number of fact sheets regarding both short- and long-term health effects of exposure to various CWAs were developed and provided to program participants. More detailed informational documents were distributed to providers.

When appropriate, the medical point of contact for each service provided the human resources point of contact for their service with information from the structured interviews. For service members and veterans deemed to have injuries resulting from a likely or confirmed symptomatic CWA exposure, the services contacted them and provided information on the requirements for consideration of the Purple Heart and assisted with the submission packet. The services were directed to ensure that all service members and veterans identified as having a likely or confirmed symptomatic CWA exposure had their clinical information documented in their Service Treatment Record, and applicable disposition information documented in the DOEHRS. Pertinent information was provided to the VA.

Each military service managed its own group of possible symptomatically exposed service members and veterans in Cohorts 2, 3, and 4 for the medical record screening and structured interview. All members of Cohort 1, all medical record screenings interviews of Army personnel, and the scheduling of all examinations at Walter Reed National Military Medical Center were handled by the USAPHC. As of April 2016, 6,023 Army service members or veterans were enrolled in one of the four CWA investigational cohorts and had a record in the DOEHRS. Medical records screenings were completed for 5,926, and 1,155 had participated in structured interviews. There was no evidence of a symptomatic CWA exposure in 5,092 individuals. Structured interviews identified 255 Army service members or veterans with symptomatic CWA exposures, and these were offered a medical examination. An additional 76 were authorized a medical examination on their request. For all services, 190 service members or veterans were examined at the Walter Reed National Military Medical Center, and 24 more were scheduled for examinations. For the 190 examined, no association between a CWA exposure and chronic health effects has been observed. A few individuals who had developed blistering after exposure to a blister agent (eg, mustard) had scars.

Burn Pits in Iraq and Afghanistan

Waste generated by military forces training in the field or deployed has long been recognized as a concern because it may attract rodents and insects and contribute to disease transmission. Open air waste burning was an accepted, expedient solution to the problem and did not draw much attention when the amount of waste was small and large numbers of troops did not stay in the same location for long periods of time.[6] When US forces entered Afghanistan in 2001 and Iraq in 2003, open-air burning was thus considered an accepted, expedient, short-term solution for solid waste disposal. Deployments to these two countries produced large volumes of waste, much of it novel waste not associated with earlier military operations. These military forces relied heavily on bottled water that was delivered in plastic bottles on large, shrink-wrapped pallets; disposable plates, cups, and eating utensils made of plastic or Styrofoam; and electronic equipment for duty and personal use.8,119 DoD estimated an average of up to 10 pounds of waste was generated per person per day, with up to 200 tons of waste burned at an installation in one day.[8] The burning pits were large and operated continuously, with plumes that contained soot and ash of varied composition, depending on what was being burned (Figure 6-12). People exposed to burn pit emissions complained of red, irritated eyes; respiratory irritation; and cough, which could persist.[8]

The installation of long-term waste disposal systems, such as incinerators, was hampered by contracting or money problems, and the open burn pits were maintained at least until 2009, some reaching many acres in size and burning all types of waste.8,119 Comprehensive burn pit guidance was slow in being developed and implemented, and existing guidance was not always followed. For example, items prohibited from being burned because of their harmful emissions, such as plastics, tires, batteries, petroleum products, aerosol cans, and hazardous and medical wastes, were not segregated. Additionally, burn pit emissions were not monitored or sampled.[120] Anecdotally, Pentagon officials noted that most of the troops returning from war zones reported exposure to burn pit smoke, and most did not have respiratory protection.

Concern mounted, and in August 2009, President Obama declared that “burn pits will not become another Agent Orange.”[121] VA Secretary Eric Shinseki asked, “How do we change what has been the 40-year journey of Agent Orange, the 20-year journey of Gulf War Illness, and prevent a similar journey for burn pit smoke?”[121] Lawsuits were filed in over 40 states in which former and current service members alleged they were exposed to air pollutants that caused health problems as a result of a contractor’s negligent management of burn pit operations.[120] Service members who had deployed to Afghanistan and Iraq complained of severe respiratory disease, including asthma and CB, and cancers such as leukemia. Affected individuals anecdotally associated or attributed these to exposures to the burn pits.8,106 However, attempts to assess possible associations between exposure to burn pit emissions and disease were hampered because data on exposures and medical conditions were lacking and epidemiological studies were conflicting or inconclusive.[8] Nevertheless, multiple long-term epidemiological studies of troops living or working near burn pits and studies of respiratory disease are ongoing.12,110,122–130

Figure 6-12. Emissions from an open burn pit drifting toward the life support area, Balad Air Base, Iraq, August 2006.
Photograph courtesy of LTC Scott Newkirk, US Army Public Health Center.

The American Legion and Veterans of Foreign Wars stood up for concerned service members and their families and called for the creation of a national burn pit registry, which would include a listing of all military personnel exposed to burn pits. On January 10, 2013, Public Law 112-260, Dignified Burial and Other Veterans’ Benefits Improvement Act of 2012 (38 USC 101 note),[131] was passed. It required the secretary of veterans affairs to establish and maintain an open burn pit registry, to notify eligible individuals of developments in the study and treatment of conditions associated with toxic airborne chemical exposures, and report to Congress on the effectiveness of actions taken to collect and maintain information on the health effects of toxic exposures.[131]

The VA Airborne Hazards and Open Burn Pit Registry was pilot tested in April 2014 and opened nationally on June 19, 2014. The purpose of the registry was to ascertain and monitor potential health effects from exposure to airborne environmental hazards with the overall goal of improving outreach, communication, and VA programs for eligible veterans. It was established as a database of information provided by veterans and people still in the military, using a website and self-reported questionnaires.132,133 It intentionally included all deployment-related airborne exposures, including burn pits, and was opened to any veteran or active duty service member who deployed to the southwest Asia theater of operations on or after August 2, 1990, and those who deployed to Afghanistan or Djibouti after September 11, 2001.[132]

The USAPHC prepared supporting documentation for the VA Airborne Hazards and Open Burn Pit Registry and noted that:

Over 3.5 million individuals were eligible to participate in the registry. Participation was voluntary and was accomplished by completing an online self-assessment questionnaire. The detailed questionnaire was designed to give a broad picture of the participant’s health and current and past exposures. Registry participants were encouraged to report deployment exposures to all airborne hazards, such as burn pit emissions, oil-well fires, pollution, and dust from sand storms they experienced, and their health concerns.[132]

The registry was considered useful because it established a baseline of health information that might be used to identify future changes in health, copies of completed questionnaires could be used to discuss concerns with healthcare providers, and completion of the questionnaire linked the individual to the VA, a link through which information could be provided on follow-up care and benefits.132,133

The VA has completed a series of reports that showcase registry participant characteristics, common health concerns, and other information.133–135 A June 2015 report summarized the information entered into the registry from April 2014 through December 2014. By June 2015, over 28,000 participants had joined the registry. The 2015 VA report noted, “the most common physician-diagnosed problems were insomnia and neurological problems and other diagnoses included allergies, high blood pressure, and lung disease such as emphysema, chronic bronchitis, and asthma.”[131] A total of 309 registrants reported physician-diagnosed CB.[131] The report presented descriptive data and did not implicate any exposures as causing specific diseases or conditions. Participants ranged in age from 20 to 79 years, with about 70% under age 45. More than two-thirds served in the Army, most were men (over 85%), and they represented a range of races and ethnicities. About 89% reported they had trouble doing at least one daily activity such as walking, running, or stair-climbing because of a neck or back problem (59%), knee problem (38%), breathing problem (34%), arthritis (29%), and/or a mental health problem (24%). Over 53% reported an interest in having the registry’s optional medical examination.131–133

The 2011 Institute of Medicine report on burn pits noted the following:

There is not yet enough medical or scientific information to conclude that long-term health effects on a population-level have occurred due to burn pit smoke. However, DoD medical leaders have acknowledged that acute symptoms related to smoke exposure may occur, including reddened eyes, irritated respiratory passages, and cough, and these may persist for some time. A small number of Service Members may experience longer-term health effects, related to combined exposures of sand, dust, industrial pollutants, tobacco smoke and other agents, and individual susceptibilities, to include pre-existing health conditions or genetic factors. Veterans and Service Members who were closer to burn pit smoke or exposed for longer periods may be at greater risk for health problems. Individual health effects will vary and may depend on a number of other factors, such as the type of waste being burned and wind direction. The high level of fine dust and pollution common in Iraq and Afghanistan may pose a greater danger for respiratory illnesses than exposure to burn pits.[8]

VA, DoD, and academic researchers continue to collaborate and study deployment-related airborne hazards, burn pit exposures, and the health of deployed veterans and service members.110,122–130 Joint national symposia have been held, and a book describing the state of the science of deployment-related airborne hazards has been published for exposed service members, veterans, and the physicians who care for them.[12] Future research plans include studying the exposures and clinical outcomes of registrants who elect to have the no-cost registry medical examination, as well as further study of the registry-reported cases of physician-diagnosed CB and other health conditions that may rise to levels of concern. The last report on data from the Airborne Hazards and Open Burn Pit Registry was in June 2015.[134] The VA plans to issue periodic summary reports on the registry, and these and earlier reports will be available on the VA website.[133]

OCCUPATIONAL AND ENVIRONMENTAL HEALTH INFORMATICS

In the 1990s, DoD officials had to respond to questions from Persian Gulf War veterans regarding their environmental and occupational exposures while deployed and the possible association of these exposures with their medical conditions.[133] Additionally, the decade following the Persian Gulf War rapidly became a decade of deployments with new health concerns, with US forces being sent to Africa, the Caribbean, the Balkans, and southwest Asia.[133] Analysis of this situation at the DoD led to initiatives aimed at better protecting the health of service members, particularly those deployed into hazardous areas, under the heading of force health protection. These initiatives were directed toward improving communication about health risks, improving medical record keeping, increasing biomedical research to improve countermeasures to protect troops, and improved health surveillance to better capture and store occupational and environmental exposure data.[133] The surveillance activities resulted in the popular use of the term “deployment health surveillance.” CHPPM was given an important role in improving OEH surveillance in support of deployment health surveillance.133,135,136

CHPPM was designated the DoD executive agent for deployment OEH surveillance measures, databases, data analyses, and support items.[135] In 1996 CHPPM formed the Deployment Environmental Surveillance Program to execute these responsibilities.[135] Deployments were occurring, and potentially important exposure data from occupational and environmental samples were being analyzed. The Deployment Environmental Surveillance Program faced the challenge of how to expeditiously and meaningfully capture and manage this information. In 1996 the program staff developed an internal database to capture, processes, analyze, interpret, and report all environmental samples collected during military deployments. However, this database was inadequate to meet the occupational and environmental informatics needs of future decades, so systems such as the DOEHRS and the MESL were developed.

Defense Occupational and Environmental Health Readiness System

Prior to 1996, in an attempt to better deal with the data challenges described above, military medical leaders looked at the possibility of building upon already operating systems. Beginning in the early 1980s, the US Army Medical Department took steps to modernize and standardize occupational health data collection, storage, retrieval, and use.[137] The Occupational Health Management Information System was developed as an integrated system that included the following:

- a Medical Information Module to assist with the management of clinical services and clinical medical surveillance programs;

- a Hearing Evaluation Automated Registry System to facilitate collection, capture, and storage of audiometric testing data; and

- a Health Hazard Information Management system to support the Army industrial hygiene effort by capturing and maintaining workplace hazard data and information on hazard controls.[137]

In the late 1990s, the DoD selected the Hearing Evaluation Automated Registry System and the Health Hazard Information Management modules to become platform components for the new DOEHRS. In 1999, the Hearing Evaluation Automated Registry System became the foundation for DOEHRS Hearing Conservation (DOEHRS-HC) module. Later, the Health Hazard Information Management system became the foundation for DOEHRS Industrial Hygiene (DOEHRS-IH) module.

The DOEHRS-HC system consisted of a web-based data repository and a desktop application to administratively support the provider. It improved personal auditory readiness by supporting education and the proper use of hearing protection, and helped to prevent significant hearing loss by detecting early hearing changes through audiometric testing. Using DOEHRS-HC in its entirety, hearing conservationists and audiologists collect, maintain, compare, and report hearing conservation, hearing readiness, and deployment data for DoD personnel. The desktop application consisted of a stand-alone government application and commercially available audiometer software. The system automated instructional programs and hearing test procedures for up to eight concurrent test stations from a single computer at a testing site. Hearing tests were recorded in the DOEHRS-HC stand-alone application and were uploaded to the DOEHRS-HC data repository. Staff used DOEHRS-HC to analyze the test results and determine if changes in hearing had occurred and if a significant hearing loss existed. The DOEHRS-HC data repository maintained approximately 60 million hearing test records for current and former service members and DoD civilian employees.

The DoD deployed DOEHRS-IH in 2006 to capture occupational exposure data. Before 2006, each military service used its own automated information system. Federal employees were covered under the Occupational Safety and Health Act of 1970 through Executive Order 12196. The DOEHRS-IH automated information system was designed to support compliance with the act by facilitating the development of an employee exposure record that met the act’s criteria. The act’s requirements for an exposure record included data obtained by monitoring or measuring toxic substances or harmful physical agents in the workplace, safety data sheets for materials used by civilian workers and military personnel in performing their jobs, and chemical inventories or records that documented where and when a toxic substance or harmful physical agent was used. DOEHRS-IH records contained information on predeployment, deployment, and postdeployment worker exposures. These data permit exposure-based medical surveillance, allocation of resources, implementation of controls, and development of training programs. Environmental, safety, and occupational health practitioners can analyze the data to prioritize preventive countermeasures to protect health.

The medical information module component of the Occupational Health Management Information System was never funded for migration to DOEHRS. Attempts were made to include functionalities from the medical information module in the Armed Forces Health Longitudinal Technology Application, the clinical documentation engine developed for DoD healthcare providers for recording clinical notes, orders, and procedures performed. An Armed Forces Health Longitudinal Technology Application template library was developed for hazard-specific medical surveillance encounters to complement the Composite Health Care System, the medical informatics system used by DoD military health system facilities. Many occupational health clinics adopted the Navy PC Matrix software, which provided much of the functionality of the medical information module of the Occupational Health Management Information System but produced only a hardcopy printout that had to be scanned and uploaded to the Armed Forces Health Longitudinal Technology Application.

Defense Occupational and Environmental Health Readiness Environmental Health Module and Military Exposure Surveillance Library

The USAPHC needed an information technology system that was capable of capturing and managing OEH data and stood up the Environmental Surveillance Integration Program (ESIP) to perform the mission. The ESIP was assigned the responsibility to assemble and archive all DoD deployment and environmental health surveillance data and reports required by DoD Directive 6490.2. ESIP staff initially developed the Occupational and Environmental Health Data Portal, a password-protected Internet site that allowed the management and archiving of electronic files associated with OEH surveillance activities. In addition, ESIP staff maintained an in-house database to record environmental sample results.

Personnel needed ESIP’s information technology system to capture, process, analyze, interpret, and report all OEH data from DoD sources. In conjunction with the restructuring of the Deployment Environmental Surveillance Program in 2006, the DoD expanded the capabilities of DOEHRS-IH to capture deployment environmental sampling data, creating an environmental health module in DOEHRS-IH. In 2011 the ESIP scientists, working with representatives from the other military services, expanded the functionality of the EH module to include sanitation inspection reports, waste management inspection reports, entomological surveillance reports, and OEH site assessments (OEHSAs). In addition, DOEHRS-IH was expanded to contain incident reporting, food protection, radiation and registry modules. The DOEHRS-IH registry module now houses data for the Persian Gulf War oil well fires, Operation Tomodachi (the response to the 2011 earthquake and tsunami in Japan), and the OIF CWA exposure investigation.4,112,138

The DOEHRS-IH Environmental Health module was to be used by all military services for the management of unclassified environmental samples and other preventive medicine surveillance surveys. In October 2007, an Occupational and Environmental Health Data Portal application was developed on the SIPRNet (the Secret Internet Protocol Router Network used by DoD for classified information) to manage classified OEH documents. Both the classified and unclassified Occupational and Environmental Health Data Portal applications were rebranded and named the MESL in October 2011. The concept for maintaining these separate systems was that the DOEHRS-IH Environmental Health module was the system of record for all OEH computable data. The NIPRNet (the DoD Non-Secure Internet Protocol Router Network for exchanging unclassified information) MESL was the official system of record for OEH non-computable data (eg, memoranda, photos, and situational reports) and computable data that DOEHRS-IH Environmental Health module could not accept (eg, pesticide application data and basecamp assessment team reports). In addition, the NIPRNet and SIPRNet MESL were the only systems with the ability to search the contents of electronic documents. There was overlap of system capabilities, but maintaining separate systems was considered necessary to acquire and manage all OEH data.

A 2015 Government Accountability Office (GAO) review concluded that policy should be clarified to note which system, DOEHRS-IH or the MESL, should be used for specific types of OEH data. The GAO report noted the following:

- inconsistent quality assurance processes among the military services that brought into question the reliability of the stored OEH surveillance data;

- inconsistent DoD and military service-specific policies that resulted in duplication and fragmentation in the storage of OEH surveillance data with confusion about utilization of the DOEHRS and the MESL; and

- an absence of documentation showing that the potential health risks identified through OEH surveillance were being addressed and actions were being taken to mitigate health threats.[139]

The GAO report generated interest at the congressional level. In response, revision of DoD Instruction 6490.03, Deployment Health, published in August 11, 2006, was initiated to address the GAO recommendations.[140] This revision specified that all unclassified OEH data shall be managed in DOEHRS-IH and all classified OEH data shall be managed in the SIPRNet version of the MESL (MESL-S).

The ultimate goal for DOEHRS-IH and MESL-S was the formation of an integrated system that could provide every service member a longitudinal record of individual environmental and occupational exposures over the course of their military career. The DOEHRS-IH is the DoD system of record for entering, assessing, managing, and reporting unclassified occupational and environmental exposure data. DOEHRS-IH was designed for use in both garrison and deployed operations. It contains environmental health surveillance data beginning with Operation Joint Endeavor in 1995 and is expected to continue to receive data for future deployment operations.[5] DOEHRS-IH is the foundation for the future DoD Individual Longitudinal Exposure Record.

Unfortunately, the DOEHRS-IH and MESL systems are not integrated into the current medical record system nor the new electronic health record system being developed by the DoD. Therefore, a medical provider requiring access to environmental surveillance or workplace surveillance data may not know about, nor can they query, these databases to obtain exposure data.

Occupational and Environmental Health Site Assessment Report and Periodic Occupational and Environmental Monitoring Summary

The OEHSA process is an ongoing, information organizing process that provides reports to support OEH risk management on military installations in operational environments.[141] The OEHSA process supports the documentation of environmental conditions and identification of potential OEH threats, and guides OEH data collection, risk assessments, and risk mitigation actions. It also supports data collection and risk assessments over time, including health risk assessment and health risk management activities. An end product of the OEHSA process is the Periodic Occupational and Environmental Monitoring Summary (POEMS).[142] POEMS reports describe exposure hazards (eg, airborne pollutants and infectious diseases); summarize the data and information collected; and provide assessments of known or potential short- and long-term (including postdeployment) health effects for people deployed to specific sites. OEHSA and POEMS reports are managed in DOEHRS.141,142 POEMS reports can be downloaded from the USAPHC website (https://phc.amedd.army.mil/topics/envirohealth/hrasm/Pages/POEMS.aspx) and are used by clinicians, medical epidemiologists, and deployed service members themselves to identify exposures and to assess possible relationships between deployment exposures and existing medical conditions. From December 2015 through January 2017, 10,052 POEMS reports were downloaded.

SUMMARY

Even though symptoms and diseases in Vietnam veterans that were considered to be related to their deployment, and particularly to exposure to Agent Orange, caused great pain, anxiety, frustration, and cost, the US Army was not prepared to avert a similar occurrence in the short Persian Gulf War of 1991.1–3,6,143 As symptoms and diseases developed in the veterans, many potentially harmful exposures were identified and suspected as contributors to the ills of those who had carried the burden of battle in the Persian Gulf War. Many committees and panels reviewed the available data and noted that while no causal link was established, health effects from exposures to pesticides, chemical and biological warfare agents, vaccines, pyridostigmine bromide, infectious diseases, DU, oil well fire smoke, and petroleum products were possible. Exposures occurred, but investigations into them were superficial and inadequate because very little personalized exposure information was collected.[143] “Defining the exposed and relevant control groups and obtaining data for them would be very difficult. The lack of exposure data limited even the most expert and well-funded investigation to identify health outcomes linked to specific exposures or risk factors.”[144] The GAO noted, “without accurate exposure information, the investment of millions of dollars in further epidemiological research on risk factors or causes for veterans’ illnesses may result in little return.”[144]

As a result, a strong effort was put forth to quickly identify and assess potentially harmful exposures in future deployments and to expeditiously provide data and information to informed military leaders who could take action to prevent or mitigate the exposures. This effort seemed to produce the intended results when US forces were deployed to Bosnia, Herzegovina, and Kosovo in the former Yugoslavia.[5] Available data was sometimes timely and sufficient to allow a commander to make decisions about troop facility locations relative to hazards. To date, however, sampling data has rarely been sufficient to assuage concerns of those potentially exposed, or to negate potential health effects. The Institute of Medicine of the National Academies and other groups studied the exposures and medical problems of Vietnam and Persian Gulf War veterans and provided recommendations for protecting the health of US service members in future deployments.1,7 These recommendations are still out of reach for full implementation. Unfortunately, and in spite of the efforts of many, history was repeated in the protracted military actions during OEF and OIF.

The various symptoms and diseases that service members bring home with them after their battles have ended may never be fully understood, successfully treated, or prevented. However, potentially hazardous exposures that are amenable to prevention or mitigation do occur during hostile deployments, and their rapid identification and assessment, with appropriate command action to avoid or mitigate the threat to service members, could prevent future anxiety and even disease. Collecting samples and storing data and information are not ends in themselves. Modeling potential exposures, identifying those who may have been exposed after an incident, and forming registries for those who may have been exposed have value but are not substitutes for preventing or mitigating a potentially harmful exposure. While acute exposures at levels high enough to immediately affect soldiers are easier to identify and easier to relate to predictions of long-term health outcomes, poorly defined lower level exposures typically involve much more uncertainty.

In 2007, the Office of the Chairman of the Joint Chiefs of Staff issued a memorandum requiring commanders to factor long-term health risk into their operational decision-making.[145] In order to do so, military leaders must identify, be knowledgeable about, and respect potentially harmful exposures. This requires the professional support of informed military occupational and environmental medicine physicians and other military occupational health professionals who can facilitate the rapid identification and assessment of the hazards and provide timely and sound advice to prevent or limit disease, injury, and even death.

ACKNOWLEDGMENTS

The authors thank contributors Dr. Kelley A. Brix, Dr. Robert F. DeFraites, Leeann S. Domanico, Jacqueline Howard, Brad E. Hutchens, Jeffrey S. Kirkpatrick, John E. Kolivosky Jr, Dr. Deborah C. Lake, Dr. Ron Teichman, Kevin Wisniewski, and Donald G. Zugner.

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52.   Mahan CM, Page WF, Bullman TA, Kang HK. Health effects in Army Gulf War veterans possibly exposed to chemical munitions destruction at Khamisiyah, Iraq: Part I. Morbidity Associated with Potential Exposure. Mil Med. 2005;170:935–944.

53.   GulfLINK, Office of the Special Assistant for Gulf War Illnesses. Case Narrative. The Gulf War air campaign—possible chemical warfare agent release at Al Muthanna, February 8, 1991. http://www.gulflink.osd.mil/al_muth_ii/. Final report November 15, 2001. Accessed June 20, 2016.

54.   GulfLINK, Office of the Special Assistant for Gulf War Illnesses. Case Narrative. Chemical warfare agent release at Muhammadiyat ammunition storage site. http://www.gulflink.osd.mil/muhammadiyat_ii/. Final report April 4, 2002. Accessed June 20, 2016.

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57.   GulfLINK, Office of the Special Assistant for Gulf War Illnesses. Case Narrative. US demolition operations at Khamisiyah. http://www.gulflink.osd.mil/khamisiyah_ii/. Updated December 7, 2000. Accessed June 20, 2016.

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59.   Cheng YS, Zhou Y, Chow J, Watson J, Frazier C. Chemical composition of aerosol from kerosene heaters burning jet fuels. Aerosol Sci Technol. 2001;35:949–957.

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90.   US Army Public Health Command. Microbial Risk Assessment for Aerosolized Microorganisms. Aberdeen Proving Ground, MD: APHC; August 2009. Technical Guide 316.

91.   US Army Public Health Command. A Microbial Risk Assessment Case Study Evaluating a Hypothetical Bacillus Anthracis Exposure to Garrison Personnel. Aberdeen Proving Ground, MD: APHC; June 2010. Technical Guide 316, Supplement A.

92.   US Army Public Health Command. Potential Exposure Guidelines for Bacillis Anthracis Causing Inhalation Anthrax—Guidelines for Peer Review. Aberdeen Proving Ground, MD: APHC; September 2009. Technical Guide 316, Supplement C1.

93.   US Army Public Health Command. Dose–Response Assessment for Inhalation Anthrax in Guinea Pigs Using Historical Army Data and Classical and Bayesian Statistical Methods. Aberdeen Proving Ground, MD: APHC; June 2010. Technical Guide 316, Supplement C2.

94.   US Army Public Health Command. Potential Impact of Selected Dose-Response Models on Development of Health-Based Biological Military Exposure Guidelines for Bacillus Anthracis. Aberdeen Proving Ground, MD: APHC; July 2010. Technical Guide 316, Supplement C3.

95.   US Army Public Health Command. Considerations for Exposure Guideline Development and Risk Management Associated With Anthrax Vaccination. Aberdeen Proving Ground, MD: APHC; March 2011. Technical Guide 316, Supplement C4.

96.   US Army Public Health Command. Peer Review of Preliminary Health-Based Military Exposure Guidelines for Bacillus Anthracis (Inhalation Anthrax). Aberdeen Proving Ground, MD: APHC; March 2011. Technical Guide 316, Supplement C5.

97.   US Army Public Health Command. Data Qualification Report for the Development of Interim Biological Military Exposure Guidelines for Aerosolized Bacillus Anthracis Causing Inhalation Anthrax. Aberdeen Proving Ground, MD: APHC; November 2014. Technical Guide 316, Supplement C6.

98.   US Army Public Health Command. Interim Biological Military Exposure Guidelines for Aerosolized Bacillus Anthracis Causing Inhalation Anthrax. Aberdeen Proving Ground, MD: APHC; November 2014. Technical Guide 316, Supplement C7.

99.   Weese CB. Evaluation of an exposure incident at the Qarmat Ali water treatment plant. US Army Med Dep J. 2009;April-June:10–13.

100.   Ciminera P, Superior MJ, Bullman T. Findings from the Department of Veterans Affairs Qarmat Ali medical surveillance program. Mil Med. 2016;181(4):307–310.

101.   Rodgers BE, Chesser RK. What we found at Al Tuwaitha [abridged]. Bull At Sci. 2009. http://thebulletin.org/what-we-found-al-tuwaitha. Published 19 May, 2009. Accessed June 20, 2016.

102.   US Army Public Health Command. Health Assessment of 2003 Al Mishraq Sulfur Fire Incident. Aberdeen Proving Ground, MD: June 2012. Fact sheet 64-007-0612.

103.   National Institute for Occupational Health and Safety. NIOSH pocket guide to chemical hazards. Updated May 18, 2016. www.cdc.gov/niosh/npg/npgd0575.html. Accessed September 26, 2017.

104.   US Army Public Health Command. Mishraq Sulfur Fire Environmental Exposure Assessment. Aberdeen Proving Ground, MD: Epidemiological consultation report 64-FF-064C-07.

105.   Baird CP, Debakey S, Reid L, Hauschild VD, Petruccelli B, Abraham JH. Respiratory health status of US Army personnel potentially exposed to smoke from 2003 Al-Mishraq sulfur plant fire. J Occup Environ Med. 2012;54(6):717–723.

106.   King MS, Eisenberg R, Newman JH, et al. Constrictive bronchiolitis in soldiers returning from Iraq and Afghanistan. N Engl J Med. 2011;365(3):222-230.

107.   Abraham JA, DeBakey, SF, Reid LR, Zhou J, Baird, CP. Does deployment to Iraq and Afghanistan affect respiratory health of US military personnel. J Occup Environ Med. 2012;54(6):740–745

108.   Shorr AF, Scoville SL, Cersovsky SB, et al. Acute eosinophilic pneumonia among US military personnel deployed in or near Iraq. JAMA. 2004;292:2997-3005.

109.   Office of the Assistant Secretary of Defense, Health Affairs. Deployment Pulmonary Health Report. Memorandum for Under Secretary of Defense, Personnel and Readiness, 11 February 2015.

110.   Rose C, Abraham JA, Harkins DK, et al. Overview and recommendations for medical screening and diagnostic evaluations for postdeployment lung disease in returning US warfighters. J Occup Environ Med. 2012;54(6):746-751.

111.   Zacher L, Browning R, Bisnett T, Bennion J, Postlewaite RC, Baird CP. Clarifications from representatives of the Department of Defense regarding the article “Recommendations for medical screening and diagnostic evaluation for postdeployment lung disease in returning US warfighters.” J Occup Environ Med. 2012;54(6):760–761.

112.   Chivers CJ. The Secret Casualties of Iraq’s Abandoned Chemical Weapons. The New York Times. October 14, 2014. http://www.nytimes.com/interactive/2014/10/14/world/middleeast/us-casualties-of-iraq-chemical-weapons.html?_r=0. Accessed May 16, 2016.

113.   Office of the Army Surgeon General. Medical Evaluation, Follow-up, and Recording of Chemical Warfare Nerve Agent Casualties Outside of Storage, Demilitarization, and Research Settings. Memorandum, 10 September 2004.

114.   US Army Medical Command. Medical Management, Evaluation, Follow-Up, and Recording of Chemical Warfare (CW) Mustard Agent Casualties Outside of Storage, Demilitarization, and Research Settings. Memorandum, 28 October 2004.

115.   Chivers CJ. Veterans Hurt by Chemical Weapons in Iraq Get Apology. The New York Times. March 25, 2015. http://www.nytimes.com/2015/03/26/world/middleeast/army-apologizes-for-handling-of-chemical-weapon-exposure-cases.html?_r=0. Accessed May 16, 2016.

116.   The Under Secretary of Defense, Personnel and Readiness. Iraq Chemical Warfare Agent (CWA) Exposure Personnel Guidance. Memorandum, November 7, 2014.

117.   The Under Secretary of the Army. Iraq Chemical Warfare Agent (CWA) Exposure Review Implementation Guidance. Memorandum, March 20, 2015.

118.   Gaydos JC, Kreiss K: Discussion Summary: Exposure Characterization—Questionnaires and Other Tools. In: Baird CP, Harkins DK, eds. Airborne Hazards Related to Deployment. In: Banks DE, Jones TK, eds. A Specialty Volume of the Textbooks of Military Medicine. Washington, DC: Department of the Army, Office of The Surgeon General, Borden Institute; 2015: Chap 29.

119.   Kyle JB. Identifying and Reducing Health Risks Associated with Open-Air Burn Pits [civilian research project]. Carlisle, PA: US Army War College: USAWC Fellow; 2013.

120.   US Government Accountability Office. Afghanistan and Iraq, DoD Should Improve Adherence to Its Guidance on Open Pit Burning and Solid Waste Management. Washington, DC: GAO; 2010. GAO-11-63.

121.   Shane III L. Obama says burn pits won’t become another Agent Orange. Stars and Stripes. April 4, 2009. http://www.stripes.com/news/obama-says-burn-pits-won-t-become-another-agent-orange-1.93801. Accessed August 26, 2016.

122.   Abraham JH, Clark LL, Sharkey JM, Baird CP. Trends in rates of chronic obstructive respiratory conditions among US military personnel, 2001-2013. US Army Med Dep J. 2014;July-September:33–43.

123.   Pugh MJ, Jaramillo CA, Leung K, et al. Increasing prevalence of chronic lung disease in veterans of the wars in Iraq and Afghanistan. Mil Med. 2016;181:476–481.

124.   Abraham JH, Eick-Cost A, Clark LL, et al. A retrospective cohort study of military deployment and post-deployment medical encounters for respiratory conditions. Mil Med. 2014;179(5):540–546.

125.   Matthews T, Abraham JH, Zacher LL, Morris MJ. The impact of deployment on COPD in active duty military personnel. Mil Med. 2014;179(11):1273-8.

126.   Sharkey JM, Harkins DK, Shickedanz TL, Baird CP. Department of Defense participation in the Department of Veterans Affairs airborne hazards and open burn pit registry: Process, guidance to providers, and communication. US Army Med Dep J. 2014;July-September:44-50.

127.   Holley AB, Sobieszczyk M, Perkins M, et al. Lung function abnormalities among service members returning from Iraq or Afghanistan with respiratory complaints. Respir Med. 2016;118:84–87.

128.   Falvo MJ, Abraham JH, Osinubi OY, et al. Bronchodilator responsiveness and airflow limitation are associated with deployment length in Iraq and Afghanistan veterans. J Occup Environ Med. 2016;58(4):325–8.

129.   Sharkey JM, Abraham JH, Clark LL, et al. Post-deployment respiratory healthcare encounters following deployment to Kabul, Afghanistan: A retrospective cohort study. Mil Med. 2016;181(3):265–271.

130.   Exposure biomarkers. J Occup Environ Med. 2016;58(suppl 1 8S):S1–S116.

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134.   US Department of Veterans Affairs, Veterans Health Administration. Report on Data from the Airborne Hazards and Open Burn Pit (AH&OBP) Registry. Washington, DC: VA; April 2015. https://www.publichealth.va.gov/docs/exposures/vaahobp-registry-data-report-april2015.pdf. Accessed September 6, 2017.

135.   Heller JM, Resta JJ. Occupational and environmental health surveillance. US Army Med Dep J. 2001;October-December:36–43.

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Chapter 7

ARMY OCCUPATIONAL HEALTH PROGRAM MANAGEMENT

TIMOTHY M. MALLON, MD, MPH*

INTRODUCTION

PROGRAM OVERVIEW

DEPARTMENT OF DEFENSE PROGRAM STRUCTURE AND MANAGEMENT

Office of the Secretary of Defense

Office of the Assistant Secretary of Defense for Health Affairs

Defense Health Agency

ARMY OCCUPATIONAL AND ENVIRONMENTAL HEALTH PROGRAM MANAGEMENT

The Army Surgeon General and Army Medical Command Structure

The Army Public Health Center

OCCUPATIONAL AND ENVIRONMENTAL HEALTH PROGRAM QUALITY

Process and Outcome Measures

Occupational Health Program Assessment Tools and Quality Improvement

OCCUPATIONAL HEALTH PROGRAM PERSONNEL

Role of the Surgeon General’s Consultant in Occupational and Environmental Medicine

Roles of Providers

Army Staffing Assessment Model for Civilian Occupational Health Providers

Making the Case for More Occupational Health Personnel

Recruiting and Retaining Occupational Health Personnel

Training, Competencies, and Milestones for Physician Professional Development

FUNDING

Budgeting

Sources of Funding

Expanding Service Delivery

Contracting for Occupational Health Services

SUMMARY

*Colonel (Retired), US Army; Adjunct Assistant Professor, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

INTRODUCTION

The Army Occupational and Environmental Health Program (AOEHP), which supports soldiers and civilian employees in deployed and garrison settings, has three basic roles.1,2 The first role is to protect the health of soldiers and civilian workers. AOEHP goals are centered on primary prevention, that is, preventing occupational injuries and illnesses from occurring. This includes identifying and managing the hazards associated with routine daily work and appropriately responding to unusual and unexpected hazards. The second AOEHP role is to ensure that military commands are in legal compliance with occupational health laws and regulations, including federal, state, and local statutes and those of foreign countries where appropriate. The third AOEHP role is to assist in the identification and appropriate follow-up of those who have suffered injuries or illnesses or experienced exposures that may put them at increased risk of disease in the future. For civilian employees, this includes advising local commanders on the implementation of Federal Employees’ Compensation Act (FECA) provisions through targeted efforts to prevent injuries and illnesses in worker populations at risk and to reduce compensation claims and costs, disability, and time off work.[3]

PROGRAM OVERVIEW

Legters and Llewellyn described military medicine as dealing with “risk (threat) assessment, prevention, and medical evacuation and clinical management of diseases and injuries resulting from military occupational exposures.”[4] Any training and mission-related work done by soldiers on fixed installations and in deployed settings may be associated with potentially harmful exposures. Therefore, the AOEHP has responsibility for protecting and preserving the health of soldiers, and thereby supporting the continued readiness of soldiers to fight and do their jobs. In contrast, the industrial base of the Department of Defense (DoD) is complex and includes government-owned and -operated facilities, government-owned/contractor-operated facilities, and contractor-owned and -operated facilities. This unique organizational structure provides the DoD and Department of the Army (DA) flexibility in meeting mission requirements by providing the capability to quickly ramp up production from peacetime to wartime levels. In these various configurations, personnel who provide AOEHP services must clearly understand what their responsibilities are regarding the workers, the industrial plants themselves, and the industrial processes inside the plants. Additionally, contingency considerations for ramping up production present unique challenges because existing heating, ventilation and air-conditioning systems and engineering controls may be inadequate to support an accelerated production process.

The program elements of a military occupational health program are varied but generally include reproductive health hazards, immunizations, hazard communication, illness and absence monitoring, vision protection, respiratory protection, hearing protection, medical surveillance for known hazards, and control of infections and blood-borne pathogens, among others. Reviews of occupational health programs are performed by the Occupational Safety and Health Administration (OSHA) and the Joint Commission. In addition, the Army inspector general team reviews surety medicine support, and installation-level occupational health services are reviewed by staff from the Army Surgeon General’s Office, the regional health commands, and the Army Materiel Command. The Army Public Health Center, located at Aberdeen Proving Ground, Maryland, provides occupational health staff assistance visits.1,2

AOEHP personnel include military and civilian physicians, physician assistants, nurse practitioners, nurses, occupational health technicians, industrial hygienists, and industrial hygiene technicians. The skill sets and competencies of AOEHP staff members have expanded greatly over the last 25 years, as seen, for example, in physician residency training programs in occupational and environmental medicine (OEM). OEM residents must spend more time in clinical rotations, gain greater clinical competence, and demonstrate attainment of these clinical competencies and proficiencies before graduating from a residency program and taking the American Board of Medical Specialties examination. This increased emphasis on clinical competence was driven in part by the expansion of the American College of Occupational and Environmental Medicine core competencies in OEM.5–7 Further, the utilization of primary care physicians, nurse practitioners, and physician assistants to support the clinical aspects of OEM programs poses challenges, such as ensuring that providers have the requisite skills and competencies, and that they participate in quality assurance programs with peer review as part of normal clinical business practice. This change was largely driven by the American Board of Medical Specialties in response to the general public’s demand for improvements in the overall quality of clinical care in America that occurred in 2012.6,7

Beyond the basic practice of occupational medicine, military-specific hazards and operational environments pose unique challenges for providers entering military occupational medicine. AOEHP providers must understand how the practice of military occupational medicine is different from the practice of occupational medicine taught in civilian medical schools and OEM residency programs. This includes understanding military hazards, the health problems they pose, the immediate medical treatment needed following exposure, and requirements for follow-up of those exposed.

Transitioning from civilian to military occupational medicine involves a steep learning curve. For physicians who trained in civilian OEM residency programs, the period of time required to become independently competent in the practice of military occupational medicine has been estimated by senior Army occupational medicine physicians to range from 6 to 24 months.[5] One reason for this is the limited opportunities to take courses required for military providers. In addition to military administrative courses, such as those related to security, these providers must become competent in the clinical identification and management of casualties exposed to chemical warfare agents, biological warfare agents, radiation incidents, and laser injuries. They must also be able to assume the role of medical advisor to an installation commander, serving as a public health emergency officer or as the on-the-scene commander of a toxic chemical incident or infectious disease outbreak.

DEPARTMENT OF DEFENSE PROGRAM STRUCTURE AND MANAGEMENT

Office of the Secretary of Defense

The governance of military occupational health is shared by multiple DoD organizations.8(p14) At the secretary of defense level, two offices are responsible for overseeing occupational and environmental health: the Office of the Under Secretary of Defense for Acquisition, Technology, and Logistics (USD [AT&L]) and the Office of the Under Secretary of Defense for Personnel and Readiness (USD [P&R]).

Historically, safety programs were viewed as installation functions related to USD (AT&L), while occupational and environmental health was considered a medical function overseen by USD (P&R). Environmental and occupational health functions have now been placed under USD (AT&L).8(p15) However, oversight of program execution and funding for the occupational and environmental health program resides in USD (P&R).8(p15) Combatant commanders, with mission and geographic responsibilities under the Unified Command Plan, and the military services also have responsibility for implementation and execution of the occupational health program in their areas.[8] The services have parallel systems for occupational health with separate monitoring, surveillance and reporting systems, and policy guidance.

The National Safety Council partnered with DoD in a 2001 review of the DoD’s safety and occupational health management systems.[9] The study focused leadership attention on quantifiable safety goals and safety metrics. These data were readily available because of OSHA-mandated reporting requirements. The National Safety Council highlighted the need for an effective DoD-wide safety and occupational health management system that would ensure coordinated policy, advocacy, and oversight of safety and occupational health.[8](p16),[9] In response, the secretary of defense established the Defense Safety Oversight Council (DSOC), chaired by USD (P&R).8(p16) The DSOC oversees safety policy and initiatives within DoD. In a 2006 policy memorandum,[10] the secretary of defense delegated responsibility for injury and accident prevention to the USD (P&R) and established performance goals for reducing preventable accidents.

With representatives from all the military services and the joint staff, the DSOC facilitates coordination between USD (AT&L) and USD (P&R) on policy implementation and program execution for safety, occupational, and environmental health programs.8(p17) It also helps to prioritize program management efforts and troubleshoot problem areas. DSOC coordination facilitates development of common goals and expedites policy development and oversight of program execution.8(p17) In 2016, there were several joint services working groups that facilitated the work of USD (AT&L) and USD (P&R).

DoD directive 4715.1E, Environment, Safety and Occupational Health (ESOH), issued in March 2005,[11] addresses the division of occupational health program management within the Office of the Secretary of Defense by defining responsibilities for safety and occupational health for both USD (AT&L) and USD (P&R). Designed to protect DoD personnel from accidental death, injury, or occupational illness,8(p19) the directive applies to pollution prevention, compliance, conservation, restoration, munitions response, safety, occupational health, environmental health, explosives safety, fire and emergency services, pest management, environmental technology, and international activities.

DoD Directive 4715.1E recognizes that no single organization exercises authority over all safety and occupational health activities and that parallel program management and coordination is a major challenge.8(p19) The directive appointed USD (AT&L) to oversee DoD environmental, safety, and occupational health programs and to establish goals, objectives, guidance, and procedures for safety and occupational health aspects of the DoD mission. It also appointed the assistant deputy undersecretary of defense for installations and environment as the designated safety and occupational health official. The USD (AT&L) was also assigned the responsibility for issuing environmental, safety, and occupational health policy and management guidance for DoD components in planning, programming, and budgeting for occupational health.8(p19)

For occupational health, USD (AT&L) sets policy, while USD (P&R) manages the relevant program and budget execution. Safety largely remains within the purview of USD (AT&L), except that 4715.1E designates USD (P&R) as the chairman of the DSOC, a mechanism intended to promote coordination at a high level in the Office of the Secretary of Defense.8(p21)

Office of the Under Secretary of Defense for Acquisition, Technology, and Logistics

The USD (AT&L)8(p15) has oversight for military installations and the environment; operational energy plans and programs; major weapon systems; missile defense programs; space and intelligence programs; nuclear, chemical, and biological defense programs; and nuclear programs. Within AT&L, there is a deputy assistant undersecretary for environment, safety, and occupational health, who is primarily responsible for environmental and occupational health policy development and program oversight.8(p15) This office is also responsible for DoD instructions on safety and occupational and environmental health, including DoD Instruction 6055.01, DoD Safety and Occupational Health (SOH) Program;[12] DoD Instruction 6055.05, Occupational and Environmental Health (OEH);[13] and DoD Instruction 6055.05-M, Occupational Medical Examinations and Surveillance Manual.[14]

Several integrated product teams have been established to support this office for installations in the United States, overseas, and deployed settings. One of these, the Occupational and Environmental Health Integrated Product Team, is charged with developing data management systems and integrating them with existing information management systems, primarily the Defense Occupational and Environmental Health Readiness System (DOEHRS) and the new Military Health System (MHS) GENESIS electronic medical record.[15] The Occupational and Environmental Health Integrated Product Team establishes and prioritizes requirements for MHS data systems and for electronic health record integration.8(p23)

Office of the Under Secretary of Defense for Personnel and Readiness

The USD (P&R) provides staff advice and assistance to the secretary of defense on total force management; National Guard and Reserve affairs; the MHS; readiness and training; military and civilian personnel requirements; morale, welfare, and recreation; and quality of life.8(p23)

Office of the Assistant Secretary of Defense for Health Affairs

The Assistant Secretary of Defense for Health Affairs (ASD HA) is responsible for administering the MHS,8(p18) which provides care to uniformed and civilian DoD healthcare beneficiaries in the United States and around the world. It encompasses fixed and deployed medical treatment facilities, and weaves together healthcare delivery, medical education, public health, private sector partnerships, and medical research and development. In addition to providing healthcare services, the MHS is prepared to support military operations, natural disasters, and humanitarian crises worldwide.[16]

A change in MHS governance occurred in 2013 when the TRICARE Management Agency was eliminated and replaced by the Defense Health Agency (DHA).[16] ASD HA oversees the DHA and controls both funding and policy development. Subject matter experts from the services support policy development by serving on working groups within ASD HA.

The ASD HA has adopted the use of the “balanced scorecard” for strategic planning to set goals for the MHS and establish benchmarks for accountability. The MHS balanced scorecard has six main focus areas: resources, learning and growth, internal process, customers, finance, and stakeholders.[17] The MHS balanced scorecard has continually evolved. It now includes MHS activities and healthcare quality measures, and is currently being used by all the services.[17]

Defense Health Agency

The DHA director is responsible for integration of service policy and program execution across all the services, including implementation, management, and evaluation of direct care provided in medical treatment facilities.[16] The DHA establishes quality performance measures in medical treatment facilities and oversees execution and evaluation of clinical programs for cost effectiveness and return on investment.

The DHA has several directorates, including medical logistics, health information technology, public health, finance, medical education, and research and development.[16] The public health directorate’s goal is to move the MHS to a “system of health,” focusing on prevention of disease, disability, and death. The plan is to increase effectiveness and decrease costs through consolidation of functions. The public health directorate includes branches for armed forces health surveillance, immunization, veterinary care, and deployment health.[16] The deployment health branch monitors the medical readiness status of all DoD personnel, ensuring the force is medically ready to deploy. Medical readiness involves tracking of deployment readiness in the whole force, including periodic health assessments, deployment-limiting conditions, dental readiness, and immunizations.[16]

ARMY OCCUPATIONAL AND ENVIRONMENTAL HEALTH PROGRAM MANAGEMENT

The AOEHP organizational structure is like that of the DoD. The assistant secretary of the Army for installations and environment and the deputy assistant secretary of the Army for environment, safety, and occupational health have primary responsibility for integrating DoD directives and policies into Army policies, doctrine, and guidance.8(p24) The assistant secretary of the Army for installations and environment, as executive agent for the DoD occupational health program, is tasked to “establish goals, policies, priorities, and oversight for the Army OEH programs.”8(p24) This office also coordinates initiatives with the DSOC and collects occupational health performance metrics, which it reports to DoD.8(p24)

The Army Surgeon General and Army Medical Command Structure

The Army surgeon general is commander of the Army Medical Command (MEDCOM) and is responsible for occupational health program funding and oversight of program execution. The surgeon general’s role is to advise the secretary of the Army and Army chief of staff on occupational health issues.1,18 Further, the surgeon general is responsible for developing policy for medical care to prevent disability from occupational injuries and illnesses and for executing the medical aspects of the AOEHP.[8]

A 2015 MEDCOM reorganization resulted in the elimination of the US Army Public Health Command, and its command element was moved into MEDCOM headquarters as the deputy. The remainder of the Army Public Health Command became the APHC, a field operating activity of the DCS PH.[19] The public health regional commands were also eliminated in the reorganization.

The DCS PH promotes readiness and prevents disease, injury, and disability in soldiers, military retirees, their families, veterans, and DA civilian employees.[19] It also oversees mission execution for veterinary and public health services for the Army. DCS PH has four directorates, public health, System for Health, Ready and Resilient, and veterinary services, that participate in public health planning, strategy, policy and guidance promulgation, and oversight across the Army and MEDCOM.[19]

The public health directorate establishes policies and regulations related to preventive and occupational medicine.[19] It coordinates with DHA regarding epidemiology and disease surveillance, and standardizes quality assurance for occupational health programs throughout the Army Medical Department. The directorate also participates in MEDCOM efforts to improve the quality of clinical public health practice, focusing on identifying and addressing emerging public health issues such as the Ebola and Zika viruses.

The Army Public Health Center

The APHC provides unique operational and strategic services and expertise to the Army and DoD.[18] The APHC assists in developing public health programs, products, and services; conducts technical studies and consultations; augments policy development; monitors public health program and service quality; leads process improvements; develops technical guidance; participates in national and international groups and missions; facilitates public health staffing training; and oversees nonappropriated fund management and business practice operations for veterinary and occupational health clinics across the DoD.[18]

The APHC provides support for comprehensive health surveillance including the implementation of the DOEHRS. The APHC provides feedback to installation and combatant commanders on their efforts to manage or eliminate occupational and environmental health risks. The APHC is also the executive agent for deployment occupational and environmental health. APHC staff recommend priorities for public health mission execution and collect data on performance indicators and measures of mission effectiveness.

The clinical public health and epidemiology directorate at the APHC supports occupational and environmental health programs and services executed Army-wide.[20] The directorate is comprised of occupational medicine, environmental medicine, hearing and vision, surety medicine, disease epidemiology, injury prevention, professional medical education, behavioral health, and public health nursing divisions.[19]

The APHC’s OEM division supports installation-level occupational and environmental health programs both in the United States and overseas, including assessment of threats encountered on the battlefield. The division provides soldiers and their commanders with information products and consultative services to address service member concerns and mitigate health risk.[19] The OEM division provides medical and epidemiological expertise to evaluate and communicate health risk related to environmental exposures.[19] It also conducts research and development of clinical practice guidelines for occupational and environmental hazards, and supports residency training of physicians in occupational medicine.[5]

The APHC has developed the Public Health Management System to track performance metrics for installation, regional, and headquarters public health programs. This system enables collection, review, and analysis of hearing, vision, industrial hygiene, and occupational health program data.

OCCUPATIONAL AND ENVIRONMENTAL HEALTH PROGRAM QUALITY

A new direction in medicine is to incorporate quality measures into healthcare delivery, including outcomes measurements that have evolved from the managed care system.20–24 DoD and service leaders, as well as military medical treatment facility commanders, are driving changes to lower costs.[16] Outcomes management has flourished in the clinical setting.[20] National databases are being developed that permit use of information and analysis of data that focus on clinical, financial, and health outcomes. This permits researchers to assess the impact of medical interventions on health outcomes, thus providing decision-makers information on cost effectiveness.21,22 Outcomes management is critically important to occupational medicine in justifying resource needs.

Process and Outcome Measures

Clinical performance measures include both process and outcome measures.23,24 The patient administration and resource management divisions of a military medical treatment facility collect information on the clinical performance of each provider to assess whether or not the relative value unit performance standards were met and to track the return on investment for occupational health clinical care.[20] Occupational health professionals need feedback on their performance to develop high-quality, cost-efficient healthcare.[20] Regulatory agencies develop policy based on data-driven information obtained from measures of clinical performance.[22] It is important for OEM physicians to understand which process and health outcomes indicators are being tracked, as well as the limitations of the data being collected and analyzed.22,24 Process measures include completion percentages for surveillance programs and worksite visits; outcomes measures include disability costs and lost workdays.23,24

The Joint Commission and the American Board of Medical Specialties have focused on performance improvement in healthcare outcomes, moving away from examining work processes alone. Medical treatment facilities must track healthcare outcomes that occur as a result of specific interventions using an evidence-based approach. For example, childhood immunization has successfully reduced the prevalence, new incident cases, and number of carriers of hepatitis B in the general population.

Metrics that can be used to measure healthcare cost savings from employee health and wellness programs include workers’ compensation claim costs; participation in health promotion and wellness programs (leading measures); and decreases in health risks, disability, and medical costs (lagging indicators).[24] Table 7-1 lists more examples. It is helpful to have leading and lagging indicators that are aligned with realistic performance goals. Employee health maintenance programs can reduce costs by preventing trips to the emergency department for injuries, hospitalizations, and certain procedures. Individuals with health risk factors such as smoking, stress, and depression can be identified and offered preventive interventions that help ensure access to care and offer health risk management. Health promotion and wellness programs should be aligned with the clinic quality improvement efforts, in which high-risk and frequent occurrences are identified and targeted for intervention. The return on these investments usually occurs in the second year of intervention rather than the first year.

Army occupational health clinics complete an annual report of various process and outcome metrics and submit the information to the APHC. For example, process measures related to the hearing program include hearing test completion percentages and number of referrals to audiology for evaluation of hearing loss. Examples of outcome measures of performance for the hearing program include the number of accepted hearing loss claims and total compensation costs for hearing loss claims. These measures reflect the success of the installation injury prevention program and FECA case management efforts. Other examples of clinical outcome measures in occupational health are overall injury and illness rates, tuberculosis transmission rates, and cases of lead poisoning. These outcome measures (ie, case rates) may require risk adjustment for confounders, including the severity of disease, demographics, and comorbid conditions related to cost measures.

Data Quality and Risk Adjustment

Concerns about data sources, adjustments, and attributable risks have been raised and should be carefully addressed.[24] The health outcomes data must be analyzed with scientific rigor to provide proper conclusions about the success of occupational health programs. Healthcare outcomes analysis relies on well-developed and integrated data information systems that allow program managers to continuously improve patient care. Until recently, the Army used self-reported performance data and health outcomes metrics to assess program performance. The move to centrally available data, including data captured in the military electronic medical record and civilian employee medical record, and use of health outcomes tracked by the federal workers’ compensation program provides more reliable and accurate information on health outcomes. Data derived in this manner has higher levels of clinical validity and reliability.

Also, APHC program managers with oversight responsibility can get access to the MHS Standard Inpatient and Outpatient Data Repository by requesting an online account through the armed forces health surveillance branch of DHA. Installation-specific, de-identified epidemiology data can be obtained from the repository for review and analysis. Analysis of these data can show how a particular organization is doing compared with the Army average in preventing injuries and illnesses. After adjusted for confounders, the data can be analyzed to assess which subgroups in the population have the highest risk of developing injuries or illnesses.

Existing Performance Measurement Systems

The Joint Commission has incorporated outcomes performance measurement into the accreditation process. Medical treatment facilities must develop performance measurement systems that track their performance in relation to a specified outcome.[24] The performance measure must address at least one dimension of care. The system must have an operational, automated, ongoing database that allows calculation of performance measures, and it must be able to assess the accuracy and completeness of the performance measure data elements and remove the effect of patient confounders by risk adjustment or stratification.[24] The system must also be able to deliver, on a timely basis, statistically valid performance information useful in comparing the healthcare facility with others and against national standards.[24]

Functional Health Status and Quality of Life Instruments

There is a paradigm shift away from disease to an emphasis on patient health and helping people live longer and enhancing the quality of their life. Improvements can be measured as gain in life expectancy and better quality of life.[25] Patient outcome measures are a focal point for public health and can be used in decisions about allocation of public health resources. The Department of Labor is now focusing on patient outcomes and functional status, and quality of life is now used as a standard measure of clinical outcomes.[25]

Occupational Health Program Assessment Tools and Quality Improvement

The APHC and the Navy and Marine Corps Public Health Center have developed self-assessment tools to permit any installation occupational health program manager to assess how well each element of their program is being executed. In addition to patient satisfaction questionnaires, the program manager can use the occupational health program status report to do a program assessment and see how their occupational health program compares with other programs in the Army. The results of the self-assessment and comparison with the service averages will help program managers identify areas needing improvement, and serve as a baseline for tracking success in both process and outcome measures.

TABLE 7-1

LEADING AND LAGGING INDICATORS OF EMPLOYEE HEALTH PROGRAMS

Leading Indicators

Examples

Program enrollment

Initial enrollment

Continuing engagement and tool usage

Session attendance, program completion

Medication adherence

Cardiovascular medications taken

Behavior change

Smoking cessation classes, nutrition, stress

Access to care

Met access standards

Patient satisfaction

80% or better on customer satisfaction scores

Lagging Indicators

Examples

Functional status

ADLs, full duty, light duty

Quality of life

Well-being index

Absenteeism

Days not present for work

Morbidity

Injury rates and disability costs trends

Healthcare claims cost

FECA medical cost trends

ADLs: activities of daily living

FECA: Federal Employees’ Compensation Act

Additionally, program evaluations are periodically conducted by the Joint Commission, the service inspector general’s staff, the surgeon general’s staff, or the regional commander’s staff. These reports outline the strengths of the program and areas for improvement. Program managers can obtain copies of prior evaluations of their occupational health program, and clinic staff can use them to prioritize work efforts. Program managers should become familiar with the Joint Commission environment of care checklist for their facility because it includes many elements of the occupational health program that are evaluated.

Occupational health program managers must prepare a business plan that identifies program goals and objectives and both process and outcome measures for each program element. The business plan must be signed by the chief of occupational health, the chief of preventive medicine/public health, the installation commander, and the medical treatment facility commander. Also, the program manager must ensure that the occupational health clinic is included in the facility’s public health or preventive medicine service quality improvement program. The selected process and outcome measures should then be evaluated on a periodic basis and reported on at the hospital quality improvement meetings.

OCCUPATIONAL HEALTH PROGRAM PERSONNEL

Role of the Surgeon General’s Consultant in Occupational and Environmental Medicine

The consultant to the Army surgeon general in OEM is the subject matter expert and is expected to be well versed in the technical and policy aspects of the specialty. He or she is the acknowledged professional and technical leader of area of concentration 60D (occupational medicine officers), which includes managing the human capital inventory and recommending changes. The consultant’s opinion will form the basis of the surgeon general’s or Army response to OEM questions, and the consultant may represent the Army for OEM issues in external venues and liaise with other services and agencies. This will touch on many aspects of AMEDD’s function. The consultant also serves as a staff officer to the surgeon general, which involves reviewing line-of-duty determinations, waivers for accession, unresolved cases, and policies.

The Human Capital Distribution Plan

The Human Capital Distribution Plan is the basis for assignments for AMEDD officers. This annual process relies on established business rules to implement a justifiable and equitable distribution of all AMEDD officers. As inventory manager for the distribution of 60D officers, the OEM consultant works to solve long-term and short-term staffing problems. The consultant identifies service member needs, desires, and family considerations that affect the assignment process, education, promotions, and command selections. The OEM consultant works closely with the preventive medicine consultant and the Medical Corps branch manager to prepare an annual list of recommendations for fill, which is then reviewed by regional commands and medical treatment facilities. If there is nonoccurrence, the OEM consultant and representatives from regional medical commands, major subordinate commands, US Army Europe, and the 8th Army attend a conference presided over by the deputy surgeon general. Each position is discussed and decisions are reached on disputed positions.

The OEM consultant provides Human Resources Command a list of officers who are leaving the service and those changing assignments, including the losing unit, gaining unit, and report date. For colonels, command surgeons, or other key personnel, the consultant discusses assignments with the chief of staff or deputy commander for clinical services to confirm releases and replacements are acceptable. The OEM consultant also participates in the accession of occupational medicine physicians by writing recommendations to the accession board following review of applicant credentials, resume, and work experience.

Managing Authorizations and Requirements

The MEDCOM manpower office manages requirements and authorizations for active duty officers and executes the annual MEDCOM Manpower Review Program. The OEM consultant may request changes in the number of 60D authorizations on the MEDCOM Table of Distribution and Allowances, but a 60D can only be added by either converting an existing authorization in another specialty to a 60D or by documenting that a new mission has been added to the specialty (a new mission is one that has not been previously tasked to the specialty nor previously staffed by MEDCOM). The deputy surgeon general must also support the addition. The OEM consultant is also afforded the opportunity to comment on any proposed decreases to the 60D authorizations.

Roles of Providers

The AMEDD Personnel Proponency Directorate establishes how many officers are needed and how many should be trained and brought into the Army at any given time. Primary care physicians, physician assistants, and nurse practitioners are utilized to provide clinical care services for the occupational health program at locations where organic occupational medicine staff are not assigned or the population served does not require an active duty occupational medicine physician. OEM physicians and industrial hygiene, safety, optometry, ergonomics, and audiology services may also be obtained from the surrounding local market on a fee-for-service basis or through contract support.

Assessing and treating injuries and illnesses is a major part of the occupational health clinic workload. In general, the occupational health nurse begins emergency care on sick or injured soldiers and civilian employees. Occupational health nurses, who are able to work without direct physician supervision, ensure that the clinic’s policy and procedure manual includes a set of standard medical directives covering routine and emergency situations that are written and cosigned by the supervising occupational health physician, occupational health nurse-in-charge, and usually the chief nurse of the supervising medical treatment facility. If the installation has worksites with major health hazards, such as toxic industrial chemicals or chemical warfare agents, the emergency response plan should include medical response guidance for each hazard present. The nature and extent of nursing care provided by the occupational health clinic must be formally determined by the installation, bearing in mind that the degree of treatment rendered by a nurse is limited by the nurse practice act in the state where the nurse is licensed. The occupational health clinic manager should check with the state nurse licensing board regarding rules for prescribing drugs.

Military and civilian OEM physicians may need to treat occupational illnesses and injuries, direct the occupational health nurse, perform preplacement and periodic history and physical exams, and perform exposure evaluations and OSHA-mandated surveillance examinations. The OEM physician collects epidemiological information on injuries and illnesses and initiates countermeasures to prevent future injuries and illnesses in high-risk populations.

Army Staffing Assessment Model for Civilian Occupational Health Providers

A supplement to the Army Staffing Assessment Model was developed that addresses civilian employee staffing requirements for preventive medicine, including the occupational health program. In addition to the number of employees on an installation, the professional staff needed by an occupational health clinic varies according to the type and number of different operations occurring on base, hazards of the operations being performed, number of personnel exposed to significant chemical and physical hazards, number of preplacement and periodic medical surveillance examinations being performed, number of fitness for duty and ability to work determinations, number of workers’ compensation cases being actively managed, and the specific numbers of employees and soldiers enrolled in the various elements of the occupational health program (eg, hearing, vision, respiratory protection). Other factors that affect the resource staffing model include:

- the types and complexity of encounters;

- administrative requirements in terms of meeting attendance (safety, infection control, workers’ compensation case management, environment of care, quality improvement);

- site visits done with or without coordination with safety and industrial hygiene staff;

- patient education activities;

- coordination with state and local health departments;

- support for disaster preparedness and response activities;

- public health emergency officer duties;

- marketing of occupational health services; and

- attendance at hospital and medical center executive meetings.

A separate component of the staffing model accounts for regional-level staff support and headquarters-level support, which are added into the overall service requirements for occupational health staff.

The occupational health program manager must engage early and often with the chief of resource management at the local hospital and medical center to ensure model assumptions are correct and that authorizations and requirements are consistent with staffing requirements predicted by the model. The program manager can check with the business operations directorate at the APHC to verify the numbers. The OEM consultant to the surgeon general can facilitate the process if necessary to ensure staffing needs are met once the shortfalls are identified.

Staffing for the Army occupational health program was recently increased through the DoD planning, programming, and budgeting process for occupational health and industrial hygiene personnel: approximately $50 million was earmarked in the 2010 to 2014 DoD budget plan for occupational health nurses, nurse practitioners, physicians, and industrial hygienists. With these resources made available, the installation occupational health program manager should review authorized and required personnel and compare authorizations with the on-board personnel strength. If there is a shortfall in personnel required to support the mission, the program manager should contact the occupational medicine division at the APHC to arrange for funding to obtain needed personnel.

Making the Case for More Occupational Health Personnel

If shortfalls in civilian personnel staffing exist, the occupational health program manager must work with the medical treatment facility’s resource manager to get approval from the program budget advisory committee to hire the needed personnel. This inherently represents a long and drawn-out process when the occupational health program is competing with other sections within preventive medicine and with other hospital departments for limited resources. The program manager must show in the justification why the additional personnel are needed and why occupational health should get the resources rather than other deserving programs in the hospital.

Successful strategies include demonstrating the beginning of a new requirement that did not previously exist, the existence of a new OSHA or other regulatory citation demonstrating the clinic or installation did not meet standards, or the existence of an increased health and safety risk with associated risk of adverse health outcomes because of personnel shortfalls. Additionally, the occupational health program manager should remind the budget committee that DoD funding is specifically appropriated annually for the operations and maintenance of occupational health programs. The key to success is how well statements are backed up with supporting facts and the quality of briefings to senior leaders in the chain of command, including the chief of resource management, chief of finance, chief of logistics, deputy hospital commander for resource management, and hospital commander.

Recruiting and Retaining Occupational Health Personnel

Once hiring new staff is approved, the occupational health program manager must ensure the job descriptions are current, including the latest training and qualification requirements for education, work experience, and specialized training. The regional personnel office then approves the job description and grades the position before the job announcement is posted.

Recruiting new occupational health providers to the specialty is a key role and responsibility of OEM providers in the Army. This role is currently critical as much of the OEM provider workforce reaches retirement age. Outreach on the part of current military and civilian OEM providers will help recruit top candidates. Workforce retention is just as important, and retaining top-quality personnel has become more difficult due to recent changes in the job market.

Training, Competencies, and Milestones for Physician Professional Development

Occupational medicine physicians must receive specific training in biostatistics and epidemiology, industrial toxicology, physiology, radiation, hearing protection, effects of environmental conditions such as altitude and high pressure, occupational safety, industrial hygiene, dermatology, psychiatric and psychological factors, respiratory diseases, biologic monitoring, ergonomics, management practices, and environmental health. In addition, all physicians must learn about administrative requirements related to the federal workers’ compensation program, OSHA-mandated surveillance examinations, Department of Transportation commercial driver medical examiner training and certification, and medical review officer requirements.

The training of physicians in occupational medicine has advanced in the last 10 years from teaching residents about the Accreditation Council for Graduate Medical Education core and specialty-specific competencies that were developed by the American College of Occupational and Environmental Medicine. Beyond the basic competencies, the American College of Occupational and Environmental Medicine has developed in-depth competencies for practitioners at every level of care from novice to expert.[6] This laid the groundwork for the development of milestones in the training of OEM physicians as they advance in the field. Residencies in OEM must demonstrate that trainees attain the milestones and certify that they have sufficient competence to practice independently without direct supervision.[7]

Army occupational health providers must take both phases of the AMEDD Center and School Fundamentals of Occupational Health Course, the Hearing Conservation Supervisors Course, and the National Institute for Occupational Safety and Health Spirometry Course. They must also attend training to become public health emergency officers with the following courses: Medical Management of Chemical and Biological Casualties, Toxic Chemical Training or Medical Support Personnel, Combat Casualty Care, and Advanced Trauma Life Support.

Occupational health program managers also need management skills to organize, plan, measure, and refine the implementation of the occupational health program. Two sources of military-relevant, case-based management training are the Fundamentals of Occupational Medicine Course, which offers scenarios and interactive exercises to help attendees develop and refine their management skills, and the 2-week Management of Preventive Medicine Course, also offered at the AMEDD Center and School, which provides attendees with interactive case studies that address commonly encountered problems in preventive medicine and public health at the installation level. Additional resources are available for junior officers who must supervise civilian employees, including a 40-hour civilian supervisors’ course and a junior officer leadership course.

FUNDING

Budgeting

The occupational health program manager must actively manage the program budget and be an honest broker regarding budget needs and expenditures of funds. Each department of public health or preventive medicine service will get an annual projected budget from the resource management office at the military hospital. The occupational health program manager must review prior year funding and personnel levels and determine whether funding and staffing levels have been adequate in the past, based on mission needs and unique circumstances locally. He or she must establish a budget based on prior year execution and decide whether more or less money is needed in the upcoming fiscal year. The department chief or chief of preventive medicine will expect input from the occupational health program manager regarding travel, services, personnel, supplies, and equipment.

The travel budget should cover the costs of staff assistance visits to one or more outlying occupational health clinics. Travel may be required for medical and nursing personnel to attend certification and recertification courses to maintain licensure or privileging in the specialty. OSHA requires occupational health providers to attend occupational health training annually. State nursing and medical licensing boards also require medical professionals to attend training and document attendance with training completion certificates that list the continuing medical education (CME) and continuing education units (CEUs) earned. Most providers must earn a minimum of 50 CMEs or CEUs every 2 years. Travel and per diem costs may be reduced in the future as more training becomes available online and through distributed learning.

Personnel costs for all civilian employees must be included in the occupational health budget unless some other bill-payer is supporting the additional staffing. The occupational health program manager should check with resource management to ensure sufficient funds are programmed to cover salary costs, benefits, performance awards, and step increases for civilian personnel. If the clinic employs contractors to operate ambulances or provide other acute or ambulatory care services, these personnel costs and related overhead costs for awards and training must also be included in the budget.

The occupational health program manager must also identify supplies and consumables used in the clinic and include these costs in the budget request. Supply costs for consumables such as paper, ink cartridges, staples, books, reading materials, and information pamphlets must be included in the budget based on historical usage with an increase to adjust for inflation. Ideally, these purchases can be made at year-end when remaining funds can be used appropriately for planned purchases. The purchase of office and medical supplies, including small items such as blood pressure cuffs and pulse oximeters, allow the program manager to use funds judiciously and ensure supplies do not run out at the start of the fiscal year if there is a delay in congressional approval of the federal budget. Further, if there are funds left at the end of the fiscal year, it may be prudent to pay ahead on contracts that span the current and next fiscal year.

The occupational health program manager can take advantage of available funds at the local treatment facility or medical center by adding larger purchases (over $3,000) to the hospital consolidated equipment list for purchases maintained by resource management. Among the purchases that should be considered for the occupational health clinic are an electrocardiogram machine, spirometer, audiometer and hearing booth, slit lamp, and automated, adjustable examination table with height, seat, and torso/head angle adjustments. Often the hospital does a bulk purchase of computers, printers, fax machines, desk-top projectors and screens, and the occupational health clinic should work with resource management to ensure all clinic needs are met. Lastly, equipment maintenance costs must be identified and included in the facility’s equipment maintenance list.

Sources of Funding

The occupational health program manager must be aware of other sources of funding that might be available to support the program. The chief of occupational health should collaborate with the resource manager at the hospital or medical center so that the occupational health program needs are identified and validated. It is important for the program manager to frequently visit key decision-makers regarding the budget and keep them updated about changes in mission requirements and enhancements. Further, if the mission in any area has expanded, the resource manager must be made aware of the changes. Often, funding may be available centrally to support the program expansion. Large equipment needs and other unmet personnel or financial requirements must be justified and clearly explained to the finance manager. At the midpoint of the fiscal year, the program manager should update the resource manager regarding budget execution, identify new unmet needs, and validate previously identified unfunded requirements. Two months before the end of the fiscal year, it is wise to coordinate with the resource manager and identify items to be added to the year-end funding list.

The APHC exercises oversight of occupational health program funding execution and has funded public health improvement initiatives for many years. Often the occupational health program manager may be able to secure funding through APHC. Also, the local installation safety and environmental offices receive funding that has historically been used to support safety and occupational health training and personnel. Specific funds for safety glasses and tobacco cessation products have been made available in the past.

Expanding Service Delivery

The occupational health program manager may be able to develop support agreements with other organizations needing services within the local area, but it is critical to coordinate with the chief of public health/preventive medicine, the hospital resource manager, the deputy chief for administration, and the chief of the patient administration before any agreements are made. There are restrictions on what services can be provided and to whom; for instance, contractors are not usually eligible for care in the occupational health clinic unless the provision of care and funding are included in the original contract (this commonly occurs when there are no private occupational health services in the area). Everyone is eligible for emergency services, but routine ambulatory care in the occupational health clinic is not normally provided, except as specified above. Occupational health services can routinely be provided to personnel from other federal agencies and to National Guard and Reserve personnel provided an inter-service support agreement is in place. Agencies such as the Defense Commissary Service have made arrangements and reimbursed the Army occupational health clinics for these services in the past. Usually, the additional funding is split between the hospital and the occupational health clinic.

Contracting for Occupational Health Services

Contracting for occupational health services, particularly in remote locations, is difficult for a variety of reasons. The commander arranging the services must have a thorough knowledge of the needed occupational health services, and the installation commander must maintain close contact with the contracting representatives regarding the delivery of services. Once a contract is set up, oversight of services provided tends to be problematic because of the lack of expertise on the part of the installation commander. The medical treatment facility that arranged for the contract support must exercise oversight of the services delivered to ensure standards of care are met and top-quality care is delivered, which is difficult if occupational health programs are understaffed. A concerted effort must be made to ensure periodic oversight is written into the contract and actually performed.

SUMMARY

This chapter has reviewed the organizational command and control relationships from the DoD level to the installation occupational health clinic level. The roles and responsibilities for managing the Army occupational health program were discussed, and the evaluation of occupational health programs was presented. Making the business case for a solid occupational health program requires both hard economic data that proves the financial benefits of effective programs, and the ability to translate this information into a form that resource management and the deputy commander for administration decision-makers will understand and accept.

Beyond traditional process and outcomes measures (eg, FECA costs, workers’ compensation, lost work days), new OEM research is examining the impact of health promotion and wellness initiatives, providing valuable information on workplace benefits versus the costs. Research data on absenteeism and “presenteeism” costs, coupled with increased receptivity by senior leaders and resource managers, support a stronger case for health promotion along with traditional disease and injury prevention programs. OEM professionals must use evidence from private industry and apply the lessons learned to their own occupational health programs and advocate for resources and staffing that benefit both military and civilian workers.

The continued growth of outcomes research in OEM represents significant opportunities to improve quality and efficiency by reducing waste and ensuring physicians meet the standards of care and patients are satisfied. The American Board of Medical Specialties’ Maintenance of Certification Committee has outlined an approach for providers to assess and improve their practice and ultimately improve patient health care outcomes, with the following suggestions:

- develop and promote the use of standardized forms for data collection;

- establish a national clearinghouse for collection and dissemination of data obtained;

- create a panel to identify outcomes, assess interventions, and provide feedback on care quality, health outcomes, and patient satisfaction; and

- emphasize the conduct, reporting, and dissemination of high-quality outcomes research.[26]

These changes are steps toward the goal of relating patient outcomes to the care received.

ACKNOWLEDGMENTS

The author would like to acknowledge contributions to this chapter by Dr Raul Mirza, MD, MPH, and Carol Tobias, OHN, both of the US APHC.

REFERENCES

1.   US Department of the Army. Preventive Medicine. Washington, DC: HQDA; 2009. Army Regulation 40-5.

2.   US Department of the Army. Preventive Medicine. Washington, DC: HQDA; 2009. DA PAM 40-11.

3.   Federal Employees’ Compensation Act. Pub L No. 93-416. September 7, 1974.

4.   Legters LJ, Llewellyn CH. Military medicine. In: Last JM, Wallace RB, eds. Maxcy-Rosenau-Last Public Health and Preventive Medicine. 13th ed. Norwalk, CT: Appleton & Lange; 1992: 1141–1158.

5.   Gaydos JC, Mallon TM, Rice WA. The US Army occupational and environmental medicine residency at Aberdeen Proving Ground, Maryland: 1960-1996. Mil Med. 2016;181(11):e1637.

6.   Cloeren M, Gean C, Kesler D, et al. American College of Occupational and Environmental Medicine’s occupational and environmental medicine competencies—2014: ACOEM OEM Competencies Task Force. J Occup Environ Med. 2014;56(5):e21–e40.

7.   Delgado S. The Preventive Medicine Milestone Project: Occupational Medicine; A Joint Initiative of the Accreditation Council for Graduate Medical Education (ACGME) and American Board of Preventive Medicine. Chicago, IL: ACGME; 2012. https://www.acgme.org/Portals/0/PDFs/Milestones/PreventiveMedicineMilestones-OccupationalMedicine.pdf. Accessed August 17, 2017.

8.   Cecchine G. Foundation for Integrating Employee Health Activities for Active Duty Personnel in the Department of Defense. Arlington, VA: Rand Corporation; 2009.

9.   National Safety Council. Department of Defense Executive Assessment of Safety and Occupational Health Management Systems. Itasca, IL: NSC; 2001.

10.   US Secretary of Defense. Reducing Preventable Accidents. Washington, DC: DoD; 2006.

11.   US Department of Defense. Environment, Safety and Occupational Health (ESOH). Washington, DC: DoD; 2005. DoD Directive 4715.1E.

12.   US Department of Defense. DoD Safety and Occupational Health (SOH) Program. Washington, DC: DoD; 2014. DoD Instruction 6055.01. http://www.dtic.mil/whs/directives/corres/pdf/605501p.pdf. Accessed June 17, 2017.

13.   US Department of Defense. Occupational and Environmental Health (OEH). Washington, DC: DoD; 2008. DoD Instruction 6055.05. http://www.dtic.mil/whs/directives/corres/pdf/605505p.pdf. Accessed May 16, 2017.

14.   US Department of Defense. Occupational Medical Examinations and Surveillance Manual. Washington, DC: DoD; 2007. DoD Instruction 6055.05-M.

15.   Defense Health Agency. Fact Sheet on the New Electronic Health Record. Washington, DC: DHA; 2016.

16.   Robb DJ. Defense Health Agency update. http://amops.org/wp-content/uploads/2015/04/Defense-Health-Agency-Update-by-Douglas-Robb-DO.pdf. Published April 2015. Accessed June 17, 2017.

17.   Assistant Secretary of Defense. MHS balanced scorecard. http://xml.govwebs.net/stratml/carmel/MHSwStyle.xml. Accessed June 17, 2017.

18.   Burke RI, Taylor CH. Army public health: one health, one medicine, one team. US Army Med Dep J. 2015;Jan–Mar:3–8.

19.   US Army Medical Command. 2017 Army medicine campaign plan. http://armymedicine.mil/Documents/Army_Medicine_2017_Campaign_Plan.pdf. Published November 3, 2016. Accessed June 17, 2017.

20.   Pransky G, Himmelstein J. Outcomes research: implications for occupational health. Am J Ind Med. 1996;29(6):573–583.

21.   Pransky G, Benjamin K, Dembe AE. Performance and quality measurement in occupational health services: current status and agenda for further research. Am J Ind Med. 2001;40(3):295–306.

22.   Grady ML, Bernstein J, Robinson S. Putting Research to Work in Quality Improvement and Quality Assurance: Summary Report. Silver Spring, MD: US Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research; 1993. AHCPR Publication No. 93-0034.

23.   Baker A, Madan I. Process quality indicators for general clinical occupational health practice. Occup Med (Lond). 2013;63(2):116–122. https://doi.org/10.1093/occmed/kqs208. Accessed June 18, 2018.

24.   Juster IA, Hamlin B. Financial outcomes. In: Program Measurement and Evaluation Guide: Core Metrics for Employee Health Management. Washington, DC: Health Enhancement Research Organization and Population Health Alliance; 2015: Chap 2.

25.   Kaplan GD, Palma-Davis L. Health impact. In: Program Measurement and Evaluation Guide: Core Metrics for Employee Health Management. Washington, DC: Health Enhancement Research Organization and Population Health Alliance; 2015: Chap 3.

26.   Hawkins RE, Lipner RS, Ham, HP, Wagner R, Holmboe ES. American Board of Medical Specialties maintence of certification, theory and evidence regarding the current framework. J Contin Educ Health Prof. 2013;33:S7–S19. doi: 10.1002/chp.21201. http://onlinelibrary.wiley.com/doi/10.1002/chp.21201/full. Accessed June 19, 2017.

Chapter 8

AGENCY MEDICAL EVALUATIONS

GREGORY J. MARTIN, MD, MPH*; WENDY E. MIKLOS, MD, MPH†; JERALD COOK, MD, MS‡; and J.C. PHILLIP SPOTTSWOOD, JD, MPH§

INTRODUCTION

MEDICAL STANDARDS OF FITNESS AND PHYSICAL EXAMINATION REQUIREMENTS

Provider–Patient Relationship

Medical Standards and Physical Requirements

Employees with Disabilities: Medical–Legal Considerations

PREPLACEMENT AND PERIODIC EVALUATIONS

OSHA-Mandated Medical Surveillance Examinations

Special Surveillance Programs and Examinations

Surveillance Examination Content

Medical Tests and Procedures

Documentation

PERSONNEL POLICY ENFORCEMENT EXAMINATIONS

TERMINATION MEDICAL EXAMINATIONS

SUMMARY

*Colonel, Medical Corps, US Army; Chief, Occupational Medicine, Madigan Army Medical Center, 9925 5th Street, Building 9025, Tacoma, Washington 98431

†Lieutenant Colonel, Medical Corps, US Army; Chief, Department of Preventive Medicine, US Army Medical Activity/Fort Carson, Department of Preventive Medicine, MCXE-PMD, 1650 Cochrane Circle, Fort Carson, Colorado 80913

‡Lieutenant Commander, Medical Corps, US Navy; Occupational Health Department Head, Robert E. Bush Naval Hospital, 1145 Sturgis Road, Twentynine Palms, California 92278

§Medical Policy and Program Specialist, Hiring Policy, US Office of Personnel Management, 1900 E Street, NW, Room 6500, Washington, DC 20415

INTRODUCTION

The US Department of Defense (DoD or DD) civilian workforce is a critical support entity for the military. DoD civilian workers complement and support military missions around the world in areas such as defense policy, intelligence, finance, acquisition, weapons systems development, and medicine. These employees play a key role in institutional memory, providing an indispensable service amid a climate of frequent military deployments and personnel turnover. The policies that govern DoD civilian personnel originate with the Civilian Personnel Policy/Defense Civilian Personnel Advisory Services (CPP/DCPAS), formerly known as the Civilian Personnel Management Service. In support of the undersecretary of defense for personnel and readiness, the CPP/DCPAS plans and formulates civilian personnel programs, implements policy support, and provides information management services for DoD agencies and military departments. The efforts of the CPP/DCPAS are assisted by the Office of Personnel Management (OPM). OPM supports the president, Congress, executive agencies, and the military with human capital policies in order to reach national strategic goals. Executive Order 13197,[1] signed by President Bill Clinton on January 18, 2001, formalized OPM’s authority to require federal agencies, including the DoD, to establish human resource management (HRM) practices consistent with merit system principles. Furthermore, OPM may collect agency workforce information, review the respective agency’s HRM programs, and report on their HRM practices.

The DoD has three subordinate military departments: the Department of the Navy (DoN), Department of Air Force (DAF), and Department of the Army (DA). Each military department has established its own human resources agency for the civilian workforce, and these agencies align with CPP/DCPAS and OPM policies and practices. The human resources agencies for each military department are the Office of Civilian Human Resources Services for the DoN, the Air Force Civilian Service for the DAF, and the Civilian Human Resources Agency (CHRA) for the DA. Each agency generally has local offices on major installations belonging to the respective military department. For example, the CHRA has local offices called Civilian Personnel Advisory Centers (CPACs) on every major Army installation. These offices assist with civilian job classification and staffing, recruitment and placement, and management–employee relations. They also support automated HRM systems, employee training and development, and employee benefits including retirement and workers’ compensation.

On DoD installations, there are usually three groups of civilian employees who have occupational health requirements. These groups are: General Service (GS) or salaried employees, Wage Grade (WG) or waged employees, and Non-Appropriated Funds (NAF) employees, who are most often involved in morale and welfare employment. Depending on the type of duty, occupational health requirements vary in breadth and depth. Guidance on requirements may originate with the CPP/DCPAS, OPM, DoD, the respective military department, a union, or from other agencies that provide oversight on workplace hazards, such as the Occupational Safety and Health Administration (OSHA), Federal Motor Carrier Safety Agency (FMCSA), and the National Fire Protection Association. When more than one occupational health requirement exists across entities, medical evaluations generally adhere to the most restrictive requirement.

MEDICAL STANDARDS OF FITNESS AND PHYSICAL EXAMINATION REQUIREMENTS

The main purpose for conducting occupational medical evaluations is for medical clearance: to determine whether workers are medically and physically able to perform the assigned duties without substantial risk of harm to themselves, to others, or to the mission. Another important purpose is for medical surveillance: to determine whether the workplace has caused an injury or illness due to an occupational hazard or exposure.[2] The types of occupational health medical evaluations include (1) preplacement evaluations, which may include baseline medical surveillance or medical certification examinations; (2) periodic evaluations, which may also include medical surveillance or medical certification examinations; (3) personnel policy enforcement evaluations, such as fitness for duty evaluations; and (4) termination medical evaluations. Occupational health providers conduct all of these evaluations.

Provider–Patient Relationship

Occupational health professionals are necessary for establishing and maintaining a healthy DoD workforce and a safe workplace. Occupational health medical evaluations are mainly administrative in nature and intended for either medical clearance or medical surveillance. The DoD occupational health professional typically does not assume a provider–patient relationship for the purposes of diagnosis and treatment. Rather, the occupational health provider determines the specific content of medical evaluations and takes into consideration job duties and requirements, environmental factors, legal and regulatory requirements, and any other relevant factors that may impact workplace safety and efficiency. Baseline screening labs or tests may be necessary, particularly for work involving hazardous duties. Because of the special nature of occupational health evaluations, most agencies have established medical standards and physical requirements for certain positions.

Medical Standards and Physical Requirements

Medical standards define the minimum health status or fitness level determined to be necessary for safe and efficient performance, such as a minimum level of visual acuity. According to Title 5 of the US Code of Federal Regulations (CFR) 339, Medical Qualification Determinations, agencies have the authority to establish medical standards for which they are the predominant employer (50% or more of the employees).[3] An applicant or employee needs only to meet the minimum standard, but if he or she does not, then the medical evaluator may disqualify the individual for failure to meet medical standards. Medical standards may also specify medical conditions that disqualify an individual from certain jobs.

The established physical requirements referred to in 5 CFR 339.203[3] should be listed in the job description. The medical evaluator may not disqualify an applicant or employee for failure to meet physical requirements. Rather, the medical evaluator must assess the individual’s physical limitations and forward a recommendation to the selecting official regarding whether the individual can perform the essential duties of the position.

In addition, 5 CFR 339 specifies OPM’s guidance for establishing medical standards and physical requirements pertaining to federal positions. Under 5 CFR 339.301(a), federal agencies are prohibited from ordering a medical evaluation for an applicant or employee unless that individual is applying for or occupying a position that is subject to specific medical standards or physical requirements or is required to enroll in a medical surveillance or certification program.[3] Psychiatric examinations are also prohibited except when (a) a psychiatric examination is specifically required for a position with written medical standards or subject to a medical evaluation program; or (b) during an authorized medical examination, there is evidence of behavior or actions that may affect the safe and efficient performance of the individual or others. The local civilian personnel officer determines which positions require preplacement medical evaluations. Many GS and NAF positions neither are strenuous nor involve significant hazards or exposures, so most positions do not require a preplacement evaluation. However, most WG positions are considered arduous or hazardous and frequently require both preplacement and periodic medical evaluations. DoD positions that require preplacement and periodic evaluations have specified medical standards and physical requirements (Exhibit 8-1), and it is crucial for the occupational health provider to understand the difference between the two.

Medical requirements may also apply to positions that have unique duties, require motor vehicle operation, involve work performed in a particular environment, or involve certain NAF or WG jobs. Information about such requirements is provided to applicants by the employing agency. Agencies can also require fitness for duty evaluations (discussed below) for workers with established medical requirements.

Employees with Disabilities: Medical–Legal Considerations

The Rehabilitation Act of 1973[4] prohibits employment discrimination against any individual in hiring, compensation, and firing actions. It requires employers to hire the best qualified individual, even if that person has a disability. A best qualified individual is considered able to perform the essential functions of the job either with or without “reasonable accommodation” in the workplace. Employers must modify the job or physical work environment to allow the disabled employee to perform the essential job tasks as long as these accommodations do not present an undue hardship for the employer. An undue hardship involves excessive expense, significant difficulty, or conditions in which the essential job tasks cannot be accomplished safely or efficiently.

In conjunction with the Rehabilitation Act, the Americans with Disabilities Act (ADA)[5] states that a qualified applicant or employee with a disability must be reasonably accommodated in the workplace provided it does not cause undue hardship to the employer. Under the ADA, a disability is defined as a physical or mental impairment that substantially limits one or more major life activities; it also applies if an individual is regarded as having a disability or has a record of such disability.[5] Prior to an offer of employment, the ADA prohibits all disability-related inquiries and medical examinations, even those that are job-related. After an applicant is conditionally offered a job, but has not yet begun work, the employer may make disability-related inquiries relevant to the job and review findings from a medical preplacement evaluation. The employer must follow equitable hiring procedures for all individuals entering the same job category when conducting reviews of this nature. A qualified applicant with a disability must satisfy requisite skills, experience, and education for the position with or without reasonable accommodation. When the disability or need for accommodation is not obvious, the employer may ask the individual for reasonable and sufficient documentation pertaining to his or her disability and functional limitations. In most cases, the request may only include medical information related to the disability and the need for accommodation, excluding the individual’s entire medical record.

EXHIBIT 8-1

US OFFICE OF PERSONNEL MANAGEMENT GENERAL SCHEDULE OCCUPATIONS WITH MEDICAL OR PHYSICAL REQUIREMENTS

GS-0006

Correctional Institution Administration Series

GS-0007

Correctional Officer Series

GS-0081

Fire Protection and Prevention Series

GS-0082

United States Marshal Series

GS-0083

Police Series

GS-0084

Nuclear Materials Courier Series

GS-0085

Security Guard Series

GS-0101

Correctional Treatment Specialist (Department of Justice)

GS-0462

Forestry Technician Series—smokejumper positions

GS-0485

Wildlife Refuge Management Series—positions with pilot duties

GS-0660

Pharmacist Series

GS-0664

Restoration Technician Series

GS-0680

Dental Officer Series

GS-1801

Canine Enforcement Officer (Department of the Treasury)

GS-1801

Surface Mining Reclamation Specialist (Department of the Interior)

GS-1811

Criminal Investigating Series

GS-1811

Treasury Enforcement Agent (Department of the Treasury)

GS-1815

Air Safety Investigating Series

GS-1822

Mine Safety and Health Series

GS-1825

Aviation Safety Series

GS-1850

Agricultural Commodity Warehouse Examining Series

GS-1863

Food Inspection Series

GS-1884

Customs Patrol Officer Series

GS-1890

Customs Inspection Series

GS-1896

Border Patrol Agent Series

GS-2152

Air Traffic Control Series

GS-2181

Aircraft Operation Series

___________________

Reproduced from: US Office of Personnel Management. General schedule qualification policies. May 2, 2014. https://www.opm.gov/policy-data-oversight/classification-qualifications/general-schedule-qualification-policies/#url=Medical-Requirements. Accessed September 30, 2016.

The ADA protects those with disabilities, not impairments, which is an important distinction with respect to function. An impairment is a physical and/or psychological condition that may or may not interfere with the worker’s ability to function at a particular job. For example, an administrative employee with a limb amputation may successfully function in an office setting. He or she would therefore be considered to have an impairment. In contrast, a police officer with the same limb amputation would be unlikely to perform all of the essential duties of the position safely. Therefore, he or she would be considered to have a disability.

Clinicians work with a variety of records and patient information in occupational health. Occupational health providers must know the differences between the records, the confidentiality issues involved, and specific rules related to each of the records. Laws that govern the confidentiality of patient records include the Privacy Act,[6] the Health Insurance Portability and Accountability Act (HIPAA),[7] and the Genetic Information Nondiscrimination Act (GINA).[8]

Occupational health practices generate medical records that document care of work-related illnesses and injuries or medical forms that are specific to workplace requirements. These records may include medical and employment questionnaires, job descriptions, preplacement examinations, medical surveillance examinations, biological and other screening results, occupational exposure evaluations, and workers’ compensation medical records. Employers may retain employee exposure records, including workplace hazardous exposure monitoring (eg, noise levels, air monitoring); biological monitoring (eg, blood lead level); analytical methodologies related to monitoring results; and safety data sheets.

HIPAA gives employers access to some protected health information if the disclosure is required to comply with laws relating to workers’ compensation. HIPAA also allows disclosure per requirements of state or federal laws and regulations. Thus, clinicians should be mindful of confidentiality when recording patient information in occupational medical records. Occupational health clinicians regularly keep personal health information (ie, medical conditions not related to work) separate from exposure records. Certain OSHA standards require employers to obtain written opinions from clinicians performing required medical surveillance examinations. These standards typically state that “the employer shall instruct the physician not to reveal in the written opinion specific findings or diagnoses unrelated to occupational exposure.” It is strongly recommended that occupational health providers inform the worker and obtain consent to include personal health information in the employee’s work medical file.

Lastly, GINA (2008) prohibits employers and health plans from discriminating based on genetic information, including family medical history.[8] Under GINA, an employer may not request, require, or purchase genetic information or family medical history from job applicants or employees at any time, including the post-offer stage of employment. In compliance with GINA, occupational health best practices avoid questions or questionnaires that pertain to genetic information or family medical history. Most occupational health clinics have taken measures to separate the occupational health record from the rest of an individual’s medical record, although this is not an absolute mandate under GINA. In the cases where the main medical record contains job-related information and accessing the main medical record is consistent with business necessity, then the employer may request that the employee sign a release in order to avoid potential litigation. The release should contain warning verbiage pertaining to Title II of GINA, which specifies that any acquisition of genetic information in response to the request will be considered inadvertent.[8]

PREPLACEMENT AND PERIODIC EVALUATIONS

A preplacement evaluation is conducted for medical clearance, to determine an applicant’s ability to safely and efficiently perform duties for a specific job without undue risk to themselves or others. Management needs the examination information in order to make a hiring decision. Preplacement evaluations may be dovetailed with medical surveillance, which is intended to assess employees for health effects from potential occupational exposures. If the applicant or employee will be involved in hazardous work, he or she will usually be enrolled into a medical surveillance program. Baseline and periodic clinical data, such as special labs or medical tests, is gathered as part of the surveillance data. Lab and medical test requirements vary depending on the type of work and pertinent agency regulations. Also, if an agency has an established substance abuse program, medical clearance may include screening for drug or substance use. Ideally, preplacement evaluations are completed before the individual commences work; however, they may be completed within 60 days of assignment unless more stringent requirements exist. Preplacement evaluations may identify individuals who are susceptible to or at higher risk for disease in response to specific occupational exposures. However, employment decisions cannot be based on the individual’s susceptibility or potential for developing a disease, injury, or sensitivity. For nonhazardous, non-laborious work, medical evaluations are generally not warranted.

Periodic medical evaluations are intended to provide medical surveillance and are conducted at scheduled intervals, usually occurring annually or less frequently. Periodic medical evaluations are most appropriately conducted for employees in certain arduous or hazardous jobs, such as law enforcement, or work that involves possible exposure to known toxic agents, such as lead. Medical surveillance, when tailored to a specific line of work, helps to identify employees with a pattern of disease or injury that indicates an underlying work-related problem. Screening techniques, such as history questionnaires, lab tests, or medical tests, are most effective when abnormalities in the target organ system are identified at a stage when exposure modification or medical treatment can halt disease occurrence or progression. The worker is likely to benefit from counseling and information about his or her occupational hazards, early detection, and appropriate intervention including possible referral to a medical specialty. Medical surveillance is also valuable for population data and studies, even if not directly beneficial to an individual worker. It should be noted that preplacement and periodic medical evaluations generally do not provide overall services for preventive health issues. Preventive medicine services are important but should be considered complementary to job-related medical evaluations. Union contracts may impact the type or frequency of medical evaluations. Medical surveillance examinations may also have a regulatory or OSHA component.

EXHIBIT 8-2

OCCUPATIONAL SAFETY AND HEALTH ADMINISTRATION REQUIRED MEDICAL SURVEILLANCE IN GENERAL INDUSTRY (29 CFR 1910)

Subpart H. Hazardous materials

1910.120—Hazardous waste operations and emergency response

Subpart I. Personal protective equipment

1910.134—Respiratory protection

Subpart Z. Toxic and hazardous substances

1910.1001—Asbestos

Appendix H. Medical surveillance guidelines for asbestos (non-mandatory)

1910.1003—Carcinogens

1910.1004—alpha-Naphthylamine

1910.1006—Methyl chloromethyl ether

1910.1007—3,’-Dicholorobenzidine

1910.1008—bis-Chloromethyl ether

1910.1009—beta-Naphthylamine

1910.1010—Benzidine

1910.1011—4-Aminodiphenyl

1910.1012—Ethyleneimine

1910.1013—beta-Propiolactone

1910.1014—2-Acetylaminofluorene

1910.1015—4-Dimethylaminoazobenzene

1910.1016—N-Nitrosodimethylamine

1910.1017—Vinyl chloride

1910.1018—Inorganic arsenic

Appendix C. Medical surveillance guidelines

1910.1025—Lead

1910.1027—Cadmium

1910.1028—Benzene

Appendix C. Medical surveillance guidelines for benzene

1910.1029—Coke oven emissions

Appendix B. Industrial hygiene and medical surveillance guidelines

1910.1030—Bloodborne pathogens

1910.1043—Cotton dust

1910.1044—1,2-dibromo-3-chloropropane

Appendix C. Medical surveillance guidelines for DBCP

1910.1045—Acrylonitrile

Appendix C. Medical surveillance guidelines for acrylonitrile

1910.1047—Ethylene oxide

Appendix C. Medical surveillance guidelines for ethylene oxide

1910.1048—Formaldehyde

1910.1050—Methylenedianiline

Appendix C. Medical surveillance guidelines for MDA

1910.1450—Occupational exposure to hazardous chemicals in the laboratories

___________________

Reproduced from: 29 CFR 1910, 1970. Occupational Safety and Health Standards. https://www.osha.gov/pls/oshaweb/owastand.display_standard_group?p_toc_level=1&p_part_number=1910. Accessed September 30, 2016.

OSHA-Mandated Medical Surveillance Examinations

OSHA is the main regulatory agency that mandates workplace safety and medical surveillance programs. OSHA standards address construction work, agriculture, maritime operations, and general industry, including blood-borne pathogens, respiratory protection, occupational noise exposure, and personal protective equipment. OSHA-required medical surveillance evaluations are specified in 29 CFR 1910 and referenced in Exhibit 8-2.

Special Surveillance Programs and Examinations

Other components of medical evaluation that necessitate special or selective history taking, physical examination, or laboratory or medical testing may be established by the respective agency, state or local regulation, union, or other association. These clinical processes are a reflection of the agency’s commitment to worker safety. Industrial hygiene and safety personnel also play a key role in ensuring worker safety and communicating valuable risk information about specific workplace toxins, substances, and exposures and the precautions necessary to protect workers. Special workplace programs may include:

- hearing conservation

- vision protection

- respiratory protection

- hazardous substances

- firefighting (physical qualifications are detailed in the National Fire Protection Association Standard 1582, Comprehensive Occupational Medical Program for Fire Departments[9])

- law enforcement (American College of Occupational and Environmental Medicine guidance for the medical evaluation of law enforcement officers[10])

- worldwide deployable civilian personnel (personnel who are required to travel to remote, sometimes hostile, areas that may not have comprehensive medical care available)

- personnel reliability program

- Federal Aviation Administration (FAA) exams for pilots, flight crew, and air traffic controllers; FMCSA exams for commercial motor vehicle operators who hold a commercial driver’s license

Effective May 21, 2014, FMCSA required medical examiners to be certified. FAA and FMCSA medical examiners must be familiar with the medical standards of fitness set forth by the certifying agency; they become certified by passing a written certification examination.

Employees may develop medical conditions that affect their ability to perform the job. The employee must report the change in health status to the agency, as well as to the certifying medical examiner. This may result in a temporary or permanent medical disqualification depending upon the nature and extent of the work limitations. Workers who do not meet medical requirements may apply for a medical waiver; the FAA and FMCSA decide whether or not to grant the waiver. If an agency grants a medical waiver, the employee may be medically certified and retain their license. If an agency does not grant the waiver, then the examinee may re-apply once the medical condition has resolved.

Surveillance Examination Content

A focused health and work history, as well as a focused physical examination, are most often appropriate for preplacement or periodic medical evaluations. Generally speaking, a comprehensive physical examination, while helpful for a person’s overall health, is not necessary. The occupational health provider should take a medical history based on complaints and risk factors, check pertinent systems, perform a focused physical examination, and, when indicated, order relevant laboratory or medical tests. All findings, whether normal, unique, or abnormal, should be documented. Useful factors to consider for exam content and developing examination protocols include:

- specific job tasks and requirements

- workplace risk factors including exposure to physical, chemical, biological, radiological, and other agents, as well as ergonomic stressors

- personal risk factors

- target organ systems

- public health and safety impact

- legal and regulatory requirements

- employee health promotion and personnel programs

- work history or previous job tasks and requirements

- environmental risk factors, including exposures within the household and from hobbies

- use of personal protective equipment

- allergies

- tobacco, alcohol, and illicit drug use

- diet and use of medications, vitamins, herbs, and supplements

- other factors set forth in National Institute for Occupational Safety and Health (NIOSH) Publication No. 79-116, A Guide to Work-Relatedness of Disease[11]

Elements from a general physical examination that may be tailored to a focused exam include:

- vital signs (pulse rate, respiratory rate, blood pressure with appropriately sized cuff, temperature, pain level)

- height, weight, body mass index, general appearance, mental status

- dermatologic system

- eyes, ears, nose, throat, mouth

- endocrine system, including thyroid

- cardiovascular system

- peripheral vascular system

- respiratory system

- gastrointestinal system

- genitourinary system

- musculoskeletal system

- neurological system

- psychiatric screen (if appropriate)

Medical Tests and Procedures

The following medical tests or procedures may be performed as part of a brief or comprehensive physical examination.

Laboratory Tests

Laboratory tests, as relevant to the employee’s line of work, should be obtained when either specified as mandatory by agency regulation or deemed necessary by the occupational healthcare provider. Blood tests may include a complete blood cell count, a basic or comprehensive metabolic panel, hepatic function, blood levels of particular substances, or other tests as indicated. Urine tests may include a standard urinalysis, a spot or random urine collection, or a 24-hour collection. Testing laboratories must be accredited by the College of American Pathologists, certified as a Medicare provider, or an active participant in the Clinical Laboratory Improvement Program of the Centers for Disease Control and Prevention or the American Association for Clinical Chemistry.

Vision and Eye Tests

Vision tests include color perception, corrected and uncorrected near and far visual acuity, depth perception, and peripheral vision. Color vision results must indicate the type of test used and the number of screens correctly identified compared to the number tested. When an employee has less than a perfect score on a panel of color vision tests, the ability to at least distinguish red, green, and amber may be specifically required depending on the governing agency. In other cases, such as for law enforcement evaluations, the Farnsworth dichotomous test for color may be required. If the employee requires corrective lenses such as glasses or contacts while at work, both corrected and uncorrected vision are usually assessed. The employee must bring his or her own glasses or contacts as well as supplies for contact removal and storage. Visual acuity should be recorded in a Snellen fraction (eg, 20/20). Depth perception should be recorded in seconds of arc, and the type of test utilized should be noted. Peripheral vision should be recorded in degrees on a lateral plane, both nasal and temporal, for each eye (eg, R nasal: 45°, R temporal: 90°, L nasal: 40°, L temporal: 85°).

Audiogram

Baseline and periodic audiograms should be conducted using equipment and test locations that meet OSHA regulations as specified in 29 CFR 1910.95.[12] Testing personnel should be certified by the Council for Accreditation in Occupational Hearing Conservation or trained in the use of a microprocessor audiometer. Ideally, audiograms should be performed in an American National Standards Institute (ANSI) approved booth (ANSI S3.1-1977) with equipment calibrated to ANSI standards (ANSI S3.6-1973). If a booth is unavailable, the test room sound pressure levels should not exceed those specified in the OSHA noise regulations (29 CFR 1910.95 App D[12]), as follows:

Rooms used for audiometric testing shall not have background sound pressure levels exceeding those in Table D-1 (below) when measured by equipment conforming at least to the Type 2 Requirements of American National Standard Specification for Sound Level Meters, S1.4-1971(R1976), and to the Class II requirements of American National Standard Specifications for Octave, Half-Octave, and Third-Octave Band Filter Sets, S1.11-1971 (R1976).

TABLE D-1: MAXIMUM ALLOWABLE OCTAVE-BAND SOUND PRESSURE LEVELS FOR AUDIOMETRIC TEST ROOMS

Octave-band center frequency (Hz)

500

1000

2000

4000

8000

Sound pressure level (dB)

40

40

47

57

62[12]

Hearing thresholds for each ear should be recorded separately at each of the specified frequencies. If the employee wears hearing aids, testing should be conducted without the hearing aids unless the position’s medical standards permit their use. The use of hearing aids during audiogram testing should be documented on the audiogram report.

Chest Radiograph

Chest x-rays or other radiographs should be done when specified and required by regulation. Radiographs should be ordered routinely, conducted by a qualified radiographic technician or radiologist and read by a radiologist. Radiographs taken to evaluate possible effects of asbestos or silica exposure must be read by a certified “B-reader” radiologist (a radiologist certified by NIOSH as demonstrating proficiency in accurate and precise classification of pneumoconioses on radiographic imaging). The radiologist’s report should be filed in the employee’s occupational health record.

Pulmonary Function Test

A pulmonary function test (PFT) or spirometry should be conducted when an employee has a known or potential exposure above the action level of regulated agents that affect the respiratory system, such as asbestos, benzene, coke oven emissions, cotton dust, ethylene oxide, and formaldehyde. The PFT may also be used to evaluate the effects of exposure to agents that can cause occupational asthma and for other lung disorders when clinically indicated. The PFT may also be administered to evaluate an individual’s ability to work safely while using a respirator. Personnel administering the PFT should have successfully completed a NIOSH-approved spirometry course. The parameters that should be tested and documented are usually forced vital capacity (FVC), forced expiratory volume in 1 second (FEV_1), FEV_1 as a percent of FVC (FEV_1/FVC), forced expiratory flow between 25% and 75% of the vital capacity (FEF25%-75%), and peak expiratory flow (PEF). Most modern machines automatically calculate expected levels based on the client’s age, height, gender, and race (sometimes), and may even track interim changes and trends for the same individual. Spirometry test results can demonstrate patterns of either obstructive or restrictive pulmonary disorders and allow for interpretation of the severity of the condition.

Electrocardiogram

Electrocardiograms (ECGs) should be standard 12-lead recordings and may be automated or manual. A written interpretation of the ECG by a credentialed healthcare provider trained in ECG analysis should be included in the person’s record. ECGs are helpful in establishing a person’s baseline health status; however, they have limited value as a cardiovascular screening tool in asymptomatic individuals.

Exercise Stress Test

An exercise stress test (EST) should be done when it is either specified as mandatory in regulation or has been deemed necessary by the occupational healthcare provider. An EST must be conducted by or under the direction of a credentialed healthcare provider with demonstrated training in ESTs and interpreted by a cardiologist. Generally, the EST is a graded, symptom-limited test using the Bruce protocol.

Documentation

Documentation requirements of the medical evaluation vary depending on agency medical–legal considerations, the types of forms in circulation, and local recordkeeping practices. For example, the CHRA currently has evaluations recorded on an Office Form (OF) 178, Certificate of Medical Examination, and a DD 2807-1, Report of Medical History. For DA NAF applicants, a DA Form 3437, Certificate of Medical Examination, is required. The CPAC office forwards the OF 178 or DA Form 3437 to be completed to the occupational health provider with a current copy of the job description detailing physical requirements and environmental factors. For healthcare services external to the occupational health practice, procedures must be taken to ensure maximum medical record confidentiality and security.

PERSONNEL POLICY ENFORCEMENT EXAMINATIONS

Personnel policy enforcement examinations are conducted under special circumstances to determine if a worker continues to meet medical standards and conditions of employment. Examples of these types of examinations are post-employment drug screening, work-related injury/illness evaluations, fitness for duty examinations, and impairment evaluations.[1] Drug screening programs, although beyond the scope of this chapter, serve as a deterrent to prevent workers employed in safety-sensitive positions from risking workplace safety. If an accident occurs at work, the employee may be required to undergo mandatory drug testing or face removal from the position.

If an employee has a work-related injury or illness, the occupational health professional assists in the proper medical documentation, medical care or referral, and medical coverage for the individual. Fitness for duty evaluations are formal requests by the supervisor through the civilian personnel office to determine if an employee is medically fit to continue or resume his or her duties. These evaluations may also be referred to as return-to-work examinations. If the worker has been either off work for a health-related reason, usually for 3 days or more, or on duty restrictions for a medical reason, whether work-related or not, then the occupational health provider may evaluate the individual’s health status and make a determination of fitness. The provider may recommend that the employee either remain or be placed off work, return to work but with duty or time restrictions, or return to work without restrictions. The provider is not responsible for making employment decisions or for making reasonable accommodations. Rather, the provider advises the employer with respect to:

1. the employee’s ability to meet physical requirements, if any, as specified for the employee’s position;

2. the employee’s ability to physically perform the essential functions of the position with or without reasonable accommodation; and

3. the employee’s ability to meet health and safety requirements without posing a risk to himself or herself or to others.

A fitness for duty exam should be as comprehensive as needed to determine if the employee meets the criteria above. Exams can usually be accomplished with the tests available at most clinics: vision tests, audiograms, labs, PFTs, ECGs, and chest x-rays. However, tests should be conducted only when medically indicated and must not be performed for investigative or punitive reasons. The provider should request and review medical documentation from the employee’s private healthcare, if any, that is relevant to the identified medical condition impacting the employee’s fitness for duty. In cases needing clarification, the provider should interview witnesses or other providers who can attest to the worker’s physical performance. If a report is requested by the employee’s supervisor or civilian personnel office, it should not contain details about the employee’s medical condition. Rather, the report should contain information such as the following:

- reason the fitness for duty exam was requested

- source and nature of the report’s information (eg, the workplace, private healthcare, occupational healthcare, interviews conducted with witnesses or other providers)

- whether the employee meets physical requirements, has any accommodation needs, and can perform safely and effectively at work

- suggestions, if any, that may allow the employee to meet job requirements

The provider should document the employee’s history and exam in the medical record, for example, in the DA, using an SF 600, SF 78, and current version of the medical history form. If an employee has behavioral problems without an underlying medical cause, it is a job performance issue; the employee’s supervisor is responsible for addressing behavioral problems that affect the workplace.

Impairment evaluations are for the purpose of disability rating and are performed to determine if the injury or illness is job related and, if so, the extent of the injury or illness. Impairment evaluations are usually performed for workers’ compensation or third-party insurers. The examiner should be a provider who can render an unbiased and objective opinion, and therefore is not involved in the employee’s healthcare. When conducting an impairment examination, the provider should render a clearly written report that includes the following:

- diagnosis

- causal relationship of injury/illness

- prognosis

- maximum medical improvement

- permanent impairment

- capacity to work (eg, none, modified duties, part-time, or full duty)

- disability

- appropriateness of care received

- recommendations

In a complicated or contentious situation, the most senior and experienced occupational health provider should perform the impairment evaluation. If the provider disagrees with the appropriateness of care received, he or she must carefully and objectively note the supporting facts and conclusions. These findings may be used to justify a formal request for an independent medical exam (IME). IMEs are conducted when there are litigious concerns or the Office of Workers’ Compensation requests clarification. An IME is conducted by a qualified independent medical examiner (a provider specially trained and qualified to perform objective medical evaluations).

TERMINATION MEDICAL EXAMINATIONS

There are two types of termination medical evaluations: termination of employment and termination of exposure evaluations. A termination of employment examination is designed to assess pertinent aspects of a worker’s health when a worker leaves employment. Medical documentation of the examination results may later support or refute a relationship, if any, between a future medical problem and a workplace exposure. These examinations are particularly useful for conditions that have chronic sequelae or long latency periods. For example, Title 29 of CFR 1910.1001(f) requires termination of employment examinations for asbestos workers.[12]

The second type, a termination of exposure examination, is performed when a worker’s exposure to a specific hazard has ceased. An exposure may cease when a worker is reassigned, when a job process is changed, to avoid the exposure, or when the worker leaves employment. Termination of exposure examinations are most beneficial when the health effect being screened for is likely to be present at the time exposure ceases. For example, Title 29 of CFR 1910.120(f)[12] requires termination of exposure examinations for hazardous waste operations and emergency response workers.

SUMMARY

DoD employees play a key role in helping meet mission requirements and provide institutional memory when active duty personnel deploy and rotate frequently. In the introduction, human resource policy and legal authority establishing the OPM and DoD human resources offices were discussed along with the requirements to comply with HIPAA and GINA. The next section reviewed DoD civilian workforce medical standards of fitness and physical examination requirements, including how the examination requirements were established and where the requirements can be found. The section also reviewed how employees with disabilities are handled under the Rehabilitation Act and ADA. In the next section, preplacement, periodic, and termination medical examination requirements were discussed. OSHA-mandated and special surveillance examinations were reviewed, including examination content and medical procedures involved. In the section on personnel policy enforcement examinations, fitness for duty examination procedures were discussed in detail. The last section discussed the rationale and requirements for termination physical examinations.

REFERENCES

1.   Clinton WJ. Governmentwide Accountability for Merit System Principles. Washington, DC: The White House; January 18, 2001. Executive Order 13197. https://www.gpo.gov/fdsys/pkg/FR-2001-01-25/pdf/01-2398.pdf. Accessed September 26, 2017.

2.   Under Secretary of Defense for Acquisition, Technology and Logistics. Occupational Medical Examinations and Surveillance Manual. Washington, DC: DoD; May 2, 2007: C1.3. DoDI 6055.05-M. http://www.dtic.mil/whs/directives/corres/pdf/605505mp.pdf. Accessed September 30, 2016.

3.   5 CFR, Part 339, 2012. Medical Qualification Determinations. https://www.gpo.gov/fdsys/pkg/CFR-2012-title5-vol1/pdf/CFR-2012-title5-vol1-part339.pdf. Accessed October 3, 2016.

4.   The Rehabilitation Act of 1973. Pub L no. 93-112. September 26, 1973. https://www.eeoc.gov/eeoc/history/ada25th/rehab_act-1973.cfm. Accessed September 30, 2017.

5.   Americans with Disabilities Act of 1990. Pub L no. 101-336. http://library.clerk.house.gov/reference-files/PPL_101_336_AmericansWithDisabilities.pdf. Accessed September 30, 2016.

6.   The Privacy Act of 1974. 5 USC. § 552a. https://www.justice.gov/opcl/privacy-act-1974. Accessed October 5, 2017.

7.   Health Insurance Portability and Accountability Act of 1996, Public Law 104-191. https://www.gpo.gov/fdsys/pkg/PLAW-104publ191/pdf/PLAW-104publ191.pdf. Accessed September 30, 2017.

8.   The Genetic Information Nondiscrimination Act of 2008. https://www.eeoc.gov/laws/statutes/gina.cfm. Accessed September 30, 2017.

9.   National Fire Protection Association. NFPA 1582, Standard on Comprehensive Occupational Medical Program for Fire Departments. Quincy, MA: NFPA; 2016. http://www.nfpa.org/codes-and-standards/all-codes-and-standards/list-of-codes-and-standards/detail?code=1582. Accessed October 4, 2017.

10.   American College of Occupational and Environmental Medicine. Guidance for the medical evaluation of law enforcement officers. https://www.leoguidance.org/. Accessed September 30, 2017.

11.   Kusnetz S, Hutchison MK, eds. A Guide to Work-Relatedness of Disease. Washington, DC: National Institute for Occupational Safety and Health; January 1979. NIOSH Publication No. 79-116. https://www.cdc.gov/niosh/pdfs/79-116-a.pdf. Accessed September 30, 2017.

12.   29 CFR 1910, 1970. Occupational Safety and Health Standards. https://www.osha.gov/pls/oshaweb/owastand.display_standard_group?p_toc_level=1&p_part_number=1910. Accessed September 30, 2016.

Chapter 9

FEDERAL WORKERS’ COMPENSATION PROGRAMS

CAMERON J.L. NELSON, MD, MPH*; SHERYL A. BEDNO, MD, MPH†; and TIMOTHY M. MALLON, MD, MPH‡

INTRODUCTION

FEDERAL WORKERS’ COMPENSATION

Computer/Electronic Accommodations Program

FECA Implementation and the Office of Workers’ Compensation Programs

DEPARTMENT OF DEFENSE FECA PROGRAM

Authorization for Medical Treatment

Role of the FECA Working Group

Occupational Health Clinician’s Role

Employees’ Choice of Physician

TRENDS IN MILITARY WORKERS’ COMPENSATION COST AND RATES

Injury Statistics

Initiatives to Reduce Costs

Improving Workers’ Compensation Case Management

REVIEWS OF MILITARY PROGRAMS

Workers’ Compensation Program Systems Analysis

Government Accountability Office Audit

FECA MANAGEMENT CHALLENGES

DEPARTMENT OF LABOR PROGRAM MANAGEMENT EFFORTS

SUMMARY

*Commander, Medical Corps, US Navy; Chief of Occupational Medicine, Naval Hospital Bremerton, Bremerton, Washington 98312

†Lieutenant Colonel, Medical Corps, US Army; Chief, Preventive Medicine Service, Womack Medical Center, Fort Bragg, North Carolina 28310

‡Colonel (Retired), Medical Corps, US Army; Adjunct Assistant Professor, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

INTRODUCTION

Much of the content of this chapter was originally published as two articles in a supplement to the Journal of Occupational and Environmental Medicine in August 2015 that was devoted exclusively to federal workers’ compensation programs.1,2 Since that work was published, improvements have been made in federal workers’ compensation program management. Medical case reviews have been coordinated to ensure that difficult questions regarding work ability and utilization review get addressed for the service leadership. This chapter also expands the earlier work by incorporating the systems analysis approach to evaluating the success of the workers’ compensation program.

Federal workers’ compensation insurance benefits provide wage replacement as well as medical cost coverage and rehabilitative care. Employees may request disability payments for permanent impairment. Workers who are unable to work must provide medical documentation that their injury is work related and limits their ability to do the essential job functions.

This chapter will review federal workers’ compensation program basics for setting up and running the program at the installation and regional levels. Beyond the basics, this chapter will include a discussion of best practices in Federal Employees Compensation Act (FECA) program management and discuss how program metrics can improve the ability to demonstrate program success or show that additional resources are needed to properly run the program. Available FECA data sources will be identified and useful comparison features and tools will be discussed so that local FECA managers can compare their program metrics with other installations, the service, and overall Department of Defense (DoD) FECA program metrics.

FEDERAL WORKERS’ COMPENSATION

The first federal workers’ compensation law, passed in 1908, included only a quarter of federal workers, those who were considered to work in “dangerous jobs.” Only traumatic injuries were covered, and there was a 15-day waiting period to file a claim.[3] FECA, passed in 1916, expanded coverage to all federal employees. The new law added coverage for occupational illnesses, provided wage replacement of up to 66 2/3% of regular pay, and established a compensation fund supported by taxpayers.[4] In 1949, amendments established “schedule award benefits” or fixed payment amounts for various types of permanent partial impairments. In 1960, the Department of Labor was established as the primary payer, and the employing federal agencies were asked to repay the Department of Labor.[5] In 1974 amendments, workers were given the right to choose their treating physician. In addition, the employing agency was required to pay the employee’s salary during the first 45 days of the claim for traumatic injuries.[5] As amended, FECA[6] was enacted and codified in Title 5, Chapter 81, of the US Code.[7]

Workers who have their claim accepted may obtain vocational rehabilitation services to help them return to work, and they may request disability benefits amounting to two-thirds of their wages. This amount increases to 75% if the worker has eligible family members.[5] Congress also set up a table of “schedule award benefits” designed to help the Department of Labor pay injured workers for permanent partial disability.[5] The amount and duration of disability benefits varies by the type of partial disability. Under FECA, the employing agency, through the Department of Labor, pays all medical costs associated with the claim. Survivors of employees who are killed on the job are entitled to compensation payments and receive partial funeral costs.[5]

Computer/Electronic Accommodations Program

The Computer/Electronic Accommodations Program (CAP), developed in 1990, is designed to improve accessibility for people with disabilities and cover the costs of assistive technology. The CAP covers the costs to modify computer and telecommunication equipment to enable people with a disability to perform essential job functions. CAP also covers costs of training to use the equipment.

FECA Implementation and the Office of Workers’ Compensation Programs

Federal workers may file a claim for wages, medical costs, and vocational rehabilitation benefits when they are injured or develop an occupational disease. They must complete the proper paperwork and submit the forms to the local or regional agency compensation specialist (CS), who then submits them to the Department of Labor’s Office of Workers’ Compensation Programs (OWCP).[8] The OWCP has published two handbooks about the process, Questions and Answers About the Federal Employees’ Compensation Act (FECA)[8] and Injury Compensation for Federal Employees,[9] as well as additional guidance for federal agencies and employees on its website.[10]

Workers are required by OWCP regulation to file a claim for compensation using the Compensation Act-1 (CA-1) form, Federal Notice of Traumatic Injury and Claim for Continuation of Pay/Compensation[11] within 30 days of the injury. OWCP regulations require federal agencies to process the form promptly, within 2 weeks of the date of the claim’s filing. OWCP regulations also call for the employing agency to pay the employee for up to 45 days for any lost wages and for medical expenses up to $1,500.

Workers who have a disease caused by their work, or “occupational disease,” have up to 3 years to file a claim per OWCP regulation from the date of notification that their disease was caused by their work. They must file a CA-2 form, Notice of Occupational Disease and Claim for Compensation.[11] They must submit an explanation of how the disease was caused by their work either on the form or in an accompanying statement. The CS forwards the CA-1 and CA-2 to the supervisor, who must review it and complete the section that asks for specific facts in the case. The supervisor will recommend moving forward or controverting the case if the reported events and facts are not supported by witness statements. Per the OWCP’s claims manual, the claims examiner must process a traumatic injury claim in 45 days and an occupational disease claim in 90 days.[8]

An OWCP regional office is located in each of the 12 federal regions of the country. Each office has a director, claims examiners, and nurse case managers.[10] The claims examiner performs case management.[10] There may be one medical director or district medical advisor. The employing agency may request a second opinion medical examination when there is a conflict in opinion between the treating provider and agency physician. The OWCP relies on the treating doctor’s opinion unless there is incomplete or inconsistent medical information.[10] The district medical advisor may decide if the medical evidence is sufficient or if authorizations for medical procedures are necessary.[10]

An agency has no appeal rights unless a procedural error can be proven, but a claimant may appeal any denied claim. The OWCP nurse case manager reviews and approves proposed medical treatments and facilitates timely return-to-work.[10] The agency CS must be aggressive in contacting the OWCP staff nurse when a case has problems because the OWCP nurses normally do not get involved until after a claim has been accepted.

DEPARTMENT OF DEFENSE FECA PROGRAM

Unlike other federal agencies, the DoD employs a liaison to work with the claims examiner in each of the OWCP regions.[12] The Defense Civilian Personnel Advisory Service (DCPAS) oversees the liaisons and ensures FECA support to DoD agencies in each region.[12] The services manage their own cases and administer the program on a day-to-day basis.

Most installation commanders require employees to notify their supervisor of an injury within 48 hours of occurrence. Ideally, the supervisor should send the worker to the occupational health clinic to report the injury and tell clinic staff where they will receive treatment. This is the prime opportunity for the occupational health clinic to offer the employee treatment.

The CS uses the Electronic Data Interchange system to review the case information and ensure necessary medical and other information has been obtained per 20 CFR Part 10.330. The installation FECA working group can assist the CS in addressing difficult cases. The occupational medicine physician can assist the CS in the return-to-work process by reviewing work limitations and informing the CS whether the injured worker can safely perform the job functions given the limitations. The CS communicates regularly with injured workers to help them stay connected, monitor their medical recovery, and ensure they are on track for returning to work in a timely fashion.

The CS should investigate any red flags. For example, if the injury occurs shortly after the worker is hired, if the employee was recently disciplined or had preexisting injuries, or if the incident was unwitnessed, then closer scrutiny may be necessary. Injured workers will receive continuation of pay on the agency payroll from day 1 to day 45. From day 46 to the end of the first year, workers are placed on the periodic roll if they are unable to return to work and there is a reasonable chance they eventually will return to work. During this time, workers receive pay and medical care while undergoing periodic examinations. After 1 year, OWCP will order a medical examination. There is less of a chance the injured worker will return to duty if the case is over a year old, and OWCP stops active review and places the employee on the long-term roll. After that the claimant is required to get a physical examination only once every 3 years.[9]

If the treating provider determines the employee may return to duty with limitations, the agency must identify jobs that can accommodate the employee’s work restrictions. The employee will be directed to report for work by the claims examiner. The injured employee may appeal the decision to the Employees’ Compensation Appeals Board, whose decisions are final and not reviewable.[13]

Authorization for Medical Treatment

When an injured federal employee sees the CS to file the CA-1, he or she also obtains the CA-16, Authorization for Medical Treatment.[11] The CA-16 is issued one time only. The CS or the agency physician completes items 1 through 13 on the CA-16 form. This form is then submitted to the treating provider to pay for treatment of acute traumatic injuries and covers the first 60 days of care. The treating physician can refer the patient to specialists without seeking preauthorization. In an emergency, the CA-16 must be completed within 48 hours after first examination or treatment. The treating physician must provide a written medical report documenting the work relatedness of the injury, the diagnosis and extent of injury, the treatment plan, and any work limitations. The treating provider is also asked to complete the OWCP Form CA-17, Duty Status Report.[11] On the CA-17, the supervisor lists the job requirements on the top of the form, and the provider completes the bottom portion by identifying the employee’s work capabilities and job restrictions.

Role of the FECA Working Group

The installation level FECA working group is an ad hoc committee that meets periodically or as needed to discuss problem cases. The FECA working group should include representatives from the safety office, industrial hygiene, occupational health, human resources, and the supervisor and/or commander of the injured employee. The FECA working group must review cases to ensure the facts of the case are accurate, the worker’s medical limitations are accommodated (or another worksite is found), and the requested care is medically necessary.[12] The FECA working group should also meet periodically to review FECA program performance. Metrics that must be reviewed include continuation of pay days per case, lost-time case rate, medical costs per claim and per 100 employees, wage replacement costs per case and per 100 employees, and disability retirement awards paid.

The FECA working group should do a root cause or near miss analysis on all incidents to determine the cause and assess whether interventions are necessary to prevent additional injuries. The group can identify jobs with higher risk of injury by reviewing the injury data and finding the most frequent and most costly injuries to target worksites for intervention. If necessary, changes in work processes can be made and safety equipment can be purchased to lower the risk of injury. The safety officer usually leads these investigations.[14]

The FECA working group must have command support. A representative from the FECA committee should attend command-wide safety meetings and brief injury rates and costs to the operational leaders, who often have the greatest control over safety practices followed by employees at the worksite. Senior leaders need to understand how these injury rates and costs impact mission funding and availability of skilled and trained personnel.

Occupational Health Clinician’s Role

The agency occupational health physician must assist the CS by obtaining medical information from the treating provider that the CS needs to send to the OWCP in support of the FECA claim. The agency physician should review the case file, determine the diagnosis, look at medical restrictions, and assist in the work ability determination of the injured employee. This may involve reviewing the medical documentation provided by the treating provider to ensure the medical information provided is sufficient to make the diagnosis, and contacting the treating provider to obtain additional information. The agency physician should be able to quickly address questions that arise about the medical necessity of a requested procedure or treatment. Additionally, the agency physician must advise the treating provider of the medical treatment and pharmacy options available at the base medical facility.

The agency physician must also assist the CS in reviewing job descriptions of positions in which an injured employee may be placed for return to work. The agency physician, with the occupational health nurse, must participate on the FECA committee to discuss difficult cases, review program strengths, and identify areas for improvement. The occupational medicine physician should encourage adoption of a “clinic-first” policy to facilitate timely filing of claims, permit work ability determinations, and facilitate development of the return-to-work plan. The injured employee may also be offered the opportunity to be treated in the occupational health clinic.

Once the injured employee has been cleared by their treating provider to return to work, the agency occupational medicine physician can perform a return-to-work examination and ensure that work restrictions, if any, can be accommodated at the job site by talking with the supervisor and the CS. Further, the examination can confirm that the employee can safely perform the position’s essential duties, and that the employee does not pose a risk of injury to themselves or others.

If the treating provider has given the employee work limitations and there is no light duty at the worksite, the agency physician can assist the CS in helping to determine an employee’s ability to perform in another position where light duty is available. The occupational medicine physician should routinely look at the disability guidelines developed by the Reed Group and the American College of Occupational Medicine Clinical Practice Guidelines15,16 to assess whether diagnostic criteria were met, whether medical care utilization is appropriate, and whether or not the employee is healing normally. If permanent work restrictions do not allow the employee to do essential job functions, the occupational medicine physician must inform the CS and supervisor, and alternatives may need to be explored. Vocational rehabilitation and job retraining may offer the employee an opportunity to continue working for the agency in a different position.

Employees’ Choice of Physician

OWCP regulations permit the employee to choose where they are treated for their work injury. An installation commander or supervisor may still require the employee to report to the occupational health clinic for a work ability determination before seeing their own physician, provided the injured worker is not delayed in being seen by their physician. Office of Personnel Management regulations permit the agency physician to examine the injured employee, but the employee’s choice of where to be treated must be honored.[17]

The occupational medicine physician is encouraged to offer the injured employee treatment in their clinic because this reduces cost for treatment; referral to a specialist can occur more quickly; and other services such as physical therapy, radiology, and laboratory and pharmacy services are readily available. These efficiencies reduce lost work time for the employee and permit more timely filing of claims forms and the collection of supporting medical information. The CS can more easily coordinate with the occupational medicine physician to determine any work restrictions and coordinate the timely return to work.

TRENDS IN MILITARY WORKERS’ COMPENSATION COST AND RATES

The DoD experienced a 600% increase in claims and costs between 1995 and 2005. The Department of Labor pays disability costs to the employee and medical costs to the treating physician. The DoD must then reimburse the Department of Labor. The costs paid by the DoD do not include the indirect costs sustained by agencies and services, such as lost productivity, training of replacement workers, and the effects of the work absence on morale when other workers have to pick up the work of the missing worker. Government Accountability Office audits of the FECA program have estimated that direct and indirect costs for total FECA liabilities are approximately $30 billion.

Injury Statistics

The DCPAS collects data from DoD agencies and the military in a database and tracks the data by year of injury. This data includes the causes of traumatic injury. However, the services and DoD agencies need to do a better job of capturing the cause of injury because “other” and “unspecified” are two of the largest categories. Accurate cause of injury information is needed to identify high-risk jobs that may require interventions to reduce injury risk. Occupational disease information is tracked in a separate DCPAS database.[1]

Initiatives to Reduce Costs

A 2004–2008 initiative by President George W. Bush and the secretary of labor, called Safety, Health and Return to Employment (SHARE),[18] was only partially successful in reducing occupational injuries, illnesses, and fatalities within the federal government. The DoD’s efforts at reducing worker’s compensation costs achieved the same level of success that other federal agencies achieved.

In 2010 President Obama and the OWCP developed the Protecting Our Workers and Ensuring Reemployment (POWER) initiative[19] and sought to provide funding support to federal agencies to get injured civil service employees back to work. DoD sought funding to pay worker’s salaries for modified duty positions to be able to return workers to work. Under this program, CS personnel can use funds to pay for positions that the injured worker can fill with job duties tailored to meet the treating provider’s work restrictions. The DoD also initiated efforts to improve the FECA database maintained by DCPAS.

Improving Workers’ Compensation Case Management

In 2016 there were 275,000 DoD civilian employees who received FECA benefits, which cost the federal government $30 billion in direct and indirect costs.[2] In order to reduce costs, the DoD must learn from successful workers’ compensation programs how to better manage cases to reduce costs and disability. The DoD should work with OWCP to make it easier for agency physicians to participate in case management. This will improve support for the CS to better address the medical questions that arise in problematic cases. Further, DoD can arrange for physician support for DoD agencies with no access to occupational medicine physicians by contracting for that support with Federal Occupational Health, a Health and Human Services organization that provides occupational medicine services to the federal government.

Feuerstein20,21 demonstrated that integrated case management could improve patient job function and reduce symptoms in upper-extremity injuries. Shepherd and LaFleur[22] used targeted injury prevention efforts to reduce injuries at a Navy shipyard. The Navy also saved $46 million by employing occupational medicine physicians to do case reviews.[23] The Army improved its management of FECA cases24,25 and successfully used contract case managers to effectively lower costs and get employees back to work.[26]

Leadership and worker commitment to the success of the FECA program make all the difference. Morale improves when employees are allowed to participate in health promotion and wellness programs. Training on FECA improves supervisor and worker compliance with the OWCP regulations and reduces costs. OWCP has case management resources that should be employed sooner to effectively reduce costs and prevent worker disability. A nurse case manager should get involved at the start of the case, rather than waiting until the employee has been off for 2 weeks. The case managers need to start at the beginning of the case to assist the injured worker in obtaining treatment and returning to work, and they should stay involved with the case until it is closed.[27] Occupational illness claims must be thoroughly reviewed like other claims to ensure all elements of the case have been successfully managed.

REVIEWS OF MILITARY PROGRAMS

Workers’ Compensation Program Systems Analysis

Dr. Bedno[28] used a systems approach to assess the workers’ compensation program at two Army installations in 2014. Because workers’ compensation cases are complex and involve quantitative and qualitative data collected from multiple sources and perspectives, she employed a case study design that used a mixed methods approach. She assessed the current state of the system for reporting and following up on injuries and illnesses in Army medical centers, including potential barriers and facilitators to reporting. The quantitative portion of the study consisted of analyzing workers’ compensation claim data for total costs and types of injuries. The qualitative portion included a document review of policies, procedures, and regulations. Nineteen semi-structured interviews were conducted with key participants in the workers’ compensation process, at the installation, region, and headquarters levels.

The results show a significant trend in decreased workers’ compensation costs between 2001 and 2013. The workers’ compensation claims for new DoD occupational injuries and illnesses in 2013 were less costly than 12 years earlier, but Bedno noted that more improvements are needed. Workers’ compensation staff need ways to show where the costs savings have occurred, and having dedicated resources may permit better tracking of efforts to reduce FECA costs.

The qualitative results show that because so many entities are involved in the reporting and management process, there is a tendency for each group to act independently. Based on the interviews and document analysis, identified gaps include data sharing, communication, and teamwork. Not only is there poor communication and lack of data sharing, but also the best or recommended practices are not shared. In most cases, data were not used to show changes in costs or injuries. The responsibility for reporting injuries and illnesses is not well-defined. Further, supervisors and workers need training to understand program basics. Although training on workers’ compensation is specified on an annual basis, no regular training was taking place. Leadership (installation- and organization-level) should ensure maximal interaction between involved stakeholders and make sure that everyone attends training annually.

Systems-level improvements are needed, starting with a senior leader commitment to reduce injuries and to make the workplace safer. Military leadership must prioritize occupational injury and illness prevention efforts among their other important issues. Leaders must also devote the necessary resources (eg, personnel, funding) to support this effort. Training on workers’ compensation is needed. Flowcharts illustrating the occupational injury and illness process should be used in training (Figure 9-1). Data should be integrated to support all injury prevention initiatives. The responsibility for injury analysis should be delegated within the installation or by region to an epidemiologist, who can assist with targeting injury prevention initiatives based on their analysis. These findings and best practices should be shared with other DoD, federal, and state partners.

Government Accountability Office Audit

The Government Accountability Office (GAO) reviewed the DoD FECA programs in 2010 and reported on the review in 2012.[29] The GAO analysts noted that DoD agencies and services could do a better job of injury prevention and program management.[29] They reported that FECA cases need better case management and that questionable cases should be controverted. Additionally, DoD needs better management controls to ensure Department of Labor charges are valid and required medical documentation is provided by the treating provider to support the claim.[29] GAO also encouraged the continuation of best practices that reduce the risk of fraud. Experienced staff must be employed to manage short- and long-term cases to identify fraud, and private investigators should assist in fraud investigations.

Figure 9-1. Worker’s Compensation Claim Management process. CS: compensation specialist
RTD: return to duty

Other GAO recommendations are as follows. The DoD needs to share information between the agencies and services to reduce duplicate payments and improve the job reassignment process.[29] The CS should check with Social Security to ensure workers are not working a second job while receiving disability benefits.[29] Further, agency physicians need to be consulted and actively engaged in the case management process by providing medical expertise when there are unresolved medical questions such as work ability, appropriateness of the treatment plan, and whether the employee can safely return to the job with the work limitations given by the treating provider.

GAO indicated that agency physicians need to ensure treating providers in the medical community get training on the Department of Labor medical documentation requirements of FECA.[29] GAO also stated that the DoD must prosecute fraud cases, but the Department of Justice must assist in this effort by encouraging the US attorney for each region to prosecute cases of obvious fraud, even if the cases do not have a high dollar value in terms of the medical and disability costs.[29] In addition, GAO indicated that the DoD needs to hire more CS staff. This would allow them to reduce their caseload and better manage the cases they are responsible for overseeing. GAO recommended that any cost savings that accumulate from better DoD management practices should be shared with installation commanders to help fund personnel, injury prevention, data collection and analysis, and criminal investigation initiatives.

FECA MANAGEMENT CHALLENGES

The POWER initiative[19] put the spotlight on the problem of increasing injury claims and costs, and the DoD responded well by reducing FECA costs. However, the DoD bill for FECA stood at $682 million in direct costs for 2014. The DoD’s integrated approach across functional areas requires the CS to take the lead role in coordinating with program stakeholders to achieve program success. This is difficult to do from a regional or headquarters level when the rest of the stakeholders are on the local installation. This regional approach limits the interaction between the CS and the FECA working group, including the agency physician.

The data in the OWCP’s Agency Query System, which provides CS information about claim demographics, case status, and claim costs, should be linked to data maintained by the Defense Manpower Data Center so that more accurate injury rates and costs can be tracked for each installation and unit, and commanders and supervisors can access their injury rate and cost data. This would keep FECA on the installation commander’s radar and improve local injury prevention efforts.

DCPAS has published FECA policy and procedures in one DoD instruction.[12] It calls for tracking compensation claims and costs, providing training, and assigning a DoD liaison to each OWCP district office. The DoD Safety and Occupational Health Working Group must encourage more aggressive efforts in the adoption of FECA best practices and facilitate injury prevention initiatives at the headquarters, agency, and service level.

Quarterly FECA working group meetings at the headquarters, subordinate command, and local command level should be adopted as a best practice. The FECA working group must engage to better manage the FECA program at the installation level because there is no CS to lead the effort locally. The FECA working group can work with supervisors to identify light-duty positions for employees who need to return to work. The FECA working group must track injury rates and costs over time and provide feedback to supervisors regarding the impact of injuries on costs and worker productivity. The FECA working group can target high-risk jobs for changes in work practices or protective equipment usage that will lower injury risk. DCPAS must encourage CS staff to more accurately code the nature and the cause of injury data (40% of all claims have no cause or nature of injury recorded).

DEPARTMENT OF LABOR PROGRAM MANAGEMENT EFFORTS

The POWER initiative, which lasted from 2010 to 2014, achieved many of its performance targets. Federal agencies increased collection and analysis of data on the causes and costs of injuries and illnesses.[19] FECA managers in federal agencies realized that workers on the long-term rolls for longer than a year pose a problem in terms of getting employees back to work. Therefore, high-risk jobs must be identified and targeted for injury prevention efforts before workers get injured. Front-line supervisors and workers in these high-risk jobs can be given improved training on safety procedures and monitored for adherence to safe practices and proper use of personal protective equipment. Thus, the employees and their agencies become the beneficiaries of safe and healthy workplaces.

Figure 9-2. Department of Defense results for Protecting Our Workers and Ensuring Reemployment (POWER) goal 1, reducing total case rates, 2009–2014.
VHA: Veterans Health Administration
Data source: US Department of Labor, Office of Workers’ Compensation Programs. POWER performance, Department of Defense. https://www.dol.gov/owcp/dfec/power/getxls.htm?id=1340000. Accessed August 8, 2017.

Figure 9-3. Department of Defense results for Protecting Our Workers and Ensuring Reemployment (POWER) goal 2, reducing lost time injury and illness case rates, 2009–2014.
VHA: Veterans Health Administration
Data source: US Department of Labor, Office of Workers’ Compensation Programs. POWER performance, Department of Defense. https://www.dol.gov/owcp/dfec/power/getxls.htm?id=1340000. Accessed August 8, 2017.

Figure 9-4. Department of Defense results for Protecting Our Workers and Ensuring Reemployment (POWER) goal 6, reducing lost production day rates, 2009–2014.
VHA: Veterans Health Administration
Data source: US Department of Labor, Office of Workers’ Compensation Programs. POWER performance, Department of Defense. https://www.dol.gov/owcp/dfec/power/getxls.htm?id=1340000. Accessed August 8, 2017.

The DoD achieved most of the targets for the POWER goals. The FECA metrics for each federal agency were published on the Department of Labor OWCP Division of Employees Compensation website.[30] The Army, Navy, and Air Force all met the POWER goals. The total claim rate and costs for the Army, Navy, and Air Force decreased significantly (Figures 9-2, 9-3, and 9-4).

The Department of Labor began, as part of the POWER initiative, an annual Return-to-Work Council meeting, designed to bring together senior level managers in the federal government who worked at the best and worst performing federal agencies with the aim of helping all agencies meet POWER goals. The council encouraged successful agencies and organizations to share their best practices as a model that the worst 14 could adopt. Ultimately, the Department of Labor wanted to see these agencies lower their medical and disability costs and reduce their injury rates.[31]

SUMMARY

Available data from the Department of Labor shows that the DoD has done an excellent job managing the workers’ compensation program over the last 10 years. However, there are still opportunities for improvement in terms of injury prevention and case management activities. Data collected by DCPAS should be disseminated to the services so that case management efforts can be improved and injury prevention efforts can be better targeted to at-risk worker populations. The DoD has been successful over the past decade in significantly reducing both claims and costs by engaging all members of the FECA team to do their share in supporting FECA efforts in a collaborative way that prevents injuries, lowers costs, and improves case management. While the costs have been reduced, DoD still spends over $600 million annually on FECA cases, and more improvements are possible.

The newest systems approach affords managers another way examine the FECA program’s execution and look for ways to improve it. This chapter highlighted some best practices that should be continued, such as use of the DoD nurse liaison at each regional office to help CSs coordinate with the claims examiner. Also, the DCPAS should make FECA data available to the FECA working group so that the safety and occupational health team can target injury prevention efforts to lower injuries and reduce long-term disabilities due to work related injuries and illnesses. The occupational medicine physician can assist the FECA working group by serving as medical consultant for questions about work ability, medical necessity for requested procedures and treatments, and coordination with the treating provider to obtain needed medical information, as well as by helping collect and analyze injury data and sharing the results of the analysis with the group and local installation leaders.

REFERENCES

1.   Nelson CJ, Bigley DP, Mallon TM. Analysis of new workers’ compensation claims in the Department of Defense civilian workforce, 2000–2012. J Occup Environ Med. 2015;57(suppl 3):S20–S26.

2.   Mallon TM, Grizzell TL, Nelson CJ. Hodgson M. Federal Worker’s Compensation Program basics. J Occup Environ Med. 2015;57(suppl 3):S4–S11.

3.   Guyton GP. A brief history of workers’ compensation. Iowa Orthop J. 1999;19:106-110. PMCID: PMC1888620.

4.   Nordlund WJ. The Federal Employees’ Compensation Act. Monthly Labor Rev. 1991;Sep:3–14. http://www.bls.gov/mlr/1991/09/art1full.pdf. Accessed October 10, 2014.

5.   Szymendera S. The Federal Employees’ Compensation Act (FECA): Workers’ Compensation for Federal Employees. Washington, DC: Congressional Research Service; 2012. http://digitalcommons.ilr.cornell.edu/cgi/viewcontent.cgi?article=1981&context=key_workplace. Accessed October 10, 2014.

6.   Federal Employees’ Compensation Act. Pub L 93-416. http://www.dol.gov/owcp/dfec/regs/statutes/feca.htm. Accessed August 28, 2014.

7.   Compensation for Work Injuries, 5 USC Part III, Subpart G, Chap 81 (2011). http://www.gpo.gov/fdsys/pkg/USCODE-2011-title5/html/USCODE-2011-title5-partIII-subpartG-chap81.htm. Accessed August 28, 2014.

8.   US Department of Labor, Office of Workers’ Compensation Programs. Questions and Answers About Federal Employees’ Compensation Act (FECA). Washington, DC: DoL; 2002. Publication CA-550. http://www.dol.gov/owcp/dfec/regs/compliance/DFECFolio/q-and-a.pdf. Accessed August 28, 2014.

9.   US Department of Labor, Office of Workers’ Compensation Programs. Injury Compensation for Federal Employees. Washington, DC: DoL; 2009. Publication CA-810. http://www.dol.gov/owcp/dfec/regs/compliance/DFECfolio/CA-810.pdf. Accessed August 28, 2014.

10.   US Department of Labor, Office of Workers’ Compensation Programs. Procedures manual website. http://www.dol.gov/owcp/procedure-manual.htm. Accessed August 25, 2014.

11.   US Department of Labor, Office of Workers’ Compensation Programs. Division of Federal Employees’ Compensation (DFEC), forms. https://www.dol.gov/owcp/dfec/regs/compliance/forms.htm. Accessed August 8, 2017.

12.   US Department of Defense. DoD Civilian Personnel Management System: Injury Compensation. Washington, DC: DoD; 2009. DoD Instruction 1400.25: Subchap 810. http://www.dtic.mil/whs/directives/corres/pdf/1400.25-V810.pdf. Accessed August 28, 2014.

13.   US Department of Labor. Employee Compensation Appeals Board decisions. http://www.dol.gov/ecab/decisions/main.htm. Accessed October 10, 2014.

14.   29 CFR § 1904.7. http://www.gpo.gov/fdsys/pkg/CFR-2014-title29-vol5/pdf/CFR-2014-title29-vol5-sec1904-7.pdf. Accessed August 28, 2014.

15.   MD Guidelines. Westminster, CO: Reed Group Ltd; 2015.

16.   American College of Occupational and Environmental Medicine. Occupational medicine practice guidelines. https://www.acoem.org/PracticeGuidelines.aspx. Published 2017. Accessed August 9, 2017.

17.   5 CFR § 339.301. Medical qualification determinations, January 1, 2012. http://www.gpo.gov/fdsys/granule/CFR-2012-title5-vol1/CFR-2012-title5-vol1-part339/content-detail.html. Accessed August 28, 2014.

18.   US Department of Labor, Division of Federal Employee’s Compensation. Safety, Health and Return-to-Employment (SHARE) initiative. https://www.dol.gov/owcp/dfec/share/perform.htm. Accessed October 8, 2016.

19.   US Department of Labor, Division of Federal Employee’s Compensation. Protecting Our Worker and Engaging in Re-employment (POWER) initiative. https://www.dol.gov/owcp/dfec/power/. Accessed October 8, 2016.

20.   Feuerstein M, Miller VL, Burrell LM, Berger R. Occupational upper extremity disorders in the federal workforce: prevalence, health care expenditures, and patterns of work disability. J Occup Environ Med. 1998;40:546–555.

21.   Feuerstein M, Huang GD, Ortiz J, Shaw WS, Miller VI, Wood PM. Integrated case management for work-related upper-extremity disorders: impact of patient satisfaction on health and work status. J Occup Environ Med. 2003;45:803–812.

22.   Shepherd SL, LaFleur BJ. The increased incidence on Mondays of work-related sprains and strains. J Occup Environ Med. 1996;38:681–688.

23.   Hammett ME, Jankosky C, Muller J, Hughes E, Litow F. Physician review of workers’ compensation case files: can it affect decision outcomes? Mil Med. 2012;177:17–22.

24.   Cloeren M, Mallon TM. Managing workers’ compensation costs in the military setting: the Army’s story. Clin Occup Environ Med. 2004;4:vii,323–339.

25.   Lovell MA, Gaydos JC. Control of workers’ compensation claims and costs in the US Army. Mil Med. 1998;163:451–455.

26.   Mallon TM, Cloeren M, Firestone LM, Burch HC. Contract case managers prove cost effective in federal workers’ compensation programs. Mil Med. 2008;173:253–258.

27.   DoD Medical Case Management Working Group. White Paper. Washington, DC: DoD; April 2004. http://www.denix.osd.mil/ergoworkinggroup/accommodation/home/unassigned/dod-medical-case-management-working-group-whitepaper/. Accessed August 8, 2017.

28.   Bedno SA. Systems Approach to Managing DoD and Army Workers Compensation Programs [dissertation]. Chicago, IL: University of Illinois; May 2015.

29.   US Government Accountability Office. Federal Employees’ Compensation Act. Preliminary Observations on Fraud-Prevention Controls. Washington, DC: GAO; January 2012. GAO-12-402. http://www.gao.gov/assets/590/587925.pdf. Accessed January 26, 2015.

30.   US Department of Labor, Office of Workers’ Compensation Programs, Division of Federal Employees Compensation. POWER initiative. http://www.dol.gov/owcp/dfec/power/. Accessed September 7, 2014.

31.   US Department of Labor. Protecting Our Workers and Ensuring Reemployment (POWER) Return to Work Council meeting, September 20, 2012. http://www.dol.gov/owcp/dfec/ppt/POWERCouncilMeeting9-20-12final.pdf. Accessed September 17, 20 14.

Chapter 10

MEDICAL SURVEILLANCE

TIMOTHY M. MALLON, MD, MPH*; CAMERON J.L. NELSON, MD, MPH†; DAVID P. DEETER, MD, MPH;‡ and JANET M. RUFF, RN, MPH§

INTRODUCTION

ASSESSING THE NEED FOR SURVEILLANCE PROGRAMS

MEDICAL SURVEILLANCE PROGRAM DESIGN

MEDICAL SURVEILLANCE AND CERTIFICATION EXAMINATIONS

DOCUMENTING THE PHYSICAL EXAM AND MANAGING RESULTS

SPECIFIC OCCUPATIONS

ASBESTOS

RADIATION

REPRODUCTIVE HAZARDS

EMPLOYEES WITH CHRONIC DISEASES OR PHYSICAL DISABILITIES

HEARING CONSERVATION

SUMMARY

*Colonel (Retired), US Army; Adjunct Assistant Professor, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

†Commander, Medical Corps, US Navy; Chief of Occupational Medicine, Naval Hospital Bremerton, 1 Boone Road, Bremerton, Washington 98312

‡Lieutenant Colonel (P), US Army; Director, Occupational and Environmental Health, and Director, Occupational Medicine Residency Program, US Army Environmental Health Agency, Edgewood Area, Aberdeen Proving Ground, Maryland 21010-5422; formerly, Occupational Health Consultant to the Surgeon General

§Senior Occupational Health Nurse Consultant (Retired), Occupational and Environmental Medicine Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

INTRODUCTION

The two missions of occupational and environmental medicine in the Department of Defense (DoD) are (1) to prevent work-related injuries and illnesses from a population health perspective and (2) to address the clinical needs of individual employees. These two missions will be discussed separately. Medical surveillance consists of systematically and periodically collecting and analyzing health data on groups of employees to monitor changes in health status over time and to achieve primary, secondary, and tertiary prevention of workplace disease and injury.

Primary prevention refers to the prevention of illness or injury. The aim of primary prevention is to reduce or eliminate risk by preventing or mitigating exposures. Hepatitis B immunizations are a good example of a primary prevention initiative to prevent cases of this disease in the workplace.[1] Performing screening tests for glucose-6-phosphate dehydrogenase deficiency in explosive workers can help identify those workers at increased risk of hemolysis because they do not metabolize methemoglobin.

Secondary prevention refers to early detection and intervention to halt or reverse the progression of disease, before long-term health consequences occur.[1] Medical surveillance data helps occupational health and safety personnel focus on effective disease and injury countermeasures. Mallon et al conducted surveillance of TNT workers at an Army ammunition plant and noted an increased incidence of anemia in chronically exposed workers, which triggered several interventions to reduce workplace exposure to TNT.[2]

Tertiary prevention refers to medical interventions that alter the course of the disease and reduce the severity or recovery time, allowing employees to return to work earlier than otherwise would be possible. Medical surveillance may guide inquiries regarding which occupations involve risk and the degree of impairment resulting from each type of injury or illness.[1]

Medical surveillance is prospective and should be effective, efficient, and economical in terms of program design, medical screening performed, and use of the surveillance data. Medical surveillance is different from medical screening; medical screening is the search for a health characteristic in an individual or a group at risk that is cross-sectional in nature. It is rare that health screenings show abnormal health outcomes results due to job-related exposures.[3]

Lead screening is a population health measure performed to detect occupational exposure in the workplace above the action level for lead, which is 30 μg/m3 as a time-weighted average (TWA).[4] Airborne concentration levels above this level trigger periodic surveillance and workplace controls, including administrative and engineering controls to reduce ongoing exposures. If blood lead levels exceed 60 μg/dL employers must medically remove workers from continued lead exposure until the blood lead level drops below 40 μg/dL.[4]

It should be noted that chronic low-level exposure to lead may generate large bone stores of lead without blood lead screening levels exceeding the action level. As a result, the Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health (NIOSH), and the Occupational Safety and Health Administration (OSHA) have initiated steps to lower the workplace and general population exposure limits to lead before workers are adversely affected. Chapter 21, Occupational and Environmental Lead, details policies related to workplace exposure limits in the occupational setting. Primary prevention, screening, and directed exposure countermeasures constitute effective medical surveillance.

ASSESSING THE NEED FOR SURVEILLANCE PROGRAMS

Before initiating a medical surveillance program, an occupational health program manager should identify the reasons for conducting medical surveillance and define which heath indices should be monitored. Most federal civilian workers today perform administrative tasks with minimal physical job demands or potential for exposure to job-related hazards. This group of workers is best targeted for health promotion and wellness initiatives and periodic health history screening to ensure that chronic disease risk is being managed appropriately.

The second group of employees have physical requirements specified in their job description that require sufficient health and fitness to perform their work safely and effectively. Medical screening in this group focuses on ensuring the employee can meet the physical requirements of the position while performing the essential job functions without undue risk to themselves or others. For example, US Department of Transportation (DoT) regulations require a commercial motor vehicle operator to be free of any medical condition that could incapacitate him or her while transporting hazardous cargo in interstate commerce. Thus, medical standards for this job might include the absence of insulin-dependent diabetes mellitus, and a medical surveillance program would screen drivers for diabetes. (Discrimination against the medically handicapped is not at issue here if it has been documented that the medical condition will indeed compromise the job, ie, by causing sudden incapacitation.) The key to designing medical surveillance for these employees is to maintain clearly defined medical standards. The sole authority for writing medical standards belongs to the Office of Personnel Management.[5] A subset of workers who undergo medical surveillance will be required to wear personal protective equipment (PPE) to protect against workplace hazards, and this group must be medically screened to ensure the PPE can be worn safely while performing job tasks.

Medical standards that assess the worker’s functional ability to perform job tasks are preferred to medical standards that require documentation of the absence of positive screening tests. For example, a medical surveillance for respirator wearers should be designed to ensure that employees are physically able to wear the respirator while performing job duties without a decrement in job performance. Previously, workers with beards were disqualified, but workers may now be able to wear a powered air purifying respirator that does not require a good face seal provided they can meet the other physical requirements to perform the job safely.

A performance-based medical standard could require employees to have intact pulmonary function. A physician or licensed healthcare provider may include normal pulmonary function testing (PFT) or negative responses on the OSHA respirator questionnaire as evidence of normal pulmonary function. Specification-type medical surveillance standards would require PFTs to be performed annually, set criteria all employees must meet, and recommend that someone with PFT results lower than 70% of expected based on employee demographics would be medically recommended for removal from the job. In contrast, a functional standard would offer someone not meeting the 70% of expected cutoff to demonstrate they can perform essential job duties while wearing the respirator. The DoD’s occupational and environmental health (OEH) clinic staffs must work closely with safety and industrial hygiene professionals and installation management personnel to develop local guidance that meets DoD and Army regulations but allows for exemptions when it makes sense to meet mission and health requirements.[6]

Job-related medical surveillance must be tailored to employees based on job titles, worksites, or documented exposures and individual susceptibility to chemical, physical, or biological agents that may be hazardous. This is particularly true when exposures exceed standards in order to detect early health effects, monitor the effectiveness of the controls, and monitor the extent of the exposure.

MEDICAL SURVEILLANCE PROGRAM DESIGN

A medical surveillance program is based on industrial hygiene sampling data, which helps the occupational health provider decide who is exposed in the workplace and when the exposure exceeds thresholds that mandate medical surveillance. The determination of who to enroll in the medical surveillance program is often challenging because industrial hygiene sampling data is often not available, and instead healthcare providers must rely on the employee to provide a good occupational history (which may include self-reported exposures). When industrial hygiene sampling data is lacking, sampling done in similar exposure groups may provide clues as to whether exposure in the local workplace may be occurring. Other factors weigh into the determination as well, such as management-union agreements that call for medical surveillance.

Additionally, some assumptions regarding exposure should be evaluated before making decisions on enrollment in the medical surveillance program and the extent of the history and physical examination.6,7 In order for a toxic substance to exert its effects, there must be a completed pathway of exposure from external exposure to internal exposure, and the presence of chemical and physical hazards in the workplace does not mean that a completed pathway of exposure exists. Further, if a completed pathway does exist, the worker exposure may not be biologically significant or it may not be sufficient to cause health effects. Finally, while health effects or end organ damage may be present, there may not be any screening test available to detect it.

Workplace exposures may trigger concern by employees, regardless of the level of exposure or potential for adverse health outcome. However, when employees face uncontrolled exposures in the workplace, steps must be taken to alleviate their concern and countermeasures implemented to eliminate the exposure. Except in cases of acute exposures to very high levels of toxic chemical or biological agents, there are few health effects that can be readily detected through medical surveillance. Thus, it is critical for OEH providers to communicate to employees and other stakeholders the low level of risk that most exposures pose. Further, not all subjects in a given population will be exposed identically, nor will they respond identically. For example, two Army ammunition plant workers standing side by side may be exposed to completely different levels of the same propellant because of different air flows around their work stations. Even if the exposures are identical, the two might experience different toxicological responses. One worker might be very susceptible to TNT’s negative effects, due to his or her cardiovascular status, while a coworker could be completely unaffected.

Once an exposure meets or exceeds the threshold for enrollment in medical surveillance, the employee should be examined for potential health effects. Knowledge of how toxic substances affect organ systems is critical to designing the medical surveillance program to look for internal dose, measures of early biologic effects, and end organ damage. When the pathway from external exposure to internal exposure is completed, the severity of the effect is determined by the route of entry, level and duration of exposure, and how the substance is metabolized in the body. OEH providers may be able to predict the likelihood of adverse health effects based on the substance’s toxicodynamics. DoD-adopted criteria for predicting health outcomes or sentinel events that are based on exposures at the OSHA permissible exposure level (PEL) and at the American Conference of Governmental Industrial Hygienist (ACGIH) threshold limit value (TLV). Employees require job-related medical surveillance when their workplace exposures exceed the OSHA PEL or ACGIH TLV specified in DoD’s Occupational Medical Examinations and Surveillance Manual.[7]

Determining Screening Examination Content

The content of the surveillance examination must be determined once the need for medical surveillance has been established. There are four parts of the medical surveillance examination:

1. medical and employment history;

2. physical examination;

3. diagnostic testing, including laboratory tests and radiological exams; and

4. special studies that include electrocardiograms (EKGs), PFTs, treadmill stress tests, and biological monitoring.

The utility of these tools is measured by their sensitivity, specificity, cost, acceptability, ease of use, accuracy, and reproducibility.[8] Few screening tools meet all criteria for widespread use.

Because the workforce is relatively healthy and job-related illnesses are rare, an interim medical and employment history is the preferred tool for tracking changes in employee health status and work ability. The interim work and medical history should identify changes in job duties or changes in health status. The interim history should address whether the employee (1) properly uses personal protective clothing and equipment, (2) has had exposures that exceeded the OSHA PEL or ACGIH TLV, (3) has experienced changes in health status, and (4) needs more in-depth health screening. The healthcare provider may use information obtained from the interim employment and health history to guide a directed physical examination for specific findings. By doing a focused physical examination, the specificity of the medical surveillance examination increases.[8]

Knowledge of the full range of possible health effects is important to identify adverse health effects in exposed workers. If the provider is unaware that isocyanates are pulmonary sensitizers, for example, he or she may not listen for wheezing in workers after isocyanate exposure and thus miss the fact that employees are developing job-related asthma.

For laboratory screenings (the third part of the medical surveillance examination) to be effective, the test’s specificity must be high and costs must be low. A “shotgun approach” to laboratory testing performed on a group of employees based solely on their job description, or on the presumption that they were exposed to a hazard, is both costly and has low positive predictive value. Laboratory screening tests may be unable to detect end organ damage such as early cancers and may be considered useless. The Agency for Health Care Policy provides evidence-based guidelines for providers on which tests are effective and which are not recommended. One way to improve the sensitivity of the test is to screen a subgroup of workers for whom industrial hygiene sampling has detected exposures that exceeded the OSHA PEL or ACGIH TLV.

Medical surveillance guidance[6] based on specific workplace hazards (the fourth part of the medical surveillance examination) has been published. Healthcare providers are in a better position to direct the medical surveillance of workers when they talk to employees, visit the workplace, discuss issues with supervisors and safety and industrial hygiene personnel, and learn where breakdowns in engineering and administrative controls occur.

Biological monitoring involves testing blood and other body fluids to measure a toxic agent or its metabolites.[8] The biological monitoring test should have high specificity, but only a few tests are currently available. Approved biomarker tests include blood tests for metals, urine tests for metals and benzene metabolites, and red blood cell cholinesterase testing for organophosphate pesticide exposure.[8] (Chapter 29, Biological Monitoring, provides a more in-depth review of biomonitoring.) Special studies include audiograms to detect noise-induced hearing loss; chest x-rays and PFTs to test for changes in pulmonary function; and EKGs, echocardiograms, and graded exercise testing to detect alterations in cardiac rate, rhythm, and cardiac function.

The timing of medical screening is essential.[8] Screening is done prior to employment to provide baseline data for comparison with future surveillance data. Periodic screening is done at routine intervals, and should include an interim history. The periodic screening examination should include tests based on the employee’s exposure history, scheduled according to the time needed for physiological or physical changes to occur. Hearing tests, for example, are done after a 48-hour noise-free period. However, if acute effects are being sought, or if the extent of exposure is being documented, screening both later in the day and later in the week may be more appropriate. The toxicokinetics of the substance will affect the decision of when to screen. The half-life of one hazardous material in the body may be minutes to hours, while that for others may be days to weeks. Delayed screening for the agent or its metabolic breakdown product (biomarker) is useless if the hazardous substance is metabolized in minutes to hours.[8]

Use of Medical Surveillance Results

The medical surveillance program must be managed, and the data collected must be used appropriately. The healthcare provider must inform the employee of the screening results and recommend appropriate medical follow-up, including a determination of whether the exposure was work related. If the abnormal screening tests indicate an unacceptably high exposure has occurred, then the employee should be considered for temporary duty restrictions with a goal of reducing or eliminating workplace exposure through temporary job reassignment or time off.

Often the healthcare provider must use professional judgement when there are no published medical standards. OEH clinic personnel should act with the assumption that a sentinel event has occurred and ensure periodic surveillance of the remaining worker population that may be at risk. In these situations, the safety and occupational health team, including the OEH clinic staff, industrial hygienist, and safety officer must employ the hierarchy of controls to prevent future exposures in the workforce. These controls include substitution, engineering controls, administrative controls, use of personal protective clothing and equipment, and medical removal when necessary. Data collected on both normal and abnormal findings provides a basis for comparison for future testing with the aim of preventing adverse health effects. Abnormal screening tests can provide indications about where breakdowns in exposure controls are occurring.

Medical surveillance efforts should be evaluated for compliance with OSHA, DoD and service- specific metrics established in DoDI 6055.05, Occupational and Environmental Health,[9] and service regulations. Use of program metrics will ensure that cost effective surveillance is conducted and adverse health effects will be detected.

MEDICAL SURVEILLANCE AND CERTIFICATION EXAMINATIONS

Medical surveillance and certification exams looking for signs or symptoms of work-related disease or injury are the key tasks of an occupational health provider. The medical surveillance examinations are often mandated by OSHA regulations located in 29 CFR, Part 1910, Subpart Z.[10] Certification examinations are done to qualify a worker for a specific, potentially hazardous or safety-sensitive duty, such as wearing a respirator, driving a forklift, or operating a commercial motor vehicle. Both types of examinations involve a medical history, physical exam, and laboratory and special testing.

Medical Surveillance Exams

The examining provider who performs a medical surveillance examination must know the possible adverse health effects of the hazard in order to recognize whether they are present. The provider also needs to know whether the worker has been exposed to the hazard, and at what levels and for how long the exposure has been occurring. Someone who worked with asbestos-containing material since the 1970s is a likely candidate for developing asbestos-related disease. Conversely, someone who had a one-time, 5-minute exposure to asbestos at levels below the PEL last year would be highly unlikely to have asbestos-related disease a year later due to the latency period of developing disease after exposure. The last thing a provider must keep in mind is that non-work-related conditions may be aggravated by work. If there is a clear connection between a disorder and work, it should be documented in the employee’s medical record. If not, the facts should also be documented in the record, including the provider’s rationale for why the condition is not work related.

Certification Exams

Occupational health providers who perform certification exams must be familiar with the requirements of the certification process. They should obtain a copy of the guidelines that list the requirements and any disqualifying conditions for the job. It should be noted that the DoT requires healthcare providers to pass a certification examination themselves before they can start performing medical certification examinations on commercial motor vehicle operators. In the case of other certification examinations, the healthcare provider must review the medical requirements of the position, the job description, the medical conditions and age of the employee being screened, and the results of prior certification examinations and any work limitations previously identified.

The healthcare provider should review the medical history form and address any positive responses in the comments section. The provider should update the master problem list (containing an individual’s past medical and surgical history) if new conditions have developed since the last certification examination. He or she should also review all test findings, and date and initial all hard copies of each page of laboratory, audiogram, chest x-ray, EKG, and PFT results. The provider should reference prior chest x-ray, EKG, or PFTs when reporting the current results. For employees exposed to respiratory hazards, such as asbestos and isocyanate, the provider should review past PFTs to get an idea of trends.

Audiograms should be annotated with “no significant threshold shift (STS)” or “permanent threshold shift (PTS)” with “mild, moderate, or severe hearing loss” in the high, mid, or low frequency. For example, “the employee has a 15-dB shift at 4,000 Hz AD [in the right ear only] compared to 1997 reference; or high frequency loss AU [in both ears] consistent with noise-induced hearing loss.” Visual acuity requirements for civilian positions are listed in the US Army Public Health Center Technical Guide 006, Vision and Safety Eyewear Guide for US Army Civilian and Military Job Series.[11] The corrected visual acuity must be sufficient to meet employment standards for the duties assigned. The vital signs should be reviewed, especially the employee’s stage of blood pressure. If stage 2 or higher, consider referral to the employees treating healthcare provider for blood pressure control.

The provider must identify all abnormal results and the plan for follow-up. He or she should note the test results in the encounter note in the electronic health record and print it (the printed document is standard form [SF] 600, Chronological Record of Medical Care) for placement in the employee’s hardcopy medical record.

DOCUMENTING THE PHYSICAL EXAM AND MANAGING RESULTS

The occupational history and physical examination should focus on identifying signs and symptoms of exposure and detecting adverse health outcomes associated with exposure to an individual’s workplace hazards. As discussed above, the healthcare provider must document any findings associated with the employee’s personal medical conditions in the employee’s health record. If the exam is complete and no test results or other components are pending, the healthcare provider should make a determination on the worker’s medical qualifications. If more tests are needed or the results are not back yet, the provider should check “pending” and advise the OEH clinic nurse and staff that some results are still pending.

Employees with non-work-related conditions should be referred to their personal physician for proper disease and injury management. The employee may be “qualified” for work or continued employment provided the condition does not interfere with the essential job duties. The referral to the treating provider must be documented in the employee’s electronic health record. The original referral letter along with a copy of any abnormal laboratory or testing results should be given to the employee to give to the treating provider.

If the employee is not found to meet the medical requirements for the position, then the healthcare provider must explain why in writing to the employee and their supervisor. Healthcare providers may only disclose the employee’s work ability to the employee and their supervisor. Further, employees must be advised of their privacy and Health Insurance Portability and Accountability Act (HIPAA) rights and notified that protected health information may only be disclosed to the supervisor or management with the express written permission of the employee, who must sign a consent form. The healthcare provider is encouraged to make the employee aware that failure to disclose health information to the supervisor may affect the manager’s ability to make hiring and retention decisions. The provider must also advise the employee what actions are necessary to requalify for the position.

If the occupational health provider thinks an employee has developed an adverse health effect that may be related to a workplace exposure, the provider must advise the worker about ways they may be able to reduce or eliminate ongoing exposures. Supervisors may reduce or eliminate exposures by adopting administrative controls that involve reassigning employees to other duties and improving work practices. Implementing engineering controls can also reduce the employee’s exposure. Less hazardous agents may be employed, and proper use of PPE may reduce exposures. The industrial hygienist may assist the occupational health provider in implementing these controls. The bottom line is that the employee must follow safe work practices and appropriately use PPE. If not, adverse health effects may likely continue.

SPECIFIC OCCUPATIONS

Department of Transportation Commercial Driver Medical Examination

The following comments were taken from DoT regulations for commercial driver exams.[12] The medical examiner must be familiar with 49 CFR, Part 391, Physical Qualifications for Drivers, and should review these instructions before performing the physical examination. The DoT Federal Motor Carrier Safety Administration now requires the medical examiner to register with the agency and pass an examination demonstrating knowledge of the regulations and medical aspects of driving. (These regulations have changed sufficiently; the reader is encouraged to check the DoT website for the latest version of the regulations and advisories to medical providers who perform these examinations.) There is specific medical guidance on certifying commercial motor vehicle operators who have diabetes, hypertension, cardiovascular disease, congestive heart failure, heart murmurs and arrhythmias, syncope, stroke, seizure, vision and hearing problems including vertigo and Meniere disease, back problems, musculoskeletal problems, and impaired respiratory function including obstructive sleep apnea.

The medical examiner must be familiar with drivers’ essential duties and the criteria for establishing work ability as a commercial motor vehicle operator. A commercial truck driver endures physical, mental, and emotional stresses each day and is subject to periodic unannounced drug testing. Commercial motor vehicle operators must operate a vehicle safely so that they do not pose a threat to themselves or others during the operation of the vehicle. The medical examiner must certify that the driver does not have a physical, mental, drug, or alcohol problem that might affect their ability to operate a commercial motor vehicle safely.

If a diagnosis suggests that a medical condition might interfere with the control and safe operation of a commercial motor vehicle, further testing and evaluation is required. The physician may order laboratory work to check the urine for protein, blood, or sugar. Deformities of the hand or fingers, or difficulty with grasp, may prevent the driver from maintaining steering wheel grip, resulting in losing control of the vehicle. If there is foot or leg deformity, the driver may not be able to operate pedals properly. A skill performance evaluation may be required when deformities interfere with vehicle operation. Drivers may apply to the state of their legal residence for a Skill Performance Evaluation Certificate under 49 CFR, Part 391.49.[12]

Commercial motor vehicle operators are usually issued a license by the state transportation department that is valid for 2 years unless any medical restrictions have been specified by the physician. Every commercial motor vehicle operator must undergo a medical certification examination every 2 years, unless specified sooner. The medical examiner may determine that more frequent monitoring of a condition is appropriate and can recommend that a certificate be issued for a shorter period than 2 years. The physician can also specify on the license that the driver must wear hearing aids or corrective lenses to drive safely, and disqualify drivers who do not have binocular vision.

Crane Operator

The crane operator medical examination guidance is found in the Navy and Marine Corps Public Health Center Technical Manual OM 6260, Medical Surveillance Procedures Manual and Medical Matrix,[6] and DoD 6055.05M.[7] Generally the employee must be 21 years old; have all extremities; have at least 20/30 vision in one eye and 20/50 in the other; be able to distinguish red, green, and yellow light perception; hear conversational speech at 15 feet; have sufficient strength, endurance, and agility; and have the needed reaction time to operate the equipment. Waivers may be granted to current operators who were previously qualified and have deviations from the current physical requirements.

Explosive Ordinance Handler and Explosives Vehicle Operator

The following guidance for explosive workers comes from Technical Manual OM 62606 and DoD 6055.05M.7 A candidate may be rejected as an explosive ordnance handler or explosives vehicle operator if they have a condition that interferes with safe performance of assigned duties. Employees may be rejected if they have uncorrected distant visual acuity worse than 20/40 in each eye; peripheral vision less than 70 degrees to each side; red, green, amber colorblindness; hearing loss in either ear averaging greater than 40 dB at 500, 1,000, and 2,000 Hz with or without an aid; cardiovascular disease accompanied by syncope, dyspnea, or congestive heart failure; uncontrolled hypertension; or loss of a leg, foot, hand, or arm. Impairment of a hand or finger that interferes with grasping, or history of epilepsy, syncope, or other conditions that cause altered consciousness may be disqualifying. Employees using drugs or alcohol may not be certified to operate a motor vehicle unless authorized by the treating provider.

For all employees (active duty, reserve, or civilian), regardless of age, the maximum periodicity for the explosives handler certification examination is 5 years; the maximum periodicity for the explosives vehicle operator examination is 2 years.[6] Medical surveillance standards for active duty service members are evolving, so healthcare providers should periodically refer to the guidance for updates.6,7

Forklift Operator

The requirements for the forklift operator history and physical examination listed in the Navy and Marine Corps Public Health Center Technical Manual OM 62606 and DoD 6055.05M7 are similar to the explosive handler physical examination requirements. The provider should use clinical judgment in checking fasting glucose, hemoglobin A1C levels, fasting lipids, and EKGs based on the employee’s occupational and medical history and physical examination. For all employees (active duty, reserves, or civilian), the maximum periodicity for the forklift operator certification examination is 5 years up to age 59; for age 60 and older the examination is required annually.

Firefighter

Firefighting is arduous work performed under dangerous conditions. Personnel who cannot safely perform firefighting duties should be restricted. The US Office of Personnel Management has established physical examination requirements for firefighters.[13] Firefighters must have corrected distant vision of at least 20/30 in the better eye, and 20/70 in the other eye. Their uncorrected distant vision must be at least 20/100 binocular, and they must have red, green, blue color vision. Firefighters must have hearing no worse than 30 dB at 500, 1,000, and 2,000 Hz.6,7 Firefighters must be free of pulmonary conditions that interfere with speech, breathing, and use of respiratory protection equipment. They must be free of heart, valvular, and coronary heart disease; angina; recurrent syncope; and history of myocardial infarction.6,7 They must be free of gastrointestinal conditions including inflammatory bowel disease, hernia, or enlargement of the liver or spleen that limits the performance of duties, as well as musculoskeletal conditions that limit movement of the spine, pelvis, or upper and lower extremities, including problems with the knees. Firefighters must also be free of neurological disease and disqualifying mental health conditions.6,7

The National Fire Protection Association (NFPA) has established guidelines for healthcare providers who perform history and physical examinations on firefighters and applicants for the position.[14] The NFPA coordinated with physician subject matter experts to develop lists of category A (disqualifying) conditions and category B (possibly disqualifying) conditions. Firefighters who have a category B condition must be evaluated on a case-by-case basis to determine if the condition prevents the individual from performing essential firefighting duties without causing undue harm to themselves or others. All OEH providers should reference the NFPA’s list of category A and B medical conditions. In addition to the history and physical examination, the healthcare provider should order height, weight, blood pressure, heart rate, and heart rhythm measurements. The provider should review the OSHA respirator questionnaire completed by the firefighter every year. Hearing and vision tests, PFTs, laboratory tests, and EKGs should be ordered every 3 years for ages 18 to 29, every 2 years for ages 30 to 39, and every year after age 40.6,9

Police and Security Guards

Police and security guards must be able to meet the strenuous physical exertion requirements listed in the job description. Police officers and security guards must be able to engage in foot pursuit and participate in first responder duties in emergencies without risk to themselves or others. They must have near and distant vision, color vision, hearing with good speech discrimination, and emotional and mental stability. The Office of Personnel Management has established physical requirements for police and security guard positions, GS-0083[15] and GS-0085,[16] respectively.

The police and security guard occupational and medical history and physical examination is required annually; the requirements are listed in DoD 6055.05M.[7] The healthcare provider should obtain vital signs, check hearing and vision, and order a urinalysis and lipid profile. An EKG should be obtained at baseline and annually after age 45. A medical condition is considered disqualifying only if the condition limits the police officer or security guard from performing the essential duties of the position.

Army Regulation (AR) 190-56, The Army Civilian Police and Security Guard Program,[17] provides practical guidance for healthcare providers on the medical screening of police and security guards who have cardiac risk factors; this document is also used by the Navy.[6] Under AR 190-56, all police and security guards must be screened for cardiovascular risk. If a policeman or security guard has known cardiac disease or significant cardiac risk factors (eg, a Framingham 5-year risk score > 15%), the individual is referred for level B screening, which assesses cardiac functioning with a stress echocardiogram or stress graded exercise test. Police and security guards with positive level B screening results should be restricted from work until they can be referred to their treating cardiologist for chronic disease risk management.

The American College of Occupational and Environmental Medicine has developed clinical practice guidelines for occupational health providers who perform law enforcement officer history and physical examinations.[18] The guidelines provide information on evaluating and managing officers with disqualifying or potentially disqualifying medical conditions; providers should consult the guidelines if questions arise regarding the medical qualifications of law enforcement officers.

ASBESTOS

Asbestos is a naturally occurring mineral that is both fibrous and noncombustible. It was used for many years in construction and engineering due to its thermal properties and ability to dissipate heat, especially for wrapping steam and hot water pipes to provide insulation. Asbestos was also used in brake linings and clutch facings because of its excellent friction properties. Asbestos has been used in textiles, paints, and coatings for over 100 years. In the 1970s regulations were passed that banned the use of asbestos in construction because health studies showed there was a causal association between exposure and lung cancer and mesothelioma. The fear of liability also limited its use. Nevertheless, heavy asbestos use and unprotected exposures continued in shipyards around the world between 1970 and 1980.

Workers exposed to asbestos during the years 1950 to 1970 were heavily exposed, and they were not afforded respiratory protection because asbestos health risks were poorly understood. Employees who removed or performed renovations on asbestos-containing material aboard ships or in buildings were at the greatest risk of exposure. Vehicle mechanics who performed brake and clutch work were also exposed, at levels high above the OSHA PEL. Employees who did insulation work, including pipe fitters and shipyard workers, were also heavily exposed. Once the health risks became known, occupational exposures in shipyards and construction were drastically reduced, and asbestos workers were mandated to wear PPE.[19]

Health Effects

Workers exposed to asbestos may experience parenchymal or pleural lung disease.[19] These disorders can occur independently, and workers who have similar exposures may develop different diseases. Asbestosis is lung parenchyma fibrosis associated with onset of cough and exertional dyspnea.[19] The cough is nonproductive at first, but may be productive in later stages, with the development of chronic bronchitis.[19] The course of asbestosis is slowly progressive and there is no known treatment. Occupational exposure to asbestos may also cause pleural disease. Workers who develop diffuse pleural thickening are usually asymptomatic, but they may complain of shortness of breath and pleuritic chest pain. Once workers develop pleural thickening, they are more likely to develop asbestosis and lung cancer.[19] As a result, occupational health providers and workers enrolled in the asbestos medical surveillance program must be vigilant for the development of other lung disease. There is no way to modify the course of either asbestosis or pleural fibrosis, but workers should be advised to continue participating in medical surveillance because of the latency period for developing cancer and asbestosis.

Also, workers must be advised to eliminate exposure to cigarette smoke and other pulmonary toxins because of the significantly increased risk of developing lung cancer in asbestos workers who smoke. The risk for lung cancer among workers with asbestos exposure is several times higher than the risk for non-exposed workers. There appears to be a multiplicative risk for lung cancer among smokers with asbestos exposure compared to the risk for nonsmokers with no asbestos exposure.20–22 Additionally, several studies report a modest (10%–15%) increased risk of gastrointestinal cancers (esophagus, stomach, pancreas, colon, and rectum) in heavily exposed asbestos workers.[23]

Lung cancer caused by asbestos is indistinguishable from lung cancer due to other causes.[19] Mesothelioma is characterized by tumors on the pleura, peritoneum, or mediastinum that grow rapidly, are fatal, and are usually associated with asbestos exposure.[19] Benign pleural effusions can also be caused by asbestos exposure; these effusions are usually small and asymptomatic, may be unilateral or bilateral, and last from weeks to months before resolving. Patients with pleural effusions must be tested to rule out lung cancer, mesothelioma, and pleural thickening.19,24

The latency period from onset of asbestos exposure to development of asbestosis is usually more than 15 years, except when the exposure exceeded the OSHA PEL by several orders of magnitude.[17] Pleural plaques and diffuse pleural thickening generally develop 20 years after exposure began,[19] but pleural thickening does occur sooner if the worker previously had benign pleural effusions. The average latency period for asbestos-related cancers is 25 years, and the latency period for mesothelioma is 30 to 35 years.[19]

Asbestos Medical Surveillance Program

Workers, both military and civilian, who are exposed to asbestos above the action level (half of the OSHA PEL) must be enrolled in the asbestos medical surveillance program (AMSP) specified in 29 CFR, Part 1910.1001.[19] Employees may voluntarily enroll in the “past worker” AMSP if they were previously enrolled in the AMSP, if they worked for the federal government and had asbestos exposure for 30 or more days, or if an occupational medicine physician and industrial hygienist determine that an employee met OSHA exposure criteria in the past.

A baseline exam includes a work history, standard respiratory questionnaire, physical examination focusing on the respiratory system, PFT, and a chest x-ray. The chest x-ray is read twice: the local “A” reading is done by a radiologist who looks for heart, lung, or other abnormalities that require urgent attention; the “B” reading is performed by a contracted, NIOSH-certified radiologist who is trained to read radiographs for signs of pneumoconiosis (Exhibit 10-1). Chest x-rays should be done in advance of the provider visit so the results can be discussed with the patient. An abnormal B reading must be discussed with the patient.[19]

Current asbestos workers and past asbestos workers age 45 and older who had more than 10 years of exposure should undergo an annual asbestos medical surveillance examination. Workers age 35 to 44 who were exposed for more than 10 years should get an exam every 2 years. Workers under age 35 with more than 10 years of asbestos exposure and all workers with less than 10 years of exposure should get the surveillance examination every 5 years. A termination examination is required at least 30 calendar days prior to last day of employment, if not performed within the last year. All asbestos medical surveillance documents must be kept for 30 years plus the duration of employment. The occupational health provider should refer to DoD 6055.05M,[7] Technical Manual OM 6260,[6] and the US Army Public Health Center Technical Guide 40-513, Occupational and Environmental Health Guidelines for the Evaluation and Control of Asbestos Exposure,[24] for required documentation of asbestos medical surveillance examinations.

DoD asbestos medical questionnaires (DD Form 2493-125 and DD Form 2493-226) are completed by the worker. The history and physical examination forms are completed by the occupational health provider. The Navy has additional forms used to document history, physical examination, and results of the chest x-ray B reading.27,28 Chest x-ray B reading results and any changes should be noted in the worker’s electronic health record.29,30 Asbestosis produces a restrictive pattern on PFT, and smoking and asbestosis usually produces a mixed pattern on the PFT. Therefore, PFT results and trends over time must be noted. End-inspiratory rales suggest asbestosis. Physical exam findings may be absent even in the presence of significant x-ray or pulmonary function abnormalities. Providers must include their written medical opinion regarding the results of the asbestos medical surveillance examination and whether exposure resulted in development of asbestos-related health outcomes.

Considerations in making a diagnosis of asbestos-related disease include latency period, duration of exposure, intensity of exposure, and chest x-ray findings.[19] The latency period (described above) serves as a firm guideline for ruling in or out a diagnosis of asbestos-related disease. Duration of exposure can be determined by the employee’s occupational history. The occupational health provider should coordinate with an industrial hygienist to obtain an estimate of the intensity of exposure for the worker by position held, industry, decades during which exposure occurred, and the employee’s self-reported use of respiratory protective equipment. The higher the intensity of exposure, the more one should consider the possibility of asbestos-related disease when faced with a consistent clinical picture. Chest x-ray findings are the most important consideration. The lack of x-ray changes consistent with asbestos-related disease should raise concerns about the diagnosis, and consultation with a pulmonologist is recommended.

RADIATION

Radiation is classified as ionizing or nonionizing depending on whether it is capable of producing ions, directly or indirectly, in passing through matter. Ionizing radiation includes gamma rays, x-rays, alpha particles, beta particles, neutrons, protons, and other particles and electromagnetic waves capable of producing ions. Occupational exposure in the services occurs in four distinct areas: medical or dental services, naval nuclear propulsion, nuclear weapons, and industrial applications. Chapters 22 and 23 in this textbook further explore ionizing and nonionizing radiation, respectively, along with the benefits and potential risks associated with its use in the DoD.

EXHIBIT 10-1

INTERNATIONAL LABOR ORGANIZATION GUIDANCE FOR THE CLASSIFICATION AND INTERPRETATION OF CHEST X-RAYS

The plain chest x-ray is the standard imaging technique for detecting asbestos-related lung disease, although computed tomography is more sensitive. Usually there are no chest x-ray findings until 20 years after the onset of exposure unless the patient has had a benign pleural effusion. Asbestos-related pulmonary fibrosis is linear and most commonly involves the lower lobes of the lungs. It begins peripherally and moves centrally. With advanced disease, it can involve the middle and upper lobes. Irregular opacities, class s and t, in mid and lower lung fields and at low grades of perfusion are the common findings of asbestosis. Diffuse pleural thickening and extensive pulmonary fibrosis are classic features of advanced asbestosis. Discrete pleural plaques can be seen face-on, laterally, or on the diaphragm. They occur most commonly in the middle of the diaphragm and on the posterior and lateral chest wall between ribs 6 and 10. Pleural plaques can be bilateral or unilateral, round or irregular. Non-calcified plaques are more common than calcified ones; however, they tend to calcify with time. Apical pleural thickening up to 10 mm is a common variant of normal; most definitions only consider thickening that occurs below the fourth rib as abnormal. Diffuse pleural thickening or pleural fibrosis is often a sequelae of benign asbestos-related pleural effusions. Findings are classified according to the standards listed below.

Opacities

- Small opacities are 1 cm or less; large opacities are more than 1 cm.

- Small opacities are judged by their shape as either round (p, q, r) or irregular (s, t, u), increasing in size from “p” to “r” and from “s” to “u.”

- The predominant type of opacity is called primary; the second most predominant type is secondary.

- Large opacities are judged in increasing size as A, B, C (seen in silicosis and black lung).

- A concentration of opacities (called a profusion) is described as one of 12 ordered subcategories, within four main categories (0, 1, 2, 3), indicating an increase in concentration as the number increases.

Pleural Changes

- Pleural thickening is classified as either discrete (called plaques) or diffuse.

- Calcifications if present and costophrenic angle blunting if present are noted.

___________________

Data sources: (1) US Navy. Periodic Health Evaluation: Navy Asbestos Medical Surveillance Program History and Physical Examination. NAVMED Form 6260/5; 1990. http://www.med.navy.mil/sites/nmcphc/Documents/oem/amsp_6260_5_front.pdf. Accessed August 1, 2016. (2) Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. Chest radiography: ILO classification. http://www.cdc.gov/niosh/topics/chestradiography/ilo.html. Accessed August 1, 2016. (3) International Labour Organization. Guidelines for the use of the ILO international classification of radiographs of pneumoconioses, Revised edition. http://www.ilo.org/safework/info/publications/WCMS_168260/lang--en/index.htm. Published 2011. Accessed August 12, 2017.

Regulations

Occupational exposure to ionizing radiation is covered in OSHA regulations 29 CFR, Part 1910.1096,[31] Toxic and Hazardous Substances, Ionizing Radiation. In addition, the Environmental Protection Agency has issued radiation protection guidance that applies to the DoD under Executive Order 12196.[32] DoDI 6055.08, Occupational Ionizing Radiation Protection Program,[33] directs the services to establish and maintain occupational ionizing radiation protection programs and ensure that unnecessary exposure is avoided. The DoDI takes efficiency, cost, and mission requirements into account and requires the services to maintain occupational and environmental exposures to ionizing radiation as low as reasonably achievable. The services have published guidelines for their programs.[34]-[42]

Ionizing Radiation Medical Examination

The ionizing radiation medical examination[42] is performed on radiation workers who are identified by their command as being occupationally exposed to ionizing radiation. Normally, these employees work directly with ionizing radiation and have a significant potential for exposure. They receive special training before they are allowed to participate in the program. The radiation medical examination is documented on form NAVMED 6470/13.[43] There are preplacement, periodic, postexposure, and termination radiation physical examinations.

Occupational health providers may only perform radiation medical examinations after they have attended a radiation health training course.42,44–47 The exam includes a focused medical history of cancer and significant exposures to ionizing radiation as well as a focused physical examination designed to locate cancers of the thyroid, breast, testes, prostate, and skin. Laboratory testing should include a white blood cell count, hematocrit, and urine dipstick. A positive history or abnormality on physical or laboratory evaluation should be annotated as disqualifying or not disqualifying. Ionizing radiation medical examinations that are considered disqualifying must be sent to the Navy Bureau of Medicine and Surgery’s Radiation Effects Advisory Board for final determination.[48]

OEH clinic staff should develop and maintain a working relationship with the local radiation safety officers, who serve critical roles in the execution of the radiation protection program. The radiation safety officer can assist clinic staff in obtaining employee exposure data and help clarify administrative questions that arise from radiation medical examinations. The Uniformed Services University of the Health Sciences’ Medical Effects of Ionizing Radiation Course[49] is available for providers to increase their knowledge of the biomedical consequences of radiation exposure and how to medically manage casualties.

Navy and Marine Corps[42] radiation workers get a preplacement radiation medical examination prior to beginning their duties and periodic surveillance every 5 years until age 50, every 2 years from age 50 to 60, and annually after age 60. Postexposure examinations must be completed on any individual who has exceeded the radiation exposure protections standards.[42] Termination medical examinations must be completed for all radiation workers 6 months prior to separation from active duty or termination from employment. Army ionizing radiation worker examinations are done at baseline but are not performed periodically. A reported overexposure must be evaluated on a case-by-case basis to assess the need for medical examination and further medical follow-up. The circumstances surrounding the exposure and estimated organ and whole-body dose help determine the extent of follow-up needed.[49]

Air Force ionizing radiation workers do not undergo routine examinations unless their dose exceeds the radiation protection dose limits. Medical surveillance of overexposures is conducted and the results are evaluated on a case-by-case basis by the major commands’ command surgeon’s office in coordination with the Air Force Medical Support Agency’s Bioenvironmental Engineering Division.[38] Doses greater than 5 rem during military operations require long-term periodic health monitoring performed by the Air Force School of Aerospace Medicine. Submission of bioassay samples to determine the absorbed dose may be necessary and annual medical examinations may be needed based on the latency period of the cancers involved.

REPRODUCTIVE HAZARDS

Workplace exposures may pose reproductive and mutagenic hazards to pregnant workers and their fetuses. Raising awareness of workplace reproductive hazards through education and medical surveillance tends to minimize or reduce the risk to the pregnant employee, her fetus, and male employees. Both males and females are at risk from workplace reproductive hazards based on studies of the biology of reproduction.50–52 The services’ reproductive hazards programs have focused on nursing, dental, medical, and veterinary personnel. In addition to evaluating pregnant women for potential exposures to chemical, physical, and biological hazards, exposures to nosocomial hazards (such as cytomegalovirus, herpes virus, and rubella) in the medical treatment facility must also be evaluated. Pregnant women should avoid unnecessary or regular contact with patients who either have hepatitis or who could be carriers of the hepatitis virus. Maternal infection with hepatitis B virus in the latter stages of pregnancy may cause significant illness or death in the newborn.

A pregnancy surveillance program must be conducted in accordance with established DoD 6055.05M7 and service guidelines.50,53,54 One of the first steps in implementing a pregnancy surveillance program is for the occupational health provider, in coordination with military and civilian personnel offices and supervisors, to implement policies and procedures ensuring that personnel who are pregnant or planning to become pregnant get screened in the OEH clinic as soon as possible. The program for military women must be coordinated with the obstetrical/gynecological clinic staff as well.

The industrial hygienist should identify work areas or occupations that contain potential reproductive hazards through the health-hazard inventory and alert the occupational health provider and supervisor in each work location of hazards present in the worksite. All personnel including women of childbearing age and male employees assigned to the area must be informed of reproductive hazards and their potential health effects. The occupational health provider should obtain a reproductive history including problems of infertility for affected employees, and must also inform workers of their right to work in spaces free of reproductive hazards and job-reassignment in the event of pregnancy to protect the mother or her fetus. Counseling and education on reproductive hazards must be documented in the employee’s medical record.

When a pregnant employee contacts OEH clinic staff to inform them of her pregnancy, a physician or licensed healthcare provider must interview the employee and have her supervisor fill out the service-specific forms.55,56 The occupational health provider, in conjunction with the industrial hygienist, must then determine whether the employee may continue working safely in her current job. The providers should inquire about the employee’s job duties, expected delivery date, prior pregnancies, home exposures, and work hours. If there is any question about workplace exposures, the industrial hygienist should do a worksite evaluation to assess the potential for exposures to reproductive or developmental hazards. The occupational health provider should ask the employee to contact the OEH clinic immediately if any changes occur in the work environment.

Coordination between OEH clinic staff and the pregnant employee’s attending physician is essential. The occupational and environmental medicine physician is familiar with the demands and exposures of the job, and the attending physician, while unfamiliar with the work hazards, knows the employee’s medical status and prior reproductive history. When questions arise about the need for job-reassignment, collaboration leads to better decision making about transfers or other job accommodations.

The need for collaboration between the employee’s treating physician and the occupational healthcare provider continues after the pregnancy. The treating physician must clear the employee’s return to work after maternity leave, and the occupational health provider must be aware of and ensure workplace hazards do not pose a risk to the mother who may be breast-feeding the newborn infant. The occupational health nurse should evaluate the pregnancy outcome and document the results in the individual’s employee health record.

EMPLOYEES WITH CHRONIC DISEASES OR PHYSICAL DISABILITIES

Surveillance of personnel with chronic diseases or physical disabilities ensures that the employees’ optimal health status is maintained and that no adverse effects result from interactions of the job with the chronic illness or disability. If this surveillance is effective, these employees are more likely to remain active and productive members of the workforce.

OEH clinic staff should identify employees who have chronic diseases or disabilities that may affect or be affected by their work assignments. For each employee, OEH staff should review any documents that may contain information regarding functional level, including (but not limited to) SF 177, Statement of Physical Ability for Light Duty Work[57]; SF 93 (or DD 2807-1), Report of Medical History58,59; and SF 88 (or DD 2808), Report of Physical Examination.60,61 Providers also can identify affected employees by reviewing the master problem list, which may be documented on a DD 2766, Adult Prevention and Chronic Care Flowsheet,[62] performing preplacement, periodic, and return-to-work examinations. Once employees with chronic condition have been identified, they should be medically evaluated to determine if they can perform the essential duties of their job. If the employee is unable to perform all of their job duties, the occupational health provider should notify both the employee and the supervisor in writing, placing a copy of the notification letter in the individual’s employee health record. This may be accomplished by use of DD Form 68963 or another locally acceptable form.

The frequency of follow-up evaluations varies depending on the employee’s condition. A follow-up evaluation may consist of either a telephone call by the occupational health provider to the employee to inquire about their health status, or a follow-up visit to the OEH clinic for further medical evaluation, which is documented in the employee health record. Documentation should include clinical data regarding the disease or physical disability, its current treatment, and the name of the employee’s personal physician. The condition should also be added to the master problem list.

HEARING CONSERVATION

Service members and civilian employees working in hazardous noise environments face the single most injurious hazard in terms of cost and frequency of occurrence for active duty and civilian workers. Occupational health providers should become familiar with the DoD Hearing Conservation Program,[64] the Army Medical Department Hearing Program,[65] and the Navy Medical Department Hearing Program.[66] Chapter 12, Army Hearing Program, addresses hearing conservation in greater detail. Successful hearing programs have many unique features. First, it is critically important to convey to service members and civilian employees the importance of wearing hearing protection to prevent noise-induced hearing loss and maintain warfighting capability. Next, hearing tests must be done regularly, and personnel must be referred to audiologists and ear, nose, and throat specialists when appropriate. Lastly, people with significant hearing loss must be removed from ongoing noise exposure.

All persons who are routinely exposed to noise levels greater than 84 dB (8-h TWA) or 140-dB peak sound levels of impulse noise (from activities such as firing a weapon or striking a nail with a hammer) should be identified and enrolled in the hearing conservation program.64–66 This is the definition of the noise action level. Persons who are exposed to noise below the action level should not be enrolled in the hearing program.

Noise-induced hearing loss is a type of sensorineural hearing loss; it occurs in both ears and is usually greatest at 4,000 Hz. Conductive hearing loss occurs across most, if not all, frequencies. Normal hearing thresholds go up to 25 dB. Mild hearing loss is 30 to 40 dB; moderate hearing loss is 45 to 65 dB, and severe hearing loss is 70 to 90 dB. Profound hearing loss is 95 dB or higher.64–66 Any individual who has average hearing loss of 90 dB in both ears at 3,000, 4,000, and 6,000 Hz that add up to 270 dB or more should not be assigned or hired to work in a hazardous noise environment (this is the “270 rule”).64–66 Environments in which the noise exposure level is 104 dB TWA or greater require double hearing protection. These areas should be appropriately labeled, and individuals working in them should be informed they require double hearing protection. Occupational health providers should work with audiologists to assess which worksites are likely to have cases of noise-induced hearing loss so that prevention interventions such as ear plug fitting and patient education regarding hazardous noise can be targeted to these high-risk groups.

SUMMARY

This chapter has discussed the common medical surveillance programs conducted by occupational and environmental medicine providers across the DoD, which promote the health and wellbeing of service members and civilian employees from a population perspective. The concepts of primary, secondary, and tertiary prevention were reviewed. The chapter included both the need for and design of surveillance programs. Designing an effective surveillance program has to be tailored to the workers, their exposures, and the biological effects of exposures. Medical surveillance also establishes the work ability of service members and civilian employees to assure that personnel can perform their job safely. Those employees who work with potentially hazardous chemical, physical, or biological agents require medical surveillance only when workplace exposures exceed safe levels specified by OSHA, the ACGIH, and the DoD. The surveillance is designed to detect service member and civilian exposures that produce exposure-related health effects and to monitor the effectiveness of workplace controls.

Job-related medical surveillance in occupational and environmental medicine consists of systematically and periodically collecting and analyzing health data on groups of service members and civilian employees for the purpose of early detection of personnel who are at increased risk of developing disease or identifying those who have developed workplace-related diseases and injuries. The screening examination content and use of medical surveillance results were discussed. The differences between certification and surveillance examinations were examined and the approach to dealing with adverse health outcomes was discussed. The differences between screening and surveillance were reviewed: screening is performed when excessive exposure to lead, for example, occurs and elevated blood lead levels result; screening conducted over time is medical surveillance. Surveillance done when high airborne lead levels are encountered includes comparison of annual blood lead levels to monitor for trends. Lastly, several specific medical surveillance examination types were covered, including DoT commercial drivers, firefighter, police, forklift, ionizing radiation, reproductive hazards, hearing, and asbestos.

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24.   Headquarters, Department of the Army. Occupational and Environmental Health Guidelines for the Evaluation and Control of Asbestos Exposure. Washington, DC: HQDA; July 10, 2013. DA PAM 40-513.

25.   Department of Defense. Asbestos Exposure, Part I: Initial Medical Questionnaire. DD Form 2493-1; 2000. http://www.dtic.mil/whs/directives/forms/eforms/dd2493-1.pdf. Accessed August 1, 2016.

26.   Department of Defense. Asbestos Exposure, Part II: Periodic Medical Questionnaire. DD Form 2493-2; 2000. http://www.dtic.mil/whs/directives/forms/eforms/dd2493-2.pdf. Accessed August 1, 2016.

27.   US Navy. Periodic Health Evaluation: Navy Asbestos Medical Surveillance Program History and Physical Examination. NAVMED Form 6260/5; 1990. http://www.med.navy.mil/sites/nmcphc/Documents/oem/amsp_6260_5_front.pdf. Accessed August 1, 2016.

28.   US Navy. Periodic Health Evaluation: Navy Asbestos Medical Surveillance Program History and Physical Examination. NAVMED Form 6260/7; September 2016. https://www.med.navy.mil/sites/nmcphc/Documents/oem/6260-7_fields_with-DigitalSignature4_RC2.pdf. Accessed August 19, 2017.

29.   Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. Chest radiography: ILO classification. http://www.cdc.gov/niosh/topics/chestradiography/ilo.html. Accessed August 1, 2016.

30.   International Labour Organization. Guidelines for the use of the ILO international classification of radiographs of pneumoconioses, Revised edition. http://www.ilo.org/safework/info/publications/WCMS_168260/lang--en/index.htm. Published 2011. Accessed August 1, 2016.

31.   29 CFR, Section 1910.1096. Ionizing radiation. https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=10098. Accessed August 1, 2016.

32.   Exec Order No. 12196. 3 CFR, 1987. http://www.archives.gov/federal-register/codification/executive-order/12196.html. Accessed August 2, 2016.

33.   Department of Defense. Occupational Ionizing Radiation Protection Program. Washington, DC: DoD; December 15, 2009. DoD Instruction 6055.08. http://www.dtic.mil/whs/directives/corres/pdf/605508p.pdf. Accessed August 2, 2016.

34.   Headquarters, Department of the Army. The Army Safety Program. Washington, DC: HQDA; 2013. Army Regulation 385-10.

35.   Headquarters, Department of the Army. Army Safety Program. Washington, DC: HQDA; 2010. DA Pamphlet 385-10.

36.   Headquarters, Department of the Army. Army Accident Investigations and Reporting. Washington, DC: HQDA; 2015. Department of the Army Pamphlet 385-40.

37.   US Army Medical Command. USMEDCOM Radiation Safety Program. Ft Sam Houston, TX: MEDCOM; May 2. 2012. MEDCOM Reg 40-42.

38.   US Air Force. Ionizing Radiation Protection. Washington, DC: USAF; 2001. AF Instruction 48-148. http://static.e-publishing.af.mil/production/1/af_sg/publication/afi48-148/afi48-148.pdf. Accessed August 19, 2017.

39.   US Air Force. Air Force Culture. Washington, DC: USAF; August 7, 2012. AF Policy Directive 1. http://static.e-publishing.af.mil/production/1/af_cc/publication/afpd1/afpd1.pdf. Accessed August 19, 2017.

40.   Department of the Navy. Department of the Navy Policy for Safety, Mishap Prevention, Occupational Health, and Fire Protection Programs. Washington, DC: USN; 2005. SECNAVINST 5100.10J.

41.   Department of the Navy. Occupational Ionizing Radiation Protection Program. Washington, DC: USN; 2013. OPNAVINST 6470.2C. http://doni.daps.dla.mil/Directives/06000%20Medical%20and%20Dental%20Services/06-400%20Special%20Medical%20Fields%20Support/6470.2C.pdf. Accessed August 2, 2016.

42.   Department of the Navy, Bureau of Medicine and Surgery. Radiation Health Protection Manual. Washington, DC: BUMED; 2011. NAVMED P-5055. http://www.med.navy.mil/directives/Pub/5055%20(Feb%202011).pdf. Accessed August 2, 2016.

43.   US Navy. Ionizing Radiation Medical Examination. Form NAVMED 6470/13; 2011. http://www.med.navy.mil/directives/ExForms/NAVMED%206470%2013.pdf. Accessed August 2, 201 6.

44.   Department of the Navy, Bureau of Medicine and Surgery. Radiation Health Training for Designated Medical Department Personnel. Washington, DC: BUMED; 2016. BUMED Instruction 1500.27.

45.   Navy Medicine Operational Training Center. Undersea Medical Officer Candidate course. http://www.med.navy.mil/sites/nmotc/numi/Pages/UMOC.aspx. Accessed August 2, 2016.

46.   Navy Medicine Operational Training Center. Radiation Health Officer Program. http://www.med.navy.mil/sites/nmotc/numi/Pages/OfficerProgram.aspx. Accessed August 2, 2016.

47.   Navy Medicine Operational Training Center. Radiation Health Indoctrination course. http://www.med.navy.mil/sites/nmotc/numi/Pages/RadiationHealthIndoctrination.aspx. Accessed August 2, 2016.

48.   Department of the Navy, Bureau of Medicine and Surgery. Appointment, Functions, and Responsibilities of the Bureau of Medicine and Surgery Radiation Effects Advisory Board (REAB). Falls Church, VA: BUMED; 2012. BUMED Instruction 6470.21A. http://www.med.navy.mil/directives/ExternalDirectives/6470.21A.pdf. Accessed August 2, 2016.

49.   Uniformed Services University of the Health Sciences. Armed Forces Radiobiology Research Institute. Medical Effects of Ionizing Radiation (MEIR) Course. https://www.usuhs.edu/afrri/meircourse. Accessed August 19, 2017.

50.   Headquarters, Department of the Army. Preventive Medicine. Washington, DC: HQDA; 2005. DA Pamphlet 40-11.

51.   Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. The effects of workplace hazards on female reproductive health. https://www.cdc.gov/niosh/docs/99-104/default.html. Accessed August 19, 2017.

52.   Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. The effects of workplace hazards on male reproductive health. https://www.cdc.gov/niosh/docs/96-132/default.html. Accessed August 19, 2017.

53.   Headquarters, Department of the Army. Standards of Medical Fitness. Washington, DC: HQDA; 2007. DA Regulation 40-501.

54.   Navy and Marine Corps Public Health Center. Reproductive and Developmental Hazards: A Guide for Occupational Health Professionals. Portsmouth, VA: NMCPHC; April 2010. Technical Manual NMCPHC-TM-OEM 6260.01C. http://www.med.navy.mil/sites/nmcphc/Documents/policy-and-instruction/oem-reproductive-and-developmental-hazards-a-guide-for-occupational-health-professionals.pdf. Accessed August 2, 2016.

55.   US Navy. Occupational Exposures of Reproductive or Developmental Concern: Supervisor’s Statement. NAVMED Form 6260/8; 2003. https://navalforms.documentservices.dla.mil/unlocked/NAVMED%206260%208.pdf. Accessed August 2, 2016.

56.   US Navy. Occupational Exposures of Reproductive or Developmental Concern: Workers Statement. NAVMED Form 6260/9; 2003. https://navalforms.documentservices.dla.mil/unlocked/NAVMED%206260%209.pdf. Accessed August 2, 2016.

57.   US Office of Personnel Management. Statement of Physical Ability for Light Duty Work. SF 177; 1984. http://www.justice.gov/sites/default/files/usao-nj/legacy/2013/11/29/statementofphysicialabilitysf177.pdf. Accessed November 30, 2013.

58.   US General Services Administration. Report of Medical History. SF 93; 1996. http://www.gsa.gov/portal/forms/download/116410. Accessed November 30, 2013.

59.   Department of Defense. Report of Medical History. DD Form 2807-1; 2015. http://www.esd.whs.mil/Directives/forms/. Accessed August 13, 2017.

60.   US General Services Administration. Report of Medical Examination. SF 88; 1994. http://www.gsa.gov/portal/forms/download/116402. Accessed August 2, 2016.

61.   Department of Defense. Report of Physical Examination. DD Form 2808; 2005. http://www.dtic.mil/whs/directives/forms/eforms/dd2808.pdf. Accessed August 2, 2016.

62.   Department of Defense. Adult Prevention and Chronic Care Flowsheet. DD Form 2766; 2000. http://www.med.navy.mil/sites/nmcphc/Documents/health-promotion-wellness/Healthy_Living/Clinical_Health_Services/PHA/DD_2766.pdf. Accessed August 2, 2016.

63.   Department of Defense. Individual Sick Slip. DD Form 689; 1963.

64.   Department of Defense. Hearing Conservation Program. Washington, DC: DoD; December 3, 2010. DoD Instruction 6055.12. http://www.esd.whs.mil/Portals/54/Documents/DD/issuances/dodi/605512p.pdf. Accessed August 19, 2017.

65.   Department of the Army. Army Hearing Program. Washington, DC: HQDA; 2015. DA Pamphlet 40-501. https://army-pubs.army.mil/epubs/DR_pubs/DR_a/pdf/web/p40_501.pdf. Accessed August 19, 2017.

66.   Navy and Marine Corps Public Health Center. Navy Medical Department Hearing Program Procedures. Portsmouth, VA: NMCPHC; 2008. Technical Manual NMCPHC-TM 6260.51.99-2. http://www.med.navy.mil/sites/nmcphc/Documents/oem/TM6260_51_99-2_September2008.pdf. Accessed August 2, 2016.

Chapter 11

HEALTH HAZARDS TO HEALTHCARE WORKERS

MELISSA A. McDIARMID, MD, MPH*; KEVIN P. MICHAELS, MD, MPH†; MARLENE SANCHEZ, MD, MPH‡; GARY E. HERR, MS, MPH§; MICHAEL J. TESTA, MS¥; DANIEL J. CALDWELL, PhD, MHS¶; and TIMOTHY M. MALLON, MD, MPH**

INTRODUCTION

HISTORY

PERSONNEL AND POPULATIONS

TYPES OF HAZARDS

Chemical Hazards

Biological Hazards

Radiation Hazards

Physical Hazards

Psychosocial Hazards

STRATEGIES FOR HAZARD ABATEMENT

WORKPLACE VIOLENCE

SUMMARY

ATTACHMENT: BLOOD-BORNE PATHOGEN EXPOSURE CONTROL PLAN

*Professor of Medicine, Epidemiology and Public Health, and Director, Division of Occupational & Environmental Medicine, University of Maryland School of Medicine, 11 S. Paca Street, Suite 200, Baltimore, MD 21201

†Colonel (Retired), US Army; Medical Director, Providence Hospital, Department of Occupational Health, 5100 Rangeline Service N, Mobile, Alabama 36619

‡Commander, US Navy; Director of Public Health, Department of Occupational Medicine, Naval Health Clinic Hawaii, 480 Central Avenue, Building 1750, Joint Base Pearl Harbor-Hickam, Hawaii 96860-4908

§Major, US Army; Chief, Environmental Health and Industrial Hygiene, Preventive Medicine Services, William Beaumont Army Medical Center, El Paso, Texas 79920

¥Major, US Army; Chief, Healthcare Hazards Division, US Army Public Health Center, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010-5403

¶Lieutenant Colonel, US Army; Chief, Exposure Assessment Section, Occupational Health Research Detachment, Wright Patterson Air Force Base, Ohio 45433-7400; formerly, Chief Medical Systems Safety and Health Branch, Industrial Hygiene Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

**Colonel (Retired), US Army; Adjunct Assistant Professor, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814

INTRODUCTION

This chapter is being published as an update to Chapter 5, Health Hazards to Healthcare Workers, in the previous edition of this textbook.[1] The chapter has been updated to reflect new and emerging technology and medical equipment. Much of the chapter has also been revised to focus on protecting the healthcare worker in stateside military treatment facilities (MTFs) and deployed locations. The references and figures have been updated as well.

Healthcare workers are exposed to many types of health threats, such as the physical, biological, chemical, and environmental hazards listed in Table 11-1. Healthcare facilities, in the best of circumstances, are complex environments that may threaten the worker’s health. Deployments during humanitarian and civic crises, natural disasters, and traditional wartime operations pose additional challenges and health threats. To counter these threats, the occupational medicine physician must discern potential hazards, define the extent of exposure, and coordinate with safety and industrial hygiene personnel to develop and implement strategies to eliminate or reduce exposure through appropriate control measures.

In order to accomplish these tasks, the occupational health clinician must work closely with the hospital safety officer and industrial hygiene staff to identify those workers at risk who must enroll in medical surveillance. Further, the occupational health clinician must coordinate with each employee’s supervisor to ensure worker participation in the medical surveillance program. Surveillance efforts are documented in the medical treatment record to comply with the Occupational Safety and Health Administration (OSHA) and The Joint Commission’s environment of care requirements.

HISTORY

In the past, healthcare facilities were considered safer than industrial sites because employees were not thought of as workers exposed to a wide variety of hazards; however, that perception is far from reality. There are inherent dangers that come with caring for those who are sick and injured; these dangers range from physical injury to illness and death. Measles, diphtheria, and scarlet fever were substantial risks during the 20th century. In the past 2 decades, healthcare workers have been exposed to and died from occupationally acquired hepatitis B (HBV), human immunodeficiency virus (HIV) infection, and multidrug-resistant tuberculosis.1–3

Among US industries, hospitals and nursing/personal care facilities have the highest nonfatal injury and illness case rates. Among service-providing industry sectors, healthcare workers and nursing assistants in particular experience the highest risk of injury, with 200 cases per 10,000 workers, which is twice the next highest injury rate and seven times higher than the population average of 28.2 cases per 10,000 full-time workers.[4] The estimated annual death rate for health-care workers is low at 9 per 10,000 workers compared to 34 per 10,000 workers in the US population.[5]

Most healthcare changes have resulted in improved health and safety conditions for healthcare workers. Handwashing, introduced by Dr Philipp Ignaz Semmelweis (1818–1865), reduced puerperal fever patient mortality in the mid-1800s. During the mid to late 1800s, Florence Nightingale (1820–1910), who believed hospitals were hazardous to both patients and their caregivers, opened windows to allow ventilation and tried to reduce hospital overcrowding.1,6 The current emphasis on standard precautions is critical to protecting the patient and healthcare worker against blood-borne pathogens and airborne infectious diseases. However, there are many other hazards the occupational medicine physician must discern and protect against, and new hazards continue to appear in hospitals.[7]

For example, while caring for their patients, physicians have been exposed to infectious diseases including severe acute respiratory syndrome, the H1N1 virus (also known as swine flu), the virus that causes Middle Eastern respiratory syndrome (coronavirus), and the Ebola virus, which pose huge respiratory and blood-borne hazards, as well as radiation risks secondary to radiographs, fluoroscopy, and radio-pharmaceuticals. Flammable anesthetic gases pose explosion risks and reproductive hazards to operating room personnel. Stressors to the musculoskeletal system through repetitive tasks such as moving patients or computer work pose ergonomic hazards for healthcare workers and administrative staff. Workplace violence has become widespread, and patient attacks on healthcare workers continue to be a problem in many facilities.[8]

Addressing health hazards and providing good medical surveillance in the workplace are essential to maintaining a healthy and vital healthcare workforce. Organizations such as OSHA, the National Institute for Occupational Safety and Health (NIOSH), and the Centers for Disease Control and Prevention (CDC) provide guidelines listed in Table 11-2 that include recommendations for protecting healthcare workers, including vaccination, isolation precautions, personal protective equipment (PPE), and education. There have been many successes, such as the 1991 OSHA blood-borne pathogen standard,[9] which, combined with childhood immunizations for HBV, has led to the marked reduction of HBV among healthcare workers.[10] However, more can be done to protect the healthcare worker.

TABLE 11-1

OCCUPATIONAL HAZARDS IN MILITARY HEALTHCARE FACILITIES*

*Musculoskeletal strain, psychological stress, and safety (such as electrical and explosive) hazards are not included.

TABLE 11-2

HAZARDS OF SELECTED SOLVENTS, REAGENTS, AND DISINFECTANTS

Chemical

Main Biological Effects

Type of Work

Work Site

Benzene

Carcinogen (leukemia) Neurotoxicity

Chemistry procedures

Laboratory

Benzidine-based dyes

Carcinogen (bladder) Neurotoxicity

Biological stains
Chemistry procedures
Print dyes

Histology lab
Chemistry lab
Print shop

Xylene

Neurotoxicity
Cardiovascular effects
Reproductive effects
Liver and kidney damage

Solvent
Tissue processing

Histology lab
Chemistry lab

Toluene

Neurotoxicity
Cardiovascular effects
Reproductive effects
Liver and kidney damage

Solvent
Tissue processing

Histology lab
Chemistry lab

Chromic acid

Carcinogen (lungs)

Tissue processing

Histology lab

Glutaraldehyde

Mutagenicity
Respiratory effects
Dermatitis

Tissue fixation
Disinfection
Dermal treatment
X-ray file processing

Histology lab
Central supply
Dermatology
Radiology

Azide

Neurotoxicity
Cardiovascular effects
Respiratory effects

Blood chemistries

Serology lab

Data source: 29 CFR Part 1910.1000, Occupational exposures to hazardous chemicals in laboratories.

PERSONNEL AND POPULATIONS

All military and civilian personnel must be medically screened to ensure they meet the medical requirements for deployment. These requirements include updated and country-appropriate immunizations, a 6-month supply of the individual’s medications, PPE, specific training on health threats, and appropriate medical surveillance documentation, including a medical summary of the individual’s medical diagnosis. However, recent deployments have changed to include an increasing number of government service civilians, contractors, and coalition partners who provide specialized services to support military operations. After action reports and studies estimated that 19,000 civilians and contractors worked beside US troops during the first Persian Gulf War.[11]

Contractors who deploy with active duty and civilian employees must meet the combatant commanders’ guidance requirements for medical fitness standards and entry into theater. Contractors, however, are sometimes not screened as rigorously before deployment as military and civilian personnel. Thus, contractors may not meet medical deployment requirements, may not be free of infectious diseases such as active tuberculosis, and may inadvertently put the unit and mission at risk. Service regulations define health conditions that prevent someone from deploying; however, providers who screen contractors and civilian employees are often not aware of restrictions or disqualifying conditions. Further, foreign nationals are hired to provide contract support for basic installation operations including food service, grounds maintenance, and Army and Air Force Exchange Service and commissary operations in deployed areas of operation. Often, these foreign nationals receive little to no health screening, and they have transmitted tuberculosis and other infectious diseases to deployed troops.[11]

Strict requirements are necessary because the austere and hostile conditions limit available resources on the typical deployed operating base. For example, there may be a limited number of refrigerators and cooling units to store temperature-controlled medications. In addition, because the fighting force’s health is first priority, care at deployed MTFs is limited to emergency care only for civilians and contractors. Thus, individuals with disqualifying disease conditions require an exception or waiver to deployment policy.[12]

Additionally, deployed US medical personnel often work with coalition and host country populations. In Operation Enduring Freedom in Afghanistan and Operation Iraqi Freedom in Iraq, the United States acted in coalition with 60 other countries. Thirty of the coalition partners were from developing countries. Baseline health; language barriers; medical credentialing; health maintenance (medications, surgical procedures, etc); environmental and personnel exposures; and readiness requirements are some of the issues healthcare providers face while working with coalition and host nation partners in the deployed MTF. For example, required medical clearance, immunizations, and prophylaxis for malaria, while standard for a deployed US service member or civilian employee, may not be routine or required in coalition or host nation forces. The coalition forces may also have a higher incidence of tuberculosis and other infectious diseases endemic to their place of origin.[11]

TYPES OF HAZARDS

In healthcare and research facilities, workers are routinely exposed to chemical, biological, radiological, physical (including ergonomic), and psychosocial hazards. Since September 2001, hazards from terrorist activities have added another dimension to protecting the healthcare facility, patients, and staff.[13] The potential terrorist threat includes weapons of mass destruction such as chemical and biological warfare agents, radiation hazards from dirty bombs, and high-yield explosives. Comprehensive risk identification, hazard reduction or elimination plans, and a response plan in the event of a terrorist incident are required components for every healthcare facility using good industrial hygiene practices and physical security measures.

Chemical Hazards

Healthcare workers are exposed to chemicals by skin contact, inhalation, or ingestion. Exposure effects range from no effects to acute or chronic and long-term effects. The chemical may be a mild irritant, or it may produce more severe reactions such as tumors or cancer because of mutagen, teratogen, or carcinogen properties. The extent of health effects depends on the exposure concentration and duration, the exposure route, and the substance’s physical and chemical properties. When a healthcare worker is exposed to two chemicals simultaneously, health effects can potentiate or decrease, depending on the mixture’s chemical properties. In most cases, acute exposures from chemical accidents, spills, leaks, fires, and ventilation failures pose a greater risk than chronic exposure because they happen more frequently and the chemicals’ concentrations can be significantly higher.

In the healthcare setting, the most common toxic effect of chemical exposure, and the most prevalent occupational illness, is contact dermatitis. Nurses who administer drugs and housekeeping staff who routinely use cleaners and disinfectants have the most frequent contact dermatitis cases. Several cleaners, disinfectants, and solvents increase the risk of developing contact dermatitis among kitchen, radiography, pathology, nursing, surgical, and maintenance staff (see Table 11-2).14–16

Healthcare workers are often exposed to potentially hazardous aerosols and vapors (see Table 11-1). Chemicals with mutagenic, teratogenic, and carcinogenic properties, and those with acute toxicity, including anesthetic gases, antineoplastic agents and hazardous drugs, glutaraldehyde, formaldehyde, mercury, and methyl methacrylate are further discussed below.

Anesthetic Gases

Anesthetic gases, such as nitrous oxide, halothane, methoxyflurane, enflurane, desflurane, sevoflurane, and isoflurane, can be released into healthcare facility work areas including operating rooms, labor and delivery rooms, dental and veterinary clinics, and recovery rooms.17–22 Studies show that exposures to anesthetic gases are kept well below the permissible exposure limit and threshold limit value.[7] However, workers have reported short-term neurotoxic effects at low exposure levels including drowsiness, irritability, depression, headache, nausea, fatigue, and impaired judgment and coordination.17–22 These symptoms can be dangerous for operating room staff, including nurses and doctors, who need unimpaired judgment and coordination to perform successful operations. When workers experience these symptoms, the occupational health clinician should consult with a safety and industrial hygiene professional to check equipment for leaks.

Assessing the long-term effects of exposure to anesthetic agents on human health is difficult and controversial. There are few epidemiological studies on the low-dose exposure to waste anesthetic gases (WAGs) and related health effects, most of which are retrospective epidemiological and animal studies. A 1985 study suggested that chronic exposure to WAGs is associated with an increased risk of spontaneous abortion in exposed women and the wives of exposed men.[23] Recently studies have shed more light on exposures in the workplace,24,25 and other potential adverse reproductive effects include infertility, low birth weight, and congenital abnormalities.[26]

Whether anesthetic gases are carcinogenic is subject to analysis because of structural similarities between the known human carcinogens (dibromoethane, dichloroethane, bis-chloromethyl ether, and chloromethyl methyl ether) and several of the halogenated inhalation anesthetics now in use.27–33 In addition, anesthetic compounds can be transformed into reactive metabolites, which may combine with tissue macromolecules to initiate a carcinogenic event.31–33 Several studies have noted elevated rates of some cancers in hospital personnel who are chronically exposed to anesthetic gases. Anesthesiologists had a higher cancer rate for reticuloendothelial and lymphoid malignancies than the general population, and nurse anesthetists had a threefold increase in malignancies compared to the general worker population.28,33

Although no federal standard for WAGs exists, OSHA, NIOSH, and the American Conference of Governmental Industrial Hygienists recommend control of occupational exposure to WAGs.20,22 The Army promulgated Guidelines for the Recognition, Evaluation, and Control of Occupational Exposure to Waste Anesthetic Gases (Technical Bulletin, Medical, 510) to ensure exposures are controlled and medical surveillance is performed on healthcare workers exposed to anesthetic gas.[34] There are preplacement, periodic, and postexposure surveillance requirements.

Exposure to WAGs can be controlled by ensuring employees are aware of their sources. Exposures usually result from careless work practices such as improperly sealing the patient’s mask, failing to eliminate anesthetics before removing the patient’s mask or endotracheal tube, or failing to wash anesthetic gas from the patient’s lungs with oxygen. Properly functioning scavengers and ventilators control exposure to waste anesthetic gases and have reduced or eliminated significant exposures in healthcare workers.[7] However, leaking anesthetic equipment, inadequate waste-gas collection and scavenging systems, and poor general ventilation have also led to exposures. The WAG scavenging system’s exhaust should be as far away as possible from the environmental control unit’s air intake.

Antineoplastic Agents and Hazardous Drugs

NIOSH defines hazardous drugs as those that exhibit carcinogenicity, teratogenicity, reproductive toxicity, organ toxicity, and genotoxicity.[35] Antineoplastic agents inhibit tumor growth by disrupting cell division and killing actively growing cells.[35] They can be divided into five drug classes: alkylating agents, antibiotics, antimetabolites, mitotic inhibitors, and a miscellaneous class.35,36 Antineoplastic agents (cytotoxic drugs) make up most of the hazardous drugs on the NIOSH list, which also includes antiviral drugs, hormones, and bioengineered drugs.[36] OSHA established guidelines for healthcare workers for the safe handling of antineoplastic agents.[37] These guidelines recommend the use of laminar flow biological safety cabinets during drug preparations, as well as PPE, worker education, specific standard operating procedures for drug handling, and medical surveillance for workers. The guidelines also call for the preparation of antineoplastic agents in a class II, type B, biological safety cabinet that is vented to the outside of the facility.[37]

While there is agreement that the guidelines have reduced hazardous drug exposures in the workplace, sampling for contamination in healthcare facilities shows widespread contamination exists.[38] Furthermore, these exposures result in reproductive hazards and genetic changes including alterations on chromosomes 5 and 7.39,40 The Army has developed safe handling procedures for hazardous drugs and antineoplastic agents, which are commonly used in the larger medical centers and hospitals, but are rarely used in deployed settings.[41]

Alkylating agents act by covalently binding to deoxyribonucleic acid, thus interfering with normal deoxyribonucleic acid replication. Antibiotics work as deoxyribonucleic acid intercalators and interfere with transcriptional processes in protein synthesis. Antimetabolites block synthesis of essential cellular building blocks such as folate, purines, and pyrimidines, thereby inhibiting protein synthesis. Anti-mitotic agents act primarily as spindle poisons and block mitosis and normal cell division. The miscellaneous category contains agents with various effect mechanisms. Several of these agents are mutagenic, carcinogenic, and toxic to the reproductive system (see further discussion below).[42]

Patients treated with these drugs have had significant adverse outcomes including hematopoietic effects and occurrences of second malignancies (usually hematological), impaired reproductive function, immunosuppression, and malformed infants born to treated mothers.[42] These reports, together with laboratory evidence of the mutagenic activity of antineoplastic agents, have triggered concern about possible long-term health risks to healthcare personnel who handle these drugs.

A meta-analysis of 14 studies performed from 1996 to 2004 in the United States and Europe noted an association between exposure to antineoplastic drugs and adverse reproductive outcomes such as fetal loss, low birth weight, and spontaneous abortion.[43]

Another study in China reported significant decreases in full-term births, premature births, spontaneous abortions, and congenital malformations.[44] These findings suggest a significant reproductive risk may exist for workers who handle antineoplastic agents during pregnancy.

A study performed by Skov in Denmark noted a link between cancer and healthcare worker exposure to antineoplastic agents. A significantly increased risk of leukemia was observed in oncology nurses for the period 1943 to 1987, and an increased risk of leukemia was observed in physicians who worked a minimum of 6 months in the department administering drugs.[45] Thus, occupational exposure increases the risk of mutagenicity and cancer risk in nurses and pharmacists following exposure.[41]

Glutaraldehyde

Glutaraldehyde is routinely used in healthcare facilities as a cold sterilant for heat or moisture-sensitive equipment and instruments. It is typically packaged in a 2% solution and supplied in jugs, which are dumped into the sterilizers situated throughout the hospital in endoscopic units, operating rooms, intensive care units, and dialysis units. There are OSHA best practices for the safe use of glutaraldehyde and a NIOSH alert on glutaraldehyde.46,47 Glutaraldehyde’s entry route into the body is through inhalation and dermal absorption.48,49 Glutaraldehyde is a mucus membrane and respiratory irritant that causes respiratory and skin sensitization, asthma, rhinitis, contact dermatitis, and wheezing.48,49 NIOSH recommends fully automated and enclosed sterilizers that use glutaraldehyde to disinfect sigmoidoscopies and colonoscopy scopes.[47]

Formaldehyde

Formaldehyde is used as a tissue preservative in hospital laboratories and autopsy suites and as a disinfectant in dialysis units and central supply where most medical instruments are sterilized and packaged for the next use.[50] Formaldehyde use in hospitals has been poorly controlled. As with other hazardous chemicals, the effects of formaldehyde depend on the duration and extent of the exposure. Low levels of exposure (<1 ppm) may cause direct irritation of the skin, eyes, nose, throat, and lungs.[50] Higher concentrations (10–20 ppm) may cause coughing, chest tightness, increased heart rate, and a sensation of pressure in the head. Concentrations of 50 to 100 ppm are associated with pulmonary edema and death.[51]

Repeated exposure to formaldehyde vapors causes sensitization in some healthcare workers, which may occur days, weeks, or months after the first exposure. Immunogenic responses include eye irritation, upper respiratory irritation, or an asthmatic reaction at exposure levels too low to cause symptoms in most people. Reactions can be quite severe, with swelling, itching, wheezing, and chest tightness.[51] Direct contact with formaldehyde solutions can cause severe eye injury and corneal damage as well as dermatological symptoms. Skin contact with solutions as dilute as 4% can trigger primary irritation. Dermatitis (including red, sore, cracking, and blistered skin) is a common complaint.[52] As a reactive alkylating agent, formaldehyde is a potent human carcinogen.[52] Several animal studies have demonstrated that formaldehyde is a mutagen and a carcinogen. In addition, human epidemiological studies have associated formaldehyde exposure with cancers of the lung, nasopharynx, oropharynx, and nasal passages.[52]

OSHA currently regulates formaldehyde: the permissible exposure level for an 8-hour time-weighted average is 0.75 ppm; the 15-minute short-term exposure limit is 2.0 ppm; and the action level (the level at which workers must be enrolled in medical surveillance programs) is 0.5 ppm.[51]

Occupational exposures can be reduced by:

- substituting safer products,

- using laboratory hoods,

- wearing appropriate PPE,

- instituting good work practices,

- installing and maintaining general ventilation, and

- training healthcare workers about relevant hazards and exposure precautions.[49]

Mercury

Mercury has been removed from almost all industrial and healthcare settings because of its acute and chronic toxicity, which prompted the establishment of occupational exposure standards and controls. Service members may still be exposed to mercury in dental clinics.53–55 Mercury dust is generated in dental clinics when mercury-containing amalgam is cut, or ground out when older fillings containing mercury are removed.53–55 Mercury is adsorbed through inhalation and skin contact. Good work practices including wear of appropriate PPE, periodic air monitoring, use of local exhaust ventilation, and employee education can prevent mercury exposure.53–55

Methyl Methacrylate

Methyl methacrylate is an acrylic cement derived from mixing a liquid containing methyl methacrylate monomer with polymethyl-methacrylate powder. It is used in orthopedic and dental applications, and prepared immediately before use. [56] Healthcare workers are exposed through inhalation and skin contact. Personnel at risk of methyl methacrylate exposure include technicians who work with dentures and hearing aids, orthopedic surgical personnel who use methyl methacrylate cement for fixation of prostheses, and pathology personnel who imbed histological preparations.[56]

Methyl methacrylate is an eye, skin, and mucous-membrane irritant that causes contact dermatitis, pulmonary sensitization, and occupational asthma.[57] NIOSH reported that health effects including dermatitis, genitourinary, and respiratory complaints were common in workers exposed to methyl methacrylate at concentrations lower than 50 ppm.[56] Exposure can be reduced by mixing methyl methacrylate under hoods equipped with local exhaust ventilation; wearing PPE including goggles to protect the eyes, gloves to protect the hands, and an impermeable apron to protect the body; practicing careful personal hygiene; and providing health education regarding the hazards of methyl methacrylate.56,58

Biological Hazards

The occurrence of occupational diseases in the healthcare industry has recently received considerable attention with the outbreak of Ebola in Africa and Middle East respiratory syndrome. Healthcare workers can become infected by patient contact or through contact with patient specimens in the laboratory. Bacterial, viral, fungal, and parasitic organisms pose a constant threat to the unprotected healthcare worker and patients. Medical, dental, and laboratory workers as well as housekeepers, laundry, maintenance, and supply personnel are at risk of infection through contact with patient waste, soiled laundry, and contaminated equipment.

Tuberculosis, varicella, and rubella continue to pose a risk to healthcare workers and patients despite major efforts to control these diseases. In addition, emerging diseases, such as Middle East respiratory syndrome, severe acute respiratory syndrome, and Ebola pose new threats to workers and patients. Healthcare facilities must be prepared to respond to these new threats as well as the traditional biological warfare threats, smallpox, and anthrax. Further, methicillin-resistant Staphylococcus aureus (S aureus) has become a major problem in many healthcare facilities.

In Southwest Asia, military healthcare facilities encountered another hard-to-control organism when Acinetobacter baumannii was found in the wounds of surgical patients. This threat quickly became a nosocomial infection risk and forced staff to reemphasize the importance of infection control practices in the deployed setting.[59]

Hepatitis B and Hepatitis C

Healthcare workers may become infected by blood-borne pathogens directly through needlesticks or splashes of blood-containing fluids to the mucous membranes, or indirectly, through contaminated work surfaces. Hepatitis B (HBV), hepatitis C (HCV), and human immunodeficiency virus (HIV) pose the greatest risk of blood-borne pathogen infection for healthcare providers.[60] The CDC notes that the risk of HBV transmission in the occupational setting is greater than that for HIV or HCV, and practices that reduce the transmission of HBV also prevent the transmission of HCV and HIV.[60] HBV can cause persistent infections, chronic liver disease, and hepatocellular carcinoma. In acute illness, it causes fever, anorexia, jaundice, and acute liver failure.[60] HCV infections generally cause chronic infection, and 10% to 15% of infected patients will develop cirrhosis. HIV infection may cause an initial infection with flu-like symptoms. Untreated HIV will damage the immune system and progress to AIDS (acquired immune deficiency syndrome).[60]

There are 66,000 new cases of HBV; 16,000 new cases of HCV; and 1,000 new cases of HIV infection worldwide each year due to needlestick injuries.[61] Healthcare providers are at risk of blood-borne pathogen infection in intensive care units, operating rooms, emergency rooms, inpatient units, and transport teams. Almost all workers at a facility are at risk, including physicians; surgeons; nurses; nursing assistants; laboratory staff; technicians; students; and service employees in departments such as laundry, dietary, environmental services, and maintenance. Personnel who handle medical waste are also at increased risk. Paramedics, emergency medical technicians, and public safety employees who work in prehospital evaluation and patient management must also comply with the OSHA regulations and utilize standard precautions.[60]

The most common causes of needlestick injury are manipulating a needle inside a patient (26%); disposing of a needle or scalpel (21%); bumping into a coworker (10%); and recapping needles (5%).[62] These percentages vary by country because the levels of engineering controls and patient safety education among health-care providers differ. Devices most often involved in needlestick injuries are disposable syringes (30%), suture needles (20%), winged steel needles (12%), scalpel blades (8%), intravenous catheter stylets (5%), and phlebotomy needles (3%).[62]

Title 29 Code of Federal Regulations 1910.1030, Blood-borne pathogens,[9] was published in December 1991 and amended in April 2012. These OSHA regulations require employers to develop a written exposure control plan; use engineering controls (safe needles, sharps containers, needleless systems); issue PPE to healthcare workers; offer HBV vaccinations; provide safe work practice training to employees; and provide postexposure evaluation and follow-up for workers who have a blood-borne pathogen exposure.[9] The regulation also outlines housekeeping and decontamination procedures for cleaning and discarding sharps and regulated wastes. Healthcare providers must follow standard precautions that include treating blood and body fluids from all patients as if they were infectious, whether or not an infection has been confirmed. The regulations also require good hand hygiene, proper use of PPE, safe injection practices, safe handling of potentially contaminated equipment or surfaces, and respiratory hygiene.[9]

Needleless systems that can replace or eliminate unnecessary sharps in cost-effective ways are now required.63,64 For example, towel clips in surgery can be eliminated and hollow bore needles can be replaced. Attention to best practices can eliminate the risk posed by exposed needles on a syringe after use and needles attached to tubing, such as butterflies, that can be difficult to place in sharps containers.[65] Sharps containers must be present in all areas where sharps are generated. Containers must be closable, puncture-resistant, leak-proof, spill-proof, and contamination-free. The level of sharps inside the container must be visible and the container must be changed when three-quarters full. The sharps container must be placed no higher than 54 in from the floor with easy access.[65]

Needleless systems and other engineering controls have greatly reduced needlestick and sharps injuries. The needlestick injury rate has gone from 5 per 10,000 to 0.06 per 10,000 between 2001 and 2010.[63] Infusion therapy needleless devices have decreased needlestick injuries related to intravenous connectors by 62% to 88% over the same timeframe.[64] Needleless systems deliver medication and fluids through a needleless catheter port. Jet injection systems, which inject medications below the skin or into the muscle, are also needleless. Syringes must have needlestick prevention features like needle retraction or a shield that caps the used needle. Healthcare providers are strictly prohibited from recapping used needles. Safe needle and self-blunting features have reduced phlebotomy needlestick injuries by 80%.[65] Blunt tip suture needles have reduced the risk of injury by 69% in operating rooms and surgical suites.[66]

The Department of Defense requires personnel in fixed and deployed hospital settings to follow 29 CFR 1910.1030. Additionally all medical treatment facilities must have an exposure control plan that has been reviewed and accepted by the executive hospital leadership and is available to all employees. Refer to Attachment 11-1 for a model copy of a blood-borne pathogen exposure control plan that can be adapted to specific work settings.

Human Immunodeficiency Virus

The CDC issued guidelines on August 21, 1987, for preventing HIV transmission in healthcare facilities, which state that healthcare workers should assume all patients are infectious for HIV and other blood-borne pathogens.[67] The CDC reported that as of December 31, 2013, there have been 58 confirmed and 150 unconfirmed occupational transmissions of HIV in the United States.[68] The CDC estimates that healthcare workers who experience a needlestick injury will become infected in 2.3 out of 1,000 cases.[68] In 2013, the CDC updated guidelines to manage healthcare worker exposures to HIV and postexposure prophylaxis.[69] In 2017, Markelz published recommendations that update the CDC guidance regarding the proper medications, dosing, and required follow-up for affected healthcare providers.[70]

Tuberculosis

Mycobacterium tuberculosis (M tuberculosis) is a bacterium that causes tuberculosis. M tuberculosis grows slowly in the lungs and can remain dormant for a long time.71–73 M tuberculosis is transmitted through airborne particles called droplet nuclei, which are formed when individuals with pulmonary or laryngeal tuberculosis cough, sneeze, shout, or sing. The droplets are 1 μm to 5 μm in size, remain airborne for prolonged periods of time, and spread throughout the healthcare facility.71–73 Patients who are immunocompromised, or who have HIV, diabetes, poor nutritional status, silicosis, or end-stage renal failure are at a higher risk for developing tuberculosis. Other risk factors include overcrowded living conditions, smoking, indoor air pollution, alcohol use, corticosteroid therapy, malignancy, and genetic susceptibility.71–73

Latent tuberculosis infection in the patient population can range from 20% in the developed world74,75 to about 70% in the developing world.[76] The annual rate of M tuberculosis infection in hospital workers ranges from 0.1% to 2% in unexposed hospital administrative personnel to from 1% to 10% among healthcare providers who perform high-risk procedures in pulmonary care, surgical services, and laboratory services.[74] However, the risk of tuberculosis transmission varies depending on the healthcare setting, the prevalence of tuberculosis in the general population, and the type of exposure. The annual incidence of M tuberculosis in healthcare providers is 60 per 100,000, compared to the general population incidence of 25 per 100,000.[77] Active M tuberculosis is symptomatic in three-quarters of the cases, and patients may exhibit clinical signs of persistent cough for 2 or more weeks, low-grade fever, weight loss, and night sweats. Most patients contract pulmonary tuberculosis, but M tuberculosis can infect any organ, so the signs and symptoms may vary.[73]

The OSHA “General Duty Clause”[78] requires healthcare facilities to adhere to the CDC’s guidelines for control of tuberculosis transmission in healthcare facilities. Administrative measures mandated by the CDC are critical to reducing the transmission risk of tuberculosis.71,79 The CDC guidelines include a written infection control plan, prompt detection and isolation of suspected cases, staff training materials, rapid reporting of diagnostic tests, and tuberculosis education materials for patients and their families. Healthcare facilities must perform an individualized, location-specific risk assessment of M tuberculosis within the facility. This risk assessment triggers a number of requirements that moderate- and high-risk facilities must meet, such as whether routine tuberculin skin testing should be performed on healthcare providers and whether isolation rooms must be available. Healthcare providers who have a positive reaction must be evaluated for treatment of active or latent M tuberculosis infection.71,79

Environmental controls help prevent the transmission of M tuberculosis in healthcare facilities. These controls include local exhaust ventilation, general mechanical ventilation, room air high-efficiency particulate filters, and ultraviolet germicidal irradiation units. Local exhaust ventilation is used in locations where patients undergo aerosol-generating procedures, such as sputum induction and pentamidine inhalation therapy.71,79,80 Local exhaust ventilation is also used in autopsy rooms to reduce exposure to pathogens and embalming vapors. Class II biological safety cabinets should be used in laboratories where M tuberculosis tests are performed and infectious aerosols may be generated.[81]

Patients thought to have the M tuberculosis infection should be moved to an airborne infection isolation room. The isolation room should have twelve air changes per hour.[80] Older buildings are still allowed to have six air changes per hour. If the room uses recirculated air, it should pass through high-efficiency particulate air filters. All patient rooms and patient isolation rooms should be maintained at a slight negative pressure .[80] Ultraviolet germicidal irradiation can be effective if installed properly and carefully maintained.[82] The room airflow rate must be slow enough to properly irradiate the air, and the humidity must be kept below 70%.[81]

Healthcare providers do not always don their respirators before entering the room of a patient suspected of having M tuberculosis. Healthcare providers who perform high-risk procedures must wear an N95 high-efficiency particulate filtering respirator at a minimum. Healthcare workers also need extra encouragement to perform annual respirator fit testing and seal checks.[79] The Institute of Medicine reviewed respirator use in healthcare facilities by comparing the effectiveness of N95 respirators and surgical masks. The N95 respirator was found to be superior to surgical masks in filtering efficiency and protection when fitted and used correctly.83–86

Latex

Natural latex rubber is made from the white sap of commercially grown rubber trees. Latex contains the proteins hevein and chitinase, which are thought to cause allergic reactions in some people. For this reason, latex rubber gloves are being phased out of the healthcare industry.

Prepowdered gloves that are treated with cornstarch adsorb latex allergenic proteins. Repeated glove donning and removal generates a large amount of latex allergen. These particles remain airborne for up to 24 hours and travel throughout ventilation systems.[87] In addition, some common medical devices contain natural latex, including blood pressure cuffs, bulb syringes, catheters, dental coffer dams, elastic bandages, endotracheal tubes and airways, enema syringes, ventriculoperitoneal shunts, finger cots, intravenous-access injection ports, manual resuscitators, penrose surgical drains, pulse oximeters, stethoscope tubing, stretcher mattresses, tourniquets, and vascular stockings .[87]

The population at greatest risk for latex allergies includes healthcare personnel who wear latex-powdered gloves and people who have undergone multiple surgical procedures as a result of injury, disease, or chronic conditions (eg, spina bifida, genitourinary congenital defect).[87] Others at risk are those who have severe allergic reactions to certain foods such as banana, kiwi, avocado, and nuts, and individuals who are atopic.[87] Latex can cause allergic or irritant dermatitis, which can be seen several days after initial exposure or may not show up for several weeks. Allergic symptoms include rhinitis, conjunctivitis, asthma, urticaria (hives), facial edema, bronchospasm, and in some cases, anaphylaxis and death.88–90

Irritant dermatitis is a nonallergic condition that affects the skin and is usually reversible. Patients complain of dry, itchy, scaly skin, which becomes aggravated by repeated handwashing and contact with irritating alcohol-based hand sanitizer.88–90 Healthcare facilities have taken great steps to protect latex allergic patients and staff by converting to powder-free and latex-free gloves.[89] Vinyl, nitrile, polymer, and neoprene gloves have nearly replaced latex gloves for routine use in healthcare facilities and pose no risk to latex-sensitive people.[90]

Methicillin-Resistant Staphylococcus Aureus

Staphylococcus aureus (S aureus) causes both skin infections and more severe systemic blood infections. S aureus is found in hospital settings that are resistant to methicillin and other antimicrobials.91–93 Mortality is higher in hospital acquired methicillin-resistant S aureus (MRSA) infections, so efforts are underway to prevent patient infections. Between 1% and 4% of healthcare providers have MRSA colonization, which commonly occurs as a result of poor hand hygiene.[91] MRSA is a multidrug-resistant organism that is difficult to treat with typical antibiotics. MRSA can also be contracted from patients; identifying infected patients has reduced infection rates more effectively than other control efforts.[91] Humans can contract MRSA from their own nasal bacteria, or by contact with an infected person’s sore or from an asymptomatic carrier. Hands are the most common means of transmission.[93] Objects such as clothing and equipment can also be a source of infection. Workers with open wounds, those with chronic illness, and immuno-compromised individuals are more likely to contract MRSA. A recent study noted several MRSA outbreaks caused by a single healthcare provider who transmitted it to patients.[94]

There are no OSHA standards for MRSA. The CDC recommends the following control measures to prevent the spread of MRSA:

- contact precautions,

- proper hand hygiene,

- recognition of previously colonized and infected patients,

- rapid reporting of lab results, and

- the proper training of healthcare providers on control measures.[93]

Healthcare providers should only be tested if there is a persistent cluster of infections in one unit, and all other efforts to identify the source have failed.[94] Employees with staph infections can continue working in most patient care areas. However, infected employees should cover their wounds and follow normal precautions (handwashing, use of gloves, etc).

Radiation Hazards

Ionizing and nonionizing radiation are present in fixed and deployed medical, dental, and veterinary facilities. The radiation safety officer should be consulted to ensure that recommended safe exposure levels are not exceeded within these medical facilities. Distance, time, and shielding are important in determining whether healthcare workers are adequately protected. Ionizing radiation sources are used for diagnostic and therapeutic purposes. Nonionizing radiation sources are used in food preparation and germicidal treatment of room air with ultraviolet light. Refer to Chapter 22, Ionizing Radiation, and Chapter 23, Nonionizing Radiation, for a discussion of workplace controls.

Physical Hazards

Noise

Noise can be a problem in healthcare facilities when it exceeds the OSHA permissible exposure level of 85 dBA, which is an 8-hour time-weighted average. Most healthcare workers are not routinely exposed to this much noise.95–97 However, high noise levels are a problem in food service, laboratory, maintenance, and engineering facilities. Incinerator rooms, orthopedic cast rooms, administrative areas (printers), and dental clinics (high-speed hand drills) may also have high noise levels.95–97

Healthcare providers who deploy may encounter high noise levels when they retrieve patients from air evacuation aircraft and personnel carriers. Fixed- and rotary-wing aircraft, high-mobility multi-wheeled vehicles, air conditioners, and generators all produce high noise levels that range from 80 to 106 dBA. Deployed personnel who work in conditions with high noise levels have a significantly elevated risk of developing hearing loss.[98]

Musculoskeletal Strain

Lower back pain and other musculoskeletal injuries are among the most common injuries among healthcare workers and the most common reason for lost time and limited duty.99–101 Most workers are injured while lifting or transferring patients. 99–102 Healthcare workers are at increased risk of injury when they use excessive force to lift, push, pull, or transfer patients to a bed, chair, toilet, diagnostic and treatment tables, and stretchers. The risk is increased when providers do not ask for assistance or there are not enough staff to assist.99–102 Patient handling risks occur in most patient treatment areas. In addition, maintenance and housekeeping staff are at risk of injury when they perform manual material handling. They may be asked to move or lift heavy medical equipment, linen, garbage, cleaning supplies, furniture, tools, food carts, and other equipment.99–102

There are no federal ergonomic or lift standards in the United States. Both NIOSH[101] and OSHA[102] have guidelines for the safe handling of patients in health-care and nursing facilities that call for the elimination of manual patient handling.101–102 The Facility Guidelines Institute planning guide calls for one ceiling or portable lift for every 8 to 10 patients.[103] There is an excellent return on investment for lifting equipment; it pays for itself in less than 3 years.[104] Several studies have reviewed the medical evidence and reported on the efficacy of lift-assist devices for patient transfers, including total lifts, sit/stand lifts, and stand aids.105,106 Selection depends on the patient’s weight-bearing status and medical condition. Electrically powered ceiling lifts are preferable to portable floor-based lifts because they are easier to turn and need less storage space. Slide sheets with handles are effective when moving patients up in bed or transferring patients from the bed to a stretcher, and when rolling the patient from one side to another to make an occupied bed.[107]

In the deployed environment, personnel are routinely asked to set up medical treatment facilities and tents for sleeping. However, these soldiers may be impaired due to sleep deprivation, jet lag, or lack of acclimatization to altitude or temperature. They are likely also unaccustomed to the task they are asked to perform. Additionally, military healthcare personnel may be wearing body armor and a Kevlar (DuPont; Wilmington, DE) helmet, which add to the lifted weight and decrease maneuverability. Other contributing factors include understaffing, lack of regular training on proper lift procedures, inadequate safety precautions or lift-assist devices, and lack of awareness of lift-assist devices. During deployments, all personnel responsible for setting up and establishing operations of the hospital facility are at risk of sustaining back problems.[108]

The Army has implemented a program to increase awareness of back pain and strain and prevent back injury. The use of lift-assist devices has reduced manual lifting and helped Veterans Administration healthcare facilities reduce back injuries and lower Federal Employee Compensation Act costs. (Refer to Chapter 9, Federal Workers’ Compensation Programs, for more information regarding the Federal Employees Compensation Act.)

Environmental Extremes

Soldiers often face environmental extremes and austere environments during operations. Cold, heat, and altitude are encountered in all parts of the world and are still significant barriers to conducting military operations. Medical personnel typically work in environmentally controlled fixed facilities prior to deployment. Acclimatization to a new environment prevents or reduces illness or injuries in medical staff.[109]

Facilities and Medical Maintenance

Field medical operations may be conducted using tents and standard material, supplies, and equipment. Additionally, field medical operations are sometimes carried out in existing facilities (such as buildings located in the training area or area of operations) using material, supplies, and equipment found in the fixed facility. The deployed MTF must have a functioning field sanitation program. Basic services such as water, waste, electricity, and environmental control are essential.[108] The volume of solid waste and wastewater can be significant due to laundry, showers, bedpan washing, handwashing, waste from radiograph units, and disposable supplies.

Appropriate and meaningful evaluations of field MTFs can prevent morbidity and mortality, as well as preserve valuable human resources. Evaluations must be performed by knowledgeable, preventive medicine personnel who are experienced in this area.[108] When conducting a survey, specific aspects of the field sanitation program should be reviewed, including:

- the water supply (water containers and trailers), to ensure it is being monitored and properly disinfected;

- food operations, to confirm basic food sanitation guidance is being followed;

- waste disposal operations (medical and chemical waste, wastewater, and solid waste), to ensure acceptable policies are established and followed;

- arthropod and other animal-control measures, to ensure they are appropriate and adequate;

- safety and health training programs, to ensure relevance to fixed or field environments;

- WAGs, laboratory chemicals, and radiation, to ensure that potential hazards are recognized and controlled; and

- autoclave operations, to ensure sterilization procedures are adequate, and that explosive and burn hazards are controlled.

Psychosocial Hazards

Healthcare workers face a large amount of stress and pressure to meet the physical and psychological needs of patients. Healthcare workers and their supervisors must recognize when stress becomes a problem in the workplace and employ stress-management techniques. Shift work may also be a stressor, particularly when it is assigned without consulting the employee about family circumstances or other considerations.

Emotional Stress

Healthcare workers most at risk for severe emotional stress are those employed in burn units, emergency rooms, operating rooms, and intensive care units. Most emotional stress studies have focused on physicians and nurses, but laboratory and food-service workers may also be affected.110–114 Excessive stress may lead to physical or emotional exhaustion.110–114 Stress indicators in workers who demonstrate adaptive reactions include delayed gratification, compulsiveness, and expressing the need for support. These behaviors may lead to physiological and psychological problems including loss of appetite, ulcers, migraine headaches, fatigue, sleep disorders, and oversleeping. Emotional stress may also disrupt social and family life, causing apathy, in-decisiveness, and a reluctance to accept responsibility. It can also lead to more serious conditions including substance abuse, mental illness, and suicide.110–114 To address these problems, Department of Defense leadership has incorporated programs to address stress in the redeployment cycle of service members, including methods for coping with burnout, caregiver fatigue, and work-related stress.

Shift Work

Shift work is a major cause of stress in healthcare facilities, especially when the supervisor employs a rotating work schedule. Shift work disrupts the circadian rhythm and can cause fatigue due to sleep deprivation. Shift work also disrupts social and family life, which may affect the worker’s psychological health and physical well-being. There is insufficient evidence to demonstrate conclusively that shift work causes a specific illness in workers; however, shift workers have more health complaints than other workers, such as digestive problems, chest pain, wheezing, nervousness, colds, and fatigue. Studies also note an association between shift work and a higher incidence of cancer, myocardial infarction, and diabetes mellitus.[115] Generally, shift workers have lower job satisfaction and productivity, and have more subjective health complaints and personnel turnover. Workers adapt better if the shift transition is done slowly over 3 or more weeks to permit adaptation. Shift changes should be progressively later, going from day to evening and then to night shift.[115]

STRATEGIES FOR HAZARD ABATEMENT

The first step in controlling or eliminating a workplace hazard is to conduct an inventory of the hazards present in the healthcare facility. The facility safety officer should conduct a joint worksite visit with the industrial hygienist, environmental science office, and occupational health staff to identify any hazards, observe controls in place to minimize exposure, and see what, if any, protective equipment are being used to protect workers. The worksite visit should document in detail whether:

- engineering interventions are available and used to control the hazard;

- proper ventilation of the spaces is occurring if the hazard is respiratory;

- PPE is available and used by workers;

- worker training to recognize and avoid hazards has been provided;

- safe work practices are written and utilized; and

- safety and occupational health programs are enforced.

Once the hazard inventory is completed, the risks should be prioritized, and those posing the greatest hazard targeted for elimination first. Workers must be trained about the hazard and the steps necessary to prevent exposure. They need training on safe work practices and how to properly use safety equipment and PPE, including respiratory devices, to protect against toxic chemicals and other workplace hazards. Additional evaluation methods include environmental or workplace sampling and medical surveillance to assess the success of workplace controls. Guidelines for workplace hazards control are listed in Table 11-3.

TABLE 11-3

GUIDELINES FOR THE CONTROL OF HAZARDS IN HEALTHCARE FACILITIES

CDC: Centers for Disease Control and Prevention

HIV: human immunodeficiency virus

MDRO: Multidrug-resistant organisms

MERS-Cov: Middle East respiratory syndrome coronavirus

MMWR: Morbidity and Mortality Weekly Report

NIOSH: National Institute for Occupational Safety

OSHA: Occupational Safety and Health Administration

USPHS: US Public Health Service

WORKPLACE VIOLENCE

Workplace violence, which NIOSH defines as violent acts (including physical and threats of assaults) directed toward persons at work or on duty, includes harassment, intimidation, or other threatening disruptive behavior.[116] The burden of workplace violence is high: nearly two million American workers are victims of workplace violence each year,117,118 and these incidents are on the rise. It fact, homicide is the fourth-leading cause of fatal occupational injuries in the United States and the leading cause of death for women in the workplace. According to the Bureau of Labor Statistics Census of Fatal Occupational Injuries, of the 4,547 fatal workplace injuries that occurred in the United States in 2010, 506 were workplace homicides.117,118 A study of the Department of Justice’s National Crime Victimization Survey from 1993 to 1999 noted that the average annual rate for nonfatal violent crime for all occupations was 12.6 per 1,000 workers.117,118

Healthcare professionals, along with public service workers, law enforcement, and those who work alone or in small groups, are at higher risk of workplace violence. The average annual workplace violence rate for physicians is 16.2 per 1,000; for nurses, 21.9; for mental health professionals, 68.2; and 69 for mental health and custodial workers.117,118 The cost of workplace violence can be staggering, with lost production, loss of focus, and mission impact. Prevention is key; a work environment that minimizes hostility, creates a secure and physically safe workplace, provides education, and conducts early interventions is helpful in minimizing and preventing workplace violence.[119] For more information, refer to the workplace violence section of the Department of Labor’s website: https://www.osha.gov/SLTC/workplaceviolence/.

SUMMARY

This chapter reviewed common exposures and hazards present in healthcare facilities. Healthcare workers face myriad workplace exposures to chemical, biological, physical, and psychosocial hazards. The facility or unit commander, staff, supervisors, and healthcare workers all have a responsibility to participate in safety and occupational health programs designed to protect the employee and patient health at military healthcare facilities. The MTF is unique because there is greater risk of exposure to chemical and biological warfare agents and highly explosive devices. Therefore, workers require extra training and preparations to respond to casualties who have been exposed to these agents. Furthermore, new and emerging threats, such as severe acute respiratory syndrome and Ebola, require healthcare workers to stay current with new developments in biological threats. If these or similar diseases occur at their facility, workers must be aware of their risks and precautions.

This chapter dealt primarily with hazards routinely encountered in fixed US MTFs. However, the principles discussed here are equally applicable in deployed military healthcare settings. The challenge in deployed settings is that many of the engineering controls in place at US facilities are difficult to institute. However, proper screening of deploying personnel and healthcare providers should minimize or eliminate the exposure potential to many of the biological and blood-borne pathogen hazards discussed here. Protective measures for healthcare workers translate into protective measures for their patients. An ill or impaired healthcare worker can spread disease to coworkers and other service members, thus affecting the morale and health of all. The impact could adversely affect the deployed force’s fighting strength, which could be catastrophic.

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XXXX MILITARY MEDICAL CENTER
OCCUPATIONAL MEDICINE SERVICE
STANDARD OPERATING PROCEDURES

SOP Title: Blood-borne Pathogen Exposures Program

SOP No

Version 1.0

Effective Date: 17 NOVEMBER 2018

Page 1

1. Purpose: To implement an effective blood-borne pathogen (BBP) postexposure program at the XXXXXX military medical center by establishing a process to inform the workforce of the proper procedure for reporting and evaluation of blood-borne pathogen exposure incidents.

2. Scope: Applies to all workers (military, government civilians, contractors, and volunteers) with potential exposures to blood or bodily fluids.

3. Background: Healthcare workers are at risk of exposure to blood-borne pathogens such as hepatitis B (HBV), hepatitis C (HCV), and the human immunodeficiency virus (HIV). The risk of infection is decreased by completing the HBV three-shot immunization series and by following the proper procedures and utilizing the appropriate personal protective equipment with all patients. Despite these preventive measures, exposure incidents still occur. It is important to immediately report the incident and be evaluated right away. If postexposure medications are needed due to a significant HIV exposure, then it is most effective if started within 2 hours of the exposure. Nonresponders to the HBV vaccine also require HBV immune globulin following exposure to HBV.

4. Responsibilities:

a. The assistant chief of staff for public health, chair of the Public Health Advisory Committee, is the blood-borne pathogen program coordinator.

b. The occupational medicine service chief is responsible for:

1) Overseeing this program and reviewing this standard operating procedure (SOP) on an annual basis.

2) Designating a clinical provider to implement the program as the blood-borne pathogen surveillance program manager (BBP-SPM).

c. The BBP-SPM is the clinic’s primary point of contact for liaison with other departments for:

1) Annual computerized training requirements.

2) Training provided by clinic staff.

3) Working with the contracting department to ensure that contract personnel working at XXXXXX are screened appropriately by their organization.

4) Policy and procedures to ensure the timely evaluation of BBP exposures by the occupational medicine service or emergency department (ED).

5) Prompt reporting of BBP exposures to the safety office and unit supervisors.

6) Quarterly reports to the Infection Control Committee of all BBP incidents.

d. The clinic’s senior occupational health nurse will ensure the prompt evaluation of exposed employees by a clinic provider or ED if a clinic provider is not present.

e. The inpatient provider (of the source patient) is responsible for ordering source labs in the Center for Healthcare Services (CHCS)/Essentris system and ensuring the exposed employee is referred to either the occupational medicine clinic or the ED for evaluation. The source patient and employee should have baseline labs ordered and, if necessary, Infectious Disease (ID) should be consulted to assess the need for employee postexposure prophylaxis.

f. The occupational medicine service staff is responsible for the initial BBP assessment screening and education during business hours. When the occupational medicine service is closed, the exposed employee will report to the ED for evaluation and treatment. The employee will then follow up in the occupational medicine service the same day or next business day.

g. All personnel with blood and bodily fluid exposures in the eye will report directly to the ED for evaluation and treatment; follow up in occupational medicine same day or next business day.

5. Policy: The occupational medicine service will assist the XXXXXX staff to work in a safe and healthy workplace by the proactive implementation of federal, military, and professional guidance regarding the reduction of risk for BBP exposures at XXXXXX.

6. Procedures:

a. The occupational medicine service staff schedules the worker, performs the initial assessment screen, and orders baseline postexposure labs for the exposed employee. The following steps will be performed in a timely fashion at the direction of the senior occupational health nurse when an employee presents to the occupational medicine service after a BBP incident:

1) Determine if an occupational medicine provider is available in the clinic; otherwise a referral by (telephone) phone ___-___-____ to the XXXXXX ED will be made. The exposed employee will be escorted with a direct transfer to the nursing staff of the ED.

2) If seen by the occupational medicine service: entry into GENESIS with vital signs and a 15-minute observed wash of the exposure site (if indicated) as the occupational medicine provider is notified.

3) The location of the exposure source will be identified and contact made with the supervisor to ensure the source remains in the hospital. This will allow the supervisor and/or the occupational medicine service to attain informed consent for the collection of source laboratory studies.

b. The clinic’s designated occupational medicine provider is responsible for appropriate care and a follow-up plan for BBP exposures:

1) Incidents reports by either online or hard copy are forwarded to XXXXXX safety as soon as possible.

2) If the source is inpatient, labs (HIV Rapid, Hep BsAG (hepatitis B surface antigen) and Hep C AB (hepatitis C antibody) must be ordered in Essentris using order set: bbpexp-source. If the source is outpatient, labs must be ordered in CHCS using order set: bbpexp-source.

3) For the exposed employee, postexposure baseline labs (HIV, Hep B sAG, Hep B sAB, Hep C AB and alanine aminotransferase (ALT) must be ordered in CHCS using order set: bbpexp. In Essentris it is: bbpexp-exposed.

4) The occupational medicine provider refers the exposed employee depending on review of all labs (exposed and source):

a) HBV – depending on vaccination status of the exposed employee and immune status of source, hepatitis B immune globulin (HBIG) and/or vaccine may be indicated.

b) HIV – if source Rapid is positive or source is known to have HIV, then refer exposed employee to infectious disease.

c) HCV – if source positive with/without elevated liver function tests (LFTs), refer to gastroenterology.

d) Refer pregnant women to obstetrics (especially in the case where source may have positive labs and the exposed employee may require treatment (HBIG, HIV prophylaxis).

e) Determine tetanus, diphtheria, and acellular pertussis vaccine (Tdap) status in accordance with the Centers for Disease Control and Prevention (CDC) recommendations.

5) Another resource is the National Clinicians’ Postexposure Prophylaxis Hotline (PEPline) through the University of California, San Francisco, School of Medicine National Clinicians’ Postexposure Prophylaxis Hotline; 24/7 telephone number: 1-888-448-4911. http://www.nccc.ucsf.edu/

6) Employees who would benefit from HIV postexposure prophylaxis will be escorted to the ID (infectious disease) clinic and a walk-in consult will be made to the on-call attending physician.

7) The treating occupational medicine provider will ensure the BBP-SPM is notified and provided the appropriate clinical records for reporting and clinical follow-up.

c. The BBP-SPM is responsible for the reporting, follow-up, and tracking of exposed personnel. Refer to Tables 1 and 2.

1) A physician’s written opinion compatible with OSHA, service, and local guidance will be provided to the exposed employee as soon as appropriate.

2) The BBP-SPM will complete follow-up visits and make appropriate tracking entries in AHLTA and local database.

3) Quarterly summaries of all exposures will be reported to the XXXXXX Infection Control Committee. This report will include data on XXXXXX and tenant command personnel receiving occupational health services at the XXXXXX occupational health center (OHC) for BBP exposures both onsite and offsite in the course of their duties.

7. Explanation of Abbreviations and Terms:

AG

antigen

ALT

alanine aminotransferase

AR

Department of the Army Regulation

BBP

blood-borne pathogens

BBP-SPM

blood-borne pathogen surveillance program manager

BUMED

Navy Bureau of Medicine and Surgery

CDC

Centers for Disease Control and Prevention

CFR

Code of Federal Regulations

CHCS

Center for Healthcare Services

DoD

Department of Defense

DODI

Department of Defense Instruction

GENESIS

The DoD electronic health record (formerly AHLTA)

HBIG

hepatitis B immune globulin

HBsAg

hepatitis B surface antigen

HBV

hepatitis B virus

HCV

hepatitis C virus

Hep B sAB

hepatitis B surface antibody

Hep C AB

hepatitis C antibody

HIV

human immunodeficiency virus

ID

infectious disease

INST

instruction

LFT

liver function test

MMWR

Morbidity and Mortality Weekly Report

NMCPHC-TM

Navy and Marine Corps Public Health Center Technical Manual

OASD

office of the assistant secretary of defense

OHC

occupational health center

OSHA

Occupational Safety and Health Administration

PEPline

postexposure prophylaxis hotline

PWO

physician’s written opinion

SOP

standard operating procedure

Tdap

tetanus, diphtheria, and acellular pertussis vaccine

USPHS

United States Public Health Service

8. Tables:
TABLE 1. FOLLOW-UP OF WORKERS FOR HIV AND HCV EXPOSURES

Test

Known Positive or Positive Risk Factor

Known Negative

Unknown

HIV

6 wk, & 4 mo

None

6 wk, & 4 mo

LFT, HCV, RNA

6 wk, 3 & 6 mo
Perform at 6 wk, 3 mo; AB at 6 mo

None

6 wk, 3 & 6 mo

TABLE 2. SCREENING FOR HEPATITIS B POSTEXPOSURE PROPHYLAXIS

Vaccination and/or Antibody Response Status of Exposed Person^1

Treatment When Source Patient is:

HBsAg^2 Positive

HBsAg^2 Negative

Source Unknown or Not Available for Testing

Unvaccinated^3

HBIG^4 ×1; initiate HBV^5 vaccine series

Initiate HBV vaccine series

Initiate HBV vaccine series

Previously vaccinated

Known responder^6

No treatment

No treatment

No treatment

Known nonresponder^7

HBIG^4 ×1 and initiate revaccination^8 or HBIG ×2

No treatment

If known high-risk source, then treat as if source were HBsAg positive

Antibody response unknown

Test exposed person for antibody to HBsAg

1. If adequate Ab to HBsAg^6 no treatment needed

2. If inadequate Ab to HBsAg^7, give HBIG X1 & vaccine booster

No treatment

Test exposed person for antibody to HBsAg

1. If adequate Ab to HBsAg no treatment needed

2. If inadequate Ab to HBsAg, give booster & ck titer in 1-2 mo

Notes

1Persons who have previously been infected with HBV are immune to reinfection and do not require postexposure prophylaxis.

2HBV surface antigen

3People who have not yet received all three HBV shots should get HBIG and complete the series.

4HBV immune globulin; dose is 0.06 ml/Kg intramuscularly.

5HBV vaccination includes three shots of HBV vaccine.

6A responder is a person with adequate levels of serum antibody to HBsAg with antiHBs > 10mIU/mL.

7A nonresponder is a person with inadequate antibody response to vaccination, ie serum anti-HBsAg < 10 mIU/mL.

8The option to give one dose of HBIG and reinitiate the vaccine series is preferred for nonresponders who have not completed a second three-dose vaccine series. Two doses of HBIG are preferred for persons who previously completed a second three-dose vaccine series but failed to respond.

9. References:

Regulation/Citation

Document Title

29 CFR 1910.1030 OSHA

29 Code of Federal Regulations; Blood-borne pathogens
http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=standards&p_id=10051.

USPHS (2013)

Updated US Public Health Service guidelines for the management of occupational exposures to human immunodeficiency virus and recommendations for postexposure prophylaxis. Infect Control and Hosp Epidemiol. 2013. Sep 34(9):875-892.

USPHS (CDC)

Updated US Public Health Service Guidelines for the Management of Occupational Exposures to HBV, HCV, and HIV and Recommendations for Postexposure Prophylaxis. MMWR Recomm Rep. 2001 Jun 29;50(RR11);1-42. (www.cdc.gov).

USPHS (CDC)

Updated recommendations for use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis (Tdap) vaccine from the Advisory Committee on Immunization Practices, 2010, MMWR January 14, 2011 / 60(01);13–15.

http://www.cdc.gov/mmwr/preview/
mmwrhtml/mm6001a4.htm.

DoD

OASD Policy. Hepatitis B Immunization Policy for Department of Defense Medical and Dental Policy. 23 Oct 96.

DODI 6055.05-M

Occupational Medical Examinations and Surveillance. Table C2.T14, Blood borne Pathogens.

AR 40-501

Standards of Medical Fitness.

AR 40-501 BUMEDINST 6230.15.

Joint Instruction Immunizations and Chemoprophylaxis 29 SEP 2006.

BUMEDINST 6220.14

Bloodborne Pathogen Control Program.

NMCPHC-TM OM 6260

Medical Surveillance Procedures Manual and OEM Medical Matrix 11th Edition November 2010, NMCPHC-TM OM 6260.

NMCPHC-TM-OEM 6260.7

Bloodborne Pathogen Exposure Control Manual
Navy and Marine Corps Public Health Center
Technical Manual NMCPHC-TM-OEM 6260.7
November 2010.

NNMCINST 6220.5G

NNMC Infection and Control Program.

HIV Prophylaxis Following Occupational Exposure: Guideline and Commentary; Barry S. Zingman; January 30, 2013.

NNMC

Infection Control Manual.

HIV Prophylaxis Following Occupational Exposure: Guideline and Commentary; Barry S. Zingman, MD; January 30, 2013.

Chapter 12

ARMY HEARING PROGRAM

DOUG W. OHLIN, PhD*; SHARON L. BEAMER, AuD, CCC-A†; and MARJORIE GRANTHAM, PhD‡

INTRODUCTION

HEARING ANATOMY AND PHYSIOLOGY

NOISE-INDUCED HEARING LOSS

Mechanisms

Susceptibility

Ultrasound and High Frequency Exposures

Ototoxins

TINNITUS

INCIDENCE OF HEARING LOSS IN THE ARMY

PREVENTING NOISE-INDUCED HEARING LOSS

Garrison-Based Hearing Conservation Programs

Noise Hazard Evaluation

Engineering Controls

Hearing Protection

Monitoring Audiometry

Health Education

Program Evaluation

IMPROVING HEARING LOSS PREVENTION EFFORTS

Department of Defense Hearing Center of Excellence

Mission-Critical Hearing Studies

Expanded Program Components

HEARING CONSERVATION ON THE BATTLEFIELD

Sound Localization

Sound Identification

SUMMARY

*Formerly, Chief, Hearing Conservation Program, US Army Center for Health Promotion and Preventive Medicine, Aberdeen Proving Ground, Maryland 21010; Deceased

†Program Analyst, Navy Bureau of Medicine and Surgery, 7700 Arlington Boulevard, Falls Church, Virginia 22042

‡Colonel (Retired), US Army; Technical Science Writer, Ho-Chunk Technical Solutions, Austin, Texas 78723

INTRODUCTION

For nearly 70 years, the US Army has been involved in efforts to identify noise hazards in the military work environment and to protect soldiers and civilian workers from the harmful effects of noise hazards. These efforts have evolved over the years as the disciplines of audiology, hearing science, bioacoustics, psycho-acoustics, and acoustical engineering have matured, and as more has been learned about the mechanisms of noise-induced hearing loss (NIHL).1–3 The advent of key legislation, such as the incorporation of the Walsh-Healy Public Contracts Act, Noise Standard (1969), in the Occupational Safety and Health Act (OSHA)[4] of 1970, and the development of military documents that paralleled the federal regulations, played a pivotal role in the development of Army hearing conservation programs.

As early as 1941, researchers at Fort Knox, Tennessee, investigated the effects of noise on personnel efficiency and the cause of temporary hearing loss associated with tank noise. By 1944, the researchers made a recommendation that personnel regularly exposed to gunfire, such as gun crews, be provided hearing protection.[5] As a result, the Army procured a single-flanged earplug to be issued to those who required hearing protection in World War II.

Under the direction of the Army, the Industrial Hygiene Agency, based at Johns Hopkins University in Baltimore, Maryland, maintained an emphasis on noise hazard identification and hearing conservation for the military and private sector, which continued for 27 years. Over the course of 2 decades, from the 1940s through the 1960s, the work of the Industrial Hygiene Agency expanded. The agency was relocated to Aberdeen Proving Ground, Maryland, and, by the late 1950s, was renamed the US Army Environmental Hygiene Agency. In 1969, the establishment of the Bio-Acoustics Division, which included audiology, broadened the scope of hearing conservation efforts from the noise-identification approach of industrial hygiene to a focus on medical and engineering approaches to hearing loss prevention.

In addition to the Bio-Acoustics Division, research facilities such as the US Army Aeromedical Research Laboratory at Fort Rucker, Alabama, and the Human Engineering Laboratory at Aberdeen Proving Ground emerged to investigate hearing loss from noise as well as hearing protective equipment, sound detection, and the effects of noise on mission performance. The development of military hearing conservation programs can also be linked to the creation of several key documents, including Department of Defense Instruction 6055.12, Hearing Conservation,[6] in 1987, and Department of the Army Pamphlet (DA PAM) 40-501, Hearing Conservation,[7] in 1991. These documents have been updated over time8–10 and continue to guide hearing conservation activities in the Army.

This chapter addresses the nature of NIHL and misconceptions associated with it, as well as the salient features of an effective hearing conservation program and the role of the Army Hearing Program. Also discussed are tinnitus, ototoxins, and sound identification in combat, as well as strategies for communicating to individuals, hearing program personnel, and commanders the importance of good hearing in the context of training and, ultimately, in combat.

HEARING ANATOMY AND PHYSIOLOGY

A brief review of hearing anatomy, with an emphasis on the inner ear and focused on the site of lesion from hazardous noise, will provide basic terminology for subsequent discussion of NIHL. (This section provides a limited discussion of the anatomical correlates and complex physiological processes underlying NIHL. The reader is referred to numerous references on hearing anatomy, including the chapter 7 in the 1993 edition of this Textbook of Military Medicine[11] for a detailed treatment of the topic.)

Anatomical illustrations and explanations of the hearing mechanism begin with the anatomical divisions of the outer, middle, and inner ear (Figure 12-1). Acoustic energy (in the outer ear) is converted to mechanical energy (in the middle ear), and, finally, the hydraulic energy transmitted into the inner ear results in a chemo-electric impulse, which is transmitted to the brain.

The layperson’s knowledge of the anatomy of the hearing mechanism usually does not extend beyond the eardrum (tympanic membrane). As a result, hearing problems are sometimes associated with outer ear components. Misconceptions abound that loud noise can build up extra layers of skin on the eardrums, and the ears can be toughened to withstand noise damage. Hearing loss involving the outer ear may be attributed to the build-up of ear wax (cerumen) or to eardrum perforation but, because most disorders of the outer ear are medically treatable, the implication is that NIHL is also treatable and reversible. The phenomenon of temporary threshold shift (TTS), that is, a temporary hearing change that recovers with time, also contributes to this notion. When hearing “bounces back,” an individual may believe the false notion that no damage was done and that hearing will always come back. Even when anatomical knowledge extends beyond the eardrum, there is a potential for misunderstanding that the hair cells in the inner ear can be restored to normal functioning.

Figure 12-1. The human ear.
Drawing courtesy of National Institutes of Health Medical Arts Branch.

Noise-exposed personnel need to know that the 25,000 to 30,000 hair cells in the inner ear are systematically destroyed by loud noise, resulting in diminished hearing sensitivity and acuity (Figure 12-2). Once these cells are destroyed, it is not a reversible condition. In addition, personnel must understand that this damage may not necessarily be associated with pain. The fact that hearing loss is a relatively painless, bloodless, and unseen process is one of the greatest risk communication challenges for the occupational health professional.

Hearing anatomy and hearing physiology influence the relationships between the intensity and spectrum of noise exposures, hearing loss at different frequencies, and the resulting inner ear hair cell damage. For instance, although the hair cells in the inner ear are arranged in a tonotopic manner (high frequencies are in the base of the cochlea and low frequencies in the apex), noise exposures to broadband stimuli do not cause equal damage in the ear at all of the frequencies present in the stimuli. Nor do they inflict damage equally across the basilar membrane in the cochlea, in the inner ear. Maximum hearing shifts occur between 3,000 and 6,000 Hz, with most shifts represented by a 4,000-Hz notch, or area of greatest hearing damage. The following explanations for the 4,000-Hz notch have been proposed: (a) the 4,000-Hz region of the basilar membrane has the poorest blood supply; (b) mechanical forces and stresses are greatest in this area of the cochlea; (c) the acoustic reflex (of the middle ear) is not effective at the higher frequencies (over 1,000 Hz); and (d) the shape and length of the ear canal affects gain at 2,000 to 4,000 Hz.11,12

Figure 12-2. Scanning electron micrographs of the normal (a) and damaged (b) cochlear sensory epithelium. In the normal cochlea, the stereocilia of a single row of inner hair cells (IHCs) and three rows of outer hair cells (OHCs) are present in an orderly array. Damage to the cochlea, such as exposure to loud noise, will result in missing and abnormal hair cells. Micrographs are courtesy of Elizabeth M. Keithley, PhD. Reproduced with permission from: Ryan AF. Protection of auditory receptors and neurons: Evidence for interactive damage. Proc Natl Acad Sci 2000;97(13): doi: 10.1073/pnas.97.13.6939.
http://www.pnas.org/content/97/13/6939.figures-only. Accessed December 13, 2017.

The acoustic reflex referred to in explanation c is one of the physiological processes that can have a diminishing effect on the acoustic energy reaching the inner ear. The anatomical mechanisms involved in the acoustic reflex are two muscles, the stapedius and the tensor tympani, that contract reflexively to sound. Together they stiffen the middle ear system, that is, the middle ear bones (ossicles) and the eardrum, and impede the transmission of lower frequencies to the inner ear. The value of the middle ear reflex as a protective mechanism is often diminished because it fatigues rapidly; it is sensitive to the lower frequencies; and its latency (50–100 ms) is too slow to protect hearing from impulse noise. Its protective role may be more significant for anticipated impulse noise exposures.[13]

NIHL is permanent. It can occur gradually after repeated exposures to noise or after a single unprotected exposure, such as weapons fire or an improvised explosive device (IED) blast. Individuals who experience NIHL may initially be unaware of the damage to the ear. Typically no pain or physical symptoms are associated with the onset of NIHL. In the early stages of the NIHL, low frequency hearing remains intact while high frequencies (above 2,000 Hz) are typically affected. Initial symptoms, such as difficulty communicating in background noise, may be subtle but will impact work performance near aircraft, weapons fire, or industrial operations.

The difference between NIHL as an occupational illness and as acoustic trauma has implications for the mode of damage, time of onset, and audiometric configuration, as well as the condition’s status as a federally reportable medical event. NIHL as an occupational illness is a relatively slow process involving TTSs, which may eventually become permanent. A TTS reaches its maximum at the cessation of the noise exposure, then recovers from that point on. The mode of damage is metabolic. In simple terms, the cochlea is overdriven and cells are poisoned by the resulting cellular waste products.[14]

Acoustic trauma is the result of an explosion or high-level impulse noise, sometimes from a single exposure but more often the result of multiple impulses. IEDs have produced some of the most recent cases of acoustic trauma in deployed combat actions. The discharge of shoulder-fired rockets (Figure 12-3) without hearing protection can produce similar results during training in garrison or in forward deployments. While TTSs may also be present in cases of acoustic trauma, this type of TTS usually increases after cessation exposure, eventually reaching asymptote before recovery begins.

Figure 12-3. Impulse noise exposures of shoulder-fired rockets can inflict significant hearing damage from only one firing. US Marine Corps photo by Lance Corporal Robert D. Williams Jr.

Depending on the level of exposure, the TTS from impulse noise (weapons fire and explosions) may result in more significant auditory problems. The mode of impulse noise damage is mechanical. Inner ear hair cells and supporting cells are torn from their structural supports. Acoustic trauma usually presents as unilateral hearing loss, that is, more pronounced in one ear. For example, when a right-handed shooter fires a rifle, the head shadow effect attenuates the more hazardous, high-frequency components, and the right ear is more protected, while the left ear, closest to the blast energy, sustains the greatest hearing damage.

There are differences in how hearing loss is reported as an occupational illness and as acoustic trauma. A significant threshold shift (STS) is a 10-dB or more average hearing shift at 2,000, 3,000, and 4,000 Hz from the baseline, in either ear, without correction for age. An STS is federally reportable when the thresholds at those frequencies exceed a 25-dB average hearing threshold level. Although hearing loss as an occupational illness and as acoustic trauma have the same quantitative criterion, different reporting mechanisms (forms) are used to report acoustic trauma and hearing loss for civilian personnel. Military personnel use the same form for both types of hearing loss, but a different form than used by civilians.

NOISE-INDUCED HEARING LOSS

Mechanisms

The effects of noise on the auditory system have been well documented in the past several years. Noise changes the structure and function of the auditory system through mechanical and metabolic processes, resulting in NIHL. It is the delicate structures of the inner ear, or cochlea, that are most affected by hazardous noise. The organ of Corti (Figure 12-4), located in the cochlea, is the key organ of hearing and contains the hair cells, or stereocilia, which are particularly vulnerable to the effects of noise. When the stereocilia become damaged to the point that they can no longer repair themselves, cell death occurs. The mechanism for hair cell death can be through apoptosis, in which the cell nucleus condenses and results in the shrinking of the cell wall, or necrosis, where the cell and nucleus swell, causing the cell membrane to break down.[14]

Figure 12-4. This illustration depicts the structures in the organ of Corti.
Illustration available through Creative Commons. Author: Madhero88. File: Organ of corti.svg. March 12, 2017. Wikimedia Commons, the free media repository. https://commons.wikimedia.org/w/index.php?title=File:Organ_of_corti.svg&oldid=236859964. Accessed November 15, 2017.

Intense acoustic energy, such as from a gunshot or a blast, can cause the hair cells to be torn from their supporting structures. The metabolic stress from the damage to hair cells can also release toxic molecules that, although a normal byproduct of cell energy production, affect the antioxidative properties of the cell when produced in large quantities. This oxidative stress can then lead to necrotic cell death. Hair cell death can occur within minutes of noise exposure and progresses rapidly, making early intervention to prevent damage to the hair cells crucial.14–19 Knowledge about the nature of hair cell death is important, and potential treatments and prevention measures are being studied and developed.20,21

Susceptibility

Soldiers go to war with the hearing they have at the time, which is not always the hearing they had when they joined the Army. In 2015, 10% of discharges for conditions existing prior to service were for hearing loss. Between 2010 and 2014, Army inductees were granted more waivers for hearing loss at the time of enlistment than inductees in the other services.[22] The Army and Marine Corps granted the most waivers for hearing loss (3.5% and 2.2%, respectively), followed by the Navy, at 1.2%, and the Air Force, with less than 1% of requests for hearing loss waivers granted.[21] Acceptance of such hearing loss speaks volumes about the challenges facing occupational health professionals in the implementation of Army hearing conservation programs. Recent studies, for example, have shown that individuals with hearing loss at the time of entering the military are up to 8 times more likely to require a disability exam for hearing loss upon leaving service.[23]

There is marked variability in hearing threshold changes following noise exposure among individuals with the same noise exposure history.[24] This variability makes it challenging to apply damage-risk criteria to prevent NIHL. An understanding of what makes some soldiers more susceptible to NIHL would allow the Army to more effectively counsel enlistees about career decisions, intensify and target hearing conservation efforts to more susceptible individuals, and more frequently monitor hearing thresholds of those most susceptible. Risk factors for increased susceptibility to NIHL range from anatomical differences and genetic factors25–27 to environmental factors, such as the use of ototoxic drugs and exposure to chemical solvents,28–31 heat,[32] and vibration.[33]

Ultrasonic and High Frequency Exposures

Exposure criteria for high frequency and ultrasonic noise are included in DA Pam 40-501, Army Hearing Program.[10] The Army has adopted the exposure criteria recommendations of the American Council of Governmental Industrial Hygienists.[34] Ultrasonic exposures are rare, yet the resulting damage, as noted earlier, is not limited. Ultrasonic noise is defined in DA-PAM 40-501 as “sound above the normal range of audibility for the human ear, although subharmonics of ultrasonic noise may be audible.”[10] Although ultrasonic sound may not be heard, there is still potential for hearing loss and other possible effects on health.

Ototoxins

Inhalation exposure to some chemicals may cause hearing loss, independent of noise exposure. Additionally, some chemicals may not cause hearing loss independently but may exacerbate NIHL.[34] Certain chemical substances have shown ototoxic effects at high airborne exposure levels but may not be ototoxic in the concentrations observed in typical occupational settings. Some potential ototoxic chemicals (eg, toluene, xylene, n-hexane, organic tin, carbon disulfide, mercury, organic lead, hydrogen cyanide, diesel fuel, kerosene fuel, jet fuel, JP-8 fuel, organophosphate pesticides, chemical warfare nerve agents) may be absorbed through the skin, which may significantly contribute to the systemic dose if dermal exposures are not properly controlled.[35]

Because the exposure threshold for such ototoxic effects is generally not known, audiometric monitoring is necessary to determine whether the substance is damaging the hearing of exposed workers. While audiometric data are useful for any worker exposed to any measurable level of a potential ototoxic chemical, yearly audiograms are highly recommended for workers whose airborne exposures, without regard to respiratory protection worn, are at 50% or more of the occupational exposure limit (which is more stringent than the Occupational Safety and Health Administration permissible exposure limit or American Conference of Governmental Industrial Hygienists threshold limit value) for the substance in question, regardless of the noise level.[34] The 50% action level, although somewhat arbitrary, ensures the collection of data from exposures below the occupational exposure limit. If there are dermal exposures to toluene, xylene, n-hexane, organic tin, carbon disulfide, mercury, organic lead, hydrogen cyanide, diesel fuel, kerosene fuel, jet fuel, JP-8 fuel, organophosphate pesticides, or chemical warfare nerve agents, where such exposures may result in a systemic dose equivalent to 50% or more of the occupational exposure limit, yearly audiograms are also recommended.

If a worker is currently participating in a hearing conservation program due to excessive noise, the reviewers of the audiometric data should be alert to possible additive or synergistic effects between the noise exposure and the chemical substance and, if necessary, suggest reducing the exposure to one or both. The exposure level and known nature of the ototoxin should be entered in the comment sections of Defense Department (DD) forms 2215, Reference Audiogram, and 2216, Hearing Conservation Data.

Activities where noise and ototoxins often combine include:

- painting

- printing

- boat building

- construction

- furniture making

- manufacturing of metal, leather, and petroleum products

- fueling vehicles and aircraft

- firefighting

- weapons firing

Table 12-1 shows the prevalence of ototoxins at US Army facilities.

TABLE 12-1

POTENTIAL OTOTOXIC CHEMICALS IN THE OCCUPATIONAL ENVIRONMENT

Hazard

Count of US Army Worksite Occurrences

No. of US Army Installations Represented in Worksite Counts

Acrylonitrile

16

8

Arsenic

86

19

Carbon disulfide

9

3

Carbon monoxide

9,393

316

Chemical warfare agents

2,494

15

Cyanide

68

46

Ethyl benzene

475

57

Fuels

1,675

36

Heptane

190

7

Mercury compounds

11

7

Manganese

349

46

Methyl ethyl ketone

592

52

n-Hexane

457

43

Organic tin (Sn)

19

3

Organophosphate pesticides

3

2

Paraquat

1

1

Lead compounds

1,798

71

Perchloroethylene

103

25

Stoddard solvent

650

49

Styrene

85

27

Toluene

1,303

64

Trichloroethylene

126

28

Xylene

1,076

63

Reproduced from: US Army Public Health Command. Occupational Ototoxins (Ear Poisons) and Hearing Loss. Factsheet 51-002-0713. https://usaphc.amedd.army.mil/PHC%20Resource%20Library/Ototoxin_FS_51-002-0713.pdf. Accessed January 30, 2017.

TINNITUS

Communication limitations and social isolation are only part of the suffering endured because of NIHL. Many individuals experience an accompanying condition called tinnitus. Some individuals report tinnitus to be more debilitating than the hearing loss itself. The consequences of tinnitus can be a stronger motivator for wearing hearing protection than any resulting hearing loss.

For some, tinnitus is a buzzing, roaring, or rushing sound in their ears. For those with NIHL, tinnitus is usually a chronic high-pitched ringing or hissing sensation. In this discussion, tinnitus is defined as “the perception of a sound that results exclusively from the activity within the nervous system without any corresponding mechanical, vibrating activity within the cochlea.”[36]

Most people have experienced a transient ringing in the ears. Of the estimated 40 million Americans with hearing loss, however, 10 million also suffer from tinnitus.[37] Since 2002, tinnitus has been the most prevalent Department of Veterans Affairs (VA) service-connected disability among all new compensation cases. Individuals exhibit a range of reactions to tinnitus. Although tinnitus does not cause hearing loss, it can interfere with concentration, sleep quality, and attention span. Depression and insomnia have been linked to both tinnitus severity and loudness.38,39

A hearing conservation consideration for those with tinnitus is the increased awareness of tinnitus when hearing protectors are fitted in quiet surroundings such as a clinic or audiometric test booth. The complaint is that hearing protectors made their ringing worse. This is one consequence of blocking the ear canal. When external sound is blocked or significantly attenuated, sounds inside the head seem louder. Counseling should reassure the individual that the hearing protectors merely enable them to hear their tinnitus better in a quiet setting, not in the noise-hazardous work or training environment. Hearing protectors do not make tinnitus worse. Once back in the workplace, background noise may mask the tinnitus. Although there are no guarantees that the tinnitus will eventually go away, it is important to counsel patients on the possibility that failing to use hearing protectors in hazardous noise levels may result in tinnitus becoming worse.

Tinnitus must also be factored into the medical surveillance element of hearing conservation programs. Audiometers in the Defense Occupational and Environmental Health Readiness System–Hearing Conservation (DOEHRS-HC) application are defaulted to a pulsed tone mode. Pulsed tones accommodate those in the program who already have some degree of tinnitus. The pulsed tone makes it easier to separate tinnitus from the audiometer test tones for a more reliable and accurate hearing evaluation.

Tinnitus is known to be associated with cochlear damage in the inner ear. Animal studies have shown changes in the tonotopic characteristics of the cochlea from noise exposure.40,41 A resulting increase in firing of the brain’s auditory centers is the mostly likely mechanism for noise-induced tinnitus.40–46 For counseling purposes, when workers experience tinnitus following unprotected, hazardous noise exposure, they have probably incurred damage to the inner ear.

Excision of the cochlea or a section of the auditory nerve are radical treatments that provide only short-term relief of tinnitus.47,48 The tinnitus eventually returns, sometimes worse than before, along with other complications such as loss of balance or complete loss of hearing in that ear. If the tinnitus persists despite such radical interventions, then what is the recommended course of treatment? The short answer is that chronic, noise-induced tinnitus is not treatable, but management strategies are available that may help control reactions to tinnitus. Tinnitus treatment programs include individual or group counseling, with goals such as making the tinnitus less noticeable or bothersome. For individuals with hearing loss and tinnitus, hearing aids that allow the listener to hear speech and environmental sounds better may make tinnitus less noticeable. Sound generators that produce gentle, repetitive, soothing sounds such as waterfalls or soft music can be also be used to assist with relaxation. Some sound generators can be worn in the ear and resemble a hearing aid in appearance, producing gentle sounds such as a hissing noise. Because each person’s experience with tinnitus is different, treatments programs should be customized for the individual sufferer.

INCIDENCE OF HEARING LOSS IN THE ARMY

Determining the true extent of NIHL in the military has proven to be a challenge. In the early days of hearing loss prevention, estimations of the extent of NIHL in the Army were based on a 1975 hearing loss prevalence study,[49] hearing loss data from the Army’s Hearing Evaluation Automated Registry System, and compensation expenditure statistics from the VA and Department of Labor. The 1975 study reported that over 50% of soldiers in combat arms occupational specialties with more than 15 years of service experienced significant hearing loss, and most of these soldiers were not assigned a physical profile appropriate for their degree of hearing loss.[49] These metrics, however, did not provide a prospective, longitudinal approach to examining the incidence of NIHL in the Army, so a more epidemiological approach was pursued to improve the data’s quality and consistency.[50]

Currently, epidemiological data are used to determine the incidence of NIHL and tinnitus in the military. The Armed Forces Health Surveillance Center maintains a central repository of inpatient and outpatient medical encounters used for disease and injury surveillance of US military personnel.[51] A key set of International Classification of Disease (ICD-9-CM) codes that reflect NIHL and other auditory injuries are being examined by the center’s staff to estimate the extent of noise-induced hearing injuries. The ongoing analysis of this data will be used to monitor the effectiveness of hearing conservation progress and drive performance improvement of the programs.

Adopting a more outcomes-focused approach to determining causes and analyzing prevention efforts will translate into more effective hearing loss prevention programs. If unanticipated changes in hearing injury occur, for example, an increase in hearing loss injury rates, the information can be used to inform intervention strategies. Prevention strategies include hearing health education, noise hazards risk communication, engineering controls for noisy equipment, and deployment of hearing protection devices (HPDs) that are more suited for the type of noise exposure. This “public health process” is very different from past risk management strategies, in which data were used to predict the likelihood of hearing loss occurrence and determine the severity of injuries, but not to address intervention strategies.52–54

The US Army Active Duty Noise-Induced Hearing Injury Summary, Calendar Years 2007 to 2011,[55] shows a stable sensorineural hearing loss (SNHL) rate over the 5-year period studied. This is compared to a slight, but statistically insignificant, decline in noise-induced hearing injury (NIHI) during the same period. The report also noted an overall STS rate increase between 2007 and 2011, as well as an increase in tinnitus. Although slight declines in STS and tinnitus in 2008 and 2010 were noted, the changes were not considered to be statistically significant. In earlier studies, authors advised caution in interpreting NIHL data, however, because clinicians tend to medically code hearing loss as SNHL rather than NIHL.56,57 Despite continued problems with coding NIHI, if the reduction in NIHI from 2007 to 2011 had been significant, the data could have been used as an indicator of performance change.

This study was the initial venture into the use of NIHI surveillance data for informing performance improvement. It has produced information now being utilized by leaders and decision-makers to improve Army hearing loss prevention. For example, the data analysis has informed increased momentum for improvements in HPDs for specific noise hazards as well as the deployment of mission-specific hearing protectors on a large scale, increased awareness of noise hazards through enhanced health communication strategies being developed at the Office of The Surgeon General level, and increased efforts to elevate hearing conservation and readiness needs as reportable metrics during command safety inspections. More actionable and robust surveillance information will continue to emerge as the quality of the surveillance data improves through more exact coding of NIHI.

The VA provides data, on an annual basis, on compensation and pension expenditures. This data is reported in terms of number of new claims, overall claims, and expenditures for compensation. For many years, hearing loss and tinnitus have remained the two most prevalent compensable service-connected disabilities reported by the VA. By the end of 2012, over 970,000 veterans had a service-connected disability for hearing loss, and over 774,000 had received compensation for tinnitus.[58] A closer look at VA data shows that hearing loss and tinnitus are the two most prevalent disabilities for veterans from World War II, the Korean War, Vietnam, and during peacetime. Tinnitus is number one, and hearing loss is number eight, for Persian Gulf War veterans. For Army veterans, there was a 39% increase in new hearing loss compensation cases between 2007 and 2012, and a staggering 75% increase in new tinnitus compensation claims during the same time. In addition to monetary compensation, there are additional expenditures for hearing prosthetics devices, such as hearing aids, used to treat hearing loss. For example, in 2011 the VA issued over 596,000 hearing aids for a net procurement of $221 million.[59]

In addition, researchers from the National Center for Rehabilitative Auditory Research noted that 11.7% of veterans reported tinnitus, compared to 5.4% of their non-veteran counterparts.[58] Compensation for hearing loss through the VA has steadily risen over the past three decades, with nearly $1 billion in compensation for auditory-related conditions reached by 2005.58–60

PREVENTING NOISE-INDUCED HEARING LOSS

Garrison-Based Hearing Conservation Programs

Most NIHL occurs in training and, to a lesser extent, in combat. Over a military career, a soldier spends considerably less time in combat firefights than training in garrison. Soldiers can lose more hearing from one unprotected firing exercise than from years of listening to loud music. Noise is generally defined as unwanted sound. Hearing conservation programs are designed to protect and preserve the ability to hear wanted sounds vital to maintaining situational awareness and effective communication. Guidance and requirements for implementing a hearing loss prevention program are in DA Pam 40-501.

A comprehensive hearing conservation program includes the following program elements:

- noise hazard evaluation (and posting of signs and decals)

- engineering and administrative controls

- HPDs

- monitoring audiometry

- health education

- command emphasis and enforcement

- program evaluation

Recordkeeping and audiometric follow-up are important functions that should be incorporated in the elements listed. Most hearing conservation professionals acknowledge the need for all of these elements, but their individual specialties often determine which aspect of the program is emphasized; for example, industrial hygienists may focus on noise hazard evaluation. However, a singular focus on noise hazards alone may have consequences for overall program success, perhaps leading to the removal of individuals from the education, monitoring, and hearing protector aspects of the program, or employing the most lenient exposure criteria. Sometimes emphasis is placed on preventing hearing loss claims rather than preventing hearing loss. A numbers-driven emphasis on monitoring audiometry may reduce attention to other components of hearing loss prevention.

In the early 1970s, medical leaders decided to focus on hearing protection and health education. Most noise hazards had been identified, and no engineering controls existed to reduce tank and howitzer noise levels. Audiometric monitoring was conducted, but testing itself does not prevent hearing loss. The protection and education strategy proved successful because sufficient numbers of Army audiologists were available to carry the hearing conservation message to the field.

Also successful have been setting written standards for implementing each element of the hearing conservation program, as well as the supporting responsibilities of leaders and medical care providers. Military audiologists have proven most successful in the role of program manager, coordinating with a team of industrial hygienists and technicians, occupational medicine physicians, physician assistants, public health nurses, safety managers, unit leaders, and hearing technicians.

Noise Hazard Evaluation

Evaluating and documenting noise hazards are primarily the industrial hygienist’s role. Safety personnel and supervisors can also alert industrial hygienists to any new operation or change in an operation that may affect noise levels, but it is the industrial hygienist’s responsibility to inspect all potentially noise-hazardous areas at least annually. Military-unique noise hazards are well documented in health hazard assessments performed during the development of noisy technology. Noise levels, administrative controls, and hearing protection requirements are documented in operations manuals.

Weapons fire is the most hazardous noise soldiers will encounter—a hazard that soldiers and their leaders widely underestimate. Weapons fire noise measurement requires specialized instrumentation that is not available at most installations. While all weapons exceed the 140-dB peak impulse noise exposure criteria, the Army’s loudest weapons systems, such as shoulder-fired rockets, may have restrictions on the allowable number of rounds that may be fired safely in a 24-hour period, the type of hearing protection required when exposed, and the firing conditions under which the weapon may be fired. Reflective surfaces and enclosures, which are characteristic of mission operations on urban terrain (MOUT) training and urban warfare, significantly increase the hazard.

The US Army, like the Air Force, Navy, and other NATO forces, uses the 3-dB exchange rate (“3-dB rule”) for steady-state noise; that is, for every 3-dB increase in noise exposure level, the allowable exposure time is halved. OSHA, however, uses a 5-dB rule. Under the 3-dB rule, 8 hours is permitted at 85 dBA. At 88 dBA, the permissible noise exposure is dropped to 4 hours, and so on. The 3-dB rule is considered more protective for exposures without quiet breaks. At least five to seven quiet breaks are assumed for an 8-hour exposure under the 5-dB exchange rate.

Engineering Controls

A typical response to the need for engineering controls is to install carpeting and acoustic tile. If the desired goal is to reduce the overall noise level in a room, some noise reduction will result when the acoustic absorption properties of the carpeting and tile are a proper match for the spectrum of the noise. However, if the goal is to reduce noise at its source, there will be no noise reduction. Vibration isolation is another area where engineering controls may be attempted. However, if the vibration mounts reinforce the resonant frequency of the machine being isolated, the machine could vibrate right off the mounts, resulting in safety violations and possible injury or loss of equipment and lives. The Tacoma Narrows Bridge disaster in 1940 is an example of this principle: despite attempts to install a hydraulic system to stabilize the structure, the “bounce” in the bridge could not be controlled and it eventually collapsed.[61] Reputable acoustical engineer and noise reduction consulting firms exist, but a more expedient and less expensive alternative is to consult an acoustical engineer on the Army Hearing Program staff at the US Army Public Health Center. Some consultations can be handled through a phone call, while others may require an onsite visit and detailed, one-third octave band measurements. For a brief introduction to engineering noise control principles and procedures, see DA Pam 40-501.[10]

Hearing Protection

Soldiers or civilian workers who are exposed to hazardous noise must use the proper hearing protection. HPDs are available in a variety of styles, sizes, materials, and noise reduction ratings. The goal is to find an HPD that is comfortable for the user and provides the right amount of protection for the working environment. HPDs may be hand-formed, such as foam earplugs, or pre-formed, such as the triple- or quad-flanged earplug. Earplugs can also be linear or non-linear in their attenuation of sound. Non-linear HPDs provide protection from hazardous noise while facilitating effective communication and situational awareness. It is crucial that the user receive training on the insertion, use, and care of HPDs. This is mandated by OSHA as part of the hearing health education element of any hearing conservation program. In addition, the HPD’s fit must be checked for each of an individual’s ears because the ears may require different sizes. The reader is referred to DA Pam 40-501[10] for hearing protection requirements in the Army Hearing Program.

Monitoring Audiometry

The military services have standardized audiometric testing requirements and procedures. The DOEHRS-HC system integrates these business rules with test protocols to produce an audiogram designed to be transparent no matter where or by whom it was administered. Test results are automatically recorded and compared to baseline results for STSs. Certified hearing technicians review results for conditions requiring referrals and further testing. Audiometric technicians must be certified after approved training, and must have accounts to export data to a Department of Defense (DoD) data repository. Local program managers perform essential oversight functions for all testing conducted and must also have DoD data repository accounts. Data exports are required at least monthly (see the Program Evaluation section below).

Health Education

Specific hearing health education requirements are outlined in DA Pam 40-501.[10] A focus on the hearing mechanism itself is required by regulation and law.4,8,62–65 The anatomy of the ear, its vulnerabilities, and the permanency of damage to the hair cells in the inner ear should be emphasized. Education on the possibility of permanent nerve damage should increase the use of earplugs among noise-exposed personnel.

Health professionals should also be aware of other behavioral obstacles associated with hearing and noise that can confound the best intentions of hearing conservation program education efforts. Such obstacles include misconceptions that reliance on technologies and other senses leads to a lessened dependence upon hearing; the association of loud equipment with power and efficiency; the ability to mentally adapt to noise, such as when drivers continuously raise the volume of the radio over the course of a trip; and the previously mentioned technical and anatomical misinformation, such as believing that the eardrum is the main ear part damaged by noise and that it can be repaired.[66]

The consequences of providing earplugs to noise-exposed personnel without fitting and without care and use instructions are significant. Moreover, unless inserted earplugs are closely scrutinized for proper insertion and given a gentle tug for seal tension, only the user knows whether they are inserted correctly. This is why it is critical to teach noise-exposed personnel how to fit, and check the fit of, their own hearing protectors. If a drop of blood ran out of the ear for every decibel of hearing lost, individuals would need little convincing. Instead, the process is relatively painless, bloodless, and insidious, which continues to challenge individual motivation to protect hearing.

Medical professionals often advocate preservation of good hearing as a quality of life issue, that is, hearing is the most precious learning and social sense. However, some noise-exposed personnel consider hearing loss prevention as a very low life priority, and it is critical to understand what motivates workers to protect themselves. For example, many who suffer from tinnitus often state that, given the choice between regaining normal hearing and stopping their tinnitus completely, they would stop the tinnitus. Education about preventing tinnitus or ensuring it does not become worse, through proper hearing protector fit and use, effectively motivates some noise-exposed personnel.

Program Evaluation

Annual self-assessments of federal occupational safety and health programs are required.[51] Many programs conduct onsite visits to assess the effectiveness of the hearing conservation program. Although onsite visits to noise-hazardous areas and operations are recommended, they cover only a single point in time. Local program managers have several other tools available to evaluate program processes and effectiveness over time. The audiometric and demographic data available through DOEHRS-HC provides measures of program participation, quality assurance, and program effectiveness. Installation program managers are required to report updated denominator data, that is, numbers of military and civilian personnel enrolled in the hearing program, every year. These data and the number of personnel tested are used to generate audiometric monitoring compliance reports. Reports on STS can be queried by installation, unit, hearing protector, job code, and rank. Other available reports include a quality assurance report on negative STS (ie, improvement in hearing thresholds) designed to evaluate the efficacy of reference audiograms. Reporting requirements are detailed in DA Pam 40-501.[10]

IMPROVING HEARING LOSS PREVENTION EFFORTS

The Army Hearing Conservation Program formed the cornerstone of hearing loss prevention efforts for more than 30 years. As noted above, the program was primarily a garrison-focused activity addressing noise hazard identification, engineering controls, hearing protectors, monitoring audiometry, health education, enforcement, and program evaluation. When all components of the program were working in concert, significant changes in the incidence of NIHL could be expected. Although there have been advances in hearing loss prevention efforts, NIHL continues to be the number one occupational health hazard for the military. While several studies have explored the effectiveness of various program components, such as reduction in noise levels in the work environment or use of HPDs, the quality of evidence in the literature is considered low in systematic review.[67]

Continued concern regarding hearing loss in the military prompted Congress to require a study of hearing loss among veterans. The study, conducted by a committee of the Institute of Medicine (IOM), was published in 2006.[66] The IOM report concluded that there was insufficient evidence in available data to determine the extent to which noise in the military contributed to hearing loss. The committee also concluded that military hearing conservation programs beginning in 1970 were not adequately protecting personnel from the effects of noise exposure, while the hearing conservation efforts prior to 1970, when no mandatory hearing conservation programs were in place and the quality of HPDs was poor, were even less effective. Although the quality of HPDs has improved since 1970, their effectiveness still depends on appropriate fitting and proper use. The IOM committee estimated that only half of military personnel who were issued HPDs actually used them. The committee made the following recommendations:

- Improve the deployment and consistent use of HPDs by military personnel.

- Include tinnitus screening at the time of hearing tests, at the onset of service, and throughout the individual’s career.

- Ensure hearing tests are performed prior to noise exposure for all new military service members at all basic training sites.

- Require hearing tests for all personnel at the end of military service.

- Include 8,000 Hz as a test frequency in hearing testing for early detection of NIHL.

- Enforce requirements for annual monitoring audiograms, as well as for follow-up audiograms if STS is detected in annual monitoring audiograms.

- Improve the reporting capabilities of DOEHRS to include tracking of tinnitus, and implement the system’s industrial hygiene database to provide information on exposures to hazardous noise and other chemical, physical, biological, and ergonomic hazards.

- Develop an interface to allow VA personnel to access the data in DOEHRS-HC.[66]

Additional guidance for improvement in hearing loss prevention efforts came in the 2011 General Accounting Office (GAO) report, Hearing Loss Prevention: Improvements to DoD Hearing Conservation Programs Could Lead to Better Outcomes. The GAO study’s goal was to examine DoD efforts to prevent hearing loss, specifically, the identification and mitigation of hazardous noise, the evaluation of hearing conservation program performance, and the sharing of DoD and VA data on auditory injury among service members and veterans. Following a review of DoD policies and guidance, examination of hearing conservation program performance data, and interviews with DoD personnel and officials, the GAO recommended that DoD address concerns regarding the type, timing, and tracking of hearing health education; the development of performance indicators evaluating the effectiveness of hearing loss prevention efforts; and the collection and analysis of performance data that inform improvement in hearing conservation programs.

Department of Defense Hearing Center of Excellence

When the 2011 GAO report was produced, the DoD Hearing Center of Excellence (HCE) was under development but not fully implemented. The HCE was legislated by Congress in the fiscal year 2009 National Defense Authorization Act. It directed the DoD to partner with the VA, institutions of higher education, and other appropriate public and private entities to create the center. The HCE’s primary missions were to develop a data registry to track hearing loss and auditory injuries in the military and share the data with the VA; facilitate research related to auditory injury and hearing loss prevention; and develop best practices and clinical education. The HCE is focused on the prevention, diagnosis, mitigation, treatment, and rehabilitation of hearing loss and auditory injury. The HCE has developed hearing health education resources, provided funding for auditory research, and established a network of partners to assist with hearing loss prevention and quality clinical care. Development is underway for the Joint Hearing and Auditory System Injury Registry to track diagnosis, treatments, interventions, and follow-up for each case of hearing loss or injury incurred by a service member on active duty. The database will allow sharing of information with the VA to improve delivery of audiologic services, including rehabilitation and fitting of auditory prosthetics for veterans.

Mission-Critical Hearing Studies

Soldiers rely on visual cues, such as hand gestures and verbal communications, to relay information in combat environments where noise discipline is important, or where noise levels preclude hearing with open ears (ie, with hearing protectors in or on the ears). Although advances have been made in electronic equipment to assist in communication, many devices were not designed both for effective communication in military-unique high noise levels and to protect and preserve mission-critical hearing.

The effects of diminished hearing on combat communications in a tank simulator were studied in 1990 at the US Army Human Engineering Laboratory at Aberdeen Proving Ground. With good speech intelligibility, 94% of targets were “killed”; with poor speech intelligibility, targets “killed” decreased to 41%. The time needed to execute the mission increased from 6 seconds with good speech intelligibility to 40 seconds when speech intelligibility was poor, and gunner accuracy plummeted from 90% to 42%. This was the first published study that addressed the effects of the degradation of speech intelligibility on soldiers’ workload and performance.[68] More recent work at the Army Research Laboratory at Aberdeen Proving Ground has shown that effects of hearing loss on speech recognition performance are also exacerbated when the listener is engaged in a walking task.[69] In other words, if soldiers experienced a hearing loss, then their ability to understand speech may be compromised if they were moving.

Without good hearing it becomes difficult to localize, that is, locate and identify the source of sound, gauge the distance to the source of sound, and understand verbal orders or communication over electronic systems such as radios. Through the use of mathematical models, the effect of reduced hearing on the ability of a solider to complete key military tasks can be predicted.[70] The ability to detect sounds decreases rapidly as hearing loss increases. A soldier’s ability to detect a rifle bolt being closed before firing, for example, decreases from 1,000 m with normal hearing to 46 m with a hearing loss (equivalent to hearing with an H3 hearing profile[68]). Similarly, the ability to hear a voice at normal volume decreases from 180 m to 32 m. Hearing loss in military personnel can have a profound effect on mission performance, and has serious consequences for the survivability and lethality of the soldier. Good hearing can mean life or death in combat and in training. With this in mind, the goal of the Army Hearing Program is to maximize soldiers’ hearing and communication abilities and, as a result, contribute to survivability, lethality, and mission effectiveness.

Expanded Program Components

Over their 30-year course, garrison-level Army hearing conservation programs did not effectively translate into hearing loss prevention in the deployed environment. A more holistic approach to preventing NIHL emerged in 2008, when the Army “Hearing Conservation Program” was renamed the Army “Hearing Program” to address the continuum of soldiers’ hearing and communication needs. Added to the original OSHA model were three other hearing conservation components: hearing readiness, clinical hearing services, and operational hearing. Clear communication is crucial on the battlefield. The continuum of the soldier’s hearing and communication needs and mission requirements are addressed now through the four components of the Army Hearing Program: (1) hearing readiness, (2) clinical hearing services, (3) operational hearing services, and (4) hearing conservation.[10]

Hearing readiness ensures that soldiers have the required hearing capabilities to perform their assigned jobs, that is, the best hearing possible. The goal of hearing readiness is to identify changes in hearing through monitoring audiometry; provide hearing protection and assistive listening technology (hearing aids) when indicated; and provide health education to reduce damage from noise exposure. All soldiers are required to have a hearing test.[10] Hearing tests are currently performed using the DOEHRS-HC microprocessor audiometers. Through interfacing with other military health systems such as the Medical Protection System (MEDPROS), DOEHRS-HC provides a means to track data at both an individual and Army unit level.10,71

Clinical hearing services were incorporated into the Army Hearing Program to treat and manage soldiers when hearing loss is identified. Clinical hearing services assist in determining if the soldier is fit for duty from an auditory perspective. Only an audiologist or qualified physician can diagnose NIHL and determine fitness for duty. Diagnostic audiologic assessment may include not only measures of auditory acuity through pure tone testing, but also measures to assess ability to understand speech in noise or evaluate balance problems. Treatment plans for soldiers with NIHL may include fitting of hearing aids or other assistive listening devices, audiologic rehabilitation, tinnitus management, or physical therapy or other balance management.[10]

Operational hearing services mitigate NIHL during military operations while facilitating effective communication. Noise assessment, reduction of hazardous noise through engineering controls, and ensuring optimum communication capabilities are the focus of operational hearing services. There is an emphasis on improving communication through the use of nonlinear and multifunctional HPDs, such as the Tactical Communication and Protective Systems (TCAPS), that enhance communication and reduce the impact of noise during military operations. TCAPS is designed to amplify low-volume sounds while providing hearing protection from impulse noise such as weapons fire. Devices such as the TCAPS protect soldiers in training and combat environments while allowing them to maintain effective communication. A more detailed description of current HPDs for the operational environment can be found in DA PAM 40-501.[10]

Along with hearing readiness and hearing conservation, operational hearing focuses on ensuring that soldiers have the required hearing capabilities to perform their assigned jobs. However, operational services also include mission-specific hearing protector research, development, and testing, in collaboration with auditory researchers across the DoD and Army acquisition.[10]

Hearing conservation programs currently are primarily intended for work environments where operations change very little over the work day, and industrial-based settings, such as maintenance facilities or weapons manufacturing. Because the majority of employees in these settings are civilian workers and not active duty military, hearing conservation efforts are primarily in support of civilian employees. The seven elements of the hearing conservation program—noise hazard identification, engineering controls, hearing protectors, monitoring audiometry, health education, enforcement, and program evaluation—continue to serve as the foundation of hearing loss prevention efforts for garrison-based operations.[10]

HEARING CONSERVATION ON THE BATTLEFIELD

While an effective garrison-based hearing conservation program is critical (soldiers fight the way they train), hearing conservation efforts must continue forward, to the battlefield. Soldiers must use all available senses to survive and perform on the modern battlefield. While vision is critical to the soldier’s effectiveness, hearing is used to detect, locate, and recognize the enemy. Combat veterans value hearing as a 360-degree warning sense, in the absence of other sensory input, whereas vision is acknowledged as providing slightly more than 180 degrees of information. Soldiers must also communicate face-to-face and via radio in secure modes during mission operations. Operational environments, such as during night reconnaissance; movement in nuclear, biological and chemical defense modes; or in the presence of smoke, dust, and haze; confound the soldier’s mission effectiveness. Cave clearing and MOUT operations are particularly hazardous to hearing. These are environments in which subtle sounds must be heard, yet hearing must be protected from expected and unexpected blasts. In addition, unprotected exposure to hazardous noise from small arms, artillery fire, armored vehicles, and aircraft can result in an inability to hear for hours, even days, and either immediately or eventually result in a permanent hearing loss, degrading the soldier’s and the unit’s mission capabilities.

Sound Localization

Environmental and occupational threats to individual safety exist in almost any industrial setting, but none more so than the military environment. Increased operational tempo and the lethality of urban warfare require special emphasis on communication and situational awareness. Sound localization, the ability to pinpoint the direction (and distance) of sound, is a vital component of a soldier’s situational awareness.

The outer ear, or pinna, which serves as a collector of sound, also modifies the incoming acoustic signal, amplifying some frequencies and attenuating others. Subtle differences between ears in phase (time) and intensity enable the brain to locate sound in space. Generally, differences in phase provide the cues for localization of higher frequency sounds, whereas intensity differences between ears provide the cues for lower frequency sound localization. The balance between direct and reflected sound is used to judge distance.[70] However, background noise levels can mask reflected sound and, as a result, the source may sound closer than it really is.[72] Noise sources collocated with the sound can also affect the ability to determine directionality, under certain conditions. For example, the directionality of a high frequency sound source like a backup alarm on a fork lift may not be perceived if the alarm is not at least 10 to 15 dB above the background noise.[73] The importance of having two normal-functioning ears for this ability cannot be overemphasized.

Sound Identification

For years, Army audiologists have advocated for the association of hearing conservation measures with mission accomplishment. For example, if hearing protection is worn properly, there is less of a tendency to flinch when firing small arms, and the soldier will shoot more accurately—something members of rifle and pistol teams have always known. However, the preservation of hearing can be associated with something more important than a high marksmanship score, because the ability to accurately identify sound is often a life-or-death matter in combat. This ability is also critical to support the latest “actionable intelligence” initiative in the US Army, where every soldier is a sensor.[74]

The importance of identification of enemy weapons by sound was noted in a 1952 report by the Office of Naval Research that included interviews with soldiers who had been exposed to combat sounds such as various weapons, aircraft, mortar, and artillery rounds. The soldiers reported that, in combat, “sound was more important than all other means of equipment identification.”[75] The soldiers also “regarded the sound of enemy weapons as such an important means of identification that they rarely made use of captured equipment because it resulted in their being fired upon by friendly troops.”[75]

In 2004, the National Ground Intelligence Center (NGIC) conducted interviews with soldiers returning from Iraq and Afghanistan and confirmed the earlier reports by World War II soldiers. Soldiers interviewed by NGIC made the following observations:

- “Unlike visual information, information carried by sound comes to us from all directions, through darkness and over or through many obstacles to vision.”

- “Aggressive action produces sound the enemy cannot hide or camouflage.”

- “Sound is often the first source of information a Warfighter has before direct contact with the enemy.”[76]

Although some of these observations may be obvious to anyone with a background in acoustics, these soldiers gained such insights first hand, through combat experience. Understanding combat-relevant sounds is a vital component to situational awareness that can provide a tactical advantage for accomplishing the mission.

Combat veterans value hearing as a 360-degree warning sense, which inherently underscores the problem. These survivors learned, through chance encounters, the value of their hearing and of combat-relevant sounds. For example, returning Vietnam veterans reported that bird calls in the lower jungle canopy meant that Viet Cong could be in the area because the birds had come down from the upper canopy to feed on rice spilled by the enemy soldiers.[76] After experiencing weapons firing, the soldiers knew the difference between the noise signatures of an AK-47 versus an M-16. Good hearing in both ears also facilitated the localization (ability to pinpoint direction) of sniper fire and other relevant sounds.[76]

Data from the late 1980s through the 1990s that examined listening performance in tank simulators and detection of combat sounds indicated a correlation between good hearing and mission performance, but results of these studies had limited application and reach.77,78 Sound identification training significantly extends the auditory advantage to individual soldiers. “Combat-relevant sound identification gives the U.S. Soldier the edge in any hostile encounter by capitalizing on the underutilized sound-identification capability of the ear.”[78] More recent data has shown that a soldier’s ability to effectively communicate is compromised when hearing loss is present and they are engaged in a walking task.[69] This has important implications when considering communication systems a soldier may need for dismounted operations.

Army Hearing Program staff are interested in how hearing combat-relevant sounds and effective communication are affected by use of hearing protection, existing hearing loss, and the combination of the two. Work is currently underway at the Walter Reed National Military Medical Center, the Audiology and Speech Center, and the Army Research Laboratory to answer these questions. Preliminary results are providing insights into a soldier’s survivability and lethality in combat under less-than-optimal auditory conditions.

SUMMARY

There is no shortage of explanations for why military hearing conservation is such a challenge. Behavioral obstacles and limited resources demand dedication and persistence in overcoming these challenges. Nevertheless, medical interest in hearing loss prevention programs can heavily influence command interest and the soldier’s mindset. If properly informed and adequately resourced, occupational health professionals can impact program compliance at all levels. A dedicated professional, such as an Army audiologist, must be available to serve as an advocate and coordinator for installation hearing programs and military hearing conservation programs in general. Effective hearing loss prevention programs involve the coordinated application of all four components of the Army Hearing Program: hearing readiness, operational hearing services, clinical hearing services, and hearing conservation. Although implementation of these program elements requires a multidisciplinary approach, hearing conservation programs are, ultimately, command programs.

The benefits of an effective, well-resourced hearing conservation program have been documented.[52] Unfortunately, reduced hearing loss and cost savings have not been enough to maintain the critical mass of military audiologists required to sustain a viable program. Focus on hearing loss prevention forward may ensure dedicated resources and provide a new direction for the program. Hearing conservation measures must be linked not only to readiness, but to mission accomplishment. Hearing cannot be protected unless the importance of what has to be heard is also taken into consideration.

The comprehensive and well-documented 1952 study recommended sound identification training for the warfighter.[75] Fifty-two years later, in 2004, a training program was initiated,[74] and the following year a multiservice task force investigated the feasibility of warfighter hearing protection in combat. Warfighter hearing protection sounds like a recent concept, but a memorandum published in 1918 advocated “ear protectors for the benefit of Soldiers in actual combat…. Although study of this subject was made and the advantages of various types of protectors were tested, no definite action looking into adoption of these articles was taken.”[79] We look forward to the next generation of leaders to apply lessons learned in preventing NIHL.

REFERENCES

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35.   Morata TC. Chemical exposure as a risk factor for hearing loss. J Occup Environ Medicine. 2003;45:676–682.

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39.   Folmer RL, Griest SE. Tinnitus and insomnia. Am J Otolaryngol. 2000;21:287–293.

40.   Bauer CA, Turner JG, Caspary DM, Myers KS, Brozoski TJ. Tinnitus and inferior colliculus activity in chinchillas related to three distinct patterns of cochlear trauma. J Neurosci Res. 2008;86:2564–2578.

41.   Mulders WH, Robertson D. Hyperactivity in the auditory midbrain after acoustic trauma: dependence on cochlear activity. Neuroscience. 2009;164:733–746.

42.   Alkhatib A, Biebel UW, Smolders JW. Reduction of inhibition in the inferior colliculus after inner hair cell loss. Neuroreport. 2006;17:1493–1497.

43.   Snyder RL, Bonham BH, Sinex DG. Acute changes in frequency response of inferior colliculus central nucleus (ICC) neurons following progressively enlarged restricted spiral ganglion lesions. Hear Res. 2008;246:59–78.

44.   Vogler DP, Robertson D, Mulders WH. Hyperactivity in the ventral cochlear nucleus after cochlear trauma. J Neurosci. 2011;31:6639–6645.

45.   Mann ZF, Kelley MW. Development of tonotopy in the auditory periphery. Hear Res. 2011;276:2–15.

46.   Wang F, Zuo L, Hong B, et al. Tonotopic reorganization and spontaneous firing in inferior colliculus during both short and long recovery periods after noise overexposure. J Biomed Sci. 2013;20:91.

47.   Hazell JWP. Models of tinnitus. In: Vernon JA, Moller AR, eds. Mechanisms of Tinnitus. London, England: Allyn and Bacon, 1995: 62–73.

48.   Feldmann H. Mechanisms of tinnitus. In: Vernon JA, Moller AR, eds. Mechanisms of Tinnitus. London, England: Allyn and Bacon; 1995: 43–55.

49.   Walden BE, Prosek RA, Worthington DW. The Prevalence of Hearing Loss Within Selected U.S. Army Branches. Washington, DC: Walter Reed Army Medical Center; 1975.

50.   US Government Accountability Office. Hearing Loss Prevention: Improvements to DOD Hearing Conservation Programs Could Lead to Better Outcomes. Washington, DC: GAO; 2011. GAO Report No. 11-114.

51.   Helfer TM. Noise-induced hearing injuries, active component, U.S. Armed Forces, 2007-2010. MSMR. 2011;18(6):7–10.

52.   Fausti SA, Wilmington DJ, Helt PV, Helt WJ, Konrad-Martin D. Hearing health and care: the need for improved hearing loss prevention and hearing conservation practices. J Rehabil Res Dev. 2005;42(4 Suppl 2):S45–S62.

53.   Verbeek JH, Kateman E, Morata TC, Dreschler WA, Sorgdrager B. Interventions to prevent occupational noise-induced hearing loss. Cochrane Database Syst Rev. 2012;10:CD006396.

54.   Petruccelli B, Knapik J. Army epidemiology and health surveillance. Army Med Dep J. 2006;Apr-Jun:22–30.

55.   Helfer T, Canham-Chervak M, Kropp L, Deaver K, Hall S. U.S. Army Active Duty Noise-Induced Hearing Loss Injury Summary, Calendar Years 2007-2011. Aberdeen Proving Ground, MD: US Army Public Health Command; 2013.

56.   Helfer T, Canham-Chervak M, Canada S, Mitchener TA. Noise-induced hearing injury surveillance in the U.S. military, 2003-2005. In: Canham-Chervak M, Jones B, eds. Preventing Injuries in the U.S. Military: The Process, Priorities, and Epidemiologic Evidence. Aberdeen Proving Ground, MD: US Army Center for Health Promotion and Preventive Medicine; 2008. Technical Report No. 12-HF-04MT-08: 3-61-3-69.

57.   Helfer T, Canham-Chervak M, Canada S, Mitchener TA. Epidemiology of hearing impairment and noise-induced hearing injury among US military personnel, 2003-2005. Am J Prev Med. 2010;38(1 Suppl):S71–S77.

58.   US Department of Veterans Affairs. Annual Benefits Report Fiscal Year 2012. Washington, DC; VA; 2012.

59.   Beck LB. Update on VA audiology program. Paper presented at: Joint Defense Veterans Audiology Association Conference; February 25, 2013; Nashville, TN.

60.   Folmer RL, McMillan GP, Austin DF, Henry JA. Audiometric thresholds and prevalence of tinnitus among male veterans in the United States: Data from the National Health and Nutrition Examination Survey, 1999-2006. J Rehabil Res Dev. 2011;48(5):503–516.

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62.   Executive Order 12196. Occupational safety and health programs for federal employees. October 1, 1980.

63.   29 CFR, Part 1960. Basic program elements for federal employee occupational safety and health programs and related matters. July 1, 2010.

64.   29 CFR, Part 1910.95 Occupational noise exposure. September 9, 2009.

65.   Bragdon CR. Noise Pollution: The Unquiet Crisis. Philadelphia, PA: University of Pennsylvania Press; 1971.

66.   Humes LE, Joellenbeck LM, Durch JS, eds. Noise and Military Service Implications for Hearing Loss and Tinnitus. Washington, DC: National Academies Press; 2006.

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68.   Garinther GR, Peters LJ. The Effects of Speech Intelligibility (SI) on Crew Performance in an M1A1 Tank Simulator. Aberdeen Proving Ground, MD: US Army Human Engineering Laboratory; 1990.

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76.   Monroe JN. Sound Identification Recordings for Warfighters [CD-ROM]. Charlottesville, VA: US National Ground Intelligence Center, 2004.

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78.   Ohlin DW. Let’s hear it for our troops: saving hearing—and money—in the military. ASHA. 1998;40(4):50–53.

79.   Richardson CW. Office memorandum to the surgeon general, subject: Ear protectors for the benefit of soldiers in actual combat. February 20, 1918. Cited in: Lynch C, Weed FW, McAfee L, eds. The Medical Department of the United States Army in the World War, Vol XI, Surgery, Pt 2. Washington, DC: US Army Surgeon General’s Office; 1927.

Chapter 13

RESPIRATORY PROTECTION

TIMOTHY M. MALLON, MD, MPH*; CAMERON J.L. NELSON, MD, MPH†; BRANDON GARDNER, DO, MPH‡; GREGORY J. MARTIN, MD, MPH§; and JOHN P. BARRETT, MD, MPH¥

INTRODUCTION

RESPIRATOR CLASSIFICATION

RESPIRATORY PROTECTION PROGRAMS

RESPIRATOR SELECTION GUIDELINES

MEDICAL CONSIDERATIONS AND EVALUATION

RESPIRATOR TESTS AND CHECKS

MAINTENANCE

TRAINING

PROGRAM EVALUATION

RECORD KEEPING

SUMMARY

*Colonel (Retired), US Army; Adjunct Assistant Professor, Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814

†Commander, Medical Corps, US Navy; Chief of Occupational Medicine, Naval Hospital Bremerton, 1 Boone Road, Bremerton, Washington 98312

‡Major, Medical Corps, US Army; Chief, Occupational Medicine Branch, US Army Medical Department Center and School, 3599 Winfield Scott Road, Fort Sam Houston, Texas 78234

§Colonel, Medical Corps, US Army; Chief, Occupational Medicine, Madigan Army Medical Center, 9925 5th Street, Building 9025, Tacoma, Washington 98431

¥Colonel, Medical Corps, US Army; Deputy Chief, Epidemiology Division, Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814

INTRODUCTION

The Occupational Safety and Health Administration (OSHA) has established requirements for worker respiratory protection. OSHA regulation requires employers to develop and put in place a respiratory protection program that includes engineering and administrative controls to prevent workplace hazards, and to use respirators only after all other means to reduce or eliminate occupational exposures to airborne contaminants have been exhausted. Respirators are only intended to be an interim measure to reduce workplace exposures when other controls are neither feasible nor effective at reducing exposures below the OSHA permissible exposure limit.[1]

When an employer develops a respiratory protection program, the first order of business is to define the hazardous exposures present in the workplace and establish their exposure levels. This usually involves arranging for an experienced, certified industrial hygienist to conduct an industrial hygiene survey. Once the workplace hazards and levels are identified, appropriate respiratory protection and other personal protective equipment is selected. The National Institute for Occupational Safety and Health (NIOSH) published 42 Code of Federal Regulations (CFR) Part 84, Approval of respiratory protective devices,[2] that factors in considerations for respirator selection such as hazard properties, concentration, and warning properties in terms of odor and color.2,3 The local industrial hygienist assesses the program annually and recommends improvements to the installation safety and occupational health council or person in charge of the respiratory protection program.

Respirator use is the least desirable method of controlling workplace exposures because respirators must be properly selected, fit tested, maintained, and worn; and their use must be monitored.[2] Respirators can be hot and uncomfortable to wear, particularly for an 8- to 12-hour shift. Respirators can pose a safety hazard if they impair the ability to hear, see, or communicate effectively. Also, employees with cardiopulmonary health conditions may require a special screening, which is done as part of the medical clearance, to assess their suitability to wear a respirator.[1] If the respiratory protection program is not well executed, it can pose a health hazard to employees and give them a false sense of security.

Workers should only wear NIOSH-approved respirators.[1] The M40 military protective mask is a tight-fitting, full facepiece, air-purifying respirator developed to protect against chemical, biological, and radiological contaminants on the battlefield. These masks, however, are not approved by NIOSH for use in the industrial workplace for protection against toxic industrial chemicals.[3]

RESPIRATOR CLASSIFICATION

Respirators are designed to protect workers from inhaling harmful airborne substances and allow employees to work in oxygen-deficient spaces. There are two basic types of respirators: the air-purifying respirator removes contaminants from the air; and atmosphere-supplying respirators provide clean breathing air from an uncontaminated source.2,3 There is a combination respirator which is a subset of each of the two categories. Respirators can also be categorized as tight- and loose-fitting. Respirators are designed to work properly with either a tight-fitting facepiece that forms an airtight seal or a loose-fitting facepiece that forms a partial seal.2,3 Both air-purifying and atmosphere-supplying respirators can have facepieces that maintain either positive or negative pressure. There are some respirators that maintain positive pressure in the facepiece relative to the ambient air pressure outside the mask during the entire breathing cycle.2,3 Some respirators maintain a negative pressure in the facepiece when the wearer inhales and often leak ambient air into the facepiece.

Air-Purifying Respirators

When someone wearing an air-purifying respirator inhales, contaminants such as gases, vapors, aerosols, particulates, or a combination of these are removed from the air as it passes over and is absorbed by filter elements.2,3 There must be sufficient oxygen in the space to support life, and the hazard level has to be low enough that it does not overwhelm the respirator’s filtering capacity too quickly. A filtering respirator’s useful life span is calculated using the contaminant’s concentration rate, the wearer’s breathing rate, the workplace temperature and humidity levels, and the filter element’s removal capacity. Wood wrote an article that addressed how to estimate the service life of organic vapor cartridges, and Cothran identified software that estimates the service life of respirator cartridges.4,5

Selecting an air-purifying respirator depends on the needed level of protection and the types of hazards in the working environment. Available styles are described below.

Figure 13-1. This 3M half-face filtering respirator (model 6200) is designed with two attached filtering cartridges and intended to be worn with safety goggles.
Photograph courtesy of 3M Corporation, used with permission.

- Mouth bit. This respirator is used for escape-only situations and regenerates breathable air for emergency escape from areas containing harmful gasses. It is tight fitting and has a short tube designed to fit in the mouth. The wearer must use a nose clip to seal the nostrils to prevent inhalation of ambient air during evacuation from the contaminated environment. The mouth seal and nose clips form the respirator’s seal.[2]

- Half-face. This respirator is also tight fitting; it covers the facial area from the top of the nose to the bottom of the chin. Half-face respirators (Figure 13-1) generally have two filter cartridges, but a few have a single cartridge.[2]

- • Half-face filtering respirator. Much like the half-face respirator, the half-face filtering respirator covers the area from above the nose to underneath the chin; however, the entire respirator is made of filtering material. While considered tight fitting, these devices do not have a good elastomeric sealing surface. Almost all filtering facepiece respirators are exclusively designed to protect against particulates and bioaerosols commonly present in the healthcare industry. Filtering facepiece respirators also protect against tuberculosis and similar sized pathogens.[2] The respirator wearer should never confuse a surgical mask with a half-face filtering respirator. A high efficiency particulate air (HEPA) respirator protects against tuberculosis and the transmission of small viruses and particles, while a surgical mask only reduces the amount of aerosol droplets when the wearer sneezes. Figure 13-2 is an example of a half-face N95 filtering HEPA respirator.2,3

- Full-face. This respirator is unique because it covers the whole face from the scalp to underneath the chin. It fully covers the eyes and protects against splashes from irritating chemical vapors, aerosols, dusts, fumes, and particulates. Figure 13-3 shows an example of a full-face filtering respirator with canisters.2,3

- Powered air-purifying respirator (PAPR). This respirator (Figure 13-4) is ideal for people who have difficulties wearing a respirator, including those with a respiratory impairment. PAPRs use a blower to force air through the filter and reduce the labor of breathing through a respirator. PAPRs can have either tight- or loose-fitting facepieces, hoods, or helmets. NIOSH requires PAPR blower units to provide at least 4 cubic feet per minute of air to a tight-fitting facepiece and at least 6 cubic feet per minute of air to a loose-fitting facepiece, helmet, or hood.2,3 PAPRs with hoods and helmets are well suited for wearers who have facial hair and are unable to get a good facial seal. PAPRs that maintain positive pressure inside the mask have loose-fitting facepieces with partial sealing surfaces at the temple, cheek, or chin. In order to obtain a tight seal, respirator wearers should remove any facial hair that contacts the respirator’s sealing surface.2,3 NIOSH requires PAPRs to have HEPA filters. The HEPA and P100 filters for negative pressure, air-purifying respirators are magenta or purple in color.[2]

- Particulate. Particulate respirators capture air particles such as dusts, mists, and fumes. They are more effective when particles accumulate on the filter and plug spaces between the fibers. Particulate respirators do not protect against gases or vapors. The filters should be replaced when the user finds it difficult to breathe through them.

- Gas and vapor removing.

- Air-purifying respirators that remove gases and vapors tend to remove specific chemicals or a combination of contaminants via cartridges or canisters containing sorbents. Sorbents are often granular, porous materials that remove contaminants by a variety of mechanisms including adsorption, absorption, and catalytic reaction. The cartridges must be replaced when the sorbents lose effectiveness.2,3 These respirators are not designed to protect against airborne particles.

- Air-purifying aerosol respirators have filters that protect the wearer against gases and vapors.2,3 The filtering facepiece respirator may have either a replaceable or permanent cartridge. There are a number of filter cartridge configurations, including randomly laid nonwoven fiber materials, compressed natural wool, and synthetic felt or glass fibers loosely packed into a filter container. Alternatively, any of the above materials may be compressed into a flat sheet that is then pleated and placed into a filter canister. Expanding the filter’s surface area by pleating the filter material increases its capacity and efficiency and decreases its resistence.2,3

- Combination. Combination respirators are used in atmospheres that contain both particulate and gas hazards. They use both particulate filters and gas or vapor filters, and tend to be heavier than other respirators.

Figure 13-2. This 3M half-face N95 filtering respirator (model 8210V) is designed for wear in hospitals and intended to be worn with safety goggles.
Photograph courtesy of 3M Corporation, used with permission.

Figure 13-3. This 3M full-face filtering respirator (model 6800) is designed for wear with filtering cartridges attached. Prescription glass inserts may be added to improve worker wearability.
Photograph courtesy of 3M Corporation, used with permission.

Filtration Mechanisms and Classification

A number of mechanisms provide the respirator wearer with clean air. The four commonly used mechanisms in fibrous filters are interception, sedimentation, impaction, and diffusion. Some filters employ a combination of mechanical means to remove particles; the contribution of each depends on flow rate, particle size, and aerodynamic diameter. In addition to mechanical methods, some respirators use an electrostatic attraction to remove particles.

Figure 13-4. The 3M powered air-purifying respirator (model 6884) is designed for wear in settings where neither a tight-fitting facepiece nor a negative pressure respirator can be worn.
Photograph courtesy of 3M Corporation, used with permission.

NIOSH classifies air-purifying respirators based on how well they resist oil. Those that are not resistant to oil are labeled “N”; those that are resistant to oil are labeled “R”; and those that are oil proof are labeled “P.”[2] Each of these classifications has three filter efficiency ratings: 95%, 99%, and 99.97% (essentially 100%).2,3 Particles that are between 0.1 and 0.4 μ in size are the most difficult to filter because they are too small for large particle removal mechanisms and too large for the diffusion filtering mechanism to remove effectively. Tuberculosis bacilli are 1 to 4 μ long and 0.3 to 0.6 μ in diameter. Anthrax bacilli are 1 to 8 μ long and 1 to 1.5 μ in diameter, while the spores are 1 μ in diameter. Filters rated at 95% efficiency remove more than 99.5% of tuberculosis- and anthrax-sized bacilli and spores.

Oil aerosols, including cutting oils, hydraulic oil, lubricating oil, engine oil, dioctyl phthalate, corn oil, and transformer oil, tend to degrade filter efficiency. Refer to the Guide to the Selection and Use of Particulate Respirators Certified Under 42 CFR Part 84 for a list of respirators that may resist oil saturation.[3] OSHA now requires employers to estimate the cartridge life for particulate respirators.[1] Wood described the process and Cothran identified a computer software program that calculates service life for cartridges.4,5

Atmosphere-Supplying Respirators

Atmosphere-supplying respirators provide an air source independent of the ambient environment.2,3 These respirators are used when: (a) a cartridge change-out schedule cannot be established, (b) an end-of-service-life indicator is not feasible because of the hazard’s properties, or (c) the contaminant concentrations are at or near the immediately dangerous to life or health (IDLH) levels, which make an air-purifying respirator inadequate. There are three types of atmosphere-supplying respirators: air-line or supplied-air respirators, self-contained breathing apparatus (SCBA), and combination air-line SCBA.2,3

- Full-face air-line. Full-face air-line respirators use compressors to supply breathing air pressures no more than 125 psi and restricted to 300 ft of hose.2,3 Figure 13-5 shows a full-face air-line respirator. The manufacturer must specify the operating pressure and maximum hose length. Air-line respirators are not permitted for use in IDLH atmospheres where the wearer is unable to escape when the air supply fails. Air-line respirators have a variety of facepieces including half-face, full-face, and loose-fitting hood, and they operate in continuous, demand, or pressure-demand modes.

- Self-contained breathing apparatus. An SCBA has an independent air supply that permits the wearer freedom of movement. Pressure-demand SCBAs are approved for IDLH and oxygen-deficient atmospheres. SCBAs are designed to be either closed- or open-circuit devices.

- Closed-circuit. These respirators recirculate the wearer’s exhaled breath within the respirator after carbon dioxide (CO_2) is removed and oxygen is replaced.2,3 Closed-circuit SCBAs are smaller and more lightweight (weighing less than 35 lb) than open-circuit SCBAs and have a longer service life (up to 4 hours). Reoxygenation can be performed through a tank of compressed gas or through oxygen generation.

- Open-circuit. An open-circuit respirator (Figure 13-6) discharges exhaled air into the atmosphere. Contaminants in the facepiece are purged instead of recirculated. The SCBA uses a large air tank carried on the wearer’s back, making it heavier than the closed-circuit model and limiting the use to one hour. Open-circuit SCBAs are demand or pressure-demand devices.2,3 NIOSH approves SCBA for firefighting using guidelines that generally require full-face, pressure-demand SCBAs equipped with 30-minute cylinders that meet National Fire Protection Association requirements.6,7

- Escape-only. These respirators are intended for emergency use only. NIOSH guidelines call for mouthpiece respirators to be equipped with nose clips to prevent inhalation of hazardous atmospheres.[2]

- Combination air-line/self-contained breathing apparatus. Figure 13-7 is an example of a supplied-air respirator and an SCBA cylinder that serves as an auxiliary air supply.2,3 Pressure demand combination air-line/SCBAs are approved for IDLH atmospheres.[2]

Figure 13-5. The full-face air-line respirator provides the wearer breathing air in hazardous environments. The respirator can be worn for a full work shift.
Photograph courtesy of Brandon Gardner, Major, Medical Corps, US Army; US Army Medical Department Center and School, Fort Sam Houston, TX.

Figure 13-6. The full-face open circuit self-contained breathing apparatus is designed for wear in extremely hazardous environments for short periods up to 30 minutes.
Photograph courtesy of Brandon Gardner, Major, Medical Corps, US Army; US Army Medical Department Center and School, Fort Sam Houston, TX.

Figure 13-7. The air-line filtering respirator with emergency escape canister permits the wearer to work a full shift and escape the area if there is a release of immediately dangerous to life hazards.
Photograph courtesy of Brandon Gardner, Major, Medical Corps, US Army; US Army Medical Department Center and School, Fort Sam Houston, TX.

After the September 11, 2001 terror attacks, NIOSH established certification standards for SCBAs worn by firefighters and other first responders.[6] SCBAs must protect the wearer from harmful chemicals, pathogens, and radioactive materials. Respirators approved for chemical, biological, radiological, and nuclear (also known as CBRN) environments are rigorously tested and certified to protect against both toxic industrial chemicals and chemical and biological warfare agents. The list of approved respirators is maintained on the NIOSH website.[8]

Respirator Service Life

OSHA respirator regulations eliminated odor thresholds to determine when a respirator has reached the end of its service life. Regulations now require that chemical canisters and cartridges are changed before their end-of-service-life based on a color change.[3] This data, along with the logic for the change-out schedule, must be described in the employer’s written respirator protection program. Some cartridges have a colorimetric end-of-service-life indicator that changes color when the filter sorbent is saturated.

RESPIRATORY PROTECTION PROGRAMS

Major requirements of OSHA’s respiratory protection standard, 29 CFR 1910.134, requires that employers develop and implement a written respiratory protection program with worksite-specific procedures for respirator use.[1] Each military installation commander must appoint an installation respirator program director and an installation respirator specialist.[9] The program director is responsible for preparing local regulations in conjunction with the local medical authority. Elements of the OSHA respiratory protection program include the following:[10]

- procedures for respirator selection;

- medical evaluation of employees prior to respirator wear;

- fit testing procedures;

- procedures for routine and emergency use;

- procedures and schedules for cleaning storing, inspecting, and maintaining respirators;

- procedures to ensure air quality, quantity, and flow for atmosphere-supplying respirators;

- employee training about the respiratory hazards at work;

- employee training in all aspects of the program; and

- regular evaluation of program effectiveness.

All work areas where respirators are worn should have specific written standard operating procedures that identify which respirator to wear and under what conditions, and address emergency situations. OSHA regulations also permit workers to voluntarily wear respirators to control nuisance odors or dust. NIOSH-approved respirators are not required for voluntary use, nor do the devices have to be fit tested. The filtering facepiece dust masks and air-purifying respirators are the most commonly worn. The employer does not need a written respiratory protection program if only filtering facepiece dust masks are worn. The employer should ensure the dust masks are clean and do not pose a safety hazard. Each user must be given a copy of Appendix D of 29 CFR 1910.134, (Mandatory) information for employees using respirators when not required under standard,[1] which addresses voluntary respirator use.

RESPIRATOR SELECTION GUIDELINES

OSHA requires wearers to use NIOSH-approved respirators. There are several factors to consider when selecting the correct respirator for a given circumstance.[2]

- Nature of the hazard. Includes physical and chemical properties of the contaminants.

- Oxygen deficiency. NIOSH approves air-purifying respirators only for use in atmospheres containing 19.5% oxygen or greater at sea level.[2] OSHA defines oxygen-deficient atmospheres (less than 19.5% oxygen by volume) as IDLH and requires personnel entering these atmospheres to wear either a pressure-demand SCBA or combination pressure-demand air-line/SCBA.[1]

- Physical properties. Physical properties include physical state (gas, vapor, dust, fume, mist, etc), particle size, molecular weight, boiling point, and vapor pressure.

- Chemical properties. The hazard solubility in water, reactivity with other chemicals, and sorbent materials in respirator cartridges or canisters must be considered when selecting a respirator filter. The hazardous decomposition products and oil content in the aerosol are important because these materials will degrade filter efficiency.

- Physiological effects. Physiological effects on the body include skin absorption, eye and mucus membrane irritation, simple or chemical asphyxiation, anesthesia, sensitization, carcinogenicity, and hazards to reproductive systems.

- Warning properties. Warning properties include odor, taste, and irritant effects. The odor properties are least important because OSHA regulations now require that air-purifying respirators be equipped with approved end-of-service-life indicators.[2]

- Concentration and relevant exposure limit. The concentration of a compound is an important factor in determining the appropriate respiratory protection. OSHA established the permissible exposure level, and the American Conference of Governmental Industrial Hygienists established the threshold limit value. The DoD requires the services to use the most protective exposure limit choosing between the permissible exposure limit and the threshold limit value. For military chemical warfare agents (nerve and blister agents), the Army has published airborne exposure limits.[11] If concentrations are unknown, the atmosphere should be considered IDLH, and a full-face pressure-demand SCBA or full-face pressure-demand combination air-line/SCBA should be worn. This is similar to the maximum use concentration above which filtering respirators should not be worn.

- Nature and location of the work operation or process. The work area, materials, workers’ duties, and actions that must be taken in an emergency all factor into the selection of a respirator. Other considerations include exertion level and climate because workers must be monitored for either heat or cold stress.

- Time period the respirator is to be worn. Many factors affect respirator wear time. Air-purifying respirators have different breakthrough (the penetration of contaminant through an air-purifying element) times, which can vary depending on the hazard air concentrations, temperature, and humidity. If workers use SCBAs, the fixed air supply and cylinder weight can increase the wearer’s breathing labor and thus shorten the wear time.

- Fit testing and employee’s health. Individuals must wear respirators that are properly fit tested and, because respirators increase the work of breathing and stress the heart and lungs, should only wear them after being medically cleared to do so.

- Employee acceptance. Many factors influence whether an employee will accept and properly wear a respirator; chief among these is the influence of a supervisor who adheres to OSHA regulations and advocates for employee health and safety. Further, the respirators should fit well and comfortably, provide little resistance to breathing, allow adequate visibility (including prescription inserts, when necessary), afford good communication with others, and allow the worker to perform tasks safely.

- Respirator characteristics, capabilities, and limitations. Respirator wear is required to protect the worker from workplace hazards and must not impair the workers’ vision, hearing, or communication, or restrict movement. Peripheral vision can be impaired during full-face respirator wear. Workers with vision impairments may obtain prescription glass inserts that can be fitted to the facepiece of the full-face respirator. Full-face respirator wear can also impair mobility in confined areas; working in pairs can minimize difficulties when one worker directs the movements of the second worker. Workers who have hearing difficulty may struggle to hear speech in noisy conditions and should be tested for hearing capability. Further, respirator wearers can demonstrate hearing capability during trial use by wearing the respirator while performing job tasks.

MEDICAL CONSIDERATIONS AND EVALUATION

Respirator wear is a burden to the human body. It presents medical considerations including psychological and physiological issues that can interfere with task performance and reduce work efficiency. Left undetected or untreated, some issues may even be life threatening.

Physiological Effects of Respirator Wear

Respirator wear increases air flow resistance and breathing labor. Filtering respirators increase breathing labor by 20% to 30%, and SCBA units increase it by 100%. The body must work harder to breathe because it takes effort to overcome the inhalation and exhalation valves and to pull air through the respirator dead space and into the lungs. A normal breath measures about 500 mL of air. At rest, humans normally take 12 breaths per minute, which equals 6 L of air inhaled per minute. The normal anatomical dead space is about 150 mL. Respirator wear increases the anatomical dead space because some exhaled air remains inside the respirator; half masks retain 250 mL while full-facepiece respirators retain 750 mL. An increased amount of dead space reduces the volume of fresh air and oxygen moving into the alveoli. As a result, CO_2 levels increase inside the respirator by 2% to 5%. The alveolar partial pressure of CO_2 (Pco_2) increases, and alveolar partial pressure of oxygen (Pao_2) decreases. Some diseases impair the body’s response to increased CO_2 concentrations; these must be detected during the baseline medical examination.

Medical surveillance should detect conditions that restrict or constrict the lungs and increase cardiac demand, such as asbestosis, silicosis, chronic bronchitis, or emphysema. Table 13-1 lists the specific disqualifying conditions for respirator wearers in accordance with National Fire Protection Association Standard 1582.1,7 Wearing a respirator also increases heat production because air inside the respirator is heated from sorption chemical reactions in the filter cartridge during breathing. The body’s ability to dissipate heat decreases and the skin is covered by a respirator and protective coveralls, thus hampering the evaporative cooling process.

Psychological and Physiological Problems

Many respirator wearers report they feel like they are suffocating in the facepiece, even though they have air. Some workers also get anxious or feel claustrophobic while wearing a respirator. Wearers may also report a feeling of increased pressure on the face. Wearing a respirator involves carrying additional weight, increased breathing labor due to increased pulmonary resistance, decreased hearing and vision, and heat stress. Bulk weight is the single most important work factor for those using an SCBA; the extra weight increases the work and physiological demands on the cardiopulmonary system. As a minimum, respirator wearers must have the physiologic capacity to perform at 10 METS (metabolic equivalents) when testing is conducted on a treadmill, particularly if the worker has any cardiovascular (CV) conditions.

TABLE 13-1

SPECIFIC DISQUALIFYING CONDITIONS FOR RESPIRATOR USE

Medical Condition

Problem

Solution

Eye glasses

Eye glasses worn inside the full-face negative pressure respirator prevent a good seal around the mask because outside air leaks in around the temple-bars on the glasses.

Inserts must be provided by the employer for myopic employees who use a respirator.

Contact lenses

Not allowed by federal regulation with any full-face respirator due to their possible contamination and dislocation, which could lead to injury.

Inserts must be provided if the employer cannot obtain full-face mask allowing wear of glasses.

Facial hair

Facial hair that extends between the face and facepiece border does not permit a proper seal.

Shaving or wear of a powered air purifying respirator with loose-fitting hood.

Facial deformity

Marked facial furrowing or deformity due to the loss of teeth, surgery, or scarring may make a proper facial seal impossible.

Wear of a powered air-purifying respirator.

Respiratory conditions

Employees with emphysema may not be able to overcome the increased resistance to breathing caused by the negative pressure respirator. People with chronic bronchitis who take inhaled medication or have a sputum-producing cough may find constant respirator wear difficult.

Wear of a powered air-purifying respirator.

Cardiovascular

Employees with angina, significant arrhythmias, or myocardial infarction during last 12 months are not qualified to wear a respirator.

Perform a cardiovascular assessment and risk factor modification.

Hearing

Employees’ hearing must be adequate to ensure communications and response to instructions/alarms.

Perform a hearing check while the respirator is worn.

Ruptured ear drum

Perforations in the tympanic membrane allow toxic vapors to enter and be absorbed in the respiratory system.

A hooded respirator may provide protection.

Neurological

Inability to coordinate movements and conditions affecting consciousness will disqualify the employee.

Epilepsy controlled with medications for 1 year is not disqualifying.

Endocrine

Medical conditions where the employee may suffer sudden loss of consciousness (eg, hypoglycemia from too much insulin) may be disqualifying.

Perform assessment of hypoglycemic episodes.

Medications

Prescription drugs may affect judgment, performance, or reliability or alter state of consciousness.

Determine if medication is safe for respirator use.

Psychological

A psychological condition that results in poor judgment or reliability should be disqualifying.

History of claustrophobia or anxiety and respirator intolerance may require a trial of wear for 30 minutes.

Heat stroke

May require work restrictions depending on the environment and protective equipment.

Risk factor modification.

Dermatitis

Dermatitis aggravated by using occlusive materials may be disqualifying.

A loose-fitting powered air-purifying respirator may permit the wearer to use the respirator with dermatitis.

Data sources: (1) 29 CFR Part 1910.134. Respiratory protection. (2) National Fire Protection Association. NFPA 1582: Standard on Comprehensive Occupational Medical Protection for Fire Departments. Quincy, MA: NFPA; 2013.

Purpose of the Medical Evaluation

OSHA[1] and US Army regulations[9] require that employees are medically qualified or cleared to wear a respirator, and that they are fit tested and trained. Employees are medically evaluated to ensure they can safely wear a respirator and they have no medical conditions that would put themselves or others at risk.[1] The medical clearance must be done prior to issuing the respirator to the employee. The baseline assessment is a comprehensive history and physical examination that includes a pulmonary function test, physical examination, baseline laboratory work, and a completed OSHA respirator questionnaire. The medical evaluator can perform a use test to ensure personnel who wear respirators in the workplace are safely able to do so while performing their jobs.

The medical evaluation is designed to identify serious conditions including heart problems such as hypertension or prior myocardial infarction, stroke, or angina; respiratory diseases such as asthma, bronchitis, emphysema, or chronic obstructive pulmonary disease; restrictive lung diseases such as asbestosis; neurological conditions that impair sensory function or involve psychological disorders; and musculoskeletal disorders. Personnel who wear a respirator for escape-only purposes do not require medical clearance. However, they must be briefed on the use of the escape respirator and escorted by personnel who can assist them in an emergency.

Who Should Perform the Medical Evaluation?

The medical evaluation must be performed by a physician or other licensed healthcare professional.[1] OSHA defines licensed healthcare professionals as physicians, occupational health nurses, nurse practitioners, and physician assistants who are licensed to perform the respirator assessment in the state in which they practice. OSHA requires the medical examiner to use its mandated medical questionnaire, which is published in Appendix C of 29 CFR 1910.134, OSHA respirator medical evaluation questionnaire (mandatory).[1] If the employee gives a positive response to any of the specific questions, a more thorough medical evaluation is required. OSHA regulations require the healthcare provider’s written opinion regarding the employee’s fitness and a list of any limitations to respirator wear. If medical follow-up is warranted, the licensed healthcare provider must indicate what is needed to assist the examiner in making a recommendation. Some medical conditions prohibit the wear of a negative pressure air-purifying respirator, and in these situations the powered air-purifying respirator may be a suitable alternative.

Frequency of Medical Evaluations

OSHA[1] and US Army regulations[9] require employers to medically reevaluate respirator wearers at least annually using the OSHA respirator questionnaire. The American National Standards Institute (ANSI) recommends a more comprehensive history and physical examination every 5 years for individuals below age 35, every 2 years for those age 35 to 45, and annually thereafter. Special evaluations should be performed after prolonged absences from work for medical reasons or whenever a functional disability is identified. A health assessment may be required more frequently than annually for changes in the health status of the employee when:

- medical signs or symptoms are present that interfere with the ability to use a respirator;

- a supervisor, healthcare professional, or safety/industrial hygiene professional observes that the worker has problems using a respirator;

- difficulties observed during employee fit testing suggest the need for reevaluation; or

- a change in work conditions increases the employee’s physiological burden, such as increased work effort, a change in protective clothing, respirator type, or temperature/humidity changes.

Military personnel who have completed an annual periodic health assessment are deemed fit for full duty and medically qualified to use all respirator types. Civilian employees must complete the questionnaire in Appendix C of 29 CFR 1910.134. Then the examiner reviews the questionnaire responses. The employer must provide the examiner with a copy of the written respiratory protection program, a copy of regulation 29 CFR 134.10, Respiratory protection, and the following information about the job:

- type and weight of the respirator;

- duration and frequency of respirator use (including use for rescue and escape);

- expected physical work effort;

- other protective clothing and equipment; and

- temperature and humidity extremes.

Cardiovascular Risk Assessment and Evaluation Procedures

The healthcare provider must perform a CV risk assessment for respirator wearers in high risk positions (eg, firefighters, police, security guards, and other first responders). The CV evaluation consists of a level A and B screening. Level A screening determines if workers have any CV risk factors. If the CV risk factors are significant, such as a Framingham Risk Score (a risk assessment tool that estimates a patient’s 10-year risk of developing CV disease) greater than 15%, then level B screening is required. Individuals who have coronary heart disease, or a coronary heart disease-risk equivalent, must undergo a level B screening evaluation. The level B CV evaluation consists of a noninvasive treadmill stress test that includes myocardial perfusion scintigraphy (thallium or sestamibi) or stress echocardiography.

Workers with an intermediate Framingham Risk Score (between 10% and 15%) should be referred to their primary care provider for chronic disease management to include dietary counseling, exercise prescription, and reduction of other risk factors. Workers with a Framingham Risk Score greater than 15% should be temporarily restricted from wearing a respirator until the level B screening is completed. Workers with a score above 15% but below 20% may be given a temporary medical clearance for 3 months to use an air-purifying respirator. Individuals should be reevaluated every 3 to 5 years, or sooner if they develop new symptoms or their cardiac risk increases. Individuals who fail level B screening should not use a respirator except for escape purposes.

Pulmonary Function Testing Basics

Spirometry has long been used to screen respirator wearers by measuring lung function, specifically the volume and speed of inhaled and exhaled air. Spirometry is readily available in doctors’ offices because it is inexpensive, compact, and portable. Acute illness, smoking or bronchodilator use, upper or lower respiratory tract infection, operator experience, and individual motivation can affect spirometry results and require additional testing.

Testing Procedures

For each spirometry trial, the patient inhales maximally and then exhales completely. A minimum of three trials are needed to ensure reproducibility. Unreproducible results should be repeated. The volume-time tracing plots volume on the y-axis and time on the x-axis. The flow volume loops plot inspiratory and expiratory flow on the y-axis and time on the x-axis. Normal tracings are available for comparison with the flow and volume loops generated during testing. The results are adjusted for gender, height, age, and race, then compared to norms and presented as a percent of the predicted value. The normal range of the forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV_1) is any value greater than or equal to 80% of the predicted value. The normal FEV_1/FVC ratio (Tiffeneau-Pinelli index) is between 80% and 85%. Spirometry results may suggest that workers need further testing. If the FVC is less than 80%, or the FEV_1 is less than 70% of the predicted value, the individual should be restricted from respirator use for further evaluation. Any patient who complains of a persistent cough, wheezing, or shortness of breath should get a chest radiograph and pulmonary function test.

Abnormal pulmonary function test results can have an obstructive, restrictive, or mixed pattern. The obstructive pattern is altered because there is some pathology that restricts air movement out of the lungs. This causes the volume-time curve to look flatter than normal: the FEV_1 decreases, the FVC is normal, and the FEV_1/FVC ratio is less than 80%. When individuals have a restrictive pattern, interstitial lung disease causes reduced lung volumes and both the FEV_1 and FVC are reduced, but the FEV_1/FVC ratio is normal or slightly increased. The volume-time curve appears normal but is decreased in size. Workers may also have a mixed pattern, where features of both obstructive and restrictive disease are present. A mixed pattern pulmonary function test will show a decreased FEV_1 and FVC; the FEV/FVC or FEV_1% will be reduced as well.

Causes of Obstructive and Restrictive Patterns

Obstructive lung disease is associated with decreased airflow, which results from bronchoconstriction, inflammation of bronchial linings and increased mucus secretion, and loss of lung elasticity. Asthma and smoking are associated with an obstructive pattern. Restrictive lung disease is associated with decreased lung volumes but normal rates of airflow. A restrictive pattern may be seen with diseases that may affect specific parts of the lungs. For example, pleural diseases decrease lung volumes by restricting the expansion of the lungs. Alveolar diseases such as pneumonia and pulmonary embolism decrease lung volume by displacing air or preventing air from filling the alveolar spaces. Interstitial lung diseases such as sarcoidosis, pulmonary fibrosis, silicosis, and asbestosis decrease lung volume by filling the interstitium of the lung.

RESPIRATOR TESTS AND CHECKS

Fit Testing

Respirators are sometimes classified as tight-fitting or loose-fitting. Tight-fitting respirators need a tight seal between the respirator and the user’s face or neck in order to work properly and provide optimal protection. To ensure a tight seal, the employer performs a fit test on a worker using the same make, model, and type of respirator as those used on the job. Tight-fitting respirators shall not be worn when conditions prevent a good seal. OSHA and Army regulations require tight-fitting respirators to be fit tested prior to initial use, when there are changes in facial features, and annually. Facial hair, temple bars on eyeglasses, missing dentures, facial deformities, and jewelry may interfere with the seal. Personnel with beards or eyeglasses may wear devices that are not tight-fitting, such as air-line respirators and PAPRs. Loose-fitting devices do not need to be fit tested. Personnel who perform fit testing must follow ANSI Z88.10 Section 5, Respirator Fit Testing Methods.[12] OSHA regulations require respirator wearers to be fit tested initially before wearing the respirator and at least annually thereafter. If there has been a change in the facial conformation, then personnel should be tested sooner.

Quantitative and Qualitative Fit Tests

Quantitative fit testing determines the leakage around the wearer’s face and sealing surfaces; the results do not rely on a subjective response from the worker. Quantitative fit testing requires expensive equipment, trained personnel, and probed respirators or special filter adapters. Figure 13-8 shows quantitative fit testing equipment attached to a respirator. Qualitative fit testing uses a test chemical to elicit a response from the wearer. These tests are fast, easy to perform, inexpensive, and usually involve an odor test, taste test, or irritant smoke. All respirator wearers are screened to ensure they can detect the fit test agent. Figure 13-9 shows qualitative fit testing equipment.

Figure 13-8. Quantitative fit testing will measure the concentration of particulates outside the mask and compare it with the concentration inside the mask to assure mask seal quality.
Photograph courtesy of Brandon Gardner, Major, Medical Corps, US Army; US Army Medical Department Center and School, Fort Sam Houston, TX.

Negative and Positive Pressure Respirators

Negative pressure respirators include a safety factor of 10 per ANSI Z88.2 para. 9.1.1-2015, American National Standard Practices for Respiratory Protection.[13] Negative pressure respirators must pass the fit test with a fit factor at least 10 times greater than the assigned protection factor.[8] The respirator fit factor is measured during fit testing and expressed as a ratio of the test agent’s concentration level outside the respirator to the test agent’s concentration level inside the respirator facepiece.[2] Respirators with higher fit factors provide greater protection against contaminants. Positive pressure respirators, including PAPRs, must be fit tested in the negative pressure mode by temporarily converting the facepiece into a negative pressure air-purifying respirator or by using a “surrogate” negative pressure facepiece. OSHA allows positive pressure respirators to be fit tested either qualitatively or quantitatively.[1]

Figure 13-9. Qualitative fit testing is done by releasing a chemical with a recognizable odor into the hood space surrounding the respirator and determining whether the odor is detectable in the respirator’s facepiece.
Photograph courtesy of Brandon Gardner, Major, Medical Corps, US Army; US Army Medical Department Center and School, Fort Sam Houston, TX.

Figure 13-10. A positive seal check is a function check of the respirator performed by the wearer who exhales forcefully while covering the exhaust port of the respirator.
Photograph courtesy of Brandon Gardner, Major, Medical Corps, US Army; US Army Medical Department Center and School, Fort Sam Houston, TX.

User Seal Checks

Users of tight-fitting respirators must be trained to perform user seal checks, which is a function test done before each use. To perform the check, a worker generates positive pressure in the mask by exhaling with force while covering the exhaust port, as shown in Figure 13-10. For a negative pressure seal check, the wearer covers the inlet valves of the filter cartridge and inhales deeply, as shown in Figure 13-11. Seal checks are not substitutes for quantitative or qualitative fit tests and should be done per the manufacturer’s recommendations.

Figure 13-11. A negative seal check is a function check of the respirator performed by the wearer who inhales forcefully while covering the intake ports of the respirator.
Photograph courtesy of Brandon Gardner, Major, Medical Corps, US Army; US Army Medical Department Center and School, Fort Sam Houston, TX.

MAINTENANCE

Cleaning and Storage

OSHA regulations require proper respirator maintenance and cleaning, which help prevent skin irritation and encourage worker acceptance of respirator wear. Some contaminants, such as particulates and aerosols, build up on the sealing surface and may enter the breathing zone. In addition, the contaminant buildup on the respirator will cause it to deteriorate. Lastly, a dirty facepiece may obscure vision.

Respirators must be stored in an area free of dust, harmful chemicals and biological agents, sunlight, vibration, shock, extreme heat or cold, insects, and excessive moisture. Plastic reclosable storage bags make great storage devices. Respirators should be packed and stored so the facepiece and exhalation valves rest in a normal position. Respirators must be stored properly without using straps or deforming the facepiece, which can cause facepiece failure. Respirators designated for emergency use should be stored in clearly marked compartments dedicated to emergency equipment and must be accessible at all times.

Inspection and Function Checks

All respirators, even new ones, should be inspected to make sure they are free from defects and not damaged in shipment. All respirators must be inspected before each use and after each cleaning. Emergency use respirators must be inspected before each use, at least monthly in accordance with the manufacturer’s instructions, and before being carried into the workplace. Each employee must inspect and maintain their own respirator. This includes a functional check of respirator connections, and a check of the condition of all parts, including the facepiece, lenses, head straps, valves, connecting tubes/hoses, filters/cartridges/canisters, and air cylinders.

Color Coding

Air-purifying respirator canisters, cartridges, and filters are color coded for rapid identification and to ensure consistency among respirator manufacturers. The standards in ANSI Z88.7-2010, Color Coding of Air Purifying Respirator Canisters, Cartridges, and Filters, permit rapid selection of respirator cartridges.[14]

Breathing Air for Supplied-Air Respirators

OSHA requires that all compressed air meets the specification for Grade D breathing air per 29 CFR 1910.143(i) (1), Nonwater carriage disposal systems.[15] Breathing air stored in cylinders or produced by compressors must be tested, and vendors must have a certificate stating the air meets Grade D breathing air requirements. Organizations that generate their own breathing air, such as fire departments, should sample and analyze air quarterly. The Compressed Gas Association G-7. 1-1997 technical bulletin, Commodity Specification for Air,[16] requires the collection and testing of breathing air. Compressed oxygen must never be used in supplied-air respirators because it poses an explosion risk if oil or grease were previously introduced during compressed-air operations.

TRAINING

Prior to respirator use, OSHA requires employers to train their employees, including personnel who issue respirators and supervisors of respirator wearers, on all aspects of the respiratory protection program. The training goal is to further assure proper respirator selection, use, and maintenance. OSHA regulations require training programs tailored to the educational level and language skills of the employee. Each person who wears respiratory protection in the workplace must be given instruction that includes:

- an explanation for respirator use including hazard identification, the extent of employee exposures to those hazards, and potential health effects if the respirator is not properly worn;

- a discussion about what engineering and administrative controls are being used (if any) and why respirators are still needed for protection in the workplace;

- an explanation of why a particular type of respirator has been selected, along with the function, capabilities, and limitations of that device (especially with regard to IDLH environments);

- instruction on how to inspect, check, don, wear, and remove the respirator, and what to do if a problem is discovered;

- instruction on how to use the respirator in an emergency situation, such as during a malfunction or if the environment becomes IDLH;

- training on proper respirator cleaning, maintenance, and storage procedures;

- information on adverse health conditions (such as asthma) that may limit or prevent the effective use of respirators; and

- a review of the OSHA Respiratory Protection Standard so that employees understand their employer’s obligations with respect to employee protection.

Employees who are trained in respirator donning and wear must physically handle the respirator and practice donning, adjusting the straps, performing seal checks, and determining a proper fit.

PROGRAM EVALUATION

Under the OSHA respirator rule, employers must ensure that the written respiratory protection program is properly implemented in their workplaces and that employees are properly using respirators.[1] Employers must ask respirator users about program quality and identify any program problems. This assessment must include all program elements including proper fit testing, safe respirator wear, respirator suitability for the hazards present, situational use, and maintenance. Problems identified through this assessment process must be corrected immediately.

RECORD KEEPING

The OSHA Respirator Standard requires employers to keep a copy of the written respiratory protection program on hand. Employers must record and retain written information regarding medical evaluations, fit testing, training, and the respirator program in general.[1] Employers can use this information to promote employee involvement in the respirator program, to audit program adequacy, and to provide a record for compliance purposes. Employees can use this information to assess their own health risks.

Medical Evaluation Records

The healthcare provider must keep a medical evaluation record on file for each employee who is required to wear a respirator. This record must include a copy of the OSHA medical questionnaire and the licensed healthcare provider’s written opinion and recommendations regarding the employee’s ability to wear the respirator. These records must be retained and made available per OSHA regulations at 29 CFR 1910.1020, Access to employee exposure and medical records.[17]

Fit Test Records

OSHA requires the employer to keep fit test records on file until the next fit test is administered. If an employee no longer needs to wear a respirator because of reassignment or change of duties, a record must contain annual fit test results and the respirator type used for the employment period.

Training Records

The minimum training documentation includes training dates and the names of the trainees and training administrator. Training records are maintained by the installation respirator specialist.

SUMMARY

This chapter reviewed OSHA requirements for employers to have a respiratory protection program in place when they require employees to wear a respirator. OSHA standards place primary emphasis on utilizing engineering, administrative, and work practice controls to reduce or eliminate occupational exposures to airborne contaminants. However, respirators are often required as an interim measure in those instances where workplace controls are not feasible in reducing exposures. Respirators are the least desirable method of exposure control, and they only provide effective protection if properly selected, fit tested, maintained, and worn. Factors to consider when selecting a respirator include the hazard, hazard properties, hazard concentration, and hazard warning properties (color, odor, etc). Workers require medical clearance prior to use of a respirator, and respirators must be approved by NIOSH. The local industrial hygienist should document any apparent deficiencies in a respiratory protection program and bring them to the attention of the unit commander, site supervisor, or person in charge.

ACKNOWLEDGMENTS

The authors would like to acknowledge the contributions of Irene Richardson, MS, CIH, who was a civilian industrial hygienist at the US Army Center for Public Health when the chapter was written.

REFERENCES

1.   29 CFR Part 1910.134.

2.   42 CFR Part 84.

3.   National Institute for Occupational Safety and Health. Guide to the Selection and Use of Particulate Respirators Certified Under 42 CFR Part 84. Cincinnati, OH: NIOSH; 1996. DHHS (NIOSH) Publication 96-101.

4.   Wood GO. Estimating service lives of organic vapor cartridges. Am Ind Hyg Assoc J. 1994;55(1):11–15.

5.   Cothran T. Service life software for organic vapor cartridges. Occup Health Saf. 2000;69(5):84–86.

6.   NIOSH interim guidance on the use of chemical, biological, radiological and nuclear (CBRN) full facepiece, air-purifying respirators/gas masks certified under 42 CFR Part 84. Centers for Disease Control and Prevention, National Personal Protective Technology Laboratory website. http://www.cdc.gov/niosh/npptl/guidancedocs/interapr070805.html. Accessed August 9, 2016.

7.   National Fire Protection Association. NFPA 1582: Standard on Comprehensive Occupational Medical Program for Fire Departments. Quincy, MA: NFPA; 2013. http://catalog.nfpa.org/NFPA-1582-Standard-on-Comprehensive-Occupational-Medical-Program-for-Fire-Departments-2013-Edition-P1435.aspx#sthash.qotWZ18G.dpuf. Accessed August 8, 2016.

8.   Certified Equipment List. Centers for Disease Control and Prevention, National Personal Protective Technology Laboratory website. https://www.cdc.gov/niosh/npptl/topics/respirators/cel/. Updated August 1, 2016. Accessed August 9, 2016.

9.   US Department of the Army. The Army Respiratory Protection Program. Washington, DC: DA; 2013. Army Regulation 11-34.

10.   US Department of Labor, Occupational Safety and Health Administration. OSHA Technical Manual, Section 8, Chapter 2, Respiratory protection. https://www.osha.gov/dts/osta/otm/otm_viii/otm_viii_2.html#6. Accessed August 8, 2016.

11.   US Army Chemical Management Activity. Current and revised chemical warfare agent AELs. https://www.cma.army.mil/Pages/CMA-Home.aspx. July 26, 2017.

12.   American National Standards Institute. Respirator Fit Test Methods. Falls Park Ridge, IL: American Society of Safety Engineers. ANSI/ASSE Standard Z88.10-2010, Section 5.

13.   American National Standards Institute. Practices for Respiratory Protection. Park Ridge, IL: American Society of Safety Engineers. ANSI/ASSE Standard Z88.2-2015.

14.   American National Standards Institute. Color Coding of Air-Purifying Respirator Canisters, Cartridges, and Filters. Park Ridge, IL: American Society of Safety Engineers. ANSI/ASSE Standard Z88.7-2010.

15.   29 CFR 1910.143(i)(1).

16.   Compressed Gas Association. CGA G-7.1-1997, Commodity Specification for Air. Austin, TX: Trace Analytics Inc; 1998. Technical Bulletin No. 9401A (rev. 01.99). http://www.airsystems.com/Reference/CGA%20Air%20Grade%20Specifications.pdf. Accessed August 8, 2016.

17.   29 CFR 1910.1020.

Chapter 14

INDUSTRIAL HYGIENE PROGRAM MANAGEMENT

SANDRA PARKER-MONK, CIH,* and JOHN W. YASALONIS, CIH†

INTRODUCTION

HISTORY

ORGANIZATION OF THE INDUSTRIAL HYGIENE PROGRAM

PRACTICING ARMY INDUSTRIAL HYGIENE

The Department of Defense Exposure Assessment Model

Army-Specific Requirements

Defense Occupational and Environmental Health Readiness System

Industrial Hygiene Metrics

SUMMARY

*Program Manager, Occupational Health Sciences, Army Public Health Center, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010

†Formerly, Lieutenant Colonel, US Army; Industrial Hygiene Consultant to The US Army Surgeon General, Headquarters, Department of the Army, 5109 Leesburg Pike, Falls Church, Virginia

INTRODUCTION

The intent of this chapter is to describe how the Army applies the art and science of industrial hygiene in its unique and challenging environment. The theory and practice of industrial hygiene is relatively consistent in private industry and the public sector. Both the American Industrial Hygiene Association (AIHA)[1] and the American Conference of Governmental Industrial Hygienists (ACGIH)[2] define industrial hygiene as “the science and art devoted to the anticipation, recognition, evaluation, and control of those environmental factors or stresses, arising in or from the workplace, which may cause sickness, impaired health and well-being, or significant discomfort and inefficiency among workers or among the citizens of the community.”

A fully competent industrial hygienist requires an interdisciplinary education covering the basic sciences, toxicology, ergonomics, and physiology. When Army industrial hygienists couple their scientific knowledge with the art of industrial hygiene, they perform true preventive medicine: eliminating hazards before they cause harm. At all Army installations, industrial hygienists help protect the health and welfare of civilians and soldiers by reducing workplace risk. Controlling hazards, such as degreasing solvents, noise, or carbon monoxide, helps ensure the soldier is in a state of maximum combat readiness.

In this chapter, the term industrial hygienist denotes a qualified professional. The US Army’s military industrial hygienists are environmental science/engineer officers (area of concentration 72D). The Office of Personnel Management classifies civilian industrial hygienists as general schedule (GS) 690 and industrial hygiene technicians as GS 640 (health aide and technician). Defense contractors may also provide industrial hygiene support.

HISTORY

The US Army became seriously involved in the development of industrial hygiene practice during World War I, when workers in military gas mask manufacturing plants needed protection from chemical agent gases and typical industrial, chemical, and physical hazards: varying (and various) gas concentrations, solvents, dust, and noise.[3] Both government- and contractor-operated factories received industrial hygiene evaluations during World War I, but those efforts ceased with the war’s end.

In October 1942, the Department of the Army (DA) established the US Army Industrial Hygiene Laboratory at Johns Hopkins University to conduct occupational health hazard surveys and investigations at Army industrial plants, arsenals, and depots.[4] Workers at these facilities had potentially hazardous exposures to military-unique and industrial maintenance operations. The laboratory concentrated on four technical and scientific areas: field survey, chemical sampling analysis, engineering design, and medicine/toxicology. Compared to World War I, fatalities caused by occupational diseases were brought to extraordinarily low numbers during World War II, and the fact that industrial hygiene personnel identified hazards and recommended control requirements played a significant role in reducing the rates.

The Army Industrial Hygiene Laboratory was transitioned into the US Army Environmental Hygiene Agency, then the US Army Center for Health Promotion and Wellness, then the US Army Public Health Command, and finally the Army Public Health Center (APHC), the de facto provider of industrial hygiene consultation to the Army today.

ORGANIZATION OF THE INDUSTRIAL HYGIENE PROGRAM

The Army occupational safety and health program is divided organizationally and financially at the DA level into occupational safety and occupational health. The safety program (defined in Army Regulation [AR] 385-10, The Army Safety Program[5]) is managed and executed by safety personnel at Army commands, service components, direct reporting units, and installations. The occupational health program is a medical program (defined in AR 40-5, Preventive Medicine[6]) executed primarily by medical department activity and medical center personnel, who support all the commands, components, units, and installations.

The Army occupational health program is divided into two main functional areas: industrial hygiene and occupational healthcare (which includes medicine and nursing). DA Pamphlet 40-503[7] describes the Army industrial hygiene program, which includes support of occupational healthcare personnel by:

- quantitatively defining the level of worksite exposures to hazardous materials, allowing clinic personnel to (a) make informed patient care decisions regarding medical surveillance and (b) target the hazards most likely to cause health effects on workers;

- recommending controls for existing hazards that, when implemented, can eliminate or greatly reduce medical surveillance requirements; and

- operating the Defense Occupational and Environmental Health Readiness System (DOEHRS), a comprehensive health database that provides exposure and other worksite data to occupational healthcare personnel in an easily accessible and usable form.

The primary differences between the safety and industrial hygiene missions are that:

- occupational safety personnel are mainly concerned with the prevention and control of traumatic injury to personnel, and with accidents that result in loss of material, and

- industrial hygienists are mainly concerned with factors at the worksite that cause chronic or acute illness, disease, or injury to personnel.

The programs are most effective when staff of both work together to execute their responsibilities. For example, if acid bubbles out of a lead acid battery on high charge and burns a worker’s unprotected hands, it is an occupational safety issue; however, if the worker inhales the resulting acid mist, and consequently sustains respiratory illness, these are industrial hygiene and occupational healthcare issues.

Personal protective equipment (PPE) also involves dual medical and safety responsibilities. For example, the issue and use of respiratory protective equipment has traditionally been the domain of supervisors and occupational safety personnel. However, selecting the proper respirator requires a detailed industrial hygiene exposure evaluation, and the potential user must be medically evaluated before being required to wear a respirator.

PRACTICING ARMY INDUSTRIAL HYGIENE

The Department of Defense Exposure Assessment Model

Army industrial hygienists provide information on the mission and health impact of health risks to commanders, who can then make decisions that minimize risk. Industrial hygienists collect information on potential hazard sources; exposure pathways; and magnitude, frequency, and duration of worker exposures. They analyze this information to identify the risk of negative health effects from these exposures; determine options for controlling the sources, pathways, and exposures; and quantify the risk. Industrial hygienists also provide exposure information to occupational medicine staff and other healthcare professionals to support medical surveillance. This exposure information contributes to the longitudinal medical record.

In 2000, the Army collaborated with the military services and other DoD components to create a common industrial hygiene business practice that incorporated the best practices of industry and professional associations. The result was the DoD industrial hygiene exposure assessment model (Figure 14-1).[8] This model describes the industrial hygiene exposure assessment process to collect and evaluate exposure data, including exposures at any workplace where Army personnel are employed. Workplaces vary from fixed installations during peacetime operations to wartime deployments.

The elements of the exposure assessment in Figure 14-1 outline the sequence used by industrial hygienists. The process is sequential, with information from earlier steps essential to completing later steps, as follows:

Figure 14-1. Department of Defense industrial hygiene exposure assessment model.
SEG: similar exposure group

Step 1. Define scope of support and resources.

- Through data collection, research, and interviews, identify organizations to be served and the scope of the industrial hygiene services needed. Develop a schedule with required resources for providing services.

Step 2. Perform basic characterization.

- Anticipate and identify potential exposures. Identify the types of operations performed and exposure situations, and the types of hazards that require assessment at each exposure location, by reviewing results of previous workplace assessments, reviewing medical surveillance and injury/illness events and summaries, and meeting with the supervisor and employee representative. Identify the hazard sources using Material Safety Data Sheets or equipment inventories.

- Assess the hazard sources. Describe their operating characteristics (eg, power settings used for an electrical generator) and existing controls (eg, engineering, PPE, administrative). Then qualitatively assess whether or not there are significant personnel exposures to toxic chemicals and/or harmful physical agents based on all available information.

Step 3: Establish similar exposure groups.

- A similar exposure group (SEG) is a tool to effectively and accurately use limited industrial hygiene resources. The industrial hygienist groups similarly exposed workers into an SEG, performs a risk assessment of all hazards and exposures for the SEG, and administratively assigns the exposures and controls to all members of the SEG. A worker may belong to more than one SEG (eg, one SEG for exposures from arc welding, and another SEG for exposure to kerosene-fueled heaters from living in a tent). This allows the industrial hygienist to leverage scarce resources and still collect, analyze, and archive quality information.

- The industrial hygienist establishes SEGs at a level of detail needed to separately identify and evaluate exposures. The hygienist may choose to group more workers together into a single SEG to save time, or separate workers into smaller groups to more accurately identify workers needing training, protective equipment, and medical surveillance. The hygienist may establish SEGs by:

- unit organizational structure, treating an organization or sub-unit as one SEG;

- geographic location or event (eg, space with heat stress, base camp on an old fuel spill, downwind of an uncontrolled chemical release); or

- individual work operation and task (eg, paint removal, sanding, solvent cleaning).

Step 4: Develop a workplace monitoring plan.

- The industrial hygienist develops a workplace monitoring plan with the following objectives:

- monitoring performance of the exposure controls (eg, static pressure in ventilation duct, interlocks on x-ray rooms, testing for carbon monoxide in fuel-heated spaces);

- collecting exposure data to monitor effectiveness of controls (eg, using exposure control charts);

- collecting additional data to improve the accuracy of exposure estimates (eg, reduced standard deviation); and

- complying with periodic monitoring required by regulatory agencies (eg, Occupational Safety and Health Administration [OSHA] regulations on cadmium).

- The information needed in the monitoring plan includes:

- hazard and SEG being monitored;

- purpose of monitoring (eg, monitor controls, exposure trends, improve exposure estimate);

- procedures for measuring exposures or controls;

- number of measurements;

- type of sample or measurement (eg, breathing zone, general area sample, peak noise level, full-shift, duration of task, air velocity in duct);

- location type (eg, general area, breathing zone, source zone);

- location description (eg, center of base camp, representative living quarters);

- conditions required during monitoring (eg, doors open or closed);

- standards used to compare to results (eg, ventilation baseline criteria, occupational exposure limit [OEL]); and

- data analysis procedures (eg, pass/fail criteria, run-chart trend analysis).

Step 5: Characterize exposures.

- The industrial hygienist uses state-of-the art sampling and monitoring techniques to characterize worker exposures. This may be done by what is often a sequential process:

- directly measure exposures (eg, air sampling, noise dosimetry);

- record information on person sampled (eg, name, employee identification number, job title, job series identification number);

- record sample type and location (eg, personal breathing zone, general area, dosimetry, bulk, wipe);

- record PPE worn by person sampled (eg, respirators, gloves, eye protection, face and body protection);

- record environmental conditions (eg, indoors or outdoors, doors open or closed, ambient temperature, pressure, wind speed and direction);

- submit the samples for analysis; and

- determine the time-weighted average or other exposure level and compare to OELs.

Step 6: Assess exposures and provide control plan.

- Industrial hygienists compare the documented exposures to appropriate OELs to determine the need for corrective actions and follow-up surveillance. They calculate and assign prioritization codes to all potential exposures in an SEG. They evaluate effectiveness of controls for each potential route of exposure (eg, breathing zone levels with local ventilation operations, noise attenuation of hearing protection, chemical permeation of gloves). They develop options for controlling exposures, considering inherent effectiveness and reliability of the controls. Control options include:

- eliminating or modifying the process;

- material substitution within the existing process;

- engineering controls (isolation, interception);

- PPE; and

- administrative controls (including training, physical security of hazard source).

- And finally, the industrial hygienist determines if periodic monitoring of the hazardous agent or the controls is required.

Step 7: Report and record.

- Army industrial hygienists use DOEHRS to collect, analyze, and archive all information relevant to occupational exposures. The industrial hygienist uses many means of communication (eg, memoranda, email, meetings) to convey information to decision-makers, workers, supervisors, safety managers, and occupational medicine providers.

Step 8: Reevaluate.

- The exposure assessment process is cyclical. It is often necessary to repeat the exposure assessment process with the goal of improving previous assessments, and thereby continuing to reduce risk.

Army-Specific Requirements

The Army implements the DoD policy to reduce, to as low as reasonably achievable, health risks to each employee from recognized chemical, physical, or biological hazards that cause or are likely to cause death, illness, injury, or reduced mission effectiveness. The lowest OEL for the vast majority of occupational health hazards are listed by the American Conference of Governmental Industrial Hygienists (ACGIH) in TLVs and BEIs (threshold limit values and biological exposure indices).[9] This reference is updated annually based on current science, and the guidelines are developed to assist in the control of health hazards. They are not developed for use as legal standards.

The permissible exposure levels (PELs) developed by OSHA are legally binding. Because the standard promulgation process is so lengthy and new standards are subject to administration stays and legal actions, the OSHA PELs are often less stringent than ACGIH TLVs. The Army believes that its soldiers and civilians are best served by the most stringent standards, affording them the best protection in the workplace, so it is Army policy to use the most stringent OEL available.[7]

Within the Army, there are many military-unique workplaces, operations, types of equipment, and systems. Army personnel are engaged in testing and maintenance of military-unique equipment and systems such as military weapons, military-unique aircraft, military-unique ships, missiles, early warning systems, military space systems, ordnance, and tactical vehicles. They also perform operations such as peacekeeping missions; field maneuvers; combat training; military flight and missile operations; military-unique research, development, test, and evaluation activities; and actions required under national defense contingency conditions. Often the Army must develop a military-unique OEL because an appropriate level does not exist, as well as accompanying sampling and analysis protocols.

For example, after elevated concentrations of orthochlorobenzylidene malononitrile (commonly referred to as CS or tear gas) were found during mask confidence training (MCT) at a basic training site, the Army developed procedures for capsule dispersal to establish an initial CS training concentration in the chamber and maintain that concentration. Also, a new requirement was established for industrial hygienists to conduct semiannual monitoring and hazard assessments for all sites that conduct MCT using CS in test chambers. The organization responsible for the chamber had to implement a periodic cleaning schedule using wet methods to reduce the residual CS build-up in the chamber. Personnel tasked with cleaning the CS chambers were required to wear full-face respirators approved by the National Institute of Occupational Safety and Health for CS exposure, water-resistant disposable coveralls with a hood, water-resistant protective footwear, and gloves. Industrial hygienists assist with respirator fit-testing and selection of appropriate protective equipment.

Defense Occupational and Environmental Readiness System

The Army and all DoD components must collect and analyze health information to support the risk management process during all phases of military operations.10,11 They must also maintain and control access to personnel exposure and medical surveillance records for the duration of employment plus 30 years.[12] DOEHRS is used to carry out this directive. The data collection modules in DOEHRS follow the steps in the exposure assessment model, including a method for establishing SEGs and assessing the statistical validity of exposure monitoring.

DOEHRS data collected at the garrison level, in the field, or on deployments is routinely added to an Army corporate database. This database not only provides a longitudinal exposure record for workers, it also allows for data analysis. Analytical review of the data can answer questions about the prevalence of hazards (eg, how many soldiers are exposed to beryllium); prevalence of risk (eg, how many workplaces have high risk assessment codes); and the accomplishments of local industrial hygiene programs.

Industrial Hygiene Metrics

To ensure timely delivery of quality industrial hygiene services, the Army conducts frequent reviews of their programs by assessing program workload, health outcomes, management effectiveness, and resource utilization. Reviews include program assistance visits and self-reported metrics. A program review involves an organization such as APHC assessing a local program, noting deficiencies, and making recommendations for improvement.

DoD Instruction (DoDI) 6055.5, Occupational and Environmental Health,[8] lists several metric measurements that provide insight into the effectiveness of the local industrial hygiene program. The reduction of work-related occupational and environmental exposures is a real measure of success. The metrics include:

- percentage of shop hazard characterizations completed,

- index of unacceptable exposures,

- percentage of hazards by risk level, and

- percentage completion of the monitoring plan.

SUMMARY

The fundamental goal of Army industrial hygiene is to ensure the health and welfare of the soldier and civilian in an increasingly complex and fast-paced world. Army industrial hygienists must not only maintain a scientific edge, they must also embrace new technologies, effectively communicate risk and risk remediation, and leverage scarce resources to accomplish the mission.

REFERENCES

1.   American Industrial Hygiene Association website. http://www.aiha.org. Accessed October 27, 2016.

2.   American Conference of Governmental Industrial Hygienists website. http://www.acgih.org. Accessed October 27, 2016.

3.   Bayne-Jones S. The Evolution of Preventive Medicine in the United States Army, 1607–1939. Washington, DC: US Department of the Army, Office of The Surgeon General; 1968.

4.   Heaton LD, Anderson RS, Hoff EC, eds. Preventive Medicine in World War II. Vol 9, Special fields. Washington, DC: US Department of the Army, Office of The Surgeon General; 1969.

5.   US Department of the Army. The Army Safety Program. Washington, DC: DA; 2010. Army Regulation 385-10.

6.   US Department of the Army. Preventive Medicine. Washington, DC: DA; 2007, Army Regulation 40-5.

7.   US Department of the Army. The Army Industrial Hygiene Program. Washington, DC: DA; 2013. DA Pamphlet 40-503.

8.   US Department of Defense. Occupational and Environmental Health. Washington, DC: DoD; 2008. DoD Instruction 6055.05.

9.   American Conference of Governmental Industrial Hygienists. TLVs and BEIs: Threshold Limit Values for Chemical Substances and Physical Agents. Cincinnati, OH: ACGIH; 2016.

10.   US Department of Defense. DoD Safety and Occupational Health (SOH) Program. Washington, DC: DoD; 1998. DoD Instruction 6055.1.

11.   National Science and Technology Council. Improving the Health of Our Military, Veterans, and Their Families. Washington, DC: Executive Office of the President, Office of Science and Technology Policy; August 1998. Presidential Review Directive 5.

12.   29 CFR, Part 1910.1020. Access to employee exposure and medical records.

Chapter 15

ERGONOMICS

JOHN PENTIKIS, PhD,* and JAY CLASING, PhD†

INTRODUCTION

THE US ARMY ERGONOMICS PROGRAM

ERGONOMICS RISK FACTORS

RECOGNIZING HAZARDS

ERGONOMICS RISK FACTOR MANAGEMENT

PERSONAL PROTECTIVE EQUIPMENT CONSIDERATIONS

WORKSITE TASK ANALYSES

MANUAL MATERIAL HANDLING

SUMMARY

ATTACHMENT: BASIC ERGONOMICS ASSESSMENT SURVEY FORM

*Ergonomist, US Army Public Health Center, 8977 Sibert Road, Aberdeen Proving Ground, Maryland 21010-5403

†Lieutenant Colonel, Medical Specialist Corps; Manager, Industrial Hygiene Field Services Division, US Army Public Health Center, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010-5403

INTRODUCTION

Ergonomics, the science that explores the working relationship between humans and their working environments, began to evolve in the United States in 1950 due to design problems encountered in military equipment such as airplanes, radar and sonar stations, and tanks.1,2 Ergonomists study anatomical, physiological, and psychological aspects of workers in their working environments with the goal to optimize worker health, safety, comfort, and efficiency. Ergonomists apply knowledge about human capacities and limitations in worksite, job, task, tool, equipment, and environment design in order to fit the workstation to the worker’s comfort and productivity. Ergonomic risk factors are common in today’s industry and can lead to injury. Specifically, nonneutral postures and repetitive motions put individuals at risk for repetitive motion injuries.[3] Repetitive high force motions cause work-related musculoskeletal disorders (WMSDs) when individuals adopt nonneutral body postures for extended periods of time.

THE US ARMY ERGONOMICS PROGRAM

Program Regulations

The US Army Occupational Safety and Health Program consists of an occupational safety and an occupational health program at the Department of the Army level. Army Regulation AR 385-10, The Army Safety Program,[4] defines the role of the US Army Occupational Safety Program at the major Army command and installation levels. Army Regulation 40-5, Medical Services Preventive Medicine,[5] states that the occupational health program is a medical program that is executed along medical command lines at medical centers and Army community hospitals (US Army Medical Department Activity).[4]-[6] Table 15-1 lists Army regulations and pamphlets that apply to the ergonomics program.

In 1987 the Occupational Safety and Health Administration (OSHA) issued its first directive on the subject of ergonomics; in 1992, it began the rule-making process, and in 1995 started drafting the ergonomics standard. OSHA issued its Ergonomics Program Standard on November 14, 2000 (29 CFR Part 1910.9000), which became effective on January 16, 2001. The ergonomics standard was later repealed on March 20, 2001 via Senate Joint Resolution 6. Currently, OSHA cites employers under the Occupational Safety and Health Act of 1970, Section 5 of the General Duty Clause[7] when ergonomic issues put workers at risk for injury.

Program Organization

At the installation level, the commander is responsible for executing the ergonomics program. This is accomplished by establishing an ergonomics subcommittee, integrating ergonomics into day-to-day operations, approving an ergonomics policy, supporting an ergonomics program, and designating an installation ergonomics officer. Based on DA PAM 40-21,[8] the chief of preventive medicine should serve as the chair of the ergonomics subcommittee. Another member of the healthcare team, an industrial hygienist or safety officer, may serve as chair of the ergonomics subcommittee team if that person is more qualified or there is no assigned preventive medicine physician.

TABLE 15-1

REGULATORY BASIS FOR AN ERGONOMICS PROGRAM

Regulation

Description

DoD Safety and Occupational Health (SOH) Program, DoD Instruction 6055, August 1, 1998.

DoD instruction that provides policy, procedures, and responsibilities for administration of a comprehensive DoD OSH Program.

Department of the Army Pamphlet 40-21 15 May 2000, August 15, 2003.

Pamphlet that provides guidance for establishing the ergonomics program as an integral part of the Army Occupational Safety and Health program at all Department of Army facilities.

Army Safety Program, AR 385-10, February 24, 2017.

Army regulation that implements safety requirements of federal and defense regulations.

Preventive Medicine, AR 40-5, May 25, 2007.

Army regulation that implements occupational health requirements of federal and defense regulations.

AR: Army Regulation
DoD: Department of Defense
OSH: Occupational safety and health

An ergonomist must have the requisite training and experience to quantitatively define the level of worksite risk (pounds lifted, repetition rates, push/pull force requirements, etc) and to recommend controls for existing hazards. Typically the installation ergonomics officer is also the occupational medicine physician; the daily ergonomics program support tasks fall to the industrial hygiene staff. The safety officer, installation compensation specialist, occupational therapist, physical therapist, union representative, civilian personnel office representative, and healthcare team are key players in ergonomics team meetings. Figure 15-1 lists ergonomics program components.

ERGONOMICS RISK FACTORS

Occupational Risk Factors

Repeated biomechanical stress and microtrauma can cause WMSD injuries that evolve over time into a painful, debilitating state involving muscles, tendons, and nerves. Back pain, tendonitis, tenosynovitis, bursitis, and nerve entrapment syndromes are all examples of work-related injuries that can be caused by ergonomic risk factors. Ergonomic risk factors such as poor posture, repetition, duration, forceful exertions, mechanical compression, vibration, and cold temperature can decrease blood flow to muscles, nerves, and joints and lead to nerve compression, tendon damage, muscle strain, and joint damage. Prolonged exposure to these risk factors can lead to permanent damage and debilitating medical conditions. There is often a multiplicative risk of developing WMSDs when individuals perform a single task with multiple ergonomic risk factors. Those tasks should be targeted for engineering redesign and administrative controls.

Position or Nonneutral Postures

The terms “position” and “nonneutral posture” are used interchangeably in ergonomics literature. Nonneutral postures are defined as extreme or excessive bending or twisting of the back and upper and lower extremities. Examples include prolonged elbow or shoulder elevation often seen in overhead work; low lifting, which bends the back forward; and typing on a standard keyboard. Some common causes of nonneutral postures are inadequate workspace design, poor hand tool design, and improper lifting.

Repetition

Repetition is the act of performing the same task over and over. Machine- and production-based operations in industrial settings require workers to complete tasks that last less than a few minutes. These tasks can put workers at risk when performed for 2 or more hours per day. Muscles, tendons, and nerves need sufficient time to properly recover; repetitious work may not allow sufficient recovery time and tissue injury may occur.[9] Also, there may be more than one type of ergonomic risk factor present, and repetitious work, when combined with the other risk factors such as forceful exertions, mechanical compression, poor posture, vibration, and cold temperature, may exacerbate the tissue injury.

Figure 15-1. Multiple factors comprise ergonomics. Consideration of all factors ensures workers benefit from ergonomic interventions.
Data Source: California Department of Industrial Relations, Cal/OSHA Consultation Service. Ergonomics in Action: A Guide to Best Practices for the Food-Processing Industry. Oak-land, CA: DIR; 2003.

Duration

Duration is the length of continuous effort required to perform a task. The longer the duration, the longer the recovery time needed to ensure the design of non-fatiguing jobs. The amount of necessary recovery time is dependent on the level of effort required to perform the task.[10] A general rule of thumb is that highly repetitive tasks, regardless of effort, should be designed for 50 minutes of work and 10 minutes of rest per hour. Overtime work should be avoided whenever possible because it lengthens the workday and decreases the body’s recovery time the following day.

Forceful Exertions

Individuals must exert force to accomplish an occupational task. The force applied to lift weights, overcome friction, and correct for poor postural alignment while working can stress muscles and tendons beyond their capacity and lead to damage of muscles, tendons, ligaments, cartilage, bones, and nerves.

Mechanical Compression

Mechanical compression is contact between the body and any external object. Damage to soft tissues can occur when they are exposed to high force requirements (excessive force spread over a small surface area), which increase fatigue and risk for WMSDs. A common example of mechanical compression is using the base of the palm as a hammer. Due to the velocity and impact of the palm contacting an object, irritation and swelling to the underlying muscles, nerves, tendons, and blood vessels may occur. Medical compression worksite incidents commonly occur when workers use tools that have sharp or hard handles, carry objects on the shoulder, and type on a keyboard while resting the wrist on a hard-edged surface.

Vibration

Workers who come in contact with vibrating machines, vehicles, and equipment are exposed to occupational vibration. Vibration can either transmit energy to the whole body through a seat or platform, or to the hands or affected body part through direct contact (known as segmental vibration). Permanent tissue damage can occur during prolonged whole-body or segmental vibration exposure.

Cold Temperature

Cold temperatures lower the core body temperature and can reduce sensory and motor nerve conduction and impair circulation to peripheral tissues. Exposure to temperatures between 50°F (10°C) and 68°F (20°C) reduces manual dexterity, and can accentuate symptoms of nerve impairment such as numbness and tingling.

Individual Risk Factors

Age, gender, smoking, level of physical activity, strength, and abnormal anthropometric measurements are well-known individual risk factors for ergonomic WMSD. Preexisting conditions such as arthritis, bursitis, and joint pain predispose individuals to ergonomic injuries. Also, inefficient work methods such as holding a tool incorrectly may cause an individual to exert excess force. People with individual risk factors may be more susceptible to ergonomic injuries.

RECOGNIZING HAZARDS

From an ergonomics perspective, all work hazards can be traced to one or more ergonomic risk factors. Job analysis is useful for identifying problematic tasks and jobs that illustrate safe levels of task factors and effective work design. Minimizing or eliminating known ergonomic risk factors reduces the risk of WMSD. A well-trained ergonomist can target risk factors, make workstation improvements quickly at little or no cost, and plan for risk factor corrections that require more time and resources.

Active Surveillance

The ultimate goal of active surveillance is to identify hazards and improve workstations before an injury occurs. Injury prevention is critical to reducing injuries and disability in the workforce and lowering workers’ compensation costs. The presence of one risk factor should trigger an active surveillance survey. Trained ergonomics personnel should survey all workstations and observe task performance at least once a year and conduct walk-through surveys for any new or significantly changed job, process, equipment, or method. Worker interviews during walk-throughs can help identify issues with tasks, tools, and workstation design. For example, an interview may reveal that workers manually move 50-lb boxes because a lift table dedicated to that task is broken.

Symptom questionnaires and worksite surveys allow workers to self-report ergonomic risk factors often before injuries occur. The ergonomist can gain insight about worksite issues and prioritize job tasks that require more detailed assessments. It is important to note that workers need a basic knowledge of musculoskeletal disorders for self-reported techniques to work.[11] The attachment at the end of this chapter is an example of a short ergonomics survey tool that health and safety personnel may use to identify ergonomic risk factors.

Health and safety personnel must conduct surveillance to identify WSMD cases with correctable ergonomic risk factors. For example, a laboratory worker seeks medical care for hand and wrist pain and the occupational history indicates worksite ergonomic risk factors exist at the workstation. The health and safety team can perform an ergonomic assessment and risk factor modification to minimize or eliminate identified risks. A worksite intervention may be necessary to determine if other workers are similarly affected.

Passive Surveillance

Safety and occupational health personnel conduct periodic passive surveillance by collecting and analyzing monthly illness and injury reports that identify service members and civilian employees who have experienced a WMSD. Data is analyzed to identify high risk occupations and worksites to target for further evaluation. The ergonomics committee then prioritizes work based on the number and severity of injuries and ergonomic risk factors. Although passive surveillance takes less time than active surveillance, it is not preferred because it focuses on secondary rather than primary prevention. Data regarding military and civilian injuries and illnesses are recorded on OSHA Form 300, Log of Work-Related Injuries and Illnesses, and DA Form 285, the Army Accident Report. Data can also be retrieved from the Office of Workers’ Compensation First Report of Injury Log, a workers’ compensation state form that the installation injury compensation specialist maintains in the human resource office.

ERGONOMICS RISK FACTOR MANAGEMENT

Currently, there is a debate over the extent to which roles worksite and job design play in the development of WMSDs. Some experts insist personal risk factors are more important than worksite risk factors in determining who will develop an injury. For example, research suggests the heavier a person is, the higher the risk for carpal tunnel syndrome.12,13 People who are less physically active are also at greater risk for developing carpal tunnel syndrome. Other research shows there is a strong association between WMSDs and the known risk factors of repetition, force, vibration, nonneutral posture, mechanical stress, and environmental factors. The most reasonable approach to risk factor management is to include three critical elements in program management: ergonomics, wellness, and health. Table 15-2 identifies worksite contributions for WMSD prevention. Figure 15-2 illustrates key components to WMSD reduction.

Ergonomics Contributions

Ergonomists maintain worker comfort and enhance productivity by applying knowledge about human capabilities and limitations in worksite design. Effective job or worksite design (or redesign) enables the safety and occupational health team to prevent or reduce exposure to WMSD risks. Based on the hierarchy of controls, the following is a list of ergonomic interventions in order of priority, from most to least successful as defined by DA PAM 40-21:

TABLE 15-2

WORKPLACE CONTRIBUTIONS FOR WORK-RELATED MUSCOSKELETAL DISORDERS PREVENTION

Ergonomics Contribution

Wellness Contribution

Health Contribution

Process elimination
Engineering controls
Substitution
Administrative controls

Fitness
Excessive weight
Stress management
Smoking cessation

Medical case management
Job limitations
Job specification
Work hardening

Figure 15-2. The Venn diagram illustrates the key components for injury reduction.

- Process elimination. Eliminating a demanding work process essentially eradicates the ergonomic hazard. For example, adopting an automatic bar code scanner would eliminate the ergonomic risk factors associated with a hand-held bar code scanner.

- Substitution. Use of poorly designed hand tools can increase the risk of repetitive motion injury. Substituting a new work process or tool (without WMSD hazards) for a work process with identified WMSD hazards can effectively avoid the hazard. For example, hand tools that require awkward wrist positions (extreme wrist flexion, extension, or deviation) can be replaced with tools that allow a neutral wrist posture.

- Engineering controls. Ergonomic engineering controls redesign the equipment or worksite to fit the limitations and capabilities of workers. Equipment or worksite redesign typically offers a permanent solution—for example, a computer workstation that can be adjusted to a wide range of anthropometric dimensions.

- Administrative controls. Administrative controls help reduce the magnitude, frequency, and duration of exposure to repetitive motion injury risks. Administrative controls change the way jobs are assigned, scheduled, and performed. Workers can be rotated to different jobs or shifts to vary the demands and work routine. Administrative controls include education and training; decisions related to employee rest, break, work schedules; exercise programs; and on-site instruction in lifting techniques. Administrative controls can also include the adoption of policies and procedures to protect the worker like requiring the use of pneumatic hand tools and vibration-damping gloves, and requiring supervisors to enforce the use of protective equipment.

- Personal protective equipment. Personal protective equipment (PPE) refers to items that provide a barrier to a hazard and are worn by workers. There is insufficient research to support the efficacy of most PPE advocated for ergonomics application. In the absence of more definitive research, the following is advised:

- Back belts are not considered PPE and their use is not recommended by the National Institute of Occupation Safety and Health (NIOSH) or the US Army Surgeon General.

- Knee and elbow pads can protect superficial soft tissues from mechanical insult or contact stress. Although workers may perceive reduced discomfort wearing these devices, research has not substantiated that they are able to reduce pressures inside the knee or elbow joints during weight bearing.

- Antivibration (AV) gloves must meet ISO 10819:2013 standards. Hand-arm vibration should first be eliminated at the source or reduced to its lowest level that is practicable through the hazard abatement process. AV gloves are to be used as a final resolution.

Wellness Contribution

Fitness

Increased worker conditioning and strength helps prevent injuries and can reduce fatigue. Workers with stronger muscles use a smaller percentage of their strength than a person with weaker muscles. Healthy and fit workers can work longer between recovery breaks because they accumulate lactic acid more slowly than someone who is less fit. Worksite fitness programs designed to reduce employee WMSD risk should exercise the same body parts used to accomplish the work task to ensure the appropriate muscle groups and soft tissues are engaged. For instance, if lifts from the floor frequently take place during the day, then appropriate hamstring muscle stretches and exercises should be a part of the exercise program.[14] Moderate exercise 30 minutes a day, such as walking at a comfortable speed and using light weights for upper body toning, helps condition workers and reduces WMSD risk.

Excessive Weight

Excessive weight can increase the risk of back and lower extremity injury.[15] The extra pounds overweight individuals carry contribute to fatigue because they place additional pressure on the spine and strain on the back muscles. From a biomechanics viewpoint, a large stomach exerts a constant forward pull on the back muscles, which increases the amount of force on the lower back. Excess weight places the back, especially the L4-L5 disc and the L5-S1 disc regions, at risk for an injury. Furthermore, excess weight also stresses the hips, knees, and ankles. A heavier worker will often experience more hip and knee pain when walking compared to a normal weight individual.[16]

Stress Management

Research has indicated that high stress levels associated with working conditions are linked to adverse outcomes such as increased tardiness, absenteeism, and turnover rates.[17] Social factors, both at and away from work, can also cause stress such as workload, deadlines, interpersonal relationships, domestic and financial problems, and personality types (perfectionists, workaholics, etc). Stress can either aggravate local WMSDs, such as carpal tunnel syndrome, or cause diffuse muscle conditions, such as pain, weakness, numbness, tingling, and tissue swelling.[14]

Smoking Cessation

Studies show there is a causative effect between smoking and WMSDs. Smoking is a strong risk factor for back pain and is thought to cause disc disease due to malnutrition of spinal disc cells. Smoking increases the amount of carboxyhemoglobin-induced anoxia and vascular disease that affects the spinal disc cells. Nicotine enters most body fluids and has detrimental effects on a variety of tissues.[18] Smoking causes vasoconstriction that has been linked to other WMSDs.

Health Contribution

Health contribution refers to controls a healthcare provider implements to reduce the worker’s injury risk. The controls can be applied proactively before an injury or retroactively after an injury has occurred.

Medical Case Management

Medical case management has several components: injury treatment, worksite evaluation, risk factor elimination, WMSD treatment, and expedited return to work. The case management team focuses on early intervention because literature shows that the longer employees are out of work, the less likely they are to return. The likelihood an employee will return to work after 6 months is 50% and after a year no more than 10%.[17] There are morale and personal benefits as well as reduced medical and workers’ compensation disability costs associated with the timely return of an injured employee. Common medical case management practices include self-care and treatment plan oversight, utilization management, and facilitating an injured employee’s return to work.

Job Limitations

The medical case management team works with the treating provider to accommodate worksite job limitations. Worksite accommodations facilitate the timely return to work, prevent injury aggravation, and afford rest and healing time. Restricted duty assignments are coordinated among the supervisor, human resources, occupational health, and safety office. In addition, trained ergonomists should evaluate the workstation for hazardous conditions and redesign opportunities.

Job Specification

A job specification details all the elements that form a job description. An ergonomist should review a job description before it is posted to ensure the physical demands can be performed successfully. A task that exceeds an individual’s normal capabilities may lead to an injury.

PERSONAL PROTECTIVE EQUIPMENT CONSIDERATIONS

PPE should meet the worker’s job requirements and act as a physical barrier between the worker and the hazard. However, PPE may not be the answer to controlling most WMSD hazards; incorrect or ill-fitting equipment may worsen stressors. PPE can cause heat stress, introduce new physical demands because of its weight, and cause worker fatigue, requiring additional rest periods to counteract increased physiological stress. Because PPE is ineffective in preventing nonneutral postures, forceful exertions, and repetitive motions, the choices are limited for ergonomic hazards. PPE is good at preventing vibration hazards; protective barriers such as gloves or vibration dampening wraps or seat pads prevent the transfer of energy. A trained ergonomist should be consulted when selecting PPE.

Figure 15-3. This is an example of improper back belt use. The worker wears a back belt throughout the course of the work day even though tasks may not involve lifting. Using a back belt in this manner can lead to muscle atrophy.
Photograph courtesy of Christina Graber, Army Public Health Center, Aberdeen Proving Ground, MD. Used with permission.

Medical equipment including wrist rests, back belts, and back braces is prescribed by a healthcare provider. The Department of Defense policy and the research literature do not support the blanket use of back belts to prevent back injuries.16,19,20 In fact, wearing a back belt throughout the workday (as shown in Figure 15-3) causes dependency and muscle atrophy.[21] Figure 15-4 also illustrates improper back belt use and how it can lead to a back injury. The credentialed healthcare provider who prescribes medical equipment, such as the back belt, must educate the worker on proper fit and use, and monitor the worker’s wear of the device.

Figure 15-4. In this example, the back belt rides too high and does not support the back during the lift.
Photograph courtesy of Christina Graber, Army Public Health Center, Aberdeen Proving Ground, MD. Used with permission.

WORKSITE TASK ANALYSES

Once job problems are identified and prioritized, further worksite analysis is important in developing solutions. Many techniques are available for workplace analysis, and they vary greatly in sophistication, time investment, detail, and appropriateness. Generally speaking the ergonomist first identifies the parts of the body at risk. Second, the ergonomist analyzes the tasks and workstation design and how they affect the body. Third, once the analysis is complete the ergonomist can develop potential solutions.

Posture Assessment

Any deviation from neutral posture, regardless of gender, size, or physical condition, puts the worker at risk. Ergonomists should directly observe workers to identify stressful or poor postures and contributing factors. Workstation factors, work location, material orientation, and tool shape, along with job task frequency and duration all contribute to workplace stress and poor posture. A basic postural assessment can be completed using a video or digital camera, tape measure, and either a goniometer or protractor. Engineering controls can reduce workplace stressors and allow work to be performed closer to the body; specifically, the shoulders should be relaxed, the arms hanging at the side, and the arms extended no more than 15 to 20 in. The work surface location should be adjusted to ensure work can be performed in a neutral posture. Hand tools should allow the worker to complete tasks in a neutral hand position, that is, no flexion, extension, ulnar deviation, or radial deviation.

Repetition Assessment

Repetitive motions have been linked to a variety of WMSDs in the upper extremities. Unfortunately, the causes of these disorders are complex and no single causative factor has been identified. Ergonomists must perform task analysis to determine whether machine pacing, high-frequency work, or rapid movements contribute to WMSDs. Ergonomists also assess work pace and advise management to consider the costs and benefits of adopting incentives that allow the worker to dictate work pace. Research has shown that when machines pace the work, WMSD injuries increase.[22] The best way to lower WMSD risk is to reduce repetition through automation and decrease production demands. Two administrative controls that are often employed are worker rotation (rotating workers throughout the day to jobs that do not stress the same body parts) and job enlargement (increasing the scope of a job by adding related tasks and variety).

Duration Assessment

Work duration influences the length of the workday and the body’s recovery time before the next work shift starts. Research shows that longer workdays reduce the body’s ability to recover; workers fatigue more easily, and muscle soreness is more prevalent.[23] To compensate for longer work shifts, a workload should not exceed the employee’s physical capacities. A duration assessment considers the length of the shift and any overtime, break schedule, and the nature of the work (light assembly, heavy manual material handling, monitoring or inspection, etc). The ergonomist looks for ways to control long duration tasks by developing appropriate work, rest, and break schedules.

Forceful Exertion Assessment

Forceful exertions refer to job tasks that produce loads on the joints and soft tissues of the musculoskeletal system. The use of force to lift, carry, or operate a tool is common in many jobs. The amount of muscle force needed to perform a task is dependent on the posture and muscles; less force is needed to complete a task with larger muscle groups and proper posture. The goal of ergonomic work design is to complete the task with the least amount of fatigue in active muscles during the work shift. The ergonomist observes all tasks that require lifting; lowering or other manual material handling; holding or using force to overcome resistance (such as squeezing a hand tool); and measures the force and duration of the activity. The exerted force is measured using a hand dynamometer and pinch gauge to estimate forceful hand exertions, a weight scale to measure weights of objects, and a force gauge with high capacity to record forces.

Forceful exertion is controlled by improved posture and minimized load handling. Ergonomists ensure workers use proper posture and decrease functional load and travel of the handled items. They ensure that all lifted items are stable and can be lifted with two hands kept close to the body. Whenever possible, they design jobs to make use of gravity and employ engineering controls. The ergonomist identifies and selects hand tools that are low in weight and have grip handles that allow the hands to function in a neutral posture, and use hoists or tool balancers to support hand tool weight.

Mechanical Compression Assessment

Any outside object that comes in contact with the body creates mechanical compression. The fingers and hands are a common target for mechanical compression; hands are constantly in contact with tools, parts, or equipment. The hand is sometimes used as a hammer when a worker pounds an object in place with a closed fist. Prolonged exposure to mechanical compression of the hands can cause soft tissue damage to the fingers, palm, and wrist.[24] Other body parts are also at risk if they are exposed to hard surfaces, sharp edges, or heavy weights (for example, carrying a heavy item on the shoulder). Mechanical compression is assessed by: (a) identifying contact points between the body, work objects, and work surfaces; (b) determining the contact force; (c) establishing the contact location, either qualitatively (ie, sharp edge or hard surface) or quantitatively (square inches, linear feet, etc); and (d) determining contact duration and frequency.

Good tool design can minimize the impact mechanical compression has on the hands. When considering a hand tool, it is important to select handles that:

- extend past the palm,

- are made of a soft, compressible material, and

- are rounded and have no finger grooves.

Workers are advised to avoid using the hand as a tool when performing tasks.[25] Mechanical compression for other body parts is minimized by spreading force requirements over a larger surface area. For instance, carrying a bag that has a 2-inch shoulder strap will place half as much force on the shoulder as a bag with a 1-inch shoulder strap.

Vibration Assessment

Vibration in the workplace is a common occurrence for individuals who work with powered hand tools or drive heavy vehicles or equipment. Energy is transmitted from a vibrating source to the body through the hands, seat, or feet. Prolonged exposure to vibration can cause permanent tissue damage similar to that seen in Raynaud syndrome.

Segmental Vibration

The use of vibrating hand tools can lead to small blood vessel spasms of the hand, wrist, and arm. This impaired circulation can directly affect muscle function, and continued work can lead to permanent vibration injury or WMSD. For over 20 years it has been demonstrated that replacing worn out pneumatic power tools with new tools that employ vibration-dampening technology increases worker productivity and lowers vibration risk.[25] Vibration equipment is available that allows the ergonomist to conduct segmental vibration surveys. These surveys also involve worker observation and determine exposure frequency. Whenever possible, the ergonomist should compare exposure duration and intensity with known standards such as the American Conference of Governmental Industrial Hygienists threshold limit value for vibration exposure.[26] Segmental vibration exposure is best controlled by eliminating the vibration source. Well-maintained tools, dampening gloves, and tool handles coated with vibration-dampening material also help control vibration exposure.

Whole-Body Vibration

Whole-body vibration is transmitted to the body through vehicle or machinery seats and affects the vertebrae, intervertebral discs, and supporting back muscles. Soldiers sitting in an armored vehicle driving over an unpaved road experience vibration transmitted to the feet from the floor boards and to the buttocks through the seat. Whole-body vibration in combination with other WMSD risk factors such as long-duration tasks in nonneutral postures increases the risk of a back disorder. Whole-body vibration analysis involves observing the worker; determining exposure frequency, intensity, and duration; and comparing these measures with known standards. Whole-body vibration exposure is best controlled by eliminating the vibration source or decreasing the exposure time.

Cold Temperature Assessment

Working in cold temperatures has been linked to repetitive motion injuries of the hands and can reduce manual dexterity. Duration studies in cold environments are conducted with a stopwatch and thermometer. During a cold temperature assessment, the ergonomist measures temperatures to determine if they fall within a certain range and checks with workers to ensure they have adequate clothing and equipment. Workers should have well-fitting gloves to increase finger temperature, clothing that maintains core body temperature on the torso, and hand tools that do not conduct cold.

MANUAL MATERIAL HANDLING

Background

On average, approximately 30% of all workplace injuries are attributed to manual material handling (lifting, lowering, carrying, pulling, or pushing) activities; the majority of injuries are to the back.[27] In workers under age 45, back injuries are the most prevalent cause of disability and the diagnosis with the highest cost in the 30 to 50 age group. Approximately 1% of the US population is chronically disabled and 1% is temporarily disabled due to back injury.[28] From a search using the Defense Medical Epidemiologic Database (DMED), the US Army is approaching 500,000 ambulatory visits a year due to back injuries.[29] These ambulatory visits now exceed 300 cases per 1,000 soldiers annually, and in many instances the case rate exceeds 400 cases per 1,000 soldiers annually.[30] Figures 15-5 and 15-6 contain detailed information on ambulatory back injury cases and case rates. Unfortunately, the DMED does not contain costs associated with ambulatory visits; however, lost work time and disability payments can be three times as much as medical costs.[31] Other common injuries include pinched or trapped hands and fingers, crushed feet and toes, and trauma resulting from a slip, trip, or fall.

Lifting

Although back injury prevention training has existed since the 1950s, there has been no appreciable decrease in back injury rates.[32] Preventing lift-related back injuries is difficult because factors that increase the risk are many and often present at the same time. Figure 15-7 contains a diagram of all the risk factors present when a lift takes place. Back injury prevention or lifting technique training conveys valuable information; however, the best way to prevent a back injury is to reengineer the job to eliminate or reduce physical demands. While lifting technique training can improve body posture, it is not a replacement for task redesign. In order for training to be meaningful, it must target the worker’s activities, be continually reinforced, and take place in a work environment that will not exceed work capacities and physical limitations.

Figure 15-5. Department of Defense Ambulatory data for back injury cases from 2007 to 2012.
Reproduced from Defense Medical Epidemiology Database, Armed Forces Health Surveillance Branch of the Defense Health Agency.

Case Study 1: Engineering Control

This case study demonstrates how engineering controls can minimize WMSD risk factors, improve worker safety, increase productivity, and lower injury risk. Two employees had to lift a trash barrel approximately 4 ft to dump a barrel of waste. Figure 15-8 shows how waste was removed at an office building, before the ergonomic intervention. WMSD risk factors present were forceful exertions from lifting the barrel of waste; poor upper extremity postures from lifting the barrel; and mechanical compression from the barrel. Workers risked back and shoulder strain while tipping the barrel over to empty it. A number of ergonomic interventions, such as the use of a specialized dolly, as pictured in Figure 15-9, can improve a job. Now the job can be performed in half the time with only one worker and all risk factors are eliminated.

Case Study 2: Administrative Control

Figure 15-10 shows a smoke ejector fan stored approximately 7 ft off the ground on top of a fire truck before the ergonomic intervention. Three firefighters had to lift and lower the 86-lb smoke ejector fan and were exposed to several WMSD risk factors: forceful exertion from lifting or lowering the smoke ejector fan; poor posture from lifting with the hands above the shoulders; and mechanical compression of the hands and torso from contact with the fan and fire truck. Workers risked back and shoulder strain as well as trauma to the body if the fan fell on a body part or if they fell off the truck during the manual material-handling procedure.

Figure 15-6. Department of Defense Ambulatory data for back injury case rates from 2007 to 2012.
Reproduced from Defense Medical Epidemiology Database, Armed Forces Health Surveillance Branch of the Defense Health Agency.

Figure 15-11 illustrates how an administrative ergonomics intervention can improve a job through a decision to store the heavy object in a lower location. Although the weight of the fan has not decreased, lifting and lowering the fan to its new storage spot is easier. This ergonomic intervention allows only two workers to lift and lower the fan (more people can assist if needed) approximately 2 ft off the ground. Relocation of the fan has reduced the forceful exertion and improved worker posture as well as decreased manpower and time.

Individual Risk Factors

Individual risk factors change over time. A 55-year-old worker does not have the same capabilities as a 25-year-old worker because capacity declines as people age.[33] A worker who is physically fit can better meet the job’s physical demands and is at less risk for injury than a less fit coworker.[34] Gender and body build differences also contribute to individual risk factors. On average, women have approximately two-thirds the lifting strength of men.[35] Women also work closer to their aerobic capacities than men when performing the same task and therefore, are at a greater risk for injury.[34] Taller people are weaker in lifting strength and are more susceptible to back pain because they lean forward more and have to reach farther.36,37 Lastly, the literature suggests that the ability to handle weight or exert force is limited by a worker’s muscle strength.38,39 Weaker workers who perform lifting activities are more likely to suffer lower back pain.[40]

Figure 15-7. There are multiple risk factors to consider when a lift takes place to ensure a worker will benefit from ergonomic interventions.

Objects and Weight Distribution

Although an object’s weight is a good predictor of low back stress, it is not an absolute measure. Frequency, duration, and posture should be considered when determining a safe lifting weight. The National Institute for Occupational Safety and Health indicates that people should not lift more than 51 lb under ideal conditions.[41] From a biomechanical perspective, objects that weigh the same do not place the same amount of stress on the back. Unevenly distributed loads cause handling problems, and workers experience back stress when they react to unexpected weight shifts. Slowed reaction times may lead to strained back ligaments and injured intervertebral discs. Objects whose center of gravity is farther from the spine place more stress on the back.42,43

Figure 15-8. Waste removal process before ergonomic intervention.
Photograph courtesy of Christina Graber, Army Public Health Center, Aberdeen Proving Ground, MD. Used with permission.

Figure 15-9. Waste removal process after an ergonomic intervention. Notice how the use of an engineering control reduces the risk of worker injury.
Photograph courtesy of Dump Dolly LLC (San Angelo, TX). Used with permission.

Figure 15-10. Lowering of a smoke ejector fan before ergonomic intervention. Notice the firefighters’ poor postures and force requirements as they reach to move the fan.
Photograph courtesy of Christina Graber, US Army Public Health Center, Aberdeen Proving Ground, MD. Used with permission.

The size and shape of an object contribute to the lifting stress. Any item that cannot fit between the knees is too large to lift safely. Collapsible containers such as bags cause problems when lifted, so the shape should be as small as possible. Good handles or couplings are essential to provide load and postural stability during lifting.[44] Research has shown that containers with handles can increase lifting capacity[45] and containers without handles decrease lifting capacity.46,47

A 25-lb object held 25 in from the body requires more force to lift than a 50-lb object held 10 in away. Biomechanical studies demonstrate that holding objects farther from the spine decreases the maximum amount of weight individuals can safely lift.48,49 Studies have also shown that lifting items on or close to floor level greatly increases lumbar back stress.50,51 A properly designed ergonomic workstation ensures that all lifts begin and end between mid-thigh and mid-chest, and ideally occur at knuckle height.

Frequency

Frequency is the most critical task element that determines an individual’s capacity to perform manual material handling.[34] Manual material handling activities that are frequent or repetitious need to be redesigned. Two ways to decrease the frequency material is handled is either to increase the weight limits of objects or increase the task duration. OSHA recognizes task duration as one of the key criteria when designing weight limits for lifting tasks. Furthermore, there is a positive linear relationship between duration and the body’s metabolic demands. When given a choice, workers will decrease the amount of weight they handle and take more time to complete the task.[34]

Figure 15-11. Firefighters relocate a smoke ejector fan after an ergonomic intervention. Notice how relocating the fan from the top of the fire truck to the rear bumper allows for easier access.
Photograph courtesy of Christina Graber, Army Public Health Center, Aberdeen Proving Ground, MD. Used with permission.

SUMMARY

The need for ergonomics will not disappear as technology and equipment improvements allow soldiers to serve more efficiently and civilian employees to work faster than ever. History has shown that technological advances need to be matched by improved workstation design and worker training. The US Army’s ergonomics initiatives are an essential element in meeting goals to maximize troop readiness and reduce civilian employee lost work time and injury costs. The goal of an ergonomics program is to prevent WMSDs through active and passive surveillance. Industrial hygienists, safety officers, and other stakeholders determine if WMSD risk factors exist. Physical therapists, occupational therapists, and occupational health nurses treat symptomatic workers for injuries and rehabilitate them. Command and management support changes in work practices and workstation design to minimize or eliminate identified WMSD risk factors. If any link in the ergonomics chain is weak, soldiers and civilian workers will not receive the support and resources they need to maximize productivity.

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32.   Brown JR. Factors contributing to the development of low back pain in industrial workers. Am Ind Hyg Assoc J. 1975;36(1):26–31.

33.   Aberg U. Physiological and mechanical studies of material handling. Ergonomics.1961;4:282.

34.   Mital A, Nicholson AS, Ayoub MM. Factors to be considered in designing manual materials handling tasks. In: A Guide to Manual Materials Handling. London, England: Taylor & Francis; 1993: 15–16, 22–24.

35.   Roebuck JA, Kroemer KHE, Thomson WG. Engineering Anthropometry Methods. In: Wiley Series in Human Factors Book 3. 99th ed. New York, NY: Wiley; 1975.

36.   Chaffin DB, Herrin GD, Keyserling WM, Foulke JA. Preemployment Strength Testing in Selecting Workers for Materials Handling Jobs. Cincinnati, OH: National Institute of Occupational Safety and Health; 1977. Publication 77-163. https://www.cdc.gov/niosh/docs/77-163/pdfs/77-163.pdf. Accessed October 16, 2017.

37.   Merriam WF, Burwell RG, Mulholland RC, Pearson JC, Webb JK. A study revealing a tall pelvis in subjects with low back pain. J Bone Joint Sur Br. 1983;65(2):153–156.

38.   Yates JW, Kamon E, Rodgers SH, Champney PC. Static lifting strength and maximal isometric voluntary contractions of back, arm, and shoulder muscles. Ergonomics. 1980;23(1):37–47.

39.   Kroemer K. Testing individual capacity to lift material: repeatability of a dynamic test compared with static testing. J Safety Res. 1985;16:1–7.

40.   Chaffin DB. Human strength capacity and low-back pain. J Occup Med. 1974;16(4):248–254.

41.   Waters TR, Putz-Anderson V, Garg A, Fine LJ. Revised NIOSH equation for the design and evaluation of manual lifting tasks. Ergonomics. 1993;36(7):749–776.

42.   Chaffin DB, Moulis EJ. An empirical investigation of low back strains and vertebrae geometry. J Biomech. 1969;2(1):89–96.

43.   Anderson CK, Chaffin DB, Herrin GD, Mathews LS. A biomechanical model of the lumbosacral joint during lifting activities. J Biomech. 1985;18(8):571–584.

44.   Mital A, Ayoub MM. Effect of task variables and their interactions in lifting and lowering loads. Am Ind Hyg Assoc J. 1981;42(2):134–142.

45.   Garg A, Saxena U. Container characteristics and maximum acceptable weight of lift. Hum Factors. 1980;22:487–495.

46.   Snook SH, Ciriello VM. The design of manual handling tasks: revised tables of maximum acceptable weights and forces. Ergonomics. 1991;34(9):1197–1213.

47.   Smith JL, Jiang BC. A manual materials handling study of bag lifting. Am Ind Hyg Assoc J. 1984;45(8):505–508.

48.   Snook SH. The design of manual handling tasks. Ergonomics. 1978;21(12):963–985.

49.   Bean JC, Chaffin DB, Schultz AB. Biomechanical model calculation of muscle contraction forces: a double linear programming method. J Biomech. 1988;21(1):59–66.

50.   Punnett L, Fine LJ, Keyserling WM, Herrin GD, Chaffin DB. Back disorders and nonneutral trunk postures of automobile assembly workers. Scand J Work Environ Health. 1991;17(5):337–346.

51.   Garg A, Chaffin DB, Herrin GD. Prediction of metabolic rates for manual materials handling jobs. Am Ind Hyg Assoc J. 1978;39(8):661–674.

ATTACHMENT: BASIC ERGONOMICS ASSESSMENT SURVEY FORM

Adapted from: Goddard DE, Neufeld KL. Basic Ergonomics Assessment Survey Form. Aberdeen Proving Ground, MD: US Army Proponency Office for Preventive Medicine; 2003.

Chapter 16

AEROSPACE MEDICINE

ALFRED C. EMMEL, MD, MPH*; RAYMOND R. BATZ, DO, MPH†; and JOHN J. VENEZIA, DO, MPH‡

INTRODUCTION

AEROSPACE HAZARDS, ILLNESS, AND INJURY

The Atmosphere and Altitude

Pressure Illness

Thermal Stress

Three-Dimensional Motion

Noise

Sleep and Rest

Weaponry and Injury

Ergonomics

Travel Health Hazards

Common Industrial Hazards

PREVENTION, FITNESS, AND PERFORMANCE

General Environmental

Readiness and Deployment

Personal Protective Equipment

Visual Performance and Protection

MILITARY AVIATION ADMINISTRATION

Safety and Health

Flight Medicine

SUMMARY

*Colonel (Retired), US Air Force; Attending Physician, Emergency Medicine and Occupational Medicine, Presbyterian Hospital, 1100 Central Avenue, SE, Albuquerque, New Mexico 87106

†Captain, Medical Corps, US Navy; Force Surgeon, III Marine Expeditionary Force, PSC 559 Box 6853, FPO AP 96377, Okinawa, Japan

‡Major, Medical Corps, US Army; Associate Program Director, Department of Occupational Medicine, US Army School of Aviation Medicine, 340 Hulse Road, Naval Air Station, Pensacola, Florida 32508

INTRODUCTION

Aerospace medicine is a subspecialty under the American Board of Preventive Medicine that focuses on the health of crews, passengers, and support personnel of aviation and space vehicles. Segments of this population often work and live in remote, isolated, or austere environments. Not surprisingly, the aerospace working environment is replete with physical and psychological stress. Hazards are unique and, not infrequently, immediately dangerous to both life and health.

Aerospace medicine is often considered a subset of occupational medicine with some aspects of family practice and emergency medicine. Aerospace medicine’s unique focus is on aviation occupational and environmental hazards, the prevention and treatment of illnesses and injuries related to these hazards, and the design of airframes and equipment to prevent injuries, foster fitness, and promote health.

This chapter will discuss the practice of aerospace medicine in terms familiar to the occupational specialist by introducing the major hazards, illnesses, and injuries, and the prevention programs that maximize the health, safety, and general well-being of the aviation and space community.

AEROSPACE HAZARDS, ILLNESS, AND INJURY

The Atmosphere and Altitude

Structure of the Atmosphere

The atmosphere provides life on earth with essential elements and protection from harmful agents. Sunlight penetration provides energy and warmth, while harmful high-energy solar and cosmic radiation are largely shielded. Life-essential oxygen and water are maintained as necessary elements, while more harmful carbon dioxide is recycled.[1]

Figure 16-1. Diagram of the atmosphere showing increasing altitude.
Reproduced from: US Department of the Army. Aeromedical Training for Flight Personnel. Washington, DC: DA 2009. Training Circular TC3-04.93. August 31, 2009: 16.

All these events take place in a massive, four-layer gaseous blanket, with the true vacuum of space occurring at an altitude of approximately 1,000 miles. The innermost layer, the troposphere, is most familiar and the site of 99% of human activities. The other remaining layers, in order of occurrence, are the stratosphere, ionosphere (or mesosphere), thermosphere (not pictured), and exosphere.[2] Figure 16-1 provides an overview of the layers of the atmosphere along with their associated altitudes.

The troposphere is approximately 60,000 ft thick. It is not uniform in density from top to bottom: air density at the earth’s surface diminishes rapidly with increasing altitude, reaching half its overall density at 18,000 ft. At this altitude, the oxygen-deficient environment is insufficient to fully saturate hemoglobin. Moreover, as altitude increases, temperatures decrease, reaching freezing temperatures at 8,000 ft and -2°C to -60°C at the higher altitudes where large and fast aircraft travel. Likewise, as temperatures drop, so does humidity, to a low of 5% or less at the upper reaches of the atmosphere. From a physiological perspective, the human body is generally able to adapt to an altitude up to 12,500 ft; above that, the human body is unable to compensate and is considered physiologically deficient.[2]

Altitude-Induced Hypoxia

High altitude exposure and the accompanying decrease in relative ambient pressure lead directly to hypoxia and decompression illness. With increased altitude, the partial pressure of oxygen is decreased unless it is augmented by a mechanical system. Many aircraft cabins are sealed and therefore can maintain a cabin pressure compatible with normal physiological function. Most pressurized aircraft maintain a cabin pressure between 6,000 and 8,000 ft above mean sea level. When flying in an unpressurized aircraft above 10,000 ft, the aviator should breathe oxygen from an aviator’s mask to prevent hypoxia.[2] At higher altitudes, oxygen must be delivered under pressure to maintain sufficient partial pressure of oxygen to saturate hemoglobin.

Military aviators are specifically trained to recognize the symptoms of hypoxia so they can immediately initiate lifesaving interventions in the event of in-flight hypoxia. Progressive symptoms of hypoxia include headache, difficulty performing tasks requiring fine motor skills or higher intellectual functioning, malaise, light-headedness, sleepiness, nausea, giddiness, loss of color vision, blurred vision, tunnel vision, loss of vision, unconsciousness, and finally death, if the hypoxia is not corrected.[2] Hypoxia can also occur if an aircraft loses pressure, either slowly or rapidly, depending on the altitude. If pressure loss is undetected, the time of useful consciousness an aviator has to don an aviation mask and descend to a safe altitude or otherwise remedy the problem will be short. The time of useful consciousness is determined by the altitude to which the aviator is exposed. Table 16-1 lists the times of useful consciousness for various altitudes.[2] In aviation, a flight level is defined as a vertical profile of airspace at standard pressure, expressed as a nominal altitude in hundreds of feet. In-flight treatment for altitude-induced hypoxia involves switching the oxygen regulator to deliver 100% oxygen and descending to an altitude below 10,000 ft above sea level.[2] If symptoms persist upon landing, the aviator should be treated with 100% oxygen via a tight-fitting aviator mask.

TABLE 16-1

TIMES OF USEFUL CONSCIOUSNESS

Altitude in Flight Level

Time of Useful Consciousness

Altitude in Feet

FL 180

20–30 min

18,000

FL 220

10 min

22,000

FL 250

3–5 min

25,000

FL 280

2.5–3 min

28,000

FL 300

1–2 min

30,000

FL 350

0.5–1 min

35,000

FL 400

15–20 s

40,000

FL 430

9–12 s

43,000

FL 500 and above

9–12 s

50,000

Adapted from: US Department of Transportation. AC 61-107A – Operations of Aircraft at Altitudes Above 25,000 Feet MSL and/or Mach Numbers (MMO) Greater Than .75. Washington, DC: US Deptartment of Transportation, Federal Aviation Administration; 2009.

Pressure Illness

Barotrauma

Boyle’s law is associated with a proportional inverse relationship between volume and ambient pressure.[2] Ambient pressure changes with altitude and translates directly to gas volume changes inside physiological tissues. Because a volume of gas is inversely proportional to the pressure surrounding it, this situation can lead to trapped gas disorders.[2] Pain can occur when the increased pressure inside a tissue cavity cannot equilibrate with the environment. Chapter 18 of this textbook, Physiology and Medical Aspects of Diving, provides more information regarding gas laws pertinent to understanding the physiological effects of pressure changes on the human body. Trapped gas disorders are either associated with ascent or descent.

Barotrauma of the sinuses and middle ear (sinus block and ear block, respectively) are usually associated with trapped gas during descent, due to the pressure gradient between the area of trapped gas and the environment. The Valsalva maneuver is typically used to equalize pressure associated with descent when the pressure of the trapped gas is lower than that of the hypopharynx.[3] In this situation, the eustachian tube, a collapsible tube that connects the middle ear to the hypopharynx, acts as a one-way valve to allow pressure equilibration with exhalation against a closed nose and glottis. Unfortunately, the Valsalva maneuver is not effective in managing ascent because the relative pressure in the middle ear is increasing. During ascent, a healthy and patent eustachian tube is required to equilibrate the pressure, often augmented with a swallow. Ear block occurs with descent if the aviator is not able to equalize pressure with Valsalva or any other maneuver via the eustachian tube. Such tube dysfunction is usually caused by inflammation or congestion of the proximal tube due to upper respiratory infection, allergic rhinitis, or other inflammatory disorders. Similarly, sinus block occurs if the ostia, which allow the cranial sinuses to drain and equalize pressure, are not sufficiently patent to allow for normal physiological equilibration during descent.[4] Eustachian tube dysfunction and sinus ostial drainage obstruction associated with allergy or upper respiratory infection are contraindications to flight duties.

Dental and gastrointestinal pain are typically associated with trapped gas during ascent (also see Chapter 18 of this textbook). Dental cavity and root abscesses are rare but severely debilitating causes of ascent-associated pain. Good dental hygiene and a high regard for dental readiness are vitally important in prevention. At higher altitudes, trapped gastrointestinal gases begin to cause discomfort, and may be controlled with eructation (burping) and flatulence. However, on occasion this pressure can only be resolved with descent. To minimize the risk of discomfort, it is important to avoid gas-producing foods and rapid food consumption (increasing swallowed air).

Decompression Sickness

Decompression sickness (DCS) is one of the most potentially dangerous effects of high altitude exposure. DCS occurs when nitrogen bubbles exit solution to enter the tissues and fluids of the body. As discussed in Chapter 18, Henry’s law states the concentration of a gas in solution is directly related to the partial pressure of the gas above the solution and is the primary mechanism for DCS development.[2] Bubbles cause both mechanical and biochemical effects. Bubbles mechanically block small vessels; biochemically, they trigger an inflammatory response, leading to vasoconstriction.

DCS is classified into two types. DCS type I refers to pathology of the integument and musculoskeletal systems caused by bubble formation.[2] Due to the kinds of tissues involved, type I is not thought to be as debilitating as type II DCS. Type II DCS encompasses the more severe forms, including all DCS with neurological or cardiopulmonary symptomatology.[5] The exception to this statement is bilateral pain involving the trunk or hips and should be considered type II DCS. Though nitrogen bubbles are a common etiology in all DCS cases, it is important to realize altitude-related DCS is a unique clinical entity when compared to diving-related DCS.

Approximately 65% of altitude cases and 85% of diving cases of type I DCS involve limb pain. The onset of pain is gradual but develops into a throbbing ache in the affected limb.[2] Usually direct pressure over the painful area exerted by a blood pressure cuff is sufficient to relieve the pain. Pain from ischemia and nerve entrapment would be made worse by applying direct pressure. The pain experienced with type II symptoms is much worse. There is an acute onset of sharp shooting or encircling pain, accompanied by tingling or burning when the central nervous system is involved. These symptoms represent type II DCS disease and must be treated more aggressively.[5]

The skin is often affected, and there are two distinct skin manifestations. The most common symptom is a transient, multifocal itching or crawling sensation. This sensation is common in the hyperbaric chamber and does not require recompression. Venous obstruction and vasospasm can present as confluent rings of pallor, surrounded by areas of cyanosis that blanch to touch.[6] This condition is known as cutis marmorata, which is thought to be more serious. It responds well to recompression, but swelling of the lymphatics may persist.[2] The primary care or occupational health provider should discuss all type I DCS cases with an aerospace medicine physician to ensure type II DCS cases are prevented.

Service members who have type II DCS must be treated immediately, particularly when they exhibit neurological symptoms at any level. The neurological symptoms may range from mild paresthesias to numbness, or weakness limited to one limb.7,8 More severe symptoms may affect the spinal cord in one in ten type II altitude DCS cases. The clinical presentation of DCS is discussed in greater detail in Chapter 18 of this textbook. Spinal DCS is more common in diving environments than flight decompression cases—see Chapters 17, Military Diving Operations, and 18. Cerebral decompression cases occur commonly in altitude cases of type II DCS.9,10 The common symptoms in cerebral decompression range from mild to life threatening and include fatigue, confusion, personality changes, headache, tremor, hemiplegia, and scotomata.9,10 Vertigo, tinnitus, and hearing loss may be symptoms of inner ear DCS, which may mimic round window rupture. Any neurological symptom after a dive or flight should raise the healthcare provider’s suspicion of type II DCS or arterial gas embolism (AGE). Intravascular bubbling may cause cardiopulmonary symptoms of substernal pain, cough, and dyspnea,9,10 present in only 5% to 10% of altitude DCS cases, and may cause circulatory collapse and death if not treated immediately.

Factors that reduce the risk of DCS include adequate cabin pressurization and prohibition from flight for at least 24 hours after diving activities, including SCUBA (self-contained underwater breathing apparatus) or compressed air dives as well as hyperbaric (high-pressure) chamber exposure.9,10 Flight prohibition may be reduced to 12 hours for urgent operational requirements provided there are no symptoms following the dive and the subject is examined and cleared by a flight surgeon (a military medical officer who serves as the primary care physician for an aviation unit). Factors increasing the risk of DCS include a history of DCS.[2] This issue becomes especially important if one works as an inside observer of hyper- or hypo-baric chamber operations, in which exposure seems to be more associated with DCS than actual high-altitude flight. There is limited scientific evidence suggesting that being over 40, being female, exercising strenuously, and having excess body fat may increase the risk of bubble formation and DCS.[2] Hypoxia, alcohol hangover, dehydration, and fatigue have clearly been implicated in an increased incidence of DCS. Patent foramen ovale has also been implicated in stroke and type II DCS, as reported in cases of divers and astronauts, and is likely associated with venous return of bubbles formed in skin or joints moving directly into the arterial vasculature supplying the central nervous system.[11]

AGE is produced when gas emboli enter directly into the arterial circulation, with potentially life-threatening consequences. The most susceptible organs include the heart and the central nervous system. AGE symptoms usually occur within 1 to 2 minutes of surfacing after breathing compressed air. Unconsciousness occurring within 10 minutes of surfacing must be assumed to be AGE and treated immediately.9,10,12 If AGE symptoms are present and resolve spontaneously, they may recur later with increased severity. Therefore, AGE symptoms should be treated promptly, even if they have resolved spontaneously. When deciding whether the etiology is DCS or AGE, it is safer to err on the side of treatment for AGE. In any event, the standard therapy for both conditions is recompression with oxygen.9,10,12

Table 16-2 provides oxygen treatment parameters for recompression therapy.[12] Two basic treatment approaches exist. The first is to treat the patient with 100% oxygen for shorter duration under increased pressure, and the alternative treatment utilizes 100% oxygen for a longer time period.9,12 To triage and refer altitude DCS cases, type II DCS requires that all cases be recompressed urgently or evacuated promptly if recompression is not locally available.9,12 Type I DCS patients should be treated with 100% oxygen for 2 hours and remain under observation for recurring symptoms.9,12 If there are no recurring symptoms, the patient should be limited to light duty without flight or high altitude exposure for 1 week. Instruct the patient to return promptly for hyperbaric therapy if symptoms recur. If symptoms develop at altitude and do not resolve on descent or develop after flight, place the patient on 100% oxygen while arranging evacuation or recompression. If evacuation is delayed and symptoms resolve on 100% oxygen, the patient should remain on supplemental oxygen for 24 hours and on limited duty for 1 week, with no physical training for 72 hours. Recurring symptoms must be treated by hyperbaric therapy.

For an aero medical evacuation (MEDEVAC) of DCS cases, the medical representative must contact a provider familiar with the treatment protocol at a facility with adequate therapeutic capability prior to transport. Additionally, MEDEVAC aircraft should be pressurized to a pressure altitude of 500 ft or less. The patient should be placed on 100% oxygen via aviator mask, in a supine position with neutral head position and uncrossed extremities for transport. To monitor mental status, it is important the medical attendant not allow the patient to sleep. Intravenous therapy access should be maintained with a physiological crystallite solution. Inflatable cuffs should be filled with water rather than air.

Recommended aeromedical disposition for type I patients includes restriction from flight/diving duties for 1 week; type II patients should be restricted from such duties for 1 month. With any suspicion of air embolism, the patient should undergo further examination to rule out cardiac septal defects or pulmonary overinflation syndrome etiologies such as pulmonary bullae.9,12 Persistent neurological sequelae of DCS or AGE should be considered a disqualifying factor for flight duties.

TABLE 16-2

OXYGEN TREATMENT TABLE FOR TYPE I DECOMPRESSION SICKNESS*

Depth (feet)

Time (minutes)

Breathing Media¶

Total Elapsed Time (h:min)

60

20

O_2

0:20

60

5

Air

0:25

60

20

O_2

0:45

60–30

30

O_2

1:15

30

5

Air

1:20

30

20

O_2

1:40

30

5

Air

1:45

30-0

30

O_2

2:15

*Treatment of type I decompression sickness when symptoms are relieved within 10 minutes at 60 feet and a complete neurological exam is normal.

†Descent rate: 20 ft/min.

Ascent rate - Not to exceed 1 ft/min. Do not compensate for slower ascent rates. Compensate for faster rates by halting the ascent.

‡Time on oxygen begins on arrival at 60 feet.

§If oxygen breathing must be interrupted because of CNS Oxygen Toxicity, allow 15 minutes after the reaction has entirely subsided and resume schedule at point of interruption.

¥Treatment Table may be extended two oxygen breathing periods at the 30-foot stop. No air break required between oxygen breathing periods or prior to ascent.

¶Caregiver breathes 100 percent O_2 during ascent from the 30-foot stop to the surface. If the tender had a previous hyperbaric exposure in the previous 18 hours, an additional 20 minutes of oxygen breathing is required prior to ascent.

Source: Navy Treatment Table 5. US Navy Diving Manual, Volume 5. Diving Medicine and Re-compression Chamber Operations. Diagnosis and Treatment of Decompression Sickness and Arterial Gas Embolism. Section 20-5: 20-13–20-17. https://www.uhms.org/images/DCS-and-AGE-Journal-Watch/recompression_therapy_usn_di.pdf. page 20-40.

Thermal Stress

Hypothermic Injury

Injuries due to cold may be local or systemic. In all cases, preventive measures including provision for adequate clothing as well as education on proper responses to emergency conditions may protect against such injury. Frostbite is the most common injury during freezing conditions. Hands, feet, face, and ears are most susceptible to injury due to rapid vasoconstriction and high surface area of the exposed skin.[13] Another form of localized damage is trench foot (or immersion foot), which is associated with poor foot hygiene and long exposure to unfavorable cold and wet conditions. Trench foot is the manifestation of neuromuscular damage, venous thrombosis, and hyperemia in a poorly protected lower extremity.

Cold and wet conditions can also lead to systemic hypothermia in otherwise healthy active adults. As the body’s core temperature drops below 34°C, central nervous system depression occurs.[13] As core temperature drops below 31°C, physiological functions slow, including those measured with vital signs, and more severe hypothermia ensues, ultimately leading to apnea and death, if unchecked. In the resuscitation of a hypothermic patient, slow rewarming is the rule and the provider must watch for complications of hypothermia including electrolyte imbalance, cardiac dysrhythmias, and plasma volume decreases so the capillary area is reduced for fluid exchange. A practical reminder is that a hypothermic patient is not truly dead until vital signs confirming death are taken after the individual’s core temperature has been raised through resuscitation efforts.

Another planning consideration for cold exposure is the wind chill factor. Wind speed and cooling power are proportionally related; however, no matter how uncomfortable one may feel, it is rare for frostbite to occur when the ambient air temperature is above freezing.

Heat Stress

Heat stress occurs when the body fails to adapt to high temperature extremes that result in pathology, associated with the individual’s relation to environmental conditions, work load, and clothing.[14] Sweating is an individual’s physiological response to increased warming. Adaptive behavior to heat stress includes moving to a cooler area, decreasing workload, or changing to lighter weight clothing; however, these mitigating actions may be impractical due to the aviator’s restrictive work environment. Cockpit temperatures may exceed 50°C.[14] Many heat sources, such as radiant, convective, electrical, metabolic, and aerodynamic, may add to heat stress in the cockpit. Heat stress is heightened with protective equipment such as a helmet, gloves, anti-G suit, and chemical defense suit. Dehydration contributes to heat stress pathology as well. Without rehydration, the simple act of sweating, one of the primary means the body uses to maintain homeostasis, will eventually accelerate the pathology of heat stress. Dehydration degrades an individual’s ability to handle workload. Water loss should be limited to less than 1% to 2% of body weight in all individuals, with consideration of even tighter controls for those piloting aircraft.

Risks for occupational exposure to warm environments may be mitigated through acclimatization over the course of 8 to 14 days. Exposure to warm conditions in a controlled nature with mild exercise for 1 to 2 hours results in acclimatization, manifested by more profuse sweating at a lower temperature.[15] Acclimatization allows more effective heat loss and improved thermostasis. There is a mistaken notion that acclimatization results in less sweating and water loss, which is the opposite of what actually occurs.

Three-Dimensional Motion

Acceleration, Loss of Consciousness, and Ejection Injury

Consider that ground travel is largely linear and one-dimensional and water travel is two-dimensional due to the influence of water currents and winds on intended linear travel. Air travel takes on a third dimension because travel includes altitude changes and exceeds the capacity of human sensory, postural, and locomotive systems. Additionally, human-operated aircraft start, travel, turn, and stop faster than any other moving objects, adding to motion-related flight hazards.

Motion stress can be categorized as transient or sustained acceleration. Figure 16-2 depicts the forces acting in all directions. Transient accelerations are short (1–2 second) events typical of ejections and collisions that reach the upper limits of human anatomical tolerance at 20g to 50g. Sustained accelerations encompass the centripetal/centrifugal motion of turning an aircraft at high speeds.[16] In fighter aircraft, sustained acceleration can reach the upper limit of human physiological tolerance at 8g to 9g for up to 30 seconds at a time, and repeatedly for up to 20 minutes or more in a single sortie.

Transient Acceleration

Aircraft ejections are a form of transient acceleration. Adverse effects of transient acceleration are largely anatomical, and characterized by acute physical injury. Common ejection injuries include bony and soft tissue injuries to the face, eyes, and upper and lower extremities, as well as spinal compression fractures.[16] These injuries occur at the moment of ejection and at ground upon landing. Transient acceleration prevention systems are designed to limit bodily injury to the face, head, arms, legs, and spine during ejection, parachute landing, and crash events. Injuries to these anatomical areas have decreased dramatically with improvements in safety systems.

When an aircraft crash is imminent, the aviator may decide to activate an emergency egress system, such as an ejection seat powered by a rocket, catapult, or other ballistic force. There are many types of ejection systems that work under varying altitude and velocity conditions. Some ejection seats, such as the Advanced Concept Ejection Seat II, require no minimum airspeed or altitude to safely eject the occupant from an aircraft.[17] At the other end of the spectrum, egress ejection systems have ensured aviator survival at speeds in excess of Mach 1 and altitudes greater than 50,000 ft.[17]

Ejection seats can be found in both single seat and multi-place aircraft. Upon ejection, the aviator and the seat are propelled up a rail at a high rate of acceleration out of the cockpit and into the elements. The aviator should expect injuries during this sequence. Upon ejection, explosive charges blow the top off the cockpit canopy and propel the seat upward, causing minor to major burns. Due to the positive G forces in the z-axis, the spine is compressed, which can result in fractured vertebrae and herniated discs.[17] These injuries can be exacerbated if the aviator does not assume the correct position before ejection, aligning the spine with the ejection seat’s vector. Also, flying debris from the cockpit can cause trauma to the aviator during the ejection sequence. Once the flyer enters the wind stream, he or she may be subjected to flail injuries, hypoxia, hypothermia, frostbite, and decompression illness.[17] Although engineering designs were implemented to decrease the opening shock of the parachute, the aviator may still experience soft tissue injuries when the parachute opens.

Figure 16-2. Crash forces in Gx, Gy, Gz axes.
Reproduced from: US Department of the Army. Aeromedical Training for Flight Personnel. Washington, DC. DA 2009. Training Circular TC3-04.93, August 31, 2009: 72.

The final insult to the ejected aviator is the landing. Aviators are instructed in proper parachute landing fall technique to absorb the impact with their feet, calves, thighs, buttocks, and upper body. If performed improperly or in rough terrain, significant bony and soft tissue injuries can be expected with ground contact. Following an ejection, the examining physician should consider radiographs of the crew member’s entire spine and other injured areas. As with all military aviation mishaps, the physician must remember that blood and urine specimens as well as a detailed medical history are necessary, as soon as practical, as part of the safety investigation. The treating physician should follow the patient for several weeks to ensure no musculoskeletal or other injuries are inadvertently missed because some injuries may not be immediately apparent.

Sustained Acceleration

The adverse effects of sustained acceleration are largely physiological, characterized by partial or complete G-induced loss of consciousness (G-LOC). G-LOC is extremely dangerous because the unconscious pilot may not be in control of the aircraft for 30 to 60 seconds or longer, possibly leading to catastrophic or fatal results.[16] There are a variety of strategies to prevent G-LOC associated with sustained acceleration. These strategies eliminate acute loss of consciousness events, using combinations of life support equipment, muscle strength training, and breathing maneuvers. Additionally, special accelerative centrifuges are used to train and verify crew readiness for the high-G flying environment.[16] Of secondary importance is the potential for long-term degenerative effects on the spine following 10 or more years of high-G flying exposure.[18]

A loss of consciousness is one outcome of sustained acceleration occurring in the z-axis. Many military aircraft are capable of high-performance flying, including sustainment of high G-forces in multiple axes. G-forces can be exerted in any plane, but are commonly defined by the x, y, and z-axes. Aviators most commonly encounter G-force problems in the z-axis. Gz is a gravitational force that is applied to the vertical axis of the body. If it is experienced from foot to head, it is termed negative Gz and happens when an aircraft pushes into a dive or enters an outside loop. Under increasing negative Gz force, blood flow from the jugular veins to the heart decreases while arterial blood flow to the head increases. “Red out” is a visual condition that occurs when the body experiences a negative Gz force sufficient to cause increased blood pressure in the head and eyes. Red outs are potentially dangerous and can cause retinal damage and hemorrhagic stroke.[19]

Conversely, positive Gz force is experienced from head to foot and happens when an aircraft enters a high-speed turn or pulls out from a steep dive. Under increasing positive Gz force, blood tends to move from the head toward the feet and pools in the lower extremities. “Black out” is a visual condition that occurs when the body experiences a positive Gz force sufficient to lower blood pressure in the eyes to cause a complete loss of vision while conscious. Further sustainment of the positive Gz force may cause G-LOC, as discussed above. If G-LOC occurs while flying in a single seat aircraft, the outcome may be fatal. The aviator will regain consciousness once the positive Gz force load is reduced. This process generally takes seconds to a full minute and may be followed by a latent period of partial consciousness, during which the aviator is unable to make or execute sound decisions.[19]

Many factors affect tolerance to positive G forces. Aviators are trained in the anti-G straining maneuver (AGSM).[19] This maneuver involves activating the lower and upper extremity muscle groups and exhaling against a closed glottis in order to increase blood pressure in the extremities, thereby maintaining adequate venous return to the heart and effective blood pressure in the brain. AGSM allows the blood to return to the heart and remain oxygenated. Aviators are taught AGSM in the centrifuge before actually performing it in the aircraft. Aviators in high-performance aircraft are also fitted with an anti-G suit, a snug-fitting garment that covers the lower extremities and the abdomen. The anti-G suit contains bladders that are inflated with air, providing resistance around the lower extremities and abdomen. Upon onset of positive Gz force, the garment automatically inflates, augmenting the aviator’s AGSM.[18]

To ensure aviators are performing a correct and adequate AGSM, a physician or physiologist reviews AGSM performance by reviewing cockpit audio recordings. These reviews are performed periodically on a preventative basis and any time an aviator experiences G-LOC. Life support equipment must also be evaluated for functionality. Physiological factors that can contribute to G-LOC include dehydration, decreased muscle tone and mass, physical illness, fatigue, and tall stature.[19] The examining physician must search for the etiology of the G-LOC event in order to make recommendations, so the aviator does not experience a similar event. A subset of G-LOC is almost G-induced loss of consciousness. Almost G-induced loss of consciousness generally occurs during and after short-duration, rapid-onset, positive Gz force and is characterized by transient incapacitation, but not loss of consciousness.

Spatial Disorientation

Spatial orientation is the ability to maintain body orientation in relation to the surrounding environment at rest and in motion. Humans sense position and motion in three-dimensional space through sight, sound, and touch (pressure). Because the human body is designed to maintain spatial orientation on the ground in a 1g environment, the three-dimensional flight environment creates a sensory conflict that makes spatial orientation difficult for aviators to maintain.[20] About 10% of all general aviation accidents are due to spatial disorientation, and 90% of these cases are fatal.[20]

During spatial disorientation, the pilot incorrectly perceives linear and angular position and motion relative to the earth. Sensory function limitations may lead to the loss of control. Anxiety reactions may exacerbate the situation and contribute to recurrence. Preventing the cascade of events leading to a spatial disorientation mishap begins with understanding the aircraft’s orientation of flight.[20] Once in the cockpit, aviators must relearn perception skills using ambient and peripheral vision and cockpit instrument displays. Aircraft instruments allow the aviator to appropriately interpret aircraft orientation in a three-dimensional environment.

Visual cues provide for 80% to 90% of the aviator’s decision-making information and are integral to spatial orientation. Ambient and peripheral vision are typically used during daylight. Ambient vision relies on movement, horizon lines, and other visual cues to provide spatial orientation.[20] Peripheral vision provides critical information to the parts of the brain that specialize in tracking movements. Visual stimuli are compared with vestibular, auditory, and somatosensory inputs to corroborate perceived movement and aircraft orientation. During flight without visual cues, for instance in bad weather, discrimination of cockpit instrument markings is critical for spatial orientation.[20] Focal vision, the central vision of the eye, is required to appreciate this fine detail on aircraft instruments. Instrument-derived orientation may conflict with the perceived aircraft orientation provided by sensory-vestibular system or “seat of the pants” flying, but with appropriate training, the pilot interprets the instruments to correctly identify aircraft orientation.

Flight-related sensory inputs also come from the kinesthetic sensors of joints and supporting tissues. Kinesthesias receptors in the skin, capsules of joints, muscles, ligaments, and deep supporting structures are stimulated mechanically and provide sensory input associated with forces acting on the body.[20] Physicians must consider the occupational consequences of aviators who have lost a limb or experienced a significant orthopedic injury or change in weight. These anatomic changes may limit an individual’s capacity to assess spatial orientation, though aviators will likely compensate and accommodate over time. Good spatial orientation relies on the effective perception, integration, and interpretation of visual, vestibular, and proprioceptive sensory information.

Alternobaric vertigo, the pathology associated with positive middle ear pressure that causes vertigo, is another cause of spatial disorientation.[21] There is a well-established association between alternobaric vertigo and eustachian tube dysfunction, typically seen while flying in high-performance aircraft. Because alternobaric vertigo is caused by a positive middle ear pressure, it arises with ascent or from overly vigorous auto inflation of the ear, which can occur during a Valsalva maneuver to clear a congested middle ear.[21] It usually presents with rotary vertigo and without hearing loss. Symptoms are self-limited and resolve when the upper airway inflammation and eustachian tube dysfunction symptoms resolve. Persistent symptoms may indicate perilymphatic fistula; patients should be referred to an otorhinolaryngologist.[21] Risk of vertigo from middle ear pressure is one of the main reasons aviators should not fly with an upper respiratory infection.

Other factors affecting spatial disorientation include weather, fatigue, alcohol or medication use, dehydration, and poor mission preparation.[2] As previously discussed, in foul weather critical visual cues and inputs to the brain are lost, potentially resulting in spatial disorientation. Fatigue, dehydration, and alcohol and medication use are preconditions that reduce the vigilance required to maintain situational awareness. Poor mission planning and preparation may lead to spatial disorientation. Impromptu missions in combat or for aero MEDEVAC may limit advance preparation for the flight due to fatigue or sleep deprivation and this may increase the risk of spatial disorientation.

Pilots who become spatially disoriented may lose situational awareness. However, pilots may lose situational awareness for other reasons besides spatial disorientation. For instance, pilots who get vertigo may lose situational awareness due to the spinning sensation, though they may maintain spatial orientation. Mishaps due to spatial disorientation claim many more lives than other mishaps.

To avoid spatial disorientation, aviators must consider their limitations, remedy correctable factors, properly use capabilities, recognize high risk situations, and stay alert. Aviators must apply operational risk management before flights, avoiding unnecessary risks and weighing operation risk in terms of benefit and cost. Aviators must be well rested, well hydrated, and well fed prior to the flight briefing. Flights during bad weather or conditions such as brownout (sandstorm or rotor wash causing poor visibility due to sand and dust disturbance) should be avoided if possible. In one study, meteorological conditions (eg, brownout, whiteout, or inadvertent entry to instrument weather conditions) accounted for more than 25% of flight mishaps due to spatial disorientation.[2] Physicians and other aeromedical consultants must educate and caution aviators against task saturation and excessive physiological or mental in-flight stress. In the long run, it is important for aviators to remain alert. Vigilance in flying includes maintaining the visual scan while aviating, navigating, and communicating. Transferring controls when the pilot is spatially disoriented in a multi-crew aircraft is another safety measure.[2]

Aviators must maintain vigilance to retain spatial orientation in-flight because the visual, vestibular, and proprioceptive stimuli all rapidly vary in magnitude, direction, and frequency. The various sensory inputs must be reconciled, or a sensory mismatch may occur that can lead to spatial disorientation. Aviators flying under instrument flight rules must get significant training to overcome the spatial illusions and successfully master flying in all conditions and prevent flight mishaps.

Motion Sickness

Motion sickness, which occurs when a person is exposed to real or apparent and unfamiliar motion stimuli, may be an additional component of spatial disorientation. The condition is characterized by dizziness, fatigue, and nausea, which may progress to vomiting, pallor, and cold sweat.[22]-[24] Motion sickness may initially manifest as a headache or somnolence that advances to stomach symptoms. As nausea increases in severity, the individual experiences pallor and sweating. Further worsening leads to an avalanche phenomenon associated with increased salivation, bodily warmth, lightheadedness, and subsequent vomiting. Hyperventilation and air swallowing associated with yawning and sighing may precede emesis. Excessive vomiting may be associated with electrolyte disorders, dehydration, and hoarseness.

Incidence rates vary based on stimulus, strength, and operator susceptibility. Only 1% of passengers become airsick in large, civil transport aircraft during a typical commercial flight. However, during heavy turbulence, one third to one half of airline passengers experience some degree of motion sickness. Experienced aviators, including 59% to 63% of US Navy student pilots, 10% to 75% of paratroopers, and 67% to 85% of shuttle astronauts (during or after flight), have experienced motion sickness.[22]

Motion sickness can significantly complicate operational safety. A pilot suffering from dizziness, fatigue, or nausea is more inclined to lose situational awareness and more prone to spatial disorientation. These symptoms disrupt normal physiology and preoccupy the operator, possibly eroding flight communications and duty performance. Pilots are not the only personnel who can be adversely affected by motion sickness; other crew members such as navigators and mission specialists may become incapacitated during flight and thus compromise mission effectiveness. Additionally, passengers’ conditions at the time of disembarkation are important; those suffering from airsickness may be unable to function in a wide variety of operational duties following flight. Fear and anxiety can lower the threshold for symptoms; therefore, anticipatory briefings on motion sickness and situational awareness are important for passengers as well as the pilot and crew.

Treatment of motion sickness includes fresh air or oxygen, rest, fluids and electrolytes maintenance, parenteral use of antiemetics, and a light diet with adequate hydration.[22] Unfortunately, medications to prevent and treat motion sickness often have undesirable side effects such as drowsiness, altered cognition, sedation, blurred vision, dizziness, and dry mouth.[22] Side effects of prophylactic medications compromise the effectiveness of the drugs and are associated with poor performance. Waiting to use medications until crew or passengers experience symptoms does nothing to alleviate the symptoms and the affected individual may need rest before returning to full duty. Therefore, prevention may be considered the best way to manage motion sickness; early intervention is better than ignoring motion sickness symptoms.[22]

To prevent motion sickness through ergonomics, maintain a supine position as space allows (this reduces incidence by 20%), minimize unnecessary movements, and maintain a view of the horizon, if possible.[22] Adapt the aircraft to minimize low frequency movements (below 0.5 Hz), minimize foul odors such as engine exhaust, and provide cool air in warm conditions to optimize comfort. As individuals become acquainted with and adapt to these provocative stimuli, motion sickness symptoms usually become less frequent.

Noise

Noise-Induced Hearing Loss

Hazardous noise is intense and ubiquitous to military aviation activities. Please refer to Chapter 12, Army Hearing Program, for a more in-depth discussion. Hearing loss was well recognized by the US military in the 1940s following World War II; frequent exposure to artillery, tanks, trucks, ships, and aircraft produced significant hearing disabilities. However, it was the advent of the turbojet engine that eventually forced the military to address hazardous noise and hearing loss.[25] The military aviation community first initiated hearing conservation programs in the 1950s. Not long after, the Occupational Safety and Health Administration adopted hearing conservation regulations for general industry in the early 1970s.

These early jet engines raised occupational noise levels for aircraft maintainers and operators to an extremely dangerous (and often painful) range of 120 to 140 dB. At those noise levels, even very short term exposures caused harmful effects, including permanent, high frequency hearing loss. For persons in the immediate proximity of modern US Navy and Air Force jet aircraft, such as mechanics and crew chiefs, noise levels of 120 to 150 dB remain common and continue to challenge hearing conservation.[25] Even takeoff and landing noise for bystanders, including city dwellers, can be as high as 100 dB. Alternate power units can run extensively during ground-based preflight activities and create noise in the range of 113 dB. Beginning in the 1960s, sonic booms from supersonic aircraft (eg, military, Concorde) became a major concern and eventually led to regulations that protected nearby airport residents. These environmental noise exposures are largely engine related. Of equal concern to the aviation community is cockpit noise.

Cockpit or internal noise comes from various sources, including high-pitched hydraulic systems, cabin pressurization or air-conditioning systems, internally reflected jet engine noise, and in-flight aerodynamic turbulence across the fuselage and control surfaces. All these noise sources are worse in military aircraft because designers chose to favor performance over sound-damping insulation. Modern jet fighters have cockpit noise as high as 120 dB or more.[25] Rotary aircraft, although possessing a different spectrum than fixed-wing aircraft, produce a combination of rotor, exhaust, and gearbox noise inside and immediately outside the aircraft that routinely reaches 125 dB.[25]

Furthermore, it is likely the combination of noise exposure and other ototoxic substances, such as solvents and fuels, can produce hearing loss[25] by lowering the threshold at which it occurs. Other significant hearing loss effects include chronic tinnitus, acute fatigue, and impaired communications. These latter issues directly impact human performance. Further research on hearing loss prevention in the aviation environment is needed because crews currently rely on traditional personal protection measures such as noise-dampening helmets, headsets, and earplugs.

Noise Prevention

Controls for aircraft noise, first initiated over 60 years ago, remain critical for present-day operations. Air Force programs in the 1950s were among the first industrial activities to incorporate containment measures during engine testing, mandatory use of personal protection with ear plugs and muffs, and medical surveillance with periodic pure tone audiometry. These methods remain the mainstay of modern programs even as new technologies, such as active noise reduction, are incorporated into military operations.

The US Environmental Protection Agency implemented the Noise Control Act of 1972 and Quiet Communities Act of 1978 to protect an estimated 16 million people routinely exposed to environmental aircraft noise.[26] The Environmental Protection Agency coordinated all federal noise control activities through its Office of Noise Abatement and Control. This office was phased out in 1982 as part of a shift in federal noise control policy that transferred the primary responsibility of noise regulation to state and local governments. At the same time, the Federal Aviation Administration rewrote Federal Aviation Regulation Parts 36, 91, and 150 to modify aircraft design, airport design, and the scheduling of aircraft operations. At present, the Federal Aviation Administration is developing new standards for a more stringent aircraft design standard.

Unlike the civilian aviation industry, which has reduced noise via quieter engines and aircraft interiors, military aviation has largely relied on alternative or more limited engineering controls, biological monitoring, and especially the use of improved personal protective equipment (PPE). These limited controls have been necessary to maintain engine and aircraft performance. Through its formal occupational health program, the Air Force currently monitors 42% of its active duty workforce for potential hearing loss.[25] Nonetheless, a 2006 Institute of Medicine report noted 10% to 18% of military service members continue to have significant hearing threshold shifts, a rate that is two to five times that of the civilian industry.[27] A recent Navy flight deck study demonstrated that 79% of noise-exposed flight deck personnel had only 0 to 6 dB of effective hearing protection. This inadequate protection was attributed to poorly fitting earplugs as well as the lack of hearing protection. When properly used, helmet and headset attenuation can yield protection up to 45 dB; however, this protection can be offset by bone conduction if the helmet is in contact with the skull. The Navy flight deck study also demonstrated that 75% of subjects did not have properly fitted helmets and ear cups to provide maximal protection.[27]

The optimal solution to hearing problems in the aviation community is for aircraft manufacturers to adhere to noise-reduction criteria that maintain performance and maximize protection for the crew and support team. The new FA-35 Lightning II Joint Strike fighter, for example, shows recent noise testing levels in excess of the 145 dB range. Noise levels in the crew’s quarters below the flight deck are consistently above 100 dB.[27] Engineering controls in the crew’s quarters and quieter engines must be part of the acquisition process. Until these engineering changes are made, the military aviation community will continue to experience higher incidents of noise-induced hearing loss than other occupations. Thus, medical surveillance must continue, and improved personal hearing protective devices must be issued to crew members.

The best PPE provides significant active noise reduction by reducing ambient exposure to loud noise as high as 140 dB to as low as 85 dB. The new hearing protection known as the Attenuating Custom Communications Earpiece System was incorporated into fighter aircraft helmets by Air Force and Navy research labs. The Attenuating Custom Communications Earpiece System provides noise reduction and improves the clarity of voice communications. The system’s noise-canceling microphones and custom-fitted communication ear plugs also provide aviators and maintenance personnel sufficient, effective, and comfortable hearing protection. Figure 16-3 shows an aviator’s helmet and communication ear plugs.

Sleep and Rest

Fatigue, Sleep Deprivation, and Circadian Rhythm Disturbance

The average adult requires 8 hours of sleep each 24-hour period.[28] Several factors contribute to poor sleep. Sleep loss results in a predictable pattern of symptoms, though symptoms may manifest differently among individuals. For example, for some individuals, the loss of only 2 hours of sleep a night for two consecutive nights has been shown to impair performance. After several days of partial or interrupted sleep, most people suffer some degree of impaired performance.[16] Long-range flight operations and multiple-day missions are operational realities in military aviation.

Figure 16-3. Aircrew helmet with communicating ear plugs. Photograph courtesy of Christianne N. Opresko, Major, Medical Corps, US Air Force; Eglin Air Force Base, FL.

Fatigue results from sleep deprivation are associated with prolonged periods of work and the operational stresses of flight.[16] Flight surgeons must be familiar with flight operations and crew stresses including sleep deprivation; circadian desynchronization; prolonged sitting; heat stress; noise; vibration; motion sickness; hypoxia; dysbarism; drugs such as caffeine, alcohol, and antihistamines; bladder distension; barotrauma; G-stresses; and psychological stress.[16]

General George E. Marshall, who was chief of staff of the US Army under presidents Franklin D. Roosevelt and Harry S. Truman, noted the operational consequences of sustained operations during World War II, observing that crews were disoriented, sleepy, and unable to give and receive orders due to fatigue and sleep deprivation that led to attention lapses and poor memory.[16] Aircraft operations can be affected by poor night vision, equipment limitations, and aviator endurance. Advances in aircraft technology make sustained operations longer than 18 to 24 hours possible, so the flight duration is often limited by human endurance.

Sleep deprivation and circadian rhythm disturbances impair performance during sustained operations, so it is critical to identify signs of performance degradation to manage sleep loss and fatigue. Sleep loss and fatigue degrade performance in the following ways:[16]

- Mood and motivational changes. Decreased initiative and irritability may be reported in individuals who experience fatigue and insufficient sleep.

- Attention deficit. Tired individuals have a shortened attention span and cannot concentrate on specific tasks with the same vigilance as when they are rested.

- Memory lapse. The inability to remember recent events may be a sign of sleep loss. Sleep-deprived individuals, after 48 hours of continuous work, are only able to recall 40% of information.

- Delayed responses. During continuous work without sleep, both speed and accuracy suffer. Also, sleep loss causes unpredictable slowing of response times and nodding off, both of which can be dangerous.

- Performance blindness. Deficits accumulate that can go undetected until performance suffers. People can become more rigid in their approach to job tasks and problems they encounter, and flexibility may be critical.

- Interpersonal skills and communication. A major factor in safe flight operations is the crew’s ability to maintain command, control, and communications among all members of the crew. Communication problems due to fatigue and sleep loss often result in improper task prioritization and poor coordination. Breaks seem to increase performance and mood, and built-in breaks may have sustained benefit during long-term flight operations. Even short periods of sleep, such as strategic naps, help increase alertness. Studies have shown 2 hours is the minimum amount of sleep needed to boost performance.

Operators can partially offset sleep difficulties arising from irregular work and rest patterns through physician-prescribed hypnotics. Hypnotics can aid airmen during rest periods scheduled at unusual times of the day and under circumstances that may not be conducive to sleep. A hypnotic should decrease sleep latency, preserve normal sleep architecture, and be free of residual sequelae. The Air Force studied F-16 pilots who flew an average of 149 hours over a 3-month period, and found that sleep aids zolpidem and temazepam were effective when prescribed and monitored by a flight surgeon.[16]

Stimulants are another class of drugs that improve performance during sustained operations. These medications can help an individual maintain vigilance during long duty periods without rest or sleep. Currently the military services use dextroamphetamine and modafanil for long-duration tactical and strategic missions in single-seat fighters and B-2 aircraft. Like hypnotics, direct physician oversight is critical. Caffeine is widely used by crew to maintain alertness, and is generally safe and effective.[16] However, prolonged use of caffeine over time can cause insomnia, nervousness, gastritis, nausea and vomiting, and increase both the heart and respiration rates. Higher doses of caffeine cause headache, anxiety, agitation, chest pain, and ringing in the ears, and very high doses can cause arrhythmias and death.[29]

Fatigue Management

Flight surgeons are in a key position to watch for the onset of sleep deprivation and operational fatigue and recommend corrective actions. Recommendations should include appropriate rest schedules and lodging accommodations to reduce light, attenuate noise, and maintain climate control. Whenever possible, critical mission segments (eg, aircraft recovery) should not be scheduled during the circadian trough. Additionally, flight surgeons can aid commanders and their assigned crew with environmental and life stressors that can add to operational fatigue. Some of these stressors include inadequate diet and irregular meal schedules, uncomfortable or improperly sized equipment, personal and family difficulties, and poor physical conditioning. Several monitoring tools are at the flight surgeon’s disposal, including software that plots a crew member’s past activities and their relationship to circadian rhythm and sleep cycles. The sleep data can be used to track operational fatigue and adjust operations to protect individual safety and mission execution. When appropriate, hypnotics and stimulants may be prescribed to mitigate acute, in-flight fatigue.

Weaponry and Injury

The extreme hazards from the intentional use of modern weaponry are self-evident. Aviators and their maintainers must be familiar with these threats and minimize their effects during air operations and on the ground. Among the broad array of chemical, biological, radiological, nuclear, and high-yield explosives weaponry, those of special interest to the aviation community are chemical, laser, and other directed energy threats. The challenge to protect the aviator with a suitable barrier from chemical exposures in and out of the cockpit has been daunting, focused currently on using specialized PPE or mission oriented protective posture gear, to minimize restrictive effects while providing adequate protection. Lasers present a threat as both a tool (targeting, alignment devices) and a weapon. Laser beams pointed at an aircraft cockpit in-flight not only create a form of intense operational flash blindness from the scattered canopy or windshield illumination, but may also create temporary retinal or permanent corneal injury.[30] Special aviator medical screening programs using Amsler grid interpretation and retinal photography provide monitoring and determine the incidence of laser eye injuries. Laser eye injury management and an assemblage of laser eye protection (LEP) devices are available for use. Additionally, microwave and particle beam forms of directed energy have been developed as weapons and present challenges for crew protection.

Ergonomics

Most aircraft restrict the pilot’s in-flight mobility. Especially during long flights aviators find themselves in an ergonomically challenging workplace. Contributing factors to musculoskeletal disorders, especially neck and back pain, include long periods of stationary work, safety harness wear, exposure to whole-body mechanical vibration (especially in rotary-wing aircraft), PPE such as flight gear, survival equipment, and possibly night vision goggles (NVGs) and body armor. Aviators and their flight surgeons must closely monitor back pain because it is a long-term exposure risk and common complaint among the general population.

Travel Health Hazards

The need for military aviation personnel to respond to events anywhere in the world, on short notice, for prolonged periods of time, and in remote and austere living conditions makes them world travelers. These military professionals must be protected from diseases indigenous to developing countries, by immunization (for yellow fever, typhoid, tetanus, hepatitis, measles, etc); prophylactic treatments (for malaria and traveler’s enteritis); and good hygienic practices in bathing, eating, drinking, clothing, and shelter. Medications and immunizations must not interfere with the aviator’s job performance (some drugs require pretesting or use restrictions).

Common Industrial Hazards

Like many other industrial settings, the aviation environment is replete with general and specific hazards and respective prevention programs. In addition to noise, confined spaces and heights (platform, hoist, and crane operations) are of concern. Lead and asbestos are present in older buildings and must be mitigated according to laws and policies.

Fuels, propellants, and solvents such as jet fuel, hydrazine, and benzene are of special importance in the aviation environment. Jet fuel comes in various mixtures; Jet Propellant 8 is the most predominantly used fuel. Jet Propellant 8 poses an exposure risk for people who inspect and maintain fuel tanks. The concern for fuelers is the combination of chronic below threshold fuel exposures paired with hazardous noise potentially causing more pronounced hearing loss. In addition, Jet Propellant 8 has been found to produce immune suppression in laboratory animal studies, so use of an Air Force protective overgarment is recommended. Hydrazine, an F-16 engine starter propellant, is an acutely toxic substance. It is a mucosal irritant, readily absorbed through the skin in its normal liquid state, and capable of causing skin and eye burns, neurological and hepatic damage, nausea, vomiting, and convulsions, with potential histological damage to liver and kidneys. Among the many solvents used in the aviation environment, benzene, a known carcinogen, is a principal ingredient of concern, and is found in cleaning products and fuels. In all cases, medical surveillance programs generally follow Occupational Safety and Health Administration regulations and National Institute for Occupational Safety and Health guidelines.

Corrosion control involves the removal and replacement of paints, coatings, and platings on both mechanical and nonmechanical portions of the aircraft. Removing old protective layers by sand or bead blasting or using chemicals may result in worker exposures to these agents, heavy metals, and isocyanate paints. Silica and methylene chloride are also used for paint stripping. Exposure to these materials is controlled through the use of local exhaust ventilation, substitution, and respiratory protective equipment. Medical surveillance follows Occupational Safety and Health Administration regulations and National Institute for Occupational Safety and Health recommendations. The paints and coatings used in aviation often contain cadmium and chromates, both of which have superb anticorrosion characteristics. Cadmium is used for plating moving parts; chromium is used in paints that coat the fuselage, wing, and tail surfaces. Because aircraft parts maintenance is a constant process, tight controls and periodic medical surveillance are necessary. Isocyanates used in paints have superior bonding and abrasion resistance but are known pulmonary sensitizers, even at low doses, and even relatively short exposure times require close monitoring for isocyanate sensitization.

Composite materials are increasingly being used in place of traditional aluminum for aircraft fuselages and wing fabrication. These can consist of boron, carbon/graphite, and glass fibers imbedded in a polymer (epoxy or polyester) matrix.[31] Hazards are directly related to the components themselves. The fibers can become particulate irritants to skin, mucus membrane, and lungs; respiratory protection is critical to avoid inhalation. Polymers must be controlled for their largely irritant and sensitizing effects. Exposures occur not only during manufacture and repair, but also following aircraft mishaps during the crash investigation, when burning materials can release fibers and particulates.[31]

Ionizing radiation methods are used for nondestructive investigation of aircraft structural integrity. Workers are monitored via dosimetry, similar to methods for medical radiology. Radar systems that emit nonionizing microwave radiation may cause physical effects with short-range exposures. Workers must be aware and take protective measures to avoid short- and long-term exposures. Chapter 22 of this textbook, Ionizing Radiation, addresses precautions and protective measures.

PREVENTION, FITNESS, AND PERFORMANCE

Workplace injuries can happen to any employee regardless of the type of work. Each year hundreds of thousands of people are injured at work. These injuries cost both employees and employers billions of dollars annually in health costs and lost work time. Injury data and near-miss incident reviews must be analyzed to find ways to prevent future workplace injuries through the adoption of proper safety procedures and workplace practices.

General Environmental

Whether in garrison or on deployment, occupational medicine providers need to perform several services to ensure force protection and human performance enhancement. These safeguards include ensuring food and water quality, optimizing the unit’s medical readiness to fight, and supporting the operational mission.

One of the basic functions of aerospace medicine involves safeguarding the food and water military personnel consume. Systematic surveillance ensures food safety and quality at the time of procurement or receipt, during storage, and at the time of serving. Likewise, water sources, storage, and distribution systems are routinely monitored for bacteria and chlorine residuals. In the Air Force, ensuring food and water quality and safety is the key task for deployed preventive aerospace medicine teams. In the Army, this is a joint effort of the Preventive Medicine and Veterinary Corps services. During Operations Iraqi Freedom and Enduring Freedom, personnel who performed food receipt inspections identified food spoilage in the hot Middle East environment and guarded against tampering when convoys transported food across long distances.

Personnel ensured water quality through source analysis—bottled water was purchased only from approved vendors after source water was treated with reverse osmosis filtration and chlorination. High temperatures rapidly neutralized chlorine, which then required frequent monitoring for appropriate chlorine residuals. Also, storage in bladders and water distribution through tent cities posed a challenge to maintaining potable water. The distribution system’s integrity in field conditions is paramount in preserving potability.

The population at risk must be optimally fit to effectively execute deployed operations. Optimization begins with the home station ensuring all military members manage their diet, weight, aerobic, and strength fitness. The services’ fitness programs provide for unit level fitness activities, testing, and management for noncompliant members. Each member undergoes a periodic health assessment to screen for health maintenance, health changes, disease risk factors, counseling, and medical interventions. Immunizations are given as needed depending on the deployed location. Every service member has an individual medical (mobility) readiness status, which indicates deployment readiness based on system-defined health parameters. In aggregate, the command (ie, Air Force Wing) has visibility of its population, ensuring its medical readiness and ability to deploy anytime.

Air Force bioenvironmental engineers and Army environmental science officers are charged with supporting surveillance for chemical and biological attacks in concert with civil engineering readiness. Sampling, substance identification, and plume characterization are bioenvironmental engineering’s key roles. Its capabilities are crucial to an airbase’s ability to survive and operate following an attack of any kind. Chemical gas mask fit testing is another service provided by bioenvironmental engineers. Depending on the military threat, deployed troops may be issued chemical and biological antidotes.

Readiness and Deployment

Assessment

Military medicine is now linked with individual medical readiness. Individual medical readiness is assessed throughout the year, but is particularly focused during an annual preventative health assessment (PHA) visit. During this encounter, the primary care clinician documents readiness, consolidates evidence-based clinical preventive services, conducts occupational health and risk screening, reviews the health record, makes referrals for specialty physical examinations, conducts deployment health assessments, and performs individualized counseling, testing, and treatment. The PHA visit has replaced the annual Air Force physical; however, in the Army, the PHA is only part of the annual flight physical. All service members are required to receive an annual PHA during which the six elements of individual medical readiness are measured and documented in MHS Genesis (the new electronic health record for the Military Health System). The six elements of individual medical readiness include:

1. absence of deployment-limiting conditions;

2. dental readiness;

3. laboratory tests (human immunodeficiency virus, DNA, blood type);

4. immunizations;

5. medical equipment; and

6. completion of the PHA questionnaire.

Readiness tracking allows for real time data updates during the PHA. In the case of those on flight status, the review should encompass a hearing status update, visual acuity check, and update on occupational hazards. Readiness assessments are also done both before and after deployment. International Classification of Diseases, Tenth Revision coding guidance for all readiness assessments may be found in the Military Health System medical coding guidlines.[32]

New Accession Exams

New accession exams are performed on every new recruit or employee. These comprehensive physical examinations include blood tests and radiographs. The labs and physical exams are tailored to the existing occupational hazards. Air Force pilots are evaluated at the 711th Human Performance Wing Human Systems Integration Directorate with specific tests including echocardiography as well as an exam by a team of aeromedical specialists. In the Navy and Army, all aviation applicants are evaluated by the Naval Aerospace Medical Institute and the Army Aeromedical Activity, respectively, to ensure quality control and database exam records that can be used for comparison later. The entry examination ensures the member meets all physical demands of military service, screens for existing physical problems that would prevent the member from performing duties, and establishes a medical baseline to detect service-connected physical problems.

Flight exams are performed annually in conjunction with the PHA. These exams are more stringent as the risk to the pilot and aircraft increases from flying class I to flying class III. The sole pilot of a high-performance jet aircraft undergoes a class III flight physical.

Modified Duty Programs

Modified duty programs involve a brief or prolonged illness. To place someone “on quarters” is a medical recommendation given to military members who cannot perform their required duties because of a medical condition.33,34 Quarters are a temporary administrative program lasting 24 to 72 hours. If the member has a condition that exceeds this timeframe, then medical leave can be used. If the medical condition is ongoing and requires a longer work absence, the member can obtain a temporary physical profile. With a physical profile, the active duty member can be restricted from participating in certain or in some cases all of their duties. These restrictions protect the member by ensuring prompt and appropriate medical care and preventing deployment or leave status where medical supervision may be limited or inadequate. An active duty member can stay on this program for 365 days before a medical evaluation board (MEB) is required. An MEB is a detailed summary of medical care submitted on behalf of the military member to the military treatment facility’s commander or a designee. A panel of three appointed physicians reviews the individual’s history and physical findings, considers other specialty care providers’ medical opinions on the likelihood of recovery or resolution of a particular medical condition, and then makes one of three recommendations.35,36 The MEB can recommend a member return to active duty without restrictions, convene a physical exam board consisting of a panel of specialists who meet with the member, or recommend to medically retire a member, bypassing the need for a physical exam board.[36]

Profiles noting a physical restriction are issued for documentation as well as protection (ensuring a member does not perform duties that could cause injury). Hearing loss is an example. As hearing worsens, a member’s profile rating may change from excellent hearing (H1) to lower levels (H2 or H3). Many jobs require a minimum hearing level for worker safety. An individual who is unable to meet those requirements may need a waiver to continue working in the specialty or at a specific job site. A waiver is very much like the MEB process in that a summary of medical care is completed; however, the panel of physicians is generally smaller and the individual’s physical ailment is permanent and unlikely to change.[33]

A similar profile program for aviators is the duty not involving flying (DNIF) status. All personnel on flying status need a medical disposition from a flight surgeon for flying duties. A member who cannot safely fly is placed in a DNIF status. The status of the crew member is recorded on the DD Form 2992, Medical Recommendation for Flying or Special Operational Duty, used by all services. Flight surgeons record flight status as either qualified or disqualified and the DD Form 2992 is maintained in the crew member’s flight records. There is no definitive length of time a person remains in DNIF status, but a general rule is no longer than a year. After a year, an MEB or physical exam board should be considered.[33] Once the MEB is complete, an aeromedical summary, which includes waiver recommendations to the approving authorities, is submitted for review by the respective services’ aeromedical review sections. The Air Force uses the grounding management information system or aeromedical services information management system, tracks all DNIF crew, and generates a weekly report for review by the flight surgeon staff. The use of information management systems ensures aviators receive proper medical follow-up. All of these programs ensure commanders have a fit and healthy force able to safely accomplish the flying mission.[37]

Fitness Testing Programs

Fitness testing programs are used to ensure military members are fit for duty. Fitness and overall good health practices are vital to any organization but especially in the military during arduous and austere operating conditions. Every active duty member is required to pass a physical fitness test that measures strength, physical conditioning, and aerobic fitness. The fitness testing program is also based on the military member’s profile status. If the member is restricted from certain physical requirements, then a fitness program is tailored to meet individual needs. If the member is unable to perform and maintain a minimum level of fitness, then the MEB or physical exam board process is initiated.

Counter Fatigue Programs

Counter fatigue programs are available for all aviators; those on flying status undergo ground testing for counter fatigue medications prior to use during flight in operational environments.[38] Although dextroamphetamine has traditionally been used, modafanil has recently also been shown to attenuate many of the cognitive deficits associated with inadequate sleep with fewer side effects than dextroamphetamine. The sleep aids temazepam, zolpidem, and zaleplon have been used successfully in the treatment of circadian rhythm disturbances, especially when transitioning through several time zones or when the time zone changes are rapid. These medications are used in conjunction with missions that do not allow for adequate sleep/rest cycles or adequate time zone adjustment.[38]

Circadian rhythm or “jet lag” fatigue is of particular operational concern, especially with the need to rapidly deploy troops who are fully mission capable upon arrival. Researchers with the Warfighter Fatigue Countermeasures program at Wright Patterson Air Force Base, Dayton, Ohio, have developed counter-fatigue measures such as optimal crew work/rest schedules, sleep-enhancing techniques and circadian rhythm adaptation, and assessment of alertness enhancing medications. One such measure is the Fatigue Avoidance Scheduling Tool. This interactive software program allows mission planners, flight surgeons, and aerospace physiologists to assess the effects of work/rest cycles, circadian rhythms, performance declination with sleep loss, and sleep inertia.[38]

Personal Protective Equipment

PPE is used as the only measure of protection when engineering and administrative controls are not feasible. Employees and employers must be educated regarding workplace hazards and the controls necessary to protect workers. Physicians, industrial hygienists and safety professionals must assess the potential risk for workplace-associated injuries. They should review each of the basic hazards and determine the hazard type, risk level, and seriousness of potential injury. They should also consider the possibility of simultaneous exposure to several hazards. Assessment should then lead to selection of the appropriate controls to include engineering controls, administrative controls, product substitution, and/or appropriate PPE selection.

A variety of devices are available to provide a barrier between the worker and hazardous exposure. Eye protection equipment comes in such forms as safety glasses, goggles, and face shields. There are many types of skin protection such as gloves, aprons, and full body suits made of materials impervious to chemicals. For example, flight gloves and suits are made of flame-resistant Nomex (DuPont, Wilmington, DE) material.

If the air in the workplace contains fine particles, sprays, mists, or toxic gases, there is almost certainly a risk of exposure to a worker’s respiratory system. Workers in these areas should wear respirators. Air-purifying respirators filter contaminants out of the air, while supplied-air respirators provide an air source free of contaminants or additional oxygen in oxygen-deficient working environments.

If any substance in the workplace can fly, splash, or drip into the eyes, the worker likely requires eye protection. This protection may be as simple as safety glasses with splash guards or more involved, such as heavier duty goggles or face shields to protect against impact or trauma risks to the eyes or face.

High noise levels can cause hearing loss.[19] Often workers and employers are unaware of the degree of noise exposure. Noise exposure can be intermittent and perceived as nonthreatening. Protecting a worker’s hearing is complicated by the perceived inconvenience of wearing hearing protection. A proper assessment of noise exposure, hearing protection training, and periodic follow-up testing for hearing loss are all essential parts of the hearing program.[19]

Visual Performance and Protection

While visual cues are valuable on the ground, they are absolutely essential to flight operations. As such, vision constitutes a critical portion of entrance physical examinations, where candidates are expected to possess excellent visual acuity, color vision, depth perception, and binocular vision.

Color Vision

Color perception allows a person to quickly distinguish objects from each other, interpret important information (eg, traffic signals and sports jerseys), and process information more efficiently. Even small changes in color perception can affect interpretation and situational awareness. Technological advances and harsh environmental conditions challenge the warfighter’s ability to assess color; therefore, it is critical for healthcare providers to be aware of color vision physiology, abnormal color vision, and color vision testing.

Color vision is an extraordinarily complex process involving physics, biology, and psychology. The physics of color begin with light that is either reflected off a surface or emitted from a source. A person considered to have normal color vision has three classes of cone photoreceptors within the retina, with each tuned to a range of short (blue), medium (green), or long (red) wavelengths of light. After the cones receive light stimulation, the biology of color vision begins.[39] The remaining retinal layers convert light energy into neural signals via electrochemical processes. These neural signals are then transmitted to the visual cortex for further processing. Color perception and visual processing mostly occur within the occipital lobe of the brain.

The main components in color vision are hue, brightness, and saturation. Hue is the name given to a particular wavelength interpretation, for example, red and blue. Brightness is the perception that a given hue is emanating light; for example, a red car may appear dim red when dusty and bright red when newly polished.[39] Saturation is the amount of color concentration. For example, pink, red, and scarlet are varying degrees of the same hue at the same brightness, but with different amounts of red. Color vision is subject to misinterpretation or illusions resulting from the brain’s rules of interpretation.[39] For example, objects in the distance are more faded in color than near objects. On a clear day, a distant mountain that appears crisp and sharp in color will often be interpreted as being much closer to the observer than it really is. It is important to note without a psychological interpretation of wavelength, color does not exist. For individuals who do not have the same mechanisms or processes as most people, color still exists, but in a skewed form.

While most people are considered color normal, roughly 6% to 8% of males and 0.4% of females experience some form of color blindness.[39] Total color blindness (ie, monochromatism) is exceptionally rare and is due to the complete lack of retinal cone cells. Medications, genetics, disease, and ocular appliances (eg, colored spectacle lenses or LEP) may alter color perception. The severity of color deficiency can range from mild to severe. A color-deficient person may confuse stimuli in the short end of the spectrum (blue-yellow deficiency) or, more commonly, in the medium and long ends of the spectrum (red-green deficiency).[39]

Even mild color vision alteration may affect occupational safety. Color-deficient individuals require more processing time for color-based information, and they are known to make significantly more errors than color-normal individuals. In 2002, the National Transportation Safety Board made a significant discovery following a commercial airliner mishap. The safety inspectors found the main cause of the aircraft mishap was the pilot’s color vision deficiency.[40] The pilot was unable to distinguish the runway lights during an approach, and as a result, the aircraft collided with trees 3,100 ft short of the runway. Such mishaps underscore the importance of color vision testing, not just upon entry into the military, but also during routine physical exams, with the diagnosis of certain health problems, or after brain or ocular injury.

Color vision testing assesses an individual’s ability to name colors, distinguish between different colors, and match different objects of the same color.[41] Tests vary considerably in their ability to identify a color deficiency, determine superior color vision, or determine if a person is able to perform a particular color-dependent task. The most common and reliable color vision tests include the Ishihara pseudoisochromatic plate, Farnsworth-Munsel 100 Hue, and Farnsworth Lantern.[41] All color vision tests require specific lighting conditions, a proper test environment, and a skilled administrator to ensure accurate results. It is also important to maintain the tests in a cool, dry environment free from the sun and fingerprints; a color vision test that has been faded by the sun or exposed to fingerprints suffers pigment alteration, which may result in color-deficient individuals passing a test they would otherwise fail. The cone contrast test has replaced the pseudoisochromatic plate and Farnsworth Lantern tests as a more sensitive screening tool for general red-green color deficiencies.[41]

The growing importance of color vision in the military aviation environment (from pilots to air traffic controllers) is important for testing and safety. In the past, most color demands in the cockpit were minimal. Cockpits had a small number of red or green lights. Most color was outside of the aircraft: blue lights on the night taxiway; flashing red, green, or white lights on other aircraft; and occasionally red and green flares. Little time was spent processing color information, because these lights centered around safety and navigation. Today’s multifunctional aircraft displays are not comparable to past cockpits. Pilots in military aviation environments are required to assess cockpit displays, external navigation aids, and aeronautical charts for air-to-ground and air-to-air operations. Additionally, aircraft carrier operations require the color detection of flight deck jerseys, signal wands, deck lights, and signal lights and beacons. Cockpits feature polychromatic, multifunctional displays that present flight management and control data with over 256 color shades. These colors are often superimposed on each other, requiring excellent discrimination. Color use in aviation has increased dramatically, as has the time spent examining color displays, tools, and the environment.

Though color vision requirements in aviation have become more sophisticated, color vision testing has not. Current studies have found large variabilities in color vision tests, administration, and integrity.[41] Universal tests and standards are needed to reduce the variabilities in color vision testing results. Additionally, there is debate regarding the proper assessment of perceptual color in the aviation environment. The Commission Internationale de l’Eclairage (International Commission on Illumination) has developed a metric for quantification and measurement; however, while the metric provides a standard for clinical assessment, its application to aviation remains unclear.

The Research and Technology Organization of the North Atlantic Treaty Organization recently called for a more objective color vision assessment that takes into account special flight circumstances.[42] These circumstances include ambient lighting, display size, object versus aperture color, task requirements, and the importance of color. Current tests built specifically for the aviation environment are promising. These tests range from lanterns with a wider range and stronger system for representing the spectral array found in aviation, to tests that mimic actual demands, such as map reading, head-up display stimuli, and air traffic control signal lights.

Lastly, few aviation communities utilize testing of blue-yellow color discrimination despite its importance. A number of pharmaceuticals affect color perception, especially of blue-yellow,[42] and the blue-yellow axis is the most affected by aging-related color vision changes. Additionally, demands of the flight environment subject all visual pathways to disruption; again, the blue-yellow pathway is most affected. It is important that future research examining color perception and aviation include the blue-yellow axis. If there is any doubt regarding an individual’s color vision status, it is best to refer the case to a color vision specialist, who can administer and interpret more specialized and sensitive color vision tests.

Laser Eye Protection

Many eye components are prone to laser-induced damage. The retina is the most vulnerable,[19] due to the intense concentration of visible and near-infrared wavelengths of light onto the retina by the eye’s optical components. Symptoms can range from no impairment to severe visual loss and pain, depending on the severity and location of the insult. It is important to note most laser-induced retinal insults are painless, because the retina has no pain receptors. Overall, lasers can affect vision by producing glare, interfering with dark adaptation, inducing flash blindness, or causing temporary or permanent vision loss.[19]

Due to the risk of enemy and friendly laser fire, all branches of the US military utilize some form of LEP, usually in spectacle or visor format. The overall goal of LEP is to block laser threat wavelengths from reaching the eye while concurrently allowing a maximum amount of nonthreat wavelengths to pass through. Because some useful wavelengths of light are blocked in this process, LEP is always a visual compromise. Users can expect slightly reduced daytime visual performance and color perception and significantly reduced nighttime visual performance (unaided). Another drawback is the fact that one pair of today’s LEP cannot protect the user from all laser threats.[19] Therefore, LEP must be carefully selected, based on the power and wavelength of the laser threat. The latest military LEP combines older dye-based protection with newer, high-tech reflective technology.[43] The result is an expensive but highly capable LEP that protects against multiple hazardous laser systems and minimizes the impact to visual performance. Figure 16-4 provides an example of coated thin film LEP on the visor of a crew helmet.

Night Vision Goggles

NVGs are electro-optical sensors, which use an image intensifier tube to amplify visible and near infrared light energy. The image intensifier converts incident photons into electrons, which are then multiplied and converted back into viewable photons.[44] The result of this intensification process provides the user with a two-dimensional, monochromatic image of the nighttime scene. Most importantly, the scene detail is increased from a 20/200 to 20/400 scotopic (ie, nighttime) image to near-photopic (ie, daytime 20/30) visual acuity levels.[44] Just as the human eye’s spatial discrimination varies with illumination and contrast, so too does the NVG image quality. Actual acuity with NVGs depends on the NVG specifications and the night environment. Military specifications for NVG acuity can vary, but most NVG systems provide 20/30 visual acuity or better under ideal environmental conditions and after proper focusing techniques.

Figure 16-4 Laser eye protective film on the visor of an aircrew helmet.
Photograph courtesy of Alfred Emmel, Colonel (Retired), Medical Corps, US Air Force; Presbyterian Hospital, Albuquerque, NM.

Two important components of NVGs are the objective lens and the diopter (or eyepiece) lens. The objective lens focuses the reflected light energy from an object onto the image intensifier.[44] Improper objective lens focus will result in poor visual acuity and suboptimal sensor performance. Once the amplified electrons are converted back into photons, the diopter lens focuses the output image onto the user’s eye. Proper diopter focus is required to avoid eyestrain or eye fatigue. The diopter lens can correct for simple, mild myopia (nearsightedness) and hyperopia (farsightedness). There are three main NVG designs: monocular, biocular, and binocular. The AN/PVS-14 used by some ground forces is a monocular design. It has one image intensifier, housed between the objective and diopter lenses, and the user views objects in direct line-of-sight with one eye. The AN/PVS-7, the most common NVG used by ground forces, has a biocular design. Its single image intensifier amplifies the night scene, and, through combining optics, the intensified image is presented to both eyes simultaneously. The AN/AVS-9, used by Navy and Marine Corps flight personnel, has a binocular design; each eye has its own independent NVG monocular.[44]

The NVG design limits the user’s ability to estimate distance and depth. All NVGs should be focused and aligned so the user experiences no accommodation or ocular convergence. With monocular designs, only one eye sees the image and there is no binocular information available to estimate distance or depth. With binocular design, each eye sees the same image and binocular designs provide for limited binocularity and stereopsis. Beyond 600 ft, where binocular cues cease to provide useful information, humans naturally use monocular cues for distance and depth estimations. These same cues provide the majority of the distance estimation and depth perception to NVG users.

Spatial orientation requires more conscious mental processing with NVGs than with normal photopic vision due to the reduced field of view. During the daytime, peripheral or ambient visual cues provide humans with location information through subconscious or preconscious perception of a horizon. NVGs intensify only a 40-degree horizontal field of view at a time. To compensate for this reduced field of view while using NVGs, crew members and other operators must scan the scene to see the horizon, read flight instruments, and more consciously process orientation cues.

In short, while NVGs provide enhanced visual acuity at night, visual drawbacks compared to daytime can easily introduce orientation challenges. Proper NVG training, hands-on experience, and proper preflight adjustments are critical to maximizing NVG performance and reducing the propensity toward user spatial disorientation.

Refractive Surgery

For centuries, prescription lenses have been used by ametropic warfighters to maximize visual performance and mission effectiveness. With no other available options, the benefits of wearing spectacles—or more recently, contact lenses—have outweighed the disadvantages. However, glasses often become fogged, get displaced, restrict peripheral vision, induce painful hotspots under head gear, and significantly reduce the hearing protection afforded by earcup seals in aviation and flight line helmets. It is difficult to incorporate spectacles under helmet-mounted displays, chemical/biological masks, visors, LEP, and NVGs. Contact lenses can be dislodged or dislocated, and quickly become uncomfortable in extreme environments (eg, high altitudes, dry climates). Most importantly, contact lenses demand frequent care under sanitary conditions. Because this is rarely possible during wartime, contact lens use is typically discouraged or prohibited in the field. The multiple drawbacks of traditional prescription lenses, in combination with recent advancements in medical and laser technology, have permitted refractive surgery to quickly become a viable alternative for many thousands of military personnel.

In its most common forms, refractive surgery permanently reshapes the eye’s anterior surface (ie, the cornea) to reduce or eliminate a patient’s reliance on prescription lenses. Civilian surgeons in the United States have been performing corneal refractive surgery since the late 1970s. The earliest form of surgical correction, radial keratotomy, relied on a surgeon’s steady hand to create multiple (typically eight), deep radial incisions into the periphery of the anterior corneal surface. The natural healing process that followed flattened the central cornea and thereby reduced the patient’s myopia or astigmatism.[19] Because radial keratotomy incisions never fully recede, long-term complications include fluctuating refractive error, complaints of halos at night, and structural weakness of the cornea in response to trauma.[19] The advent of laser-based refractive surgery, associated with significantly better visual outcomes and lower complication rates, all but eliminated radial keratotomy as a reasonable option.

Photorefractive keratectomy (PRK) utilizes an excimer laser to remove precise amounts of corneal tissue to reshape the anterior ocular surface.[19] Another popular procedure, laser in situ keratomileusis (LASIK), uses the excimer laser in a similar manner. However unlike PRK, a corneal flap is created and folded away prior to ablation. The surgeon then exposes the corneal bed to laser treatment, and returns the flap to its original position.[19] Visual outcomes and surgical complications are approximately equal in PRK and LASIK. PRK is associated with higher initial discomfort and a longer healing time, and often with complaints of halos at night during the first year of recovery. The primary disadvantage to LASIK is its corneal flap; sharp objects (eg, fingernails, tree branches) on exceedingly rare occasions have dislodged flaps, even years postoperative. With this in mind, warfighters who have undergone LASIK treatment should exercise extra diligence in wearing eye protection.[19]

The Navy began performing corneal refractive surgery in the early 1990s. Since then, PRK in the military environment has become widely accepted. Refractive surgery for the warfighter has been shown to increase readiness, enhance operational performance and safety, and improve retention rates. Most importantly, wavefront guided (custom) treatments continue to improve postoperative visual performance for both PRK and LASIK by reducing higher-order optical aberrations.

MILITARY AVIATION ADMINISTRATION

Aerospace medicine paralleled the development of aviation. The military requirement to have a combat edge over its enemies often fueled aviation development. As aircraft technology evolved from balloons to reusable space vehicles, the challenge to keep pilots and crew functioning normally in complex airframes and extreme, unforgiving environments was daunting. Aerospace medicine requires knowledge in several areas: human factors in the cockpit and workplace design, physiological tolerance criteria, environmental cooling systems, performance psychology, selection and training, PPE, and escape and survival are among the subjects specialist flight surgeons must understand to fulfill their primary aim of preventing disease, injury, and disability in flying personnel.

Safety and Health

A good aviation safety and health program should begin with staff consisting of a safety specialist and consulting occupational health professional at a minimum. In the aerospace community, the team typically includes an aviation safety officer and flight surgeon. A successful safety program contains several basic elements, including management commitment, good facility and equipment design, safety and health training and education, safety and health inspections, accident investigation, and health hazard evaluations.

Management Commitment

The three military services have dedicated aviation safety centers: the Combat Readiness Center at Fort Rucker, Alabama; the Naval Safety Center at Norfolk, Virginia; and the US Air Force Safety Center at Kirtland Air Force Base, Albuquerque, New Mexico. These safety centers develop flight safety programs based on best practices as well as Occupational Safety and Health Administration and Environmental Protection Agency standards applied to the aviation industry. From these headquarters, the aviation safety programs are delegated to the major commands and their subordinate units to implement. By regulation, the local aviation unit commanders must comply.

Facility and Equipment Design

All three services have human systems research, development, and acquisition organizations. The US Army Aeromedical Research Laboratory at Ft Rucker, Alabama, conducts research on crew health, performance, and protection.[45] The Naval Medical Research Unit at Wright-Patterson Air Force Base near Dayton, Ohio, conducts research on biomedical sciences and spatial orientation systems.[46] The US Air Force Research Laboratory, also located at Wright-Patterson Air Force Base, conducts research on directed energy biological effects, biosciences and protection, warfighter interface, and warfighter readiness.[47]

Using applied science, the various aeromedical research labs develop state-of-the-art technology designed to give military aviation its combat edge while simultaneously protecting personnel in the weapon system. Examples include the Gentex HGU-56/P Rotary Wing Aircrew Ballistic Helmet System designed to protect the head in a helicopter crash, the tactile vest designed to give pilots situational awareness, and active noise reduction in headsets, which improve communications and reduce hearing loss.

Safety and Health Training and Education

Education on flight safety and health hazards usually occurs during a unit commander’s monthly safety briefing. Normally, the briefings are conducted by or under the supervision of the flight surgeon. Some topics include altitude physiology, spatial disorientation, aviation protective equipment, exogenous factors, noise, vibration, G-forces, aviation toxicology, and visual systems. There are periodic safety stand-downs during which flying operations cease. During such events, the unit dedicates time to perform safety checks on the work environment and attend to medical or health issues.

On a larger scale and from a programmatic perspective, there are aviation safety officer courses as well as aviation safety modules in the three services’ basic flight surgeon course. These courses address the theory of errors and instruct methods to mitigate human factors that are often the root cause of aircraft accidents. One such method is crew resource management, which emphasizes open and unbiased communication among all crew members. Open communication broadens the sphere of situational awareness, which helps minimize the likelihood of an accident. Another method is operational risk management, in which the crew evaluates the various risks associated with a planned sortie, and then thoughtfully plans how to mitigate them. If the risks cannot be sufficiently reduced, the crew can cancel that sortie or determine an alternative course of action.

Safety and Health Inspections

Safety and health inspections are control measures used to evaluate the effectiveness of established programs. At the local level, flight line visits and the flight medicine program (annual physicals that include screening for hearing, vision, and occupational exposures) are among the conducted inspections.

From a major command or higher headquarters perspective, units undergo periodic inspections to ensure compliance with health and safety policy and regulations. These inspections are usually conducted by personnel outside the inspected unit. In this way, findings and recommendations have less bias or undue influence. In the Army, the aviation readiness management survey is a high-level tool to ensure aviation line commanders are in compliance with the service’s aviation safety program.

Mishap Investigation

Mishaps create the motivation for all safety and health actions. A mishap is an undesirable event that must be investigated to help prevent recurrences. It serves no purpose to investigate mishaps without initiating some type of corrective action to prevent future occurrences. All mishap investigations should attempt to answer who and what was involved and where, when, how, and why the mishap occurred.

The three services’ safety centers conduct accident investigations using full time staff members assigned to an accident investigation team consisting of an engineer, pilot, aviation safety officer, flight surgeon, and senior officer as board president. Using oral reports, maintenance records, health records, and forensics, the team determines whether the mishap was due to material failure or human factors. The aviation safety officer and flight surgeon are responsible for analyzing human factors. The Department of Defense Human Factors and Classification System tracks causal factors throughout four distinct layers: unsafe acts, preconditions for unsafe acts, unsafe supervision, and organizational influences.[48] The process acknowledges deficits at each layer. This model, developed for naval aviation mishap analysis by Shappell and Weigmann, has been adopted throughout Department of Defense for use in developing the final official report at the conclusion of the investigation.

Health Hazard Evaluations

A health hazard evaluation can be used to determine the risk level associated with exposures as well as measure the effectiveness of any hazard control mechanism. At the program level, evaluations are conducted during the research and development phases of the systems lifecycle management process. At the unit level, evaluations should be conducted by the flight surgeon.

Flight Medicine

The flight surgeon is integral in conserving fighting strength. In addition to clinically treating the crew member’s medical condition, the flight surgeon must determine whether that medical condition will affect the individual’s ability to safely perform aviation duties. In good faith, the flight surgeon will abide by the guidelines set forth by HIPAA (the Health Information Portability and Accountability Act). Operational risk and a commander’s need-to-know may dictate the flight surgeon report directly to the commander about the nature and ramifications of a crew member’s medical condition.[49]

Aviation Fitness Evaluation

The US military’s need for a resolute and deployable fighting force means it must be able to select the best qualified and most fit individuals. This is especially true for aviators. Recruits and candidates must meet the military’s stringent medical fitness standards and undergo an initial flight physical (ie, the accession physical). If the individual does not meet the medical fitness standards, then that individual will not be employed as a crew member.

Annual physical evaluations are conducted throughout the crew member’s career to ensure medical fitness for flight duties. These evaluations are based on respective military services’ aeromedical waiver guide and the US Preventive Services Task Force guidelines as they pertain to the aerospace mission of the three military services.

Determining Flight Status

Military medicine, by design, exists primarily to support the military community service members who are fit and able to engage in the business of war. The military’ aviation community is particularly sensitive to medical conditions that affect the aviator’s ability to perform safely. Regulations, instructions, and policies address conditions that adversely affect flight safety.

Determining Work Relatedness

Because military service members are subject to duty at any time, most incidents (injury or disease) are considered work related. The military provides training programs, through the various services’ safety centers, to foster a culture of safety. Determining work relatedness following crew injury is no different from investigating injuries in any other military occupation. The flight surgeon should get an initial impression from the patient and validate the mechanism of injury or disease development, then document the medical findings in the crew member’s electronic health record. If the service member was command referred, the commander may get medical information from the flight surgeon, but it is best if the physician asks the patient to sign a release of medical information under HIPAA.

Air Evacuation

Due to the nature of military operations, wounded combatants must be rapidly cleared from the battlefield because rapid treatment in the golden hour is paramount. The military has an echelon-based medical system starting with an individual service member providing self-aid or buddy aid, to combat medics, forward surgical teams and field hospitals, and eventually extending back to major medical centers in the continental United States, which provide definitive and rehabilitative care. The concept is to medically evacuate the wounded to a level of care where they can be treated and returned to the fight. If a return to duty is not possible, then the service member will be medically evacuated to a level where providers can treat the injury and determine the service member’s fitness for duty.

Air evacuation is a means to accomplish rapid evacuation of personnel who have serious and life-threatening wounds. Although air evacuation is relatively seamless, the services have distinct roles. The Army has the primary mission to provide tactical MEDEVAC, and the Air Force provides fixed-wing, strategic aero MEDEVAC.

Army rotary-wing aircraft are generally used to evacuate wounded from a hot landing zone to a forward surgical unit or a combat support hospital. The number of patients transported range from one to four, due to the helicopter’s tight configuration. A “9-line” MEDEVAC request via radio or other messaging system will mobilize the helicopter, with its flight medic, to the evacuation point. Short distance intra-theater medical treatment facility transfers go through the chain of medical command and usually follow the civilian standard of care regarding interhospital transfers. Because the Army MEDEVAC helicopter is a dedicated asset, response time is fairly rapid.

The Air Force evacuates from forward surgical units and combat surgical hospitals to rearward theater hospitals and hospitals based in the continental United States. The number of patients transported depends on the number of attendants on the wide body airframe and the stability and criticality of the patient. C-17 and C-130 aircraft can transport 50 or more litter and ambulatory patients. Because of the strategic nature of large cargo jets, it takes time to assemble a designated aeromedical evacuation wide-bodied fixed-wing aircraft for evacuations. The Air Force further supports aero MEDEVAC with ground-based en route patient staging facilities per AFTTP 3-42.51 dated 7 Apr 2015 (formerly aeromedical staging facilities). US Transportation Command (TRANSCOM) supports patient movement by tracking theater bed availability, reviewing and validating patient movement requests, and tracking patient location via the TRANSCOM Command and Control Evacuation System.[50] To initiate a patient movement request, the requesting medical treatment facility coordinates with one of TRANSCOM’s patient movement requirements centers (Ramstein Air Base, Germany; Osan Air Base, Republic of Korea; Hickam Air Force Base, Hawaii; and Scott Air Force Base, Illinois).

Whether transported via tactical or strategic air evacuation, the patient is exposed to environmental stressors, but unlike the crew, the patient’s physiology is abnormal. The flight surgeon must consider this altered physiological state when preparing a patient for air evacuation. For example, a patient with an open wound and significant bleeding experiences hypemic hypoxia and the oxygen saturation falls to 87%. When the aircraft files over a mountain pass at 2,000 ft, the patient’s oxygen saturation falls even further to between 70% and 72% oxygen saturation. If the air evacuation is longer than 30 minutes, the patient’s status will require 100% supplemental oxygen. The patient is monitored by pulse oximeter to measure oxygen saturation. To provide responsive and effective support to the operational mission, air evacuation routes and availability must be preplanned and patient movement must be executed efficiently. Flight surgeon involvement is absolutely paramount in all aspects of preparation, response, and after action.

SUMMARY

The aerospace medicine specialty was created to address unique health and medical aspects of the aviation work environment. It focuses on individual health and how it interacts with altitude, pressure, thermal stress, acceleration, noise, vibration, fatigue, flight deck ergonomics, and various other hazards crews are exposed to when performing their flight duties. These factors, along with other physiological conditions, may contribute to spatial disorientation and threaten the aviator’s ability to safely operate aircraft. As with many industries, the aviation community is exposed to toxicological hazards such as solvents, fuels, propellants, and materials that form the aircraft itself.

To ensure flight safety, aviation crew members must meet medical standards for accession and retention. If current health precludes them from meeting these standards, there are several administration actions, from being placed on temporary quarters to permanent suspension of flight duties, which are at the professional discretion of the flight surgeon. The flight surgeon is the medical staff officer to the commander, imbedded in the aviation unit safety program. The flight surgeon consults or participates in MEDEVAC and is involved in aviation mishap investigations as the medical expert focused on the human factors component.

While the flight surgeon is responsible for assessment, treatment, and safety, overall safety responsibility lies with commanders. Prevention programs, improvements in systems safety and design, PPE, and support in the form of equipment, maintenance, facilities, and services are components of a safety-oriented environment. A successful unit safety program includes self-disciplined crew members, leaders who enforce standards, training skills to performance standards, procedures that are clear and practical, and collaboration between leaders and military personnel.

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18.   Newman DG. High G Flight: Physiological Effects and Countermeasures. Burlington, VT: Ashgate Publishing Company; 2016: 89–96.

19.   US Department of the Army. Aeromedical Training for Flight Personnel. Washington, DC: DA 2009. Training Circular TC 3-04.93.

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21.   Wicks RE. Alternobaric vertigo: an aeromedical review. Aviat Space Environ Med. 1989;60(1):67–72.

22.   Rodgers D, Van Syoc D. Clinical practice guideline for motion sickness. Aerospace Medical Association. http://www.asams.org/guidelines/Completed/NEW%20Motion%20Sickness.htm. Published November 14, 2011. Accessed October 3, 2016.

23.   Parmet AJ and Ercoline WR. Fundamentals of Aerospace Medicine, 4th ed. Ed. Davis JR, Johnson R, Stepanek J, Fogarty JA. Philadelphia, PA: Williams and Wilkins; 2008: 195–203.

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Chapter 17

MILITARY DIVING OPERATIONS

MICHAEL G. ZAKAROFF, MD*; RYAN W. SNOW, MD†; RICHARD D. VANN, PhD‡; and JAMES VOROSMARTI, JR, MD§

INTRODUCTION

CENTRAL NERVOUS SYSTEM OXYGEN TOXICITY IN DIVERS

UNDERWATER BREATHING APPARATUSES

THE ROLE OF RESPIRATION IN DIVING INJURIES

DECOMPRESSION PROCEDURES

SATURATION DIVING

THERMAL PROTECTION AND BUOYANCY

MEDICAL STANDARDS FOR DIVING

HYPERBARIC OXYGEN THERAPY AND RECOMPRESSION CHAMBERS

SUMMARY

*Lieutenant, Medical Corps, US Navy; Diving Medical Officer, Mobile Diving and Salvage Unit One, Pearl Harbor, Hawaii 96818

†Lieutenant, Medical Corps, US Navy; Diving Medical Officer, Explosive Ordnance Disposal Mobile Unit Five, Santa Rita, Guam

‡Captain, US Navy Reserve (Retired); Divers Alert Network, Center for Hyperbaric Medicine and Environmental Physiology, Box 3823, Duke University Medical Center, Durham, North Carolina 27710

§Captain, Medical Corps, US Navy (Retired); Consultant in Occupational, Environmental, and Undersea Medicine, 16 Orchard Way South, Rockville, Maryland 20854

INTRODUCTION

Divers breathe gases and experience pressure changes that can cause different injuries from those encountered by most military personnel. This chapter discusses the operational hazards, equipment, and procedures of military diving. The pathophysiology, diagnosis, and treatment of diving-related disorders, including decompression sickness, are discussed in a later chapter. The US Navy has responsibility for all diving by US forces, and most US military divers are in the Navy. All diving operations by US forces must be conducted in accordance with the US Navy Diving Manual and related directives. US Navy diving and salvage forces include T-ARS-50 Safeguard-class salvage ships, explosive ordnance disposal (EOD) units, mobile diving and salvage units, underwater construction teams, and teams assigned to submarine tenders and shore-based ship repair facilities. The diving and salvage forces conduct salvage, search and recovery, underwater mine clearance, underwater construction, security inspections, and ship’s husbandry tasks such as hull cleaning and maintenance.

Salvage divers receive basic training at the Naval Diving and Salvage Training Center (NDSTC) in Panama City, Florida, and qualify in the Mark (Mk) 21 Mod 1/Kirby Morgan (KM) 37 NS mixed-gas diving helmet (Figure 17-1) to a depth of 300 feet of seawater (fsw; equivalent to 90 meters of seawater [msw]). EOD technicians undergo dive training at NDSTC as well and qualify in the Mk 16 Underwater Breathing Apparatus (UBA), which is used for mine clearance. About 100 US Navy divers are specialized in saturation diving using personnel transfer capsules (PTCs) and deck decompression chambers (DDCs).

Naval special warfare combat divers, known as SEALs (sea, air, land) are trained for reconnaissance and direct action missions at rivers, harbors, shipping, and coastal facilities in restricted or denied waters. SEAL divers operate from surface craft, submerged submarines, and miniature wet submersibles known as SEAL delivery vehicles (SDVs). Insertion by fixed- or rotary-wing aircraft is also possible. SEALs qualify in open-circuit and closed-circuit oxygen scuba (self-contained underwater breathing apparatus), with some receiving additional training in the Mk 16 closed-circuit, mixed-gas scuba rig.

SEALs are part of the Special Operations Forces, which include US Army, Air Force, and Marine Corps divers; divers from these services have narrower training and missions and dive less frequently. SEALs train at the Naval Special Warfare Center in Coronado, California, while divers from other services train at NDSTC or at the US Army Special Forces Underwater Operations School in Key West, Florida. Other military divers include US Air Force Pararescuemen and combat controllers, US Army port facility maintenance divers, and US Coast Guard divers for rescue and pollution response. The military also employs civil service divers and contracts with commercial diving companies for specific projects.

Training in diving medicine for military physicians is conducted by the US Navy for all US forces and occasionally for foreign militaries. Instruction includes 6 weeks of practical diving training and 3 weeks of diving medicine at NDSTC. Navy undersea medical officers receive 12 weeks of additional training in submarine-specific issues at the Naval Undersea Medicine Institute in Groton, Connecticut.

The unique medical support requirements for diving are a result of the physiological, engineering, and environmental challenges present underwater. Military diving physicians require broad training for the wide range of missions they may support, but military physicians may also be consulted concerning civilian diving casualties, because many military personnel or their dependents are recreational divers. In addition to physiological hazards, divers must cope with threats posed by various forms of marine life. Medical officers need to be mindful of all the problems, not just the respiratory ones that military divers and swimmers may encounter in the marine environment.

Figure 17-1. Both divers are wearing the KM 37 NS helmet with an attached divers underwater color television system.

CENTRAL NERVOUS SYSTEM OXYGEN TOXICITY IN DIVERS

Cerebral oxygen toxicity occurs with inspiration of high partial pressures of oxygen and is a serious concern during certain diving or chamber operations. A seizure is the most spectacular and objective sign of central nervous system (CNS) oxygen toxicity, but there is no evidence that seizures lead to permanent damage if the oxygen exposure is promptly discontinued. Other symptoms of CNS oxygen toxicity include irritability, twitching, dizziness, incoordination, and visual or auditory disturbances. These symptoms do not necessarily precede convulsions.

Factors that elevate cerebral blood flow also augment oxygen delivery to the brain, which appears to increase susceptibility to oxygen toxicity. These factors include immersion, exercise, and hypercapnia.[1] Carbon dioxide may be present in the inspired gas or may be retained in the body owing to inadequate ventilation caused by high gas density or external breathing resistance. The primary treatment for all forms of oxygen toxicity is to reduce the partial pressure of inspired oxygen to a nontoxic level.

Oxygen exposure limits have been established to reduce the risk of convulsions for divers breathing pure oxygen or the oxygen in nitrogen-oxygen gas mixes. Chamber trials and experience in open water indicate that convulsions occasionally occur near or within the accepted oxygen exposure limits. Oxygen exposure limits are more conservative for nitrogen-oxygen mixes than for pure oxygen. Nitrogen-oxygen mixes are used at greater depths and have higher gas densities. The higher gas densities are believed to cause greater carbon dioxide retention within the body, which increases susceptibility to oxygen toxicity.

UNDERWATER BREATHING APPARATUSES

A UBA provides the diver with a continuous and reliable supply of physiologically safe breathing gas. There are two broad categories of UBAs, surface supplied (or tethered) and self-contained. Each type has a number of subcategories with advantages and disadvantages that lend themselves to a particular operational utility.

Open-Circuit, Self-Contained Underwater Breathing Apparatus

The most familiar and common UBA currently in use is the open-circuit, compressed-air scuba. Open-circuit scuba consists of one or more tanks of gas compressed to a pressure of 137 to 341 ata (absolute atmospheres) or 2,000 to 5,000 psi gauge (psig). A first-stage pressure regulator attached to the tanks reduces their high pressure to an intermediate pressure of about 7 ata (100 psig) over the ambient water pressure. During inhalation, a second-stage regulator, held in the diver’s mouth, reduces the intermediate pressure to ambient. The system is described as “demand” and “open-circuit” because air flow is available for inhalation on demand and the exhaled gases are vented directly to the surrounding water.

Based on Dalton’s law of partial pressures, the partial pressures of oxygen and nitrogen change with depth for divers breathing air or 100% oxygen (Figure 17-2). With pure oxygen, there is a significant risk of CNS oxygen toxicity at 33 fsw (10 msw), while with compressed air, which is only 21% oxygen, CNS oxygen toxicity does not usually appear until depths greater than 190 fsw (57 msw).[2]

Figure 17-2. Nitrogen and oxygen partial pressures for air and 100% oxygen at various depths.
O_2: oxygen
ata: absolute atmosphere
fsw: feet of seawater

Surface-Supplied Diving

UBAs became possible with the invention of the air compressor in the 18th century during the Industrial Revolution, but the first practical equipment did not appear until about 1828, when the Deane brothers in England developed an open helmet that rested on the diver’s shoulders.[3] Hand-driven pumps on the surface supplied the helmet with air through a hose, and excess air escaped around the shoulders, but the helmet would flood if the diver leaned over too far. Further developments by the Siebe Gorman diving company of England in the mid-19th century added a closed suit to the helmet, which prevented flooding and improved thermal protection. This became the traditional “hardhat” deep-sea diving dress, which remained the primary equipment for military and commercial diving until the 1970s. The US Navy diving helmet, the Mk V (Figure 17-3), was introduced in 1905, with improvements in 1916 and 1927, and was the system of choice until 1980.

The current diving helmets in use by the US Navy are the Mk 21 Mod 1 and KM 37 NS (see Figure 17-1). These masks are nearly identical and incorporate a demand regulator from open-circuit scuba, but use an oronasal mask that allows spoken communications instead of a mouthpiece. The oronasal mask is a significant improvement and has much less respiratory dead space than previous diving helmets. This permits lower gas-supply flow rates while limiting carbon dioxide retention. The Mk 21 Mod 1 helmet has a depth limit of 190 fsw (57 msw) when used for air diving. Its principal applications are search, salvage, inspection, ship’s husbandry, and enclosed-space diving. The Mk 21 Mod 1 can also be used to a depth of 300 fsw (90 msw) with helium-oxygen mixtures.

Figure 17-3. The US Navy Mk V Mod 1 diving helmet.

Figure 17-4. The US Navy Mk 20 Mod 0 surface-supplied, open-circuit, lightweight system with full facemask is limited to a depth of 60 fsw (18 msw) for applications such as diving in mud tanks and enclosed spaces.

Another tethered diving system in the US Navy inventory is the lightweight Mk 20 Mod 0 (Figure 17-4), which is used to a maximum depth of 60 fsw (18 msw) for diving in mud tanks or enclosed spaces. For saturation diving, the Navy uses the Mk 21 Mod 1 helmet and Mk 22 Mod 0 band mask (Figure 17-5) with a hot water suit and hot water shroud for heating breathing gas.

Closed-Circuit Oxygen Scuba

The term “closed-circuit” describes a UBA in which 100% of the breathing gases remain within the unit, as opposed to escaping into the aquatic environment around the diver. The gas exhaled is carried via an exhalation hose to a canister containing a chemical absorbent that removes the exhaled carbon dioxide. The gas then travels to a breathing bag, where it is available again to the diver. Metabolically consumed oxygen is then replaced by an oxygen addition system.

Figure 17-5. The US Navy Mk 21 Mod 0 helmet with hot water suit, hot water shroud, and come-home bottle (left) and Mk 22 Mod 0 with hot water suit, hot water shroud, and come-home bottle (right) for heating breathing gases. These are the primary underwater breathing apparatuses for saturation diving. Reprinted from: US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011: 15-2, 15-3. NAVSEA 0994-LP-100-3199.

Closed-circuit UBAs have no escaping bubbles (except during ascent or inadvertent gas release), making them ideal for Naval special warfare and EOD operations. They also offer extended dive duration and weight advantages over open-circuit scuba. Closed-circuit UBAs are significantly more complex than open-circuit scuba, and malfunctions are more frequent. Among the disadvantages are a generally greater breathing resistance, additional training requirements for divers and maintenance personnel, and costs of initial purchase and subsequent maintenance. The Mk 25 Mod 2 (Figure 17-6) is the closed-circuit UBA used by most US Navy combat swimmers. It uses 100% oxygen without any inert gas diluent. Figure 17-7 shows the gas flow path.

By using 100% oxygen at shallow depths, there is no need for decompression, and if proper procedures are followed, the risk of decompression sickness is theoretically zero. However, there are several potential serious hazards associated with closed-circuit oxygen scuba:

- dilutional hypoxia from failure to initially purge nitrogen from the lungs and the breathing loop;

- increased risk of CNS oxygen toxicity at depths greater than 25 fsw (7.5 msw);

- carbon dioxide poisoning caused by overexertion, skip-breathing, increased breathing resistance, or exhaustion of the carbon dioxide absorbent; and

- flooding of the breathing loop, leading to both loss of buoyancy and chemical burns from wet absorbent (known as a “caustic cocktail”).

Figure 17-6. The Mk 25 Underwater Breathing Apparatus. May 18, 2006 - A US Navy SEAL (Sea, Air, Land) hangs on to a pier during a Combat Swimmer Training dive. US Navy photo by Senior Chief Mass Communication Specialist Andrew McKaskle (Released).
Reproduced from: http://www.navy.mil/view_image.asp?id=37909.

Figure 17-7. Gas flow path of the Mk 25.
Reprinted from US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011: 19-10. NAVSEA 0994-LP-100-3199.

Furthermore, the location of the breathing bag or bags relative to the lungs can cause carbon dioxide retention and reduce the diver’s exercise capacity. When the diver is in a prone swimming position, a back-mounted bag is at a lower pressure than the lungs. This imposes a negative static lung load (as when breathing through a snorkel) and requires extra work during inspiration but less work during expiration. A chest-mounted bag imposes a positive static lung load, which assists inhalation but imposes extra work during exhalation. Of the two types of lung load, a small positive load causes less carbon dioxide retention and is preferable to a negative load.

Due to the very serious risk of CNS oxygen toxicity, strict operational limits are placed on depths and durations of closed-circuit oxygen dives. Further information on Mk 25 diving operations and procedures can be found in Chapter 19 of the US Navy Diving Manual.[2]

Closed-Circuit, Mixed-Gas Scuba

Closed-circuit, mixed-gas scuba affords the mobility of a free-swimming diver with the depth advantage of mixed gas. Figure 17-8 shows the US Navy Mk 16 UBA, which has a back-mounted breathing bag. Closed-circuit, mixed-gas rebreathers have one or more oxygen sensors (the Mk 16 has three) that measure the inspired oxygen partial pressure. This partial pressure is compared to the desired oxygen set point by a digital computer, which adds oxygen to the breathing bag when the partial pressure falls below the set point. For the Mk 16 Mod 1, the oxygen set point is 0.75 ata at depths shallower than 33 fsw (10 msw), and 1.3 ata deeper than 33 fsw (10 msw).

Perhaps the greatest advantage of a closed-circuit mixed-gas rebreather is gas conservation. At a fixed depth, the gas consumption of a closed-circuit rebreather equals the diver’s metabolic rate (between 0.5 L/min for rest and 3.0 L/min for work), which a small oxygen supply can support for hours. The purpose of the diluent supply (Figure 17-9) is to fill the counterlung during descent, but the diluent can be quickly exhausted by multiple vertical excursions. The diluent can be air for depths shallower than 150 fsw (45 msw), and 12% oxygen in helium (He_2O_2 88/12) to prevent nitrogen narcosis for depths up to 300 fsw (90 msw). Both air and 12% oxygen (but not a smaller percentage of oxygen) can be breathed in an open-circuit mode at the surface in the event of equipment malfunction.

Figure 17-8. Students at the Naval Diving and Salvage Training Center conduct training with the US Navy Mk 16 Mod 1 UBA.
Photo courtesy of the US Navy.

Closed-circuit mixed-gas rebreathers are significantly more complex than closed-circuit oxygen rebreathers, and malfunctions are more frequent. Divers who make emergency ascents to the surface are at risk for arterial gas embolism (AGE) or decompression sickness (DCS), and those who lose consciousness underwater are at risk of drowning. Loss of consciousness usually occurs during descent or ascent, usually due to CNS oxygen toxicity or hypoxia, respectively. Closed-circuit mixed-gas scuba is still evolving and will remain a specialty most appropriate for divers who are highly trained, well-funded, and willing to assume risks beyond those encountered with open-circuit scuba.

Figure 17-9. Schematic diagram of the Mk 16. This mixed-gas rebreather has a single, back-mounted bag, which contains three sensors that measure the oxygen partial pressure. The dotted lines represent electrical signals to and from the computer. If the mean partial pressure falls below the set point (0.75 ata shallower than 33 fsw [10 msw] and 1.3 ata deeper than 33 fsw [10 msw] for the Mk 16 Mod 1), the computer adds oxygen to the breathing loop.

THE ROLE OF RESPIRATION IN DIVING INJURIES

Risk of injury in diving can be mitigated in several ways, primarily through proper planning before the dive. However, there are several factors challenging divers, some of which are within their control (experience, practice, gear, team, etc), and some which are not (innate physiology, laws of physics). Also, a diver’s ability to consciously influence fundamental physiological processes such as respiration adds complexity to the diving environment.

Divers who make emergency ascents to the surface are at risk for AGE or DCS, and those who lose consciousness underwater are at risk of drowning. Loss of consciousness when breathing air or nitrogen-oxygen has been called “deep-water blackout,” as opposed to shallow-water blackout. The causes of these events can be difficult to determine, but nonfatal occurrences and unplanned laboratory incidents indicate that respiration plays an important role, as Edward H. Lanphier, MD, describes in Case Study 17-1.

Case Study 17-1. Carbon Dioxide Retention and Dyspnea. We were testing a new bicycle ergometer at 7.8 ata (224 fsw, 67 msw) in the dry chamber. Nitrogen narcosis is very evident on air at that pressure, but we were doing OK until we started breathing on the measuring circuit that gave us only about half the air we needed. Herb stopped pedaling after about three minutes, out cold with his eyes rolled back. I took the bike. I knew I wasn’t getting nearly enough air, but I was too narc’d to think straight and was determined to finish the test. I pedaled myself right into oblivion and coming around slowly afterwards with a horrible feeling of suffocation was the worst experience of my entire life. Both of us surely would have drowned if such a thing had happened when we were underwater.[4]

Carbon Dioxide Retention and Dyspnea

Respiration is designed to maintain physiologically acceptable levels of oxygen and carbon dioxide in the blood and tissues, and healthy people breathing free air at sea level adjust their ventilation unconsciously to match their exertion. This is not always so during diving, where the effects of nonphysiological levels of oxygen, nitrogen, and carbon dioxide can interact and are exacerbated with increasing depth by work, breathing resistance, and gas density.5,6

Exercise capacity at sea level is limited by the cardiovascular system, whereas the respiratory system is usually the limiting factor during diving. Immersion shifts blood from the legs to the thorax, which reduces vital capacity and maximum ventilatory capacity. A regulator decreases the ventilatory capacity still further by increasing the work of breathing. Work of breathing is caused, in part, by resistance to gas flow in the airways and the breathing apparatus, and may be exacerbated by wasted work due to overbreathing the regulator. Resistance increases with depth as the gas density increases, but this effect is also dependent on the gas mixture used (helium is less dense than nitrogen). Ultimately, regardless of the cause, carbon dioxide is retained when ventilation is inadequate.[6]

Carbon dioxide is the primary ventilatory stimulus in diving. The hypoxic ventilatory drive is generally absent, because most diving gases are hyperoxic. Blood is designed to carry oxygen and carbon dioxide at normoxic pressures, not at elevated oxygen partial pressures. At sea level pressure, where venous oxygen is low, carbon dioxide is tightly bound to hemoglobin. At high oxygen partial pressures during diving, carbon dioxide is more loosely bound to hemoglobin, causing its tension in the blood and tissues to rise (known as the Haldane effect). However, the actual effect on increasing the carbon dioxide tension at depth has been disputed.[7]

Dyspnea generally results if increased ventilation does not reduce the elevated carbon dioxide tension. However, because dyspnea has a perceived component, it may not be solely due to retained carbon dioxide. There may be an additional neurologically mediated effect at higher pressures, over 1,000 fsw (305 msw), similar to the effects of high pressure nervous syndrome (HPNS).[6]

Multiple factors (see Case Study 17-1) may contribute to inhibited ventilation, and divers sometimes consciously override the hypercapnic ventilatory stimulus and hypoventilate (skip-breathe) to conserve air. Besides the risk of pulmonary barotrauma from breath-holding while breathing compressed gas, skip-breathing can contribute to hypercapnia, which, among other problems, can be responsible for headaches after diving.[8]

The importance of adequate respiration may not be adequately stressed during diver training, and a diver who expects the same respiratory performance at depth as on land may be surprised by the breathlessness that can occur if sudden exertion is required in an emergency. As Case Study 17-1 indicates, dyspnea is a frightening experience, and panic is a common response. Newly trained divers are particularly susceptible to making emergency ascents when dyspnea occurs. A diver overcome by a desire to surface and breathe free air may ascend too rapidly and risk AGE, DCS, or both.

An episode of respiratory insufficiency underwater can be a learning experience, but it is not an ideal lesson (Case Study 17-2). Because the normal unconscious regulation of respiration at sea level may be compromised during diving, divers should beware of incipient dyspnea, ventilate adequately, and minimize exertion. Sufficient ventilatory reserve should be maintained so that sudden, unexpected activity does not cause breathlessness and panic. If breathlessness occurs, the best way to avoid becoming in extremis is to stop all activity and let breathing return to normal.

Case Study 17-2: Deep-Water Blackout. During a dive to 180 fsw (54 msw) in a water-filled pressure chamber, a diver performed moderate exercise while swimming against a trapeze at an oxygen consumption of 2 L/min. He was using an Mk 15 UBA (similar to the Mk 16; see Figure 17-8) with an oxygen partial pressure of 1.4 ata in nitrogen. Despite orders from the diving supervisor to slow down, he increased his workload until he became unconscious. He revived immediately on removal from the water.

Interactions Between Gases and Impaired Consciousness

Carbon dioxide retention is exacerbated as depth increases by increased ambient pressure and greater work of breathing. Inspired carbon dioxide partial pressures of 10% to 15% surface equivalent are narcotic and can affect a diver’s consciousness.[2] When the oxygen partial pressure is elevated, hypercapnia loses its effectiveness as a warning signal of respiratory depression or impending unconsciousness. The narcotic effect of excess carbon dioxide is additive to nitrogen narcosis, and narcosis can cause the hypercapnic ventilatory drive to be overlooked (see Case Study 17-1). Elevated carbon dioxide increases cerebral blood flow and raises oxygen delivery to the brain, increasing the risk of CNS oxygen toxicity.

Figure 17-10. Factors affecting carbon dioxide retention and consciousness. Various factors contribute to increased Pco_2 in blood (center of diagram). Gas density increases as depth increases, which raises the work of breathing and decreases ventilation. Nitrogen narcosis increases with depth and can lead to altered mental status, either because it suppresses ventilation or because ventilation is altered by absolute increased pressure (dashed line).
Pn_2: pressure of nitrogen gas

Thus, diving can impair consciousness through the combined effects of nitrogen narcosis, carbon dioxide intoxication, and oxygen toxicity. These effects are exacerbated by exercise and gas density, which further increase carbon dioxide retention. Figure 17-10 illustrates the interactions among gases, exercise, and depth that increase the risk of unconsciousness. Deep air (as opposed to heliox) diving is dangerous because interactions of depth, work, oxygen, nitrogen, and carbon dioxide affect respiration and consciousness. Carbon dioxide is the primary factor controlling respiration during diving when the hypoxic ventilatory drive is absent in the presence of hyperoxia. Various factors contribute to increased Pco_2 in blood (center of Figure 17-10). Gas density increases as depth increases, which raises the work of breathing and decreases ventilation. Nitrogen narcosis increases with depth and can lead to altered mental status; however, debate exists as to whether nitrogen narcosis suppresses ventilation, or whether ventilation is altered due to absolute increased pressure.[9] Some divers reduce ventilation voluntarily to save gas, whereas others have poor ventilatory response to elevated carbon dioxide. Elevated carbon dioxide potentiates CNS oxygen toxicity, and carbon dioxide itself is narcotic.[10] Carbon dioxide is more likely additive to Voluntary inert gas narcosis rather than synergistic, although this is still in debate.[9] In the presence of hyperoxia, dyspnea caused by carbon dioxide is less effective as a warning of altered consciousness. The risks of unconsciousness from oxygen toxicity, carbon dioxide toxicity, and nitrogen narcosis (all of which increase with depth) are exacerbated by physiological interactions among them.

Figure 17-11. Variation in individual susceptibility to symptoms of central nervous system oxygen toxicity. The time to symptom onset is illustrated for a single individual who was exposed to 100% oxygen at 70 fsw (21 msw) on 20 days over 3 months. The average onset time was 44 minutes, with a range of 7 to 148 minutes.
Data source: Donald K. Oxygen and the Diver. Welshpool, Wales: SPA Ltd; 1993.

Individual Susceptibility to Impaired Consciousness

Susceptibility to carbon dioxide retention, oxygen toxicity, and nitrogen narcosis vary widely from one individual to another. Some divers have poor ventilatory response to inspired carbon dioxide and are believed to be at an elevated risk of CNS oxygen toxicity due to increased cerebral oxygen delivery.6,11 Studies also have shown wide variability of the latent period before CNS toxicity for the same individual. Experiments by the British found that the time to symptom onset varied randomly from 7 to 148 minutes for a single diver who made 20 exposures at 70 fsw (21 msw) while breathing 100% oxygen (Figure 17-11).[12]

A few individuals have made compressed air (21% oxygen) dives to depths of 300 to 500 fsw (90-150 msw) and have returned safely, despite nitrogen and oxygen stresses that would incapacitate most people. Other divers in these conditions have developed severe DCS or drowned, probably owing to loss of consciousness. There is no way to predict who is susceptible or resistant or how individual susceptibility varies from day to day.

DECOMPRESSION PROCEDURES

Other than avoiding diving altogether, the most effective way to reduce DCS risk is to employ methods that make the practice of undergoing changes in barometric pressure safer. This involves utilizing a system of techniques and procedures that are based in theory and also, ideally, proven by experimental data. One of the most often cited and commonly used sources of diving procedures is the US Navy Diving Manual.[2] In particular, it contains an extensive set of dive tables specific to different types of diving that guide the diver on how to safely allow the body to equilibrate to the surface after being under increased atmospheric pressure for a period of time. Several other diving authorities have developed similar tables and algorithms, all with varying allowed bottom times and ascent procedures. The discussion in this text is based on the US Navy tables, which are the most commonly used tables in military diving.

In relation to DCS, diving today is a relatively safe activity, especially when compared with the practices at the turn of the 20th century, when permanent paralysis and death were common (Case Study 17-3).

Case Study 17-3. Fatal Decompression Sickness in 1900. A Royal Navy diver descended to 150 fsw (45 msw) in 40 minutes, spent 40 minutes at depth searching for a torpedo, and ascended to the surface in 20 minutes with no apparent difficulty. Ten minutes later, he complained of abdominal pain and fainted. His breathing was labored, he was cyanotic, and he died after 7 minutes. An autopsy the next day revealed healthy organs but gas in the liver, spleen, heart, cardiac veins, venous system, subcutaneous fat, and cerebral veins and ventricles.[13]

According to the current US Navy standard air decompression tables, this diver should have had up to 532 minutes of decompression time.[2] Decompression risk is relatively low for divers who follow standard decompression tables such as those published in the US Navy Diving Manual, but even divers who adhere to accepted tables may develop the less serious forms of the disease and, occasionally, severe problems. Decompression tables specify rules for the time at depth, decompression stops, and surface intervals between dives. More recently, diver-worn digital computers have automated the process of decompression calculations, making them simpler and less prone to the kinds of errors divers make when working with tables. Additionally, these computers can more accurately calculate actual depth and time, thereby allowing the diver more time in the water, particularly on a multilevel dive. However, neither dive tables nor dive computers guarantee freedom from risk of DCS.

In 1993, the rate of ascent to the first decompression stop was changed in the US Navy Diving Manual from 60 fsw/min (18 msw/min) to 30 fsw/min (9 msw/min).[2] The safety stop, a development in recreational diving during the 1990s, interrupts ascents from no-stop dives with a 3- to 5-minute stage at 10 to 20 fsw (3-6 msw). Slower ascent rates and a safety stop may reduce the incidence of venous gas emboli, but their effect on the risk of DCS is uncertain.

No-Stop (No-Decompression) Dives

No-stop (ie, no-decompression) dives are the simplest, safest, and most common form of exposure. No-stop dives are short enough that the diver can return directly to the surface with an acceptably low risk of DCS. Although the slowest ascent rate possible conveys the least risk, an acceptable and practical alternative is the prescribed ascent rate of 30 fsw/min (9 msw/min), per the US Navy Diving Manual. Table 17-1 is the US Navy table for no-stop air dives. It lists the maximum time (in minutes) allowed at a corresponding depth. The repetitive group designation letters in the table are used to determine allowed bottom time for subsequent repetitive dives.

In-Water Decompression Stops

If the bottom time at a given depth exceeds the stated no-stop limit for a decompression table or dive computer, the diver must remain at a shallower depth (a decompression stage or stop) long enough to allow inert gas to be eliminated harmlessly through the lungs. If the decompression stops are too short, excessive formation and growth of bubbles in the blood and tissues may result in DCS. In-water decompression stops are traditionally at 10-fsw (3-msw) intervals, with the shallowest stop at 10 or 20 fsw (3 or 6 msw). Decompression tables show the required stops and time at particular depths; these requirements vary depending on the decompression gas used.

Experiments and observations have found that decompression time can be reduced by 30% to 50% with about the same or a lower risk of DCS if oxygen is used instead of air during in-water decompression stops, but this benefit comes with the risk of CNS oxygen toxicity.[14] In-water oxygen decompression is not recommended deeper than 30 fsw (9 msw). A typical protocol requires the diver to breathe air at deeper stops, then switch to 100% oxygen at 30 fsw (9 msw). A backup decompression plan should be available for times when in-water oxygen cannot be used. Air should be available as a backup breathing gas in the event of CNS toxicity symptoms, and an emergency plan should be in place to manage convulsions. To reduce the risk of CNS toxicity, the US Navy tables stipulate that 5-minute air breaks be taken for every 30 minutes of oxygen breathing.

TABLE 17-1

US NAVY NO-DECOMPRESSION LIMITS AND REPETITIVE GROUP DESIGNATORS FOR NO-DECOMPRESSION AIR DIVES

•: Highest repetitive group that can be achieved at this depth regardless of bottom time.
Reproduced from: US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011: 9-63. NAVSEA 0994-LP-100-3199.

Surface Decompression

During salvage of silver and gold in World War I, the weather or the military situation sometimes forced British divers to surface before completing their required in-water decompression stops.[14] Experience showed that this could be done safely if the divers were rapidly recompressed in a shipboard pressure chamber within 5 to 10 minutes of reaching the surface. Surface decompression was initially conducted with air, but subsequent studies by the US Navy found that decompression with oxygen was more effective.[14] Surface decompression with oxygen is typically conducted with recompression on 100% oxygen to a depth of 50 fsw (15 msw). It is acceptable to breathe 100% oxygen at a depth of 50 fsw (15 msw) in a dry chamber, in contrast to the 30 fsw (9 msw) depth limit for divers in the water, because dry divers are at a lower risk of oxygen toxicity.[14] As with in-water decompression, air breaks of 5 minutes are given for every 30 minutes of oxygen breathing.

Repetitive and Multilevel Diving

If two dives are made in close succession, inert gas remains in the body from the first dive. The second dive must therefore include reduced bottom time or longer decompression time to avoid increased DCS risk. The second exposure is known as a repetitive dive, and the time between the two dives is called the surface interval. The US Navy Residual Nitrogen Time Table for Repetitive Air Dives[2] indicates how to account for previous dives when planning repetitive dives. A no-stop repetitive air dive may be considered a new dive with no reduction in bottom time when the required surface interval has been met, which can range between just over 2 hours to nearly 16 hours, depending on the profile of previous dives. Repetitive diving is common among recreational divers, and four or more no-stop dives per day are not unusual over several days. Repetitive multi-day diving was once thought to increase the risk of DCS, but more recent data point to some amount of acclimatization that decreases DCS risk. The mechanism for this occurrence is poorly understood, but there has been a demonstrated decrease in venous gas bubble load after multi-day repetitive dives. However, multi-day diving also increases oxidative stress, leading to blood vessel endothelial dysfunction, which can increase DCS risk.15–17

Multilevel diving is a variant of repetitive diving in which the diver does not return directly to the surface but ascends in stages that take advantage of the longer no-decompression times at shallow depths (see Table 17-1) while avoiding mandatory decompression stops. Commercial, recreational, and military diving (with submersibles, in Special Operations) are frequently multilevel. There are a number of multilevel dive tables, but multilevel dives are most efficiently conducted when dive computers are used.

Dive Computers

The common term for a digital computer that a diver carries underwater for decompression guidance is a dive computer. (An alternative term sometimes used by the US Navy is a decompression computer.) The computer is usually worn on the wrist where it can be easily viewed. There are many different commercially available dive computers, but all are programmed with models, or algorithms, derived from the same or similar mathematical calculations as decompression tables. A decompression model is a mathematical representation of the kinetics of inert gas exchange in body tissues with rules to preclude ascents that might result in unsafe bubble formation or growth. Because the understanding of decompression physiology is incomplete and because there are differences among individuals, no decompression model is totally effective in preventing DCS. However, with current algorithms the incidence appears to be less than 1%.[18]

Dive computers accurately track depth-time profiles and minimize the human errors that can occur in table selection. They are most useful when conducting multilevel dives. Standard dive tables are based on maximum depth attained and total bottom time, and assume the diver spends the entire dive at that maximum depth. By using a dive computer that calculates inert gas exchange in real time, a diver may safely extend the no-decompression limit on a multilevel dive beyond the limits prescribed in the standard tables. Currently, only the Cochran Navy AIR III (Cochran Consulting Inc, Richardson, TX) decompression computer is authorized for use on military dives in lieu of standard dive tables, and only for no-decompression dives at altitudes less than 1,000 ft (305 m) above sea level. Dive computers are reasonably reliable, but hardware failures occasionally occur, so backup computers or tables are recommended. Despite their particular advantages and ease of use, dive computers are not a substitute for proper dive planning.

Nitrogen-Oxygen Diving

Many breathing devices can be used with gases other than air. The most common mixtures are of nitrogen and oxygen (called NITROX), in which the oxygen percentage is greater than the 21% in air. Such mixes are also known as enriched air NITROX. NITROX can be used with open and closed-circuit UBAs, but the oxygen fraction varies with the depth. NITROX mixes that contain less nitrogen than air reduce the risk of DCS if used with standard decompression procedures; however, the bottom time is often extended instead, which negates the reduction in decompression risk. The advantages of fixed percentage NITROX are as follows:

- extended bottom times for no-decompression diving,

- reduced decompression time,

- reduced residual nitrogen in the body after a dive,

- reduced possibility of decompression sickness, and

- reduced nitrogen narcosis.

The disadvantages of using NITROX include:

Figure 17-12. Oxygen partial pressures in air and 36% nitrogen-oxygen mixture (NITROX). The 36% NITROX provides a decompression advantage over air by reducing the nitrogen partial pressure to which a diver is exposed. Thus, 36% NITROX at 33 fsw (10 msw) has the same nitrogen partial pressure and is the decompression equivalent of breathing air at 20.5 fsw (6.2 msw). This is known as the equivalent air depth (EAD). The EAD at 66 fsw (20 msw) is 47 fsw (14.3 msw), and the EAD at 95 fsw (29 msw) is 71 fsw (21.6 msw). NOTE: the normal working limit for 36% NITROX is 95 fsw (29 msw) because at this depth the oxygen partial pressure rises to 1.4 ata; the risk of CNS oxygen toxicity increases significantly above this pressure.
ata: absolute atmospheres
CNS: central nervous system
fsw: feet of seawater
msw: meters of seawater

- increased risk of CNS oxygen toxicity,

- decreased allowable maximum depth due to risk of CNS oxygen toxicity,

- production requires special equipment,

- equipment requires special cleaning techniques,

- long-duration dives can result in pulmonary oxygen toxicity,

- working with NITROX systems requires special training, and

- NITROX is expensive.

Figure 17-12 illustrates the oxygen and nitrogen partial pressures at various depths with air and with 36% NITROX. The 36% NITROX has a clear decompression advantage over air, owing to its lower nitrogen partial pressure, but the depth limitation due to increased risk of oxygen toxicity is also obvious. Ignoring depth limits in NITROX diving has led to fatal convulsions. NITROX diving can be conducted with reasonable safety, but additional training in physics, physiology, and gas mixing and analysis is advisable. The decompression requirement is obtained by calculating the equivalent air depth of a given NITROX mixture (Table 10-1 in the US Navy Diving Manual[2]) and using that depth on the standard air table. NITROX is not suitable for deep diving because of the increased risk of CNS oxygen toxicity. Per the US Navy Diving Manual, the normal working limit for oxygen partial pressure exposure is 1.4 ata, which makes 100 fsw (30 msw) the greatest allowable depth with 32% oxygen (including a safety factor for rounding gas percentages to the nearest whole number and potential errors in gas analysis).

Helium-Oxygen and Trimix Diving

For dives deeper than 150 fsw (45 msw), heliox (a mixture of helium and oxygen, commonly referred to as “mixed gas”) or trimix (a mixture of helium, nitrogen, and oxygen) are used to eliminate or reduce nitrogen narcosis. The oxygen fraction in these mixtures is often less than 21% and is determined to keep oxygen partial pressures below 1.3 to 1.4 ata, which are potentially toxic to the CNS at deep depths. The US Navy Diving Manual contains helium-oxygen tables for use with surface-supplied and closed-circuit diving operations.

Omitted Decompression

A diver who surfaces before completing a required decompression stop is subject to increased risk of DCS. Decompression may be omitted as a result of water conditions, equipment failure, personal injury, uncontrolled ascent, or running out of air. Out-of-air situations are more common with scuba than with surface-supplied equipment. If omitted decompression does occur, the diver should be treated in a recompression chamber or decompressed in the water, depending upon the amount of decompression missed, presence of symptoms, and tactical situation. Due to the risk of omitted decompression, no-decompression dives are safer than planned decompression dives.

Flying After Diving and Diving at Altitude

DCS can occur independently of diving during altitude exposures above about 18,000 ft (5,500 m; a barometric pressure of 0.5 ata).[19] Nitrogen dissolved in the tissues at sea level has a tension of about 0.79 ata and leaves solution to form bubbles at altitude. Flying after diving increases the risk of DCS because additional nitrogen remains in the tissues after a dive. To reduce the DCS risk from flying too soon after diving, divers are advised to wait long enough at sea level for nitrogen dissolved in their tissues to be eliminated harmlessly through the lungs. The US Navy Diving Manual Table 9-6 lists preflight surface intervals required before flying is considered safe. These surface intervals range from 0 to 21 hours for a commercial flight depending on the severity of the previous diving exposure. The US Air Force requires a 24-hour wait after any diving before flight.

Diving at altitude also increases the risk of DCS. Because the bodies of sea-level residents are in equilibrium with the 0.79 ata of nitrogen in atmospheric air, rapid ascent to an altitude of 18,000 ft (5,500 m), where atmospheric nitrogen is only 0.4 ata, causes a supersaturation of 0.39 ata. The supersaturated nitrogen dissipates over about 24 hours and must be accounted for during that time. Dives conducted within 12 hours of initial ascent to altitude are considered repetitive dives. US Navy Diving Manual Table 9-5 lists the repetitive group designator associated with altitudes up to 10,000 ft (3,048 m).

After equilibration is complete, the no-decompression times are still shorter than normal because bubbles grow larger at reduced barometric pressure than at sea level. Therefore, a dive conducted at an altitude of 5,000 ft (1,524 m) to a depth of 60 fsw (18 msw) is equivalent to an 80-fsw (24-msw) dive at sea level. US Navy Diving Manual Table 9-4 lists equivalent sea level depths for air diving at altitudes up to 10,000 ft (3,048 m), as well as altitude diving procedures relevant to military diving.

Safety of Decompression Practices

The question of how safe diving is with the use of dive tables or computer algorithms is extremely difficult to answer despite significant advances in the understanding of decompression physiology. The inability to accurately predict DCS lies in the incomplete understanding of the human physiologic response to diving and the unique interactions of gas exchange, bubble dynamics, and, tissue response. Additionally, DCS has long been considered a binomial event, meaning it either does or does not happen, making it difficult to capture sub-threshold events. The true nature of DCS is more likely a spectrum that is difficult to gauge until the point of significant symptoms. In historical findings, the measured DCS incidence rates in a set of US military dives has been shown to range from 0.029% to 1.25% over a wide variation of dives.20,21

Much work has been done in attempting to model the complex system of human decompression by either trying to replicate the components of gas exchange and bubble dynamics coupled with empirical parameters (deterministic modeling), or by using modern statistical methods of analyzing diving databases and applying estimated parameters (probabilistic modeling).[22] At present, insufficient experimental or observational data are available to confirm the estimated probabilities of DCS, although the estimates are suspected to exceed the true values. As such data and more powerful computing techniques become available, probabilistic algorithms are expected to replace the algorithms currently used by dive tables and dive computers.

SATURATION DIVING

The term “saturation diving” refers to diving operations (dry or wet) conducted with divers remaining at a particular depth for a period of time such that their bodies become equilibrated, or saturated, to a maximum partial pressure of inert gas. After about 24 hours at any depth, the inert gas tension in the body reaches equilibrium with the inert gas partial pressure in the ambient atmosphere, and the decompression time achieves its maximum length, independent of dive duration. Although saturation dives are logistically complex, they prevent the stresses of multiple bounce dive decompressions in circumstances where long working times are desirable. The overall advantage is that the work can be completed in less time on station because the efficiency of bottom time per diver is greater. Saturation diving is used most often in commercial diving, occasionally in scientific diving, and by the US Navy for salvage or submarine rescue.

Saturation divers usually live in a DDC at a “storage” pressure near to or shallower than the dive site depth at which they work. If the chamber is on a surface ship, the divers transfer to a PTC through a mating hatch in the DDC, and the PTC is lowered to the dive site. Figure 17-13 shows a saturation diving system with one PTC and two DDCs. The US Navy currently uses a portable system known as SAT FADS (Saturation Fly Away Diving System), which can be mounted on different types of vessels and is certified to an operating depth of 1,000 fsw (305 msw).

Saturation diving may also be conducted from seafloor habitats, but few of these are now in use because they are expensive and difficult to maintain. The longest running sea-floor operation is the Aquarius Habitat off the coast of Key Largo, Florida. Owned by the National Oceanic and Atmospheric Administration and managed by Florida International University, Aquarius Habitat primarily conducts marine science research, but it has also been used for saturation diving training by the US Navy and for simulated astronaut training by NASA.

If a diver is stored at a given depth and the worksite is deeper than the storage depth, he or she makes a descending, or downward, excursion to the worksite. Ascending, or upward, excursions from storage depth are usually made from underwater habitats. The US Navy Diving Manual provides tables for excursions from various saturation depths after which divers may return to the storage pressure without decompression stops. Downward excursions are most common, with the DDC storage depth chosen as shallow as the operation of the excursion tables allow. This minimizes the pressure at which the divers must live and the length of the final decompression to the surface. Oxygen partial pressures during excursions can range from 0.4 to 1.2 ata, depending on the breathing apparatus used and the type of operation. Because helium is expensive and not readily available, and because open-circuit equipment (scuba or surface-supplied) uses large gas volumes as the depth increases, exhaled gases are sometimes returned to the PTC or the surface, where they are reconditioned for reuse by removing carbon dioxide and adding oxygen.

Atmospheric Control

A saturation chamber is a closed environment whose atmosphere must be carefully controlled to maintain diver health. As the saturation depth increases, the oxygen percentage must decrease so that the oxygen partial pressure does not exceed 0.5 ata, which is the approximate threshold for pulmonary oxygen toxicity in long-duration exposures. At a depth of 1,000 fsw (305 msw), for example, the oxygen percentage must not exceed 1.6% in order to maintain a Po_2 of 0.5 ata. The US Navy uses a goal Po_2 range of between 0.44 and 0.48 ata.

Figure 17-13. The dive bell component of the Flyaway Saturation Diving System, which is used to transport saturation divers to and from a large compression chamber on the surface and the ocean depths where they perform their work. Gulf of Mexico, May 9, 2012 - Navy Diver 1st Class Alvin Carter, right, a reserve component sailor certified to mix gases for breathing in deep-water diving, watches as a winch hoists a manned dive bell from a depth of more than 600 feet, more than 65 miles south of the coast of Panama City Beach, FL. US Navy photo by Mass Communication Specialist 2nd Class Charles E. White (Released).
Reproduced from: http://www.navy.mil/view_image.asp?id=123795/.

The balance of the pressure is made up by inert gas, which is nitrogen for dives to depths of about 120 fsw (37 msw) and helium at greater depths. Most saturation diving occurs deeper than 200 fsw (61 msw), with helium as the inert gas. At depths of 1,000 fsw (305 msw) and deeper, a trimix of helium-nitrogen-oxygen or a mix of hydrogen-helium-oxygen is sometimes used to reduce the risk of HPNS, but it is uncertain if the nitrogen ameliorates the HPNS or only relieves some of its symptoms. The Navy currently has procedures only for helium-oxygen.[2]

Accurate gas analysis is essential to maintaining safe levels of oxygen and carbon dioxide. The carbon dioxide level is typically controlled to less than 0.5% surface equivalent or a Pco_2 of 0.005 ata, by absorbent material in a closed-loop life-support system. At a depth of 1,000 fsw (305 msw), for example, the percentage of carbon dioxide must not exceed 0.016%. Chamber ventilation must be adequate to keep the atmosphere mixed. In a helium atmosphere, heavier gases such as carbon dioxide and oxygen tend to pool in low or poorly ventilated areas, and toxic levels of carbon dioxide have occurred in bunks isolated by curtains.

Toxic atmospheric contaminants such as carbon monoxide or hydrocarbons can be eliminated only by flushing the chamber and piping systems with fresh gas, but this is costly and may be impossible on a ship with limited gas supplies. Contaminants must be prevented from entering the chamber. Carbon monoxide is produced at a rate of 8 to 10 mL per person per day by the metabolism of hemoglobin and must be monitored, but unsafe levels from this source are unusual.

Hydrocarbons can be introduced from petroleum lubricants, leaks in life-support refrigeration units, or improperly cleaned piping. Petroleum lubricants are a fire hazard as well as source of pollution. Divers produce methane at a rate of 300 to 500 mL per person per day. Some chamber systems lock out human waste immediately; others hold it in a sanitary tank. Human waste allowed to sit in a sanitary tank produces ammonia, indole, skatole, sulfur dioxide, hydrogen sulfide, chlorine, and carbon dioxide; therefore, sanitary tanks should be vented externally to prevent contaminating the chamber atmosphere. Many naturally occurring contaminants can be removed by filters in the life-support loop. Mercury is prohibited, and instruments or components such as mercury thermometers and electrical mercury switches must be avoided. The basic rule for preventing contamination is “if in doubt, keep it out.”

Fire

Although the concern for fire is significant in any enclosed environment used for human occupation, the chance for combustion is remote at oxygen percentages lower than 6%. This means that fire is of the greatest concern at depths less than 231 fsw (70 msw). Many of the same materials that pose a risk of atmosphere contamination are also fire concerns (petroleum products, hydrocarbons, flammable gases). Applying the same rules to saturation systems as to standard recompression chambers will provide significant safety from fire. A variety of fire suppression systems exist, typically employing the use of water under pressure either through handheld or wall-mounted devices.

Infection

Hygiene is important in a closed environment. High humidity fosters an environment that promotes the development of superficial infections. A common recommendation for preventing external otitis is to instill a solution of aluminum acetate with 2% acetic acid into each ear every morning and evening, and before and after diving. The external ear canals are filled with this solution for 5 minutes while the diver lies on one side and then the other. Bed linen should be changed every 48 hours and daily showers taken whether diving or not. Chamber surfaces require daily cleaning with a nonionic detergent solution, and the bilges should be rinsed and drained at the same time. Food spills and the like should be cleaned immediately. Divers should wear their own thermal protection suits to prevent the spread of skin infections. Suits should be rinsed with nonionic detergent and water and be hung to dry.

Hyperbaric Arthralgia

Hyperbaric arthralgia is joint discomfort or pain that occurs during compression and decreases in intensity during 24 hours or more at constant depth. Symptoms include joint cracking, a sensation of “dry and grainy” joints, and a feeling similar to sprain. In order of severity, affected joints are the shoulders, knees, wrists, hips, and back. Least affected joints are the ankles, fingers, and elbows. Hyperbaric arthralgia can occur during short bounce dives but is more common during deep saturation dives. Its frequency, severity, and duration increase with depth and compression rate, but task performance is usually not affected. The condition is less common with the slow compression rates used to alleviate HPNS. The origin of hyperbaric arthralgia is unknown, but suggested causes are changes in the nature of bubble formation with increasing pressure and changes in joint fluid osmolarity leading to dehydrated articular cartilage. There is no evidence that hyperbaric arthralgia leads to joint degeneration or aseptic bone necrosis.

High Pressure Nervous Syndrome

HPNS begins at about 300 to 600 fsw (90–180 msw) and is manifested by tremor, decreased motor and intellectual performance, dizziness, nausea, vomiting, and occasionally psychosis. Focal reflex changes sometimes occur, and balance may be affected. Deeper than 1,000 fsw (305 msw), electroencephalograms may show slow theta waves, and alpha activity may be depressed. Divers easily fall into microsleep if not continually aroused. HPNS symptoms can be reduced, but not eliminated, by slowing or interrupting compression as depth increases. Although there is considerable individual variability, HPNS imposes a limit of not much more than 2,000 fsw (610 msw) as the maximum depth that humans can tolerate under dry conditions. The maximum depth at which practical work in the water is possible is less than 2,000 fsw (610 msw) owing to excess work of breathing in the UBA, particularly during exhalation.

Temperature Control

Saturation diving using helium-oxygen mixtures poses additional problems because of heat loss from the body due to the high thermal conductivity of helium. A significant amount of heat is lost through respiration, and the loss may be too great to be overcome by metabolic compensation alone. Therefore, various thermal protection mechanisms are employed (see further discussion below).

Heating the breathing gas (raising its temperature by 16° to 28° C [30°–50° F]) mitigates respiratory heat loss. Without using a heating device, divers would succumb to respiratory symptoms and hypothermia with relatively little warning due to the rapid cooling effect of breathing cold helium mixtures.

The usual thermal protection of wetsuits and dry suits is not sufficient at saturation depth sea temperatures and helium environments. In addition to breathing gas heating, active external heating of the body is required, typically through hot water suits. Hot water is received through the diver’s umbilical, circulates through the suit, and discharges to the sea.

Decompression

Saturation decompression must occur very slowly to prevent DCS. For helium-oxygen, the US Navy uses a continuous reduction of pressure according to the following scale:

- 6 fsw/h from 1,600–200 fsw (1.8 msw/h, 480 to 60 msw);

- 5 fsw/h from 200–100 fsw (1.5 msw/h, 60-30 msw);

- 4 fsw/h from 100–50 fsw (1.2 msw/h, 30-15 msw); and

- 3 fsw/h from 50–0 fsw (0.9 msw/h, 15-0 msw).[2]

To minimize decompression during sleep, the US Navy schedule stops decompression from midnight to 0600 and from 1400 to 1600, during which the oxygen partial pressure is maintained at 0.4 to 0.48 ata. Saturation divers are required to remain near a recompression chamber for at least 2 hours after decompression and within 30 minutes’ travel time to a chamber for 48 hours. Flying is prohibited for 72 hours after saturation diving.

THERMAL PROTECTION AND BUOYANCY

Global water temperature is typically below body temperature, and except for short exposures, unprotected divers are at risk of hypothermia, as discussed above in relation to saturation diving. Hyperthermia, on the other hand, is an unusual hazard for divers. The US Navy Diving Manual gives allowable exposure durations as a function of temperature and the means of thermal protection. Buoyancy control is closely linked to thermal protection, because almost all thermal protection methods use gas for insulation.

Most heat loss occurs by convection through the skin and lungs; as a result, the ambient temperature in a saturation chamber must be 29.4° C to 32.2° C (85° F–90° F) for normal body temperature to be maintained. The range of thermal comfort narrows with increasing depth. Water vapor diffuses slowly at high pressure, and evaporation provides little cooling, which makes the skin feel wet without evidence of sensible water. The comfort range for relative humidity is 50% to 70%.

Historically, hard-hat divers wore heavy woolen underwear beneath a canvas outer suit. The suit was supposed to remain dry but frequently leaked. Because the suit was filled with air, the diver wore heavy boots and weights to achieve the negative buoyancy needed to walk on the bottom. To maintain proper buoyancy, the suit had to be inflated during descent and deflated during ascent. Hard-hat divers could suffer severe injury from suit squeeze (ie, barotrauma that occurs when a poorly fitting suit is insufficiently expanded) if the air supply was inadequate to maintain suit volume during descent. During ascent, gas was vented from the suit to avoid uncontrolled positive buoyancy (ie, blow-up), in which the diver was propelled to the surface and risked air embolism, DCS, or mechanical injury from collision.

The wetsuit is the most common form of thermal protection used today. Made of air-filled, closed-cell neoprene foam, wetsuits are satisfactory for several hours at temperatures of 10° C to 15.5° C (50° F–60° F) but provide less protection with increasing depth as the air-filled cells compress. Minor suit squeeze sometimes occurs with tight-fitting wetsuits. As a diver descends, wetsuit compression reduces buoyancy by several pounds. A buoyancy compensator to which gas can be added or removed is typically used to make adjustments from slightly positive to slightly negative buoyancy, according to whether ascent or descent is desired. With open-circuit scuba, buoyancy increases by several pounds as compressed gas is consumed from the tanks. Swimming with fins, the common mode of propulsion with scuba, helps a diver remain warm for several hours.

The next level of thermal protection, the variable-volume dry suit, is a waterproof outer garment over insulating underwear that is sufficiently warm for brief periods of ice diving. Dry suit diving requires training in buoyancy control to avoid suit squeeze or blow-up. For an untethered scuba diver in deep water wearing a dry suit, a suit squeeze could make the diver negatively buoyant, resulting in a fatal uncontrolled descent. Conversely, over-inflation of the suit can lead to an uncontrolled ascent or blow-up, resulting in serious or fatal AGE or DCS. Dry suits can be inflated from the diver’s breathing gas or from a separate gas supply. Helium is a poor choice as an insulator because its thermal conductivity is 5.7 times greater than that of air, and its heat capacity 4.4 times greater than that of air.[23] These characteristics cause heat loss to increase with depth. Dry suits provide inadequate thermal protection during 6- to 8-hour exposures in -1.1° C to 4.4° C (30° F–40° F) water for inactive divers, such as the operators or passengers of SDVs. Additionally, a diaper or other urine-collection device is required if the dry suit is to remain dry during a dive of several hours’ duration. Because of its greater bulk, a dry suit is more difficult to swim in than a wetsuit.

Wetsuits and dry suits provide passive insulation, which delays but does not prevent body cooling. Active heating is the most effective thermal protection. The most common active heat source is hot water (not to exceed 43° C [109° F]) supplied from the surface or a PTC to a loose-fitting wetsuit, through which the water flows before it exits at the hands and feet (see Figure 17-5). An even distribution of flow and careful temperature control are critical for adequate heating without causing hot spots or thermal burns. During deep helium-oxygen diving, the breathing gas must be heated to prevent convective heat loss through the lungs, which can cause a progressive hypothermia that may go unnoticed.

Hyperthermia can occur in special circumstances. At remote diving sites in hot climates, recompression chambers that treat diving casualties and DDCs that support saturation diving may be outdoors and exposed to the sun. Hyperthermia can occur when diving in very warm water, such as in the Arabian Gulf where water temperatures can exceed 32° C (90° F). Divers in confined waters (eg, in or around power plants) may also be exposed to temperatures that can cause hyperthermia. This is a particular problem in hazardous environments such as nuclear reactors, where special suits and breathing apparatuses are worn to prevent inward leaks of water contaminated by radioactive material. These suits may incorporate closed-circuit cooling water to prevent overheating. In addition to being leak-proof, suits used in water or other liquids that are contaminated with biological agents or toxic chemicals must be made of materials that will not degrade during exposure. Before the diver undresses, the suits must be thoroughly washed down to prevent harmful exposure to the diver or support personnel.

MEDICAL STANDARDS FOR DIVING

As with many activities, diving is associated with inherent risks. These are due to operating in a foreign environment under physical (temperature, pressure) and physiological (micro-bubble emboli, inflammatory) stress, conditions that are not normally familiar to the human body. To maximize safety, it is imperative that any alterations from a normal physiological state be assessed and determined to be compatible with safe diving practices. The guiding principle is that any abnormality that could unnecessarily be made worse by diving, which could place the diver in immediate undue risk in the diving environment (or cause the diver any detriment), should represent a contraindication to diving.

In the military, diving medical officers (DMOs) examine candidates for initial diving training, provide advice to diving officers concerning the medical aspects of diving operations, examine divers before or after dives, offer routine medical care, and treat divers for diving injuries. Some conditions (eg, epilepsy) are absolute contraindications for diving, while others (eg, upper respiratory infection) are temporarily disqualifying or disqualifying until corrected. Table 17-2 summarizes the generally accepted recommended absolute and relative contraindications for recreational and commercial diving. No list on this matter is complete, and there are exceptions to every rule, so each diver should be evaluated for his or her specific conditions by a qualified examiner. Conditions that might be allowed for recreational divers may be disqualifying for military divers. US Navy regulations outlined in the Manual of the Medical Department, NAVMED P-117, Chapter 15, guide the military diving medical standards for all US military services.[24]

TABLE 17-2

RECOMMENDED ABSOLUTE AND RELATIVE CONTRAINDICATIONS TO DIVING

System

Absolute Contraindications

Relative Contraindications

Ears and upper respiratory

Open tympanic perforation

Inability to equalize the middle ear

Tube myringotomy

Inner ear surgery (eg, stapedectomy, ossicular chain)

Permanent obstruction of the external canal

Meniere disease or other inner ear disease

Chronic mastoiditis or mastoid fistula

History of vestibular barotrauma

Inability to retain mouthpiece

Deafness in one ear

Middle ear barotrauma

Recurrent or chronic sinus, external canal, or middle ear infections

Allergies of the nose and upper respiratory tract

Pulmonary

History of spontaneous pneumothorax

Reactive airway disease (asthma) of any origin

Chronic obstructive pulmonary disease

Restrictive lung disease

History or radiographic evidence of pulmonary blebs, bullae, or cysts

Childhood asthma without residual hyperactivity or air trapping

Pneumothorax due to barotrauma, penetrating injury, or surgery without air trapping

Cardiovascular

Aortic or mitral stenosis

History of myocardial infarction

Angina or coronary artery disease

Cardiac septal defects

Complete or fixed second-degree heart block

Wolf-Parkinson-White syndrome with paroxysmal atrial tachycardia or syncope

Exercise-induced tachyarrhythmias

Fixed-rate pacemaker

Hypertension with evidence of end-organ damage

Drugs that inhibit normal exercise

Peripheral vascular disease that limits exercise

None

Neurological

Seizure disorder

Brain or spinal cord tumor

Cerebrovascular accident or transient ischemic attack

Demyelinating disease

Spinal cord trauma with neurological deficit

Head injury with sequelae

Intracranial surgery

Central nervous system aneurysm or vascular malformation

Migraine headaches with neurologic symptoms

Episodic loss of consciousness

History of head trauma with loss of consciousness but no sequelae

Chronic headaches

History of neurological decompression sickness with residual symptoms

Hematological

Unexplained anemia

Polycythemia or leukemia

Sickle cell disease

Acute anemia

Endocrine

Insulin-dependent diabetes mellitus

Diabetes mellitus treated by diet or oral agents with history of hypoglycemia

Non–life-threatening hormonal excess or deficiency

Renal insufficiency

Obesity

Reproductive

Pregnancy in any stage

None

Psychiatric

Inappropriate motivation

Claustrophobia or agoraphobia

Active psychosis or psychosis while receiving psychotropic drugs

Panic disorder

Alcohol or drug abuse

Suicidal ideation with or without severe depression

Significant anxiety state

Manic state

None

Ophthalmological

Radial keratotomy

Uncorrected visual acuity inadequate to find diving buddy or boat if corrective lenses

Corrected visual acuity inadequate to read instruments

None

Gastrointestinal

Uncorrected abdominal wall hernia

Paraesophageal or hiatal hernia

Chronic or recurrent obstruction

Severe gastroesophageal reflux

Peptic ulcer disease

Malabsorption

Functional bowel disorders

Inflammatory bowel disease

Musculoskeletal

Low back pain with neurological symptoms

Disability that would hamper work in the water or with diving equipment

Juxtaarticular aseptic bone necrosis

Acute sprain or strain

Acute trauma

Data sources: (1) Bove AA, Davis JC, eds. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Saunders, 2004. (2) Davis JC, Bove AA. Medical Examination of Sports SCUBA Divers. Flagstaff, AZ: Best; 1986. (3) Linaweaver PG, Vorosmarti J. Fitness to Dive: 34th UHMS Workshop Report. Kensington, MD: Undersea and Hyperbaric Medical Society; 1987.

The US Navy Diving Manual provides general guidelines for return to diving after DCS or AGE, but each case requires review by a DMO.[2] Current guidelines state that divers successfully treated for type I DCS may be cleared by a DMO for return to diving duty after 7 days post treatment. Divers successfully treated for AGE or type II DCS, with no residual symptoms, may be cleared by a DMO to return to diving duty 30 days after treatment. If symptoms persist, follow-on treatments may be recommended at the discretion of the DMO. Return-to-duty determination will likely require further workup and specialist review.

HYPERBARIC OXYGEN THERAPY AND RECOMPRESSION CHAMBERS

Decompression illness is a relatively rare phenomenon, and most civilian recompression facilities are used more frequently to provide hyperbaric oxygen therapy (HBOT) for other indications. HBOT is recommended for conditions caused by gas bubbles, inadequate perfusion, and metabolic poisons. The recognized expert on this subject matter is the Undersea and Hyperbaric Medical Society (UHMS), which regularly reviews current literature and publishes a peer-reviewed journal on diving and hyperbaric medicine. According to the UHMS and the Centers for Medicare and Medicaid Services, HBOT constitutes breathing oxygen in a pressurized chamber. The current recommendation is that the Po_2 should be 1.4 ata or higher. Breathing 100% oxygen at 1 ata or exposing isolated parts of the body to 100% oxygen is not considered HBOT.[25]

The field of HBOT has undergone significant changes in its lifetime, and there are numerous claims for its ability to treat many types of ailment. The UHMS has fought hard to keep the field rooted in evidence-based medicine, but many treatment centers continue to promote HBOT for unapproved indications. The Food and Drug Administration continues to monitor these practices and has issued warnings to consumers to be skeptical of overzealous claims.[26] The following indications are approved uses of HBOT as defined by the UHMS’s Hyperbaric Oxygen Therapy Committee:[25]

- air or gas embolism

- carbon monoxide poisoning

- carbon monoxide poisoning complicated by cyanide poisoning

- clostridial myositis and myonecrosis (gas gangrene)

- crush injury, compartment syndrome, and other acute traumatic ischemias

- decompression sickness

- arterial insufficiencies

- central retinal artery occlusion

- enhancement of healing in selected problem wounds

- severe anemia

- intracranial abscess

- necrotizing soft tissue infections

- osteomyelitis (refractory)

- delayed radiation injury (soft tissue and bony necrosis)

- compromised grafts and flaps

- acute thermal burn injury

- idiopathic sudden sensorineural hearing loss

The above conditions, except for severe anemia, intracranial abscess, acute thermal burn injury, and idiopathic sudden sensorineural hearing loss, are covered for reimbursement by the Centers for Medicare and Medicaid Services[27] (the exceptions may be covered by third-party insurers). In light of recent military conflicts involving injury due to explosions, there is increasing interest in the possible benefits of HBOT for traumatic brain injury, and several studies are ongoing. Under certain circumstances the US Navy will treat some of the approved indications; however, most Navy chambers are designed for supporting military diving operations and lack the medical support infrastructure needed to treat more complicated medical patients.

There are two principal types of hyperbaric chambers: multiplace and monoplace. Multiplace chambers are made of steel or aluminum, can accommodate two or more people, and are usually compressed with air. Their depth capability is often greater than 60 fsw (18 msw). Multiplace chambers generally have two or more compartments, known as “locks,” that allow personnel to be transferred in or out while at pressure (Figure 17-14). Typically the inner lock is larger and kept at depth, while the outer lock is smaller and available to “travel” from surface pressure to depth as required. Depending on size, an inner lock may accommodate as many as 12 patients who receive 100% oxygen by mask or hood. The lock is periodically ventilated with air to keep the carbon dioxide level below 1.5% surface equivalent and to maintain the oxygen level below 25% to limit the fire hazard.[2] Critical care nursing can be provided if mechanical ventilation or intravenous drug infusions are required.

Figure 17-14. Double-lock hyperbaric chamber.
Santa Rita, Guam, February 25, 2015 - US Naval divers monitor a patient during a demonstration for patient care due to decompression illness in the hyperbaric chamber. US Naval Base Guam is home to the only recompression chamber in the region and provides treatment to military and civilian personnel from Guam and the Micronesia Islands. US Navy photo by Mass Communication Specialist 2nd Class Chelsy Alamina (Released).
Reproduced from: http://www.navy.mil/view_image.asp?id=192715.

A monoplace chamber is generally an acrylic cylinder compressed with 100% oxygen that accommodates a single patient in the supine position. Its depth capability is often 45 to 60 fsw (13.5–18 msw). Monoplace chambers do not allow for direct patient access, although air breaks during oxygen breathing often can be given by mask for conscious patients. Monoplace chambers have been used effectively for decompression illness therapy, but depending on depth capability, they may not be able to provide therapy in accordance with the standard treatment tables. Because of their lower cost, there are many more monoplace chambers than multiplace chambers. Lightweight, inflatable monoplace chambers that can be compressed with air have proven effective but are cumbersome to use. In addition to treatment, they can be used as hyperbaric stretchers to provide transport to more robust facilities.

SUMMARY

Military diving operations have special medical requirements because of the physiological stresses imposed by barometric pressure, breathing gas composition, and immersion. Personnel at risk include several thousand divers in the US military (Navy, Marine Corps, Army, Air Force, Coast Guard) in addition to military divers from other nations. For US forces, the US Navy Diving Manual provides guidance on the conduct of diving operations and associated medical assistance. Diving history provides a useful context in which the interactions of mission and environment can be appreciated from a medical perspective. UBAs, which provide a reliable source of breathing gas and extend the dive time, introduce additional problems that can occur with increasing depth, including the need for thermal protection and alterations of consciousness from interactions of oxygen, carbon dioxide, and nitrogen.

Ascent from depth must become progressively slower as the surface is approached to avoid DCS from bubbles that form in the diver’s body. Decompression schedules and diver-worn computers provide guidance concerning how to ascend with acceptable DCS risk. After 12 to 24 hours at depth, divers become saturated with inert gas and may remain at depth indefinitely without accruing additional decompression time. Saturation dives require special pressure chambers in which the divers live while not actively working underwater. Failure to follow the decompression prescriptions of dive schedules or computers increases the risk of DCS or AGE (which sometimes occur even if these prescriptions are followed). The pulmonary, cardiovascular, and neurological systems require close evaluation during medical examinations to determine fitness to dive for initial training or for the return to diving after DCS or AGE.

REFERENCES

1.   Clark JM, Thom SR. Toxicity of oxygen, carbon dioxide, and carbon monoxide. In: Bove AA, Davis JC, eds. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Saunders, 2004: 241–259.

2.   US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011. NAVSEA 0994-LP-100-3199.

3.   Bevan J. The Infernal Diver. London, England: Submex; 1996.

4.   Lanphier E. The story of CO_2 build-up. aquaCorps. 1992;3(1):67–69.

5.   Lanphier EH, ed. The Unconscious Diver: Respiratory Control and Other Contributing Factors. Bethesda, MD: Undersea Medical Society; 1982. Publication 52WS (RC) 1-25-82.

6.   Camporesi E, Bosco G. Ventilation, gas exchange, and exercise under pressure. In: Brubakk A, Neuman T, eds. Bennett and Elliot’s Physiology and Medicine of Diving. 5th ed. Edinburgh, Scotland: Saunders; 2003: 77–114.

7.   Cherry AD, Forkner IF, Frederick HJ, et al. Predictors of increased PaCO_2 during immersed prone exercise at 4.7 ATA. J Appl Physiol. 2009;106(1):316–325.

8.   Cheshire WP Jr, Ott MC. Headache in divers. Headache. 2001;41(3):235–247.

9.   Bennett P, Rostain J. Inert gas narcosis. In: Brubakk A, Neuman T, eds. Bennett and Elliot’s Physiology and Medicine of Diving. 5th ed. Edinburgh, Scotland: Saunders; 2003: 300–322.

10.   Arieli R, Ertracht O. Latency to CNS oxygen toxicity in rats as a function of PCO_2 and PO_2. Eur J Appl Physiol Occup Physiol. 1999;80(6):598–603.

11.   Davis RH. Deep Diving and Submarine Operations: A Manual for Deep Sea Divers and Compressed Air Workers. 7th ed. London, England: Saint Catherine Press; 1962.

12.   Donald K. Oxygen and the Diver. Welshpool, Wales: SPA Ltd; 1993.

13.   Deep-Water Diving. London, England: His Majesty’s Stationery Office; 1907.

14.   Vann RD, Thalmann ED. Decompression physiology and practice. In: Bennett PT, Elliott DH, eds. The Physiology of Diving and Compressed Air Work. 4th ed. Philadelphia, PA: WB Saunders; 1992: 376–432.

15.   Doolette DJ. Health outcome following multi-day occupational air diving. Undersea Hyperb Med. 2003;30(2):127–134.

16.   Obad A, Marinovic J, Ljubkovic M, et al. Successive deep dives impair endothelial function and enhance oxidative stress in man. Clin Physiol Funct Imaging. 2010;30:432–438.

17.   Pontier JM, Guerrero F, Castagna O. Bubble formation and endothelial function before and after 3 months of dive training. Aviat Space Environ Med. 2009;80:15–19.

18.   Dear G de L, Uguccioni DM, Dovenbarger JA, Thalmann ED, Cudahy E, Hanson E. Estimated DCI incidence in a select group of recreational divers. Undersea Hyperb Med. 1999;26(suppl):19. Abstract 34.

19.   Vann RD, Butler FK, Mitchell SJ, Moon RE. Decompression illness. Lancet. 2010;377:153–164.

20.   Flynn ET, Parker EC, Ball R. Risk of Decompression Sickness in Shallow No-Stop Air Diving: An Analysis of Naval Safety Center Data, 1990-1994. Bethesda, MD: Naval Medical Research Institute; 1998. NMRI Technical Report 98-108.

21.   Berghage TE, Durman D. US Navy Air Decompression Schedule Risk Analysis. Bethesda, MD: Naval Medical Research Institute; 1980. Report No. NMRI 80-1.

22.   Ball R, Schwartz SL. Kinetic and dynamic models of diving gases in decompression sickness prevention. Clin Pharmacokinet. 2002;41(6):389–402.

23.   Hamilton RW. Mixed-gas diving. In: Bove AA, Davis JC, eds. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Saunders, 2004: 95–126.

24.   Bureau of Medicine and Surgery. Navy Medicine, Manual of the Medical Department, NAVMED P-117, Chapter 15. February 2017. http://www.med.navy.mil/directives/Pages/NAVMEDP-MANMED.aspx. Accessed November 15, 2017.

25.   Gesell LB. The Hyperbaric Oxygen Therapy Committee Report. Durham, NC: Undersea and Hyperbaric Medical Society; 2008.

26.   US Food and Drug Administration. Hyperbaric Oxygen Therapy: Don’t Be Misled. www.fda.gov/ForConsumers/ConsumerUpdates/ucm364687.htm. Accessed August 23 2017.

27.   Centers for Medicare and Medicaid Services. National Coverage Determination for Hyperbaric Oxygen Therapy (20.29). Washington, DC: CMS; 2006. Pub no. 100-3.

Chapter 18

PHYSIOLOGY AND MEDICAL ASPECTS OF DIVING

RYAN W. SNOW, MD*; MICHAEL G. ZAKAROFF, MD†; JAMES VOROSMARTI, JR, MD‡; AND RICHARD D. VANN, PHD§

INTRODUCTION

PHYSICAL PRINCIPLES

UNDERWATER PERTURBATIONS OF VISION AND HEARING

BAROTRAUMA

PATHOPHYSIOLOGICAL EFFECTS OF COMMON DIVING GASES

DECOMPRESSION SICKNESS

PREDICTING AND PREVENTING DECOMPRESSION SICKNESS

TREATMENT OF DECOMPRESSION SICKNESS AND ARTERIAL GAS EMBOLISM

BREATH-HOLD DIVING

SUMMARY

* Lieutenant, Medical Corps, US Navy; Diving Medical Officer, Explosive Ordnance Disposal Mobile Unit Five, Santa Rita, Guam

† Lieutenant, Medical Corps, US Navy; Diving Medical Officer, Mobile Diving and Salvage Unit One, Pearl Harbor, Hawaii 96818

‡ Captain, Medical Corps, US Navy (Retired); Consultant in Occupational, Environmental, and Undersea Medicine, 16 Orchard Way South, Rockville, Maryland 20854

§ Captain, US Navy Reserve (Retired); Divers Alert Network, Center for Hyperbaric Medicine and Environmental Physiology, Box 3823, Duke University Medical Center, Durham, North Carolina 27710

INTRODUCTION

Diving as a military activity is sufficiently common that any military physician has a significant probability of involvement in diving operations or in treating or examining divers during his or her career. In addition, military physicians may be called on to treat civilian recreational divers with diving-related problems when no appropriate facilities exist in the civilian community.

Diving is not new to military operations. The first recorded use of breath-hold divers for military purposes dates from the 5th century BCE, when Scyllus and his daughter Cyane saved the fleet of Xerxes by freeing the ships’ anchors, allowing them to get underway rapidly when threatened by a sudden storm.[1] The Syracusans are said to have trained divers to swim underwater and damage enemy ships.[2] Divers of Tyre were employed to cut the anchor ropes of Alexander the Great’s ships during the siege of Tyre in 332 BCE.[3] However, not until the 19th century, after many technological advances, did diving become a military, as well as an industrial, specialty. Military diving operations today include Special Operations; explosive ordnance disposal and mine clearance; salvage of ships; location and retrieval of aircraft or other equipment lost in the water; clearance of wrecks and debris from harbors and waterways; ship-hull maintenance and repairs (ship’s husbandry); repair of piers, locks, dams, and other associated structures; and reconnaissance. The military services employ military and civilian divers to fulfill these varied missions worldwide. See also Chapter 17, Military Diving Operations, for additional discussion.

Figure 18-1 shows the relationship of the depth of the oceans to the attempts humans have made to enter them. Water is an unforgiving and difficult environment in which to work. Most diving operations are done in cold water with a minimum of visibility. The diver’s ability to work is also degraded by the physically challenging equipment used, the respiratory effects of increased breathing resistance, and other physiological changes due to pressure. The risk of injury or illness is largely dependent on the differential in ambient pressure experienced by the diver. Many advances in technology and procedures have helped mitigate the dangers of diving, but there will always be challenges to putting humans in the sea. This chapter discusses the physics and physiology of diving as they relate to humans living and working in the underwater environment, while highlighting common health effects and mitigation strategies.

PHYSICAL PRINCIPLES

Certain fundamental physical principles need to be understood before the deleterious effects of diving can be appreciated. Foremost among these are the behaviors of gases under pressure. Barometric pressure is the force per unit of surface area exerted by the atmosphere. Under natural conditions, this pressure is the result of gravity acting on the column of air that stands several miles above the surface of the Earth; its value was initially measured against a column of mercury and is thought to have been first described by Italian physicist Torricelli in the mid-1600s. It was given an average value of 760 mm Hg at sea level.

The primary unit of pressure in the International System of Units (SI units) is the Pascal (Pa, a unit derived from newtons per square meter), where 1 atmosphere (atm) equals 101.3 kPa. Other units are also sometimes used (Table 18-1).

Many pressure gauges (eg, blood pressure gauges) read zero at ambient (surface) pressure, thereby measuring only differential pressure. However, physiological calculations require the use of absolute pressure, where zero corresponds to a complete vacuum. Therefore, every expression of pressure must be designated as gauge (g) or absolute (a). Conversion between the two requires knowledge of ambient barometric pressure at the time the measurement was made.

Actual pressure underwater differs between fresh and salt water and varies slightly from one area of the ocean to another, depending on local salinity and temperature. One atmosphere is equivalent to 10.13 m of depth in seawater (msw) or 33.08 ft of depth in seawater (fsw). In fresh water, 1 atm = 10.38 msw, or 33.83 fsw.

The following formula may be used when converting from diving depth to atmospheres:

absolute pressure = (D + De) / De

where D represents the depth in units of length and De represents the number of those units equivalent to 1 atm. When solving for pressure using atmospheres (atm) as the base unit of measure, absolute pressure is described as atmospheres absolute (ata). NOTE: this equation assumes a pressure of 1 atm at the surface of the water and requires correction for high-altitude diving.

Figure 18-1. Various forms of diving and other submarine activities in relation to ocean depth. (a) Breath-hold diving is usually not deeper than 100 feet of seawater (fsw) or 30 meters of seawater (msw), although some divers can go deeper. (b) Self-contained underwater breathing apparatus (scuba) diving with air is usually limited to a normal working depth of 130 fsw (40 msw). (c) Surface-supplied air diving is usually limited to a normal working depth of 190 fsw (58 msw) for the US Navy, and 220 fsw (67 msw) for commercial or technical diving. (d) Surface-supplied helium–oxygen diving without a diving bell is usually limited to a depth of about 300 fsw (91 msw). (e) The deepest seafloor habitat operation is at 610 fsw (185 msw). (f) The deepest saturation diving at sea operation is at 1,752 fsw (534 msw). (g) The deepest dive in an armored 1-atm suit is at 2,000 fsw (610 msw). (h) Research submersibles can operate to depths of about 2,000 fsw (610 msw). (i) The bathyscaphe Trieste has been to the deepest-known depth of the ocean, 35,814 fsw (10,916 msw), in the Marianas Trench. More recently the Deepsea Challenger descended to 35,756 fsw (10,898 msw) in the Challenger Deep area of the trench. Note that the ordinate, marking depth, has been shortened. If this graphic were drawn to scale, a page at least 1.26 m long would be required to display ocean depth to the bottom of the Marianas Trench.

Gas Laws

Changes in barometric pressure and in the composition of inspired gas affect the human body in ways that reflect the physical behavior of gases in gaseous mixtures and liquid solutions. A good grasp of gas laws and related physical principles is therefore prerequisite to understanding the physiological effects of the pressure changes imposed by flying and diving.

Pressure Effect (Boyle’s Law)

The volume of a given mass of gas varies inversely with absolute pressure when temperature is held constant. In mathematical terms:

P_1 / P_2 = V_2 / V_1

or the formula can be rewritten:

P_1 • V_1 = P_2 • V_2

TABLE 18-1

PRESSURE EQUIVALENTS

1. Fresh water (FW) = 62.4 lb/ft^3; salt water (FSW) = 64.0 lb/ft^3.

2. The SI unit for pressure is kilopascal (kPa); 1 kg/cm^2 = 98.0665 kPa and by definition 1 BAR = 100.00 kPa @ 4°C.

3. In the metric system, 10 MSW is defined as 1 BAR. Note that pressure conversion from MSW to FSW is different than length conversion; ie, 10 MSW = 32.6336 FSW and 10 m = 32.8083 ft.

Reproduced from: US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011: 2-32, Table 2-10. NAVSEA 0994-LP-100-3199.

where P represents pressure, V represents volume, and the subscripts 1 and 2 refer to the condition before and after a pressure change. For example, if a flexible container is filled with 1 L of gas at 1 ata and then subjected to increasing pressure, at 2 ata the volume will be halved (0.5 L) and at 3 ata it will be one third of its original volume (0.33 L). Ascent to an altitude of 18,000 ft (0.5 ata) would cause the volume to double (2 L).

Because gas in body cavities is saturated with water vapor at body temperature, Boyle’s law is often applied in the following form:

(P_1 – PH_2O) / (P_2 – PH_2O) = V_2 / V_1

where PH_2O represents water vapor pressure at body temperature (47 mm Hg). The addition of the term PH_2O is important when doing respiratory studies and in high-altitude work but is insignificant when calculating pressure volume relationships in diving.

Temperature Effect (Charles’s Law)

The volume of a given mass of gas is directly proportional to its absolute temperature when pressure is held constant. According to Charles’s law, this relationship can be expressed mathematically: V_1 / V_2 = T_1 / T_2, or the formula can be rewritten:

V_1 • T_2 = V_2 • T_1

where T_1 and T_2 represent initial and final temperature, respectively. For this purpose the temperatures must be expressed in absolute units, which can be calculated as T°K (Kelvin) = T°C (Celsius) + 273.

Universal Gas Equation

Boyle’s and Charles’s laws are often expressed in a single equation for calculating the effects of concurrent changes in pressure and temperature, as follows:

(P_1 • V_1) / T_1 = (P_2 • V_2) / T_2

The gas laws listed above are discussed in terms of a flexible container that fully accommodates alterations in volume due to changes in pressure and temperature. However, considering real-world applications for gas in a rigid container when volume is held constant, the increasing ambient pressure will eventually cause structural collapse of the container, whereas decreasing pressure will force the walls to burst. For this reason, the inability to ventilate semi-rigid, gas-filled body compartments such as the lungs and middle ear during severe pressure changes can cause incapacitating or fatal injury in the form of a diving “squeeze” or overinflation.

Partial Pressure in Gaseous Mixtures (Dalton’s Law)

The total pressure exerted by a mixture of gases is equal to the sum of the pressures that each gas would exert if it alone occupied the container. According to Dalton’s law, this can be expressed mathematically:

Pt = P_1 + P_2 + P_3 + Pn

where Pt represents the total pressure of the mixture, and P_1 + P_2 + P_3 + Pn represent the component partial pressures. The partial pressure of a single gas in a mixture can be calculated from the following relationship:

Px = Fx • Pt

where Px represents the partial pressure of gas x, and Fx represents the fractional concentration of that gas in the mixture. At 1 ata, oxygen and nitrogen exert partial pressures of 0.21 and 0.79 atm, respectively. On raising barometric pressure to 3 ata, these partial pressures triple, to 0.63 and 2.37 atm.

Gases in Solution (Henry’s Law)

The quantity of a gas that dissolves in a liquid is directly proportional to its partial pressure in the gas phase, and inversely proportional to the absolute temperature, assuming that no chemical reaction takes place. When the partial pressure of the gas is reduced, a proportional amount of that gas will emerge from solution and may form bubbles in the liquid phase. This is the primary initial mechanism for the development of decompression sickness (DCS).

Transmission of Pressure in a Liquid (Pascal’s Law)

Pressure exerted at any point on a confined liquid is transmitted uniformly in all directions. As opposed to hollow organs, which may contain an airspace, solid organs are mostly liquid, and therefore, pressure exerted on them is distributed equally throughout the body and does not change tissue volume.

Buoyancy

As stated in Archimedes’s principle, any object immersed in liquid will be buoyed up by a force equal to the weight of the water displaced. For example, an object that weighs 100 lb in air and displaces 90 lb of water will be 10 lb heavier than the water displaced and, therefore, sink. If the amount of water displaced is equal in weight to the object, its depth remains constant because it is neutrally buoyant.

Buoyancy is important to a diver because it affects the amount of work needed to change or maintain depth. A positively buoyant diver rises, and a negatively buoyant diver sinks. If the buoyancy is not appropriate, a catastrophic accident can occur. The desired state of buoyancy depends on operational requirements. For example, a combat diver swimming into an enemy harbor at 20 fsw will try to achieve neutral buoyancy, both to make the best speed and to conserve breathing gas. If negatively buoyant, the diver might swim too deep and develop oxygen toxicity; if positively buoyant, the diver might break the surface and be detected. On the other hand, a diver doing salvage work on a hull of a ship may want to be strongly negatively buoyant so that he or she can handle the equipment and tools required without being unsteady or easily movable in the water.

Control of buoyancy is achieved by various methods. The most common is by adding or removing gas from the diving dress (a garment that provides thermal and mechanical protection) or the buoyancy compensator (an inflatable vest for adjusting buoyancy). Weights or weighted equipment are also used to provide initial negative buoyancy for entering the water. When a diver wishes to return to the surface, he or she may establish positive buoyancy by dropping weights or inflating the buoyancy compensator. Certain types of protective clothing, such as the closed-cell neoprene suit, are positively buoyant at shallow depths but become less so at greater depths as the material collapses.

UNDERWATER PERTURBATIONS OF VISION AND HEARING

Vision

Vision underwater is affected by the mask a diver wears, absorption of light by the water, intensity of light, and turbidity of the water, which depends on the amount of material suspended in it. Looking through a diving mask or helmet magnifies objects underwater by 25% to 35% and therefore makes them look closer than they are (Figure 18-2). This displacement of the image is a result of refraction of light as it passes from water through the faceplate material to gas, and it can be confusing to novice divers. A mask or helmet also restricts the peripheral vision of the diver by as much as 50%. Masks or helmets with larger viewing areas increase the field of view but introduce visual distortion.

Stereoacuity, or depth perception, is the ability to determine the relative distance between objects. It is also adversely affected underwater as a result of narrowed field of view due to mask, change in refraction of light causing relative magnification, decreased contrast due to increased light absorption, and decreased clarity of image due to increased turbidity. This is especially noticeable in clear, well-illuminated water and worsens with decreasing illumination and increasing turbidity.

Figure 18-2. When seen underwater, images are displaced toward the diver. The closer apparent position is caused by the refraction of light rays as they pass through the water, the material of the face mask, and the gas inside the mask.

Absorption of light affects underwater vision by decreasing available illumination. In clear water, only about 20% of incident light penetrates to a depth of 33 ft (10 m). Available light also decreases with a decreasing angle of incidence of sunlight to the water surface (as the sun approaches the horizon), as more light is reflected instead of penetrating the surface. However, in clear water with a high sun angle, useful illumination may be found as deep as 198 to 297 ft (60–90 m). As the turbidity increases, the penetration of light decreases. In many rivers, lakes, and harbors, there may be no usable light even within a few feet of the surface.

Changes in color perception occur because water selectively absorbs the very short and very long wavelengths of light. At fairly shallow depths, the red-orange spectrum is lost, and most objects appear blue-green. For example, at a depth of about 10 ft (3 m), blood appears greenish rather than red. If an underwater light source is used, however, the colors appear normal.

Vision in dry, hyperbaric environments is not significantly changed. The only vision-related problems that may arise in repetitive or prolonged saturation dives (see Chapter 17, Military Diving Operations) are a slight loss in visual acuity and a tendency to esophoria.

Hearing

In a dry, hyperbaric environment the only effect on hearing appears to be an increase in the hearing threshold with increasing depth. This is not due to changes in bone conduction, which remains normal at depth, but to changes in conductivity in the middle ear as a result of increasing gas density. This occurrence reverses with decreasing pressure, and occurs in both nitrogen–oxygen and helium–oxygen environments.

Hearing underwater is a completely different situation. Because the densities of tissue and water are similar, a submerged head is “transparent” to sound energy. In addition, water in the external ear canal damps the vibrations induced in the tympanic membrane. Therefore, hearing underwater occurs through bone conduction rather than through the middle ear, with a 50% to 75% decrease in the hearing threshold.

Sound is difficult to localize underwater. It travels much faster in water than in air, reducing the difference in time at which sound arrives at each ear. The human brain is uniquely tuned to interpret this time difference in air, but at shorter intervals, as experienced underwater, localization can often be impossible even though the sound is heard well.

Speech intelligibility is a problem in diving. In water, it is almost impossible for divers to converse without a communications device because too much power is required for through-water sound transmission by voice alone. Divers wearing rigid helmets can converse by touching helmets, so that sound is transmitted directly from helmet to helmet. While speech intelligibility decreases somewhat as the density of a nitrogen–oxygen mixture increases, speech is almost impossible when a helium–oxygen mixture is used. This is because helium shifts the resonance of vocalizing structures and gas-filled cavities, drastically changing the timbre of the vowels. This results in a high pitched, nasal quality referred to as “Donald Duck” speech. Most saturation divers find that their understanding of such speech improves after several days under pressure, but it is still poor.

Permanent hearing loss was a common problem among divers in the past because of high noise levels in helmets and chambers. Although divers who wear a “hard hat” (the classic rigid diving helmet) may still have this problem, newer diving equipment is quieter and hearing loss is not common. If a hyperbaric chamber does not have muffling for the compression and exhaust systems, divers inside the chamber and operators outside should use individual hearing protection to prevent temporary or permanent hearing loss.

A submarine’s sonar uses sound signals propagated into water for certain aspects of operation (eg, active sonar). Standards for diving operations near active sonar sources are defined in appendix 1A of the US Navy Diving Manual.[4] Exposure to sonar can produce both auditory and nonauditory effects. Exposure to high sound pressure in water is similar to exposure to loud noise in air, causing either a temporary threshold shift or permanent sensorineural hearing loss. Whether decreased hearing is temporary or permanent depends on the sound pressure level and the frequency of the sonar signal.

Unless a sonar signal is unexpectedly energized at close range, there is little danger because a diver who is swimming in the area of a sonar source can hear or feel the signal and stay clear of the danger zone. Divers exposed to sonar have reported feeling vibrations (in parts or the entire body), vertigo, nausea, general discomfort, disorientation, decreased ability to concentrate, fatigue, and transient joint pain. The vibration is a mechanical phenomenon, whereas the vertigo, nausea, and discomfort indicate effects on the vestibular system. Similarly, nausea, vomiting, and vertigo are occasionally described in patients with vestibular signs or symptoms induced by loud noise (the Tullio phenomenon). The combination of disorientation, decreased concentration, and fatigue are similar to symptoms of motion sickness and probably result from sound stimulation of the vestibular system. The cause of joint pain is uncertain. Adherence to the published exposure standards should prevent these symptoms.

BAROTRAUMA

Barotrauma refers to injury caused by changes in pressure. Barotrauma can occur on descent or ascent when a gas-filled cavity fails to equilibrate with changing ambient pressure (see also Chapter 16, Aerospace Medicine). Almost any gas-filled cavity in the body can be affected by barotrauma. For example, gastrointestinal barotrauma can occur if gas is swallowed. The gas expands during ascent, causing abdominal distress, cramping, flatus, or eructation. No therapy is usually required because the gas will be expelled over a short time, but several cases of gastric rupture after decompression have required emergency attention.5,6

Less obvious body cavities are restored dental caries and gingivitis, which can also become gas-filled. Often referred to as aerodontalgia, dental barotrauma results from poor or eroded fillings or gum infection, and can occur on both ascent and descent. On descent, an air space can be filled with gum tissue or blood, and pain may occur. Descent also may cause the thinned filling or cementum over a carious tooth to collapse. If gas has become trapped under a filling during a dive, the pressure change during ascent may cause the cavity walls to explode.

Barotrauma that occurs when pressure increases is commonly referred to as a “squeeze.” For example, suit squeeze occurs in a poorly fitted wetsuit or in a dry suit with an insufficient gas supply to keep it slightly expanded. There may be no symptoms at all, or the diver may notice some pinching of the skin. Upon removal of the suit, irregular linear wheals or ecchymosis may be seen where the skin was pinched in folds of the suit material. No therapy is required. Mask squeeze can occur if a diver fails to equalize the pressure in the mask during descent. The space inside the mask is subjected to a relative vacuum and the skin under the mask becomes puffy and edematous, and may show small hemorrhages. Mask squeeze is more common around the eyes and in the conjunctivae. A severe squeeze will bruise the entire area under the mask.

Middle Ear Barotrauma

Descent

The most common form of barotrauma is middle ear squeeze. Anyone who has flown in an airplane or ridden in an elevator in a tall building has felt fullness in the ears during descent to ground level. This usually resolves by swallowing or yawning, which opens the eustachian tube and allows pressure equalization of the air on both sides of the tympanic membrane: ambient air and the air within the middle ear (see also Chapter 16, Aerospace Medicine). The consequences of not achieving equilibration are much worse in diving, where pressure changes far exceed the 1-atm maximum change in descent from altitude. The initial symptom of fullness in the ear progresses to pain if descent continues without equalization. The tympanic membrane retracts and small hemorrhages occur (Figure 18-3). If the process continues, the relative vacuum in the middle ear causes serum and blood to fill the space, and eventually the tympanic membrane ruptures. If cold water then enters the middle ear, sudden severe vertigo may occur, producing disorientation, nausea, vomiting, and panic. Predisposing factors to eustachian tube dysfunction and middle ear squeeze are conditions that prevent easy opening and closing of the eustachian tube, such as upper respiratory tract infections, allergies, mucosal polyps, mucosal irritation from smoking, otitis media, or anatomical variations.

Figure 18-3. Photograph showing moderate barotrauma of the middle ear. Note the hemorrhaging around the handle of the malleus and surrounding tympanic membrane, and the slight retraction and dullness of the tympanic membrane.

The diver should begin equilibration as soon as descent begins and continue every few feet. If the pressure differential is allowed to become too large, the eustachian tube will collapse to a point where it is “locked” and cannot be opened by any method. Methods of opening the eustachian tubes, or clearing the ears, include sliding the jaw around, opening the mouth, yawning, swallowing, and performing the Valsalva and Frenzel maneuvers. The Valsalva maneuver consists of closing the mouth, blocking the nostrils, and exhaling gently to increase internal gas pressure. A forceful Valsalva maneuver may produce pressure high enough to cause rupture of the round window with cochlear and vestibular damage (see Inner Ear Barotrauma, below). The Frenzel maneuver consists of closing the mouth, glottis, and nose, and contracting the muscles of the mouth and pharynx or swallowing. If these maneuvers do not work, the diver should ascend a few feet and try again. If repeated attempts do not allow equilibration, the dive should be aborted.

Prevention of middle ear barotrauma includes not diving when any condition exists that prevents proper eustachian tube function. Some divers often have “sticky ears,” a condition in which eustachian tube function is present but equilibration is difficult to achieve. Nonsedative oral decongestants can be helpful but may not always be effective. Topical decongestants should be used with care because overuse can make matters worse.

There is no specific therapy for middle ear barotrauma except the prohibition of significant pressure change or the use of autoinflation techniques until the problem resolves. In the case of tympanic membrane rupture, close observation is needed to detect infection when it first occurs. For severe barotrauma, serial audiograms are recommended to exclude hearing loss that may require further investigation and therapy. Generally, a diver who has had an ear squeeze without perforation can return to diving within 2 weeks. The basis for return is complete resolution of signs and symptoms as well as demonstration of the ability to equilibrate pressure in the middle ear. If rupture has occurred, a month or longer may be needed before return to diving can be allowed. Recurrence is common if exposure to pressure is allowed too soon after rupture.

Ascent

Middle ear barotrauma of ascent is infrequent because the middle ear can normally vent passively through the eustachian tube when its pressure reaches about 50 cm of water over ambient. When it does occur, middle ear barotrauma of ascent is usually a consequence of middle ear barotrauma of descent. If blockage is severe, ascent without trauma may be impossible. Symptoms are pressure, pain, tinnitus, vertigo, or hearing loss. The Valsalva maneuver should be avoided while ascending because it increases pressure in the middle ear space and can also lead to pulmonary barotrauma (see below). If pain or vertigo develops on ascent, the diver should halt the ascent and descend a few feet to relieve symptoms before attempting ascent at a slower rate. There is usually little to observe clinically, but hyperemia or hemorrhage in the tympanic membrane may occur. No specific therapy is required unless the vertigo persists after pressure equalization. Continued vertigo requires immediate investigation, especially if there is hearing loss.

Inner Ear Barotrauma

Any diver who has had difficulty equalizing the ears or has had barotrauma of the middle ear may also develop inner ear barotrauma, probably due to a rupture of either the round window or the vestibular membrane. Tinnitus is the most common manifestation, but hearing loss may occur at the time of barotrauma or within a few days. Some divers may experience vertigo, nausea, and vomiting. Hearing loss is usually sensorineural and is probably due to cochlear membrane rupture or hemorrhage.[7] If deafness is instantaneous and present in all frequencies, it is probably due to severe round-window rupture. If it is mild and develops over several days, a round-window fistula may be present. If air leaks into the perilymph, the deafness may change with head position. Immediate referral to an otolaryngologist is recommended to prevent permanent hearing loss. Bed rest with head elevation is required. The diver should be cautioned not to do anything that will raise the pressure of the cerebrospinal fluid, such as nose blowing, performing a Valsalva maneuver, straining at the stool, or coughing.

If there is no improvement within 24 to 48 hours or if the casualty’s condition deteriorates, then surgical therapy should be considered. If improvement is steady, bed rest is continued for 1 week after improvement plateaus. Aeromedical evacuation, if required, should occur in an aircraft that can be pressurized to sea level. If helicopter transfer is the only method available, the pilot should be instructed to fly as low as is safely possible, preferably below 1,000 ft (305 m).[4] If deafness, vertigo, or tinnitus persist despite all therapy, the casualty should be advised against any future diving. Inner ear barotrauma and inner ear DCS can have similar symptoms (see Decompression Sickness, below), and their differentiation is important because DCS is treated by recompression, which is contraindicated in barotrauma.

Sinus Barotrauma

Sinus barotrauma during descent is probably the next most common problem after ear squeeze and involves the same predisposing factors. Symptoms include a feeling of pressure or tightness and pain over the face during descent. If the maxillary sinuses are affected, pain may be referred to the teeth. Often the diver may not realize that a mild squeeze has occurred until ascent, when the ostia may open, expelling blood and fluid.[7] Sometimes fluid, blood, or gas can be felt escaping from the sinuses. Divers who are unfamiliar with the problem can become extremely worried if this occurs. Although pain is usually relieved on ascent, it may persist for several hours. Persistent pain indicates that equilibration has probably not occurred and there is a risk of acute sinusitis. Valsalva maneuvers will usually allow equilibration of the sinuses. Nasal decongestants may also be used.

Sinus barotrauma rarely occurs during ascent. However, if the pressure in the sinuses is high enough, there may be a painful rupture of the ostia or mucosa into the nasal cavities. Treatment is the application of nasal decongestants.

Palsies of the fifth and seventh cranial nerves can result from sinus barotrauma (cranial nerve V) or middle ear barotrauma (cranial nerve VII).[8]

Pulmonary Barotrauma

Descent

Pulmonary barotrauma of descent occurs under two circumstances:

1. When a hard-hat diver accidentally descends faster than the gas can be supplied to the helmet or suit.

2. In breath-hold diving at depths so great that gas in the lungs is compressed to less than the residual volume.

The second circumstance is a very rare event in conscious divers because chest pain alerts the diver of excessive depth. For most people the maximum breath-hold depth is about 100 fsw (30 msw), although competitive free divers have exceeded 650 fsw (200 msw). See Breath-hold Diving, below.

Ascent

Pulmonary barotrauma of ascent is potentially the most severe type of barotrauma and can occur in all types of diving and in submarine escape (as well as in rapid decompression to high altitudes). Pulmonary barotrauma of ascent is caused by overinflation of the lung as the gas expands during ascent, either by breath-holding or by some local pathology that prevents gas from escaping from a portion of the lung. Pulmonary barotrauma is believed to be the second most common cause of mortality in divers (drowning is the most common). It has been reported in ascent from a depth as shallow as 3 to 6 ft (1–2 m) of water.9,10 During naval submarine escape training, ascents are done under close supervision after medical screening, with emergency medical care immediately available. Predisposing conditions for pulmonary barotrauma are breath-holding during ascent, previous spontaneous pneumothorax, asthma, blebs, pulmonary tumors, pleural adhesions, infections, pulmonary fibrosis, or any other disease that weakens the lung tissue or interferes with the free passage of gas.4,11,12

Pulmonary barotrauma may result in local or wide-ranging damage to lung tissue, characterized by disruption of the alveolar-capillary membrane and consequent passage of alveolar gas into (a) the mediastinum, causing mediastinal or subcutaneous emphysema; (b) the pleural space, causing pneumothorax; and (c) the capillaries, with probable resultant cerebral arterial gas embolism (AGE). These traumata can occur alone or in combination. Patients with pulmonary barotrauma but no signs or symptoms of AGE should be kept under observation for at least 24 hours, even if no therapy is required, to ensure that medical attention is available if the patient worsens, or if a new condition such as DCS emerges.

Pulmonary Tissue Damage

There may be no symptoms with local pulmonary tissue damage, but if the damage is widespread, the diver may surface with cough, hemoptysis, and dyspnea. Respiratory failure may result if enough alveoli have been ruptured. Severe symptoms of pulmonary damage require immediate respiratory support with 100% oxygen, as in the treatment of nonfatal drowning or acute respiratory distress syndrome. If pulmonary barotrauma is suspected, positive pressure ventilation should be avoided unless it is absolutely necessary for survival because it may cause further lung damage or other complications. Recompression is not needed unless symptoms or signs of AGE or DCS are present.

Mediastinal Emphysema

Mediastinal emphysema occurs when gas enters the mediastinum along perivascular sheaths or tissue around the airways. The gas may extend to the subcutaneous tissue of the neck (subcutaneous emphysema), the pericardium (pneumopericardium), or the retro-peritoneal space (pneumoperitoneum). There may be no symptoms in mild cases, or symptoms may appear immediately or over hours, depending on the severity of the condition. Signs and symptoms include crepitus under the skin, faint heart sounds, paralysis of the recurrent laryngeal nerve, tachycardia, hypotension, cyanosis, coma, fullness in the throat, retrosternal discomfort, voice changes, dyspnea, dysphagia, syncope, shock, and unconsciousness. Crepitus that is heard over the precordium and is related to heart sounds is called Hamman sign. Gas that has dissected into the pericardial sac or between the pleura and pericardium may cause cardiac tamponade. A chest radiograph will confirm the diagnosis, or it may be the only evidence of mediastinal emphysema.

Mediastinal emphysema in divers is generally not life-threatening and usually requires no treatment. Breathing 100% oxygen will accelerate absorption of the inert gas in mild cases and is required for life support in severe cases. Severe cases may benefit from recompression to reduce the volume of gas in the tissues. Compression on 100% oxygen to a depth of relief (normally 5–10 ft [1.5–3 m]) for 1 hour should suffice.[4]

Pneumothorax

Pneumothorax occurs when increased pressure in the lung ruptures the pleura with results similar to a spontaneous pneumothorax. A hemopneumothorax may occur if blood vessels are torn. Symptoms include sudden onset of chest pain (possibly pleuritic) and dyspnea. Bilateral pneumothoraces may be present after a fast ascent, as in submarine escape training or in an emergency ascent from a dive. Signs include increased respiratory rate, decreased breath sounds, and increased resonance. If a tension pneumothorax is present, the classic tracheal shift to the unaffected side may occur, with shock and severe respiratory distress. If the pneumothorax is small, no therapy is necessary, although breathing 100% oxygen at the surface should accelerate pleural gas absorption.

If the patient is under pressure and decompression continues, a tension pneumothorax will result. If the patient is in a chamber, treatment includes recompression to reduce symptoms, 100% oxygen breathing (or a gas mix with increased partial pressure of oxygen), and the insertion of a chest tube or valve to allow decompression while avoiding expansion of the pneumothorax. If the diver is in the water when the pneumothorax occurs, however, none of the above treatments are possible.

If the patient is on the surface and severe symptoms are present, recompression should not be initiated unless required for treatment of AGE or DCS. Treatment at sea level does not differ from that for a pneumothorax resulting from other causes. If recompression is required for therapy of AGE or DCS, insertion of a chest tube should be considered before recompression. For emergency recompression, a needle with a nonreturn valve may need to be inserted prior to or during decompression. If recompression is needed and a chest tube with drainage is in place, care is required to prevent water and gas from being sucked into the chest during compression. If the system allows gas or fluid into the chest, the chest tube should be clamped close to the chest wall until treatment depth is reached. Due to the possibility of infection, chest tubes should not be used in a recompression chamber unless absolutely necessary.

Arterial Gas Embolism

AGE can be life threatening or result in permanent injury, and requires immediate recompression. AGE is a complication of pulmonary barotrauma caused by the entry of gas through tissue tears into the pulmonary venous system, with further distribution through the left side of the heart to the arterial system. The gas bubbles generally come to rest in the cerebral circulation, or uncommonly in the coronary circulation. In the coronary system, immediate death can result through cardiac failure. In the cerebral circulation, the typical signs are of sudden arterial block, as in a stroke. The onset of signs and symptoms is sudden and dramatic, appearing almost always during the ascent or within 10 minutes of surfacing. The most common signs are altered mental status, unconsciousness, disorientation, and paresis. Paresis can occur in any distribution but is most often unilateral.

Other symptoms, depending on the anatomical location of the blockage, include vertigo, visual disturbances, dysphasia, sensory abnormalities, and convulsions. If the coronary system is involved, cardiac chest pain and dysrhythmias may be present. AGE, whether in the brain or elsewhere, causes ischemia in the surrounding tissue and induces coagulopathies, hemorrhages, and endothelial damage.[13] If recompression treatment is delayed, reperfusion injury may occur once the circulation has been reestablished.

Studies may show abnormal electrocardiographic, electroencephalographic, and brain scan findings, but if AGE is suspected, there is no reason to delay treatment while these tests are obtained. Immediate recompression is the key to adequate treatment of this syndrome. If treatment is delayed, the chances for a good outcome decrease and therapy becomes more difficult. In severe cases death may occur despite immediate and aggressive therapy. In mild cases the symptoms may resolve without any therapy. In some cases a patient may improve after initial symptom onset but relapse despite treatment.[14] There is no way to predict which case will resolve and which will not. Therefore, all cases of suspected AGE should be recompressed as soon as possible. Iatrogenic AGE can occur during interventions such as vascular catheterization, mechanical ventilation, open heart surgery, brain surgery, and kidney dialysis.13,15 Treatment in these cases is no different from that in cases resulting from ambient pressure changes.

The treatment for AGE is immediate recompression, as discussed in further detail below. The US Navy Diving Manual recommends initial recompression to 60 fsw (18 msw) on 100% oxygen. If the symptoms resolve, treatment may be completed in accordance with US Navy Treatment Table 6. If the patient does not respond satisfactorily, further compression to a depth not to exceed 165 fsw (50 msw) is an option for attempting to reduce the size of remaining bubbles.[4] If immediate recompression is not available, 100% oxygen breathing by mask should be immediately initiated.

Transportation to a recompression facility should be done as gently and quickly as possible to prevent further distribution of bubbles to the brain or elsewhere. Air evacuation, if required, should occur at an altitude below 1,000 ft (305 m) and preferably in an aircraft that can be pressurized to sea level.[4] Other supportive therapy should be used as required.

In certain cases, there may be difficulty in determining whether the diver has AGE or cerebral DCS (see Decompression Sickness, below).

PATHOPHYSIOLOGICAL EFFECTS OF COMMON DIVING GASES

The nature of diving requires the creation of an artificial environment, one that simulates the very narrow parameters required to sustain life, where small variations can have drastic effects. With increasing depth comes increasing complexity due to changes in physiologic responses as the body is exposed to changing stressors.

The pathophysiology of all metabolically active gases (oxygen, carbon dioxide, carbon monoxide) depends on the gas’s partial pressure, not on its percentage in the breathing mixture. For example, at 1 atm, a mixture containing 5% oxygen is not compatible with life, but at 5 atm this mixture is perfectly adequate. Just as life-sustaining gases need to be adequately controlled, so do gases considered to be contaminants. A small fraction of contaminants at sea level can cause significant levels of toxicity at high pressure because the partial pressures increase with depth, as described by Dalton’s law (see Gas Laws, above). The current US Navy standards for the purity of air, oxygen, nitrogen, and helium are found in the US Navy Diving Manual.[4] Breathing gases that do not meet these standards are not to be used for diving. This section deals with the pathological conditions associated with commonly used breathing gases and some common contaminants (carbon dioxide, carbon monoxide).

Oxygen Toxicity

Oxygen, at its most fundamental requirement for life, is used for cellular respiration and the production of adenosine triphosphate, the body’s energy currency. However, it has long been known that breathing high partial pressures of oxygen (greater than that experienced in atmospheric air at sea level) can lead to toxicity issues that particularly affect the lungs, central nervous system (CNS), and eyes. The risk is dose dependent. Effects can be seen even on shorter dives and should be a serious consideration for longer exposures such as during saturation dives and hyperbaric oxygen therapy.

Pulmonary Oxygen Toxicity

Pulmonary oxygen toxicity was first described by Lorrain-Smith in 1899 as the result of breathing pure oxygen with a partial pressure of oxygen (Po_2) of 1 ata at sea level for a prolonged time.[16] Clinically, the symptoms of pulmonary oxygen toxicity follow the tracheobronchial tree and progress to the interstitial lung tissue. Patients typically first report the symptoms of a mild “tickle” in their throat and mild cough. This is followed by tracheal and substernal burning with cough on deep inspiration. Persistence of high dose oxygen can eventually lead to dyspnea and death. Even though the patient may be breathing pure oxygen, the cause of death is asphyxia. A measurable sign of pulmonary oxygen toxicity is a decrease in vital capacity (VC), with increasing loss of inspiratory capacity and increasing residual volume. The pathophysiology can be divided into two phases. The first is an exudative phase (< 5 days) and includes an initial general inflammatory response that results in endothelial damage, inflammatory cell infiltration, exudative fluid leakage, hemorrhage, and consolidation. This is followed by the second, proliferative phase (> 5 days) characterized by alveolar type 2 cell and fibroblast proliferation, alveolar membrane thickening, and eventual fibrosis of interstitial lung tissue. The first phase is considered reversible, while the second phase is not.[17]

It has also been shown that there is an association between CNS and pulmonary oxygen toxicity at higher partial pressures of oxygen (> 2 ata) such as those that are known to cause CNS toxicity.[18] The injury pattern, however, is different than that seen with the classic presentation of pulmonary toxicity, which can be induced by lower partial pressures of oxygen (1 ata). Studies in rats have shown that oxygen-induced seizures are associated with pulmonary changes consistent with hydrostatic injury.[19] Mechanisms proposed include an increased output of the sympathetic nervous system in response to increased oxygen tensions, resulting in hemodynamic changes that lead to pulmonary edema and protein leakage.

Several markers for monitoring pulmonary oxygen toxicity have been proposed, most notably, the reduction of lung VC. This effect can be estimated by the unit pulmonary toxicity dose (UPTD),20,21 which is based on the experimental measurement of changes in VC in human subjects. One UPTD is the degree of pulmonary decrement produced by breathing 100% oxygen continuously at 1 ata for 1 minute. A common benchmark is 1,425 UPTDs, which produces a VC decrease of 10%. This concept assumes no decrement in lung function when breathing oxygen at a partial pressure of 0.5 ata or less. The results of such calculations should be considered as an estimate of pulmonary effects, because there are large individual differences, but it is useful as a tool to limit prolonged oxygen breathing at partial pressures higher than 0.5 atm. Likewise, actual measurements of VC can vary between subjects, and results must be interpreted in context. Recently some experts have recommended using the parameter of diffusing capacity for carbon monoxide as a marker of pulmonary oxygen toxicity.[17]

Although pulmonary oxygen toxicity is an uncommon problem in routine air diving operations, gas content must be carefully planned in saturation diving, where divers are exposed to a Po_2 in the range of 0.4 to 0.5 ata for days to weeks with intermittent exposures to higher levels for diving excursions (see Chapter 17, Military Diving Operations). Care must also be taken to monitor divers using 100% oxygen rebreathers during special operations missions (see Chapter 17, Military Diving Operations). Pulmonary oxygen toxicity can also occur in prolonged recompression therapy for DCS or AGE, as well as during hyperbaric oxygen therapy. Therapy will often be planned to give at least 1 to 2 days’ rest for each 5 to 6 days of treatment. Shallower depths may also be used to limit the oxygen exposure. Tradeoffs are made between benefits of high partial pressure oxygen used to promote healing versus the pulmonary damage incurred.

Central Nervous System Oxygen Toxicity

CNS oxygen toxicity, discovered by Paul Bert in 1878, has been referred to as acute oxygen poisoning because of its rapid onset. CNS toxicity can occur while breathing oxygen under pressure at a Po_2 of 1.6 ata but typically requires pressures higher than 2.0 ata Po_2. There can be significant individual variability in susceptibility, as discussed below.

The most significant and potentially troublesome symptom of CNS oxygen toxicity, particularly for the diver, is the tonic-clonic convulsive seizure. Other symptoms of CNS toxicity can include facial muscular twitching, nausea, vertigo, tunnel vision, hearing changes, anxiety, and behavioral changes, but these symptoms do not usually precede seizures. Occasionally patients have reported aura, but typically there is no warning prior to the onset of seizure. There is some evidence in rat models for increased respiratory rates preceding seizures,[22] but anecdotally, this has not been a reliable predictor. The treatment for CNS toxicity is to remove the patient from the high-level oxygen source and prevent self-injury. Rarely, a convulsion may occur within minutes after oxygen breathing stops. This is known as the “off effect” and has no accepted explanation, but it likely represents the culmination of a process that began during oxygen breathing.

Because oxygen toxicity is dose-related, oxygen can safely be used as long as time and depth are limited. This allows the use of oxygen at greater than 1 ata partial pressure to reduce inert gas absorption at depth, both to accelerate inert gas elimination during decompression and for recompression therapy. The latent period prior to the onset of symptoms can be extended by periodically breathing a gas with a reduced oxygen partial pressure. Therefore, treatment tables at 60 fsw (18 msw) utilize oxygen breathing periods of 20 minutes, separated by 5-minute air breaks (see Chapter 17, Military Diving Operations).

A number of factors affect sensitivity to oxygen toxicity, including extreme variation among individuals and within the same individual from day to day. There is no guarantee that someone who did not have an oxygen convulsion today will not have one tomorrow. Immersion and exercise decrease the latent period, which increases the risk for a working diver compared with that for a diver at rest in a dry hyperbaric chamber.[23] Increased inspired or arterial carbon dioxide decreases the latency,[24] and individuals prone to retain carbon dioxide may be at greater risk. Modern underwater breathing apparatuses have less breathing resistance and dead space than earlier equipment, but heavy work at greater depth may cause carbon dioxide retention and potentiate oxygen toxicity. Increased gas density also decreases ventilation and can lead to retention of carbon dioxide.

The mechanism by which oxygen causes these pulmonary and CNS derangements is still not completely understood. The most accepted explanation is that oxidative stress mediated by reactive oxygen species, such as superoxide and hydrogen peroxide, act through intermediate reactions, and may interfere with cellular metabolism and signaling. Nitric oxide is of particular interest as an intermediate reactant; it can form peroxynitrite from its reaction with superoxide.[25] Plasma membrane is a significant site of free radical interaction, causing disruption by lipid peroxidation, amino acid oxidation, and protein crosslinking.[26]

Other well-known effects of oxygen include vasoconstriction-induced reduction in peripheral blood flow, decreased carbon dioxide carrying capacity of hemoglobin, and increased red blood cell fragility, but these subtle changes do not generally cause concern. Some evidence suggests that high oxygen tensions can also cause DNA strand breaks, but this damage is short lived as repair mechanisms are activated, and no mutagenic effects have been seen.[27]

Ocular Oxygen Toxicity

Though less common, the deleterious effects of oxygen on the eye tend to be cumulative and occur over a prolonged period, similar to pulmonary oxygen toxicity. This can occur in hospitalized patients who receive 100% oxygen for prolonged periods or in divers. Additionally, the condition known as retrolental fibroplasia, a disease of the growing eyes of a premature newborn exposed to elevated levels of inspired oxygen, causes a disruption of normal retinal growth patterns. In adults the common ocular manifestations are decreased peripheral vision and myopia. Both conditions tend to resolve after cessation of high dose oxygen.[28]

Carbon Dioxide Toxicity

Carbon dioxide is a naturally occurring gas produced by cellular respiration. It can have significant effects on divers, if not adequately controlled. These effects include hyperventilation, dyspnea, tachycardia, headache, lightheadedness, and dizziness, progressing to mental confusion and unconsciousness (Table 18-2). Carbon dioxide was once used as an inhalation anesthetic (beginning in 1824), but was surpassed by newer medications with fewer side effects.[29] As with other gases, the effects are dependent on the partial pressure of the gas, not the percentage. Increased carbon dioxide levels and toxicity can be caused by the following conditions:

- increased carbon dioxide in the breathing gas due to compression of contaminated gas in an open-circuit breathing apparatus or failure of the carbon dioxide absorbent in a closed-circuit apparatus;

- increased respiratory dead space owing to poor equipment design or inadequate ventilation of the chamber or helmet;

- voluntary hypoventilation (when divers hold their breath after inhalation or “skip-breathe” to increase the duration of the open-circuit gas supply);

- increased partial pressure of oxygen, which decreases the ventilatory response to carbon dioxide; or

- increased breathing resistance, either intrinsic (in a diver’s lungs) or extrinsic (due to breathing equipment); the latter is more common than the former. Added breathing resistance decreases ventilatory response to elevated carbon dioxide.

TABLE 18-2

ACUTE EFFECTS OF INCREASED INSPIRED CARBON DIOXIDE

Partial Pressure of CO_2 (ata)

Effect

0.0003

None, normal atmospheric partial pressure of CO_2 at sea level

0.0003–0.04

None, exposures less than 8 hours

0.04–0.06

Mild hyperventilation and confusion, headache

0.06–0.10

Moderate dyspnea and confusion

>0.10

Unconsciousness, muscle twitching

Data source: Lambertsen CJ. Carbon Dioxide Tolerance and Toxicity. Philadelphia, PA; University of Philadelphia Institute for Environmental Medicine; 1971.

Carbon Monoxide Toxicity

Carbon monoxide sources in the environment are largely due to incomplete combustion of hydrocarbons (fuels) or other carbon compounds. Contamination of compressed air is rare but dangerous when it occurs. The most common source of divers’ gas contamination is from an air compressor whose intake is near the exhaust of an internal combustion engine, even the compressor’s own power source. Compressors lubricated with oil are also a potential source of carbon monoxide if the oil does not meet specifications or the compressor is operating at elevated temperatures. Physiologically, a small amount of carbon monoxide is produced during the metabolism of hemoglobin, and habitual smokers exhale even larger quantities for up to 24 hours after their last cigarette.[30] Any amount of contamination is concerning at increased ambient pressures, particularly when divers are exposed to prolonged bottom times such as in saturation diving.

Contamination of breathing air with carbon monoxide from any source prevents normal saturation of hemoglobin with oxygen and, through a cascade of events, can cause long-term neurologic sequelae. Exhibit 18-1 lists common symptoms of acute carbon monoxide toxicity. Many texts contain a table that correlates symptoms to measured levels of carboxyhemoglobin, but this table has been shown to be an outdated tool in the management of poisoned patients due to the poor correlation of carboxyhemoglobin levels with actual patient presentations.[31] The more important finding is to link the triad of exposure, symptoms, and abnormal elevation of carboxyhemoglobin to make decisions about treatment.

The acute toxic effects of carbon monoxide at depth depend on its partial pressure, and the symptoms are the same as at sea level. Because carbon monoxide binds to myoglobin as well as to hemoglobin, carboxyhemoglobin concentrations do not always correlate with symptomatology. The length of exposure, inspired carbon monoxide partial pressure, and physical activity are also important. A short exposure of a resting person to a high level of carbon monoxide may produce a lower blood level than a long exposure of a working person to a relatively low inspired carbon monoxide concentration.

EXHIBIT 18-1

COMMON SYMPTOMS OF ACUTE CARBON MONOXIDE TOXICITY

- headache

- dizziness

- nausea/vomiting

- confusion

- fatigue/weakness

- vision changes

- chest pain

- shortness of breath

- loss of consciousness

- death

Because carbon monoxide and oxygen compete for binding sites on hemoglobin, oxygen breathing, particularly at increased partial pressure, is considered to be an effective treatment for carbon monoxide poisoning. It has long been thought that breathing 100% oxygen at sea level (Po_2 of 1 ata) decreases the morbidity and mortality associated with carbon monoxide poisoning. This led to the idea that hyperbaric treatment with oxygen breathing (Po_2 > 1 ata) might further improve outcomes. Several studies (of varying quality) have been conducted, some showing benefit, others showing no difference, in breathing 100% oxygen at sea level versus hyperbaric oxygen therapy. A recent review concluded that there is insufficient evidence to routinely recommend hyperbaric oxygen therapy for the treatment of carbon monoxide poisoning.[32] Some experts, however, while acknowledging the limitations of previous studies, still recommend hyperbaric oxygen therapy for poisoned patients with loss of consciousness, ischemic cardiac changes, neurological deficits, significant metabolic acidosis, or carboxyhemoglobin over 25%.[33]

Nitrogen Narcosis

Nitrogen narcosis, “the rapture of the deep,” is the progressive intoxication that develops as a diver descends and the partial pressure of nitrogen increases. Depending on individual sensitivity, common lore states that each 1- to 2-ata increase in air pressure is equivalent to one martini, the so-called “martini law.” While perhaps not absolutely correct, this analogy does reflect the subtle changes that begin at 50 to 100 fsw (15–30 msw) while breathing compressed air that have been described as feeling similar to alcohol intoxication.[34] Most commonly there is a general decrease of cognitive function and memory accompanied by motor impairment that worsens as depth increases. This continues to about 350 fsw (105 msw), where most divers lose consciousness.[35]

Factors that exacerbate nitrogen narcosis are inexperience, anxiety, alcohol, fatigue, and increased inspired carbon dioxide.[36] Ameliorating factors are suspected to be experience, mental discipline, and fixation on a task, but these are anecdotal at best. The evidence for adaptation to narcosis with frequent exposure is lacking and controversial, with some studies showing the contrary.[36] Because narcosis is a threat to diver safety, most agencies limit air diving with a scuba to 130 fsw (40 msw), and with hard-hat surface-supplied air diving to near 165 to 180 fsw (50–55 msw).

The mechanism of nitrogen narcosis, which is thought to be similar to anesthesia, is still under study. Anesthetic potency shows some relationship to lipid solubility, which was formerly thought to cause cell membranes to swell, thereby influencing ion transport. This is consistent with the lack of narcosis from helium, with its low solubility and low surface tension. More recent trends under consideration, supported by advanced laboratory techniques, have focused on a membrane protein binding theory, which may better explain discrepancies in the lipid solubility model.[37] Overall consensus is that there are likely multiple mechanisms that contribute to anesthesia.

Helium

Much experimentation has been done on breathing gas alternatives since the dawn of diving. Finding gases that benefit the diver while incurring the least amount of side effects has been the goal. Although the noble gases (group 18 in the periodic table of elements) are chemically inert, they can be physiologically active.

Substitution of helium for nitrogen in breathing gas has four major effects. The first is the effect on the voice due to decreased density of helium gas passing by the vocal cords. The second is the absence of narcosis. The third is decreased work of breathing, owing to the lower density. This, and the lack of narcosis, make helium particularly useful at depths greater than 150 fsw (45 msw). The fourth effect is loss of heat through the skin and the lungs, owing to helium’s high heat capacity and conductivity. Both the skin and the breathing gas must be heated during prolonged helium–oxygen diving to prevent hypothermia. Hot water is usually used for this purpose. Hypothermia can also occur in a dry, helium–oxygen filled chamber if the temperature is not raised above the normal comfort level for air. The required temperature increases with increasing gas density. A full discussion of these effects can be found in the section on saturation diving in Chapter 17, Military Diving Operations.

Although helium is the gas of choice for deep dives, a deleterious effect called high-pressure nervous syndrome (HPNS) begins at depths typically greater than 600 fsw (180 msw). HPNS is characterized by CNS hyperexcitability, including tremors, poor sleep (with microsleep), loss of appetite, decreased manual dexterity, and impaired but stable cognitive function.[38] Limited accounts of psychotic symptoms have been reported at depths greater than 2,000 fsw (600 msw).[39] Initially, HPNS was believed to be caused by helium (“helium tremors”), but it is unclear if pressure is more likely the responsible agent.

Several studies in the 1970s involving deep dives showed that the onset of HPNS was dependent on rate of compression and overall depth. Protocols that slowed descent proved beneficial. Additionally, because the excitatory effects of pressure and the narcotic effects of nitrogen are partially counteractive, combinations were used to ameliorate each effect. This phenomenon, known as the pressure reversal of anesthesia, was first discovered in tadpole experiments with ethanol as the narcotic. It is achieved by adding nitrogen to helium–oxygen mixtures when diving to greater depths.[40]

Hydrogen

Interest in hydrogen diving has been ongoing since engineering advances in handling hydrogen–oxygen mixtures reduced the danger of explosion. These techniques take advantage of the fact that hydrogen cannot ignite if mixed with less than 5.5% oxygen. Hydrogen is inexpensive, readily available, and less narcotic and less dense than nitrogen. The decompression properties of hydrogen appear to be between those of helium and nitrogen. Up to 20 ata of hydrogen have been used to reduce both HPNS and breathing resistance at depths greater than 2,000 fsw (610 msw), but hydrogen narcosis, perhaps exacerbated by HPNS, appears to be a limiting factor.[41]

Other Inert Gases

Of the other noble gases, neon has been used in deep diving experiments because of its lack of narcotic effect. However, it is not used for diving operations because it is expensive and has a higher density than helium (or hydrogen), which causes greater respiratory work. Argon, xenon, and krypton are narcotic at 1 ata and therefore not appropriate for diving. Because of its high insulating properties, argon is sometimes used to inflate dry diving suits.

DECOMPRESSION SICKNESS

DCS refers to the overt illness that follows a reduction in environmental pressure with the development of endogenous gas bubbles. The condition is distinguished from AGE, in which bubbles originate from the lungs or external sources and enter the vasculature through disruptions in the pulmonary membranes. DCS occurs in diving, caisson work, rapid ascent to high altitude, and following hyperbaric chamber work. DCS can occur at any time following the start of decompression and can be subtle or catastrophic. The initiating cause is the formation of bubbles of the inert gases dissolved in the tissues. Diagnosis can be difficult because the signs and symptoms of DCS resemble not only non-diving diseases but also AGE. Symptoms and signs may disappear spontaneously but return unpredictably hours later. DCS should be the top-most diagnosis in the physician’s mind when a patient presents with complaints following any dive.

DCS is traditionally classified into two types: Type I, which is minor, includes only limb or joint pain, itch, skin rash, or localized swelling; and Type II, which is serious, includes presentations with neurological and pulmonary symptoms or signs (see also Chapter 16, Aerospace Medicine). The term “decompression illness” is used for any diving accident involving pressure reduction, including Type I DCS, Type II DCS, and AGE. In certain cases, it may be impossible to distinguish between AGE and DCS with signs of cerebral dysfunction, or a combination of both. Table 18-3 provides some guidance, but differentiation is often not possible. Clinically, this is not a significant issue; the US Navy Diving Manual specifies the same symptom-based therapy, including saturation therapy, for both AGE and severe neurological DCS: recompression with oxygen to 60 ft (18 m), or to deeper depths with air or a breathing gas with an increased oxygen content (eg, 50% oxygen–50% nitrogen).[4] The depth and duration of therapy are determined by the clinical progression.

TABLE 18-3

COMPARISON OF DECOMPRESSION SICKNESS AND ARTERIAL GAS EMBOLISM

Factor

Decompression Sickness (DCS)

Arterial Gas Embolism (AGE)

Occurrence

A dive of sufficient depth and duration to cause significant inert gas absorption

Any dive

Onset

Immediate or delayed

Immediate

Cause

Inert gas bubbles in tissue, veins, or arteries

Bubbles in arteries only as a result of pulmonary barotrauma

Bubbles

From dissolved gas

From alveolar gas

Usual first symptom

Localized pain or numbness

Unconsciousness or paralysis

Neurological signs

Usually bilateral

Usually unilateral

Prognosis

Mild to serious

Serious

For treatment purposes, the most important point is how these symptoms respond to therapy, not the initial classification. In fact, as therapy progresses, the diagnosis may change. For example, a diver with severe pain may not notice local weakness or sensory loss until recompression relieves the pain. The pain may also mask the signs from an examiner. Immediate recompression of patients with serious signs and symptoms should take precedence over a detailed physical examination that may reveal less obvious signs. Additional information on the treatment of DCS and AGE for flight or diving environments can be found in Chapter 16, Aerospace Medicine, and Chapter 17, Military Diving Operations.

Inert Gas Exchange

When an inert gas is breathed at elevated pressure, its partial pressure in the lungs initially exceeds that in the tissues. As the time at pressure lengthens, the inert gas is progressively absorbed by the tissues until its partial pressure there equals that in the lungs. The principal factors governing the rate of gas absorption by tissue are perfusion and solubility. Lipid tissues, such as fat, with high inert gas solubility and poor perfusion, absorb (and eliminate) inert gas much more slowly than low solubility aqueous tissues, such as muscles, that are well perfused.[42] Diffusion is not as important as perfusion, but it can influence gas exchange any time areas of tissue have different inert gas tensions. For example, diffusion shunts can occur between adjacent arterial and venous vessels, resulting in slower inert gas exchange in a tissue than would be expected on the basis of perfusion alone.

Bubble Formation

Bubble formation that follows decompression isolates inert gas from the circulation and reduces the effectiveness of perfusion in eliminating the inert gas in the vicinity of the bubble. An effective method for accelerating the elimination of an inert gas from tissues or bubbles is to increase the partial pressure of oxygen in the inspired gas, which increases the difference between inert gas in the lungs and in the tissue.[42]

In experiments with animals performed during the 1870s, Paul Bert[43] of France demonstrated that the most severe forms of DCS are caused by bubbles in the blood and tissues. Bubbles are less obvious in the milder forms of DCS, which led to the suggestion of other etiologies, but none of these theories has been sustained. The presence of bubbles, after even very shallow or short dives, can be detected using ultrasound devices.[44]

In both living and nonliving systems, a primary factor that determines whether a bubble will appear is the level of supersaturation, or the sum of the partial pressures of all vapors and dissolved gases, minus the local absolute pressure. The level of supersaturation that leads to bubble formation is a clue to how bubbles form. Supersaturation of gases on the order of 100 to 1,000 atm in nonliving systems is evidence for de novo nucleation (ie, the formation of bubbles where no gas phase previously existed).42,45 During physiological decompression, however, supersaturation rarely exceeds several atmospheres, and the lowest supersaturation at which DCS occurs is about 0.5 atm.13,46 Under these conditions, bubbles probably expand from preexisting gaseous micronuclei, or gas nuclei, which exist in all aqueous fluids. It is difficult to understand the origin of gas nuclei in closed living systems, but some are probably mechanically generated by the de novo nucleation resulting from both viscous adhesion in tissue and shear forces during the relative motion of articular surfaces.[42] Such motion causes the local pressure to transiently decrease to hundreds of negative atmospheres and creates vaporous bubbles that make audible sounds as they collapse (“cracking” joints).[47] Stable gas bubbles also form as result of this process. The population of some gas nuclei in the body appears to normally be in a state of dynamic equilibrium, wherein their creation by mechanically induced nucleation is balanced by their elimination due to surface tension.

Pathophysiology of Decompression Sickness

DCS results from a reduction in ambient pressure with the subsequent formation of stable bubbles. Despite the common occurrence of bubbles in the circulatory system, bubbles probably do not originate in blood but form extravascularly and seed the microcirculation as they expand. These bubbles grow by the inward diffusion of nitrogen as they are carried in the venous blood to the heart and lungs. The pulmonary circulation is usually effective in filtering these bubbles. However, if the volume of gas becomes overwhelming, as can occur in accidental ascent from great depth, pulmonary edema and cardiac failure can result, leading to death by asphyxia.48,49

Venous bubbles have the potential for reaching the arterial circulation by passing through the pulmonary circulation or bypassing the lungs altogether through arteriovenous shunts or possibly a patent foramen ovale (PFO). Large numbers of emboli in the arterial circulation can arise due to pulmonary barotrauma of ascent. While this gas can have serious consequences if carried to the brain, the situation is worse if the barotrauma occurs at the end of a dive when the tissues contain excess inert gas. Bubbles that enter the arterial circulation can expand if they reach supersaturated tissue. This may explain a devastating form of DCS that involves both the brain and spinal cord after relatively shallow dives that end with pulmonary barotrauma (Figures 18-4 and 18-5).

Figure 18-4. This gross cross-section of a spinal cord shows hemorrhages in the white matter that are typical of decompression sickness.

Figure 18-5. Brain from a patient who died of severe decompression sickness, showing bubbles in the surface vasculature.

Bubbles have both mechanical and biochemical effects, which may be extravascular or intravascular (arterial and venous). Extravascular bubbles can compress or stretch tissue and nerves. Intravascularly, they can cause embolic obstruction, platelet aggregation, ischemia, edema, hemorrhage, and tissue death (Figure 18-6).50,51 Endothelial cell membranes are stripped by the passage of bubbles. Bubbles may block lymphatic channels, causing tissue edema. The most serious of these events are rare, except in cases of severe DCS or AGE, and mild cases are the rule when modern dive procedures are used. The human body appears to tolerate a certain volume of bubbles with no symptoms or only mild symptoms.[44]

The biochemical effects of bubbles relate to their surface active properties, which cause enzyme activation and protein denaturation leading to thrombosis and complement activation.50,52 Together, the mechanical and biochemical effects of bubbles can increase blood viscosity, postcapillary resistance, transcapillary fluid loss, and hemoconcentration.51,53 These interactions can produce reperfusion injury, which occurs when toxic oxygen species are generated after circulation to an ischemic area of the brain has been reestablished.[54] Reperfusion injury may explain a poor response to hyperbaric therapy or relapse after initially successful treatment of DCS or AGE. Relapse may also occur due to the aggregation of leukocytes on damaged endothelium.

Clinical Presentation

Whether provoked by diving or by rapid ascent to altitude, DCS is a protean disease that can present with subtle symptoms and no signs. These may or may not worsen over minutes to hours. DCS may also present as a sudden catastrophic event with multiple symptoms, signs, and multiple organ involvement. Table 18-4 lists the signs and symptoms reported by Vann and colleagues in 2,346 cases of DCS in recreational divers reported to the Divers Alert Network from 1998 to 2004.[13] The five most frequent signs and symptoms reported were pain (68.0%); numbness or paresthesia (63.4%); constitutional symptoms including headache, lightheadedness, fatigue, malaise, nausea, vomiting, or anorexia (40.8%); dizziness or vertigo (19.4%); and motor weakness (18.7%).[13] In an older study by Rivera of 933 military and civilian divers with DCS, the five most frequent signs or symptoms were pain (91.8%), numbness or paresthesia (21.2%), motor weakness (20.6%), rash (14.9%), and dizziness or vertigo (8.5%).[55]

Comparison of the two studies indicates that the number of DCS cases involving pain was less in the Vann series, and that the number of cases with neurological symptoms (numbness/paresthesia, dizziness/vertigo, and motor weakness) was greater. The reasons for these differences are not clear. In Rivera’s series, most of the divers were military and perhaps reported their symptoms (and were subsequently treated) earlier, thereby preventing more serious symptoms.[55] Military divers are also under stricter control regarding adherence to decompression schedules and may be more conservative than recreational divers in selecting decompression schedules. Recreational divers also tend to make more repetitive dives, which could predispose them to more serious problems.

Figure 18-6. Bubble formation in a blood vessel. (a) The lodging of a bubble at a vascular junction, with (b) sludging of the red blood cells (RBCs) and formation of protein debris, and (c) blood clot and extravascular fluid loss. Bubbles in blood vessels are typically not spherical.

A minor DCS symptom is pruritus, known as “skin bends,” which is most common in dry chamber dives. Itching may be accompanied by an urticarial rash and is usually localized in well-perfused, exposed skin such as the ears, although it can occur anywhere on the body. Skin bends is generally transient and does not require treatment, but the diver should be observed for at least an hour for the onset of more serious symptoms. A severe form of rash called “marbling” or “mottling” (cutis marmorata) appears as a pale area with cyanotic mottling. The area may enlarge, become hyperemic, and show swelling. While uncommon, cutis marmorata is often a harbinger of more severe DCS and warrants immediate treatment.

TABLE 18-4

FREQUENCY OF SIGNS AND SYMPTOMS OF DECOMPRESSION ILLNESS

Sign or Symptom

Percentage of Patients with a Given Sign or Symptom (n=2,346)

Pain

68.0

Numbness/paresthesia

63.4

Constitutional*

40.8

Dizziness/vertigo

19.4

Motor weakness

18.7

Cutaneous

9.5

Altered mental status

7.9

Decreased coordination

7.9

Dyspnea or cough

5.6

Bladder or bowel incontinence

2.8

Decreased consciousness

1.8

Lymphatic

1.8

*Constitutional symptoms included headache, lightheadedness, inappropriate fatigue, malaise, nausea, vomiting, or anorexia.

Data source: Vann RD, Butler FK, Mitchell SJ, Moon RE. Decompression illness. Lancet. 2010;377:153–164.

Lymphatic obstruction appears as painless local edea, usually on the trunk. If it is severe the skin may have a “pigskin” appearance. Unilateral breast swelling and swelling of specific muscles may occur. In these cases, recompression may help alleviate pain. Obstruction of the lymphatics usually disappears in a few days with or without treatment.

Joint pain and numbness are the most common DCS symptoms. The onset of pain may be gradual or abrupt, and its nature mild, severe, paroxysmal, aching, or boring. Severe cases may be associated with a cold sweat. Classically the pain is described as a deep, dull ache isolated to a particular joint. It is present at rest and usually not affected by movement. Occasionally, the pain can be reduced by the application of local pressure with a sphygmomanometer cuff. A painful joint will sometimes have an associated area of numbness or altered sensation that may reflect a peripheral nerve lesion, but this is difficult to diagnose.

Divers with neurological symptoms should be recompressed as soon as possible to achieve the most complete relief and to forestall the onset of more severe problems. Abdominal or thoracic pain occurring in a circumferential pattern (girdle pain) signals the onset of spinal cord DCS. The pain may disappear after a short time but be followed within an hour by severe symptoms, usually paralysis of the lower extremities.

In diving, DCS occurs in the upper extremities two to three times more often than in the lower extremities. The opposite is true for caisson workers, saturation divers, and workers in ground-based altitude exposures simulating astronaut extravehicular activity. The reason for this difference may be due to the weight-bearing stresses of gravity in the latter cases. In divers, these stresses are relieved by immersion in water, which could reduce the formation and expansion of bubbles in the legs. CNS symptoms vary with the site of the tissue insult and are similar to those found in CNS disease from other causes. There is a wide range of symptoms (see Table 18-4). As with AGE and neurological symptoms, any CNS symptom following diving is serious, and the patient should be recompressed as soon as possible for best results.

Symptoms of DCS generally appear shortly after the diver surfaces. In a series of several thousand air dives compiled by the US Navy, 42% of divers with DCS developed symptoms within the first hour after surfacing, 63% within 3 hours, 83% within 8 hours, and 98% within 24 hours.[4] Occasionally, the onset time is longer, but few symptoms appear after more than 24 hours. Even if a symptom does not occur until 24 hours or longer after diving, the patient should be presumed to have DCS until it is ruled out. Symptoms with very long onset times sometimes respond to recompression and should not simply be dismissed as not diving related.

Rarely, symptoms of DCS begin in the water during decompression, and usually only after long, deep dives. In water DCS is most likely to occur at the shallower decompression stops near the surface. The primary symptom will usually be joint pain, but more serious neurologic symptoms may develop. Treatment of in-water DCS depends on the type of diving equipment used. Detailed information on the treatment of DCS can be found later in this chapter, as well as in the US Navy Diving Manual.

Aseptic Bone Necrosis

Aseptic bone necrosis, also known as dysbaric osteonecrosis, is a delayed consequence of chronic exposure to a hyperbaric environment that may not be evident until years after exposure (Figure 18-7). The exact mechanism of this condition is unknown, but incidence appears related to the length of the diver’s career and magnitude of hyperbaric exposure.[56] Studies of commercial divers indicate the prevalence of bone necrosis is less than 5%.57,58 Lesions usually occur at the proximal ends of the humerus, femur, and tibia, adjacent to a joint or midshaft of the humerus and femur.[56] Often the lesions never cause symptoms and are identified only by radiography. No treatment is required for lesions, such as shaft lesions, that do not cause symptoms. The most serious lesions are juxta-articular. If these areas become necrotic and collapse, it may be necessary to replace the joint with a prosthesis.

Figure 18-7. A composite radiograph shows an abnormal pattern of calcification in both proximal tibias as a result of aseptic bone necrosis, a sequelae of decompression sickness.

Diving at Altitude and Altitude Exposure after Diving

There is increased danger of DCS whenever the barometric pressure is reduced soon after, or in association with, diving. Circumstances can include diving at altitude, mountain travel after diving, and flying after diving. DCS can occur independently of diving during altitude exposures above 18,000 ft (5,486 m; a barometric pressure of 0.5 ata).[42] Nitrogen dissolved in the tissues at sea level has a tension of about 0.79 atm and leaves solution to form bubbles at altitude. Flying after diving increases the risk of DCS because additional nitrogen remains in the tissues after a dive. To reduce the DCS risk from flying too soon after diving, divers are advised to wait long enough at sea level until nitrogen dissolved in their tissues is eliminated harmlessly through the lungs. Table 9-6 of the US Navy Diving Manual lists preflight surface intervals required before flying is considered safe.[4] These surface intervals range from 0 to 21 hours for a commercial flight, depending on the severity of the previous diving exposure. The US Air Force requires a 24-hour wait after any diving before flight.

Diving at altitude also increases the risk of DCS. There are two main factors. First, because the bodies of sea-level residents are in equilibrium with the 0.79 atm of nitrogen in atmospheric air, rapid ascent to an altitude of 18,000 ft (5,486 m), where the atmospheric nitrogen is only 0.4 atm, causes a supersaturation of some 0.39 atm. Supersaturated nitrogen dissipates over about 24 hours and must be accounted for before then. Dives conducted within 12 hours of initial ascent to altitude are considered repetitive dives.[4] Table 9-5 of the US Navy Diving Manual lists the repetitive group designator associated with altitudes up to 10,000 ft (3,048 m).[4]

Second, after equilibration is complete, the no-decompression times are still shorter than normal because bubbles grow larger at reduced barometric pressure than at sea level. Therefore, a dive conducted at an altitude of 5,000 ft (1,524 m) to a depth of 60 fsw (18 msw) is equivalent to an 80 fsw (24 msw) dive at sea level.[4] Table 9-4 of the US Navy Diving Manual contains equivalent sea level depths for diving at altitudes up to 10,000 ft (3,048 m).[4]

Factors Affecting Individual Susceptibility

Several factors are known or suspected to affect susceptibility to DCS, among them inadequate decompression; exercise and body temperature as they affect perfusion; and individual characteristics such as age, obesity, and dehydration.[59] The most common cause of DCS is inadequate decompression, which can result from ignorance or misapplication of the decompression schedules, panic, equipment failure, and other causes. Omitted decompression does not necessarily result in DCS, and DCS may occur even if the prescribed decompression is followed exactly. DCS has also occurred after dives that ordinarily do not require decompression stops. The severity of DCS does not correlate well with the amount of omitted decompression. Neurological DCS is more common after deeper dives than long, shallow dives.[59] Repetitive diving (more than one dive in 12–24 h) may increase the risk of DCS, presumably due to the increased total load of absorbed nitrogen and errors in computing the necessary decompression schedule.

Any physiological or environmental factor that changes local perfusion (eg, exercise, body temperature) also changes regional inert gas exchange. A change in perfusion may have a different effect on DCS risk depending on the phase of the dive in which it occurs (at pressure, during decompression, or after decompression). For example, a factor that increases perfusion while a diver is at depth will increase inert gas uptake, but this same factor will increase its elimination if present during decompression. Factors that increase peripheral perfusion include exercise, immersion, and heat, while cold and dehydration decrease perfusion. Immersion and exercise at pressure have been demonstrated to increase gas uptake and DCS risk.[59] When multiple factors exist that change during a dive, the results may be difficult to anticipate. Mild exercise during decompression appears beneficial, but DCS may be confounded by exercise at pressure. The most disadvantageous situation probably occurs during a decompression dive, wherein the diver works at pressure and rests during decompression. In this instance, work at pressure increases the perfusion and warms the diver, while rest during decompression decreases perfusion and causes vasoconstriction from cooling.

Temperature and exercise also have effects unrelated to perfusion. Inert gas solubility decreases as the temperature rises. As a diver warms on the surface after a dive, the inert gas solubility falls and the dissolved gas tension and supersaturation rise. This fact may explain the anecdotal observations that hot showers precipitate DCS.

Exercise may mechanically aggravate the formation and expansion of bubbles by reducing the local absolute pressure in tissue and thus increasing the local supersaturation, which expands existing bubbles or micronuclei and may cause new nuclei to form. Human experimental evidence indicates that exercise after decompression from diving or ascent to altitude increases DCS incidence.[60] Note the distinction between exercise during and exercise after decompression. Exercise during decompression increases the elimination of inert gas by raising perfusion, while exercise after decompression, when bubbles are already present, can initiate or accelerate bubble expansion.

Increasing age increases the risk of DCS.44,59 The age effect may be related to decreased inert gas exchange efficacy and increased formation of gas nuclei. Obesity may increase the risk of DCS, presumably because inert gas is more soluble in fatty than in aqueous tissue; however, this relationship has not been proven.[61] Similarly, there is no proven difference in DCS susceptibility between genders.13,62

Dehydration reduces perfusion and inert gas elimination. Divers with DCS are often found to have elevated hematocrit values, perhaps from dehydration but perhaps also from increased capillary permeability resulting from DCS.[13] Typical causes of dehydration in diving are alcohol consumption, low fluid intake, sweating in hot climates or diving suits, sea sickness, and cold- or immersion-induced diuresis.

Experience with caisson workers shows that the incidence of DCS is greatest during the first few days of repeated exposure to increased pressure.[63] This may result from a depletion of the gas nuclei that appear to be the origin of bubbles. Acclimatization to prevent DCS has been better proven in helium–oxygen diving than in air diving.[59]

Patent Foramen Ovale as a Risk Factor

Recently there has been much interest in the effect a PFO has on the incidence of DCS. A PFO is an atrial septal defect that results from the failure of the fetal foramen ovale to close after birth. Theoretically, venous bubbles may cross a PFO and enter the arterial circulation. However, in most persons the flow across a PFO is from left to right (high pressure to low pressure). In order for bubbles to enter the arterial circulation the shunt must be reversed. Factors thought to increase this flow are straining, lifting, coughing, or any other process that increases right atrial pressure. Immersion itself does not appear to increase right-to-left shunting across a PFO.[51]

The presence of a PFO has been shown to statistically increase the incidence of DCS with neurologic and cutaneous manifestations.[13] The estimated relative risk for serious neurologic DCS due to a PFO ranges from 2.5 to 6.6.[64] However, given that the actual risk of serious neurologic DCS is less than 0.02%, the presence of a PFO imparts a very small absolute risk.[65] Furthermore, a PFO is present in approximately 27% of healthy individuals.[66] Given the vast number of dives that are completed without incident, it seems the overall effect of a PFO is minor.

Due to its prevalence and the small absolute risk of serious neurologic DCS it carries, routine screening for a PFO among divers or diver candidates is not recommended. Divers who do experience serious neurologic DCS may warrant screening. However, it is unclear how to best manage those found to have a PFO, especially because the risks of operatively closing a PFO may outweigh the potential benefit.

PREDICTING AND PREVENTING DECOMPRESSION SICKNESS

Decompression Tables

The most important factors in reducing the risk of DCS are (a) limiting the time at depth to reduce inert gas uptake and (b) allowing for slow ascent so that inert gas may be harmlessly eliminated through the lungs. Death or permanent disability were common among divers and caisson workers in the 19th century, before this was understood. By the end of the century it was recognized that some type of slow decompression was necessary to prevent injury. Not until after the turn of the 20th century, when J.S. Haldane began studying the problem systematically in England, were decompression schedules similar to those used today constructed.[42] Haldane realized that the manner of decompression used at the time, steady decompression at rates between 1.5 and 5 fsw per minute, was too slow at deeper depths and too rapid at shallow; this rate allowed more inert gas to be absorbed at depth and did not provide enough time for inert gas to be eliminated in shallow water. He devised the now familiar staged decompression schedules, which use progressively longer stops near the surface. Modifications of the Haldane calculation methods are still the basis of many modern decompression schedules.

A decompression table contains multiple decompression schedules for a particular dive depth and bottom time. Each schedule defines the depths and duration of the decompression stops, and tables are available for diving with different inert gases and oxygen concentrations. With current procedures, DCS is a rare event. The DCS incidence when using the US Navy diving tables, which all US military diving operations are required to use, is about 0.1%.[59] The incidence of DCS during recreational diving is about 0.3%.[67] Granted, many of these dives are conducted well within decompression limits and do not represent the rate of DCS using the maximum exposure limit; the incidence of DCS using US Navy diving tables during decompression dives or the maximum no-decompression limit is about 2%.[13] See also Chapter 17, Military Diving Operations.

Probability of Decompression Sickness and Acceptable Risk

Any dive profile might be called “safe” if an individual diver completes it without DCS. But is a dive safe if DCS occurs in 1 of 10 divers, or in 1 of 100? The answer depends on the definition of safety. Many human activities would be impossible if absolute safety—the complete absence of risk—were required. Safety is based on the level of risk a person is willing to accept. Thus, safety is defined as the acceptable risk. The US Navy diving tables assume a risk determined to be acceptable for military diving operations; however, it should be understood that even if the tables are followed correctly, there is still a small risk of DCS.

TREATMENT OF DECOMPRESSION SICKNESS AND ARTERIAL GAS EMBOLISM

As previously discussed, AGE is the result of pulmonary barotrauma that leads to air entering the arterial circulation, while DCS is due to the formation of bubbles in blood and tissues after a reduction in ambient pressure. The immediate goal of therapy is to reduce the volume of the offending bubbles. This may be possible for patients treated shortly after symptom onset, but long delays before treatment are common, and gas bubbles may have caused physical or biochemical damage that persists after the bubbles themselves have resolved. In such situations, therapy to oxygenate poorly perfused tissue or reduce edema can still be beneficial.

The definitive treatment for DCS and AGE is increased atmospheric pressure and 100% oxygen. The additional pressure serves to reduce the size of the bubbles, and oxygen accelerates their resolution by causing nitrogen to diffuse from bubble to blood. On reaching the lungs, excess nitrogen from the blood is exhaled. Pressure (or recompression) was first used in 1909 to treat DCS (then called “caisson disease”), but oxygen was not routinely used during recompression until the 1960s.[35]

The best first aid for AGE or DCS is 100% oxygen delivered by mask. Inspired oxygen percentages near 100% are essential for the greatest effect. Because injured divers are often dehydrated due to illness or post-immersion diuresis, oral rehydration or administration of isotonic, non-glucose-containing intravenous fluids may be considered.[13] However, cases of AGE may be complicated by cerebral edema, and care should be given not to fluid-overload the patient.[4] The patient should be positioned on their back or side on a horizontal plane. In the past, it was advised that the patient be placed in the Trendelenburg position to prevent more gas from entering the cerebral circulation, but this is no longer recommended because the head-down position increases central venous pressure and cerebral venous pressure, and can cause cerebral edema.[68]

There are no proven adjuvant therapies. Aspirin and other platelet inhibitors are no longer recommend due to concerns about possible hemorrhage into neural tissues.[69] The only exception is the use of low-molecular-weight heparin in patients with lower extremity paralysis to prevent deep vein thrombosis. If convulsions are present, benzodiazepines may be considered. While not commonly used, intravenous lidocaine may be helpful in the treatment of AGE with serious neurological symptoms. Lidocaine has been shown to increase cerebral vasodilation and decrease the rise in intracranial arterial pressure.[70] It may also be useful in the treatment of cardiac dysrhythmias; however, no studies have been conducted concerning its use in divers.[13] If used, intravenous lidocaine should be dosed to produce an antiarrhythmic effect.[4] The use of parenteral steroids, once thought to reduce cerebral edema, has been shown to worsen outcomes in animals and is no longer recommended.4,69,71

Because there is no definitive test for DCS or AGE, a differential diagnosis is important to rule out other conditions that can have similar signs and symptoms (eg, stroke, myocardial infarction, or musculoskeletal injury). One of the first questions the medical officer should ask is whether the patient has a recent history of diving or altitude exposure. Signs or symptoms with onsets later than 48 hours after diving or altitude exposure are probably unrelated to decompression.

Therapy According to US Navy Treatment Tables

The standard US Navy therapy for DCS or AGE is recompression to 60 fsw (2.8 ata, 18 msw) while the patient is breathing 100% oxygen. Typically, the course of treatment is determined by the initial signs/symptoms and the response to treatment. US Navy Treatment Table 5 (Figure 18-8) may be used if:

- the only symptoms are joint or limb pain, itching, rash (except cutis marmorata), or local swelling;

- the absence of neurological findings is verified by physical examination; and

- the symptoms are completely relieved within 10 minutes of oxygen breathing at 60 fsw.

Treatment Table 5 requires 135 minutes to administer, with two oxygen periods at 60 fsw and one oxygen period at 30 fsw (1.9 ata, 9 msw). The oxygen periods are 20 minutes long, followed by 5 minutes of air breathing to reduce the risk of CNS oxygen toxicity. Ascent from 60 to 30 fsw and 30 fsw to surface occurs at 1 fsw per minute.

US Navy Treatment Table 6 (Figure 18-9) is used if:

- a neurological exam has not been conducted;

- Treatment Table 5 fails to provide complete resolution of symptoms within 10 minutes; or

- any neurological or cardiopulmonary signs or symptoms are present.

Treatment Table 6 requires 285 minutes to administer, including three 25-minute cycles at 60 fsw and two 75-minute cycles (60 min oxygen, 15 min air) at 30 fsw. Treatment Table 6 can be extended by up to two cycles at 60 fsw and two cycles at 30 fsw.

Figure 18-8. The US Navy Treatment Table 5 depth/time profile can be used only if the diving casualty has no neurological symptoms and if all symptoms are relieved within 10 minutes at 60 fsw. Consult the US Navy Diving Manual before using this or other treatment tables.
Reprinted from: US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011: 20-40. NAVSEA 0994-LP-100-3199.

Figure 18-9. In the US Navy Treatment Table 6 depth/time profile, three 25-minute oxygen cycles at 60 fsw, and two 75-minute cycles (60 min oxygen, 15 min air) at 30 fsw, are standard. Treatment Table 6 can be extended by up to two cycles at 60 fsw and two cycles at 30 fsw. The decompression requirements of inside attendants must also be considered so that they do not themselves develop decompression sickness. Consult the US Navy Diving Manual before using this or other treatment tables. Reprinted from: US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011: 20-41. NAVSEA 0994-LP-100-3199.

For patients whose symptoms worsen or do not improve after 20 minutes of breathing 100% oxygen at 60 fsw, especially if the dive profile supports a depth greater than 60 fsw, the option is available for further compression to a depth of relief not to exceed 165 fsw (6 ata, 50 msw). Compression to 165 fsw is described in Treatment Table 6A (Figure 18-10). Due to the increased risk of CNS oxygen toxicity, treatment with this table requires switching from 100% oxygen to air or a mixture of 40% to 50% oxygen in nitrogen-helium. A high-oxygen mixture is preferable because it reduces nitrogen narcosis and limits the uptake of additional nitrogen. If symptoms completely resolve within 30 minutes at the depth of relief (not to exceed 165 fsw), the patient can be decompressed at 3 fsw per minute to 60 fsw. From there, the procedures for Treatment Table 6 should be followed.

If relief at depth (not to exceed 165 fsw) is unsatisfactory after 30 minutes, the time at that depth can be extended to 120 minutes, after which decompression is accomplished using US Navy Treatment Table 4 (Figure 18-11).

Patients with residual symptoms, or those who cannot tolerate further oxygen due to pulmonary toxicity, may be given repetitive treatments on subsequent days. (Mild pulmonary toxicity is reversible within hours to a day.) Typically, one to six additional treatments are given, which may be according to Treatment Tables 5, 6, or 9, or sometimes at 30 fsw for 60 to 90 minutes. The rule of thumb is that repetitive treatments should be discontinued when no clinical improvement is observed after two successive treatments.

Decompression Sickness in Saturation Diving

DCS that occurs during or after the slow decompression from saturation dives usually manifests as mild knee or leg pain. Neurological symptoms are rare. The onset of DCS is subtle and may begin with aching or a feeling in the anterior thighs similar to that after hard exercise. This is treated by recompression and administration of high oxygen partial pressures. For occurrences under pressure, oxygen partial pressures of 1.5 to 2.8 ata in helium-oxygen are administered, with a cycle of 25 minutes of high partial pressure oxygen (1.5–2.8 ata) and 5 minutes of low partial pressure oxygen (0.3–0.5 ata).

Recompression during a saturation dive occurs in 5-fsw stages until attaining the depth of relief, at which the diver is treated with oxygen at 1.5 to 2.8 ata for at least 2 hours. After treatment, the diver is maintained at that depth for an additional 2 to 12 hours, depending on the severity of the initial symptoms and the response to recompression therapy. The standard saturation decompression schedule is then resumed. For DCS that occurs after reaching the surface and breathing air, a diver may be treated according to Treatment Table 6.

Figure 18-10. In the US Navy Treatment Table 6A depth/time profile, as long as 20 minutes may be spent at 60 fsw before making the decision to compress to a depth of relief not greater than 165 fsw. The advantage of compression to 165 fsw over 60 fsw is greater reduction in bubble volume. At 165 fsw, high-oxygen treatment gas may be utilized to reduce nitrogen uptake. Consult the US Navy Diving Manual before using this or other treatment tables.
Reprinted from: US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011: 20-42. NAVSEA 0994-LP-100-3199.

Figure 18-11. In the US Navy Treatment Table 4 depth/time profile, time at 165 fsw is from 30 minutes to 2 hours. At 165 fsw, high-oxygen treatment gas may be breathed to reduce oxygen uptake. Upon reaching 60 fsw, the diver begins breathing 100% oxygen in cycles of 25 minutes interrupted by 5 minutes of air breathing. Consult the US Navy Diving Manual before using this or other treatment tables.
Reprinted from: US Department of the Navy. US Navy Diving Manual. Rev 6. Washington, DC: Naval Sea Systems Command; 2011: 20-43. NAVSEA 0994-LP-100-3199.

DCS that occurs 60 minutes or more after an ascending excursion can be treated as described above, but DCS that occurs within 60 minutes of ascent from an excursion dive deeper than the saturation depth should be considered serious, even if pain is the only symptom. Neurological symptoms, particularly those related to the inner ear, are not uncommon after rapid ascent from excursions. Recompression to at least the excursion depth should be immediate, and high oxygen partial pressures should be administered for at least 2 hours as described above, after which the patient should be maintained at depth for 12 hours before resumption of standard saturation decompression.

BREATH-HOLD DIVING

Breath-hold diving, or free diving, requires little equipment and provides examples of the many physical and physiological constraints of the underwater environment. Free diving is the oldest form of diving and has long been performed by various cultures around the world for food gathering and the procurement of tradable goods. In modern times, the activity has become popular as a sport, either for competition or recreational spearfishing. Militaries have used free diving as a tactical option since the dawn of naval warfare. It was an essential operational technique in the Pacific during World War II and remains a fundamental skill for present-day combat swimmers.

When a free diver enters the water, he or she encounters several environmental challenges starting with the diving reflex in response to submersion. On descent, ambient pressure increases, which has the strongest effect on enclosed gas spaces within the body (lungs, sinuses). Additionally, the diver must contend with a limited supply of oxygen. Additional challenges occur with ascent, which is when divers most commonly lose consciousness in “shallow water blackout.”

Diving Reflex

The diving reflex, or diving response, is a series of physiologic manifestations found in many animals that promotes the conservation of oxygen and the preservation of life while breath-holding and submersed in water. Primarily, they include bradycardia, decreased cardiac output, increased blood pressure, and peripheral vasoconstriction.

Long considered a vagally mediated process to conserve oxygen and redirect blood flow to the critical organs of the heart and brain, some of these effects, particularly bradycardia, can also be elicited by apnea with face submersion or facial exposure to cold.72,73 Additionally, it appears that the increased ambient pressure of depth plays a role in producing a more robust response.[74] Increased vagal tone has been considered a cause of cardiac arrhythmias associated with breath-hold diving.

Transient splenic contraction, known to occur in diving animals, has also been documented in humans, and contributes to an increase in hematocrit. While this response may prolong the tolerance of the apneic period, it does not appear to be a learned skill as is tolerance to hypoxia and hypercapnea.[75]

Compression of Descent

A free diver must anticipate and compensate for the compression of gas-containing spaces in the body that occurs during descent according to Boyle’s law: the volume of a given mass of gas varies inversely with absolute pressure when temperature is held constant. The middle ear requires active inflation to avoid barotrauma (ear squeeze), which is the most common medical problem in diving, but the lungs are also affected, sometimes fatally, in breath-hold diving.

Figure 18-12 represents a breath-hold diver with a total lung capacity of 6 L and a residual lung volume of 1.5 L. If this diver performed a maximal inhalation on the surface (1 ata) and descended for a free dive, Boyle’s law predicts that the lung volume would decrease to 3 L at 33 fsw (10 msw; 2 ata) and 2 L at 66 fsw (20 msw; 3 ata). On reaching 99 fsw (30 msw; 4 ata), the lung volume equals the 1.5 L residual volume. With greater descent, the elasticity of the chest wall resists further reduction in volume and the alveolar pressure becomes less than the absolute pressure, which is transmitted equally throughout all solid and liquid tissues in accordance with Pascal’s law: pressure exerted at any point on a confined liquid is transmitted uniformly in all directions. This phenomenon causes a relative vacuum between alveolar gas and alveolar capillary blood and leads to engorgement of the alveolar capillaries as blood shifts from peripheral tissues into the thorax. Further descent is possible because these fluid shifts reduce the residual volume.

Consider the example of fluid shift for a diver with a 7.22-L total lung capacity and a 1.88-L residual volume who achieves a depth of 346 fsw (105 msw).[76] By Boyle’s law, the ratio of these volumes specifies 93 fsw (28 msw) as the depth at which the lungs are compressed to residual volume. To reach 346 fsw, the residual volume would have to be reduced to 0.63 L, representing a 1.25-L shift of blood from peripheral vessels to pulmonary capillaries. The fluid shift effect is illustrated by record free dives to depths in excess of 660 fsw (200 msw). The current world record for no-limits free diving, which uses a weighted sled for descent and an inflatable lift bag for ascent, was 702 fsw (214 msw), accomplished by Herbert Nitsch in 2007.[77] There is indirect evidence that such blood shifts do occur, but reductions in residual volume may also result from elastic compression of the chest wall and upward shift of the abdominal contents and the diaphragm.[78]

Figure 18-12. Compression of the lungs during descent on a breath-hold dive. The diver, with a residual lung volume (RV) of 1.5 L (white center of circles), begins on the surface with a 4.5-L vital capacity inhalation (black circles) to a total lung capacity (TLC) of 6 L. During descent, the lung volume (LV) decreases in inverse proportion to the absolute pressure, as described by Boyle’s law. At 4 ata (30 msw; 99 fsw), the lung volume equals the residual volume. With additional descent, the elasticity of the thorax impedes further compression, leading to a relative vacuum in the lungs. Blood from the peripheral circulation shifts into the pulmonary capillaries (gray circles), which then reduces the residual lung volume (white centers) and allows further descent to 40 and 50 msw (132 and 165 fsw).

Descent to too great a depth causes compression of the thorax beyond its elastic limit, and the resulting chest pain signals the diver to ascend. Failure or inability to heed this warning pain could cause lung squeeze, or thoracic squeeze, in which chest wall compression, intraalveolar vacuum, or both, damage the thorax and lungs. Thoracic squeeze is rare because the chest pain is a strong signal for the diver to ascend.

In an effort to further push physiological limits, free divers have developed a technique called “lung packing” or glossopharyngeal insufflation. The practice employs the use of the oral and pharyngeal muscles to compress and force air into the lungs, thereby increasing the amount of available oxygen and overall gas volume. This process creates high transpulmonary pressures and mimics the conditions of pulmonary arterial hypertension.[79] Such practices could cause pulmonary barotrauma leading to hemoptysis[80] and increasing the risk for AGE.[81]

Hypoxia and Hypercapnia

There is an inherent risk of unconsciousness during diving or breath-hold swimming if time underwater is prolonged inadvertently, by hyperventilation, or by will power. This has been a causative factor in many cases of unconsciousness or drowning.[76] Hypercapnia and hypoxia are the principal causes of the ventilatory drive that causes dyspnea. In severe hypoxia, euphoria often precedes unconsciousness, and hypoxic seizures are not uncommon. In the early 1960s, Edward H. Lanphier, MD, and Hermann Rahn, PhD, conducted experiments in a hyperbaric chamber to demonstrate the changes that occur to gases in the lungs during breath-hold and breath-hold diving. This experiment demonstrated the progressive rise in end-tidal carbon dioxide partial pressure and the fall in oxygen partial pressure during a breath-hold experiment at sea level.[82] Gases were sampled from a bag into which the subject exhaled (and re-inhaled) every 10 seconds. Hypoxic and hypercapnic ventilatory drive caused a break in breath-hold at 60 seconds at well above the 20 to 30 mm Hg (0.04 atm) alveolar oxygen partial pressure at which there is a risk of unconsciousness.

In another experiment,[83] a subject made a breath-hold dive to 33 fsw (10 msw). The end-tidal oxygen and carbon dioxide partial pressures increased during descent, as described by Dalton’s law of partial pressures: the total pressure exerted by a mixture of gases is equal to the sum of the pressures that each gas would exert if it alone occupied the container. While at depth, the oxygen partial pressure decreased owing to the subject’s metabolism, but it remained above the 50 to 60 mm Hg level at which the hypoxic ventilatory drive begins. Carbon dioxide was actually diffused from the lungs into the blood because of its higher alveolar partial pressure. Hypercapnic ventilatory drive forced the subject to ascend after 40 seconds at 33 fsw (10 msw), and the oxygen and carbon dioxide partial pressures decreased, again due to Dalton’s law.

In yet another experiment,[83] the subject dived to 33 fsw (10 msw) after hyperventilating to eliminate carbon dioxide and delay the onset of the hypercapnic ventilatory drive. This extended his dive time by 20 seconds, during which oxygen metabolism continued but without inducing hypoxic ventilatory drive. When hypercapnia finally caused the diver to ascend, his oxygen partial pressure fell to below 40 mm Hg, and he exhibited cyanosis, confusion, and loss of control. This is the most common scenario leading to shallow water blackout and subsequent drowning if the diver is not rescued in time.

Decompression Sickness of Free Diving

Free diving is not generally considered to put divers at risk for DCS due to the relatively short time spent at depth; however, several cases of DCS have been reported after free diving.[84] The most common associated risk factors include a high number of dives with short surface intervals. The assumption is that insufficient time is allowed during the surface interval to off-gas the nitrogen load that was accumulated during a single breath-hold dive. If this is multiplied over hours of free diving, a significant decompression obligation may occur that is not met, which could result in DCS.

Even more remote, but shown in case studies, is the occurrence of DCS after single breath-hold dives. These are more likely to be dives to extreme depths, not those performed by spear fishers or recreational free divers. Some modeling of the risk shows that it is negligible shallower than 300 fsw.[85]

SUMMARY

Since the earliest days of breath-hold diving, the underwater environment has posed unique risks due to the physiological effects of changes in pressure on the human body. The introduction of compressed air and artificial gas mixtures have extended diving range and duration but also created problems related to inert-gas effects and rapid ascent to the surface. A series of gas laws represented by simple equations describe the physical effects of pressure and temperature on gas volume and constituent partial pressures. Pressure change creates the potential for barotrauma in closed or functionally trapped gas pockets including the face mask, middle ear, inner ear, sinuses, and lungs, all of which are subject to problems on descent (compression or “squeeze”) and ascent (expansion and possible rupture). Inhalation of compressed air or artificial gas mixtures at increased pressure readily leads to problems with oxygen toxicity, excess carbon dioxide, carbon monoxide poisoning, and narcosis due to nitrogen and other inert gases. At extreme depth, pressure itself produces effects collectively described as HPNS.

Early work with compressed air produced syndromes (called “caisson disease” or “the bends”) that were eventually recognized as the result of relatively rapid decompression. Ascent to the surface reduces ambient partial pressure of nitrogen or other inert gases, resulting in the formation of bubbles in blood and tissues, which can cause clinical problems ranging from cutaneous mottling to joint pain and neurological dysfunction. In addition, leakage of expanding gas from the pulmonary system into the arterial circulation (AGE) can lead to circulatory collapse, severe cerebral damage, and death.

Fortunately, these problems can be avoided by correct use of diving equipment and implementation of staged decompression to allow gradual desaturation of tissues without excessive bubble formation. Treatment of decompression problems requires return to pressure in a hyperbaric chamber to shrink existing bubbles, followed by gradual decompression combined with inhalation of 100% oxygen to accelerate the elimination of inert gases from the body. All military physicians should be aware of the pathophysiology, prevention, and treatment of diving-related disorders.

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41.   Lafay V, Barthelemy P, Comet B, Frances Y, Jammes Y. EDB changes during the experimental human dive HYDRA 10 (71 atm/7,200 kPa). Undersea Hyperb Med. 1995;22:51–60.

42.   Vann RD. Inert gas exchange and bubbles. In: Bove AA, ed. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Saunders; 2004: 431–459.

43.   Bert P. Barometric Pressure. Hitchcock MA, Hitchcock FA, trans. Columbus, OH: College Book Co, 1943: 709–754, 859–890. Originally published in 1878.

44.   Dunford RG, Vann RD, Gerth WA, et al. The incidence of venous gas emboli in recreational diving. Undersea Hyperb Med. 2002;29:247–259.

45.   Zheng Q, Durben DJ, Wolf GH, Angell CA. Liquids at large negative pressures: water at the homogenous nucleation limit. Science. 1991;254:829–832.

46.   Hemmingsen EA. Nucleation of bubbles in vitro and in vivo. In: Brubakk AO, Kanwisher J, Sundnes F, eds. Diving in Animals and Man. Trondheim, Norway: Tapir Publishers; 1986: 131–164.

47.   Unsworth A, Dowson P, Wright V. “Cracking joints.” A bioengineering study of cavitation in the metacarpophalangeal joint. Ann Rheum Dis. 1971;30:348–357.

48.   Zwirewich CV, Müller NL, Abboud RT, Lepawsky M. Noncardiogenic pulmonary edema caused by decompression sickness: rapid resolution following hyperbaric therapy. Radiology. 1987;163:81–82.

49.   Vik A, Brubakk AO, Hennessy TR, Jenssen BM, Ekker M, Slordahl SA. Venous air embolism in swine: transport of gas bubbles through the pulmonary circulation. J Appl Physiol. 1990;69:237–244.

50.   Bosco G, Yang ZJ, Savini F, et al. Environmental stress on diving-induced platelet activation. Undersea Hyperb Med. 2001;28:207–211.

51.   Francis TJ, Mitchell SJ. Pathophysiology of decompression sickness. In: Bove AA, ed. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Saunders, 2004: 154–183.

52.   Pekna M, Ersson A. Complement response to decompression. Undersea Hyperb Med. 1996;23:31–34.

53.   Boussuges A, Blanc P, Molenat F, Bergmann E, Sainty JM. Haemoconcentration in neurological decompression illness. Int J Sports Med. 1996;17:351–355.

54.   Brouns R, De Deyn PP. The complexity of neurobiological processes in acute ischemic stroke. Clin Neurol Neurosurg. 2009;111:483–495.

55.   Rivera JC. Decompression sickness among divers: an analysis of 935 cases. Mil Med. 1964;129(4):314–334.

56.   Walder DN, Elliott DH. Aseptic necrosis of bone. In: Bove AA, ed. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Saunders, 2004: 421–430.

57.   Edmonds C, Lowry C, Pennefeather J. Diving and Subaquatic Medicine. 3rd ed. Oxford, England: Butterworth-Heinnemann; 1992: 199.

58.   MRC Decompression Sickness Central Registry and Radiological Panel. Aseptic bone necrosis in commercial divers. Lancet. 1981;318:384–388.

59.   Vann RD. Mechanisms and risks of decompression. In: Bove AA, ed. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Saunders, 2004: 127–164.

60.   Van der Aue OE, Kellar RJ, Brinton ES. The Effect of Exercise During Decompression From Increased Barometric Pressures on the Incidence of Decompression Sickness in Man. Washington, DC: US Navy Experimental Diving Unit; 1949: 8–49.

61.   Carturan D, Boussuges A, Burnet H, et al. Circulating venous bubbles in recreational diving: relationships with age, weight, maximal oxygen update and body fat percentage. Int J Sports Med. 1999;20:410–414.

62.   Webb JT, Kannan N, Pilmanis AA. Gender not a factor for altitude decompression sickness risk. Aviat Space Environ Med. 2003;74:2–10.

63.   Walder DN. Adaptation to decompression sickness in caisson work. In: Proceedings of the Third International Biometerology Congress. Pergamon Press, Oxford, England; 1968: 350–359.

64.   Torti SR, Billinger M, Schwerzmann M, et al. Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale. Eur Heart J. 2004;25:1014–1020.

65.   Bove AA. Risk of decompression sickness with patent foramen ovale. Undersea Hyperb Med. 1998;25:175–178.

66.   Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc. 1984;59:17–20.

67.   Pollock NW. Annual Diving Report. 2008 ed. Durham, NC: Divers Alert Network; 2008.

68.   Moon RE, Sheffield PJ. Guidelines for treatment of decompression illness. Aviat Space Environ Med. 1997;68:234–243.

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71.   Dromsky DM, Weathersby PK, Fahlman A. Prophylactic high dose methylprednisolone fails to treat severe decompression sickness in swine. Aviat Space Environ Med. 2003;74:21–28.

72.   Schuitema K, Holm B. The role of different facial areas in eliciting human diving bradycardia. Acta Physiol Scand. 1988;132:119–120.

73.   Whayne TF, Killip T 3rd. Simulated diving in man: comparison of facial stimuli and response in arrhythmia. J Appl Physiol. 1967;22(4):800–807.

74.   Marabotti C, Scalzini A, Cialoni D, Passera M, L’Abbate A, Bedini R. Cardiac changes induced by immersion and breath-hold diving in humans. J Appl Physiol. 2009;106:293–297.

75.   Engan H, Richardson MX, Lodin-Sundström A, van Beekvelt M, Schagatay E. Effects of two weeks of daily apnea training on diving response, spleen contraction, and erythropoiesis in novel subjects. Scand J Med Sci Sports. 2013;23(3):340–348.

76.   Lin Y-C, Hong SK. Hyperbaria: breath-hold diving. In: Fregley MJ, Batteis CM, eds. Handbook of Physiology. New York, NY: Oxford University Press, American Physiology Society; 1996: 979–995.

77.   International Association for the Development of Apnea. World records. AIDA website. https://www.aidainternational.org/WorldRecords. Accessed April 7, 2017.

78.   Ferretti G. Extreme human breath-hold diving. Eur J Appl Phys. 2001;84:254–271.

79.   Eichinger M, Walterspacher S, Scholz T, et al. Glossopharyngeal insufflation and pulmonary hemodynamics in elite breath hold divers. Med Sci Sports Exerc. 2010;42(9):1688–1695.

80.   Kalemoglu M, Keskin O. Hemoptysis and breath-hold diving. Mil Med. 2006;171(7):606–607.

81.   Liner MH, Andersson JPA. Suspected arterial gas embolism after glossopharyngeal insufflation in a breath-hold diver. Aviat Space Environ Med. 2010;81(1):74–76.

82.   Lanphier EH, Rahn H. Alveolar gas exchange during breath-hold diving. J Appl Physiol. 1963;18:471–477.

83.   Lanphier EH, Rahn H. Alveolar gas exchange during breath holding with air. J Appl Physiol. 1963;18:478–482.

84.   Lemaitre F, Fahlman A, Gardette B, Kohshi K. Decompression sickness in breath-hold divers: a review. J Sports Sci. 2009;27(14):1519–1534.

85.   Fitz-Clarke JR. Risk of decompression sickness in extreme human breath-hold diving. Undersea Hyperb Med. 2009;36(2):83–91.

Chapter 19

UNDERSEA MEDICINE

GRACE LANDERS, MD* AND JAMES CAVINESS, MD, MS†

INTRODUCTION

UNDERSEA OPERATIONS

ILLNESS OR INJURY KNOWN TO RESULT FROM DIVING

PHYSICAL PROPERTIES

Pressure

Oxygen Toxicity

Nitrogen Narcosis

Visibility

Sound

Temperature

Contaminated Diving

PROBLEMS WITH UNDERWATER BREATHING EQUIPMENT

Hypoxia

Hypercapnia

Dyspnea

UNDERWATER HAZARDS

Marine Life

Sound Navigation and Ranging

SUBMARINES

Submarine Types and Classes

The Submarine Environment

Monitoring the Submarine Atmosphere

Disabled Submarines

The Working Schedule and Sleep

SUMMARY

* Lieutenant, Medical Corps, US Navy; Naval Medical Center Portsmouth; Resident, Emergency Medicine, 620 John Paul Jones Circle, Portsmouth, Virginia 23708

† Occupational Medicine Physician, Branch Health Clinic China Lake, Department of Occupational Health, 1 Administration Circle, Building 1403, China Lake, California 93555

INTRODUCTION

Humans have explored the sea for as long as recorded history. President Kennedy remarked:

I really don’t know why it is that all of us are so committed to the sea, except I think it’s because in addition to the fact that the sea changes, and the light changes, and ships change, it’s because we all came from the sea. And it is an interesting biological fact that all of us have, in our veins the exact same percentage of salt in our blood that exists in the ocean, and therefore, we have salt in our blood, in our sweat, in our tears. We are tied to the ocean. And when we go back to the sea—whether it is to sail or to watch it—we are going back from whence we came.[1]

Though humans have always felt a connection to the world’s seas and oceans, these water bodies can be deadly. Surface water temperatures in most regions of the world can cause hypothermia and death for unprotected or overexposed individuals. Waves at sea create hazardous conditions for maneuvering personnel and supplies, and numerous forms of marine life can inflict severe or fatal injuries. There is no air, and in very few places is there any significant warmth. Humans have little physical aptitude for survival on or in the water, and under-the-surface survival depends completely on technology. Although advances in technology make underwater operations possible, they also expose other limits, such as the human body’s vulnerability to depth pressure.

This chapter focuses on the occupational health aspects of undersea operations. Undersea medicine encompasses an understanding of the underwater environment, a familiarity with the ship and diving systems that allow survival in such an environment, a thorough knowledge of the duties and workplace hazards present in undersea settings, and an understanding of the physiological and medical issues unique to undersea operations. As a result of increased joint operations, the remote locations of many military operations, and the military’s role in humanitarian and recovery operations that include underwater salvage and repair, it is essential that military physicians be familiar with undersea medicine.

This chapter reviews the physical properties of diving to foster an understanding of physiological consequences with respect to undersea medicine. Additionally, it examines environmental hazards that threaten the health or mission success of undersea operations and discusses unique aspects and considerations of the submarine environment. This chapter is neither a complete guide to the treatment of diving casualties nor a complete overview of diving medicine. Readers are directed to companion chapters in the Textbooks of Military Medicine series; the US Navy Diving Manual, Revision 6; and references such as Bennett and Elliott’s Physiology and Medicine of Diving, or Bove and Davis’ Diving Medicine.2–4

UNDERSEA OPERATIONS

Occupational health aspects of undersea operations are numerous and varied. The environment, the nature of the mission, the equipment, and the physiological conditions of personnel are all factors. Whereas commercial industries, such as those involved in oil and gas exploration, conduct diving and undersea operations, military undersea operations have unique constraints. Operating with stealth, under time limits, and in remote and possibly contaminated locations or under the threat of enemy fire are inherent conditions to military operations. The key to safety in these conditions is to understand and prepare for the environment and its dangers.

Onboard each US Navy submarine, including fast attack and ballistic submarines, selected crew are trained as divers and can conduct security swims of the submarine perimeter or perform limited ship management. Navy divers conduct thousands of dives annually to perform limited ship management. The Navy also has underwater construction teams; mobile diving and salvage units; explosive ordinance disposal units; and sea, air, and land units with divers. Figure 19-1 shows US Navy divers participating in a salvage operation to recover nine missing crewmen and personal items following the submarine USS Greeneville’s (SSN-772) collision with and subsequent sinking of the Ehime Maru. Figure 19-2 shows divers being lowered to the Ehime Maru wreck site.

While it may seem obvious that the majority of undersea operations are conducted by the Navy, all military branches have divers. The US Marine Corps trains combatant divers as members of elite reconnaissance units to reconnoiter and infiltrate coastal areas in advance of amphibious landings. In addition to Special Forces personnel who complete the combat diver qualification course, the US Army has four light and two heavy dive teams. Light dive teams are highly mobile and can perform both scuba (self-contained underwater breathing apparatus) and surface-supplied diving. Heavy dive teams also conduct scuba and surface-supplied diving but mainly in support of commanders controlling harbors, ports, and coastal areas. Both light and heavy dive teams provide support for the Army Corps of Engineers. The US Air Force’s special tactics elite ground combat force, comprised of combat controllers, pararescue, and combat weather personnel, are dive trained. Whether part of special tactics or in the conduct of their own occupational specialty, each service may be required to participate in dive operations.

Figure 19-1. November 2001. US Navy divers swim along the Ehime Maru wreck site in Honolulu, Hawaii, to salvage personal effects and remains from the vessel off Honolulu International Airport’s reef runway.
US Navy photo by Chief Petty Officer Andrew McKaskle.
Reproduced from: http://www.cpf.navy.mil/subsite/ehimemaru/images/011105shipsside-high.jpg.

Figure 19-2. Two divers from Mobile Diving and Salvage Unit One and a Japanese diver in MK 21 dive suits are lowered to the Ehime Maru wreck site.
US Navy photo by Chief Petty Officer Andrew McKaskle.
Reproduced from: http://www.cpf.navy.mil/subsite/ehimemaru/images/011105diveplatform-high.jpg.

ILLNESS OR INJURY KNOWN TO RESULT FROM DIVING

While diving is inherently dangerous, and the environment is deadly if equipment such as underwater breathing apparatus fails, there is very little documented evidence of occupational illness or injury from diving when correct safety and decompression procedures are followed. A number of small studies, case reports, and case series suggest there may be potential neurologic, pulmonary, and neuro-psychiatric changes associated with diving, mainly in those who have suffered decompression sickness (DCS).[5]

The only well-documented diving occupational injury or illness that occurs even when current safety procedures and decompression schedules are followed is dysbaric osteonecrosis. Dysbaric osteonecrosis is a condition in which necrotic lesions develop in the hip, shoulder, or long bones, and arise after an ischemic insult to the bone’s vascular supply. Widely accepted as a rare but serious complication of deep diving, the exact mechanism by which it occurs remains elusive. It is more common in saturation diving and is prevalent across the world in caisson workers, but it can occur without extreme depth exposures.6,7 Lesions that are juxta-articular effectively end a diver’s career.[8] Dysbaric osteonecrosis rates are very low in military divers and almost nonexistent in the submarine force, most likely due to high fitness levels and attention to diving. A recent German study of military divers found they had the same rate of dysbaric osteonecrosis as matched nondivers.[9]

Many divers and medical experts feel diving results in hearing loss, while others feel any hearing loss seen in divers is a result of barotraumas such as squeezes, and late or forceful Valsalva maneuvers. The diving instruction courses at the Naval Diving and Salvage Training Center in Panama City, Florida, have long taught the most common injury to Navy divers is the middle ear squeeze. This fact is reiterated in several review articles,10–12 and a recent study of over 700 experienced divers from the United States and Australia found 52% of divers had middle ear barotraumas, making it the most common dive-related injury.[13] A comparison of Navy divers and sea, air, and land team personnel’s hearing thresholds to data from the Navy’s hearing conservation program revealed sea, air, and land units were at significantly greater risk of hearing threshold loss greater than 40 dB for frequencies above 4000 Hz, meaning that sea, air, and land unit personnel are at a higher risk for hearing loss at this frequency versus Navy divers. For Navy divers, there was no increased risk compared to those in the hearing conservation program.[14] Although diver hearing loss is likely multi-factorial, the high incidence of ear barotraumas among divers places them at risk for hearing loss.

PHYSICAL PROPERTIES

Pressure

On land and at sea level, the pressure surrounding human bodies is that of the atmosphere, namely one atmosphere of pressure, or 1 atmosphere absolute (ata). Humans have evolved to breathe at 1 ata, and can only draw breath underwater via a snorkel to a depth of approximately 4 ft. To descend deeper than 4 ft requires compressed air. The military uses a variety of diving dress that delivers compressed air to the diver; however, delivering compressed air to the diver creates problems.

In the ocean, every 33 ft of depth adds the equivalent pressure of the entire atmosphere. Boyle’s law states for a gas at a given temperature, P_1V_1=P_2V_2. For example, if a diver starts at sea level, where P_1=1 ata, and then dives to a depth of 33 ft, P_2 now equals 2 ata. Therefore, the new volume, V_2, will be half the volume of V_1. As a result, as the diver moves below the surface, air in the lungs, middle ear, and sinuses is compressed by the increasing pressure, creating a vacuum in these body spaces. Additional air is needed to fill the vacuum, and if none is available, the body’s capillaries will rupture or leak, replacing the lost volume of air with blood. The essential mechanism behind dive-related barotraumas is compressed air within gas-filled, rigid, walled spaces of the body with a vascular supply. Dive-related barotraumas are called “squeezes.” While the middle ear is the most common site for barotraumas, sinuses, teeth, and lungs (in breath-hold dives deep enough to compress the lung below reserve volume), as well as the artificial spaces between the dive mask and face, and wetsuit and skin, are also common squeeze locations.

When ascending, the reverse effect occurs. Divers have breathed a gas supply under pressure. If they were to hold their breath and ascend, Boyle’s law dictates that on ascent, pressure falls and, conversely, volume increases. The pressurized air in the sinuses, teeth, middle ears, and lungs expands. Anything that prevents expanding gas from exiting will result in barotraumas of ascent, known as a “reverse squeeze.” The most feared type of reverse squeeze is pulmonary overinflation syndrome. The alveolar membranes can rupture under a pressure differential of 70 mm Hg, or roughly 4 ft. Pressurized air expanding in divers holding their breath will rupture through the alveoli into the chest or surrounding vasculature, resulting in pneumothorax, mediastinal air, or arterial gas embolism. In operations involving explosives or underwater photography, individuals sometimes hold their breath as they concentrate to perform a delicate action. If the diver is near the surface when a wave passes, the result could be pulmonary overinflation syndrome.

Henry’s law states the solubility of a gas in a liquid is directly proportional to the partial pressure of the gas over the liquid. Dalton’s law of partial pressure states the partial pressure of a gas is equal to its percent concentration in a gas mixture, multiplied by the total pressure of the gas mixture. In diving, the partial pressure of gas increases as the pressure increases when diving deeper into the water. For example, at sea level, at 1 ata and 21% oxygen, the partial pressure of oxygen is 0.21 ata. At 33 ft underwater and 2 ata, oxygen remains at 21% (assuming the diver is breathing simple compressed air), but the partial pressure of oxygen now doubles to 0.42 ata. Following the characteristics of Henry’s law, the amount of oxygen dissolved into the human body (where the main solvent is water) will also increase. The increased solubility of gasses, resulting in greater tissue concentration, is the direct cause of two major dive complications, gas toxicity and DCS.

Oxygen Toxicity

The exact mechanism by which oxygen causes toxicity is not completely understood, but symptoms are well described and are recalled utilizing the mnemonic VENTID-C. There is no order to the development of oxygen toxicity symptoms; convulsions may be the first and only sign.

- V: Visual symptoms. Tunnel vision, a decrease in the diver’s peripheral vision, and other symptoms such as blurred vision may occur.

- E: Ear symptoms. Tinnitus, any sound perceived by the ears but not resulting from an external stimulus, may occur. The sound may resemble ringing bells, roaring, or a machinery-like pulsing.

- N: Nausea or spasmodic vomiting. These symptoms may be intermittent.

- T: Twitching and tingling symptoms. Any of the small facial muscles, lips, or muscles of the extremities may be affected. These are the most frequent and clearest symptoms.

- I: Irritability. Any change in the diver’s mental status including confusion, agitation, and anxiety should be noted.

- D: Dizziness. Symptoms include clumsiness, incoordination, and unusual fatigue.

- C: Convulsions. It warrants repeating that the first sign of central nervous system oxygen toxicity may be a convulsion.

Nitrogen Narcosis

Nitrogen narcosis is another poorly understood phenomenon wherein nitrogen above a certain partial pressure exerts an anesthetic-like effect on brain neurons. Effects are generally seen near a depth of 100 feet of seawater (fsw) and worsen with increasing depth. Individuals vary in their susceptibility, and experienced divers are able to adapt somewhat to the effect. Narcosis is so potent that individuals have been known to become euphoric and irrational to the point of removing their dive gear, including the regulator and air supply. Because of the severe effect in deeper dives, the Navy limits diving to 150 ft if breathing compressed air. Signs and symptoms of nitrogen narcosis include loss of judgment or skill, a false feeling of well-being, lack of concern for job or safety, lack of common sense, inappropriate laughter, and tingling and vague numbness of the lips, gums, and legs.

Helium is commonly used in military mixed gas diving systems to replace some of the nitrogen gas mix because nitrogen narcosis limits the depth at which humans can safely breathe compressed air. However, helium presents a few problems of its own. It has a much higher thermal conductivity than nitrogen, which means it must be warmed at depths below 300 fsw or it will cause hypothermia. Helium also causes bronchorrhea, an excessive mucous discharge from the lung’s air passages. Additionally, special communications equipment is needed to offset the effect helium has on the human voice. On extremely deep dives, especially saturation dives, helium can cause high pressure nervous syndrome. Its mechanism remains unknown, but the syndrome results in dysfunction of the central nervous system. Clinical manifestations include nausea, fine tremor, imbalance, incoordination and manual dexterity loss, decreased alertness, abdominal cramps, and occasionally diarrhea. In severe cases, divers may develop vertigo, extreme indifference to their surroundings, and marked confusion. High pressure nervous syndrome is first noted between 400 and 500 fsw, and the severity appears to depend on both depth and compression rate. Slow compression rates may allow divers to attain depth with little evidence of high pressure nervous syndrome; however, at depths greater than 100 fsw, high pressure nervous syndrome may be present regardless of compression rate.

Visibility

Visibility and color perception are often very poor underwater. The type and extent of particles in the water will determine visual accuracy. In general, objects appear larger and closer than they are until a distance of 2 to 3 m, at which point they appear farther away than they are. Color is generally lost in the order it appears in the visible spectrum, with red going first and blue remaining deepest. This description is only a generalization because the nature of solutes in the water may impact color absorption.

Sound

Sound travels nearly four times faster in water than in air. This speed surpasses the brain’s ability to discriminate the arrival time of sound between the left and right ear, which is how the human ear normally triangulates or orients to sound. Also, sound is reflected on underwater objects and at the boundary of water layers with different densities or temperatures, which further affects hearing. Divers or surface swimmers with their heads in the water will have extreme difficulty judging the direction of sound; this is especially dangerous in the vicinity of motorized boats.

Temperature

Hypothermia

Water temperature needs to be approximately 33°C (91°F) to keep an unprotected, rested human body at a stable temperature. A wetsuit is required below 26.6°C (80°F), and temperatures below 18.3°C (65°F) will limit dive duration. Dry suits allow for greater dive duration at temperatures below 12.7°C (55°F), and a hot water suit is recommended for temperatures below 15.5°C (40°F) because vasoconstriction reduces the blood volume available for off-gassing.

Hyperthermia

Until the most recent change to the US Navy Diving Manual,[4] warm water diving was not addressed, and 31.1°C (88°F) was considered the water’s upper temperature limit. However, standard diving procedures were modified after recent Middle East operations included dive missions in water warmer than 35°C (95°F). This was especially true for combat swimmers, who often swim on the surface, then dive to perform their missions, and then swim to the surface. The Navy Experimental Diving Unit (NEDU) found that Navy sea, air, and land units simulating such a mission with 1-hour transit, 2-hour dive, and 1-hour transit in 36.6°C (98°F) water and 32.2°C (90°F) air temperatures were unable to complete the dive. This 4-hour exercise scenario was based on profiles for combat swimmers developed by Naval Special Warfare Command and the Very Shallow Water Mine Countermeasures Detachment mission.[15]

Of special interest for special warfare and special operations missions is the fact that rebreather gas adds to the diver’s thermal load; NEDU measured inhalation gas temperatures consistently -14.4°C (6°F) warmer than the ambient water temperature. Individual response in terms of heat stress symptoms was highly variable. Some individuals aborted dives due to classic heat stress symptoms, such as headache, nausea, dizziness, and cramping, whereas others showed no such symptoms even as their core temperatures reached 40°C (104°F). However, with daily acclimation, such a dive was possible within 3 days. A critical element to the acclimation process was that in-water exercises were conducted for at least 1 hour daily. The NEDU study revealed warm water dives once or twice a week are insufficient to develop and maintain warm water tolerance.[16]

The Navy developed guidelines for warm water diving based on data collected while observing heat-acclimated divers dressed in underwater demolition team swim trunks and t-shirts, who were well rested, calorically replete, well hydrated, and had no immediate heat exposure prior to starting exercise. Exercise rates for the divers replicated a moderate swimming effort. Conditions contributing to the thermal load, such as heavy work rates, significant pre- and post-dive activities, and various diver dress (dive skins, wetsuits, and dry suits), can reduce exposure limits appreciably. NEDU is developing refined guidelines for exposure limits based on diver dress. Until such further guidance, the provided limits serve as maximum exposure levels. The following operational guidelines and safety precautions were taken from the current US Navy Diving Manual and apply to warm water diving operations above 31.1°C (88°F).

- Weight losses up to 15 lb (or 6%–8% of body weight) due to fluid loss may occur, and mental and physical performance can be affected. Divers should hydrate fully (approximately 500 mL or 17 oz) 2 hours before diving.

- Fluid loading in excess of the recommended 500 mL may cause life-threatening pulmonary edema and should not be attempted.

- Rehydration with water or a glucose/electrolyte beverage should be done as soon as possible after diving. Approximately 500 mL should be replaced for each hour of diving.

- Exposure limits represent maximum cumulative exposure for a 12-hour period.

- Divers should be hydrated and calorically replete to baseline weight, rested, and kept in a cool environment for at least 12 hours before repeat exposure to warm water.

TABLE 19-1

WATER QUALITY AND PROTECTIVE GEAR RECOMMENDATIONS

Water Quality*

Protection Level†

Decontamination

Category 1

A

Yes

Category 2

A or B

Yes

Category 3

A, B, or C

No‡

Category 4

A, B, C, or D

No‡

*Categories:

1. Highest contamination. Grossly contaminated with concentrated chemical or microbiological contamination.

2. Moderate contamination. Increased levels of both chemical and microbiological contamination above what is normally expected.

3. Baseline contamination. Baseline contamination is defined as the water quality that is “normally” expected AND that has a demonstrated history of causing no acute effects on divers.

4. No contamination.

† Levels:

A. MK 21 dive helmet with double exhaust kit, vulcanized rubber dry suit with mating neck-dam, dry gloves attached to integral cuff rings on dry suit sleeves. Dial-a-breath in MK 21 is to be adjusted to slight free-flow mode while at maximum depth.

B. MK 20 full-face mask in positive pressure mode, vulcanized rubber dry suit with hood, dry gloves attached over cuff rings. The side-block assembly is to be used for an emergency gas supply.

C. Any diving helmet or full-face mask not used with a dry suit.

D. Any underwater breathing apparatus with a mouthpiece or T-bit.

‡ Routine post-dive maintenance required.

CAUTION: Any breach of personal protective equipment used to conduct a dive in contaminated water should result in termination of the dive as soon as feasible to limit exposure to the hazards.
Reproduced from: Naval Sea Systems Command. Guidance for Diving in Contaminated Waters. Washington Navy Yard, DC: NAVSEA; 2008. NAVSEA Technical Manual SS521-AJ-PRO-010: 4-6.

Contaminated Diving

TABLE 19-2

COMPARISON OF NAVY’S EXPOSURE GUIDELINES WITH THOSE RECOMMENDED BY THE SUBCOMMITTEE ON EMERGENCY AND CONTINUOUS EXPOSURE GUIDANCE LEVELS FOR SUBMARINE CONTAMINANTS

Chemical

Exposure Level

US Navy Values*

NRC Recommended*

Current

Proposed

Acrolein

1-h EEGL

0.05

0.07

0.1

24-h EEGL

0.01

0.03

0.1

90-day CEGL

0.01

0.01

0.02

Carbon dioxide

1-h EEGL

40,000

30,000

25,000

24-h EEGL

40,000

15,000

25,000

90-day CEGL

5,000

7,000

8,000

Carbon monoxide

1-h EEGL

400

55

180

24-h EEGL

50

20

45

90-day CEGL

20

10

9

Formaldehyde

1-h EEGL

3

0.4

2

24-h EEGL

1

0.1

1

90-day CEGL

0.5

0.04

0.3

Hydrazine

1-h EEGL

--†

4

1

24-h EEGL

--

0.3

1

90-day CEGL

--

0.01

0.03

Methanol

1-h EEGL

200

200

600

24-h EEGL

10

10

50

90-day CEGL

10

7

10

Monoethanolamine

1-h EEGL

50

6

4

24-h EEGL

3

3

4

90-day CEGL

0.5

0.5

0.5

Nitric oxide‡

1-h EEGL

--

--

130

24-h EEGL

--

--

50

90-day CEGL

--

--

3

Nitrogen dioxide

1-h EEGL

1

3

10

24-h EEGL

1

1

2

90-day CEGL

0.5

0.5

0.7

Oxygen (min–max)

1-h EEGL

130–220 mm Hg

--

105 mm Hg (min)

24-h EEGL

130–160 mm Hg

--

127 mm Hg (min)

90-day CEGL

130–160 mm Hg

--

140 mm Hg (min)

*All values in parts per million (ppm) unless otherwise noted.

† There is no standard value available.

‡ The Navy considers the guidance levels for nitrogen dioxide to be also protective of nitric oxide exposure.

Abbreviations: CEGL: continuous exposure guidance level; EEGL: emergency exposure guidance level; max: maximum; min: minimum; mm Hg: millimeters of mercury; NRC: National Research Council

Reproduced with permission from the National Research Council. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 1. Washington, DC: The National Academies Press; 2007: 6.

The Navy’s Guidance for Diving in Contaminated Waters, published in 2008, drives the expectations for protection in water from various contaminants.[17] Dive dress is driven by the type of contamination source present. However, in most real-world scenarios, the exact contaminant may be unknown, and often a quantitative test for contamination levels may not exist or be readily available prior to the start of dive operations. A qualitative assessment of the water quality, based on criteria developed by the California Department of Transportation, is used to determine appropriate dive dress levels that will minimize exposure. The levels are patterned after Environmental Protection Agency guidelines for personal protective equipment, with level A offering the highest protection and level D the least. Table 19-1, taken from the Navy’s Guidance for Diving in Contaminated Waters, addresses dive dress levels and water quality category descriptions. Table 19-2 compares the US Navy’s exposure guidelines to those recommended by the National Research Committee.

Controlled human exposures to many sensory irritants typically use descriptors such as “mild” or “mild-to-moderate,” and the database for sensory irritation thresholds can be highly variable. Research is needed to quantify the diverse methods and end points used in sensory irritation studies so data can be used in public health and occupational health risk assessment with greater confidence.

Certain scenarios can increase the potential exposure to chemical/biological contamination, and extra protective measures should be adopted. When possible, and especially if contamination is known to include volatile compounds, compressors for the diver’s air supply should be positioned upwind of the contaminated area. If this is not feasible, bringing in compressed gas from an offsite location should be considered.

Divers working in sediment may be at greater risk because many contaminants are heavier than water and will accumulate and concentrate in the sediment. Efforts should be made to determine water quality using available resources. State and local health agencies often have water testing and reporting procedures in place that are accessible via the Internet. The National Center for Medical Intelligence (formerly known as the Armed Forces Medical Intelligence Center) available online at https://www.ncmi.detrick.army.mil can provide some local water quality information, and information requests can be made ahead of time to enable planning efforts. Additional international sources for water quality information can be found in the Navy’s Guidance for Diving in Contaminated Waters.[17]

PROBLEMS WITH UNDERWATER BREATHING EQUIPMENT

Hypoxia

Hypoxia, a deficiency of oxygen supply in tissues, can occur during underwater diving when divers breathe mixtures of gases with insufficient oxygen content or when equipment malfunctions. Signs and symptoms of hypoxia are lack of concentration, lack of muscle control, inability to perform delicate or skill-requiring tasks, drowsiness, weakness, agitation, euphoria, and loss of consciousness.

Hypercapnia

Hypercapnia, an excess of carbon dioxide in tissues, can result in similar symptoms, such as confusion, inability to concentrate, drowsiness, loss of consciousness, and convulsions. Such effects become more severe as the amount of carbon dioxide accumulates in tissues. A diver breathing gas with as much as 10% carbon dioxide generally loses consciousness after a few minutes. Breathing 15% carbon dioxide for any length of time causes muscle spasms and rigidity. A diver who loses consciousness because of excess carbon dioxide in the breathing medium and does not aspirate water generally revives rapidly when given fresh air. The diver usually feels normal within 15 minutes, and the after effects rarely include symptoms more serious than headache, nausea, and dizziness.

Dyspnea

Dyspnea is difficult or labored breathing. Increased gas density and breathing apparatus resistance are the two main factors that impede breathing. Even in a dry hyperbaric chamber without a breathing apparatus, increased gas density may cause divers to experience dyspnea. Dyspnea usually becomes apparent at very heavy workloads and at depths below 120 fsw when a diver is breathing air. If breathing heliox, dyspnea usually becomes a problem at heavy workloads in the 850 to 1,000 fsw range. At great depths (1,600–1,800 fsw), dyspnea may even occur at rest.

UNDERWATER HAZARDS

Marine Life

Divers will likely encounter marine life during their undersea missions. While predatory marine species are frequently the focus of news and entertainment programs, attacks against operational divers are rare. Common dangerous species divers may encounter include sharks, barracuda, killer whales, and sea lions. Regardless of the species, treatment involves controlling bleeding and immediate transport to a higher level of care. Providers should control for shock, immunize for tetanus, and culture wounds prior to starting antibiotics.

Sound Navigation and Ranging

Sound pressure level, not distance, is the determining factor for establishing a permissible exposure limit to sonar (sound navigation and ranging). The probability of physiological damage markedly increases as sound pressures increase beyond 200 dB at any frequency. For this reason, diver exposure to sound pressures levels above 200 dB is prohibited unless they wear full wetsuits and hoods. Fully protected divers (in full wetsuits and hoods) must not be exposed to sound pressure levels in excess of 215 dB at any frequency for any reason. Diver exposure to low-frequency sonar (160–320 Hz) can result in vertigo, tingling, and vibratory sensations in the throat and abdomen. Low-frequency sonar is physically dangerous at higher power levels. Diver exposure to ultrasonic sonar (> 250 KHz) can result in tissue heating; however, the power dissipates rapidly with distance, and divers should be safe at a distance of more than 10 yd from the sonar’s focused beam. Exposure sound pressure levels in Tables 1A-3 through 1A-6 of the US Navy Diving Manual can be used to calculate permissible exposure limits for various diver dress and sonar.

SUBMARINES

Submarine Types and Classes

Submarines are true marvels of engineering. The submarine is a self-contained, self-generating life-support system that enables the crew to safely live and work in an otherwise fatal environment at ocean depths. The US Navy submarine force is composed of approximately 5,000 officers and 55,000 enlisted personnel. Not all of these personnel are assigned to submarines. Some work onboard submarine tenders, at shore submarine repair facilities, and as submarine group or squadron staff. The submarine fleet consists of three major submarine types: attack, fleet ballistic missile, and guided missile.

Attack Submarines

The Navy has three classes of nuclear-powered attack submarines (designated SSN) in service: the SSN 688 Los Angeles class, the SSN 21 Seawolf class, and the SSN 774 Virginia class. The aging Los Angeles-class submarines (Figure 19-3), which are being refurbished and refueled or decommissioned, are crewed by 121 enlisted and 13 officers. They measure 360 ft in length and 33 ft in width, and some have bow and sail planes designed to allow operations under ice. The Seawolf class, crewed by 126 enlisted and 14 officers, was ordered toward the end of the Cold War as a planned replacement to the Los Angeles class. They are quieter, bigger (353 ft in length, 40 ft in width), and have greater offensive capability. They have twice the number of torpedo tubes as the Los Angeles class, can carry up to 50 Tomahawk cruise missiles, and were designed with Special Operations Forces (SOF) capability. Lastly, the Virginia class is smaller than the Seawolf at 377 ft in length 34 ft in width. Virginia-class submarines have four torpedo tubes, a vertical launching system (capable of firing Tomahawk cruise missiles), and SOF capability. It was the first submarine class specifically designed for both open-ocean, blue-water and littoral, brown-water operations. The crew complement is roughly the same as the other fast attack submarines, with 120 enlisted and 14 officers.[18]

Figure 19-3. The Los Angeles-class nuclear-powered attack submarine, USS Dallas (SSN-700), with dry deck shelter.
Reproduced from US Navy news photo 040719-N-0780F-070.

Ballistic Missile Submarines

The nuclear powered ballistic missile submarine (SSBN) 726 Ohio class is the largest submarine ever constructed by the United States. The Ohio class was a cornerstone of strategic deterrence during the Cold War. The Ohio-class submarines carry half of the US nuclear warhead arsenal, are 560 ft in length and 42 ft in width, and are crewed by 140 enlisted and 15 officers. While all Ohio-class submarines have four torpedo tubes, their initial purpose was to carry nuclear ballistic missiles in their 24 vertical tubes. They originally carried the Trident I C4 missile, but subsequently were designed or retrofitted to use the improved Trident II D5 missile.[19]

Guided Missile Submarines

The Navy has 18 Ohio-class submarines, but following the Cold War, four were slated for conversion into guided missile submarines (SSGN). The first of four planned conversions took place with the USS Ohio (SSGN-726) in 2005, replacing most of the ballistic missile capability with a vertical launching system for guided missiles. Tubes 3 through 24 each have a multiple all-up round canister holding seven missiles. The multiple all-up round canisters of tubes 3 through 8 can be used to store SOF gear or other supplies. The remaining tubes were converted into lock-in/lock-out chambers for other payloads or SOF capability. With the SSGN conversion, the submarine has nearly the cruise missile capability of a surface battle group. The SSGN can carry and support a team of 66 SOF personnel for up to 90 days, whereas an SOF-capable SSN can carry only 15 (Figure 19-4). Dual dry deck shelters enhance the SSGN’s SOF capability.[20]

With increased focus on special operations, the SSGN’s larger support capability may prove especially helpful, not only in terms of the increased number of SOF personnel they can carry, but also by providing greater training capability while underway. A study of the aerobic performance of Navy sea, air, and land units subjected to a 33-day deployment aboard a fast attack submarine found a significant decrease in the sailors’ running ability following deployment.[21] Given the physical demands of SOF missions, maintaining aerobic exercise capacity while on a submarine could be mission critical.

Figure 19-4. The guided missile submarine can support and launch up to 154 Tomahawk missiles, a significant increase in capacity compared to other platforms. The 22 missile tubes can also carry other payloads, such as unmanned underwater vehicles, unmanned aerial vehicles, and Special Forces equipment. This new platform can carry and support more than 66 Navy sea, air, and land unit personnel and insert them clandestinely into potential conflict areas.
Reproduced from US Navy news photo 030814-N-0000X-006.

The Submarine Environment

All submarines are nuclear powered and can distill water, make oxygen, and power a variety of devices to remove carbon dioxide and other toxic or dangerous gases and contaminants from the atmosphere. The amount of time a submarine remains submerged is driven by the amount of food it can carry, which is typically a 2-week supply of fresh food, including fruits and vegetables. After that, meals are comprised of dry, canned, or frozen ingredients. During the Cold War, an SSBN could remain submerged for months at a time. At present, most operations allow submarines to make port calls more frequently, thus replenishing perishable stock.

The submarine is designed for independent operation and is uniquely vulnerable to fire and flooding in comparison to surface ships. Fresh air is not available, and one cannot simply jump to safety. For this reason, every crew member must demonstrate expert knowledge on all submarine systems. In the event of an emergency, any crew member must act immediately and correctly to isolate and limit the problem. Successfully mastering this level of knowledge is indicated by the submariner qualification and the authorized wear of the submarine warfare device.

Although radiation is vilified in popular science fiction films and books and is viewed with distrust by the general public, there has been no evidence of risk associated with nuclear power aboard submarines. The submarine service operates what is arguably the safest nuclear power program in the world. The fear of cancer among crew members has not proved justified. Two separate studies examined the health of submariners, and both found those who served aboard submarines had no higher rates of cancer than the general public.22,23

Monitoring the Submarine Atmosphere

Central Atmosphere Monitoring System

The submarine atmosphere is monitored by the Central Atmosphere Monitoring System (CAMS). From the first successful nuclear powered submarine operations in 1955, it took the Navy 20 years to develop a reliable and accurate method to monitor the submarine atmosphere. Atmospheric monitoring was especially critical during the Cold War, when ballistic missile submarines remained submerged for extended periods of time as part of the nation’s strategic deterrence capability. The first CAMS used mass spectrometry to monitor all vital gasses except carbon monoxide, which was monitored with infrared technology. The CAMS Mark I automatically and continuously provides air monitoring for vital gases, refrigerants, and aromatic hydrocarbons. CAMS Mark II is in use today on all submarines. The CAMS Mark II system can be programmed to monitor new contaminants or change the alarm levels based on new exposure limits.[24] In addition to CAMS Mark II, colorimetric manually operated Dräger-Tubes (Lübeck, Germany) are used to measure an additional 30 possible contaminants. When the submarine is submerged, the TGA200A trace gas analyzer (Campbell Scientific, Logan, UT), which includes a photoionization detector, is used to run daily tests for excess hydrocarbons. When battery charging operations are in progress, a thermistor monitors hydrogen levels in the battery compartment (ie, the submarine atmosphere).

2, 6-Di-tert-butyl-4-nitrophenol

In 1993, submariners reported a yellow film coating the interior surfaces of submarines, which upon contact resulted in a yellow skin discoloration. Subsequent investigations discovered the discoloration was from 2,6-di-tert-butyl-4-nitrophenol (DBNP) that was produced when oil mist from synthetic steam turbine lubricants and hydraulic fluids containing the antioxidant 2,6-di-tert-butylphenol (DBP) passed through the submarine’s electrostatic precipitators, where the DBP nitrated to become DBNP. The cleaner the precipitator, the more effectively it nitrated DBP, and the longer the precipitator was used without cleaning, the less DBNP it produced. Although the DBP was released in machinery rooms, the nature of the submarine ventilation system, being a contained atmosphere, meant it was distributed throughout the ship. The Electric Boat Division of General Dynamics, which identified the yellow substance as DBNP, determined the 24-hour exposure concentrations to be in the range of less than 3.0 to 122 ppb in laboratory and submarine settings. Thus, the submarine crew could be exposed to these concentrations for 24 hours per day for up to 90 days during underway periods.

At the time, little literature was available on the toxicity of DBNP, but it is a known uncoupler of mitochondrial oxidative phosphorylation, so Navy researchers immediately investigated and found there was little risk from dermal absorption. However, this was not true for ingestion. Prior literature indicated the median lethal dose to be 500 mg/kg in a rat model. Researchers soon found this number was dependent on the delivery medium of carboxymethylcellulose. Using a delivery medium more typical of substances likely to enter the gastrointestinal tract (such as canola oil), researchers soon found the median lethal dose to be only 50 to 80 mg/kg. Toxic effects were noted in the liver, heart, kidney, and skeletal muscle. Radiolabeled DBNP was shown to cross the blood-brain barrier. Using the median lethal dose of rats at 80 mg/kg and a very large safety factor adjustment, one group of researchers recommended a reference dose of 27.3 to .273 ppb, which indicated the Electric Boat sampling fell within this range and could be a concern for chronic exposure.[25] It is unclear to what extent submarine crewmembers were exposed to DBNP, but Naval Sea Systems Command changed the specifications for TEP 2190 turbine oil (San Ramon, CA) so that current stocks contain 10 ppm or less of DBNP precursor DBP.26,27 This example serves to illustrate the fragility of the submarine’s atmosphere system. Today’s submarines utilize a variety of products to maintain a healthy atmosphere for the crew, including oils that are safe for ingestion.

Atmosphere Management and Control

The Los Angeles-class submarines use an electrochemical oxygen generator to produce oxygen by the electrolysis of water. A direct current passes through a potassium hydroxide solution, electrolyzing water into hydrogen and oxygen. More recently, submarines have utilized their oxygen-generating plants to electrolyze water via a solid polymer electrolyte cell. This process has several advantages over the electrochemical oxygen generator in that it requires no free acids or caustic liquids; it can restart in 15 minutes rather than the 6 hours the electrochemical oxygen generator requires; it operates at lower pressure (600 psi vs 3000 psi); it involves less hydrogen (one-tenth) and produces oxygen free of hydrogen contamination; and a single oxygen generating plant can meet the oxygen needs of the entire crew.

Carbon dioxide (CO_2) is removed by either the non-regenerative lithium hydroxide (LiOH) canisters or the regenerative monoethanolamine scrubber. Each 31.5-lb canister of LiOH can remove approximately 28 lb of CO_2. Once total absorption is complete, the canister is jettisoned overboard. The regenerative system uses an aqueous solution of monoethanolamine (MEA), NH_2CH_2CH_2OH to absorb CO_2 via a Lewis acid-base reaction. This reaction can be reversed by heat, allowing the MEA to be recycled. After absorbing 70% to 90% of the CO_2 in the airstream, the MEA is heated under pressure to drive off the CO_2, which is then cooled and discharged overboard. The only system drawback is that there is some MEA leakage into the atmosphere.[28]

The predominant system for air purification aboard submarines is the CO-H_2 (carbon monoxide-hydrogen) burner. Air is brought into the burner where the CO, H_2, and hydrocarbon are converted to CO_2 and water (H_2O) by reacting with a copper oxide/manganese dioxide (CuO/MnO_2) catalyst at 315°C (600°F). Combustion products are cooled and passed over lithium carbonate (Li2CO_3) to remove acidic gases. From there, the air passes over activated charcoal. Additional air purification systems include electrostatic precipitators that charge and precipitate particulate matter, especially in the galley, and vent fog precipitators, which charge and precipitate lube oil particulates in the engine room.

The Navy has detected over 50 potentially toxic atmospheric contaminants aboard submarines.[29] In 1985, the Navy asked the National Research Council to evaluate the submarine atmosphere, which resulted in its 1988 Committee on Toxicology (COT) report, Submarine Air Quality: Monitoring the Air in Submarines and Health Effects in Divers of Breathing Submarine Air Under Hyperbaric Conditions.[30] In the report, the COT recommended exposure guidance levels for six substances of interest to the Navy: ammonia, hydrogen chloride, lithium bromide, toluene, trichloroethylene, and lithium chromate. The COT found cigarette smoke accounted for much of the particulate matter, carbon monoxide, and hydrocarbons in the submarine atmosphere.[30]

The Navy Sea Systems 1992 Atmosphere Control Manual[31] lists 65 known contaminants identified in submarine atmospheres and establishes limits for certain toxic compounds. There are 90-day limits based on time-weighted averages for continuous exposure, 24-hour limits for urgent situations such as a release or spill, and 1-hour limits for emergency situations. Because of the risk of additional contaminants from products brought onboard, all items used onboard must be certified for submarine use. The Submarine Materials Review Board at the Navy and Marine Corps Public Health Center conducts such evaluations (eg, submarine atmosphere). To ensure there are no contaminants in the air that would put the crew at risk for toxic substances, each submarine undergoes routine inspections and atmospheric evaluation. The Navy continues to actively review potential contaminants and update exposure limits for submarines. There are currently 20 contaminants given top priority for review that include respirable particulates, formaldehyde, acrolein, ozone, monoethanolamine, oxides of nitrogen, methanol, carbon monoxide, carbon dioxide, oxygen, lead, ammonia, hydrazine, benzene, toluene, xylene, hydrogen, Freon 114, and Freon 12.[29]

In 2002, the Navy again approached the National Research Council to have the COT review proposed Navy exposure limits and make recommendations. The COT review resulted in the 2004 report Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants.[32] The committee found the Navy’s proposed limits (see Table 19-2) conservative, with the exception of 1-hour CO_2, 90-day CO, 1-hour hydrazine, MEA, and 1-hour O_2 limits.[32] The Naval Submarine Medical Research Laboratory (NSMRL) and the US Naval Research Laboratory are actively updating atmospheric hazards through the Submarine Atmosphere Health Assessment Program.

Disabled Submarines

The grounding of the USS Greeneville near Saipan in August 2001; the death of a sailor aboard the USS San Francisco (SSN-711) following a high-speed collision with an underwater seamount south of Guam on January 8, 2005 (Figure 19-5); and the horrific loss of the Russian submarine Kursk are stark reminders of the possible dangers that accompany every submarine voyage.

The crew’s quick damage control actions, preserved ballast tank function, and rapid assistance by nearby Navy and Coast Guard assets helped the USS San Francisco stay afloat. If not for the heroic efforts of the crew, the submarine easily could have been lost in the 6,000-ft-deep waters. In such a case, deep water would not cause a disabled submarine (DISSUB) scenario; in shallower waters, where the depth will not crush the submarine’s hull, the likely outcome would be a DISSUB. As the sad events of the Kursk illustrated, a DISSUB is a race against time. The risks to survival include oxygen depletion, hypothermia, toxic gases from fires, pressure increase within the boat, and carbon dioxide buildup.

Oxygen Depletion and Toxic Gas

Oxygen depletion can be alleviated by venting air from compressed air banks or by having crew members breathe from the emergency air breathing (EAB) system, but this would result in internal submarine pressurization, creating a dangerous risk if the crew attempts escape (as discussed below). For this reason, the submarine has oxygen-generating chlorate candles, which can be used to replenish oxygen.

In recent studies, researchers have concluded that lower oxygen levels (16.5%) and higher carbon dioxide levels (2.5%) do not increase the risk of hypothermia.[33] A DISSUB exercise conducted pier side showed, surprisingly, that the temperature of the crew compartment increased from 21°C to 26.6°C (70°F to 80°F).[34] The study’s limitations were that the submarine was not submerged and not all power was disconnected. Two European simulated DISSUB studies had opposite results. In a United Kingdom study, a 6-day experiment found that the air temperature dropped from 22°C to 4.4°C (72°F to 40°F).[35] In a Norwegian DISSUB study, the air temperature fell to 13.8°C (57°F).[36] In no study did subjects become hypothermic, suggesting if sailors can remain dry, hypothermia is unlikely a primary concern.

Toxic gas accumulation in a DISSUB scenario is a likely threat. As a result of fire, toxic gases such as ammonia, carbon monoxide, hydrogen chloride, hydrogen cyanide, hydrogen sulfide, nitrogen dioxide, and sulfur dioxide can accumulate. In the event these gases flood into the battery compartment and interact with battery sweat or leakage, chlorine gas could be released. Exposure to these gases, alone or in combination, can cause eye and respiratory tract irritation at low levels, and as levels increase, exposures can impair nervous and respiratory system functions and lead to death.

In 1998, the NSMRL recommended that exposure levels for toxic gas management include levels that would warrant escape from a submarine. The Naval Health Research Center addressed the problem and proposed the establishment of two exposure limits: Submarine Escape Action Level (SEAL) 1 and SEAL 2. SEAL 1 is the maximum toxic gas concentration a healthy submariner can be exposed to for 10 days without irreversible health effects. A submariner can be exposed to SEAL 2 for 24 hours without irreversible health effects. Although SEAL 1 or 2 exposure could cause health effects that limit response time, they should not prohibit personnel from donning protective gear or operating the EAB.

Figure 19-5. The Los Angeles-class nuclear powered fast-attack submarine, USS San Francisco (SSN-711), is pictured in dry dock undergoing damage assessment after a high-speed collision with an underwater seamount.
Reproduced from US Navy news photo 050127-N-4658L-030.

The chief of the US Navy Bureau of Medicine and Surgery then requested that the NRC independently evaluate the scientific validity of the Naval Health Research Center’s proposed SEALs for the eight gases. The project was assigned to the Board on Environmental Studies and Toxicology COT, which formed a subcommittee on SEALs. In 2002, the subcommittee concluded the proposed SEALs were safe and conservative with the sole exception being chlorine gas, which the committee felt should be reduced by 50% for both SEAL 1 and 2. Table 19-3 is adapted from the NEDU report.[37]

The Naval Health Research Center’s recommendation was to don the EAB system and commence escape during SEAL 2 unless rescue was imminent. During either SEAL 1 or 2 conditions, escape preparations must begin when 30% of the crew is using EAB, because the EAB system pressurizes the submarine.

Escape and Rescue

After initial damage control efforts to stop fire and flooding, the primary decision facing survivors is whether to attempt escape or await rescue. SEAL 2 limits are one consideration. The Nuclear Powered Submarine Atmosphere Control Manual, Volume 1[31] provides guidance for the DISSUB senior survivor to estimate survival time based on the number of survivors, material condition of the submarine, and available supplies. In addition, it provides guidance for safe escape measures. NSMRL recently developed software that assists the senior survivor in tracking parameters to guide decision-making. The software can be used on a battery-powered personal digital assistant (handheld personal computer) and was successfully tested in SUBEX (submarine exercise) 2003.[34]

The concept of unsafe escape conditions may seem illogical, but many DISSUB scenarios anticipate the submarine’s internal atmosphere will become pressurized. Increasing atmospheric pressure in a DISSUB could result from flooding, ruptured compressed gas banks, air leaks, or prolonged EAB use. Pressurization to a depth as shallow as 23 ft for 24 hours would essentially turn the crew into divers. By breathing the submarine’s pressurized air, nitrogen would dissolve into tissues, just as it does for scuba divers, and personnel would be at risk for DCS and arterial gas embolism when they surface. Researchers have determined DCS risk is less than 5% at an internal pressurization of 11 ft.[38] Survivors would also be at risk for oxygen toxicity (discussed previously), if the DISSUB were to be pressurized to 5 atmospheres (atm) or more (165 ft).

The US Navy’s adoption of the British submarine escape immersion equipment (SEIE) suit has increased a crew’s chance of surviving an escape. Figures 19-6, 19-7, and 19-8 show sailors dressed in SEIE suits in various training exercises. The US Navy’s version, the MK 10 SEIE suit, provides considerably more protection because it contains a submarine escape and immersion suit, an inner thermal liner, and a gas-inflated single-seat life raft that can be deployed at the surface. The SEIE has been tested to water depths of 600 ft. The process of escape is slow but allows two crew members to escape together, with the cycle being repeated every 15 minutes. If the entire crew of approximately 140 survived, the escape process would take over 17 hours.

TABLE 19-3

THE NAVY’S PROPOSED SUBMARINE ESCAPE ACTION LEVEL VALUES

Gas

Navy’s Proposed SEALs (ppm)

SEAL 1*

SEAL 2*

Ammonia

75

125

Carbon monoxide†

75

85

Chlorine

1

2.5

Hydrogen chloride

20

35

Hydrogen cyanide

10

15

Hydrogen sulfide

15

30

Nitrogen dioxide

5

10

Sulfur dioxide

20

30

*The National Research Council subcommittee recommended that carbon monoxide be 125 and 150 ppm for SEAL 1 and SEAL 2, respectively.

† Except for carbon monoxide values, these values agree with the recommendations by the National Research Committee in 2002. ppm: parts per million

SEAL: submarine escape action level

Adapted from: Lillo RS, Caldwell JM. Development and Evaluation of a Hyperbaric Toxic Gas Monitor (SUBTOX) for Disabled Submarines. Panama City, FL: Naval Sea Systems Command, Navy Experimental Diving Unit; 2013: 66. NEDU TR 13-04. 66.

The Navy’s default preference has been to await rescue because escape puts the crew at the mercy of the ocean environment, without access to medical care, including decompression chambers or life-support supplies. However, escape may be the only option depending on the submarine’s condition and rescue response time. The Navy has two submarine rescue chambers and one submarine rescue diving and recompression system (SRDRS), based in San Diego, California. Both can be mobilized worldwide by air transport. The submarine rescue chamber can use any suitable vessel and is lowered to the DISSUB, at a maximum depth of 850 ft. However, it can only accommodate six submariners at a time and is limited by sea conditions. The SRDRS is the newest technology, replacing the deep submergence rescue vehicle Mystic class. The SRDRS allows personnel to be transferred under pressure, which eliminates the risk of DCS or arterial gas embolism during rescue. The submariners are transferred from the injured submarine to the remotely-operated pressurized rescue module and then to a suitable vessel (Figure 19-9). The SRDRS was successfully used to rescue three DISSUBs during Bold Monarch exercises in 2008. The SRDRS can perform to a depth of 2,000 ft, transfer 16 personnel at a time, and is designed to be deployable on station in 72 hours.[39]

Figure 19-6. Instrument mannequins dressed in MK 10 submarine escape immersion equipment suits inside an engine room logistics escape trunk await the start of General Dynamics’ Electric Boat Division fully instrumented trunk test aboard the Virginia-class nuclear powered fast-attack submarine USS Virginia (SSN-774).
Reproduced from US Navy news photo 040821-N-2653P-001.

The crew’s goal is to survive a DISSUB scenario for 7 days until rescue. In most scenarios, a DISSUB would suffer a power loss. Since the CO_2 scrubbers would be inoperable, in the absence of toxic gases reaching SEAL 2 limits, CO_2 build-up is presumed to be the limiting factor to survival. Until recently, the only method to remove or scrub CO_2 from the submarine atmosphere was to spread LiOH powder in crew spaces to absorb exhaled CO_2. While an effective scrubber, LiOH is caustic, and is likely to cause skin or respiratory tract injury as it is spread or inadvertently disturbed. NSMRL researchers tested the Battelle curtain (Battelle, Columbus, OH) as an alternative CO_2 scrubbing method. Hanging the curtain allows a crew member to safely (even without personal protective equipment) pour LiOH into channels in the curtain, thus eliminating crew exposure. Battelle curtains were successfully tested during SUBEX 2003 and are now standard issue.[34]

The Working Schedule and Sleep

Figure 19-7. Gulf of Taranto, Italy, June 21, 2005. A sailor is rescued by a diver after escaping from the Italian submarine, Primo Longobardo, in the MK 10 submarine escape and immersion equipment suit, during the North Atlantic Treaty Organization submarine escape and rescue exercise Sorbet Royal 2005. Divers from various nations work together to rescue submariners during the exercise in the Mediterranean. Twenty-seven participating nations, including 14 North Atlantic Treaty Organization nations, test their capabilities and interoperability. Four submarines with up to 52 crewmembers aboard are placed on the bottom of the ocean, while rescue forces with rescue vehicles and systems work together to solve complex disaster rescue problems.
US Navy photo by Chief Journalist Dave Fliesen.
Reproduced from Navy.mil photo 050621-N-1464F-038.

Submarine air is 0.3% to 0.5% CO_2, compared with 0.033% in ambient air at sea level. Recent findings of the Board of Environmental Studies and Toxicology suggest submariners become dependent on a physiologically higher CO_2 level for their respiratory drive after being underwater for several days. If the submarine is submerged for several days and then surfaces to ventilate the atmosphere, the crew will suffer interrupted breathing at night.[40] Such disturbances could lead to increased fatigue, poor work performance, and work-related hazards.

Figure 19-8. A sailor assigned to the Los Angeles-class nuclear-powered attack submarine, USS Key West (SSN-722), receives training with the MK 10 submarine escape immersion equipment suit.
Reproduced from US Navy news photo 041012-N-0879R-007.

Adopted in the 1960s, the submarine working day is 18 hours, with the crew standing three watch sections, each 6 hours long, followed by 12 hours off watch divided between other shipboard duties and sleep. Rotating watch schedules, limited meal service, and group living quarters challenge sleep. The submarine work schedule conflicts with the natural circadian cycle (which is just over 24 hours), impacts alertness, and affects performance. Although the crew operates on an 18-hour day, research has shown internal biological rhythms remain set at just over 24 hours.[41] The conflict between internal biological rhythm and work schedule has been shown to impair cognitive performance.[42]

NSMRL conducted a submarine watch-standing study using an 18-hour day, a normal 24-hour day, and alternate 24-hour day watch cycles to examine crew performance measures. The first phase of the study took place in 2001 at the Air Force Research Laboratory sleep laboratory at Brooks City-Base, San Antonio, Texas. The alternate 24-hour schedule showed improved sleep and performance over the 18-hour submarine day and the traditional 24-hour maritime schedule.[43] However, the alternate 24-hour watch schedule placed duty periods on a 72-hour rotation, which resulted in off-duty periods of 12 and 24 hours. Unlike ashore, on a submarine there is nothing to do during long off-duty periods. During the second phase of the study, the alternate 24-hour watch schedule was tested onboard a submarine. Results showed only 15% of personnel preferred the 24-hour schedule to the standard 18-hour schedule.[44] Although a personal preference for the familiar may explain a portion of the study’s results, more work is needed to develop a better submarine watch schedule.

Figure 19-9. The pressurized rescue module is recovered from the water after performing a submarine rescue exercise with the Chilean submarine, CS Simpson, off the coast of San Diego, California, September 18, 2008.
US Navy photo by Communication Specialist 2nd Class Alexia M. Riveracorrea.
Reproduced from US Navy news photo 080918-N7029R-115.

SUMMARY

The undersea environment is a perilous place, yet every day humans successfully live and work on and in the world’s oceans. Through careful engineering, the risks have been minimized; however, even with the best technologies and careful attention to safety, accidents and injuries happen. The military’s operational requirements place personnel in situations where they face hypothermia, hyperthermia, and possibly contaminated waters. Aboard submarines, crews depend on the safe and effective operation of a host of machinery to maintain a healthy atmosphere. The specter of fire and flooding is a constant companion, and DCS remains a threat not only to every diver, but to any crew of a submerged submarine or DISSUB.

This chapter covered the occupational hazards associated with undersea operations. In recent years, NEDU has addressed the new challenge of warm water diving operations. NSMRL is working to make the submarine atmosphere safer through schedule modifications and atmosphere controls. The US Navy Bureau of Medicine and Surgery is updating medical knowledge and protocols for undersea operations and training. The Navy developed a better submarine rescue system, the SRDRS, in addition to the maintenance of the SRC. As the Navy continues to operate in the undersea environment, it will expand its capabilities and approach to risk mitigation through direct and specific medical knowledge, research, and applied physiology.

REFERENCES

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2.   Bennett PB, Elliott DH. The Physiology and Medicine of Diving. 5th ed. London, England: Saunders; 2003.

3.   Bove AA, Davis J. Bove and Davis’ Diving Medicine. 4th ed. London, England: Saunders; 2004.

4.   Naval Sea Systems Command. US Navy Diving Manual. Rev 6. Washington Navy Yard, DC: NAVSEA; 2011. NAVSEA Technical Manual SS521-AG-PRO-010, 0910-LP-106-0957.

5.   Campbell ES. Long term effects of diving. Medscape Orthopaedics & Sports Medicine eJournal. 1997;2(5). http://www.scuba-doc.com/DCSPartII.pdf. Accessed March 8, 2018.

6.   Kindwall EP. Compressed air tunneling and caisson work decompression procedures: development, problems, and solutions. Undersea Hyperb Med. 1997;24(4):337–345.

7.   Kohama M, Nagai R, Okane T, Shingaki Y, Kinjyo Y, Oiwa H. The risk factors and radiological diagnosis of dysbaric osteonecrosis in occupational divers and acute DCI patients. Abstract taken from: the Undersea and Hyperbaric Medical Society annual scientific meetings, UHMS ASM; June 2004; North Palm Beach, FL.

8.   US Navy Bureau of Medicine and Surgery. Manual of the Medical Department. Church Falls, VA: BUMED; 2014. NAVMED P-117, Change 148.

9.   Bolte H, Koch A, Tetzlaff K, Bettinghausen E, Heller M, Reuter M. Detection of dysbaric osteonecrosis in military divers using magnetic resonance imaging. Eur Radiol. 2005;15(2):368–375.

10.   Delphia B. Common ear injuries while diving. Divers Alert Network. Alert Diver. http://www.diversalertnetwork.org. Published February 1999. Accessed May 11, 2017.

11.   Clenney TL, Lassen LF. Recreational scuba diving injuries. Am Fam Physician. 1996;53(5):1761–1774.

12.   Smith DJ. Diagnosis and management of diving accidents. Med Sci Sports Exerc. 1996;28(5):587–590.

13.   Taylor DM, O’Toole KS, Ryan CM. Experienced scuba divers in Australia and the United States suffer considerable injury and morbidity. Wilderness Environ Med. 2003;14(2):83–88.

14.   Bohnker B, Rovig G, Page J, Philippi A, Butler F, Sack D. Navy hearing conservation program: hearing threshold comparisons to Navy SEALS and divers. Undersea Hyperb Med. 2003;30(2):155–162.

15.   Hyde DE. Effects of Warm Water Diving on Combat Swimmer Operations. Panama City, FL: Navy Experimental Diving Unit; 2003. NEDU TR 03-16.

16.   Long ET, O’Connor PE, Liberatore TC. Development of Exposure Guidance for Warm Water Diving: Volume 1—Physiology and Endurance. Panama City, FL: Navy Experimental Diving Unit; 2003. TA 01-08 & 99-005C NEDU TR 03-11.

17.   Naval Sea Systems Command. Guidance for Diving in Contaminated Waters. Washington Navy Yard, DC: NAVSEA; 2008. NAVSEA Technical Manual SS521-AJ-PRO-010. http://www.navsea.navy.mil/Portals/103/Documents/SUPSALV/Diving/Contaminated%20Water%20Div%20Man.pdf?ver=2016-02-10-112554-370. Accessed March 8, 2018.

18.   Attack submarines—SSN. US Navy fact file. http://www.navy.mil/navydata/fact_display.asp?cid=4100&ct=4&tid=100. Updated April 27, 2017. Accessed May 12, 2017.

19.   Fleet ballistic missile submarines—SSBN. US Navy fact file. http://www.navy.mil/navydata/fact_display.asp?cid=4100&tid=200&ct=4. Updated January 12, 2016. Accessed May 12, 2017.

20.   Guided missile submarines—SSGN. US Navy fact file. http://www.navy.mil/navydata/fact_display.asp?cid=4100&tid=300&ct=4. Updated November 9, 2015. Accessed May 12, 2017.

21.   Fothergill DM, Sims JR. Aerobic performance of Special Operations Forces personnel after a prolonged submarine deployment. Ergonomics. 2000;43(10):1489–1500.

22.   Burr RG, Palinkas LA. Health risks among submarine personnel in the US Navy, 1974-1979. Undersea Biomed Res. 1987;14(6):535–544.

23.   Charpentier P, Ostfeld AM, Hadjimichael OC, Hester R. The mortality of US nuclear submariners, 1969–1982. J Occup Med. 1993;35(5):501–509.

24.   Wyatt JR. No more loose fillings or slow embalming: how Naval science helped submariners breathe easy. Undersea Warfare. 2001;3(2):8–10.

25.   Still KR, Jung AE, Ritchie GD, et al. Disposition of 2,6-di-tert-butyl-4-nitrophenol (DBNP), a submarine atmosphere contaminant, in male Sprague-Dawley rats. Environ Res. 2005;98(3):363–367.

26.   Alexander WK, Briggs GB, Still KR, et al. Toxicity of 2, 6-di-tert-butyl-4-nitrophenol (DBNP). Appl Occup Environ Hyg. 2001;16(4):487–495.

27.   Inman AO, Still KR, Jederberg WW, et al. Percutaneous absorption of 2,6-di-tert-butyl-4-nitrophenol (DBNP) in isolated perfused porcine skin. Toxico In Vitro. 2003;17:289–292.

28.   Norfleet W, Horn W. Carbon dioxide scrubbing capabilities of two new nonpowered technologies. Habitation. 2003;9(1-2):67–78.

29.   Cassano VA. A primer on submarine environmental toxicology. Lecture presented at: Medical Issues in Undersea Operations, Uniformed Services University of the Health Sciences; February 2003; Bethesda, MD.

30.   National Research Council, Committee on Toxicology. Submarine Air Quality: Monitoring the Air in Submarines and Health Effects in Divers of Breathing Submarine Air Under Hyperbaric Conditions. Washington, DC: NRC; 1988.

31.   Naval Sea Systems Command. Nuclear Powered Submarine Atmosphere Control Manual, Volume 1. Washington Navy Yard, DC: 1992. NAVSEA Technical Manual S9510-AB-ATM-10/(U).

32.   National Research Council, Committee on Toxicology. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 1. Washington, DC: The National Academies Press; 2007.

33.   Castellani JW, O’Brien C, Stultz DA, et al. Physiological responses to cold exposure in men: a disabled submarine study. Undersea Hyperb Med. 2002;29(3):189–203.

34.   Horn W. Exercise tests disabled submarine survival. Undersea Warfare. 2003;3(20):1. http://www.public.navy.mil/subfor/underseawarfaremagazine/Issues/Archives/issue_20/survivex.htm.

35.   House CM, House JR, Oakley EH. Findings from a simulated disabled submarine survival trial. Undersea Hyperb Med. 2000;27(4):175–183.

36.   Risberg J, Ostberg C, Svensson T, et al. Atmospheric changes and physiological responses during a 6-day “disabled submarine” exercise. Aviat Space Environ Med. 2004;75(2):138–149.

37.   National Research Council, Committee on Toxicology. Review of Submarine Escape Action Levels for Selected Chemicals. Washington, DC: NRC; 2002.

38.   Parker EC, Ball R, Tibbles PM, Weathersby PK. Escape from a disabled submarine: decompression sickness risk estimation. Aviat Space Environ Med. 2000;71(2):109–114.

39.   New submarine rescue asset joins fleet. US Navy website. http://www.navy.mil/submit/display.asp?story_id=40147. Published October 2, 2008. Accessed May 12, 2017.

40.   Margel D, White DP, Pillar G. Long-term intermittent exposure to high ambient CO_2 causes respiratory disturbances during sleep in submariners. Chest. 2003;124(5):1716–1723.

41.   Kelly TL, Neri DF, Grill JT, et al. Nonentrained circadian rhythms of melatonin in submariners scheduled to an 18-hour day. J Biol Rhythms. 1999;14(3):190–196.

42.   Wright KP Jr, Hull JT, Hughes RJ, Ronda JM, Czeisler CA. Sleep and wakefulness out of phase with internal biological time impairs learning in humans. J Cogn Neurosci. 2006;18(4):508–521.

43.   Miller J. Air Force Research Laboratory. Monthly Accomplishment Report Executive Summary. Wright-Patterson Air Force Base, Dayton, OH: AFRL; 2003.

44.   Duplessis CA, Miller JC, Crepeau LJ, Osborn CM, Dyche J. Submarine watch schedules: underway evaluation of rotating (contemporary) and compressed (alternative) schedules. Undersea Hyperb Med. 2007;34(1):21–33.

Chapter 20

HAZARDOUS SUBSTANCES IN THE WORKPLACE

PAPIYA RAY, MD, MPH,* AND CAMERON J.L. NELSON, MD, MPH†

INTRODUCTION

OCCUPATIONAL EXPOSURE LIMITS

Occupational Safety and Health Administration

American Conference of Governmental Industrial Hygienists

National Institute of Occupational Safety and Health

American Industrial Hygiene Association

METALS

Arsenic

Cadmium

Chromium

ORGANIC EXPOSURES

Cyanide

Diesel Exhaust

Diisocyanates

Methylene Chloride

Methyl Ethyl Ketone

Mustard Agents

Organophosphate Nerve Agents

Pentachlorophenol

Trichloroethylene

INORGANIC OR ELEMENTAL EXPOSURES

Asbestos

Crystalline Silica

Tritium

White Phosphorus

SUMMARY

*Occupational Medicine Consultant Physician, Federal Occupational Health, 7700 Wisconsin Avenue, Suite 7201, Bethesda, Maryland 20857

† Commander, Medical Corps, US Navy; Chief of Occupational Medicine, Naval Hospital Bremerton, 1 Boone Road, Bremerton, Washington 98312

INTRODUCTION

Military personnel are exposed to numerous metals, chemicals, and solvents in the workplace, many of which can have deleterious effects on human health. This chapter provides a short list of chemicals and other hazards common to many military installations. Included for each chemical is its use, exposure routes, toxicology, and in some cases, recommended medical surveillance. There are several governing bodies and organizations that publish standards for occupational exposures, which vary in some cases. Because the military uses different sources for exposure limits, which can vary by branch, the limits are not provided here. However, in many cases the military uses the most stringent guidelines recommended.

OCCUPATIONAL EXPOSURE LIMITS

Occupational exposure limits can be either legally enforceable standards established by regulatory agencies or guidelines determined by research groups. In either case, the goal of these exposure limits is to protect workers over their entire working lifetime. The most commonly encountered organizations are described below.

Occupational Safety and Health Administration

The Occupational Safety and Health Administration (OSHA) is a federal agency in the Department of Labor. OSHA issues workplace health and safety regulations, such as exposure limits, employee access to information, conditions governing the use of personal protective equipment, and requirements for safety procedures. It is also responsible for enforcing its standards.[1]

OSHA promulgates permissible exposure limits (PELs), which are legally enforceable standards.[2] PELs are set based on chronic exposure and indicate the maximum values for the “employee’s average airborne exposure in any 8-hour work shift of a 40-hour work week which shall not be exceeded”; otherwise known as the 8-hour time-weighted average.[2] For certain substances, OSHA has also set ceiling limits, the concentration of the substance that should never be exceeded. The OSHA action level is set at half the PEL value and indicates the level at which medical surveillance should be initiated.

American Conference of Governmental Industrial Hygienists

The American Conference of Governmental Industrial Hygienists (ACGIH) is a professional association of industrial hygienists and related professionals that publishes exposure guidelines known as threshold limit values (TLVs) and biological exposure indices (BEIs).[3] Unlike OSHA PELs, these are recommendations and not legal standards. They are based solely on health factors with no consideration of economic or technical feasibility and, therefore, tend to be more stringent than OSHA levels. In addition to the time-weighted average and ceiling limit, for certain substances, the ACGIH defines a short-term exposure limit as the concentration below which workers can be exposed for a period of up to 15 minutes.

National Institute of Occupational Safety and Health

The National Institute of Occupational Safety and Health (NIOSH) is a federal agency under the Centers for Disease Control and Prevention. It is responsible for conducting research and making recommendations for the prevention of work-related injury and illness.[4] NIOSH publishes recommended exposure limits (RELs). As with TLVs and BEIs, RELs are generally updated more frequently and are stricter than PELs.

American Industrial Hygiene Association

The American Industrial Hygiene Association (AIHA) is a professional association, like the ACGIH. Its major goals are the advancement of the study and control of industrial health hazards, and the dissemination of technical knowledge.[5] AIHA publishes workplace environmental exposure levels (WEELs), which are health-based guidelines published annually. Like RELs, TLVs, and BEIs, WEELs are not legally enforceable.

METALS

Arsenic

Forms

Arsenic is a naturally occurring metal.[6] It exists in several forms: elemental, inorganic, organic, and gaseous. Elemental (or metallic) arsenic is a steel grey solid material. Arsenic more commonly exists as inorganic salts, in one of three oxidation states: -3, +3, or +5. Organic arsenic compounds can be further described as organometals, otherwise known as organoarsenic compounds, characterized by a chemical bond between arsenic and one or more carbon atoms. In inorganic form, arsenic generally combines with oxygen, chlorine, or sulfur. Arsine is the gaseous form of arsenic.

Uses

Elemental arsenic is used as an alloying agent in ammunition and solders, an antifriction additive for bearings, and a structural strengthening agent for lead batteries. Organoarsenic compounds, namely cacodylic acid, disodium methyl arsenate, and mono-sodium methyl arsenate, are used as pesticides. Other organoarsenic compounds are used as additives in animal feed to control intestinal coccidian parasites in some poultry and swine farms. Inorganic arsenics, such as arsenic acid, arsenic pentoxide, and arsenic trioxide, are also used as pesticides in the United States. Arsenic trioxide and arsenic acid are also decolorizers and fining agents used in the production of bottle glass and other glassware. Finally, arsine gas is used in the microelectronics industry for gallium-arsenide semiconductor production and as a source of dopant arsenic atoms.

Routes of Exposure

Arsenic compounds can be ingested, inhaled, and absorbed through the skin. The efficiency of absorption depends on the form of arsenic, its solubility, and the route of exposure. In general, both organic and inorganic forms of arsenic are well absorbed through the gastrointestinal tract, but dermal uptake is low. Inhalational exposure usually occurs only with trivalent arsenic oxide or arsine gas.

Toxicology

Inorganic arsenic compounds have been recognized as a human poison since ancient times.[7] Arsenic is an irritant to the skin and gastrointestinal tract and has numerous long-term health effects. Unfortunately, little is known about the effects of organoarsenic compounds in humans. Studies in animals show that most organoarsenic compounds are less toxic than the inorganic forms but still have toxic effects on the digestive and urinary tracts.

Acute toxicity. Acute arsenic poisoning commonly occurs when arsenic is ingested in large doses as inorganic arsenic. This occurs when arsenic has contaminated drinking water wells, but it does not routinely occur in the occupational setting. Individuals who ingest large quantities of inorganic arsenic will develop symptoms within minutes to hours after exposure. Symptoms can range from gastrointestinal discomfort, including nausea and vomiting, to severe abdominal pain, abdominal cramps, and profuse diarrhea. In the worst cases, hepatic necrosis associated with markedly elevated liver enzyme levels and acute renal failure can occur. Cardiovascular effects can also result from acute arsenic poisoning.[7] Seizures, coma, and circulatory collapse leading to death may result when individuals are exposed to more than 70 mg of arsenic. Persons who recover from acute arsenic poisoning may develop delayed peripheral neuropathy, which presents as symmetrical sensory loss in the distal lower extremities.

Arsenic dusts and vapors are both respiratory and eye irritants. Inhalational exposure of arsine gas results in intravascular hemolysis. The initial symptoms of exposure include headache, nausea, and chest tightness. Shortly afterward, the triad of abdominal pain, jaundice, and oliguria develop. Death can occur if exposures exceed 10 ppm.

Chronic toxicity. The skin is the major target organ in chronic inorganic arsenic exposure. Long-term ingestion produces characteristic skin changes on the palms of the hands and feet, including hyperkeratosis and hyperpigmentation with spots of hypopigmentation. Workers chronically exposed to arsenic also experience these dermal manifestations. Individuals who have a history of chronic arsenic ingestion have an elevated risk of skin cancer, including basal cell and squamous cell carcinoma.

Peripheral neuropathy can develop in individuals who have chronic low-level arsenic ingestion. The neuropathy is sensory in nature and includes paresthesia or numbness; in severe cases, the peripheral neuropathy can affect the motor neurons. Liver damage and peripheral vascular disease can also result from chronic low-dose exposure to arsenic. Individuals may be accidentally exposed to arsenic pesticides or they may drink arsenic-contaminated water. However, the most frequent source of arsenic poisoning in the United States is eating food contaminated with arsenic.[7]

The International Agency for Research on Cancer (IARC) classifies arsenic as a human carcinogen. In addition to skin cancer, arsenic exposure has been associated with an increased risk of developing bladder, lung, liver, kidney, and prostate cancer.[7]

Medical Surveillance

Arsenic compounds, both inorganic and organic, are excreted in the urine, making urinary testing the most reliable means of detecting arsenic exposures. Although most tests measure the total amount of arsenic present, organic and inorganic forms can be parsed. Because the half-life of arsenic in the body is only 10 hours, analysis of urine can only reveal recent exposures. Arsenic also accumulates in hair and nails, and testing either can detect exposures over the previous 6 to 12 months. However, the value of hair and nail testing is questionable in industrial settings because of the difficulty in removing all external contamination.[6]

The Department of Defense (DoD) recommends medical monitoring of persons with potential for arsenic exposure at or above the action level.[8] For arsenic, the DoD instruction recommends an annual exam, in addition to a baseline and termination exam. The exams focus on the respiratory system and include work history, medical history (particularly smoking and respiratory history), physical examination of the nasal tract, pulmonary system, and skin, and a chest x-ray.

Cadmium

Forms

In its pure form, cadmium is a soft, silver-white, electropositive metal.9,10 It is found in the earth’s crust, associated with zinc, lead, and copper ores. Cadmium also exists in various inorganic forms, such as cadmium oxide, cadmium chloride, and cadmium sulfate.9,10

Uses

The most common use for cadmium is as an active electrode material in nickel-cadmium batteries. Cadmium compounds are also used for electroplating and to impart corrosion resistance to other metals. Cadmium alloys are used in solder and jewelry. Cadmium sulfides and selenides are used in materials where heat stability and alkali resistance are desired, such as in pigmented rubber, inks, plastics, and ceramics. Cadmium is also used in photoelectric cells and semiconductors.9,10

Routes of Exposure

In the workplace, most cadmium exposure occurs via inhalation. Workers breathe in cadmium dusts and fumes during smelting, plating, and welding processes. Inhaled cadmium is relatively well absorbed, with about 10% to 40% reaching the bloodstream. The efficiency of absorption is based on particle size and chemical composition.

Non-occupational exposure is mainly through ingestion from dietary sources. Meat, shellfish, and vegetables are the primary sources of contamination. Cadmium is not as well absorbed through the gastrointestinal tract; only about 5% to 10% reaches the blood.9,10

Toxicology

Cadmium affects the kidneys, lungs, bones, and heart. Its acute effects target the pulmonary and renal systems.[7]

Acute toxicity. Acute cadmium poisoning results from inhalation of large doses of soluble cadmium compounds, such as cadmium oxide, chloride, or carbonate. This mainly occurs in the occupational setting from industrial accidents. Symptoms develop after a 4- to 10-hour latent period and generally consist of sore throat, headache, myalgia, nausea, and a metallic taste. Eventually cough and dyspnea develop, and death occurs 7 to 10 days after exposure from fulminant chemical pneumonitis and respiratory failure. Exposures to concentrations above 40 mg/m^3 for 1 hour or 9 mg/m^3 for 5 hours have resulted in fatalities. Acute toxicity from high-dose ingestion is rare but results in nausea, vomiting, headache, abdominal pain, and liver and renal failure.

Chronic toxicity. Chronic exposure results in kidney damage via tubular nephropathy with an increased urinary excretion of small proteins, such as β_2-microglobulin and retinol-binding protein. This can result in nephrolithiasis and eventually progress to Fanconi syndrome. The renal dysfunction impacts calcium metabolism and, combined with effects on parathyroid function and vitamin D metabolism, leads to osteomalacia with resulting propensity for pathological fractures. Chronic inhalation of cadmium results in irreversible emphysematous lung injury. Other consequences of cadmium exposure are anemia, eosinophilia, yellow discoloration of the teeth, occasional ulceration of the nasal septum, and anosmia.

Long-term ingestion of cadmium can lead to itai-itai (or “ouch-ouch”) disease. Itai-itai disease is characterized by severe osteomalacia and osteoporosis. The symptoms of itai-itai disease include back and joint pain, height loss, a broad-based or waddling gait, and, in severe cases, fatal renal failure.

Cadmium is classified as a human carcinogen. Occupational exposure to cadmium has been implicated in lung cancer. Cadmium accumulates in the kidney and pancreas and may be associated with cancer of both organs.

Medical Surveillance

OSHA requires medical monitoring of employees who are, will be, or have been exposed to cadmium at the action level, which is one half of the OSHA PEL of 15 mg/m^3. Employees who perform welding, cutting, brazing, burning, or grinding on surfaces that were painted with cadmium-containing paints; do electrical work using cadmium-coated conduit; use cadmium-containing alloys; perform fusing of reinforced steel by cadmium welding; maintain or retrofit cadmium-coated equipment; or perform wrecking and demolition where cadmium is present must be monitored.

The OSHA standard requires baseline, annual, and termination exams. The exams must include a medical and work history, emphasizing exposure, smoking history, reproductive status, and medication use, and any conditions of the cardiovascular, respiratory, renal, hematopoietic, and musculoskeletal systems; a physical exam with focus on blood pressure and the respiratory and urinary systems, including a prostate exam; a chest x-ray; pulmonary function tests; and lab work including complete blood count, blood urea nitrogen and creatinine, blood and urine cadmium levels, and urine β_2-microglobulin.[10] The DoD requirements for medical surveillance are the same as the OSHA regulations.[8]

Chromium

Forms

Chromium is a brittle, gray metal that exists as chromite or ferrochromium in the environment.[11] Forms of chromium used industrially include chromates, chromium alloys or compounds, and chromic acid. The valence state, or electric charge due to the ions present, is the essential factor in determining toxicity. Hexavalent chromium is the most toxic form.

Uses

Chromium compounds provide heat resistance and corrosion resistance. Chrome plating is used on automotive parts, household appliances, tools, and machinery for resistance against corrosion and heat as well as for decoration. In addition, chromate pigments are added to paints, dyes, textiles, rubber, plastics, and inks. Chrome-based orthopedic devices are used for joint replacement. Also, the radioisotope 56Cr is used for erythrocyte labeling in nuclear medicine.

Routes of Exposure

Chromium may be absorbed via ingestion, inhalation, or dermal routes. The valence state influences degree and rate of uptake, with the soluble hexavalent forms absorbed most readily. Most facile absorption occurs via inhalation. Following inhalation, up to 80% of hexavalent chromium is absorbed into the bloodstream. After oral exposure, absorption of chromium through the gastrointestinal tract is low, estimated to be less than 5%. Chromium can penetrate the skin to some extent, but far less is absorbed compared to inhalation exposure.[11]

The greatest occupational hazards historically have been in chromate production, with exposure to hexavalent chromium. However, stainless steel workers and welders are also exposed to chromium fumes and compounds; production and arc welding of stainless steels releases chromium. Workers also may be exposed to chromates through their use in the paint, textile, leather, glass, and rubber industries and in lithography, printing, and photography. Electroplaters are exposed to chromic acid mists. Also, certain cements have a high chromium content.11,12

Toxicology

The water-soluble hexavalent chromium compounds, such as chromic acid or chromates, have an extremely high boiling point. However, they can be inhaled when chromium is dissolved in droplets and salt aerosols that easily penetrate the respiratory tract and act as severe irritants of the nasopharynx, larynx, lungs, and skin.7,11

Acute toxicity. Acute exposure to high concentrations of water-soluble chromium compounds, such as chromic acid or chromates, causes irritation of the eyes, nose, throat, and respiratory tract. Acute oral exposure causes nausea, vomiting, and abdominal pain. Ingestion of high levels of chromium can result in acute renal failure and death from resulting uremia.

Chronic toxicity. Chronic inhalation of chromic acid or chromates may cause ulceration, bleeding, and erosion of the nasal septum. Cough, chest pain, dyspnea, and development of chromium-induced asthma are other sequelae of long-term inhalation toxicity. Chronic exposure to chromic mist results in conjunctivitis.7,11

Dermatologic manifestations are common in chromium workers. Chrome ulcers, penetrating lesions of the skin, occur chiefly on the hands and forearms. These ulcers are thought to result from a direct necrotizing effect of the chromate ion where there has been a break in the epidermis. The ulcer is relatively painless, heals slowly, and produces a characteristic depressed scar. Sensitization dermatitis, ranging from localized erythematous or vesicular lesions at points of contact to generalized eczematous changes, has also been reported.7,11

Chromium is a recognized by IARC as a human carcinogen. It is associated with cancer of the nasopharynx, trachea, bronchus, and lung. When hexavalent chromium is introduced into the cell, it can damage the genetic material and produce DNA adducts and strand breaks. Animal and cellular studies have revealed that hexavalent chromium causes mutagenesis, produces reactive oxygen radicals, and interferes with both cellular regulation of apoptosis and repair of DNA damage, which may arrest the cell cycle.[11]

Medical Surveillance

Urine chromium levels may be useful for assessing recent exposure. However, there are no practical laboratory methods for monitoring chronic exposure aside from monitoring changes resulting from end organ damage. For example, medical surveillance may detect changes in pulmonary function when workers develop respiratory disease due to exposure.

OSHA requires medical monitoring of persons with chromium exposure at or above the action level, which is one half the OSHA PEL of 5 μg/m^3.[12] The OSHA regulation requires baseline, annual, and termination exams. The exams must include a medical and work history, emphasizing past chromium exposure, a smoking history, a history of respiratory disorders and skin disorders, and a physical exam focusing on the respiratory tract and skin. DoD requirements for medical surveillance align with the OSHA regulations.[8]

ORGANIC EXPOSURES

Cyanide

Forms

The cyano group is a negatively charged ion species with three molecular carbon-nitrogen bonds.[13] Hydrogen cyanide exists as a colorless gas at ambient temperature and has a bitter, almond-like odor. Cyanide salts, such as sodium cyanide and potassium cyanide, are white solids with a similar odor. In organic cyanides, the cyano group is bound to a carbon, such as methyl. Other forms of cyanide include the thiocyanates, which are cyanide compounds that contain sulfur. Ferrocyanides, such as sodium, potassium, and calcium ferrocyanide, have highly stable bonds with iron and do not easily break down to lethal compounds.

Uses

Cyanide is mainly used in gold and silver mining, where it helps dissolve the precious metals from the impure ores. Cyanide is also used in electroplating for stabilizing metal ions prior to their deposition. It is used in jewelry making and for sepia toning in photography. In some areas of the world, cyanide is used as pesticide.[13]

Routes of Exposure

Cyanide can be absorbed via inhalation, ingestion, and dermal uptake. Hydrogen cyanide is absorbed within seconds following inhalation exposure. Following ingestion, cyanide salts rapidly enter the bloodstream from the gastrointestinal tract. On the other hand, ferrocyanides are poorly absorbed due to the iron, and thus relatively nontoxic. Chronic dermal exposure to cyanide can occur in occupational settings. Case reports in humans and studies in animals have shown toxic effects following only dermal exposure, but little is known about the toxicokinetics of dermal absorption.[13]

Toxicology

The cyanide anion is an inhibitor of the enzyme cytochrome c oxidase, part of the electron transport chain. It disrupts the electron transport chain in aerobic respiration and interferes with adenosine 5’-triphosphate metabolism.[13] Tissues that depend highly on aerobic respiration, such as the central nervous system (CNS) and the heart, are particularly affected.

Acute toxicity. Acute inhalation, ingestion, or dermal absorption of high concentrations of cyanide results in neurological depression, convulsions, coma, and death due to depression of the respiratory centers. Those who survive acute poisoning can develop parkinsonism and dystonia.[13]

Chronic toxicity. Chronic exposure to low concentrations has been associated with respiratory, endocrine, and CNS toxicities. Workers subjected to low levels of airborne cyanide reported dyspnea, presumably caused by a decrease in pulmonary phospholipids and loss of pulmonary surfactant. CNS effects include vague symptoms such as fatigue, dizziness, headaches, and tinnitus, and more severe symptoms such as paresthesia, syncope, hemiparesis, and hemianopia. Chronic cyanide exposure also results in adverse thyroid effects. In the body, cyanide metabolized to thiocyanate interferes with iodine uptake and utilization by the thyroid gland. Chronic exposure leads to reduced thyroid hormone levels, elevated thyroid stimulating hormone levels, and goiter. [13]

Medical Surveillance

If cyanide exposure is suspected, blood and urine levels of cyanide and thiocyanate can be measured. However, there are no formal OSHA or DoD regulations regarding routine medical surveillance for workers with potential for cyanide exposure.

Diesel Exhaust

Diesel exhaust is a mixture of gases and particulates produced during the combustion of diesel fuel. Gaseous components of the exhaust include carbon dioxide, oxygen, nitrogen, water vapor, carbon monoxide, nitrogen compounds, sulfur compounds, and low-molecular-weight hydrocarbons.[14]

Exposure

Uptake of diesel exhaust, and its constituents, occurs via inhalation. Workers in the following occupations have the greatest risk for exposure: mine workers, railroad workers, bus and truck drivers, truck and bus maintenance garage workers, loading dock workers, firefighters, heavy equipment operators, and farm workers.[14]

Toxicology

The primary organ system affected by diesel exhaust is the respiratory tract. Diesel exhaust particles become deposited in the airways and activate alveolar macrophages. These macrophages release cytokines and growth factors, leading to inflammation, epithelial cell injury and fibrosis, and goblet and alveolar lining cell proliferation.[14]

Acute toxicity. Acute exposure to diesel exhaust causes acute irritation of the eyes, throat, and respiratory tract, as well as neurophysiological symptoms (lightheadedness, nausea). Symptoms of acute exposure mostly consist of respiratory effects such as cough and phlegm.14,15

Chronic toxicity. While few studies of chronic exposure in humans have been published, extensive evidence from animal studies show that diesel exhaust poses a chronic respiratory hazard. Chronic animal inhalation exposure studies reveal dose-dependent inflammation and histopathological lung changes in several animal species including rats, mice, hamsters, and monkeys. Studies have also found a statistically significant correlation between long-term diesel exhaust exposure and an increased risk of lung cancer.[15]

Medical Surveillance

Several biomarkers correlate well with diesel exhaust exposure. Metabolomics studies of various polycyclic aromatic hydrocarbons found in diesel exhaust were also correlated with postdeployment serum studies of deployed personnel exposed to diesel exhaust. Serum immune mediators and microRNAs were also found to be elevated in these service members.16–19

OSHA has not established a standard for diesel exhaust as a unique hazard; however, exposures to various components of diesel exhaust are addressed in specific standards. Likewise, the DoD does not have specific regulations or recommendations for monitoring of workers exposed to diesel exhaust.

Diisocyanates

Isocyanates are a family of highly reactive chemicals. Diisocyanates are compounds of two isocyanate groups.20,21

Uses

Previously, military vehicles were painted with standard alkyl and acrylic paints, but these paints absorbed chemical warfare agents. To avoid this hazard, the military switched to polyurethane paints, which are chemical agent-resistant coatings (CARCs). There are three types or layers of coatings in the CARC system: an epoxy polyamide primer, an aliphatic polyurethane paint, and epoxy polyamide enamel. Each of the coatings is supplied as a two-component system. When the two components are combined, a chemical reaction converts them into an impermeable coating material. The polyurethane systems contain unreacted isocyanate or diisocyanate groups in the uncured resin, which irritate the skin and sensitize the respiratory system. Once cured, polyurethanes no longer release isocyanates unless heated.20,21

Diisocyanates are also used in insulation, upholstery, and furniture. Spray-on polyurethane products containing isocyanates are used for protective coatings for truck beds, trailers, boats, foundations, and decks and to protect cement, wood, fiberglass, steel, and aluminum.

Routes of Exposure

Isocyanates can be ingested, inhaled, and absorbed through the skin. However, most occupational exposure occurs via inhalation when workers breathe in vapors, mist, or smoke released by uncured polyurethane products.20,21

Toxicology

Isocyanates are powerful irritants to the mucous membranes. They cause airway epithelial damage resulting from extensive inflammation and increased bronchial hyperresponsiveness.[7]

Acute irritation. Diisocyanates are severe irritants of the eyes and gastrointestinal and respiratory tracts. Direct skin contact can also cause marked inflammation. Symptoms include burning and watering of the eyes, burning sensations in the nose and throat, sore throat, productive cough, and in some cases tightness of chest, discomfort, a feeling of breathlessness, and a temporary reduction in lung function. The severity of symptoms depends on the extent of exposure, the tissue exposed, and individual susceptibility, but it is generally independent of the individual’s exposure history. These acute symptoms are generally reversible if the victim is removed from the source of toxicant or, in cases of skin contact, the skin is decontaminated.

Sensitization. Sensitization, however, is a systemic response and is not limited to the area of contact. Sensitization usually does not occur on initial exposure but can develop within the first few months of exposure to an isocyanate environment. Sensitization may develop as a result of repeated overexposure or a large single dosage from a spill or other accident. Once sensitized, subsequent exposures can cause very strong allergic reactions. A sensitized individual may react to extremely low airborne levels. The response is similar to asthma, that is, coughing, wheezing, tightness in the chest, and shortness of breath. The skin sensitization reaction is allergic dermatitis, which includes symptoms such as rash, itching, hives, and swelling of the arms and legs. If an individual is sensitized to isocyanates, complete removal of the individual from area of potential exposure to isocyanate vapor or mist is necessary.

Medical Surveillance

There are no practical biological methods for monitoring chronic exposure to diisocyanates aside from screening for antibody production, indicating sensitization, and changes due to end organ damage. While OSHA has set the PEL for isocyanate exposure at 0.02 ppm, it has not developed a required medical surveillance program.[21] However, it does provide general guidance on medical surveillance for employers. Likewise, the DoD does not have specific regulations or recommendations regarding monitoring of workers exposed to isocyanates.

Methylene Chloride

Form

Methylene chloride is a member of the chlorinated hydrocarbon family. It is a colorless liquid with a pleasant odor. It evaporates readily but has low flammability.[22]

Uses

Widely used as an industrial solvent and paint stripper, methylene chloride is also an ingredient in some aerosol and pesticide products, spray paints, automotive cleaners, and other household products. It is also used in the production of photographic film.[22]

Routes of Exposure

Methylene chloride can enter the body via inhalation, ingestion, or dermal absorption. Due to its high volatility, inhalation is the major route of exposure, followed by dermal uptake. Inhalation is an efficient method of absorption, with up to 75% of inhaled methylene chloride reaching the bloodstream.[22]

Occupational exposure to methylene chloride occurs in numerous industries. Workers may be exposed during a variety of industrial activities including spray painting, spray gluing, metal painting, paint stripping, and aerosol packing. Most occupational exposure occurs during metal cleaning, industrial paint stripping, and ink solvent use.22,23

Toxicology

Methylene chloride gets metabolized to carbon monoxide.[7] The toxic effects are secondary to carbon monoxide and its subsequent binding to hemoglobin, producing carboxyhemoglobin. The pulmonary, hematopoietic, and nervous systems are the major targets of exposure to methylene chloride.[22]

Neurotoxicity. The nervous system is the most important target of acute methylene chloride toxicity. Methylene chloride is a mild CNS depressant, and the accompanying hypoxia from carboxyhemoglobin aggravates the CNS effects. Symptoms include dizziness, nausea, peripheral paresthesia or anesthesia, and a subjective feeling of drunkenness. With high enough exposure, usually above 8,000 ppm, unconsciousness and death result.[22]

Hematologic toxicity. Inhalation and ingestion of methylene chloride result in increased blood carboxyhemoglobin, as previously described. In some studies, in persons with chronic occupational exposure, increases in the red cell count, hemoglobin, and hematocrit were seen, believed to be compensatory hematopoiesis from chronic hypoxia.[22]

Pulmonary toxicity. Acute inhalation of high concentrations of methylene chloride damages the Clara cells of the bronchioles. This damage can result in pulmonary infiltrates, congestion, hemorrhage, and death.[22]

Carcinogenicity. While there is no clear evidence in humans that methylene chloride exposure causes cancer, a number of animal studies have demonstrated its potential as a carcinogen. Lung and liver tumors have developed in mice with chronic overexposure. As a result, IARC has classified methylene chloride as a possible human carcinogen.[22]

Medical Surveillance

Measurements of parent methylene chloride and its metabolites in expired air, blood, and urine have been used as indicators of exposure. But because it is cleared from the body very rapidly, these methods are useful for monitoring recent exposures only.

OSHA requires medical monitoring of persons with methylene chloride exposure at or above the airborne action level of 12.5 ppm.[23] The OSHA regulation requires full medical surveillance at baseline and termination, with periodic surveillance as determined by the employee’s age. The full surveillance exam must include a medical and work history (updated annually), emphasizing neurological symptoms; history of skin, hematologic, hepatic, and cardiac disorders; risk factors for cardiac disease; and methylene chloride exposure. The physical exam should focus on the respiratory tract, lungs, cardiovascular system (including blood pressure and pulse), liver, nervous system, and skin.[23] DoD requirements for medical surveillance align with the OSHA regulations.[8]

Methyl Ethyl Ketone

Form

Methyl ethyl ketone is also known as 2-butanone. It is a colorless liquid with a sharp, sweet odor. It is highly volatile and water soluble.[24]

Uses

Methyl ethyl ketone is used mainly as an industrial solvent. Most of its use is in paints, glues, and other coatings because of its rapid evaporation and ability to dissolve many substances. It is used in the manufacturing process of the following products: fabric coatings, synthetic resins, surface coating, artificial leather, lacquer and varnish, pharmaceuticals, cosmetics, synthetic rubber, lubricating oils, vinyl coatings, adhesives, acrylic coatings, hardwood pulps, and ink. Methyl ethyl ketone is also a naturally occurring substance produced by some trees, fruits, and vegetables.[24]

Routes of Exposure

Occupational exposure to methyl ethyl ketone mainly occurs via inhalation during the production, formulation, use, or transport of this compound. Approximately 50% of the inhaled compound is absorbed into the bloodstream. It can also be ingested or absorbed dermally, but less is known about the rate and efficiency of these routes of exposure.[24]

Exposure occurs when workers apply commercial coatings containing methyl ethyl ketone, especially in enclosed, unventilated spaces. It is also released into the air as a component of car and truck exhausts.[24]

Toxicology

While methyl ethyl ketone is an irritant to the eyes, mucous membranes, and skin, serious health effects have only been seen in study animals under high-concentration exposure conditions. Inhalation causes irritation of the nasal passages and respiratory tract, with symptoms of sore throat, dry nose, and cough. Exposure to the vapor can also cause conjunctival irritation manifested as redness, tearing, and blurred vision. There have been some reports of inhalation exposure resulting in mild skin irritation, but no studies or reports of dermal exposure causing skin inflammation in humans has been reported. Animals exposed to extremely high concentrations of inhaled or ingested methyl ethyl ketone have been reported to exhibit severe respiratory, hepatic, renal, and neurological effects generally culminating in death.[24]

Medical Surveillance

Methyl ethyl ketone can be detected unchanged in the blood, urine, and exhaled air. Its metabolites, 3-hydroxy-2-butanone and 2,3-butanediol, can be detected in the urine. However, methyl ethyl ketone is metabolized and excreted rapidly, with a half-life of only 90 minutes, so testing is only good for very acute exposures. Furthermore, alcohols, hydrocarbons, and other ketones also break down to 2-butanone and its metabolites, so testing is not specific for 2-butanone exposure.[24]

While OSHA has set the PEL for methyl ethyl ketone exposure at 200 ppm or 590 mg/m^3, it has not developed specific medical surveillance program requirements. Likewise, the DoD does not have specific regulations or recommendations regarding monitoring of workers exposed to methyl ethyl ketone.

Mustard Agents

Forms

Sulfur mustards are oily, clear or yellow to brown liquids with an odor like garlic, onion, or mustard. They are liquids at room temperature but will vaporize over the course of days to weeks and at faster rate at higher temperatures. They are not water soluble but dissolve easily in oils, fats, and other solvents. HD is the most common mustard agent used. Agent H is chemically distinct from the more common HD and contains about 20% to 30% impurities. HT is a mixture of 60% HD and 40% H.[25]

Uses

Sulfur mustard agents are blister or vesicant agents developed for chemical warfare. They were first used during World War I and have been used as recently as the Iran-Iraq War (1980–1988). Sulfur mustard is no longer being produced by the United States, and Congress has mandated that all stockpiles be destroyed. It is now used only for research purposes in the United States.[25]

Routes of Exposure

Sulfur mustard gas or vapor is readily absorbed through the lungs, via inhalation, or the skin. Liquid sulfur mustard is absorbed readily through the skin. Occupational exposure may occur on Army bases where sulfur mustard was previously released and has persisted in the soil, or where old containers are currently stored. Construction workers or other such laborers are most at risk at these sites. Persons involved in the storage and destruction of this compound could also be exposed during accidental release. Researchers may be exposed to sulfur mustard, and soldiers are still at risk for exposure if it is used as a chemical warfare agent. Service members who deployed to Iraq after the first and second Gulf wars occasionally encountered buried and partially buried projectiles containing sulfur mustard. Most rounds were intact, but many were leaking and exposed unprotected service members to sulfur mustard. Finally, there have been reports of fishermen being exposed by inadvertently snaring discarded canisters containing sulfur mustard in areas of historical ocean dumping with subsequent puncturing of the canister.[25]

Toxicology

Sulfur mustard has many biological actions, but the exact mechanism of tissue injury is not known.[25] Several studies have shown that sulfur mustard can produce biochemical alterations consistent with free-radical-mediated oxidative stress, such as lipid peroxidation, antioxidant enzyme activities, and depletion of glutathione. However, DNA is the most functionally sensitive biomarker of mustard gas exposure.25,26 Mustard gas causes DNA alkylation and crosslinking in rapidly dividing cells, leading to cellular death and inflammatory reactions resulting in large fluid-filled blisters on skin and excretion of fluid in the respiratory track (which causes breathing difficulty or asphyxiation). The main effects of sulfur mustard agents are in the eyes, airways, and skin.[25]

Dermal toxicity. Mustard agent causes erythema of the skin, along with itching, burning and stinging pain. The skin is most sensitive where it is thinnest, in the warm, moist areas around the eyes and genitalia. Small vesicles form in the erythematous areas, which may later coalesce to form bullae. Bullae look like large, domed-shaped, thin-walled, translucent bubbles on the surface of the skin.[25]

Pulmonary toxicity. Mustard agent that gets into the lungs causes necrosis of the mucosa and potential damage to the airway musculature. The damage begins in the bronchus and upper airways. As the exposure continues, the lower airways and bronchioles become affected. The alveoli are the last part of the lung affected. When the mustard causes severe lung injury, hemorrhagic pulmonary edema develops. Respiratory failure or secondary bacterial pneumonia is the usual cause of death from mustard exposure. If the mustard poisoning is less severe, chronic respiratory effects can develop, including chronic bronchitis, cough, and diminished lung volumes.[25]

Ocular toxicity. The eyes are the organ most sensitive to mustard vapor. Conjunctivitis, with reddening and irritation, is the earliest symptom of exposure. As the exposure level increases, the severity of clinical conjunctivitis symptoms increases, causing photophobia, blepharospasm, pain, and corneal damage. Swelling and loosening of corneal epithelial cells lead to corneal edema and leukocyte clouding. There may also be scarring between the iris and lens, which can restrict pupillary movement and predispose victims to glaucoma.[25]

Medical Surveillance

Although tests are available to detect metabolites of sulfur mustard in blood and urine, they are not readily available in most clinical settings. Rather, samples must be sent to the Centers for Disease Control and Prevention or the Army Medical Research Institute of Chemical Defense for analysis. Also, while the tests can confirm sulfur mustard exposure, they are of little use in preventing onset or treating clinical disease.[26]

OSHA has no standards or regulations regarding medical surveillance for persons with possible exposure to sulfur mustard. However, the DoD requires workers with access to chemical, biological, and nuclear materials, such as mustard agents, to be enrolled in a “surety” medical program.[8] Surety programs place added emphasis on safety, security, and personnel reliability. The Army has published recommendations for medical surveillance programs for persons with potential exposure to sulfur mustard agents, which have subsequently been adopted by the DoD.[26]

Organophosphate Nerve Agents

Organophosphates comprise a group of chemicals that were developed for home and industrial applications. These diverse chemicals are used as insecticides and anthelmintics in agriculture, as ingredients in ophthalmic medical applications, and as chemical warfare agents by several countries. Given their relevance to military personnel, the remainder of this section will focus on organophosphate use in nerve agents. The US chemical warfare agent stockpile contains the nerve agents sarin (GB) and VX.

Forms

Nerve agents are liquids under ambient conditions. The G-type agents such as sarin are more volatile and readily vaporize and disperse as vapors under normal conditions. They are clear, colorless, and tasteless liquids that are soluble in water and most organic solvents. Sarin is the most volatile nerve agent and evaporates at the same rate as water. VX is the least volatile of the nerve agents and is a clear, ambercolored, odorless, oily liquid.[27]

Uses

Organophosphates were originally developed as pesticides, but they were repurposed as chemical weapons. Sarin was developed in 1938 by Germany, and VX was synthesized in England in 1952. After World War II, organophosphates were reintroduced as pesticides as well as medicinal and pharmaceutical agents. Organophosphate pesticides reversibly inhibit acetylcholinesterase, whereas nerve agents irreversibly inhibit acetylcholinesterase. The deadly effects of these nerve agents result from a buildup of acetylcholine, which can lead to muscle fasciculations, seizures, flaccid paralysis, apnea, and copious secretions.[27]

Routes of Exposure

Nerve agents are readily absorbed via inhalation, ingestion, and through the skin.[7] Inhalation is the usual route of exposure in combat settings, but dermal exposure is the primary route of occupational exposure. Vapors are not absorbed through the skin except at very high concentrations. Ingestion of nerve agents is relatively rare compared to inhalation exposure or skin contact; however, nerve agents are readily absorbed from the gastrointestinal tract.[27]

Toxicology

Nerve agents are cholinesterase inhibitors.[27] They inhibit the carboxyl ester hydrolases in plasma, red blood cells, and cholinergic receptors, particularly acetylcholinesterase. Once acetylcholinesterase has been inactivated, acetylcholine accumulates, resulting in overstimulation of muscarinic and nicotinic receptors of the affected organ and the CNS. Onset of symptoms occurs soon after high-level exposure, but little is known about chronic low-level exposure.[27]

Central nervous system toxicity. Nerve agents cause behavioral and psychological effects, such as irritability, nervousness, fatigue, insomnia, memory loss, impaired judgment, slurred speech, and depression. The CNS signs of a large exposure are loss of consciousness, seizures, and apnea. Symptoms usually begin within a minute of exposure to a large amount of vapor or skin contact, but may be preceded by a latent period of up to 30 minutes after exposure. CNS effects such as fatigue, irritability, nervousness, and memory impairment may persist for as long as 6 weeks after recovery from acute effects.[27]

Pulmonary toxicity. Nerve agent vapor causes bronchoconstriction and increased secretions of the glands in the airways, manifesting as excessive rhinorrhea and bronchial secretions. The exposed person may feel a slight tightness in the chest after exposure to a small amount of agent and may be in severe distress after a large amount of agent. Respiratory failure may occur due to CNS depression.[27]

Cardiovascular toxicity. Exposure to organophosphate pesticides and nerve agents can result in bradycardia due to vagal nerve stimulation, or tachycardia, due to ganglionic stimulation and hypoxia. Hypertension may also result in response to the bradycardia.[27]

Gastrointestinal toxicity. Organophosphate pesticide and nerve agent exposure may stimulate nerve cells, which increases motility and secretions by the glands in the wall of the gastrointestinal tract. Nausea and vomiting are early signs of nerve agent exposure, and diarrhea may occur with large exposures.[27]

Muscular toxicity. Nerve agent exposure stimulates skeletal muscle, which produces muscular fasciculations and twitching. Prolonged exposure to nerve agents produces fatigue and muscle weakness, rapidly followed by muscular flaccidity.[27]

Glandular toxicity. Nerve agent vapor causes the lacrimal, nasal, salivary, and bronchial glands to increase secretions. Localized sweating also occurs around the site of liquid agent contact on the skin, and generalized sweating occurs after a large liquid or vapor exposure.[27]

Ocular toxicity. Miosis, a characteristic sign of nerve agent vapor exposure, is a contraction of the muscles of the eye, causing the muscles of the iris to constrict, narrowing the opening. Miosis is accompanied by pain, blurred vision, conjunctival injection, and occasionally nausea and vomiting.[27]

Medical Surveillance

Organophosphate nerve agent toxicity is a clinical diagnosis that is made using an occupational history of exposure and physical examination that includes noting signs and symptoms of exposure. Laboratory testing is possible at chemical depots to confirm nerve agent exposure. The drop in blood pH following a nerve agent exposure reflects altered red blood cell cholinesterase activity in response to the exposure. Organophosphate pesticide applicators can also be monitored by checking red blood cell cholinesterase levels, which rise following pesticide exposure.

There are no OSHA regulations for nerve agent exposure or recommendations for medical surveillance of persons exposed to nerve agents. However, the DoD requires workers with access to nerve agents to be enrolled in surety medical programs, as described above.[8] The Agency for Toxic Substances and Disease Registry has published recommendations for medical surveillance for persons with potential exposure to nerve agents.[27]

Pentachlorophenol

Forms

Pure pentachlorophenol is a synthetic, colorless crystal. Impure varieties are dark brown or gray dust, beads, or flakes. When heated, pentachlorophenol releases a sharp, sweet, or “benzene-like” odor, but at room temperature, it produces very little odor. It exists in two forms: pentachlorophenol itself, and the sodium salt of pentachlorophenol. The sodium salt form is very water soluble compared to the other form.[28]

Uses

Pentachlorophenol is only used industrially. It is mainly used as a wood preservative for power line poles, fence posts, and similar structures. Sodium pentachlorophenol is used in plywood and fiberboard waterproofing, and in termite control. Previously it was a widely used pesticide and herbicide.[28]

Routes of Exposure

Pentachlorophenol is efficiently absorbed via inhalation, oral, and dermal exposure.[28] In the workplace, most exposure is from inhalation or skin absorption. Based on human and animal studies, over 70% of inhaled pentachlorophenol is subsequently absorbed. Oral absorption is even more efficient, with virtually all ingested chemical entering the bloodstream. Dermal uptake is the least efficient method of absorption. However, dermal absorption is based on the solution; pentachlorophenol in an oily solution is better absorbed, at approximately 60%, compared to pentachlorophenol in an aqueous solution, with less than 20% uptake.[28]

Occupational exposure occurs in the gas, electric, and wood preservative industries. Acute exposures occur in the production and application of pentachlorophenol, when opening pressurized vessels, cleaning tanks, or application to lumber. Non-occupational exposure occurs by handling treated lumber.[28]

Toxicology

Pentachlorophenol is an irritant, affecting the eyes, nasal and oral passages, airways, and skin. Exposure to concentrations above 1 mg/m^3 causes upper airway pain and cough, but persons can become acclimatized to pentachlorophenol. Acclimatized persons can tolerate concentrations up to 2.4 mg/m^3. Systemic toxicity of pentachlorophenol results from uncoupling of oxidative phosphorylation and disruption of electron transport, leading to stimulation of cell metabolism and hyperthermia.[28]

Acute toxicity. Exposure to high concentrations of pentachlorophenol can cause skin irritation. Systemic intoxication is characterized by rapid onset of diaphoresis, elevated temperature, tachycardia, tachypnea, weakness, nausea, vomiting, abdominal pain, headache, intense thirst, and pain in the extremities. Symptoms culminate in progressive coma and death within hours after onset of symptoms.

Chronic toxicity. Repeated, dilute skin exposure also leads to irritation. Chloracne has been reported after direct skin exposure, most likely the result of dioxin contaminates in commercial-grade pentachlorophenol. Chronic exposure is also connected with conjunctivitis, sinusitis, bronchitis, and polyneuritis.[28]

Carcinogenicity. IARC has determined that pentachlorophenol is a possible human carcinogen. An increased risk of non-Hodgkin lymphoma has been observed in individuals exposed to pentachlorophenol.

Medical Surveillance

Pentachlorophenol and its metabolites can be measured in the blood, urine, and tissue. Since it is excreted in the urine largely unchanged, urinalysis is a noninvasive and useful method for determining exposure. However, other compounds such as hexachlorobenzene and lindane are metabolized to pentachlorophenol in the body, and thus it is a not a specific biomarker. Also, because pentachlorophenol is cleared from the body relatively quickly, these methods are only useful for monitoring exposures that occurred in the past few days.[28]

While OSHA has set the PEL for pentachlorophenol exposure at 0.5 mg/m^3, it has not developed a required medical surveillance program. Likewise, the DoD does not have specific regulations or recommendations regarding monitoring of workers exposed to pentachlorophenol.

Trichloroethylene

Forms

Like methylene chloride, trichloroethylene is a chlorinated hydrocarbon. It is a colorless liquid at room temperatures and has both a sweet odor and taste. It is fairly volatile at room temperature but nonflammable.[29]

Uses

Trichloroethylene is a solvent and is mainly used as a degreaser. It is also used as an intermediate to make other chemicals, particularly hydrofluorocarbons. Although its use is declining, trichloroethylene is also used in dry cleaning operations. Trichloroethylene can also be found in some household products, including typewriter correction fluid, paint removers, adhesives, and spot removers.[29]

Routes of Exposure

Trichloroethylene can enter the body via inhalation, ingestion, or dermal absorption. Inhalation is the major route of exposure; trichloroethylene is rapidly absorbed into systemic circulation following inhalation, with between 60% and 80% reaching the bloodstream. Although virtually all ingested trichloroethylene is absorbed by the gastrointestinal tract, this is not a common occupational route of exposure. Occupational exposure occurs in workers in the degreasing industry, as well as in those involved in trichloroethylene production or in industries using it as an intermediate.[29]

Toxicology

The toxicity associated with trichloroethylene is caused by its metabolites. Like other chlorinated hydrocarbons, trichloroethylene causes CNS and hepatic effects.[29]

Nervous system toxicity. Trichloroethylene is a CNS depressant. It causes headache, vertigo, fatigue, short-term memory loss, decreased word associations, and anesthesia. It is also associated with trigeminal neuralgia. Like other solvents, trichloroethylene is implicated in sensorineural hearing loss, especially in settings of noise exposure.[29]

Hepatic toxicity. Liver dysfunction has been noted in workers exposed to trichloroethylene. It causes acute, reversible hepatitis and fatty liver infiltrates.[29]

Degreaser’s flush. Exposure to trichloroethylene and alcohol can lead to alcohol intolerance and potentiation of the trichloroethylene’s effects. This presents as transient redness or flushing affecting the face and neck.

Medical Surveillance

Biological monitoring for exposure to trichloroethylene is possible by measuring levels of the compound or its metabolites in exhaled air, blood, or urine. However, metabolites of trichloroethylene may also come from other sources; they are not specific to trichloroethylene exposure alone.[29]

While OSHA has established the PEL for trichloroethylene exposure at 100 ppm, it has not developed a required medical surveillance program. Likewise, the DoD does not have specific regulations or recommendations regarding monitoring of workers exposed to trichloroethylene.

INORGANIC OR ELEMENTAL EXPOSURES

Asbestos

Forms

Asbestos is the generic name given to a group of hydrated mineral silicates that occur naturally in the environment. There are two classes of asbestos, serpentine and amphibole. The most common forms used in the United States are amosite and crocidolite (amphiboles) and chrysotile (serpentine), with chrysotile making up the majority of asbestos use. All forms of asbestos are toxic, but amphibole forms of asbestos are considered to be more hazardous.[30]

Uses

Asbestos was once used widely for its insulation and fire-resistant properties. It was used in building insulation, floor and ceiling tiles, and ship-building, but its use is currently less than one-tenth of the amount consumed during the 1970s. Despite its decline, asbestos is still used in roofing products, gaskets, and friction products (such as automobile clutches, brakes, and transmission components).[30]

Routes of Exposure

Most asbestos uptake occurs via inhalation. The deposition and fate of the fiber in the lungs is largely dependent on its diameter and length. Fibers with larger diameters cannot penetrate the peripheral lung, while smaller diameter fibers can infiltrate to the pleural surface. Likewise, shorter fibers can be completely phagocytized and removed from lung by a mucociliary clearance mechanism, while longer fibers are incompletely ingested and become trapped in the alveoli.[30]

After ingestion, the majority of asbestos fibers are excreted within a few days. A small number penetrate and become embedded along the gastrointestinal tract, but very few will be fully absorbed. Similarly, while asbestos fibers can penetrate the skin, it has never been demonstrated that they can subsequently enter the bloodstream.[30]

Since asbestos is a naturally occurring product found in vermiculite and talc, persons using or exposed to these products, such as miners or gardeners, may be subject to asbestos exposure. Custodial, insulation, maintenance, and asbestos abatement workers who make repairs at installations with old buildings containing asbestos may also be exposed.

Toxicology

Because most exposure results from inhalation and absorbed asbestos stays isolated within the respiratory tract, the toxic effects of asbestos target the lungs. No acute toxic effects have been reported following exposure; rather, a latency period of 10 to 20 years is typical between exposure and development of clinical signs of early disease.[7]

Asbestosis. Workers who get asbestosis following asbestos exposure develop a diffuse interstitial pulmonary fibrosis that takes between 20 and 40 years to develop. It results from a slow build-up of scar-like tissue along the lung. Fibrotic pleural changes and calcification also occur, and pulmonary function may be restricted. Studies have suggested a difference in potency based on fiber morphology, but the results are inconclusive.[30] The amount of fiber present in the lung will also affect the degree of pulmonary fibrosis. The clinical examination may note fine rales, finger clubbing, dyspnea, dry cough, and cyanosis. The chest x-ray shows granular changes, chiefly in the lower lung fields starting 20 to 40 years after first exposure. Unfortunately, asbestosis continues to progress, even after exposure to asbestos has ceased.[30]

Pleural plaques. Workers exposed to asbestos will often develop pleural plaques. Pleural plaques are almost always asymptomatic, but there may be a small but significant reduction in lung volume. Pleural plaques serve as a marker of asbestos exposure and are associated with an increased risk for developing other asbestos-related lung disease. They are visible on standard radiographs, especially if calcified. They are not premalignant and do not require treatment.[30]

Cancer. Bronchogenic carcinoma and mesothelioma are causally associated with asbestos exposure. There is also some evidence that asbestos increases the risk of cancer in the stomach, intestines, esophagus, pancreas, and kidneys.[30]

Mesothelioma is a cancer of the pleural lining. These tumors are relatively rare in the general population but are often observed in asbestos workers. Dyspnea and chest wall pain are the most common presenting symptoms. Fatigue, fever, sweats, and weight loss are other associated symptoms. Patients may be asymptomatic, however, with only a pleural effusion as an incidental finding on chest x-ray.[30]

Cigarette smoking is strongly implicated as a co-carcinogen among asbestos workers. The incidence of lung carcinoma is much higher in asbestos workers who smoke. Cigarette-smoking asbestos workers have approximately 15 times the risk of developing lung cancer compared with nonsmoking asbestos workers. There are several proposed mechanisms for this synergism. One theory is that asbestos attracts pulmonary alveolar macrophages, which then metabolize polycyclic hydrocarbons into carcinogens. Another theory is the asbestos fibers absorb and concentrate the carcinogens in tobacco smoke and then slowly release them into the lung.7,30

Medical Surveillance

OSHA requires medical monitoring of persons with potential for asbestos exposure at or above the OSHA PEL of 0.1 fiber/cm^3 as an 8-hour time weighted average.[31] The OSHA regulation requires an annual exam, as well as a baseline and termination exam. The exams must include a medical and work history using a standardized questionnaire; a complete physical examination of all systems with emphasis on the respiratory system, the cardiovascular system, and digestive tract; a chest x-ray; and pulmonary function tests.[9] The DoD requirements for medical surveillance align with the OSHA regulations.[31]

Crystalline Silica

Forms

Silica refers to the chemical compound silicon dioxide. Silicon dioxide is found in either crystalline or noncrystalline amorphous form. Crystalline silica can be found in multiple forms, with the most abundant naturally found form being quartz. Quartz exists as colorless, odorless crystals.[32]

Uses

Crystalline silica is a component of sand, stone, rock, concrete, brick, block, and mortar, as well as of nearly every mineral deposit. Industrial silica is used in glass-making, foundry work, metallurgy, abrasive work, fillers, ceramics, water filtration, petroleum manufacture, gravel, and recreational sand.32–34

Routes of Exposure

Silica can be ingested or inhaled. Ingested silica is virtually nontoxic except at extremely high quantities. However, silica dust is easily inhaled and lodged in the airways.

Occupational exposure to crystalline silica often occurs in operations involving cutting, sawing, drilling, and crushing of concrete, brick, rock, and stone products. Processes historically associated with increased silica exposure include sandblasting, sand-casting foundry operations, mining, tunneling, cement cutting and demolition, masonry work, and granite cutting.32–34

Toxicology

Silica particles are engulfed by macrophages, leading to cytokine release, fibroblast proliferation, and collagen production. This process results in the formation of silicotic nodules and fibrosis.[32]

Silicosis. Workers exposed to crystalline silica can develop silicosis, a disabling, progressive, and sometimes fatal pulmonary disease that includes fibrosis and development of lung nodules. Silicosis onset can be extremely rapid at high doses of silica exposure. If exposure levels are low, onset can take 20 to 30 years. In simple silicosis, symptoms develop 10 to 30 years following exposure and include cough, dyspnea, and wheezing. There is also a progressive deterioration in pulmonary function. Early radiographic evidence of silicosis includes small opacities, 1 to 3 mm in diameter, that appear in the upper lung fields. The opacities increase in number and size as the disease progresses, and appear in the lower lung fields. Characteristic “eggshell calcifications” are seen on the chest x-rays of workers with silicosis.32–34

Exposure to high concentrations of silica over a short period in sandblasting and silica flour production has produced accelerated silicosis, a more rapidly progressive form of the disease. The symptoms are the same as those of chronic silicosis, but the clinical findings and radiological evidence develop more rapidly. In acute silicosis, the lungs on x-ray have a diffuse ground-glass appearance.32–34 There is at least one instance of an acute form of silicosis developing after workers were exposed to extremely high concentrations of silica over a very short period. The workers developed progressive dyspnea, fever, cough, and weight loss, and, in the most severe cases, death occurred within 1 to 2 years.33,34

Tuberculosis. Silicosis seems to increase the risk of developing mycobacterial and fungal infections. Silica dust tends to overwhelm the macrophages and they can no longer kill tuberculosis bacilli. The progression of silicosis when tuberculosis is present is much more rapid than uncomplicated silicosis.32–34

Carcinogenicity. IARC has determined that silica is a human carcinogen. Silicosis also increases the risk of developing bronchogenic carcinoma.

Other diseases. Epidemiologic studies have shown that occupational exposure to respirable crystalline silica is associated with the development of chronic obstructive pulmonary disease, including bronchitis and emphysema. Silica also stimulates the immune system via an adjuvant mechanism to cause scleroderma.

Medical Surveillance

OSHA requires medical monitoring of persons with potential for respirable crystalline silica exposure at or above the OSHA PEL of 50 μg/m^3 as an 8-hour time weighted average on 30 or more days per year.[35] The OSHA regulation requires a baseline exam and a periodic exam at least every 3 years, or more frequently if recommended by the examiner. The exams must include a medical and work history using a standardized questionnaire; a complete physical examination of all systems with emphasis on the respiratory system; a chest x-ray (including an interpretation and classification per the International Labour Office International Classification of Radiographs of Pneumoconioses by a NIOSH-certified B reader); pulmonary function testing; and tuberculosis testing. The DoD requirements for medical surveillance align with the OSHA regulations.[35]

Tritium

Tritium is a radioisotope of hydrogen, containing one proton and two neutrons. It is also called hydrogen-3.[7]

Forms

The most commonly encountered forms of tritium are tritium gas and tritium oxide (or “heavy water”). Tritium is a gas at ambient temperature and pressure. It combines with oxygen to form a liquid called tritiated water.

Uses

Tritium is used to make self-powered lighting devices called betalights, which are now used in firearm night sights, watches, exit signs, map lights, and other devices. Tritium is also an important component in nuclear weapons. It enhances the efficiency and yield of fission in bombs in a process known as “boosting.”[7]

Routes of Exposure

Tritium is readily taken into the body via inhalation, ingestion, and dermal absorption. Skin and pulmonary absorption occur readily and are equally important as routes of entry.

Toxicology

Tritium is a beta radiation emitter. Beta particles are a charged form of ionizing radiation with moderate penetrating ability; they penetrate the skin down to the germinal layer and are a radiation hazard when internalized. They contain enough energy to alter structures with which they collide, and hence, are potential mutagens or carcinogens. The beta radiation emitted during tritium decay is very weak (6 keV), but produces essentially whole-body radiation injury because of the distribution of heavy water.[7]

Medical Surveillance

Workers routinely exposed to tritium should be enrolled in a medical surveillance program and are normally required to submit periodic urine samples for bioassay. The sampling frequency is determined based on the exposure potential and may be daily, weekly, monthly, or a longer interval.

Urine bioassay samples are required after each exposure incident as well. The urine bioassay should be collected 1 to 2 hours after exposure, and the worker should empty their bladder. The sampling protocol is located in Army Public Health Command Technical Guide 211, Radiobioassay Collection Labeling and Shipping Requirements.[36] A sample taken 2 hours after exposure should be reasonably representative of the body water concentration. An early sample may still be useful to confirm tritium exposure.

Tritium-labeled molecules can be found in the skin due to contact with metal surfaces contaminated with HT. These molecules, which interact with organic hydrogen, have a longer half-life in the body than tritium oxide. Airborne metal tritides may be taken into the lungs and then slowly released into the blood. When this is the case, medical surveillance should carefully follow the elimination data and look for organically bound tritium in the urine.[37] The results of the bioassay measurements should be documented in the health record and shared with the worker, like other medical surveillance results.

White Phosphorus

Forms

White phosphorus is a waxy solid with a garlic-like smell. It is white in its pure form, but commercial white phosphorus is usually yellow. It is spontaneously combusts at temperatures l0° to 15° above room temperature.[38] Because of its high reactivity with oxygen, white phosphorus is generally stored under water.

Uses

White phosphorus is used in the production of phosphoric acid and other phosphates, which are used in fertilizers, food and drink additives, industrial cleaning compounds, and waste and water treatments. It is also used as a rat and roach poison and a component in fireworks. In the military, white phosphorus is used in incendiary mortar and artillery shells and grenades. When ammunitions containing white phosphorus are combusted, they produce smoke containing some unburnt phosphorus. In military operations, white phosphorus smoke is used as an obscurant to conceal troop movements and to identify targets or the locations of friendly forces.[38]

Routes of Exposure

White phosphorus enters the systemic circulation via ingestion. Studies in animals reveal that it is almost fully absorbed through the gastrointestinal tract. While white phosphorus and its smoke can be inhaled, there is no evidence that it penetrates through the respiratory tract. Its inhalation effects result from local contact with the particles. There is no evidence that white phosphorus can be dermally absorbed.[38]

Occupational exposure occurs in persons who work in phosphorus production or in industries using phosphorus, such as grain fumigation and other previously mentioned uses. Military personnel handling munitions or involved in warfare may also be exposed. Non-occupational exposure can occur in persons who live near white phosphorus production sites and artillery training sites. White phosphorus can also bioaccumulate slightly in fish and waterfowl, so people can be exposed by eating contaminated game or fish.[38]

Inhalational exposure. Inhalation of white phosphorus or white phosphorus smoke results in respiratory tract irritation, leading to cough and laryngitis at low levels, and wheezing, dyspnea, and pneumonia at high levels. Chronic inhalation exposure can result in “phossy jaw,” a progressive degeneration or necrosis of the soft tissue, teeth, and bones of the oral cavity, particularly the maxilla and mandible. The condition is thought to be caused by the direct effects of white phosphorus contact. The presenting symptoms are toothache and increased salivation, and the oral mucosa becomes red and dull. This is followed by tooth loss from bone degeneration, poor healing of the resulting socket, and infection.[38]

Oral exposure. Ingestion of white phosphorus results in gastrointestinal, hepatic, renal, and musculoskeletal effects. In severe cases, ingestion can result in death. The earliest effect of white phosphorus ingestion, beginning within hours of exposure, is vomiting. Other gastrointestinal effects include abdominal pain and cramping. These symptoms are caused by local irritation of white phosphorus on the gastrointestinal mucosa. Hepatic dysfunction and injury occur in most persons following ingestion. Signs and symptoms include jaundice, hepatomegaly, and elevated bilirubin and liver-associated enzymes. Liver biopsies reveal necrosis, degeneration, fibrosis, hemorrhages, and fatty infiltration. White phosphorus is a renal toxin. After ingestion, the following renal effects have been detected in patients: proteinuria, albuminuria uremia, and oliguria. There are two possible mechanisms of the renal insufficiency, direct injury to the kidney or fluid loss and shock resulting in acute tubular necrosis. “Phossy jaw” is also a result of white phosphorus ingestion.[38]

Dermal exposure. Dermal exposure to white phosphorus can result in a second- or third-degree burn. White phosphorus damages the skin via corrosion and heat. It is also oxidized into a hygroscopic metabolite that further damages the skin.[38]

Medical Surveillance

Currently there are no biomarkers to indicate whether a person has been exposed to white phosphorus. While OSHA has set the PEL for white phosphorus at 0.1 mg/m^3, it has not developed a required medical surveillance program. Likewise, the DoD does not have specific regulations or recommendations regarding monitoring of workers exposed to white phosphorus.

SUMMARY

Military members have the potential to face a greater number and variety of exposures, both “traditional” occupational hazards as well as those encountered in combat zones. As described, these exposures can occur via multiple routes and can result in acute and chronic illnesses, thereby impacting both immediate missions and long-term operations. By recognizing all possible hazards, persons who may be at risk, and how the toxicities manifest, military commanders can mitigate or even prevent their effects.

ADDITIONAL RESOURCES

Copies of the various standards or recommendations regarding exposure levels can be obtained by contacting the following agencies:

- Permissible Exposure Levels (PELs)
The OSHA standards are available for public access at https://www.osha.gov/dsg/annotated-pels.

- Threshold Limit Values (TLVs)
Copies of ACGIH recommendations can be purchased by calling ACGIH at 513-742-2020 and referencing Publication #0113 or Publication #0114. They can also be ordered online at http://www.acgih.org.

- Recommended Exposure Levels (RELs)
The NIOSH guidelines can be accessed online at http://www.cdc.gov/niosh/npg/. Hard copies or CD-ROM versions can be ordered by at the NIOSH website.

- Workplace Environmental Exposure Levels (WEELs)
The AIHA recommendations can be accessed at https://www.aiha.org/get-involved/AIHAGuidelineFoundation/WEELs.

REFERENCES

1.   Occupational Safety and Health Administration. OSHA at-a-glance. https://www.osha.gov/Publications/3439at-a-glance.pdf. Published July 1, 2011. Accessed May 4, 2017.

2.   29 CFR, Part 1910.1000, Air contaminants, 1993.

3.   American Conference of Governmental Industrial Hygienists. Statement of position regarding the TLVs and BEIs. http://www.acgih.org/TLV/PosStmt.htm. Published March 1, 2002. Accessed May 4, 2017.

4.   National Institute of Occupational Safety and Health. Factsheet. NIOSH publication no. 2013-140. http://www.cdc.gov/niosh/docs/2013-140/pdfs/2013-140.pdf. Published October 2015. Accessed May 4, 2017.

5.   Anna DH, ed. The Occupational Environment: Its Evaluation, Control, and Management. Fairfax, VA: American Industrial Hygiene Association; 2011.

6.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Arsenic. Atlanta, GA: US Department of Health and Human Services; 2007. https://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=22&tid=3. Accessed June 15, 2017.

7.   Klaasen CD, ed. Casarett and Doull’s Toxicology: The Basic Science of Poisons. 8th ed. New York, NY: McGraw-Hill Companies; 2013.

8.   US Department of Defense. Occupational Medical Examinations and Surveillance Manual. Washington, DC: DoD; 2008. DoD 6055.05-M.

9.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Cadmium. Atlanta, GA: US Department of Health and Human Services; 2012.

10.   29 CFR, Part 1910.1027, Cadmium.

11.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Chromium. Atlanta, GA: US Department of Health and Human Services; 2012.

12.   29 CFR, Part 1910.1026, Hexavalent chromium.

13.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Cyanide. Atlanta, GA: US Department of Health and Human Services; 2006.

14.   National Toxicology Program. Report on Carcinogens. 14th ed. Research Triangle Park, NC: US Department of Health and Human Services, Public Health Service; 2016. http://ntp.niehs.nih.gov/go/roc14. Published November 3, 2016. Accessed June 16, 2017.

15.   Lipsett M, Campleman S. Occupational exposure to diesel exhaust and lung cancer: a meta-analysis. Am J Public Health. 1999;80(7):1009–1017.

16.   Masiol M, Mallon TM, Haines KM, Utell MJ, Hopke PK. Airborne dioxins, furans, and polycyclic aromatic hydrocarbons exposure to military personnel in Iraq. J Occup Environ Med. 2016;58:S22–S30.

17.   Blasch KW, Kolivosky JE, Heller JM. Environmental air sampling near burn pit and incinerator operations at Bagram Airfield, Afghanistan. J Occup Environ Med. 2016;58:S38–S43.

18.   Walker DI, Mallon TM, Hopke PK, et al. Deployment-associated exposure surveillance with high-resolution metabolomics. J Occup Environ Med. 2016;58:S12–S21.

19.   Woeller CF, Thatcher TH, Twist DV, et al. Detection of serum microRNAs from Department of Defense Serum Repository: correlation with cotinine, cytokine, and polycyclic aromatic hydrocarbon levels. J Occup Environ Med. 2016;58:S62–S71.

20.   Bello D, Woskie S, Streicher R, et al. Polyisocyanates in occupational environments: a critical review of exposure limits and metrics. Am J Indus Med. 2004;46:480–491.

21.   Occupational Safety and Health Administration. National Emphasis Program–Occupational Exposure to Isocyanates. Washington, DC: OSHA; 2013. CPL 03-00-017. https://www.osha.gov/OshDoc/Directive_pdf/CPL_03-00-017.pdf. Accessed May 4, 2017.

22.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Methylene Chloride. Atlanta, GA: US Department of Health and Human Services; 2000.

23.   29 CFR, Part 1910.1052, Methylene chloride.

24.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for 2-Butanone (MEK). Atlanta, GA: US Department of Health and Human Services; 2010.

25.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Sulfur Mustard. Atlanta, GA: US Department of Health and Human Services; 2003.

26.   US Department of the Army. Occupational Health Guidelines for the Evaluation and Control of Occupational Exposure to Mustard Agents H, HD, and HT. Washington, DC: DA; 2003. DA PAM 40-173.

27.   Agency for Toxic Substances and Disease Registry. Medical Management Guidelines for Nerve Agents: Tabun (GA); Sarin (GB); Soman (GD); and VX. Atlanta, GA: US Department of Health and Human Services; 2001.

28.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Pentachlorophenol. Atlanta, GA: US Department of Health and Human Services; 2001.

29.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Trichloroethylene. Atlanta, GA: US Department of Health and Human Services; 1997.

30.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for Asbestos. Atlanta, GA: US Department of Health and Human Services; 2001. https://www.atsdr.cdc.gov/toxprofiles/TP.asp?id=30&tid=4 Published September 2001. Accessed June 15, 2017.

31.   29 CFR, Part 1910.1001, Asbestos.

32.   Silica dust, crystalline, in the form of quartz or cristobalite. IARC Monogr Eval Carcinog Risks Hum. 2012;100C:355–405.

33.   National Institute for Occupational Safety and Health. NIOSH Hazard Review: Health Effects of Occupational Exposure to Respirable Crystalline Silica. Washington, DC: Department of Health and Human Services; 2002. NIOSH publication no. 2002-129. http://www.cdc.gov/niosh/docs/2002-129/pdfs/2002-129.pdf. Accessed May 4, 2017.

34.   Occupational Safety and Health Administration. National Emphasis Program–Crystalline Silica. Washington, DC: OSHA: 2008. CPL 03-00-007. https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=DIRECTIVES&p_id=3790#g. Accessed May 4, 2017.

35.   29 CFR, Part 1910.1053, Respirable crystalline silica.

36.   US Army Public Health Command. Radiobioassay Collection Labeling and Shipping Requirements. Aberdeen Proving Ground, MD: USAPHC; 2012. Technical Guide 211.

37.   US Department Of Energy. Primer on Tritium Safe Handling Practices. Washington, DC: DOE; 1994. DOE-HDBK-1079-94. https://energy.gov/sites/prod/files/2013/09/f2/hdbk1079.pdf. Accessed August 25, 2017.

38.   Agency for Toxic Substances and Disease Registry. Toxicological Profile for White Phosphorus. Atlanta, GA: US Department of Health and Human Services; 1997.

Chapter 21

OCCUPATIONAL AND ENVIRONMENTAL LEAD

CAROL I. TOBIAS, MBA, BSN*; RICHARD L. LACHIVER, MD, MPH†; AND HAN Q. BUI, MD, MPH‡

INTRODUCTION

HISTORY OF LEAD TOXICITY

MILITARY OCCUPATIONAL EXPOSURES

Paint Stripping and Welding

Firing Ranges

Electrical Soldering and Ballast Handling

ENVIRONMENTAL EXPOSURES IN THE UNITED STATES

Air

Water

Soil

ENVIRONMENTAL REGULATIONS

Drinking Water

Ambient Air

Food Contamination

Lead in Paint

OCCUPATIONAL SURVEILLANCE

TESTS FOR LEAD EXPOSURE

Blood Lead Level

Zinc Protoporphyrin

Bone Lead Measurement

Cumulative Blood Lead Index

CLINICAL IMPLICATIONS OF LEAD EXPOSURE

Effects in Children

Effects in Adults

CHELATION

CASE STUDY

SUMMARY

*Nurse Consultant, US Army Center for Public Health (Provisional), 1570 Wise Road, Building 1570, Aberdeen Proving Ground, Maryland 21010

† Formerly; Medical Director, Occupational Health Service of York Hospital, York, Pennsylvania; Major, US Army; Program Manager for Occupational Medicine and Residency Training Director, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland

‡ Commander, Medical Corps, US Navy; Chief, Occupational and Environmental Medicine, Naval Health Clinic Quantico, 3259 Catilin Avenue, Quantico, Virginia 22134

INTRODUCTION

This chapter is an update to Chapter 12, Lead, in the previous edition of this book.[1] Much of the chapter has been revised to reflect new policies related to workplace exposure limits. The references have been updated as well. This chapter recognizes efforts by the National Institute for Occupational Safety and Health (NIOSH) to review research on occupational lead exposures that noted health effects at levels half of the current permissible exposure limit (PEL), as well as Army efforts to lower the military exposure guideline to one-half of the current PEL. The US Environmental Protection Agency (EPA) initiated efforts to lower the current childhood exposure limit (10 μg/dL) based on new research that shows significant health effects occur at levels well below the limit. It is important for occupational health providers to be aware of the research basis for the proposed changes to lower workplace and environmental exposure limits.

Lead occurs naturally on Earth. The properties of lead make it very useful in commercial applications: it shields workers from radiation, resists corrosion, melts easily at low temperatures, and hardens quickly. Lead is a poor conductor of electricity and is extremely malleable, which makes it desirable in manufacturing and other job applications. However, lead exposure can lead to short- and long-term adverse health effects, so workers and young children with elevated biological indices should be monitored over time to detect any health effects. Lead can be ingested or inhaled, and air containing lead fumes or dust can lead to overexposure in unprotected workers. Medical surveillance for exposed workers should include monitoring of blood lead, zinc protoporphyrin (ZPP), and bone lead levels.

Public health measures including education and product substitution of lead for safer alternatives will reduce the average blood lead level (BLL) in the general population over time. Safety and occupational health professionals must lead the way by ensuring safer substitutes are found and safer work practices and administrative controls are adopted. Some manufacturing practices, such as lead recycling, can lead to increased industrial exposures. Lead exposures are also continuing in military applications where no substitutes for lead have been found, such as in the primer of explosive charges for ammunition. On many older military bases, lead leaches out of corroded pipes, causing drinking water contamination. Because military equipment, supplies, and training techniques have not completely substituted for lead or engineered around exposures, it is imperative that occupational and environmental medicine professionals be aware of the continued lead hazard.

HISTORY OF LEAD TOXICITY

Based on archeological and written evidence, Greeks and Romans were aware that lead had many useful properties but was toxic to humans. It is not clear how much they knew and to what extent they went to prevent lead exposures in the general population. Hippocrates was probably the first to report “lead colic” (spasmodic and recurrent episodes of abdominal pain), in 370 BCE, and Nicander described similar effects in the 2nd and 1st centuries BCE. These early healers gave no indication they understood how exposures occurred or how the disease could have been averted. Reports from the 1st century ce document that the historian Pliny the Elder warned mariners to protect themselves when painting their ships: “Cover yourselves with … animal bladder … lest you inhale this pernicious dust.”[2]

Pliny the Elder warned about the risks associated with lead exposure; however, it is unlikely the hazards were common knowledge because lead’s health effects take a long time to develop and often only occur after long periods of exposure. Only a few of those exposed may have suspected they were affected. Social factors played a role as well. The nobility may have surmised that, because “pernicious dust” was a problem encountered only by the working class, it did not concern them.

Lead poisoning was relatively forgotten after the collapse of the Roman Empire until the Middle Ages. Medieval Europeans may have poisoned themselves with wine contaminated with lead. Beginning in the Renaissance, rapidly expanding industrialization led to increased use of lead and corresponding increases in exposures. By the 1700s, Bernardo Ramazzini had made the connection between job, exposure type, and health effects in some trades. In particular, Ramazzini noted a high prevalence of lead exposure and lead poisoning among potters.[3]

During Prohibition, episodes of lead poisoning occurred around the country due to the consumption of illegally distilled whiskey that was contaminated with lead during the distillation process, when lead leached out of the solder in automobile radiators that were used as vapor condensers in stills.[4] Today, battery manufacturing and nonferrous metal production are two industries with the highest prevalence of lead poisoning in the United States.[5] Generally, the prevalence of lead poisoning in the US population (BLL above 25 μg/dL) is 5 per 100,000.[6]

MILITARY OCCUPATIONAL EXPOSURES

The US military has found many uses for lead. Lead musket balls and cannon balls were some of the earliest uses. Shot was produced by dropping molten lead from the top of a tall tower. As it drops, the molten lead solidifies into small spheres. Numerous historical shot towers still exist in the United States. During World War I and II, military personnel were exposed to lead in the metal of ship superstructures and on the painted surfaces of decking, walls, and overheads. After the wars, many cases of lead intoxication occurred during the large-scale disarmament of Navy ships. Lead smelting remains a common industrial operation in the private sector, and deployed soldiers in base camps situated adjacent to smelting facilities in Bosnia had high lead levels (see Chapter 6, History of Army Occupational Health, 1991–2015).

Lead is used today in munitions components, electrical solders, and ballast. Many workers at Army depots may be exposed to significant amounts of lead. Workers with the highest lead exposure levels include firing range instructors, welders, sand blasters, airline brake workers, maintenance mechanics, and pipefitters. Healthcare providers must be aware of the clinical signs and symptoms of lead poisoning. Workers exposed to lead must be enrolled in biological monitoring for blood lead as part of their ongoing medical surveillance program.

Paint Stripping and Welding

Lead is no longer permitted in paints, primarily due to the problem of environmental exposure in children through pica behaviors that involve eating chips of peeling paint on woodwork. However, large quantities of lead paint remained in the military supply system after the ban, and the Navy and other services continued to use the paint until it was depleted because of its excellent corrosion resistance in a wide range of environmental conditions, including on seagoing vessels and in the presence of chemical agents.

Healthcare personnel must be aware of the ongoing potential for lead exposure from older military hardware. This equipment is maintained at depots and will pose a risk of lead exposure as long as it continues to be used. Civilian and military personnel are commonly exposed to lead in the workplace during the removal of lead-based paint in building renovations and sheet metal work. Stripping of metal surfaces is done because (a) it is safer to weld on clean, unpainted metal; (b) equipment needs a new coat of paint; or (c) paint must be removed before equipment can be repaired.

Paint is usually stripped by spraying sand (or some other abrasive material such as bits of steel, walnut shells, or recycled plastic beads) forced from a compressed air source toward a painted target. Sand blasting and stripping paint by metal bead abrasion generates large quantities of highly respirable dust. Workers direct the flow of abrasive beads into many nooks and crannies to remove paint. Blasting the undersides of vehicles is problematic because of many hard-to-reach places, and blasters must direct their spray upward to strip the paint, causing abrasive material to be reflected back at the blaster. Even though paint strippers and sand blasters wear personal protective equipment (PPE), the abrasives that remove paint can also tear body suits if the spray reflects back. Stripping paint requires a significant amount of worker movement with bending, crouching, and stretching for prolonged periods in awkward positions, which can cause respirators to become dislodged.

Paint stripping continues to be a major source of lead exposure in the workplace. Depots now use robots to perform repetitive painting operations, but there are no robots available for paint stripping operations. Workers who handle waste material generated during the sand blasting operations are also at risk for lead exposure. At even greater risk are welders who work on metal surfaces containing lead. Welding is done at temperatures of between 1,000°C and 3,000°C. These temperatures vaporize lead,[7] and lead vapor is typically even more respirable than the dust produced by abrasive blasting.[8]

To reduce exposure to lead, education is needed to remind workers and service members that the old paint contains lead and that PPE must be worn properly. Supervisors must ensure welders wear adequate respiratory protection to keep exposure levels low. The US Coast Guard successfully implemented a lead poisoning prevention program to control lead exposures during ship maintenance. In this program, changes in paint removal work practices and equipment, and the proper use of air-line respirators, reduced BLLs by 50%.[9]

Firing Ranges

The Occupational Safety and Health Administration (OSHA) general industry lead standard was published in 1978.[10] Since then, a large body of literature on the health effects of lead has been published. In 2012 the US National Toxicology Program (NTP) released a monograph on the health effects of low-level lead exposure. The NTP defined low-level lead exposure as BLLs less than 10 μg/dL, and in some cases less than 5 μg/dL.[6] In 2013 the EPA released a final report of its Integrated Science Assessment for Lead.[11] The NTP and EPA reviews provide compelling evidence of health effects occurring at levels much lower than 10 μg/dL.

In light of the knowledge about the hazards posed by occupational lead exposure, the Department of Defense (DoD) asked the National Research Council (NRC) to evaluate potential health risks from recurrent lead exposure in firing range personnel. Specifically, NRC was asked to determine whether current exposure standards for lead on DoD firing ranges protect workers adequately. The NRC found that the OSHA PEL for lead, 50 μg/m^3, was frequently exceeded on Army, Navy, and Air Force firing ranges.[12] The NRC also reviewed the epidemiologic and toxicologic data and concluded there was overwhelming evidence that the OSHA standard provides inadequate protection for DoD firing range personnel and other worker populations covered by the lead standard.[12] The NRC recommended several engineering and administrative controls[12]:

1. Ammunition substitution. Exposure to airborne lead might be reduced by replacing traditional lead bullets with nylon-clad, copper-jacketed, zinc-based, or other forms of ammunition. Training requirements may limit the use of some ammunition, and the use of jacketed and alternative bullets may significantly increase the costs of training.

2. Improvements in range design and ventilation. The NRC recommended improving the HVAC systems in existing ranges to reduce or minimize airborne lead levels. Portable filtration units may be a cost-effective way to reduce airborne lead in indoor firing ranges.

3. Range cleaning. Housekeeping is also critically important for controlling lead contamination of surfaces in and around a shooting range. Even at ranges with good ventilation and use of ammunition with lead-free primers, poor housekeeping or failing to decontaminate a range thoroughly before switching primers may adversely affect lead exposures.[13] The Navy Environmental Health Center notes in its Indoor Firing Ranges Industrial Hygiene Technical Guide[14] that although there are no established limits for surface lead contamination in workplaces, OSHA has indicated in a compliance instruction for the construction industry that an acceptable lead load for non-lead work areas should be 200 μg/ft^2. Appendix D of the technical guide suggests clearance levels of 200 μg/ft^2 for interior floors and horizontal surfaces and 800 μg/ft^2 for exterior concrete.[14]

4. Hygiene practices. Strict adherence to OSHA recommendations for personal hygiene is critical. A cross-sectional study of 119 lead handlers in a battery recycling plant in Japan detected lead contamination on workers’ hands even after they had washed their hands or bathed.[15]

More recent investigations have demonstrated that washing with soap and water is not effective in removing lead from skin. After workers in lead acid battery plants showed significant dermal-oral lead exposures despite washing with soap and water, NIOSH researchers developed a highly (nearly 100%) effective hand wipe method for removing lead from skin, using a mixture of isostearamidopropyl morpholine lactate and citric acid applied with a textured absorbent material. It is now clear that hand decontamination, rather than washing, is required to ensure complete removal of lead.[16] Preventing hand-to-mouth exposure to lead requires skin decontamination and colorimetric testing to detect residual contamination.[16] Worker education on lead must emphasize the importance of skin decontamination rather than emphasizing hand washing alone. Further, workers should be routinely tested for qualitative lead skin contamination with a colorimetric indicator.

Electrical Soldering and Ballast Handling

Several US Army depots employ personnel who solder electrical components, which generates small amounts of lead fume. However, the actual risk of lead exposure to personnel who solder is relatively low—much lower than the risk to welders. The risk from electrical soldering is greatest where ventilation is limited, such as inside enclosed or confined spaces. The European Union banned lead use in solder for electronics in 2011.[17]

Ballast is typically bulk metallic lead. Ballast handlers, who place weight on ships and planes to improve their stability, can inhale or ingest lead dust that sloughs off. Other workers who handle bare lead face similar hazards. Although the risk of exposure from handling bulk lead is not as high as the risk associated with inhaling lead fumes, exposure controls are necessary. The risk of exposure to lead ballast can be defined through an industrial hygiene survey. Controls include use of PPE and engineering measures such as adequate ventilation.

ENVIRONMENTAL EXPOSURES IN THE UNITED STATES

Air

The 1973 banning of tetraethyl lead in gasoline led to a substantial reduction of lead in the air around major US cities. Although the ban was phased in over many years, leaded gasoline is no longer available for use in on-road vehicles in this country. However, other countries around the world have not yet implemented this change, so troops may be exposed when they deploy to combat areas or provide humanitarian assistance in these places. Lead smelters have shut down as well; only one currently operates in the United States, in Herculaneum, Missouri.

Current sources of airborne environmental lead include small airplane engines, exempted from the law, that use leaded aviation gasoline, which accounts for 50% of the US lead pollution annually.[18] Other sources of lead pollution include smelting, mining, and workplaces where welding, paint stripping, and grinding of lead-based metal alloys occur. The EPA national ambient air quality standard for lead is 1.5 μg/m^3.[19] Most inhabitants of military installations are not at risk from airborne lead pollution; base industrial activities do not generate large enough quantities of airborne lead to pose a health hazard.

Water

Lead contaminates surface and ground water through intentional dumping, unintentional deposition, or washing out of ambient air by rain. Lead can contaminate surface and ground water when it leaches out of tailings from smelting, mining, and industrial wastes, as well as when industrial wastes are deliberately discharged into sewers.

EPA has set the maximum contaminant level of lead in drinking water at 0.015 mg/L.[20] Lead can enter drinking water as a contaminant when it leaches out of lead pipes bringing water into a house or worksite. Lead was banned in pipes in the construction industry in the 1990s, but houses built in the 1980s and earlier are at increased risk of having high lead levels in the pipes. Lead is only slightly soluble in water, but heat and an acidic pH increases its solubility. Further, if the plumbing system is used as an electrical ground, the resulting slight electrical charge increases the solubility of lead in drinking water. In addition, if water stands overnight in pipes, there is time for the lead to leach out and enter the tap water.[20]

Generally, plumbing that contains lead must be replaced. When it is not possible to replace the pipes, filtered or bottled water should be utilized. If the water’s pH is acidic, neutralizing it can help prevent leaching. (These short-term fixes are intended to serve until lead-contaminated plumbing can be replaced.)

The city of Flint, Michigan, was taken over by the state and in an effort to cut costs, switched Flint’s drinking water from Lake Huron to the Flint River in 2011. Unfortunately, the state chose not to pay the $100 per day cost for anti-corrosion treatment, which allowed lead to leach from old pipes into the water supply. In some locations, lead measured 10 times greater than the EPA limit for lead in drinking water. The city directed residents to use bottled water for the past 3 years, and only this year did the lead levels in the water supply fall to acceptable levels.[21]

Soil

The EPA has identified the three main sources of lead in soil: (1) Lead-based paint on exterior surfaces of buildings can flake off and enter the soil. (2) Local industrial pollution (eg, from smelters) can generate airborne lead that enters the soil. (3) Combustion of leaded gasoline in small planes and race cars can generate airborne lead that enters the soil.[22] Soil contamination, particularly around older buildings with lead-based paint, is fairly common. Children playing in the area may ingest lead when their hands or toys come in contact with their mouths. When soil contamination is present, the soil should be removed as soon as possible. In the interim, hand wipes and hygiene stations should be provided to permit removal of lead from hands.

ENVIRONMENTAL REGULATIONS

Regulations pertaining to environmental lead include the Safe Drinking Water Act[20]; the Comprehensive Environmental Response, Compensation, and Liability Act[23]; and the Clean Air Act.[24] These regulations cover exposure to lead from many sources including drinking water, air, food, and consumer items such as paint. The Resource Conservation Recovery Act covers the proper handling, storage, and disposal of lead.[25] Military preventive medicine specialists are responsible for the occupational and environmental health of the installation population. They ensure the post’s drinking water is safe; that post buildings including housing and daycare facilities are lead free; and that hazardous waste is handled properly. These specialists know the EPA and OSHA regulations pertaining to lead and work to ensure compliance and minimize lead exposures.

Drinking Water

The EPA regulates lead in drinking water and has proposed the long-term goal of zero lead in drinking water. The current lead regulations state that lead solder cannot be used in plumbing joints. Furthermore, the public must be notified if drinking water is contaminated with lead.

Ambient Air

The EPA used the Clean Air Act to require the complete phase-out of lead in gasoline, and a substantial reduction of airborne lead has been achieved. Currently, the law permits no more than 1.5 μg/m^3 of lead in the air.[24] The reduction of lead in ambient air has markedly reduced the levels of lead in soil and surface water as well.

Food Contamination

Lead can contaminate food and drink. The Food and Drug Administration (FDA) recognized that food packaged in tin cans sealed with lead solder can become contaminated when the lead in the solder leaches into the food, particularly if the food is acidic.[26] Additionally, glaze used in the production of imported ceramic pottery occasionally contains lead, and if the pottery is used in meal production, food can become contaminated.[26] The FDA has focused on lowering lead content in canned foods and controlling the entry of contaminated pottery and pesticides into the United States.[26] In July 2010, the FDA examined foods for lead content and found that some commercial juice and food products contain lead, but the levels were below the FDA-allowable levels of 6 μg for children under age six, 25 μg for pregnant women, and 75 μg for other adults.[27]

Lead in Paint

The Consumer Product Safety Improvement Act of 2008 (Public Law 110-314) lowered the acceptable concentration of lead in paint from 0.06%, or 600 ppm, to 0.009%, or 90 ppm.[28] The Department of Housing and Urban Development has developed guidelines on lead abatement in homes, which apply to on-base housing and other buildings such as childcare centers that contain lead-based paint.[29] Base environmental engineers and preventive medicine personnel must become familiar with these guidelines to ensure compliance with changes in the law.

OCCUPATIONAL SURVEILLANCE

OSHA mandates that when the BLL is over 60 μg/dL, the individual requires medical management and medical removal from ongoing exposure at work.[10] For these individuals, the BLL should be checked monthly until the BLLs have returned to background levels. The regulations allow return to work when BLLs fall below 40 μg/dL.[10] The Centers for Disease Control and Prevention’s state-based Adult Blood Lead Epidemiology and Surveillance program tracks laboratory-reported elevated BLLs. Data from 40 state programs was collected and analyzed in 2008 and 2009. When the prevalence rate in 2009 was compared to the prevalence rate in 1994, a drop of 7.7 cases per 100,000 was observed.[30] Workers in battery manufacturing, smelting, refining of nonferrous metals, painting, and paper hanging had the greatest number of exposures.[30] Additionally, people who shoot firearms and pack their own ammunition can be exposed to lead, and those who remodel and paint their own homes can run into difficulties with lead-based paint exposure. People who have been shot and retain fragments of the round in their bodies may be lead exposed as well.[30]

The California Department of Public Health requires all laboratories performing lead analyses on blood samples in California to report all results to the department. The department’s Occupational Lead Poisoning Prevention Program collects and analyzes test results for adults (age 16 years and over) and enters the data into the California Occupational Blood Lead Registry.[31] This information is used to assist in lead poisoning prevention efforts. The data from the California registry from 2008 to 2011 showed that 10% of workers tested have BLLs above 10 μg /dL.[31] The BLL distribution for workers varied significantly by industry. Of those with BLL elevations, 58% of workers worked in manufacturing, 17% worked in construction, 5% worked in demolition, 4% worked in lead remediation, and 23% worked in other industries.[31] Storage battery manufacture including smelting during battery recycling had much higher percentages of workers with BLLs above 10 μg/dL than other industries.[31]

TESTS FOR LEAD EXPOSURE

Blood Lead Level

The BLL, which shows the amount of lead present in the blood, is the most frequently used test in lead medical surveillance. Lead has a half-life of 36 days in the blood.32,33 Lead is rapidly deposited in mineralizing tissues and tends to accumulate in bone regions undergoing the most active calcification at the time of exposure.6,34,35 BLLs can rise when bone is resorbed due to advanced age, broken bones, chronic disease, hyperthyroidism, kidney disease, menopause, osteoporosis, physiologic stress, pregnancy, and breastfeeding. Calcium deficiency worsens the bone-to-blood mobilization of lead.6,34,35 The average US adult BLL is about 1.2 μg/dL.[30] A BLL over this baseline should be considered a sentinel event indicating a possible breakdown in workplace exposure controls.[30]

The Reference Chemistry Laboratory at the Department of Pathology and Area Laboratory Services at Ft Sam Houston, Joint Base San Antonio, performs the majority of BLL tests for Army medical treatment facilities. The laboratory reports elevated BBLs to the ordering physician, who contacts the patient regarding medical follow-up. The laboratory also notifies the preventive medicine department, which notifies the state public health office and assists in the investigation into the cause of the elevated BLLs.

For women who are pregnant or lactating, BLLs should be under 5 μg/dL. For everyone else, if the BLL is less than 10, no action is required. If the BLL is greater than 10 but less than 20, the individual should be counselled about the increased health risk of cardiovascular, renal, reproductive, and neurological disease.[36]

Zinc Protoporphyrin

The ZPP test, which measures the effect of lead on hemoglobin synthesis, should be obtained at the same time a BLL is ordered. ZPP is formed after free erythrocyte protoporphyrin (FEP) builds up in red blood cells when lead inhibits the enzyme ferrochelatase. Ferrochelatase catalyzes the insertion of a ferrous ion into protoporphyrin IX to form heme. If it is inhibited by lead, the protoporphyrin IX incorporates a zinc ion instead of a ferrous ion, producing ZPP.37,38

ZPP elevations in both acute and chronic exposure scenarios lag behind elevations in BLL by 8 to 12 weeks.37,38 ZPP, when ordered together with BLL, provides useful clinical information on the duration of lead exposure because ZPP rises gradually over 8 to 12 weeks, and then drops off, while the BLL rises immediately. ZPP levels remain elevated in chronic exposure cases. In acute exposure cases when exposure stops, BLL drops off fairly quickly. Combined elevations in BLL and ZPP suggest that lead exposure began 8 to 12 weeks earlier or the individual has been chronically exposed to lead.37,38 However, there is large variability in ZPP measurements and poor sensitivity at low lead exposure levels.37,38

Because of the limitations of the BLL at low lead levels, healthcare providers should consider requesting a complete blood count to look for evidence of basophilic stippling in red blood cells as early evidence of exposure when lead exposure levels are low or the lead exposure is suspected but not well documented.

Bone Lead Measurement

Lead is either excreted in the urine or stored in bone.6,34,35,39 Skeletal bone contains approximately 95% of the lead body burden.[39] Blood lead has a half-life of about 35 days, so bone lead may be a better measure of the total lead burden.6,34,35,39

Bone lead is a measured by noninvasive x-ray fluorescence testing. The detector causes fluoresce in the lead atom and emission of x-rays that are proportional to the amount of lead present in bone.40,41 The x-ray florescence produces low-level radiation and takes 30 minutes.40,41 Unfortunately, x-ray fluorescence testing is available only at a few US research centers. Efforts are underway to develop a portable system capable of quickly measuring bone lead in a few minutes.[41]

Cumulative Blood Lead Index

Because of the dearth of x-ray fluorescence equipment, BLLs will remain the mainstay of biological monitoring for lead-exposed workers for the foreseeable future. The cumulative blood lead index (CBLI) is a measure of chronic lead exposure that can be calculated by multiplying the average BLL by the number of years of exposure. This measure may be helpful in determining how long chelation therapy might be needed in patients chronically exposed to lead.[33]

CLINICAL IMPLICATIONS OF LEAD EXPOSURE

When lead enters the body it serves no useful purpose. Toxic effects can occur, regardless of age, gender, or exposure pathway.

Effects in Children

In children, lead prevents the uptake of iron, zinc, and calcium, which are essential minerals needed for brain and nerve development. Often children show no signs of lead toxicity until the end of elementary school. Lead affects the nervous system more than any other organ system, and has been shown to cause behavioral problems and attention deficit hyperactivity disorder (ADHD). Acute exposures causing high BLLs (between 70 and 80 μg/dL) may produce encephalopathy and accompanying signs of ataxia, convulsions, hyperirritability, stupor, coma, and even death. These levels also produce long-term neurological and behavioral changes.6,34,35 Childhood lead poisoning increases the risk of delayed learning, lower IQ, hypertension, renal failure, and reproductive problems later in life. Even children with BLLs less than 5 μg/dL have been shown to have behavioral problems, an increased risk of ADHD, and decreased cognitive performance based on lower IQ, academic achievement, and specific cognitive measures.6,34,35

Effects in Adults

In adults lead can cause signs and symptoms of exposure that include high blood pressure, joint and muscle pain, difficulties with memory or concentration, headache, abdominal pain, mood disorders, and problems in pregnancy. Lead can cause hypertension in both men and women and causes lower sperm counts in men.[6] Research has also shown that BLLs of 5 μg/dL have reduced renal function and that BLLs of 10 μg/dL have caused hypertension.6,34,35

Pregnancy

Sufficient evidence shows that maternal BLLs under 5 μg/dL are associated with reduced fetal growth or lower birth weight.6,34,35 Maternal BLLs may be important predictors of the risk of developing eclampsia and preeclampsia.6,34,35 There is also sufficient evidence showing that BLLs under 5 μg/dL are associated with decreased renal function, and that BLLs under 10 μg/dL are associated with increased blood pressure and hypertension during pregnancy.6,34,35

The risk for spontaneous abortion is elevated at lead levels between 40 and 60 μg/dL. A prospective cohort study of pregnant women in Mexico City noted a statistically significant dose-response relationship between maternal BLLs and risk for spontaneous abortion at BLLs between 0 and 30 μg/dL.6,34,35 There is also limited evidence that maternal BLLs less than 10 μg/dL are associated with preterm birth and spontaneous abortion.6,34,35

Neurological Effects

Lead can cause neuropathy and encephalopathy at extremely high BLLs (over 80 μg/dL). Lead exposure can cause brain damage and problems with cognition, decision-making, and executive functioning. Lead-exposed adults have had problems with aggressive behavior and difficulties with fine motor control. Lower IQ, neuropsychological defects, and reduced hearing have been documented at BLLs less than 10 μg/dL.6,34,35

Renal Effects

Lead exposure was found to be strongly associated with renal effects in several studies.6,34,35 Lead exposure in childhood has been observed to cause chronic renal disease and reduced renal function in adults who were exposed at high levels. BLLs of 1.5 μg/dL in children resulted in reduced kidney function in adolescents.6,34,35 The glomular filtration rate (GFR) was reduced in adults who were exposed to high lead levels in childhood, and reduced GFR was found to be a risk factor for chronic renal failure. BLLs less than 5 μg/dL have been associated with both decreased GFR and chronic kidney disease.6,34,35 BLLs less than 10 μg/dL in childhood have been associated with hypertension in adults. Repetitive lead exposures can cause chronic and irreversible chronic interstitial nephritis.6,34,35

Hematological Effects

Lead causes both anemia and basophilic stippling of red blood cells.31,32 High lead levels can cause hemolytic anemia by decreasing red blood cell survival. Chronic lead poisoning can also cause hypochromic, normochromic, normocytic, or microcytic anemia.32,33

Endocrine Effects

High BLLs have been found to lower vitamin D levels and stop the conversion of vitamin D to 1,25-dihydroxycholecalciferol, which regulates calcium homeostasis. Lower 1,25-dihydroxycholecalciferol levels impair cell growth and tooth and bone development.6,34,35

Gastrointestinal Effects

Children and adults who have been exposed to lead may present with severe cramping and abdominal pain. The pain may be mistaken for an acute abdomen or appendicitis. Individuals with chronic lead poisoning often have chronic constipation as well.6,34,35

Cardiovascular Effects

Lead exposure is associated with the development of hypertension. Studies of people with BLLs of 40 to 60 μg/dL seen in the occupational setting show an increased risk of hypertensive heart disease and cerebrovascular disease in later life.6,34,35 More recent studies noted an association with BLLs less than 10 μg/dL and hypertension.6,34,35

CHELATION

Chelation, which is the binding of lead to a binding agent, is the usual treatment for lead poisoning when BLLs are extremely high.36,42 The FDA has approved the oral chelation agent 2,3-dimercaptosuccinic acid (DMSA), also known as succimer, for the treatment of lead poisoning in children. DMSA has also been found to be effective in treating lead poisoning in adults.36,42 The baseline laboratory tests should include BLL, ZPP, complete blood count, neutrophil count, complete metabolic panel, and urinalysis to check for protein.[42] When BLLs are greater than 100 μg/dL, chelation should be performed in the intensive care unit, where individuals can be closely monitored. Individuals whose BLLs are between 80 and 100 μg/dL should be offered chelation if they are exhibiting symptoms of lead poisoning.6,34–36 Chelation should be deferred until the absolute neutrophil count is above 1,200.

The recommended adult dosing of DMSA is 500 mg three times a day for 5 days, followed by 500 mg twice a day for 14 days. On day 6 and 20, the BLL, ZPP, complete blood count, complete metabolic panel, and urinalysis should be repeated.[42] The most common side effects of chelation therapy are gastrointestinal symptoms, nausea, transient rash, elevated liver transaminase enzymes, and neutropenia.

Calcium ethylenediaminetetraacetatic acid (EDTA), which increases renal excretion of lead, is clinically indicated when BLL is above 80 μg/dL and is administered as an alternative to DMSA by intravenous or intramuscular injection for 3 to 5 days. Treatment with calcium EDTA should be performed in an intensive care setting to monitor for and manage side effects.6,34,35 The major site of potential toxicity is the kidney. Tubular necrosis is dose related, reversible, and associated with hematuria and proteinuria. Adequate hydration is important. Adverse side effects include hypotension and cardiac rhythm changes, including bradycardia, atrial-ventricular block, and ventricular dysrhythmias. Electrocardiograms must be monitored for the development of arrhythmias during infusion. The baseline laboratory tests BLL, ZPP, complete blood count, and complete metabolic panel should be repeated on day 3 and 5 of the treatment.6,34,35

CASE STUDY

A 33-year-old male active duty service member who immigrated to the United States in his early 20s developed acute abdominal pain while on a 2-week training mission. He was admitted to a local hospital and had a full workup that showed elevated lipase, amylase, and anemia. He was diagnosed clinically with pancreatitis. Over the next month he continued to have abdominal pain and experienced a 40-pound weight loss. He began to notice “bone pain” in his upper and lower extremities, fatigue, and insomnia. He was referred to hematology for evaluation of his anemia. Because of significant basophilic stippling, a BLL was ordered, which came back highly elevated: over 100 μg/dL. His ZPP was also markedly elevated, at over 400 μg/dL, which indicated chronic lead exposure. His personal history included a significant childhood exposure to construction sites in his country of origin. After coming to the United States, he worked for several more years in the construction industry. Lead is not considered an exposure hazard in his military occupational series.

The service member was admitted to a medical treatment facility and received lead chelation therapy in an inpatient setting. He was then followed as an outpatient for many months. Six months after presentation, his blood lead remained above 50 μg/dL. Even with this significant elevation, he had returned to full duty, was running nearly 15 miles per week, and had passed his physical training test. Ultimately the consulting occupational medicine physician (HQB) determined that the elevated blood lead was the result of a mixed exposure: chronic inhalation and ingestion exposure during childhood and as a young adult on construction sites, overlaid with an acute ingestion exposure of grown-in-China over-the-counter green tea supplements.

SUMMARY

Lead occurs naturally, and its properties make it an important commodity in manufacturing, particularly in less developed countries, where deployed service members may be exposed. Exposures in overseas locations have resulted from poor environmental controls where troops deploy, often without knowledge that lead is present in the environment. Military munitions still employ lead primers, so service members can be exposed in indoor ranges with inadequate ventilation.

Lead also remains an occupational health risk on military installations. Unprotected work with lead can cause inhalation or ingestion of fumes or dust, which must be monitored through BLLs. Workers with elevated biological indices should be considered for removal from exposure and monitored for possible short- and long-term adverse health effects.

With improved hazard communication, improved engineering controls, better utilization of PPE, and product substitutions, BLLs in the population have decreased over time. However, safety and occupational health professionals must remain aware that even with substitutions and improved work practices, exposures will continue. Breakdowns in engineering controls and new recycling initiatives will expose a new generation of workers to lead. Also, military equipment, supplies, and training techniques may still expose personnel to lead. It is imperative that occupational and environmental medicine professionals understand that lead remains a hazard in today’s workplace. To reduce exposures in the workplace and in the general population, providers must maintain current knowledge of lead properties, regulations, evolving sources of exposure, diagnostics, medical surveillance protocols, and treatments.

REFERENCES

1.   Lachiver RM. Lead. In: Deeter DE, Gaydos JC, eds. Occupational Health: The Soldier and the Industrial Base. Washington, DC: Borden Institute; 1993: Chap 12.

2.   Hunter D. The Diseases of Occupations. 10th ed. London, England: Hodder and Stoughton; 2010.

3.   Fuortes LJ. Health hazards of working with ceramics. Recommendations for reducing risks. Postgrad Med. 1989;85(1):133–136.

4.   O’Neal B. Moonshining. Texas State Historical Association, Handbook of Texas online. http://www.tshaonline.org/handbook/online/articles/jbm01. Published June 15, 2010. Accessed August 29, 2017.

5.   Centers for Disease Control and Prevention. Very high blood lead levels among adults - United States, 2002-2011. MMWR Morb Mortal Wkly Rep. 2013;62(47):967–971. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6247a6.htm. Accessed August 24, 2017.

6.   US Department of Health and Human Services, National Toxicology Program. Health Effects of Low-Level Lead. Washington, DC: DHHS; 2012. http://ntp.niehs.nih.gov/NTP/ohat/Lead/Final/MonographHealthEffectsLowLevel-Lead_NewISSN_508.pdf. Accessed June 13, 2017.

7.   Zenz C. Occupational Medicine: Principles and Practical Applications. Chicago, IL: Yearbook Medical Publishers; 1988.

8.   Levy BS. Occupational Health, Recognizing and Preventing Work-Related Disease. Boston, MA: Little, Brown; 1983.

9.   Hall FX. Lead in a Baltimore shipyard. Mil Med. 2006;171(12):1220–1222.

10.   29 CFR, Part 1910.1025. Lead in general industry. https://www.osha.gov/pls/oshaweb/owadisp.showdocument?p_table=standards&p_id=10030. Accessed August 23, 2017.

11.   US Environmental Protection Agency. Integrated Science Assessment for Lead. Washington, DC: EPA; July 2013. http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=255721. Accessed March 3, 2014.

12.   National Research Council Committee on Toxicology. Potential Health Risks to DoD Firing-Range Personnel from Recurrent Lead Exposure. Washington, DC: National Academies Press; 2012: 117–123.

13.   Scott EE, Pavelchak N, DePersis R. Impact of housekeeping on lead exposure in indoor law enforcement shooting ranges. J Occup Environ Hyg. 2012;9(3):D45–51. doi: 10.1080/15459624.2011.648571.

14.   Navy Environmental Health Center. Indoor Firing Ranges Industrial Hygiene Technical Guide. Portsmouth, VA; NEHC; 2002. Technical Manual NEHC–TM6290.99-10. http://www.med.navy.mil/sites/nmcphc/Documents/policy-and-instruction/ih-indoor-firing-ranges-technical-guide.pdf. Accessed June 13, 2017.

15.   Sato M, Yano E. The association between lead contamination on the hand and blood lead concentration: a workplace application of the sodium sulphide (Na2S) test. Sci Total Environ. 2006;363(1-3):107–113. doi: 10.1016/j.scitotenv.2005.07.009.

16.   Esswein EJ, Boeniger MF, Ashley K. Handwipe method for removing lead from skin. J ASTM Int. 2011;8(8):67–81.

17.   QNET LLC. Directive RoHS2 2011/65/EU. Elk River, MN: QNET; 2013. http://www.ce-mark.com/RoHS2.pdf. Accessed August 16, 2017.

18.   Kar A. Lead still found in gasoline? The answer for small airplanes is, surprisingly, yes. Natural Resources Defense Council expert blog. https://www.nrdc.org/experts/avinash-kar/lead-still-found-gasoline-answer-small-airplanes-surprisingly-yes. Published December 30, 2010. Accessed August 29, 2017.

19.   40 CFR, Parts 50, 51, 53, 58. National ambient air quality standards for lead: final rule. https://www.gpo.gov/fdsys/pkg/FR-2008-11-12/pdf/E8-25654.pdf. Accessed August 16, 2017.

20.   The Safe Drinking Water Act of 1974, as amended. Pub L No. 93-523. https://www.gpo.gov/fdsys/pkg/STATUTE-88/pdf/STATUTE-88-Pg1660-2.pdf. Accessed August 17, 2017.

21.   Franz J. It’s been almost three years since Flint’s water crisis began. What have we learned? [transcript]. Science Friday. Public Radio International. February 26, 2017. https://www.pri.org/stories/2017-02-26/it-s-been-almost-three-years-flint-s-water-crisis-began-what-have-we-learned. Accessed August 17, 2017.

22.   US Environmental Protection Agency and Battelle Memorial Institute. Sources of Lead in Soil: A Literature Review. Washington, DC: EPA; 1998. EPA 747-R-98-001a. http://www.epa.gov/sites/production/files/documents/r98-001a.pdf. Accessed June 13, 2017.

23.   42 USC §9601. Comprehensive Environmental Response, Compensation, and Liability Act of 1980 (CERCLA). https://www.law.cornell.edu/uscode/text/42/chapter-103/subchapter-I. Accessed August 17, 2017.

24.   42 USC §7401 et seq. The Clean Air Act of 1970. https://www.epa.gov/laws-regulations/summary-clean-air-act. Accessed August 17, 2017.

25.   The Resource Conservation and Recovery Act of 1979. Pub L No. 94-580. https://www.gpo.gov/fdsys/pkg/STATUTE-90/pdf/STATUTE-90-Pg2795.pdf. Accessed August 17, 2017.

26.   US Food and Drug Administration. Guidance for industry: The safety of imported traditional pottery intended for use with food and the use of the term “lead free” in the labeling of pottery; and proper identification of ornamental and decorative ceramicware. http://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/ChemicalContaminantsMetalsNaturalToxinsPesticides/ucm214740.htm. Published November 2010. Accessed June 13, 2017.

27.   US Food and Drug Administration. Questions and answers on lead in foods. https://www.fda.gov/food/foodborneillnesscontaminants/metals/ucm557424.htm. Accessed August 17, 2017.

28.   Consumer Product Safety Improvement Act of 2008. Pub L No. 110-314. https://www.congress.gov/110/plaws/publ314/PLAW-110publ314.pdf. Accessed August 24, 2017.

29.   US Department of Housing and Urban Development. Guidelines for the Evaluation and Control of Lead-Based Paint Hazards in Housing (2012 Edition). Washington, DC: HUD; 2012. https://portal.hud.gov/hudportal/HUD?src=/programoffices/healthy_homes/lbp/hudguidelines. Accessed August 24, 2017.

30.   Centers for Disease Control and Prevention. Adult blood lead epidemiology and surveillance—United States, 2008-2009. MMWR Morb Mortal Wkly Rep. 2011;60:841–845. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6025a2.htm. Accessed June 14, 2017.

31.   California Department of Public Health. Blood Lead Levels in California Workers, 2012–2014. Sacramento, CA: CDPH; 2017. https://archive.cdph.ca.gov/programs/olppp/Documents/CABLLReport2012-14.pdf. Accessed August 18, 2017.

32.   Centers for Disease Control and Prevention. National Biomonitoring Program, lead summary. https://www.cdc.gov/biomonitoring/Lead_BiomonitoringSummary.html. Accessed August 25, 2017.

33.   Hu H, Shih R, Rothenberg S, Schwartz BS. The epidemiology of lead toxicity in adults: measuring dose and consideration of other methodologic issues. Environ Health Perspect. 2007;115(3):455–462. doi: 10.1289/ehp.9783.

34.   Abadin H, Ashizawa A, Stevens YW, et al. Toxicological Profile for Lead. 2007. Washington, DC: US Department of Health and Human Services, Agency for Toxic Substances and Disease Registry; 2007: 344–362. https://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=96&tid=22. Accessed August 25, 2017.

35.   Tarragó O, Brown MJ. What are possible health effects from lead exposure? Agency for Toxic Substances and Disease Registry, case studies: lead toxicity. Published June 12, 2017. https://www.atsdr.cdc.gov/csem/csem.asp?csem=34&po=10. Accessed August 20, 2017.

36.   Kosnett MJ, Wedeen RP, Rothenberg SJ, et al. Recommendations for medical management of adult lead exposure. Environ Health Perspect. 2007;115(3):463–471.

37.   Martin CJ, Werntz CL 3rd, Ducatman AM. The interpretation of zinc protoporphyrin changes in lead intoxication: a case report and review of the literature. Occup Med (Lond). 2004;54(8):587–591. doi: 10.1093/occmed/kqh123.

38.   Labbe RF, Vreman HJ, Stevenson DK. Zinc protoporphyrin: a metabolite with a mission. Clin Chem. 1999;45(12);2060–2072. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1849937/. Accessed June 13, 2017.

39.   Rabinowitz MB. Toxicokinetics of bone lead. Environ Health Perspect. 1991;91:33–37.

40.   Nie LH, Sanchez S, Newton K, Grodzins L, Cleveland RO, Weisskopf MG. In vivo quantification of lead in bone with a portable x-ray fluorescence system-methodology and feasibility. Phys Med Biol. 2011;56(3):N39–51. doi: 10.1088/0031-9155/56/3/n01.

41.   Todd AC, Chettle DR. In vivo X-ray fluorescence of lead in bone: review and current issues. Environ Health Perspect. 1994;102(2):172–177.

42.   Bradberry S, Sheehan T, Vale A. Use of oral dimercaptosuccinic acid (succimer) in adult patients with inorganic lead poisoning. QJM. 2009;102(10):721–732. doi: 10.1093/qjmed/hcp114.

Chapter 22

IONIZING RADIATION

CARLOS E. CORREDOR, MSNE*; SCOTT GOODISON, BS†; DOUGLAS BARRICKMAN, BS‡; DAVID ALBERTH, MS§; MARK W. BOWER, PHD¥; CRAIG JONES, BS¶; MICHAEL W. MUELLER, MPH**; HARRIS EDGE††; AND SAMUEL G. DUNSTON, MS§§

INTRODUCTION

PROPERTIES OF IONIZING RADIATION

DISCOVERY AND APPLICATIONS OF X-RAYS

DISCOVERY AND USES OF RADIOISOTOPES

IONIZING RADIATION IN MILITARY OPERATIONS

BIOLOGICAL EFFECTS OF RADIATION

PROTECTION AGAINST RADIATION

MEDICAL RESPONSE TO RADIATION INCIDENTS

THE DEPARTMENT OF DEFENSE RADIATION SAFETY PROGRAM

MEDICAL RESPONSE TO DEPLETED URANIUM EXPOSURE

SUMMARY

* Major (Retired), Medical Service Corps, US Army; Health Physicist, Health Physics Program, Army Institute of Public Health, US Army Public Health Command, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010

† Radiation Safety Officer, Army Institute of Public Health, US Army Public Health Command, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010

‡ Major (Retired), Medical Service Corps, US Army; Radiation Safety Officer, Augusta VA Medical Center, Department of Veterans Affairs, Augusta, Georgia 30904

§ Formerly, Health Physicist, Master Consultant, Health Physics Program, Army Institute of Public Health, US Army Public Health Command, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010; Deceased

¥ Colonel (Retired), Medical Service Corps, US Army; Command Radiation Safety Officer, Regional Health Command-Pacific, Madigan Army Medical Center, 9040 Jackson Avenue, Tacoma, Washington 98431

¶ Health Physicist, Health Physics Program, Army Institute of Public Health, US Army Public Health Command, 5158 Blackhawk Road, Aberdeen Proving Ground, Maryland 21010

** Lieutenant Colonel, US Army; Health Services Command Radiation Protection Staff Officer, Fort Sam Houston, Texas 78234

†† Chief, Industrial Health Physics Branch, Health Physics Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

§§ Major (Retired), US Army; Nuclear Medical Science Officer, Laser/Microwave Division; formerly, Chief, Medical Health Physics Branch, US Army, Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

INTRODUCTION

It is unlikely Wilhelm Roentgen envisioned just how big of an impact his 1895 discovery of x-rays would have on society. Additional contributions such as Marie Curie’s discovery of radium, the discovery and development of atomic fission and fusion, and other innovations described in this chapter led to numerous military and civilian applications of ionizing radiation (Exhibit 22-1). As the use of ionizing radiation began to flourish and develop, researchers gained a better understanding of the risks associated with its use. To minimize the risk while benefiting from its use, occupational health programs developed control measures for ionizing radiation. This chapter is an update to Chapter 16 in the previous edition of this book.[1]

Most military occupational exposures are minimal due to the administrative and engineering controls in place and the nature of the sources of the radiation. Many sources, however, have the potential to deliver significant levels of exposure, and a large number of military and civilian employees are routinely exposed to low-level radiation. Thus, occupational exposure to ionizing radiation demands strict adherence to all aspects of safety. Although exposure from a nuclear detonation poses the greatest ionizing radiation hazard to soldiers, Medical Consequences of Radiological and Nuclear Weapons[2] in the Textbooks of Military Medicine series thoroughly describes this hazard; therefore, this topic will not be discussed in detail here.

PROPERTIES OF IONIZING RADIATION

In general, radiation is the emission of waves or particles. These waves or particles travel through space and can deposit energy in matter with which they interact. Some common forms of radiation include visible light, radio waves, microwaves, x-rays, gamma rays, alpha particles, beta particles, and neutrons. Radiation is categorized by the amount of energy transferred to the atoms or molecules it interacts with. If the radiation has sufficient energy to strip an electron from its orbit around an atom, it is called ionizing radiation; otherwise, it is referred to as nonionizing radiation.

Ionizing radiation is a natural part of the environment. Ionizing radiation comes from many sources, including the sun and radioactive materials naturally present in soil, water, air, and food. On average, members of the US population receive a radiation dose of about 3.1 mSv from natural sources and another 3.1 mSv from manmade sources per year. Actual exposure levels of individuals vary depending on medical procedures, which create most manmade sources of ionizing radiation.

Particulate Radiation

Energetic particles emitted from radioactive material are referred to as particulate radiation. The most common examples are alpha particles, beta particles, and neutrons. The emission of alpha particles occurs primarily from heavy radioactive elements. Alpha particles contain two protons and two neutrons (a helium nucleus). Alpha particles are more massive in size compared to other common particulate radiation and have a double positive charge. When alpha particles interact with matter, they create a large number of ionizations, but these particles do not travel far. Most alpha particles travel less than 5 cm in air, but very energetic alpha particles may travel up to 10 cm. The most energetic alpha particles can travel up to 0.1 mm in soft tissue. A few centimeters of air or a sheet of paper readily shields alpha particles. Alpha particles, with energies less than 7.5 MeV, are not able to penetrate the dead layer of skin; therefore, alpha particles pose little to no hazard if the source is external to the body. However, alpha particles can be a radiation hazard if the alpha-emitting radioactive material is ingested.

Beta particles are electrons produced in the nucleus during the radioactive decay of many radioactive materials. Electrons do not normally exist in the nucleus; therefore, after the production of electrons, these particles are immediately ejected from the atom. Beta particles are smaller than alpha particles and have only a single negative charge; for this reason, they do not interact as strongly with matter. As with alpha particles, the range of a beta particle depends on its energy. Beta particles may travel several meters in air and a few millimeters in soft tissue. Therefore, beta particles from sources external to the body are a superficial skin hazard. Additionally, beta-emitting radioactive materials taken into the body can be an internal radiation hazard. Low-atomic-number materials, such as plastic or aluminum, readily shield beta particles and are preferred over higher atomic number materials. Using lead or other high-atomic-number materials to shield betas will result in the production of x-rays.

Neutrons are electrically neutral particles released during nuclear fission and some nuclear reactions. Unlike alpha and beta particles (which have a finite range in matter), there is no theoretical limit on the distance a neutron can travel. Thus, neutrons can penetrate deep into body tissues. In fact, many of the neutrons may pass completely through barriers and interact with hydrogen atoms within the human body; therefore, neutron sources are an external radiation hazard. Neutrons interact most strongly with light elements such as hydrogen. For this reason, neutron-shielding materials are generally hydrogenous (eg, water, paraffin, or plastic).

EXHIBIT 22-1

KEY DEVELOPMENTS IN ATOMIC FISSION

1897

J.J. Thomson identified the electron. Ernest Rutherford identified alpha and beta rays emanating from uranium and later correctly identified them as helium nuclei and electrons, respectively.

1898

Villard recognized gamma rays and observed their similarities to the roentgen ray.

1905

Albert Einstein proposed his famous equation, E=mc[2], stating the relationship of energy to mass.

1910

F. Soddy suggested an explanation for atoms with slightly different weights, but identical chemical properties, and called them isotopes.

1911

Rutherford proposed the atomic theory with a distribution of mass and charge that is essentially the one accepted today.

1913

Niels Bohr suggested an atomic structure involving a central nucleus with orbital electrons in layers around it.

1919

Rutherford bombarded nitrogen atoms with alpha particles and observed the production of hydrogen and oxygen. This milestone was the first controlled experiment in which one element was artificially transformed into another.

1931

Ernest Lawrence invented the cyclotron, a chamber in which it is possible to accelerate particles to immense speeds for use as projectiles.

1932

James Chadwick of Cambridge University recognized the neutron.

1934

Enrico Fermi first split an atom of uranium by neutron bombardment. Lise Meitner, a German physicist, explained the process and termed it fission; it was realized that large amounts of energy were released in this process.

1939

Fermi approached the US Navy about the prospects for an atomic weapon, and expressed his fear that Germany would produce and use such a weapon. The importance and power of atomic fission was clear to many scientists. Some also foresaw and were frightened by the implications of its use as a weapon. A letter, drafted by Leo Szilard and signed by Einstein, was forwarded to President Franklin D. Roosevelt, and Roosevelt started the process that would result in the development of the atomic bomb.

1940

D.W. Kerst constructed a betatron, in which electrons were accelerated to energies of 20 MeV, and later to 300 MeV, by magnetic induction.

1941

The Manhattan Project began, consolidating the fragmented efforts at atomic weapons development. Brigadier General Leslie Groves (a civil engineer) was appointed as the project’s director, and J. Robert Oppenheimer (a physics professor at the University of California, Berkeley) was selected as the scientific director.

1942

On December 2, Fermi successfully initiated the first self-sustaining nuclear chain reaction in a uranium pile at the University of Chicago.

1945

On July 16, the first atomic bomb detonation (a plutonium-fueled implosion device) occurred in New Mexico. On August 6, an atomic bomb (a gun-assembly, uranium-fueled device code-named Little Boy) was dropped on Hiroshima, Japan. On August 11, a second atomic bomb (a plutonium-fueled implosion device code-named Fat Man) was dropped on Nagasaki, Japan.

1986

Chernobyl Accident. On April 27, 1986 the Number 4 reactor at the Chernobyl Nuclear Power Plant in Pripyat, Northern Ukraine, was undergoing testing that resulted in a series of uncontrolled reactions. These reactions caused a non-nuclear explosion and fire that blew the roof off the top of the building. The resulting plume spread radioactive materials across Europe, and radionuclides from the damaged reactor were detected around the world. Currently, some areas near the damaged reactor are off limits to people.

1999

Tokaimura Criticality Accident. Three workers at the Japan Nuclear Fuel Conversion Company brought too much enriched uranium together and created a limited, uncontrolled nuclear chain reaction, which lasted several hours. The three workers were taken to the hospital, where one worker died after 12 weeks, and a second worker died 7 months later.

2011

Fukushima Daiichi Nuclear Power Plant Accident. On March 11, 2011, a 9.0-magnitude earthquake, the largest ever recorded in Japan, occurred northeast of Tokyo off the coast of Honshu Island. This earthquake caused the automatic shutdown of 11 nuclear power plants at four sites along the northeast coast of Japan. About 40 minutes after the earthquake and shutdown of the operating units, the first large tsunami wave inundated the Fukushima Daiichi Nuclear Power Plant. As a result of the tsunami, electrical power was lost at reactors 1 through 4. The station blackout led to a loss of cooling and a major release of radioactive material.

___________________

Data sources: (1) Dewing SB. Modern Radiology in Historical Perspective. Springfield, IL: Charles C Thomas; 1962. (2) Pizzo PP. Non-destructive inspection. San Jose State University website. http://http://www.engr.sjsu.edu/WofMatE/Mat’sChar3.htm. Accessed November 20, 2017. (3) Kathren RL, Ziemer PL. Health Physics: A Backward Glance. New York, NY: Pergamon Press; 1980. (4) Department of the Air Force. Nondestructive Inspection Methods, Basic Theory. Washington, DC: USAF; 2016. TO 33B-1-1/NAVAIR 01-1A-16-1/TM 1-1500-335-23. (5) Graham LS, Kereiakes JG, Harris CC, Cohen MB. Nuclear medicine from Becquerel to the present. RadioGraphics. 1989;9(6):1189–1202.

Electromagnetic Radiation

Electromagnetic radiation is composed of oscillating electric and magnetic fields such as visible light, radio waves, microwaves, x-rays, and gamma rays. Of these, x-rays and gamma rays are ionizing radiation. X-rays and gamma rays differ only in their source. Gamma rays are electromagnetic radiation released from inside the nucleus of atoms that have excess energy, usually following alpha particle or beta particle emission. Electron transitions within the electron cloud of an atom produce x-rays. In many elements, the difference in energy between electron orbits is high enough that when an electron drops to a lower energy orbit, ionizing radiation is emitted. This radiation is called characteristic x-rays because it is emitted only at specific energies that are characteristic of the particular element. Another example of an electron transition producing x-rays is when a high-atomic-number material is bombarded with fast-moving electrons. This process, in which some of the kinetic energy of the electrons is converted into x-rays, is called bremsstrahlung (German for braking radiation). This is the process used to produce x-rays in medical and industrial x-ray systems. For this reason, high-atomic-number materials such as lead are not used as shielding for beta-emitting radionuclides.

As with neutrons, there is no theoretical limit on the travel range of x-rays and gamma rays. Increasing the thickness of shielding material helps to reduce the amount of radiation passing through the shield, but in theory, no amount of shielding will stop all the radiation. As the energy of the x-rays or gamma rays increases, more shielding material is needed to achieve the same level of radiation attenuation. Dense, heavy materials such as lead, steel, or even depleted uranium (DU) are the best shields for gamma rays or x-rays. Building materials such as concrete are utilized frequently for structural shielding because they are less expensive than heavy materials and are self-supporting.

Gamma rays and x-rays are both external radiation hazards. They can be internal hazards if the emitting radionuclides are in the body.[3]

DISCOVERY AND APPLICATIONS OF X-RAYS

Roentgen’s discovery of x-rays was a culmination of the research of scientists such as Wilhelm Hittorf, William Crookes, Heinrich Hertz, and Philipp Lenard. Roentgen’s discovery on November 8, 1895, occurred when he saw a barium platino-cyanide screen fluorescing on a table some distance from the cathode ray tube with which he was working.3,4 This occurrence stimulated his interest, and he worked feverishly over the next few days to comprehend and document the observed phenomenon. By turning the current on and off, Roentgen observed the relation of fluorescence to discharge within the tube. Roentgen concluded that he had found a new phenomenon emanating from the tube.

In testing this phenomenon’s ability to penetrate various materials, Roentgen was startled to see the image of the bones of his own hand on a photographic plate. After this discovery, Roentgen observed and recorded the differential development of photographic plates using materials of various densities. He even produced an image of his wife’s hand with a 15-minute exposure.[5] To document the findings of these experiments, Roentgen wrote a paper describing the rays’ means of production and their important properties. In December 1895, he submitted “A New Kind of Ray” to the Würzburg Physical-Medical Society. On January 6, 1896, Roentgen’s discovery was announced to the world, creating an immediate stir in the scientific community.[5] Although other scientists observed the photographic effects of x-rays, they failed to recognize the significance of the phenomenon.

Medical Uses

In general, the medical community, and the US Army in particular, was quick to embrace the new technology that followed the discovery of x-rays; several examples of the use of x-rays for diagnoses were available within a year. Within 3 months of Roentgen’s discovery, the curator of the Army Medical Museum, Major Walter Reed, applied to the Army surgeon general for authority to obtain a roentgen-ray apparatus.

Although Surgeon General George Sternberg initially denied Reed’s request, there is evidence that the museum possessed a roentgen-ray apparatus by June 1896. Admission records of Garfield Hospital in Washington, DC, show that a 17-year-old female patient was admitted with a penetrating gunshot wound to the hip, which had been inflicted when her brother accidentally discharged a .22-caliber weapon. Dr Joseph S. Wall accompanied the patient in a horse-drawn ambulance to the Army Medical Museum, where Dr William Gray assisted in identifying the bullet’s exact location with a Roentgen tube (Figure 22-1). The patient was exposed to x-rays for 1 hour before a roentgenogram showing the location of the bullet could be obtained. After this examination, the patient returned to Garfield Hospital, where the bullet was successfully removed.[6]

Figure 22-1. A roentgen-ray tube similar to the one possessed by the US Army Medical Museum and used to locate a bullet lodged in a patient in 1896. Simple tubes of this type were the first x-ray machines used by the Army.
Reproduced from: Henry RS. The Armed Force Institute of Pathology: Its First Century, 1862-1962. Washington DC: Office of the Surgeon General, DA; 1964: 102.

Although the Army began experimenting with x-rays soon after their discovery, other countries had actually employed them in treating military casualties in early 1896. Lieutenant Colonel Giuseppe Avaro, an Italian physician, used an apparatus to examine wounded soldiers near the end of Italy’s campaign in Ethiopia. At approximately the same time, British military physicians used diagnostic x-rays during the Nile Expedition.[3] The British were the first to employ an x-ray apparatus in battlefield treatment facilities, during the Tirah Campaign (on the Indian-Afghanistan border) in October 1897.[7] Surgeon Major W.C. Beevor operated the x-ray apparatus and used the roentgenograms to locate bullets and bullet fragments. He advocated for x-ray apparatuses to be easily accessible for examining soldiers wounded in the line of duty.[7]

The US Army surgeon general had supplied roentgen-ray apparatuses to the larger post hospitals soon after Roentgen’s discovery, but the outbreak of war with Spain in 1898 prompted an increase in supply. The most important general hospitals and three hospital ships (Relief, Missouri, and Bay State) received systems similar to the original roentgen-ray apparatus. Seventeen apparatuses were available during the Spanish-American War.[8]

Figure 22-2. Captain William C. Borden, MD, wrote in his 1900 history of the use of roentgenography in the Spanish-American War, “[This soldier was] wounded at Malate, Philippine Islands, July 31, 1898. He was transferred to the division hospital, Presidio, San Francisco, Cal., October 22, 1898.” This radiograph, viewed from the patient’s back, shows a Mauser bullet, which had passed through the spine, lying 2 in. to the right of the spine over the third intercostal space. The chest film “demonstrated that the [patient’s] symptoms were due to the original traumatism and not to the presence of the bullet.”
Reproduced from: Borden WC. The Use of the Rontgen Ray by the Medical Department of the United States Army in the War with Spain (1898). Washington, DC: Office of The Surgeon General, DA; 1900: 40.

The availability and utility of the roentgen-ray apparatus proved invaluable, according to Captain William C. Borden, who was in charge of their use.[8] Borden claimed that the roentgen-ray apparatus made exploring bullet wounds with probes or by other means unnecessary, thus obviating the dangers of infection and iatrogenic traumas (Figure 22-2). Borden also extolled the benefits of roentgen rays in the diagnosis and treatment of fractures.[8] Although the quality of the early roentgenograms may leave much to be desired by today’s standards, they were, in fact, remarkable for their clarity and utility (Figure 22-3).

By the time the United States entered World War I, radiology was becoming an established medical discipline. However, the use of x-rays was limited because the equipment and supplies were unsuited to mass use, and too few radiologists were available. In fact, in April 1917 the US Army had only one radiologist, Colonel Philip Huntington.[7] While no real distinction existed between military and civilian medical applications of roentgenology, the military’s differing circumstances required a specialized apparatus. For example, portable and bedside x-ray units, not used in the civilian sector, were tailored to military needs (Figure 22-4). The Army also recognized that x-ray capabilities were necessary in mobile hospitals and surgical units, and therefore modified a standard Army ambulance to house a field-portable x-ray apparatus and one bedside unit. In May 1918, the first x-ray ambulance was tested and found to be successful.

Figure 22-3. This famous radiograph of the hand of Prescott Hall Butler showing multiple retained shot was made by Michael I. Pupin in New York City, probably on February 14, 1896. It was “the first roentgen plate to guide a surgical operation in New York [and] is the best of all early roentgen prints as far as technical quality (and bone detail) is concerned which is quite unusual when one considers the fact that the x rays were produced in the glass of the tube, and were in no way focused.”
Reproduced from: Grigg ERN. The Trail of the Invisible Light: From X-Strahlen to Radio(bio)logy. Springfield, IL: Charles C. Thomas; 1965: 312.

Figure 22-4. The Waite and Bartlett Army bedside unit, shown at the base hospital in Grand Blottereaux in 1915, was the first stock x-ray equipment that used a Coolidge hot-cathode tube. The examiner looked into a cryptoscope, the hand-held fluoroscope.
Reproduced from: Feldman A. A sketch of the technical history of radiology from 1896 to 1920. RadioGraphics. 1989;9(6):1113–1128. Copyright: The Radiological Society of North America (used with permission).

The Army worked on refining its methods for using x-rays, and on November 25 that year published the United States Army X-Ray Manual under the direction of the Office of The Surgeon General’s Division of Roentgenology.[9] This manual served as a guide and textbook for military roentgenologists. By the end of World War I, the United States had shipped 150 complete base hospital x-ray units, 250 bedside x-ray units, 264 portable x-ray units, and 55 x-ray–equipped ambulances overseas.[10]

Radiology as a specialty made tremendous strides during the interval between World War I and World War II: equipment was improved, radiologists received formal training, and radiological technologies were developed and clinically applied. By the onset of World War II, the use of x-ray technology was well established as a diagnostic and therapeutic tool. Radiology as a recognized medical specialty became an integral part of every hospital, and radiology teams were part of auxiliary surgical groups that performed frontline surgery.

Providing radiological services was still complicated, however. Once basic equipment was supplied, radiologists and technicians had to maintain it, often with great difficulty and improvisation. Battlefield needs sparked further developments in mobile and portable x-ray systems, such as the US Army field x-ray unit, which was widely used in both front- and rear-echelon military medical facilities (Figure 22-5).[11]

Figure 22-5. A portable field x-ray unit in action in World War II. The unit shown was developed by the Picker Corporation, which became the sole supplier of the US Army field x-ray unit during World War II.
Reproduced from: Krohmer JS. Radiography and fluoroscopy 1920-1989. RadioGraphics. 1989;9(6):1129–1153; Figure 15. Copyright: The Radiological Society of North America (used with permission).

Furthermore, despite the advances in radiology and training techniques, radiologists were constantly in short supply during World War II. In an effort to meet radiological needs, training courses were provided for medical officers and technicians at institutions such as the US Army School of Roentgenology.[7] The importance of radiology during World War II was also reflected in the structure of the Army Surgeon General’s Office. The Radiation Branch, later renamed Radiology, was established on July 12, 1942, under the direction of Major Michael E. DeBakey. This branch, a part of the Surgery Division, later became the Surgical Consultants Division.[7]

Diagnostic Uses

Beginning in the 1950s, great advances in radiological technology were made, partly resulting from the military uses of radiology during World War II. During the Korean and Vietnam wars, x-rays were used extensively in the diagnosis and treatment of casualties (Figure 22-6). Also during the 1950s and 1960s, A.M. Cormack, a South African, did the original work on projection imaging that set the stage for computed tomography (CT). However, the evolution of CT technology from experimental curiosity to clinical reality was largely due to the efforts of English engineer Godfrey Hounsfield.[12] Hounsfield CT scanners were introduced into medical practice in 1974.

Figure 22-6. The x-ray section of a forward surgical hospital during the Korean War. The advances in x-ray technology and techniques that had been developed since World War II permitted field hospitals to practice quality imaging in their treatment of battlefield casualties.
Reproduced from: Howard JM, ed. The battle wound: clinical experiences. In: Battle Casualties in Korea, Studies of the Surgical Research Team. Vol 3. Washington, DC: Army Medical Service Graduate School, Walter Reed Army Medical Center; 1955.

CT makes cross-sectional imaging with x-rays possible, which greatly enhanced the physician’s ability to see abnormalities in a variety of anatomical structures. Vast technological improvements have been made in CT technology since the 1970s. Within several years, scanning times decreased from 5 minutes to 5 seconds, and later to 2 seconds.[12] New generations of CT machines incorporated new software packages and hardware designs that enhanced the efficiency and quality of cross-sectional imaging while reducing the exposure to patients.

Advances and refinements continue to produce enhanced imaging and resolution and further reduce scan times. Current CT scanners typically have a scan time of about 1 second, and electron-beam CT systems have scan times of approximately 50 milliseconds. Another advance was the creation of the spiral CT (Figure 22-7), in which scans are in a continuous spiral movement (in contrast to the traditional CT scan, in which the x-ray tube head rotates 360°, then moves to the next position and continues with additional scans). In comparison to conventional CT, spiral CT reduces radiation exposure to patients undergoing the study while providing superior two- and three-dimensional imagery. Clinical medicine has benefited from cross-sectional imaging, and the field of radiology continues to evolve as medicine advances with the computer era. Approaches being explored employ radiation sources at wavelengths not currently used for imaging. There are also new techniques being developed and implemented to combine CT, positron emission tomography (PET), and magnetic resonance.

Figure 22-7. May 10, 2006. The computerized tomography (CT) scanner aboard the Military Sealift Command hospital ship USNS Mercy (T-AH 19) uses x-rays and computers to create cross-sections of bodily tissues. US Navy photograph by Journalist Seaman Joseph Caballero.
Reproduced from Wikimedia Commons.

Therapeutic Uses

Parallel to their diagnostic uses, the therapeutic uses of x-rays date to January 29, 1896, when Emil H. Grubbe reported that he, working in Chicago in collaboration with Dr R. Ludlum, treated a breast carcinoma with 18 x-ray treatments.[13] During the next few years, Grubbe and Ludlum continued to use therapeutic x-rays on conditions ranging from malignancies to excess facial hair. This experimentation resulted in many disappointing outcomes as well as radiation injuries. However, the number of successes was sufficient to maintain the interest of scientists and physicians in the therapeutic value of x-rays, particularly for tumors.

In the early years, the efficacy of therapeutic x-rays was limited by the low kilovoltage the equipment could achieve, which only enabled the x-ray beam to penetrate shallowly.[13] Thus, brachytherapy (ie, the application of an encapsulated radioactive source or sources to deliver a radiation dose at a distance of not more than a few centimeters) using radium was more useful than external-beam therapy (teletherapy) until higher-energy external-beam systems became available.[13]

In 1937, the earliest type of super voltage teletherapy unit (Figure 22-8) was used on patients.[14] This 1-MeV unit was used at St Bartholomew’s Hospital in London, England, under the supervision of Dr Ralph Phillips and George Innes. The therapeutic use of x-rays progressed after high-energy sources became available, and in 1940, Donald W. Kerst of the University of Illinois developed the betatron (Figure 22-9), which functioned as an electron accelerator. This first betatron operated at 2.3 MeV, the second at 20 MeV, and the third at 300 MeV.

Figure 22-8. Dr Ralph Phillips and a patient to be treated using the 1-MeV therapy installation at St Bartholomew’s Hospital, London. The unit created high-energy, penetrating x-rays used for treating cancers and other tumors. The immediate benefit to the patient of the tumor’s eradication or reduction was generally thought to outweigh the risk of developing future cancers from the high radiation dose delivered.
Reproduced from: Jones A. The development of megavoltage x-ray therapy at St. Bartholomew’s Hospital. Br J Radiol. 1988;22(suppl):3-10. Copyright: The British Institute of Radiology (used with permission).

In 1948, Kerst collaborated with Dr Henry Quastler, also at the University of Illinois, in the first treatment of a tumor using these high-energy rays. Localized irradiation from the betatron was administered to a graduate student at the university whose brain tumor had been partially excised. The patient eventually succumbed to cancer, but the autopsy revealed no viable neoplastic cells in the irradiated region.[14] The same year, the Allis-Chalmers Manufacturing Company developed a commercial version of the betatron with improvements for medical use.

Figure 22-9. Professor Donald Kerst with two of his betatrons (electron accelerators) in 1940. These betatrons were compact and able to accelerate electrons to high energies. Electrons that reach sufficiently high energies are able to penetrate deeply into tissue; therefore, accelerated electrons can be used therapeutically. Additionally, the betatron-accelerated electrons were relatively monoenergetic, and their energy was easy to control.
Reproduced from: Laughlin JS. Radiation therapy. RadioGraphics. 1989;9(6):1245-1266; Figure 8. Copyright: The Radiological Society of North America (used with permission).

The development of the linear accelerator (LINAC) further advanced the therapeutic use of x-rays. Before and during World War II, oscillator tubes capable of relatively high power output at microwave frequencies were developed and applied to radar.[14] At the end of the war, the technology was refined and applied to the advancement of the LINAC (Figure 22-10), which has become the predominant modality for delivering modern radiation teletherapy treatment (see further discussion below).

Industrial Uses

Industrial radiography sprang from Roentgen’s mention of the radiograph of a piece of metal in his 1895 paper. Metallurgists seized this concept as a nondestructive inspection (NDI) method for examining metals. NDI is the characterization of an object or material with a technology that does not affect its future usefulness.[15] During World War II, General Electric Company physicist E. Dale Trout was assigned to work with the military on radiographic NDI. Trout assured the quality and integrity of the templates for all B-17, B-24, B-29, and B-50 aircraft using x-rays for NDI. He claimed that during his work with the military, every shell of 155 mm or larger, all aircraft bearings, and all rocket propellant grains were x-rayed on continuously operating equipment. Trout and the military also assembled a 1-MeV unit at Hayward, California, to radiograph the outboard struts on ships built at Mare Island and Hunter’s Point.[16]

Fluoroscopy, which produces x-ray images in real time, lends itself to use on conveyor production lines or assembly lines, and is used for NDI and noninvasive inspection of packages and luggage. In the past, fluoroscopic inspection on production lines was limited to thin, lightweight metals and nonmetallic goods, but the development of state-of-the-art image intensifiers now permits inspection of heavier materials.

The military and private industry also employ ionizing radiation to analyze materials by means of x-ray diffraction and x-ray absorption photometry. Because crystals diffract x-rays in a specific diffraction pattern, x-rays permit qualitative and quantitative analyses of crystalline materials. X-ray absorption photometry is also an analyzing technique, but it utilizes the differences in absorption of the various elements.

Figure 22-10. A linear accelerator (LINAC). The LINAC is used extensively for teletherapy treatment at military medical hospitals within the United States and at overseas military bases.
Image courtesy of Elekta.

Both the military and private industry use electron-beam generators to deliver massive doses of radiation. One device for electron-beam processing is the Van de Graaff apparatus, which is an electron accelerator. Another is the 1- or 2-MeV resonant transformer x-ray apparatus. Some applications of electron-beam processing include sterilizing foods and drugs, exterminating insects in seeds, toughening polyethylene containers (inducing cross-linkage of polyethylene molecules), and activating chemical reactions in petroleum processing.

Digital Radiography

Digital radiography (DR) is now extensively used by the military and the private sector in both industry and medicine. Industrially, DR provides another method to perform nondestructive testing using x-rays to verify a material’s integrity, density, and internal contents. The x-rays produced go through the material and then interact with a digital detector that can create and save a computerized digital image. The digital image, either still or continuous, is displayed on a computer for further analysis by the radiographer.[15]

A benefit of using DR is that the radiographer can use a smaller tube potential or kilovolt peak (kVp) value to achieve an acceptable image. By using a smaller kVp setting, the exposure to the radiographer and other nearby personnel is reduced. Also, with DR, film processing is eliminated. This reduces the cost of maintenance and has less impact on the environment. DR provides immediate results for real-time viewing; images can be stored for further use or transmitted electronically to other experts who can help verify the object’s integrity and reliability of the object being analyzed.

In military medicine, DR images can be transmitted from the battlefield to fixed facilities or a mobile device for further analysis. DR has replaced the development of x-ray film in the dark room, reducing the use of chemical solutions in hospital radiology departments. DR reduces exposure to the patient and providers by using smaller tube current and/or time of exposure settings on the x-ray system. If required, DR films can be printed.

Another form of NDI utilizing DR is CT. Much like medical CT, industrial CT uses a computer system that reconstructs an object’s image using the different cross-sections created by x-rays. CT produces both two- and three-dimensional images of the object being studied. With industrial CT, objects can be viewed internally, and dimensional and spatial analysis can be performed, as well as identification of anomalies to help verify structural integrity. The capability to view parts of the object from different angles eliminates interference caused by other internal components in standard radiography.[15]

DISCOVERY AND USES OF RADIOISOTOPES

In 1896, Henri Becquerel followed Wilhelm Roentgen in exploring the idea that naturally fluorescent minerals might emit rays similar to roentgen rays. On March 1, 1896, while studying the influence of light on the fluorescence of uranium salts, Becquerel placed a sample of uranium in direct sunlight to study the degree of development of a shielded photographic plate cassette he had placed under the uranium. When the sky became cloudy, Becquerel interrupted the test and set the cassette aside. He processed the cassette a few days later and found that its emulsion had developed identically to that of cassettes exposed to bright sunlight. Recognizing the importance of his finding, Becquerel announced to the Paris Academy of Science in November 1896 that he had detected the spontaneous emission of rays.[5] The emanations of uranium were initially named Becquerel rays; however, this discovery received surprisingly little attention until subsequent work was done by Marie and Pierre Curie. In fact, the Curies coined the term radioactivity to describe the phenomenon. Becquerel and the Curies worked together after Marie Curie took an avid interest in Becquerel’s report in 1897.

In July 1898, the Curies and Becquerel positively identified a new element and named it polonium. In December, they identified another and dubbed it radium. However, it was not until 1902 that they refined a pure sample of radium, which allowed them to establish its atomic weight as 226. In 1910, Marie Curie purified radium metal in her own laboratory and prepared the official radium standard, which is still deposited in the Bureau of Weights and Measures at Sevres, France.[5]

Medical Uses

Georg Charles de Hevesy of England published the first paper (with Fritz Paneth) on the radioactive-tracer concept in 1913, which introduced radioisotopes to medicine, and established the field that evolved into modern nuclear medicine. His discovery occurred when he attempted to separate lead 210 from nonradioactive lead and realized that small amounts of lead 210 could represent nonradioactive lead atoms in qualitative and quantitative processes. His first experiment using the tracer concept outside the laboratory resulted from a personal concern at his boarding house: convinced that the property owner was using food scraps from the plates of her boarders to make hash, de Hevesy spiked the leftover food on his plate with a radioactive tracer. His detection of the tracer in the hash verified his suspicions, but got him evicted for his efforts.[17]

In 1924, the tracer concept advanced to clinical medicine and paved the way for the use of radioisotopes as diagnostic tools. Blumgart and Weiss injected bismuth 214 solutions into one arm of a subject and then detected the solution’s arrival in the other arm, measuring arm-to-arm circulation time. In 1934, Frederick Joliot and Irene Curie discovered artificially produced radioactivity, which, coupled with the Geiger counter’s detection capabilities, markedly expanded the range of possible radionuclides for clinical tracer studies. Within a few months, Enrico Fermi produced a large number of radionuclides, including phosphorus 32. Also during this time, molybdenum 99, the parent of technetium 99m, was produced in the cyclotron (Figure 22-11). Unfortunately, another 20 years elapsed before Richards’s introduction of the molybdenum 99/technetium 99m generator made technetium 99m the radionuclide most widely used for diagnostic imaging.[17]

The demand for radioactive materials soon exceeded the capacity of the few cyclotrons then operating, but the construction of the Oak Ridge reactor in Tennessee during World War II partially resolved this imbalance. However, the reactor was constructed under the secrecy of the Manhattan Project, so the phosphorus 32 produced by the reactor had to appear as if it had been produced by a cyclotron. To protect this secrecy, the phosphorus 32 was sent from Oak Ridge to the cyclotron group at the University of California at Berkeley, and distributed from there to medical centers that ordered it. The shortage of radioisotopes ended in 1945, when isotopes became widely available for research and medical use, including reactor-produced iodine 131 from Oak Ridge.[17] The work done in the development of the atomic bomb was responsible for this availability, thus contributing substantially to the medical applications of radionuclides.

Figure 22-11. Stanley Livingston (left) and Ernest O. Lawrence (right) stand in front of a cyclotron particle accelerator that Dr Lawrence invented at the old Radiation Laboratory at the University of California, Berkeley, 1934. The cyclotron greatly expanded the number of radionuclides that could be used as tracers when the cyclotron accelerates charged particles to a very high velocity and slams them into a target, creating radioactive material in the process. National Archives and Records Administration photograph.
Reproduced from Wikimedia Commons.

The medical use of radionuclides now available was enhanced by improvements in radiation-detection instruments. H. Kallmann devised the scintillation detector in 1947, using organic crystals of naphthalene attached to the face of a multiplier tube. Although crude, the scintillation detector was more sensitive than a Geiger-Mueller tube (which used pressured air or gas in a sealed container or tube, with positive and negative connections to create electrical charges in the presence of radiation). R. Hofstadter modified the scintillation detector’s basic design to enhance its sensitivity by adding small amounts of thallium to a sodium iodide crystal. In 1958, H. Anger constructed the prototype scintillation camera at the Lawrence Berkeley Laboratory, but scintillation cameras did not become commercially available until 1964.[17]

The original commercial gamma camera, which is composed of an array (group) of scintillation detectors, has been surpassed by improvements in crystal size and the design of the scintillators. Today’s machines also utilize larger detectors, adjustable peak-energy detection, tomographic techniques, and high-speed computers. Single photon emission computerized tomography (SPECT) and PET scanning techniques allow for true three-dimensional image acquisition. All of these improvements have increased the image contrast and resolution of the camera, making nuclear medicine a much more valuable diagnostic modality.[18]

Diagnostic Uses

As part of their diagnostic armamentarium, hundreds of hospitals use radioisotope techniques, including dilution techniques, flow or diffusion measurements, and biochemical concentrations. Dilution techniques can be used to measure blood volume by injecting human serum albumin labeled with iodine 125 into the bloodstream. After the iodine 125 has been uniformly distributed in the bloodstream (the time required is patient dependent), an aliquot of blood is removed and the amount of activity in the sample is compared with the amount injected. Flow or diffusion measurements also assess cardiac output and peripheral vascular disorders.

Biochemical concentration techniques are used to diagnose liver, cardiac, and kidney function; help diagnose thyroid disorders; and locate and evaluate the extent of malignancy. For example, if thyroid cancer is suspected to have metastasized, a diagnostic dose of iodine 131, followed by whole-body imaging, can frequently show the location of the metastatic tumors. PET has become a diagnostic aid to surgeons and oncologists attempting to stage certain cancers in their patients, thereby helping to guide the appropriate therapy. PET scans have also been helpful in finding and characterizing suspicious lung nodules seen on CT scan, some as small as 10 mm in diameter. Simultaneous PET and CT scanners can pinpoint foci of cancerous cells in a patient’s body. There is also an expanding role for radionuclides in the therapeutic radiology realm.

In recent years the number of radionuclides, and the materials that they are tagged to, have increased. A partial list of radionuclides routinely compounded and used for diagnostic or therapeutic use includes iodine 123, iodine 125, iodine 131, indium 111, technetium 99m, gallium 67, gallium 68, thallium 201, xenon 127, xenon 133, cobalt 57, carbon 11, nitrogen 13, oxygen 18, fluorine 18, rubidium 82, strontium 87m, strontium 90, and radium 223. These elements are gamma ray or beta emitters, but some decay by emitting positrons.[18]

Therapeutic Uses

Pierre Curie’s observation that diseased tissue is sensitive to radiation prompted new attempts to treat malignancies with radiation. In the early years of such procedures, glass seeds containing radon were implanted in tumors. Marie Curie personally supervised not only the systematic production of radon from her own radium source, but also the construction of radon-generation systems worldwide. Only a small quantity of radium was needed to produce enough radon seeds to supply a large area. In New York in 1926, Gioacchino Failla developed gold radon seeds for permanent implantation.[5]

Brachytherapy

In 1939, Ralston Paterson and Herbert Parker of the Christie Hospital in Manchester, England, published a system for using radium implants in brachytherapy.[14] This system was based on tables that ensured a relatively uniform dose distribution through prescribed placement of sources. In time, physicians used computers to design brachytherapy systems for artificial radionuclide sources. Today, iridium 192 and cesium 137 have primarily replaced radon seeds and radium sources in brachytherapy. Modern brachytherapy is performed using sealed radioactive sources for surface, interstitial, or intracavitary application. Encapsulated sources such as cesium 137 can be inserted into body cavities using the same devices as those in existence since the initiation of radium therapy. The use of iodine 125, iridium 192, gold 198, or palladium 103 encapsulated in seeds, wires, or needles allows the radioactive source to be inserted directly into the tumor.

Radiopharmaceutical Therapy

Two principles of radiopharmaceutical therapy can be used to concentrate unsealed radioactive material in the target organ: selective absorption or differential turnover. Selective absorption is used if a tissue preferentially absorbs a particular material in order to accomplish its function (eg, the thyroid’s selective absorption of iodine). Differential turnover is used if the more rapid metabolism of a particular tissue (eg, the metabolism of phosphorus by the bone- and blood-forming elements) can be monitored. After World War II, the availability of reactor-produced iodine 131 allowed its wide use as a therapeutic agent, particularly for procedures such as thyroid ablations. Strontium 89 has been used to palliate bone pain caused by metastatic prostate, breast, lung, and renal cancer. Other radioisotopes are also currently being investigated for this purpose.[18]

Teletherapy

Cobalt 60 teletherapy, introduced in 1951, employs a penetrating beam clinically equivalent to the beam from a 2-MeV linear accelerator. The encapsulated radioactive source is usually located at least 80 cm from the patient. Teletherapeutic doses are typically divided into daily treatment fractions (over 5 to 40 days), which allows high doses to be delivered to the tumor while minimizing unwanted side effects. Cobalt units require no associated high-voltage power supply or complicated acceleration apparatus, and the head, which contains the radioactive source and the collimator, is relatively compact. The units can be installed almost anywhere. However, they also have some significant disadvantages: compared with LINACs, they contain a substantial radioactive source, with the associated potential exposure hazards to both patients and medical personnel; they give poorer depth-dose characteristics; and the penumbra from the radiation source is much larger. Teletherapy is generally no longer used in the United States. Instead, radiation therapy has been focused on the use of LINACs for cancer treatment.

The search for therapeutic uses of radioisotopes has continued; new studies are investigating californium 252 and energetic heavy particles such as neutrons, protons, and alpha particles.14,16 Despite these advances and improvements in safety, when devices intended for sophisticated medical diagnostic or therapeutic uses are mishandled, the consequences can be disastrous. One of the worst incidents of this kind occurred at Goiânia, Brazil, in September 1987 (Exhibit 22-2).19–23

Industrial Uses

Radioisotopes are useful in industry because they are portable, easily applied in physically awkward areas (such as a gooseneck pipe), and do not depend on an external power source. They are used in a range of military and industrial applications including weapons, gauges for thickness or density, tracer techniques, research, neutron activation analysis, sterilization of biological and food products, smoke detection, and illumination. The military also has used nuclear reactors to produce materials for atomic weapons, to produce electrical power, and for research.

Nondestructive Inspection

In industrial radiography, the radiation produced by radioisotopes is gamma radiation. The radioisotopes most commonly used in NDI are cobalt 60, iridium 192, and cesium 137. The potential hazards from these sources depend on whether they are used as stationary or portable units. Personnel exposure from stationary irradiation facilities can be controlled by shielding, interlocks, warning lights or buzzers, and established operating procedures. Exposures from portable sources are much more difficult to control. Portable units are often transported to construction sites to check welds on metal structures and pipes; they can be very small and are easy to misplace. An essential part of operating procedures for portable radiography is to survey the area with a radiation detector before leaving the work area to ensure that no radioactive sources remain. Numerous cases of injury and some deaths have resulted from exposure to misplaced industrial radiography sources.

Neutron radiography, another form of NDI, is used regularly to complement traditional industrial radiography.[24] Because of the high attenuation of thermal neutrons by materials with low atomic numbers (those that are hydrogenous in nature) and very low attenuation to heavy metals, the processed image of a source being studied is reversed in comparison to a typical x-ray image. Lighter materials will appear clearly defined or white on the film. Therefore, items such as sealants, adhesives, lubricants, or plastics will appear clearly on the photographic image.[24] Heavier materials, on the other hand, will appear transparent or dark on the film. Because of its high sensitivity to materials that are hydrogenous or very light, neutron radiography can be employed to study sources that have organic contents within a metal source. Items such as rubber, glue, fluids, and C4 explosive material can be detected easily on the image, whereas with x-ray radiography, they would be obscured by the more metallic and dense material of the source.

Radioactive Commodities

Radioactive commodities that are government property composed in whole or in part of radioactive materials are assigned a National Stock Number or part number. Approximately 3,000 different commodities currently meet this definition, including DU munitions, luminous light sources on fire-control devices, engine components, muzzle reference sensors, and compasses and watches (Figure 22-12). The complete list is found in US Army Technical Bulletin 43-0116, Identification of Radioactive Items in the Army.[25]

Figure 22-12. The M64A1 sight unit with M9 elbow telescope allows observers to see enemy formations from behind a wall or fortified location. Both units combined contain 5.79 Ci of tritium (3H).
Reproduced from: The US Army Center for Health Promotion and Preventive Medicine. Radiological Sources of Potential Exposure and/or Contamination. Aberdeen Proving Ground, MD: USCHPPM; June 1999. Technical Guide 238.

EXHIBIT 22-2

THE ACCIDENT AT GOIÂNIA, BRAZIL

[A]n irresponsibly abandoned radioactive source [that] was … found by innocent, unsuspecting, and uninformed persons seeking potential gain … led to this tragedy.[1]

On Sunday, 13 September 1987 … a source assembly containing a 50.9-TBq (1,375-Ci) 137Cs source was removed from a radiotherapy unit by two scavengers that was left behind in an abandoned clinic. The assembly, weighing about 100 kg, was removed from its shield, loaded onto a wheelbarrow, and taken to the home of one of the men. Neither of them had any idea of its significance. A preliminary attempt was made to dismantle the assembly with the use of a maul and punch. The men managed to break the shutter of the collimator orifice, exposing and rupturing the source in such a manner that fragments of it were spread over the adjacent areas. Small bits of the source were also withdrawn with the aid of a screwdriver. This operation took place on a plot of land shared by several families living in a housing development. The attempted dismantling, which lasted 2–3 h, could not be completed because of the strong resistance of the device.

…

About 3 h after the attempt to break open the apparatus, both men developed nausea followed by vomiting; one of them had diarrhea. The gastrointestinal disturbances persisted for 4–5 d.

…

On 14 September … the assembly was apparently offered to a junkman, according to one of the scavengers. According to the junkman’s version, however, it came into his hands on 18 September … around 4:00 pm, and was placed in a dump in his backyard. At 9:00 pm, when he went back to the dump, he noticed that the object he had purchased earlier emitted some sort of luminescence, which intrigued him sufficiently to cause him to bring it into his house. It remained in the living room until 21 September … accessible to family, friends, and curious neighbors. Later, it was taken back to the dump, broken into pieces, and distributed among various individuals, mostly relatives and friends.[2]

[Brazil’s National Nuclear Energy Commission was informed on 29 September 1987.] During this time [between the removal of the device and the discovery of the emergency by the authorities], many individuals were exposed to various mixes of external irradiation, skin contamination, and internal contamination, mainly due to ingestion.[3]

Approximately 112,000 people were monitored, of whom 249 were contaminated either internally or externally. One-hundred twenty had light surface or clothing contamination and were rapidly decontaminated. One-hundred twenty-nine had moderate to severe internal or external contamination, and 50 required close medical surveillance; 79 persons with low-dose total-body irradiation were managed as outpatients. Twenty persons out of these 50 were hospitalized at the Goiânia General Hospital … and 14 [who] required intensive medical care were transferred to a specialized unit … in Rio de Janeiro. Thirty remained under medical observation at a primary care level unit and other dispensaries.[4]

Fourteen persons developed bone marrow failure and eight of them experienced the prodromal phase of the acute radiation syndrome (ARS).[5]

…

Four … died during the first month after the accident from complications of ARS, including bleeding diathesis and infection.[5] [No information regarding the total number of deaths was given.—Eds.]

Because so much of the public and the city environs were involved, this accident is one of the largest that has occurred, probably exceeded only by the nuclear-reactor accident at Chernobyl, [USSR], in 1986.[1]

___________________

1. The Goiânia radiation accident. Health Phys. 1991;60(1):1–113.

2. Oliveira AR, Hunt JG, Valverde NL, Brandão-Mello CE, Farina R. Medical and related aspects of the Goiânia accident: An overview. Health Phys. 1991;60(1):17–24.

3. Lipsztein JL, Bertelli L, Oliveira CA, Dantas BM. Studies of Cs retention in the human body related to body parameters and Prussian blue administration. Health Phys. 1991;60(1):57–61.

4. The Goiânia radiation accident. Health Phys. 1991;60(1):1–113.

5. Brandão-Mello CE, Oliveira AR, Valverde NJ, Farina R, Cordeiro JM. Clinical and hematological aspects of 137Cs: the Goiânia radiation accident. Health Phys. 1991;60(1):31–39.

Many of these commodities use radioactive materials applied in paints to achieve luminosity.[26] The radioactive material itself is not luminous, but when its energy is absorbed by phosphors (eg, zinc sulfide activated with copper), visible light is produced. For many years, radium 226 was used in luminous paints for such items as watch dials and the instruments in military vehicles. However, radium 226 is both an external hazard and significant internal hazard (if inhaled or ingested) and has been replaced by other less hazardous radioisotopes, such as tritium (heavy hydrogen, 3H).

Radioisotopes have various applications in materials analysis, materials processing, and process control. The response of radiation sensors to radiation that has interacted with the material being measured can be connected to a feedback loop to control the manufacturing process. Also, the unique radiation scattering and absorption characteristics of individual elements and compounds can be used to measure the thickness, density, and moisture content of materials in industrial processes. Testers usually measure the density and moisture content of soils and asphalt with two radioactive sources: cesium 137 (the gamma source) and a mixture of americium 241 and beryllium (the neutron source). Several models of density and moisture testers are available commercially; the standard military model is similar to those used in civilian operations.

In many industrial processes, the rapid movement of nonconducting material through machinery will generate static electricity, which may constitute a fire or explosive hazard, or adversely affect the quality of the product. This static charge can be eliminated by producing ionized air near the charged surface. Polonium, radium, and some beta emitters are used in radioactive static eliminators, which are common in ammunition plants. Radioisotopes can also be used for quality control in materials processing in much the same way that machine-produced radiation is used.

Elements with varied levels of radioactivity are used to calibrate radiation-measuring instruments. Depending on the range and sensitivity of the instrument being calibrated, radionuclides with activities that range from a few microcuries to hundreds of curies—such as plutonium and cesium—are used. Gamma-radiation instruments are frequently calibrated with cobalt 60 and cesium 137. The most common radioactive source used to calibrate neutron instruments is a plutonium-beryllium mixture, which produces neutrons when the beryllium absorbs alpha particles from the decaying plutonium. Plutonium sources are often employed to calibrate instruments used to detect alpha particles. Due to the energy-response characteristics of these instruments, they should only be used for quantitative measurements if they have been calibrated with the same type of radioactive source as that being monitored.

Figure 22-13. The chemical agent monitor (CAM) contains up to 15 mCi of nickel 63 used to ionize air molecules as the air passes through the CAM. The CAM is used to detect nerve and mustard chemical agents.
Photograph courtesy of the US Army Public Health Center.

Other pieces of equipment typically used by the military to help detect chemical agents on personnel and equipment and in the environment are chemical agent detectors (CADs) or monitors (CAMs). These detectors are usually battery operated. The radioisotopes commonly used in CADs and CAMs (Figure 22-13) are americium 241 or nickel 63.26,27

IONIZING RADIATION IN MILITARY OPERATIONS

Nuclear Reactors

The US Army currently maintains one active nuclear research reactor, located in the White Sands Missile Range, New Mexico. The reactor is designed to simulate neutron and gamma radiation that would be encountered in tactical and strategic nuclear environments. The fast-burst reactor (FBR) system operates in both pulse and steady-state modes (to simulate battlefield conditions) and produces neutron and delayed gamma radiation. The reactor system can also be operated in conjunction with other radiation-producing systems; thus, materiel can be tested in a complete nuclear radiation environment. For example, a tank might be tested in a nuclear battlefield simulator to see if its electronic components would be adversely affected by the radiation.

An additional four reactors in the US Army inventory are inactive. The Army Corp of Engineers currently manages three of these reactors (Fort Belvoir, Fort Greely, and James River Reserve Fleet), which have been deactivated but not yet decommissioned. All fuel has been removed from them. The fourth reactor, in Aberdeen Proving Ground, Maryland, is also an FBR; it was fully decommissioned in 2015.[28]

Radiation Produced by Nuclear Weapons

Nuclear weapons are militarily unique sources of ionizing radiation; however, recent events have increased the likelihood of their use as a terrorist weapons in improvised nuclear devices. During the fission process (the process used in atomic bombs), neutrons bombard the nucleus of a heavy element, causing it to simultaneously split into nuclei of lighter elements and release energy. The most commonly used fissionable radioisotopes are uranium 235 and plutonium 239. In contrast, in fusion (the process used in hydrogen bombs), light-weight nuclei join to form a heavier nucleus. The impetus for this reaction is provided by kinetic energy derived from the violent thermal agitation of particles at very high temperatures. The amount of energy released depends on the types of particles colliding and the amount of agitation.

Nuclear explosions generate gamma and neutron radiation, which are highly penetrating (the initial nuclear radiation). In addition, radioactive material from fallout and neutron-activation products remains after a nuclear explosion (the residual nuclear radiation), emitting alpha, beta, and gamma radiation. Exposures to either initial or residual radiation possess a potential risk.

Depleted Uranium

DU is a waste product of the enrichment process of natural uranium. Enriched uranium, processed by the Department of Energy, is typically used for fuel in nuclear reactors or for nuclear weapons. Natural uranium is composed of uranium 238, but it also contains smaller amounts of uranium 234 and uranium 235.[26] DU has a lower content of uranium 235, hence the word “depleted.” The typical decay from uranium is an alpha emission; additionally, beta and gamma radiation is emitted by the daughter products of uranium decay. DU also emits this form of radiation but on a much smaller scale. DU, which is 40% less radioactive than enriched uranium, is considered more of a heavy metal hazard than a radiation hazard.

DU has high mass density and strength. Because of these properties, the military has used DU for the manufacturing of armored components of M1A1 and M1A2 Abrams tanks. The DU found in Abrams tanks provides defense against projectiles of less density than that of armored DU, avoiding penetration of the foreign round and maintaining integrity of the Abrams. DU was extensively used by the military during Operation Desert Storm/Desert Shield and more recently during Operation Iraqi Freedom and Operation Enduring Freedom.

DU is also utilized for the manufacture of armorpiercing projectiles in a sabot configuration (Figure 22-14). Because of the high density, strength, and kinetic energy of the DU sabot round, not only can it pierce through less dense material, but it is also self-sharpening and pyrophoric. Different types of DU ammunition are manufactured for the Abrams tanks, the Bradley Armored Vehicle, the Air Force A-10 Thunderbolt II, and the Marine Corps Harrier aircraft.[27]

Physical Security Systems

Although physical security systems using ionizing radiation have been used for many years, the increased threat of terrorism around the world has prompted the development of several new systems. Physical security systems range from small battery-operated x-ray systems to large, high-energy particle accelerators. Most of these systems image the contents of a package, container, or vehicle in ways similar to how medical x-ray systems are used to image the body. A few systems were also developed specifically for security screening, allowing personnel to conduct quick and nonintrusive security inspections.

Imaging Techniques

Figure 22-14. Depleted uranium (DU) is used in the construction of A1 Abrams tank armor and kinetic DU penetrators placed in 120-mm sabot rounds (used as ammunition for the Abrams).
Diagram courtesy of the US Army Public Health Center.

The simplest imaging technique is to place the item being inspected between an ionizing radiation source and some type of image receptor, as is done in common medical imaging. This is called transmission imaging because the image results from the radiation that is transmitted through the item to the receptor. Areas of high density in the inspected item block more of the radiation than areas of low density, and the image is constructed based on the amount of radiation reaching a specific part of the receptor. X-ray tubes are the most common ionizing radiation source currently used, but some systems use a sealed capsule of radioactive material (usually cesium 137 or cobalt 60). Each source has advantages and disadvantages. For a portable x-ray system used to image small items, the most common image receptor is standard x-ray film, but most systems use some type of digital image receptor.

Another imaging technique is backscatter imaging. Whenever x-rays or gamma rays impinge upon an item, a small fraction of the incident radiation is scattered backward from the item. In backscatter imaging, the radiation source and an array of radiation detectors are placed on the same side of the item being inspected. A narrow, pencil-shaped x-ray beam sweeps across the item as it moves by (or as the source moves by the item), and detectors measure the intensity of the backscattered radiation. A computer algorithm constructs an image of the scanned item.

Each method is useful for imaging specific items. Dense objects such as metal are generally very easy to see on a transmission image. Low-density items, such as drugs and explosives, may be more difficult to see in a transmission image but will show up clearly on a backscatter image. In some physical security systems, both techniques are used simultaneously.

Baggage and Mail Inspection Systems

Baggage and mail inspection systems are used in airports, building entrances, and many mailrooms, employing transmission imaging, backscatter imaging, or both. Current systems employ x-ray sources; gamma ray sources (radioactive materials) are not currently in use. Most baggage and mail inspection systems are considered cabinet x-ray systems, and their manufacture is regulated by the Food and Drug Administration Center for Devices and Radiological Health.[29] The regulations establish limits on the radiation levels permitted outside the cabinet and require safety features such as interlocks, warning lights, and labels. By design, people cannot accidentally insert any part of their body into the x-ray beam.

Cargo and Vehicle Inspection Systems

Cargo and vehicle inspection system are similar in many ways to baggage and mail inspection systems. However, they are typically much larger and use higher energy x-rays or gamma rays. These systems can be either stationary or mobile. Stationary systems are permanently installed at an inspection site, and the cargo container or vehicle is brought to the system for inspection. Stationary systems may be mounted on rails or otherwise able to move over a limited distance in order to scan a vehicle or cargo container, or the vehicle or container can be moved past the system. Other cargo and vehicle inspection systems are mobile, truck-mounted versions that can be moved to any location where cargo or vehicles may need to be inspected (Figure 22-15).

Figure 22-15. Cargo and vehicle inspection systems. The radiation beam is directed toward the detector tower mounted on the truck. This system can acquire both transmission and backscatter images. The x-ray source is located inside the truck box and the radiation beam is directed outward. Photographs courtesy of Leidos.

Most cargo and vehicle inspection systems are not cabinet systems, and although they have safety features such as warning lights, labels, and interlocks, a person can easily enter the inspection area, including stowaways hidden inside cargo container or vehicles. This creates an increased potential for exposure. For cargo and vehicle inspection systems, following correct operating procedures is a key aspect of radiation protection.

Personnel Security Screening Systems

Most personnel screening systems use low-energy x-rays and a backscatter imaging technique to identify items hidden under a person’s clothing. These backscatter systems create an image of the body surface and any items hidden on it. Due to the detail of these images, one of the primary concerns people have about this type of screening is privacy. The radiation dose to the scanned individual is very low for backscatter systems. Most US organizations involved in personnel security screening are considering back-scatter systems.

Personnel security screening systems are categorized as either general-use or limited-use systems.[30] A general-use system is considered acceptable for general screening of large numbers of people. To be considered a general-use system, the dose an individual receives for a single scan must not be greater than 0.1 μSv (10 mrem). A limited-use system is considered acceptable for occasional scanning of individuals based on a specific need. To be a limited-use system, the dose from a single scan can be greater than 0.1 μSv (10 mrem) but must not be greater than 10 μSv (1 mrem).

Transmission screening systems are capable of locating items that have been swallowed or hidden inside body cavities; however, the dose to the screened individual is somewhat higher than for a backscatter system, so use limits are required. A current transmission screening application is the prevention of diamond theft by employees at diamond mines.

Neutron analysis systems are somewhat different than the x-ray and gamma-ray systems discussed above in that they are generally not used to produce an image of the item being inspected. Instead, the item is bombarded with neutrons, causing some of the atoms in it to emit gamma rays. The gamma rays are emitted at specific energies characteristic of the elements present in the item. A radiation detector measures the energy of the gamma rays emitted, and the composition of the item can then be determined. This technique has been used in industrial applications for many years, but its application to security screening is still in the development and testing stage.

Radiation Dispersal Devices

A radiation dispersal device (RDD), commonly known as a “dirty bomb” (though a dirty bomb is only an example of these devices), is an improvised assembly or process, other than a nuclear explosive device, designed to disseminate radioactive material to cause destruction, damage, or injury. Such a weapon can be easily developed and used by a terrorist with explosives (or other means of dissemination) and access to radionuclides. The material dispersed can be obtained from any location that uses radioactive sources, such as a nuclear waste processor, nuclear power plant, university research facility, medical radiotherapy clinic, or industrial complex. The radioactive material is dispersed using explosives or other means (eg, crop-dusting aircraft).27,31

There are several likely scenarios for the development of an RDD. Most involve the use of radioactive material in solid form with radiation exposure levels low enough that the terrorist’s ability to carry out an attack is not inhibited.[32] Such weapons would not cause a significant number of acute radiation casualties; however, they might cause a large psychosocial impact and potentially overload medical and support systems with patients complaining of psychosomatic symptoms.[32]

Although the use of large sources with highly penetrating radiation in an RDD is possible, these devices would be difficult to handle safely and are easily detectable by law enforcement.[32] In addition, the shielding required by those who would fabricate and deploy these devices complicate their use as an effective terrorist weapon. Though difficult to deploy and requiring shielding, RDDs that could cause significant radiation casualties could be deployed by perpetrators with considerable technical expertise and sophisticated resources.[32]

Radiological Base Camp Assessments

Radiological base camp assessments[33] are used to determine radiological health risks associated with deployment to an area known to have radiological contamination or a history of radiation or radioactive material uses. The assessment’s purpose is to characterize external radiation exposures and to collect radiological air, soil, and water samples from their associated pathways that could have a potential negative impact on soldiers’ long-term health.

The radiological base camp assessment process[33] has evolved over the past decade due to a shift in doctrine concerning soldiers’ exposure to ionizing radiation. During the Cold War, the military used two distinct policies for protection against ionizing radiation. In garrison situations and in peacetime, military regulations for radiation protection were patterned after those of civilian regulatory agencies such as the Nuclear Regulatory Commission, Occupational Safety and Health Administration, and Environmental Protection Agency. At the strategic level and during war, only short-term radiation exposures that affected mission accomplishment were considered.

In the years following Operation Desert Shield and Operation Desert Storm, the Department of Defense (DoD) has improved its doctrine for protecting soldiers from ionizing radiation and other toxic industrial chemicals and materials. Several directives, such as Presidential Review Directive-5[34] and DoD Instruction 6490.03,[35] issued in 2006, state that the military will identify, minimize, and assess exposure to radiation and other toxic substances before, during, and after all military operations including war. To comply with these directives, the DoD has developed processes to conduct occupational and environmental health surveillance and joint medical surveillance to anticipate, manage, evaluate, and control health and safety risks encountered during the full cycle of predeployment, deployment, employment, and postdeployment activities. As part of this effort, radiological base camp assessments were performed during Operation Enduring Freedom and Operation Iraqi Freedom in several countries throughout the world (Figure 22-16).

Figure 22-16. Health physics personnel from the US Army Public Health Center perform field radiation measurements during a field exercise.
Photograph courtesy of the US Army Public Health Center.

BIOLOGICAL EFFECTS OF RADIATION

The biological effects of radiation exposure depend on the type, dose rate, and total dose an individual receives. The term exposure is generally used qualitatively to mean the circumstance in which a person moves into, or is irradiated by, radiation emanating from an x-ray machine, a particle accelerator, or a source of radioactive material. The quantitative term dose or absorbed dose characterizes the amount of radiation energy absorbed by a medium (eg, an individual or an individual’s organs or tissues). Dose is measured in units of grays (Gy) or rads, where 1 Gy is equivalent to 1 joule (J) per kilogram of absorbing medium, and 1 Gy is equivalent to 100 rads. To put these amounts in perspective, a posteroanterior-lateral chest radiograph delivers a whole-body dose of approximately 0.0001 Gy, and a CT scan delivers approximately 0.03 Gy to the irradiated area.

Health physicists use the term dose equivalent to account for the fact that certain types of radiation, such as neutrons, are more dangerous than other types. The dose equivalent is measured in units of sieverts (Sv) or rem, where 1 Sv is equivalent to 1 J/kg of body weight, and 1 Sv is equivalent to 100 rems. The dose-equivalent limit for an occupational radiation worker is 0.05 Sv, or 5 rem/year.

The amount of radioactive material is described by the term activity. Activity is measured in units of becquerels (Bq) or curies (Ci), where 1 Bq is equivalent to 1 disintegration per second (dps), and 1 Ci is equivalent to 37 billion Bq. Typical radiopharmaceutical activities used in nuclear medicine, for example, are 0.4 to 4,000 megabecquerels (MBq), or approximately 0.01 to 100 millicuries (mCi).

Recognition of Effects

Almost immediately after the discovery of x-rays came the first reports of their apparent adverse effects on health. Reports of skin reactions such as erythema and loss of hair from prolonged x-ray exposure increased during 1896.[5] These effects were initially considered trivial, and only years later were the cumulative damage and late complications of radiation exposure recognized. Borden noted that during the Spanish-American War (1898), serious burns to some patients had been induced:

It appears that the factors which influence the production of Roentgen ray burns are (a) the length of exposure; (b) the nearness of the tube to the surface of the body; (c) the physical condition of the patient; and (d) individual idiosyncrasy. Relative to the length of exposure: it should not exceed thirty minutes, for with this length of exposure any part of the body may be radiographed, provided the apparatus is working properly and good technique is used. If photographic results are not obtained with a thirty-minute exposure, the operator should look to improving his apparatus or technic rather than to lengthening the time which he exposes the patient to the action of the rays.[8]

Incidents of roentgen-ray burns had been induced by prolonged and frequently repeated exposures, one of which is shown in Figure 22-17. Borden’s account continues, describing a patient’s exposure:

Six days after the last exposure, slight redness of the skin appeared on the front of the chest and shoulder. This erythematous condition increased and, two days later, small blebs appeared. These broke and small ulcers formed which gradually spread and coalesced. The tissue necrosis deepened, extended, and was accompanied by marked pain and hyperesthesia. The inflammatory action continued until the burn nearly covered the entire right breast.

Treatment of various kinds was tried, but the greatest benefit was derived from continuous application of lead and opium lotion. The burn showed no sign of healing for four months. After that time it gradually grew better, but the healing process was very slow and the burn was not entirely healed until eleven months after its first appearance.[8]

Figure 22-17. Radiation injury to the skin of a Spanish-American War soldier as a result of an x-ray examination, 1898. The radiation exposure necessary to cause this type of burn is greater than 600 R. Current technology allows a radiologist to obtain better diagnostic information at exposures that are 1,000-fold lower than the exposure this patient received.
Reproduced from: Borden WC. The Use of the Roentgen Ray by the Medical Department of the United States Army in War with Spain (1898). Washington, DC: Office of The Surgeon General, DA; 1900.

During the early years of x-ray use, the fluoroscopic hand test (Figure 22-18) was routinely taught.[4] This procedure, in which the radiologist or an assistant placed his or her hand in the beam, was used to gauge the beam’s “hardness” or “softness.” The hardness of an x-ray beam is a relative measure of the beam’s average energy. The hardness test, using an individual’s hand to absorb the beam, was used to determine contrast while adjusting the energy output of the x-ray system. A large number of hand injuries, many of which progressed to malignancy, resulted from this procedure. Clarence Dally, Thomas Edison’s assistant, was an early casualty in 1904 (Figure 22-19).[5]

Figure 22-18. The classical posture of the radiation pioneer, shown in 1896 using his hand to test the hardness of the x-ray beam. The term “hardness” was used to describe the energy of the x-ray beam: the more penetrating the x-ray, the harder the beam. An x-ray beam that was too soft would not pass through the tissue of the hand onto the film; one that was too hard would not be stopped by dense material such as bone, and contrast on the film would be lost. Therefore, operators often used their own hand as the imaging object, adjusting the unit to balance penetrability with contrast. Repeated exposures of this type over several years cost many their fingers and hands.
Reproduced from: Feldman A. A sketch of the technical history of radiology from 1896 to 1920. RadioGraphics. 1989;9(6):1113–1128. Copyright: The Radiological Society of North America (used with permission).

Figure 22-19. Thomas Edison looks through the fluoroscope; his subject is his assistant, Clarence Dally, who died in 1904 due to his frequent exposure to x-rays.
Reproduced from: Feldman A. A sketch of the technical history of radiology from 1896 to 1920. RadioGraphics. 1989;9(6): 1113-1128: Copyright: The Radiological Society of North America (used with permission).

With the recognition that health effects were associated with radiation exposure, physicians and other scientists began to investigate. In 1901, Becquerel realized that the 200 mg of uranium that he carried in his vest pocket had burned his skin. The burn ulcerated and healed very slowly. That same year, Pierre Curie tested the effect of radium on his own arm and developed a significant lesion. In 1904, Curie and two other physicians conducted experiments with radium on animals and noted that radium killed diseased cells preferentially.[5]

Most of the general public and the industrial community were oblivious to radiation’s apparent health effects, and many projects before, during, and after World War I utilized radium. For example, just before World War I, radium 226 was used to create a self-luminous effect on expensive watches and other instruments, achieved by painting the items with a mixture of zinc sulfide and a minute amount of radium. An entire industry arose to supply the demand for these glow-in-the-dark novelties. The industry, centered in northern New Jersey, employed as many as 2,000 workers, most of them young women. The entry of the United States into World War I created a massive demand for luminous dials. After World War I, the industry sought new markets, including luminous doorknobs and light switches.[36]

The health effects of radium exposure accompanied the manufacturing of these luminous items. The radium-containing paint was applied using fine brushes, which the workers “tipped” with their lips. Thus, each worker ingested radium daily. By late 1923, the industry warned its workers against tipping their brushes, but much damage had already occurred. In 1924, the first report of human radium poisoning was recorded. A young woman employed in the industry was referred to Theodore Blum, a New York dentist and oral surgeon, when her jaw failed to heal after dental work. The inflammation and signs of necrosis indicated to Blum that the bone was dying. Aware that the woman had been employed painting figures on dials with radium-containing paint, Blum correctly attributed the condition to radium ingestion. Because radium is chemically similar to calcium, the radium that she (and other dial painters) absorbed became incorporated into bone, where it constantly bombarded the bone and its marrow with alpha particles and gamma rays.[36]

Dial painters were not radium’s only victims. Chemists and workers who extracted radium from its ores or prepared its compounds in the laboratory were also affected. However, perhaps the largest group of victims consisted of people who deliberately ingested radium for quasi-medicinal purposes. Radium ingestion was almost a fad at that time, and it could be purchased over the counter. A prominent Pittsburgh industrialist, Eben M. Byers, was a faithful user of an elixir containing 37 kBq (1 μCi) of radium 226 and an equal amount of radium 228 in one-half ounce of water.[15] His avid consumption of the elixir led to his death in 1932, which was reported nationally.[36]

Eventually, scientists involved in radiation research also became victims of its effects. Marie Curie’s death from aplastic anemia was attributed to her significant and prolonged exposures to radiation. Before she died in 1934, she developed cataracts, and her hands had sustained radiation damage.[37]

Medical professionals were able to observe and document one of the first cases of acute fatal radiation injury in May 1946. Louis Slotin, a young physicist working at Los Alamos, New Mexico, noted that a nuclear chain reaction was developing criticality too rapidly. Realizing that the impending powerful explosion must be averted, he broke up the reactor pile with his bare hands, thereby exposing himself to massive levels of radiation. He died within a few weeks.[5]

Categories and Mechanisms of Effects

The early recognition of harmful effects were associated with doses at least 10-fold higher than the current occupational limit for radiation workers (50 mSv/y). By consensus within the radiological community, these effects are categorized as somatic (to non-germ cells), genetic (to germ cells), and teratogenic (to fetal cells). Somatic effects are sustained by the exposed individual. These may be further divided into prompt effects (such as the skin reddening experienced by the early pioneers of radiation use), and delayed effects (such as cancer), which become manifest years after the exposure. Genetic effects include abnormalities that can occur not only in the offspring of exposed individuals but also in succeeding generations. Although genetic effects have been documented in animal studies, no genetic effects have been confirmed in humans. Teratogenic effects occur in children who were exposed during their embryonic or fetal stages of development. Fetal exposure to even low doses of radiation can cause central nervous system malformations, decreased birth weight and head size, and childhood cancer, and no medical interventions are available to alter the course after exposure. If a fetal exposure occurs, a qualified radiation physicist should calculate the estimated dose and assist in counseling the mother on the risks.

Exposure to ionizing radiation causes two types of biological damage: cell death and cancer induction. Cell death, which usually occurs at intermediate to high doses of radiation, is defined as the cessation of the cell’s aerobic metabolism or the loss of its ability to divide. Obviously, a casualty’s health is threatened if a large number of critical cells die. The effects of intermediate doses can range from subclinical, to protracted severe illness, to death. In general, high doses at a high dose rate are fatal. Factors specific to the exposure, such as whole- or partial-body exposure, external irradiation or internal deposition, and a chronic or acute exposure period, will determine the casualty’s response.

Unlike cell death, the mechanisms by which radiation induces cancer and leukemia are not well understood. One theory is that radiation injury to a cell allows the expression of a normally suppressed oncogene. Perhaps this process is initiated by the disruption of chemical bonds, which are weak compared to the energy of a single x-ray, gamma ray, or electron. Thus, small amounts of radiation may be carcinogenic. A latency of 10 to 20 years or longer exists before cancer is expressed; a latency of 2 to 4 years is characteristic of leukemia. This long latency, and the fact that radiation-induced cancers are indistinguishable from other cancers, combine to make low-dose exposures difficult to follow up.

Occupational Radiation Risks

The term stochastic means, for the effect in question, that a statistical distribution exists over time, and therefore includes the element of chance for all individuals. Stochastic effects occur with a certain frequency in any irradiated population, but predictions cannot be made for any specific irradiated individual. The frequency of the effect may increase with increasing dose, but the severity of late stochastic effects is not related to the exposure level. Thus, the likelihood of developing a cancer because of radiation exposure increases with increasing dose, but the cancer or hereditary defect remains an all-or-none phenomenon; an individual either develops, or does not develop, the defect. Non-stochastic effects are not statistical: every exposed individual will experience the effect at a certain dose level. For example, every individual exposed to an acute dose of 1 to 2 Sv will experience leukopenia (an abnormally low number of circulating leukocytes). The exact dose level that causes this effect in a particular individual varies, but all individuals exposed will be affected. Nonstochastic effects can be avoided in all normal circumstances simply by restricting exposures to below the threshold. Skin reddening, cataracts, and prompt death are examples of nonstochastic effects; below their thresholds, these effects do not occur.

At the relatively low levels of occupational exposure to radiation that have been achieved in the United States, it is difficult, if not impossible, to show a relationship between exposure and effect. Thus, uncertainty and controversy surround risk estimates. A common assumption in radiation protection is that the probability of the occurrence of stochastic effects is proportional to the radiation exposure, and that no threshold exists. Using this linear, no-threshold hypothesis, it is impossible to eliminate stochastic effects other than by eliminating exposure. In addition to this hypothesis, a large human biological database of radiation effects exists, including Japanese survivors of the 1945 atomic bombing, dial painters occupationally exposed to radium, people who have received therapeutic radiation or doses of radioactive material, and uranium-mine workers at risk of lung cancer. Several complications limit the application of these data to radiation-risk assessments, however. For example, all the observed effects occurred in populations who received doses much higher than those currently allowed for occupational exposures.

In a 2005 report,[38] the National Academy of Sciences estimated the lifetime excess risk of death from cancer after an acute, whole-body dose of 0.1 Sv to be 0.8%. A radiation worker whose annual exposure did not exceed 10% of the maximum permissible dose would require at least 20 years to accumulate a 0.1 Sv total dose. The report further states that the individual lifetime risk of acquiring cancer in the absence of radiation exposure is 22%. Therefore, exposure to 0.1 Sv of ionizing radiation raises the total risk to 22.8%. These risk estimates, however, have limitations: extrapolation to lower doses, for which actual data are not available, requires the assumption that the risk is a linear function of the dose. This is not an unreasonable assumption, but it cannot be validated. Departure from linearity could cause either an underestimate or an overestimate of the risk from lower doses. Also, because the confidence limits on the risk at low doses include zero, the available epidemiological data do not exclude the possibility of a threshold dose below which there is no increased risk.[38]

PROTECTION AGAINST RADIATION

As adverse radiation effects became better documented and understood, the field of radiation protection began to develop. The radiation protection that existed before World War II focused primarily on the practitioner, without considering protection for the patient. Even so, the operator dose deemed acceptable at that time would be excessive by today’s standards. While the scientific community was aware of the adverse effects of high radiation doses, they were unaware of the delayed, cumulative, long-term effects of smaller, fractionated doses received over time.

Scientists began to formulate conclusions after studying many cases of radiation-induced effects. By 1948, the consensus was that a threshold for radiation effects might not exist; therefore, an element of risk might be incurred with any exposure. The acceptance of this philosophy radically changed the approach to radiation protection. Prompted by the global fallout from aboveground nuclear weapons testing, public concern about the delayed, long-term effects of low-dose radiation mounted in the 1950s and 1960s. At the same time, data gathered from atomic-bomb survivors in Japan provided evidence of the carcinogenic effects of radiation. Federal funds were allocated for research, the results of which indicated that some radiation effects may have no threshold.[39]

The combination of the dose from global fallout and the possibility that some effects have no threshold prompted the expansion of radiation protection initiatives to include the general public as well as the occupationally exposed. For example, the US Public Health Service (USPHS) initiated a nationwide program to monitor air, water, and food for radioactivity. Responding to public concern, the scientific community also focused on limiting exposures from diagnostic x-rays. In the early 1960s, the USPHS initiated a program to reduce these exposures. Equipment was evaluated, restrictions were implemented, and x-ray operator techniques were reviewed to help ensure that quality images were produced with minimum radiation exposure to the patient as well as to the medical personnel. Information disseminated to the medical profession emphasized that medical professionals should exercise sound judgment concerning the clinical necessity for any x-ray examination they order.[39] Today, although the long-term effects of small radiation doses are understood in general, scientists are still struggling to precisely define and quantify small exposure levels and their effects.

Emergence of Radiation Protection

Only after 1900 was an effort made to build protection into x-ray tubes. H. Albers-Schonberg, who had experienced chronic x-ray–induced dermatitis, proposed restrictions on exposure frequency, a 30-cm distance between the tube and the patient, a leaded tube housing, additional lead shielding for the operator, and abandoning the hand test for the hardness of the beam.[40]

William Rollins, a Boston-area dentist, pioneered many advances in radiation protection. In 1896, he advocated using x-ray machines in rooms with lead-shielded walls, and in 1902 he suggested that fluoroscopists be provided with leaded-glass goggles and x-ray systems outfitted with shielded tube housings.[40]

World War I spawned increased x-ray hazards, as more people used and were exposed to radiation from x-ray equipment, but it also engendered huge advances in x-ray development and radiation protection. The massive scale of war-related injuries placed immense demands on x-ray capabilities. In addition, wartime pressures produced hasty training, makeshift equipment, and carelessness. At the war’s conclusion, many technologists, radiologists, and physicists with wartime experiences with radiation returned to the civilian community. Also at this time, the death rate among radiologists from radiation exposure was noted to be rather high.[36] These concerns led to more research and a sharpened focus on radiation safety. Until this time, safety practices had concentrated on protecting workers from acute exposure that would cause severe erythema but had not been stringent enough to protect against cumulative exposures that could lead to cancer.

Dr George Pfahler, a Philadelphia radiologist, and Dr J.S. Shearer, a Cornell University physicist, contributed to the understanding of the hazards that medical radiation poses to both the patient and medical personnel. Shearer, who had served in the US Army during World War I, developed a portable bedside x-ray unit for field use. He was also involved in initiating and conducting an x-ray training school in New York for Army personnel.[16]

The formation of various interest groups demonstrated that the subject of radiation protection had reached the international level. In 1925, the first International Congress of Radiology convened in London to discuss the possibility of a universal unit for radiation exposure. The radiologists were generally content with the unit skin dose (ie, the erythema dose, or the amount of radiation necessary to cause the skin to redden) as the standard, but the physicists campaigned for an ionization-based unit. The physicists’ triumph at the Congress’s 1928 meeting in Stockholm led to the adoption of the Roentgen (R), measured by the ionization in air, as the international x-ray unit. The International Committee on X-ray and Radium Protection, which was later renamed the International Commission on Radiation Protection (ICRP), also was founded at this meeting.[37] Since 1928, this group has established the basic pattern for radiation protection recommendations throughout the world. Lauriston S. Taylor of the National Bureau of Standards was also the American member of the original International Committee on X-ray and Radium Protection. On his return to the United States, Taylor immediately established the Advisory Committee on X-ray and Radium Protection, which later became the National Council on Radiation Protection and Measurements (NCRP), to promote radiation protection in the United States.[36] This organization met for the first time in 1929.

Advances in radiation protection continued in 1929 with the production of an electrically insulated, radiation-shielded x-ray tube. This unit contained radiation within a glass-lined, chromium-iron cylinder surrounded by lead; radiation was allowed to emerge only from a small aperture in the lead protective shield. This design provided both operator and patient with a significant degree of radiation protection; it also eliminated the hazard of severe electric shock that had been associated with uninsulated tubes.[37]

The Manhattan Project prompted the next surge of radiation-protection activity. Physicists recognized that the project would create a new and intense source of radiation and radioactivity. Ernest O. Wollan, a cosmic-ray physicist at the University of Chicago, was asked to form a group to study and control the resulting radiation hazards.[16] The quantities and varied characteristics of the new radionuclides created by nuclear fission would require the full-time attention of a new group of specially trained professionals: health physicists.[37]

The radiation-exposure safeguards developed and used during the Manhattan Project include remote handling of radioactive material; special clothing, laundry, and decontamination procedures; controlling access to “hot” areas; monitoring workers and workplaces; reviewing exposure records; investigating exposures; training workers; and keeping exposures as low as possible. These measures form the basis of radiation protection today.[36]

Development of Dosimetry

Rome Vernon Wagner, an x-ray tube manufacturer, introduced an early form of dosimetry at the American Roentgen Ray Society meeting in October 1907. Wagner reported his practice of carrying an unexposed photographic plate in his pocket each day, and then developing it to determine if he had been exposed to x-rays.[16] This practice led to the use of film-badge dosimeters to monitor radiation exposure.

The use of film-badge dosimeters became a recommended practice in the 1920s, and developments in dosimetry continued. Based largely on the work of New York radiological physicist Edith Quimby, by the end of the decade radiologists recognized that the film should be housed in a holder equipped with filters to determine the energy of the radiation exposure. Health physicists with the Manhattan Project refined this technique of using filters and correlating optical density with dose.[16] The US Army initially used film badges to monitor radiation exposure but replaced them with thermoluminescent dosimeters (TLDs) between 1985 and 1989. From that period on, the TLD became the device of choice for monitoring personal radiation exposures in industrial and medical settings within the US Army. All TLDs are collected and processed, and final results are recorded and archived at the US Army Dosimetry Center (ADC) at the Army’s Redstone Arsenal in Alabama.

Development of Standards

Various national radiological societies began to issue rules for radiation protection during World War I. One of the early recommendations was to limit exposures to approximately 10% of the erythema dose. As German physicist Hans Kustner had demonstrated, the erythema dose is approximately 600 R (600 cGy in modern units).16,37 In June 1915, the British organized a radiation-protection interest group charged with preparing a brief outline of protection requirements for the safe operation of x-ray equipment.[16] World War I interrupted this work, but the members regrouped after the war and drafted extensive recommendations for radiation workers, encompassing both diagnostic and therapeutic protection.[16]

After World War I, scientists focused on the concept of tolerance dose. The application of toxicological experience to radiation exposure led practitioners to believe that a safe dose existed. The concept of a tolerance dose arose from the belief that below this radiation threshold level, damage would not be permanent due to biological repair. In 1924, Arthur Mutscheller made the first real attempt to define the tolerance dose, and his work served as the basis for radiation safety standards for nearly 2 decades.[37] As the quantitative means to measure radiation exposure were developed, tolerance doses were expressed in quantitative form. Mutscheller concluded early that, while absolute safety was not feasible, improvements in safety were both achievable and essential. He proposed a tolerance dose of 6 R, which is 10% of the erythema dose per month. Swedish physicist Rolf Sievert, working independently, proposed the same tolerance dose in 1925. This concept endured for some time, even though Herman J. Muller demonstrated in 1927 that a threshold probably did not exist for radiation-induced mutations.[37] By 1928, most physicists in the health field accepted Mutscheller’s proposed tolerance dose. In 1931, the ICRP recommended shielding tables based on a tolerance dose of 0.00001 R/second.[36]

In 1934, the American Advisory Committee on X-ray and Radium Protection suggested a tolerance dose for radium exposure of 0.1 R/day to the whole body and 5 R/day to the fingers. The committee had actually calculated a dose of 0.24 R/day, but, concerned about the assumptions used to arrive at that value, it decided to take a conservative approach and proposed 0.1 R/day instead. The same year, the ICRP set the daily dose at 0.2 R/day. The basis for this calculation was the same as the American Advisory Committee’s; however, the ICRP was less conservative in its approach.[36]

In 1941, the National Bureau of Standards published Safe Handling of Radioluminous Compounds,[41] which continued the use of 0.1 R/day as the permissible level for external exposure to radiation workers. However, it also incorporated the concepts of maximum permissible body burden of an ingested radionuclide (0.1 mCi [3.7 MBq] of radium, based on the work of Robley Evans), and a maximum permissible concentration of a radionuclide in the workplace (10 pCi [0.37 Bq] of radon per L of ambient air). Also in 1941, limits were established by setting the safe level lower than the amount of radium retained in any of the radium-dial painters who developed bone cancer,[37] and the same year Taylor recommended that the permissible level for external exposure be reduced to 0.02 R/day, which is approximately 5 rem/year (50 mSv). The rem unit, which accounts for the biological effectiveness of the radiation and the maximum permissible concentration for inhaled radioactivity, was a byproduct of the Manhattan Project.[16]

After World War II, the NCRP, the Atomic Energy Commission, and the USPHS actively promoted radiation protection, focusing their attention on refining exposure limits. The concept of tolerance dose was replaced by maximum permissible dose, which did not necessarily imply a threshold. The whole-body maximum permissible exposure, previously established at 30 R/year in 1936 by the US Advisory Committee on X-ray and Radium Production,[39] changed to 15 rem/year in 1948, and then to 5 rem/year in 1958.[37] In 1949, the NCRP introduced the concept of a lower radiation level for non-occupational exposure. This level was 10% of the allowable exposure for radiation workers.

Regulatory Agencies

A decade of federal involvement in radiation protection began in 1959. Members of key agencies involved in nuclear work formed the Federal Radiation Council (FRC), charged with providing regulatory guidance concerning radiation protection to federal agencies. In 1970, the FRC was abolished, and the Environmental Protection Agency (EPA) assumed its responsibilities. Today, the regulatory structure includes the Occupational Safety and Health Administration (OSHA) and the US Nuclear Regulatory Commission (NRC) as well as the EPA.

A milestone in radiation protection occurred in 1969 with the passage of the Radiation Control for Health and Safety Act.[39] As a result of the act, the USPHS assumed responsibility for regulating the performance of imaging equipment and promulgated the first standard for diagnostic x-ray equipment.

Further regulatory control has been introduced during the modern era:

- mandatory licensing of radionuclides,

- certification of machine sources of radiation,

- requirements for improved education and training of radiation workers, and

- implementation of radiation protection programs based on the concept of keeping radiation levels as low as reasonably achievable (ALARA).

The Atomic Energy Commission, which had been established in 1946,42–44 was dissolved in 1975, and its activities relating to technology promotion were assigned to the Energy Research and Development Administration (later incorporated into the Department of Energy); its regulatory authority was assigned to the newly created NRC. Today, the Department of Energy owns the nuclear weapons in the custody of the armed forces, and it operates several research and development laboratories. The EPA is also concerned with radiation protection and regulation: it published Radiation Protection Guidance to Federal Agencies for Occupational Exposure in January 1987, and currently has several programs in place to protect people and the environment from the potentially harmful effects of ionizing radiation. OSHA sets standards for the protection of employees who use any type of ionizing radiation source in the workplace.

Occupational Dose Limits

Because the United States has various regulatory bodies and authorities, current limits vary. The EPA, the NRC, OSHA, and the individual states all promulgate limits based on recommendations of international or national scientific advisory bodies. However, for US Army personnel, allowable exposure limits in the workplace (Exhibit 22-3) are prescribed by Department of the Army Pamphlet (DA PAM) 385-24,[45] which is in accordance with Title 10, Code of Federal Regulations (10 CFR), Part 20.[46] Planned special exposures, while defined in 10 CFR, Part 20, and permitted under NRC licenses under very limited, highly controlled circumstances, cannot be performed by Army or Defense Logistics Agency NRC license holders without a waiver.[46]

The occupational dose limits presented in both 10 CFR, Part 20,[46] and DA PAM 385-24[45] are as follows.

- For the annual whole-body dose limit, the more limiting of either:

○ the total effective dose equivalent being equal to 5 rem (0.05 Sv), or

○ the sum of the deep-dose equivalent and the committed dose equivalent to any individual organ or tissue other than the lens of the eye being equal to 50 rem (0.5 Sv).

- For the annual limits to the lens of the eye, the skin of the whole body, and the skin of the extremities:

○ a lens dose equivalent of 15 rem (0.15 Sv), and

○ a shallow-dose equivalent of 50 rem (0.5 Sv) to the skin of the whole body or to the skin of any extremity.

Emergencies may require first responders or occupational radiation workers to exceed the dose limits prescribed above in order to save lives or valuable property. In an emergency, responders or workers must weigh the benefit of action against the relative risk of radiation exposure. When exposure limits will be exceeded, the incident commander, to the extent the situation allows, should consider the following[47]:

- Acute effects are likely at about 1,000 mSv (100 rem).

- The lethal dose to 50% in 60 days is about 4,000 mSv (400 rem).

- Rescuers must be volunteers and must be fully informed of the risk if the dose equivalent expected is greater than 250 mSv (25 rem). Rescuers’ dose equivalent should not exceed 500 mSv (50 rem).

- Rescuers should be briefed on the potential acute radiation effects and statistically inferred increased risk for cancer from doses that may be received during the operation.

- When emergency actions do not involve lifesaving rescue, but may include protection of valuable property or equipment, exposures should not exceed 100 mSv (10 rem).

Most Army personnel who work with radiation receive an occupational radiation dose (the total dose minus both the background dose and any additional dose from a prescribed medical procedure) that is lower than their background dose. The average background dose in the United States is around 3 mSv/year. Occupational radiation doses below the background are not necessarily acceptable from a public health planning perspective, because the risk of developing a fatal cancer from radiation exposure potentially increases with increased dose. Therefore, occupational health programs consider all occupational ionizing radiation exposure to be potentially harmful and attempt to keep exposures ALARA.

Non-occupational Dose Limits

In an attempt to limit radiation exposures from the use of sources of ionizing radiation, non-occupational dose limits were developed both for individuals in the general public and for the population as a whole. The accumulated radiation dose equivalent to the whole body for a person in the general public must not exceed 1 mSv in any calendar year (100 mrem/y). This limit excludes natural background radiation, prescribed medical and dental exposures, and the contribution from any authorized disposal of licensed radioactive material into the sanitary sewage system. Authorization to exceed 1.0 mSv/year (but not to exceed 5 mSv/y [500 mrem/y]) must be requested, through command channels, from the director of Army safety. NRC licensees must request authorization from the NRC per 10 CFR, Part 20.[46]

EXHIBIT 22-3

ARMY PERSONNEL IONIZING RADIATION EXPOSURE STANDARDS

Category

Maximum1,2,3

Member of the general public

1 mSv (100 mrem) (TEDE) in calendar year^4

Fetus/embryo of occupationally exposed declared pregnant woman

5 mSv (500 mrem) (DDE of mother + ED due to radionuclides in fetus/embryo) for gestation period, not to exceed 0.5 mSv/month

Occupational exposure of adults

50 mSv (5 rem) (TEDE) in calendar year

Lens of the eye

0.15 Sv (15 rem) (EDE) in calendar year^3

Skin or extremity

0.5 Sv (50 rem) (SDE) in calendar year

Occupational exposure of minors

10% of limits for adults

1. From 10 CFR 20. Refer to 10 CFR 20 for detailed standards.

2. Abbreviations: TEDE = total effective dose equivalent; DDE = deep dose equivalent; ED = effective dose; EDE = effective dose equivalent; CDE = committed dose equivalent; SDE = shallow dose equivalent.

3. OSHA standard for occupational exposure of adults and for the lens of the eye is 1¼ rem (12.5 mSv) in calendar quarter. OSHA standard for skin of whole body is 7½ rem (75 mSv) in calendar quarter. OSHA standard for hands and forearms; feet and ankles is 18¾ rem (187.5 mSv) in calendar quarter.

4. The dose in any unrestricted area from external sources, exclusive of the dose contributions from patients administered radioactive material and released in accordance with applicable regulations, will not exceed 2 mrem (0.02 mSv) in any one hour.

Reproduced from: US Department of the Army. The Army Radiation Safety Program. Washington, DC: DA; 2015. DA Pamphlet 385-24: 23.

MEDICAL RESPONSE TO RADIATION INCIDENTS

In today’s geopolitical climate, injury from ionizing radiation is less likely to result from a wartime nuclear detonation than from an isolated terrorist incident or an accident at a facility that uses high-energy x-ray systems or uses or stores radioactive material. Such an event could produce individual to several hundred casualties, even to several thousand in a terrorist incident. It is probable that at least some medical personnel and facilities would be available to respond, and while such an event would certainly be a catastrophe, it probably would be manageable.[47]

Types of Exposures

Radiation exposures are classified as (a) internal deposition, (b) external irradiation, (c) combined external irradiation and internal deposition, (d) hot-particle trauma, and (e) mass casualties.

Internal Deposition

Most internal deposition involves gas, vapor, or dust inhalation; other possible routes of entry such as ingestion, needle sticks, and skin absorption are less likely. Fortunately, the likelihood that acute effects will result from internal deposition is very small. However, medical intervention has little effect once the deposition has occurred. Thyroid-blocking agents are effective if administered within a few hours after radioiodine I 131 has been ingested. Dilution through the administration of large volumes of fluids can be effective for tritium, while chelating agents such as diethylenetriamine pentaacetic acid (DTPA) can be effective in enhancing the biological elimination of plutonium and certain other heavy metals. As soon as an internal deposition accident is suspected, medical personnel should seek advice from the US Army Public Health Center (APHC)[48] or the Armed Forces Radiobiology Research Institute.[49]

External Irradiation

External irradiation can cause partial or whole-body exposures. The most common partial body exposure is an extremity exposure, which usually occurs when an arm or hand is inserted into a radiation beam emitted by a medical or industrial x-ray machine. Accelerator accidents are also common sources of external irradiation. In these instances, victims can incur partial-body exposure by incorrectly assuming that the system is not operating, or that shutters and other protective devices are properly positioned. The doses resulting from partial-body external exposure can be extremely high, but the acute effects will be limited to the irradiated tissue; systemic effects are unlikely from partial-body exposures. In contrast, external irradiation of the whole body typically involves exposure to an un-retracted industrial radiography source, or to exposures from distant, large devices such as a nuclear reactor, a critical assembly, or an animal irradiator.

Combined Internal and External Exposures

Casualties who sustain both external irradiation and internal deposition should receive medical treatment for each insult simultaneously because the injuries are medically independent and the treatments are completely different. Accidents of this type usually involve an explosion or fire in a facility that handles large amounts of radioactive materials, such as a nuclear reactor, weapons plant, or waste-processing plant. Casualties with combined injuries should be treated in the following sequence:

1. Treat life-threatening physical trauma first, to the extent necessary to stabilize the patient, and to permit decontamination and attention to severe radiation injuries.

2. Perform initial decontamination and wound debridement, but terminate this phase if the patient’s condition deteriorates; begin again when the patient is medically stable.

3. Finish decontaminating the patient.

4. Complete the short-term trauma care.

5. Estimate the dose sustained from external irradiation and attempt to estimate the extent of internal deposition.

6. Implement appropriate therapy for the radiation injuries.

7. Initiate definitive medical care for physical trauma.

8. Initiate long-term follow-up care.

Hot-Particle Trauma

Hot-particle trauma occurs when a small radioactive fragment, usually metal, penetrates the skin of a victim. This local radiation dose is extremely high, and if the fragment is not removed promptly, it can cause severe local tissue damage. In almost every credible accident scenario, the victim will not become a high-level source of radiation, especially if any degree of decontamination has been performed. The exception is a victim of an explosion whose body contains large, highly radioactive metal fragments. In this event, the wounds should be quickly debrided, using long forceps or tweezers if possible, and any recovered fragments should be placed immediately in a lead-shielded container. The US Army’s Emergency War Surgery handbook, 4th edition, discusses the debridement of penetrating injuries contaminated with radioactive debris.[50]

Mass Casualties

“Mass casualties” is a relative term, depending on the ratio of casualties to the medical resources available. When medical resources are plentiful, mass casualties are triaged according to the urgency of the victims’ medical needs (as are casualties in civilian practice): medical care must be concentrated on those patients for whom intervention could possibly make the difference between life and death. Based on the resources expended in a peacetime radiation accident that produces only one casualty, an accident producing mass casualties would probably require the resources of several hospitals.

If mass casualties occur in a setting where medical resources are limited, then triage must be similar to that used by the military medical departments during wartime. Military medical departments are charged to conserve the fighting strength and to maintain the fighting power of the command. Medical care must be prioritized, with those who are most likely to survive receiving first priority, and those for whom medical care will probably make the difference between life and death receiving second priority. Patients who are unlikely to survive should receive supportive care. Radiation injuries will rarely be so severe that their treatment takes priority in triage. Even for a patient with very high levels of contamination in their body, or with a high-level radiation exposure, physical trauma will probably be the greatest immediate threat to life or limb.

Procedures for Whole-Body Exposures

The treatment of patients with significant whole-body radiation exposures is a complex medical problem. Current knowledge of ionizing radiation and its pathophysiology and treatment is based on data from the accidents in Chernobyl, USSR (1986), and Goiânia, Brazil (1987 [see Exhibit 22-2]); wartime detonations of atomic bombs in Hiroshima and Nagasaki, Japan (1945); and a vast amount of laboratory experimentation. Medical Consequences of Radiological and Nuclear Weapons discusses the subject in detail.[2]

Low-Dose Exposures

Medical intervention is rarely necessary for patients who have sustained low doses (< 50 cGy) of radiation. Minimally irradiated patients should be placed in a holding area or available hospital beds. The most important therapy is assuring and reassuring these patients that their exposure was non-threatening. Most patients will be asymptomatic, although chromosomal aberrations can usually be found, and many patients will have transitory, minor drops in their platelet and leukocyte concentrations. With low-dose exposures (less than about 100 mSv), the risk of fatal cancer increases to about 1.0% over the normal incidence of fatal cancers (approximately 25%) to approximately 26%.[51] Long-term follow-up, which must be continued throughout the patient’s life, should focus on solid tumors and, less likely, on leukemia.

Intermediate-Dose Exposures

Medical care is usually necessary for patients who have sustained intermediate doses (50–500 cGy) to survive acute radiation injury syndrome. Those exposed to the lower end of this dose range will have moderate-to-severe depression of all of the formed blood elements, which can lead to death from overwhelming infection. Exposure to the upper end of the range additionally causes denudation of the crypts of the small intestine, which leads first to an inability to absorb fluids and nutrients from the small intestine, and then to the consequent dehydration, electrolyte imbalance, and potential death.

Patients generally experience three distinct phases of response to intermediate doses: the prodromal phase, the latent phase, and manifest illness. In the prodromal phase, patients experience nausea, vomiting, anorexia, diarrhea, and malaise. In the latent phase, which follows the prodromal, the patient stabilizes or begins to feel better. The manifest illness phase is characterized by the appearance of the hematopoietic and gastrointestinal signs and symptoms that can lead to death.

Triage is usually based on the severity of the symptoms and the time of onset of the prodromal phase. The earlier and more severe the prodromes, the higher the dose received. Doses at the upper end of the intermediate range cause the onset of the prodromal phase within a few hours. The prodromal phase will continue for a few days, followed by a latent period of up to 3 weeks. Doses at the lower end of the range cause a later appearance of prodromes. The lower-dose prodromal phase is shorter in duration than that associated with the upper-dose range, and the latency for lower-range doses is longer than for upper-range doses.

Immediate care for casualties who have received doses of approximately 50 to 300 cGy is primarily supportive. Medical efforts should be directed toward any physical trauma, with attention to possible infection due to the depression of leukocytes. However, medical care for casualties who have received doses of approximately 300 to 500 cGy is intensive. These patients must be hospitalized and closely observed for any decrease in blood values, the onset of aplastic anemia, and gastrointestinal bleeding and other sequelae of small bowel injury.

Statistically, a dose between 300 and 500 cGy will kill 50% of irradiated individuals within 60 days, even if antibiotics and other supportive care are provided. Although any specific individual may respond differently, the 450-cGy value is a reasonable lethal-dose estimate for an individual if special factors affecting radiation sensitivity are not known to be present and no medical care is provided.[47]

High-Dose Exposures

Gastrointestinal complaints from patients who have received high doses (> 500 cGy) of radiation will dominate the early (days to hours) clinical picture, with hematopoietic complications arising if the patient survives the gastrointestinal onslaught. Patients have a slim but real chance of surviving doses at levels of 1,000 cGy if they receive intensive therapy including bone marrow transplantation. At doses exceeding approximately 2,000 cGy, the patient will die of cardiovascular or cerebral collapse within hours to a few days. Medical care in this instance should be palliative or symptomatic.[47]

Protecting the Medical Team

Protection of the medical staff against external irradiation is afforded by minimizing the amount of time they are near the radiation, maximizing the distance from the source, and placing a shield between staff and the radiation source. Contamination (whereby radioactive material on or in the casualty becomes deposited on or in the medical worker’s body) is an unlikely hazard to the medical response team. However, to be prudent, early preventive measures for the medical team include:

- wearing surgical gowns, booties, caps, gloves, and masks;

- careful removal of the victim’s clothing; and

- thorough decontamination of the victim’s exposed areas and, as time permits, decontamination of the whole body.

The risk to the members of the medical team who treat a victim of a radiation accident depends on the victim’s level of radiation contamination and is usually low. Medical personnel receive annual refresher training to reinforce concepts for treating various radiation injuries and to allay any fears that the risk levels may be higher than they are.

Low Risk

Victims exposed to an x-ray beam pose no risk to the medical team. Likewise, those who have sustained internal deposition from an accidental needle stick present little or no risk to the medical team because the contamination is not removable and radiation levels near the victim would almost certainly be very low.

In general, externally contaminated patients pose a low risk to the medical team. The primary hazard to medical personnel is that the victim’s external contamination will transfer to the medical personnel and deposited internally via ingestion, inhalation, or accidental needle stick. Although radiation levels near accident victims are usually low, measurable amounts of radioactive contamination can be found on clothing, skin, and hair. In treating radiation victims, these preventive measures should be followed:

- Remove the casualty’s clothing and decontaminate the patient as thoroughly as possible at the accident site or en route to the hospital.

- Allow a trained radiation safety specialist (health physicist, medical physicist, or nuclear medicine specialist) to monitor the patient throughout the course of medical treatment.

- Designate presumed-contaminated and clean areas within the treatment area, and keep the casualties confined to the presumed-contaminated areas.

- Wear hospital gowns, booties, disposable rubber or plastic gloves, surgical caps, and surgical masks while treating casualties.

- Monitor all medical personnel as they leave the presumed contaminated area and decontaminate them if necessary.

Moderate and High Risk

Radiation casualties who pose the greatest risk to medical personnel include those who have severe physical trauma with high levels of external contamination or imbedded radioactive projectile fragments. These casualties can themselves emit high levels of radiation, although it is very unlikely. They require significant medical attention, and their level of physical trauma may make the removal of the radioactive material prior to treatment difficult or impossible to achieve.

All the preventive measures taken with a low-risk casualty apply in moderate-risk or high-risk situations, but additional measures are necessary to protect medical personnel from radiation emitting from a casualty’s body. Because special shielding is unlikely to be available except in designated and prepared hospitals, protection must be achieved through distance and time. When distance is employed, nonessential personnel should be kept out of the treatment area, and anyone should step away from the patient when their presence is not mandatory. When time is employed, only essential procedures should be performed initially, as quickly and carefully as possible. Additionally, the radiation safety officer may restrict the amount of time that members of the medical team can remain in the treatment room, based on survey meter measurements and readings from personal dosimeters.

Controlling Contamination in the Medical Treatment Facility

The guiding principle in controlling contamination in a medical treatment facility (MTF) is to confine the radioactive contamination to a small, known area. Any contaminated area must be removed from routine use until it has been completely decontaminated. This procedure could have a severe impact if the contaminated area is a critical component such as an operating room; therefore, a small, non-critical room should be used to treat contaminated patients. Vigorous efforts must also be exerted to keep contamination from spreading beyond the treatment area. Extensive decontamination is expensive and time-consuming, and frequently is accompanied by public relations problems with the hospital staff and general public. Preventive measures used to avoid extensive complications include the following:

- a written, periodically rehearsed response plan for radiation accidents;

- maximal patient decontamination at the accident site, en route to the hospital, and within the ambulance after its arrival;

- prior designation of the receiving and treatment areas for radiation casualties;

- a prepared radiation emergency-response kit that contains protective paper, absorbent pads, radiation signs, anti-contamination gear, and a brief standard operating procedure (SOP) on radiation injury treatment;

- preparation of the receiving and treatment areas before the casualties arrive at the MTF to facilitate containment of contamination and subsequent decontamination;

- tight control by police or security personnel over entry into and exit from the receiving and treatment areas; and

- prior designation of an area where hospital public affairs personnel can meet with media and local government officials.

The Fukushima Incident

On March 11, 2011, a 9.0-magnitude earthquake occurred off the east coast of Japan. As a result of the earthquake, a large tsunami destroyed Fukushima and the towns surrounding the city. The tsunami wave also affected three nuclear power reactors located in Fukushima. It was the largest earthquake and tsunami ever recorded in Japan. Electrical power was lost to the Fukushima Daiichi nuclear power station because of the increased water levels overflowing the Fukushima reactors (Figure 22-20).

Figure 22-20. Reactor buildings 3 and 4 at Fukushima Daiichi nuclear power station following the fire and explosion that occurred when cooling water was disrupted due to flooding following the earthquake and tsunami.
Reproduced with permission from the Tokyo Electric Power Company.

The plant’s emergency generators began providing critical electrical power; however, an hour after the earthquake, a wave over 30 feet high crossed over the lower protective sea walls of the facility and flooded the station, resulting in extensive damage and a complete loss of power to five of the six nuclear reactors. Despite heroic repair efforts by the plant’s workers, cooling to the reactors was eventually lost. Explosions occurred in Fukushima reactors 1 through 3, which resulted in the release of significant amounts of radioactivity into the atmosphere and the ocean.

In response to the Fukushima incident, the US DoD established the Operation Tomodachi Registry (OTR). The OTR includes nearly 75,000 DoD-affiliated individuals who were on or near the mainland of Japan during the period from March 12, 2011, to May 11, 2011, along with their corresponding whole-body and thyroid radiation doses. Over 58,000 individuals were associated with one of thirteen shore-based locations, which included DoD military installations and major cities where the majority of the DoD-affiliated population worked or lived. Nearly 17,000 individuals were associated with US Navy fleet-based locations, which included 25 Navy ships in the area during this period.[52]

THE DEPARTMENT OF DEFENSE RADIATION SAFETY PROGRAM

The primary goals of all radiation protection programs are to (1) maintain both individual and collective exposure ALARA, and (2) minimize the release of radioactive effluents into the environment. Through these goals, the DoD Radiation Safety Program[45] seeks to protect all personnel from unnecessary exposure to ionizing radiation in accordance with national and international scientific recommendations.53,54 These recommendations include the following:

- Justification. No procedure shall be adopted unless its introduction produces a positive net benefit.

- Optimization. All exposures shall be maintained ALARA.

- Limitation. Dose equivalent limits for individuals shall not exceed the limits recommended for the appropriate circumstances by the DoD and NRC.45,46,53

Program Responsibilities

Although there are differences in implementation between the uniformed services’ radiation safety programs, their broad contours are very similar. Within the US military, installation and activity commanders are responsible for the Radiation Safety Program (referred to as the Radiation Protection Program in Navy and Air Force regulations) at their respective commands. Both the Navy and Air Force maintain master licenses through the NRC for their radioactive material, allowing these two services to issues use permits directly to their subordinate commands. The Army maintains a number of independent licenses directly with the NRC for radioactive commodities, including at research laboratories, field activities, and MTFs with nuclear medicine departments. The commander is designated as the NRC licensee and can be held personally liable for program deficiencies. In clinical settings, the physician, dentist, or veterinarian in charge is similarly held personally responsible for maintaining the equipment in safe operating condition, and for protecting patients, the general public, and workers from unnecessary exposure to radiation. The Radiation Safety Program is managed for the commander through the Radiation Safety Committee (RSC) and the radiation safety/protection/health officer (hereafter referred to as the RSO).

Radiation Safety Committee

Organizations that use radioactive material under a specific NRC license, DoD permit, or other military radiation authorization must appoint an RSC,45,46 an advisory body that assists the commander in establishing local rules and procedures for the safe use of radioactive materials and machine-produced ionizing radiation sources. The committee accomplishes this task by reviewing any matter affecting radiation safety and making recommendations for senior management approval. Although the RSC’s membership varies among organizations, the core should include a top-management representative (deputy commander or equivalent) who is not a radiation user, the RSO, a representative from each unit in the installation (or department in an MTF) that uses radioactive material, and a medical representative. The RSC is responsible for establishing policy and providing oversight to:

- ensure the safe use of radiation sources and radiation-producing devices;

- ensure compliance with regulations;

- ensure that the use of the radiation is consistent; and

- identify problems and their solutions within the program.

To meet these responsibilities, RSC members should possess experience and competence in the safe use of radioactive material, and be familiar with the institutional Radiation Safety Program and applicable regulations. In general, the RSC meets at least once in each 4-month period at the call of the chair45,46 and keeps written records or minutes of the meeting. Within the Army system, an RSC must exist before an organization applies for an NRC license. For medical programs that employ radioactive material for human use, specific requirements for the composition of an RSC and its responsibilities are listed in 10 CFR, Part 35[55]; DA PAM 385-234[45]; Army Regulation 385-10, US Army Safety Program[56]; and the NRC license application specific to the individual licensee.46,55

Radiation Safety Officer

Because the commander bears the ultimate responsibility for the radioactive materials used under his or her command, the commander will designate, in writing, a qualified individual as the RSO to manage the Radiation Safety Program.45,46 The qualifications of the RSO depend on the complexity of the operations and the range of potential health hazards. These factors also determine the amount of training, equipment, and support staff necessary for the RSO. Because the RSO must make decisions that affect the current and future lives and well-being of personnel, he or she should report directly to the commander. According to 10 CFR, Part 35,[55] the commander shall provide the RSO sufficient authority, organizational freedom, time, resources, and management prerogative, to:

- identify radiation safety problems;

- initiate, recommend, or provide corrective actions;

- stop unsafe operations; and

- verify implementation of corrective actions.

The RSO’s role is to provide specialized assistance and guidance in developing the radiation safety aspects of the Radiation Safety Program.45,46 The RSO determines if established programs are being maintained and are adequate for present needs. However, the RSO’s oversight function in no way diminishes the responsibility of the user or supervisor to conduct operations in a safe and legal manner. Although the RSO usually takes charge of regulatory compliance actions (such as surveys and personnel dosimetry), it is the licensee and/or the commander, not the RSO or the radiation safety staff, whom the NRC holds personally responsible for assuring both the safe performance of licensed activities and adherence to NRC requirements.

Program Elements

A radiation protection program may include some or all of the following elements, depending on extent and type of the radiation hazard and the number of monitored personnel: (a) administrative controls, (b) engineering controls, (c) medical surveillance, (d) personnel monitoring, (e) respiratory protection, and (f) recordkeeping.

Administrative Controls

Administrative controls are procedures used to minimize the radiation exposure of personnel. These procedures require the cooperation of radiation protection and operations personnel and include measures such as SOPs, training, and designation of restricted areas.

Standard operating procedures. An SOP is a model procedure for the administrative control of radiation exposure. This document must specify, in as many specific steps as possible, safety policies concerning operational limitations and requirements throughout the radiation area. For example, the fluoroscope, if not properly controlled, is potentially the most dangerous of the common x-ray applications to both the patient and examiner because its x-ray tube is energized for a longer time to view dynamic processes. However, techniques and equipment are available that can reduce radiation exposure as much as 50% to 75%, and the SOP should specify the use of such techniques and equipment. In general, an SOP for ionizing radiation control should include:

- type of protective apparel required,

- posting requirements,

- radiation monitoring devices required,

- personnel dosimetry requirements,

- bioassay types and frequency required,

- recordkeeping requirements,

- reiteration of any other applicable administrative requirements, and

- any other special procedures or equipment required.

In this manner, entire complex radiation protection programs can be reduced to a series of written procedures. In fact, the NRC has adopted a licensing approach similar to this for medical licenses.

The SOP should be dated, signed, and reviewed at least annually (more often if changes are made). The review should include the radiation supervisor, the RSO, and the RSC. In many instances, it is necessary to document the review with signatures. Reviewed and updated SOPs are useful tools that provide for:

- program continuity regardless of personnel changes,

- uniform performance throughout large groups of people,

- opportunity for personnel to become familiar with procedures and operations before actually using radiation sources, and

- response planning prior to an actual emergency.

Training. Training is the cornerstone of the administrative control of ionizing radiation, and strong management support is essential to an adequate radiation safety training program. Although the RSO is responsible for implementing program policies and providing subject matter expertise to develop the policies and procedures relating to radiation safety for all staff members, management’s commitment to radiation safety should also be obvious. The scope of training varies greatly depending on job requirements. For example, physicians who treat patients with radioisotopes are required to be board certified in radiology, nuclear medicine, radiation therapy, or another appropriate discipline, or they must meet the experience requirements detailed in 10 CFR, Part 35.[55] All personnel who work in radiation areas or controlled areas should receive extensive training specific to the potential hazards and appropriate mitigation of hazards in these areas.

Other personnel such as firefighters, security forces, housekeeping personnel, facility engineers, nurses, and medical maintenance personnel should also receive training; even though they do not work with radiation directly, they might be required to enter radiation areas. All personnel should receive training before entering or beginning work in a radiation area or controlled area. They should also receive training annually thereafter, more often if policies and procedures change. Exhibit 22-4 lists some safety subjects common in radiation protection training (this list is not exhaustive). Program requirements, the audience, and their educational needs dictate the depth of these subjects. In some instances, particularly if a serious, acute health hazard exists, training with mock sources or facilities will familiarize personnel with the actions required in an emergency.

EXHIBIT 22-4

ELEMENTS OF IONIZING RADIATION PROTECTION TRAINING

- Radiation biology and the risk from occupational exposure

- Specific training on risks to pregnant workers

- Types of radiation and their characteristics

- Differences in internal and external radiation exposure

- Locations of radiation sources

- Dosimetry requirements

- Detection and control of contamination

- Dose limits

- Individual responsibilities

- Signs and symbols

- ALARA concept

- Rules and procedures, including the SOP

- Egress controls

___________________

ALARA: as low as reasonably achievable

SOP: standard operating procedure

One area of training that requires special consideration is the instruction of women who might become pregnant. Because a fetus is highly sensitive to ionizing radiation, the RSO or other qualified individual should advise women of childbearing age about the special need to limit their exposure. Additionally, pregnant women, and those planning a pregnancy, must be counseled on the options available to limit the fetus’s exposure to radiation.[57]

Designation of restricted areas. Another form of administrative control is the identification and labeling of areas to which entry is controlled or restricted. The designation of restricted areas not only heightens awareness of the hazard, but also ensures that personnel in the area are monitored and have obtained specialized training. The DoD, NRC, and OSHA have all established special controls, particularly training requirements, that apply whenever personnel enter a controlled radiation area.

Engineering Controls

Engineering controls are safety systems such as warning devices, shields, interlocks, and ventilation that are built into the source itself or its holding facility. The design and construction of safety systems employs the fail-safe principle whenever possible. A fail-safe system causes the device to shut down without exposing personnel to radiation during any malfunction, including the malfunction of the fail-safe system itself.

The proper design of facilities is another important engineering control. Properly designed facilities provide a higher margin of safety than administrative rules and procedures. Although the design of facilities cannot eliminate the possibility of accidental exposure to radiation, it can minimize the probability and severity of accidents. Design considerations include:

- general facility layout, incorporating traffic-flow patterns and work areas;

- specific equipment and system requirements;

- appropriate shielding for radiation workers and the general population;

- proper ventilation to control the movement of airborne contaminants; and

- nonporous, easily cleaned surface materials for radioactive material handling areas.

A qualified health physicist must be consulted in the planning, design, and construction phases of new or modified radiation facilities. During the design phase, the health physicist should implement the general principles of radiation control. The most common methods of controlling an internal radiation hazard (radioactive material) are to (a) confine and contain and (b) dilute and disperse. An example of the confine and contain method is a glove box inside a shielded room that is ventilated with filtered and recirculated air. An example of the dilute and disperse method is the mixing of radioactive gases with a large volume of clean make-up air, which is then discharged through an exhaust stack into the atmosphere at a height above any air intakes or occupied areas. Common engineering methods to control an external radiation hazard (and to maintain exposure ALARA) include increasing the shielding around the source, increasing the distance between the radioactive source and the employee (remote handling), and decreasing the amount of time that the employee is near the source (which is also subject to administrative control).

Medical Surveillance

Routine medical examinations for individuals occupationally exposed to ionizing radiation are usually not necessary. A reported overexposure does not necessarily indicate the need for a medical examination. The circumstances associated with the reported overexposure and the estimated organ or whole-body dose should help determine the type and extent of any examination, as well as the types of laboratory or medical tests. The supporting medical commander to units on installations, in consultation with the unit and installation RSO, will determine if a medical examination is necessary for individuals occupationally exposed to radiation. The medical commander and RSO will refer any individual suspected of having received a radiation dose in excess of the limits specified in DA PAM 385-24 to a physician.[45] The supporting medical commander and the supporting occupational health physician will determine the appropriate level of examination and treatment. Personnel potentially exposed to nonionizing radiation should receive appropriate medical examinations as specified in DoD Instruction 6055.11[58] and TSG policy directives.

The following factors should be considered when determining an appropriate medical examination:

- total actual or suspected dose,

- types of radiation to which the individual was exposed,

- portion of the body exposed,

- target organ dose,

- time elapse between the exposure and notification, and

- other appropriate factors.

Copies of reports documenting reported overexposures must be forwarded to APHC for archiving whether or not an actual overexposure occurred. Documenting a determination that a suspected overexposure did not occur is as important as documenting actual overexposures.45,46

Personnel Monitoring

Personnel monitoring includes monitoring devices, such as thermo-luminescent dosimeters (TLDs) and self-reading pocket dosimeters, and bioassays. Dosimetry measures exposure to radiation, and a dosimeter is a device used to provide a quantitative estimation of the dose received. Each person who might receive an accumulated dose equivalent in excess of 10% of the applicable dose limits must wear a dosimeter. In addition, any employee who enters a high-radiation area must wear a supplementary dosimeter, usually a self-reading electronic one (Figure 22-21). Electronic dosimeters are similar to pocket dosimeters in that they contain a small ion chamber, but their readout is in the form of a digital display, and they are not as sensitive to being physically jarred as pocket dosimeters. Dosimeters used should provide accurate, reproducible readings; be capable of measuring all radiation exposures that personnel encounter; and be simple, convenient, small, and inexpensive.

Figure 22-21. Three types of dosimeters. The instrument on the left is an IM 93A/UD pocket dosimeter used in a tactical military environment. The IM-93A/UD can detect gamma radiation between 0 and 600 R. The middle instrument is a thermoluminescent dosimeter (TLD) used in both medical and industrial settings within the Department of Defense to determine radiation doses workers are exposed to. TLDs also have been used in tactical environments. The four tissue-equivalent materials within a TLD can show the radiation dose from different forms of radiation. The range of the TLD is from 0.5 mSv to 10 Sv. On the right is the AN/UDR-13 electronic dosimeter, which is used extensively in the military. The compact and rugged AN/UDR-13 is capable of detecting gamma and neutron radiation doses, as well as the dose rate for gamma radiation. This dosimeter’s capability is 1 to 999 cGy for dose detection, and 0.1 to 999 cGy/h for dose rate. Photograph courtesy of the US Army Public Health Command, Aberdeen Proving Ground, Maryland.

The dosimeter-wearing period is usually either every month or every 3 months for occupational doses; at the end of every month or every quarter, a new dosimeter is provided to the worker. Depending on specific radiological occupational exposure, other wearing periods may be arranged. The ADC, part of the US Army Materiel Command, supplies dosimeters to all Army, National Guard, and Defense Logistics Agency personnel.[59] Personnel at Army government-owned, contractor-operated (GOCO) facilities and contractor personnel who work in Army facilities and require dosimeters must use those supplied by the ADC unless a written contract specifically exempts them. (Non-GOCO contract personnel working under provisions of an Army radiation permit may use contractor-supplied dosimetry.)[59]

Bioassays are considered the final quality control used to ensure adequate protection of workers against internal radiation exposure. A bioassay determines the type, quantity, location, and retention of radionuclides in the body either directly (by in-vivo measurement) or indirectly (by in-vitro analysis of material excreted or removed from the body). Requirements for bioassays are usually components of occupational health programs dealing with metals and other industrial chemicals.[60] Although the requirements of a bioassay program are beyond the scope of this chapter, International Commission on Radiation Protection Report No. 78, Individual Monitoring for Internal Exposure of Workers,[61] provides comprehensive information. Additional information is available in NCRP Report 87, Use of Bioassay Procedures for Assessment of Internal Radionuclide Deposition,[60] and the Health Physics Society document Design of Internal Dosimetry Program.[62]

Respiratory Protection

A respiratory protection program involves much more than issuing a respirator to an employee. The preferred methods to reduce risk of exposure to airborne contaminants are (a) reducing the air concentrations of hazardous substances by substitution with a less toxic substance and (b) engineering and administrative controls. However, an appropriate respirator must be selected for each type of exposure, and respirators must be appropriately fitted to the employee. Qualified medical and safety personnel are essential to an effective respiratory protection program. Employee training must include how to use and properly maintain the respirator. Medical clearance is also an essential part of the respiratory protection program.45,46

Respiratory protection is required wherever unsealed radioactive material is processed in such a manner that inhalable air concentrations pose a significant health threat to the radiation worker. As a guideline, respiratory protection must be evaluated whenever an individual is potentially exposed for 40 hours per week, for 13 weeks, to air concentrations equal to or greater than those listed in 10 CFR, Part 20.[46] Whenever respiratory protection is required, a bioassay program is also required.

The careful design of an air-sampling program can alert the RSO to trends or situations that require intervention, such as the necessity for respiratory protection, or to provide assurance that processes are functioning as designed. When air sampling is conducted to ensure that adequate personnel protection is in place, it is imperative that the sample be representative of the situation under investigation. To accomplish this, a worker should wear a personal air sampler near his or her respiratory zone to collect an air sample. In addition, ambient air at the worker’s height should be sampled to approximate the air concentration of the contaminant in the worker’s breathing zone. The sampler should collect respirable-sized particles rather than the larger, heavier particles that settle out of the air onto the collector. The sample size must be large enough to represent a reasonably accurate estimate of the mean concentration of airborne particles and meet the sensitivity requirements of the radiation detector.

Recordkeeping

Keeping the evidence necessary to demonstrate the reliability and effectiveness of a radiation protection program is referred to as documentation. Complete documentation should include information on radiation exposure patterns and working conditions. For medical or legal reasons, significant information from these records (such as those that establish personnel exposure history or characterize effluents and residual radiation) are retained indefinitely.

MEDICAL RESPONSE TO DEPLETED URANIUM EXPOSURE

Department of Defense Policy for Handling Exposures to Depleted Uranium

In its natural form, uranium is only slightly radioactive, and although DU is 40% less radioactive than natural uranium, its chemical or metal properties are the same as other forms of uranium.[59] DU must be taken into the body to be a potential health hazard. The potential for DU exposure among service members occurs through occupying vehicles penetrated by DU munitions, rescuing occupants of these vehicles, or performing other operational duties involving these vehicles (equipment removal, repair, salvage, etc). Exposures may also occur when a wounded individual retains fragments that contain DU in his or her body, breathes air containing DU dust, or transfers DU dust unintentionally from contaminated surfaces to the mouth or open wounds.

Since the end of the 1991 Persian Gulf War, the Army Medical Department has been actively involved in assessing potential health risks from exposure to DU during military operations. Army policy guidance stems from DoD Health Affairs Policy 03-012 (issued May 30, 2003).[63] This policy calls for the referral of all service members who have embedded DU fragments or other evidence of significant DU exposure to the Department of Veterans Affairs (VA) DU Follow-Up Program. This program was developed during the Gulf War for ongoing monitoring of exposed service members, in order to identify any long-term implications of DU exposure. The policy requires the services to:

- Identify all service members who may have had internal exposure to DU.

- Members may identify themselves as being exposed on the Post-deployment Health Assessment (Defense Department [DD] Form 2796) or by reporting for medical care.

- The services must actively try to locate units involved in operations or incidents that might involve DU exposure.

- Have service members answer the DU Exposure Questionnaire (DD Form 2872) to help assess the level of risk associated with a possible exposure.

- Review the circumstances of the exposure and assess the level of risk.

- Level 1. Personnel who may exceed occupational safety levels by taking in a sufficient amount of DU into the body.

- Level 2: Personnel who are routinely exposed to DU-damaged vehicles or fires involving DU munitions.

- Level 3: Personnel with incidental exposures to DU.

- Obtain DU bioassay material from all personnel found to have Level 1 or Level 2 exposure.

- Urine uranium assays (for total uranium and DU) should be done as soon as operationally feasible, and preferably within 180 days of the most recent incident.

- The Army tests specimens at the Laboratory Sciences Directorate of the APHC; Air Force testing is done at the Radioanalytical Laboratory at the Air Force School of Aerospace Medicine at Wright Patterson Air Force Base; and Navy and Marines testing is performed at the VA Medical Center in Baltimore, Maryland.

- Uranium in urine results must be normalized to urine creatinine values, and a specimen aliquot must be retained indefinitely.

- Level 3 exposure cases may be tested by request of the healthcare provider or the service member.

- Notify the service member of the testing results and ensure that the results are placed into the medical record.

- Offer those with significant levels of DU exposure, as evidenced by the bioassay material, referral to the VA DU Follow-Up Program.

- Managed by the Baltimore VA Medical Center.

- The VA follows a cohort of exposed individuals with medical exams, questionnaires, and additional medical testing for long-term effects of DU.

- Effectively communicate the current medical condition and future risks associated with DU exposure to service members and their family, using established risk-communication principles, addressing:

- the reason they are being evaluated for DU,

- the timeliness and nature of the assessment process,

- potential individual risk from DU exposure,

- the (generally) low incidence of significant DU exposure in theater, and

- the medical follow-up available to service members.

- File an annual report of DU bioassay results with the Defense Health Agency. Health Affairs Policy 04-004[64] added additional requirements to the overall guidance for handling DU exposure cases:

- Embedded DU fragments that are removed from service members must be analyzed for metal composition.

- The Army tests specimens at the Laboratory Sciences Directorate, APHC; all others are performed at the Joint Pathology Center in Silver Spring, Maryland.[65]

Toxicology of Depleted Uranium Exposure

About 98% of any form of uranium entering the body via ingestion is not absorbed; rather, it is eliminated in the stool. The fraction of uranium absorbed in the blood is generally greater following inhalation. Of the uranium that is absorbed in the blood, approximately 70% is filtered by the kidney and excreted in the urine within 24 hours; this amount increases to 90% within a few days.[66] The remaining 10% is absorbed into the bones and organs, from which it leaches out into the blood over time.[67] The target organ for uranium toxicity is the kidney. The metal selectively injures the middle segments of the kidney’s proximal convoluted tubule. Experimental animal models exposed to uranium develop acute tubular necrosis that often leads to renal failure.[68]

Results of Depleted Uranium Exposure Follow-Up

Since 2003, the APHC has conducted DU analysis for over 3,000 urine specimens from almost 2,900 service members involved in overseas contingency operations. These individuals submitted 24-hour urine specimens along with exposure and specimen collection information vital for proper interpretation. Service members with verified DU intakes have been referred to the DU monitoring program at the Baltimore VA Medical Center.

The group with the longest follow-up period comprises 32 individuals who were victims of friendly fire involving DU weapons and had retained fragments of DU within their bodies. This cohort, followed at the Baltimore VA Medical Center, is regularly reported on in the medical literature. For evaluation, these victims were grouped according to their level of urine uranium concentrations. The low-level group had urine levels of less than 10 μg of uranium per gram of creatinine, and the high-level group had greater than or equal to 10 μg of uranium per gram of creatinine. There has been no detectable dose-related difference between these groups. Both groups have persistent elevations in urinary uranium levels, which may be to be due to ongoing mobilization of the retained DU. Renal function remains normal; however, there have been subtle changes indicative of early abnormalities in the proximal tubules of the kidneys. No significant uranium-related health effects have been observed in blood count, blood chemistries, neuropsychological measures, semen quality, or genotoxicity measures.65,66

Additional information on the physical aspects and toxicological profile of DU can be obtained through the World Health Organization[69] and the US Department of Human and Health Services.[66]

SUMMARY

Humans have always been exposed to ionizing radiation—from both outer space and the earth itself—and only during the past 100 years have humans harnessed the power of this radiation for their own purposes. Military medicine can be particularly proud of its role in the technological development, clinical application, and safe utilization of this potent force. Soon after its discovery, radiation was recognized as both beneficial and dangerous. Early radiologists and physicists developed cancers, some of which were fatal. As the deleterious effects of radiation became better known, researchers turned their attention to attempting to understand the mechanisms of radiation damage.

Medicine, industry, and the military have become heavily dependent on the applications of ionizing radiation. Radiographic and nuclear medicine examinations are now integral to the healthcare system. NDI of critical welds, explosive ordnance disposal, production-line quality control, and materials analysis all employ sources of radiation. Self-luminous commodities containing radioactive material, such as compasses and indicator dials, are used throughout the armed forces. To counteract radiological threats from the potential use of weapons of mass destruction, US government agencies have had to implement the latest detection system technology. Each of these technologies can be used safely, but they can create a health hazard to radiation workers and to the public in general if not handled properly.

Although radiation is not detectable by the physical senses, it is relatively easy to detect and quantify with instrumentation. Physicists, physicians, and biologists have worked closely to establish quantitative estimates of risk and derive safe dose levels, and the scientific community has provided guidance and technological advances that have helped improve radiation protection. Federal, state, and local governments, with the help of scientific advisory groups, have also played significant roles in the control of radiation exposures. Recent progress in radiation protection includes stricter regulatory control, improved education and training, and implementation of programs aimed at maintaining exposures ALARA. As a result, current radiation-protection regulations and recommendations, civilian and military, provide a solid framework for the safe use of radiation sources.

However, despite regulations, safety equipment, and training, accidents do happen. These incidents have provided a rich case history for determining the optimal medical treatment of future radiation accident victims. With proper training and planning, medical teams can treat accident victims with minimal risk to the treatment team and with excellent likelihood of successful outcomes for the patients.

At high doses, radiation can cause severe injury and even death. However, such large doses are rarely encountered in the military (apart from situations involving nuclear weaponry). The levels of radiation doses received from military sources are more likely to be in the range where cancer induction and teratogenic effects are currently of statistical concern only. The challenge for the DA Radiation Safety Program and the DA Preventive Medicine Program[63] is to protect workers, the public, and the environment, while enabling the benefits of radiation to be exploited.

ACKNOWLEDGMENTS

The authors would like to acknowledge the contributions of P. Mark Moscato, MS, and Brian E. Livingston, CHP, to the compilation and development of this chapter.

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Chapter 23

NONIONIZING RADIATION

BRYAN D. KOBE*; KIERAN T. LERCH, MS†; ERNEST C. BRUMAGE, MS‡; JOHN J. DEFRANK§; PENELOPE K. GALOFF¶; CHARLES W. HICKS JR¥; AND DAVID H. SLINEY, PHD**

INTRODUCTION

CHARACTERISTICS OF ELECTROMAGNETIC RADIATION

Physical Properties

Interaction With Matter

RADIO FREQUENCY RADIATION

Radio Communication and Radar Technology

Microwave Radar

Radar During World War II

Physical Properties That Determine Energy Transfer

Direct Biological Effects

Low-Level Effects of Radio Frequency Electromagnetic Radiation

Indirect Biological Effects

Radio Frequency Radiation Protection

Emission of Radio Frequency Radiation

Military Applications

The Radio Frequency Radiation Safety Program

LASERS AND OPTICAL RADIATION

Specific Properties of Lasers and Optical Sources

Direct Biological Effects

Indirect Biological Effects

Laser Protection Standards

Military Applications

Laser and Optical Radiation Exposure Incidents

The Laser Safety Program

SUMMARY

* Electronics Engineer, Occupational Health Sciences Directorate, Nonionizing Radiation Division, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

† Physicist, Occupational Health Sciences Directorate, Nonionizing Radiation Division, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

‡ Physicist, Occupational Health Sciences Directorate, Nonionizing Radiation Division, US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

§ Chief, Nonionizing Radiation Division, Occupational Health Sciences Directorate US Army Public Health Center, Aberdeen Proving Ground, Maryland 21010-5403

¶ Physical Scientist, Laser Branch, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

¥ Chief, Microwave Branch, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

**Chief, Laser Branch, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

INTRODUCTION

This chapter updates Chapter 15, Nonionizing Radiation, in the previous edition of this book.[1] This update includes a discussion of new nonionizing radiation equipment and lasers that have been added to the Department of Defense (DoD) equipment inventory and are used daily in military operations. Physicians need to be aware of the unique hazards that nonionizing radiation poses and be able to detect signs of exposure and injury related to these exposures.

Electromagnetic radiation is a wave phenomenon consisting of oscillations in the electric and magnetic fields of space. Scientists and engineers commonly characterize electromagnetic radiation, like all wave phenomena, using two parameters, frequency and wavelength. These parameters, continuously varying from the sub-atomically small and unperceivably fast to the cosmically large and glacially slow, are used to define what is known as the electromagnetic spectrum. The spectrum is divided up into frequency (or, interchangeably, wavelength) regions based on the physical processes that generate the radiation they contain and the manner in which that radiation interacts with matter. The most physically significant division in the spectrum is that between ionizing radiation and nonionizing radiation.

Figure 23-1. Nonionizing radiation electromagnetic spectrum.

Ionization of matter occurs when an electron absorbs enough energy to overcome its attraction to the positively charged nucleus of an atom or molecule, and ionizing radiation refers to radiation energetic enough to ionize matter. Once ionized, atoms or molecules are known as ions, and because ions are charged particles, they are more chemically active than in their electrically neutral state (prior to ionization). Chemical changes that occur in biological systems because of ionization may be cumulative and can be detrimental or even fatal.

All other radiation is categorized as nonionizing. The division between the two categories falls within the ultraviolet (UV) frequency range, but the exact boundary varies with context. Laser safety standards, designed to control nonionizing radiation hazards, usually begin at a wavelength (λ) of 180 nanometers (nm), corresponding to a frequency around 1.7 petahertz (PHz).

Another important division in the electromagnetic spectrum is at the wavelength of 1 mm between the optical and radio frequency (RF) radiation regions. These regions may be divided into smaller frequency bands ad infinitum. The radiation produced in this portion of the electromagnetic spectrum does not possess energy sufficient to ionize matter. This nonionizing radiation excites atoms by raising their outer electrons to higher orbitals, a process that may store energy, produce heat, or cause chemical reactions (photochemistry).

The biological effects of nonionizing electromagnetic radiation are caused by thermal stress (the accumulation of heat) and photochemical denaturation of proteins and other molecules in cells. When heat is dissipated, the effects of thermal stress do not persist (they are not cumulative). When the thermal stress is extreme, however, persisting injuries from RF radiation such as erythema, cataracts, or burns may occur. Extreme exposures to lasers and other optical sources may cause damage to components of the eye and burns to the skin.

Figure 23-1 shows the nonionizing radiation portion of the electromagnetic spectrum. The divisions of the electromagnetic spectrum are arbitrary, overlapping regions on a continuum. The generally accepted divisions are:

x-rays; λ = 0.01 to 10 nm

UV; λ = 10 to 400 nm

visible light; λ = 400 to 700 nm

infrared (IR); λ = 700 nm to 1 mm

microwave; λ = 1 mm (300 GHz) to 1 m (300 MHz)

RF; λ = 1 m (300 MHz) to 100 km (3 kHz)

CHARACTERISTICS OF ELECTROMAGNETIC RADIATION

Two complementary concepts in modern physics describe electromagnetic radiation: the wave model and the particle model. The wave model simplifies the way in which electromagnetic radiation interacts with matter on a macro scale, for instance, with reflection and refraction. It characterizes electromagnetic radiation as the propagation of energy through transverse oscillations of the electric and magnetic fields. Electromagnetic waves are measured by four key parameters: wavelength, frequency, polarization, and amplitude (field strength). The frequency of a wave is its number of oscillations per second measured in hertz (Hz). The wavelength is the distance between successive waves, which correlate to any part of the wave, for example, peak to peak or trough to trough. The wavelength must be one full oscillation of the periodic wave. Polarization is the relative orientation of the electromagnetic field, commonly with respect to the electric field component. Waves may be linearly polarized (vertical, horizontal), or circularly polarized, when the orientation of the field rotates with respect to distance and time. The amplitude is the absolute field strength of the electromagnetic radiation, and is given in terms of volts per meter (V/m) for the electric field strength and amperes per meter (A/m) for the magnetic field strength.

Frequency and wavelength of an electromagnetic wave relate to each other through the following equation:

c = λ • f

where c denotes the wave velocity, λ denotes the wavelength, and f represents the frequency. The velocity of the wave will change with propagation through various media, but will never exceed the speed of light in a vacuum (3 · 10[8] m/s). If a wave is propagating in free space, the respective wave velocity is simply the speed of light in a vacuum.

The particle model, on the other hand, proposes that electromagnetic radiation consists of particles, called photons, which possess only discrete amounts of energy (quanta). Photons only exist in motion, which for the photon is traveling at the speed of light. Photons may interact with other particles, exchanging energy and momentum through elastic and inelastic collisions. Higher frequency electromagnetic radiation has higher particle energy. Max Planck related the actual particle energy of a quantum to frequency of the radiation through the following equation:

E = h • f

where E represents energy, h denotes Planck’s constant (Js), and f denotes the frequency of the electromagnetic radiation. The particle model is useful in conceptualizing certain phenomenon such as scatter, and widely describes the phenomenon of stimulated emission. Stimulated emission is a quantum mechanical phenomenon that results in the emission of two photons in the same direction with the same energy and spatial coherence when an incoming photon interacts with an atom or molecule in an excited state. This principle is the essence of the laser. Laser, or light amplification by stimulated emission of radiation, is a technology, not necessarily a type of radiation. However, current use of the term refers to both the technology and the highly collimated beam of nonionizing radiation it produces.

When measuring nonionizing radiation, energy and power are used to quantify its intensity. Energy, measured in joules (J), is the ability to perform work on a system. Power, measured in watts (W), is the ability to perform work on a system per unit of time; in other words, power is the rate at which energy is transferred. Thus, the power unit of the watt may be also expressed as joules per second (J/s). All types of electromagnetic radiation share certain properties that make them alike, but when the radiation interacts with matter their differences become evident. For example, a thin sheet of black paper absorbs visible light, but RF radiation passes through the sheet of paper as if it were transparent.

Physical Properties

All types of electromagnetic radiation, both ionizing and nonionizing, share the properties of divergence, interference, coherence, and polarization.

Figure 23-2. Divergence calculation from nonionizing radiation sources.

ϕ = (b-a)/r

The upper graphic depicts a common flashlight and represents its divergence for illumination. The lower graphic compares the measure of divergence to a laser, showing a much narrower beam, and thus, a much smaller divergence.

Divergence

The term divergence describes how the radiation emission from a source spreads out with respect to distance. It may be visualized and calculated through the graphic and equation in Figure 23-2, the divergence calculation from nonionizing radiation sources, where ϕ represents the divergence (in radians), b represents the diameter of the radiation beam at a measurement distance, r from the source, and a denotes the diameter of the beam at the starting point of the measurement. Divergence is bounded from below by a value known as the diffraction limit. It is impossible for divergences of sources to be less than the diffraction limit, but with laser sources the divergence can very nearly equal it. Other factors that contribute to divergence include the source size, the geometry of the emission aperture, and the medium of electromagnetic propagation.

Isotropic and collimated radiation exemplify two contrasting concepts. By definition, radiation emitted from an isotropic source diverges uniformly in all directions surrounding the source. The intensity of the radiation decreases with the square of the distance from the source. For example, if the distance to the source were doubled, the radiation would decrease by a factor of 4. If the distance to the source were tripled, the radiation at that distance would decrease by a factor of 9. A common example of an isotropic radiation source is the sun. Light is emitted in all directions regardless of spatial orientation of the source. A standard household incandescent light bulb has a near isotropic intensity, lighting up a room regardless of spatial position of the source. Figure 23-3 shows the inverse-square relationship of the radiated power with respect to the distance to the source.

Figure 23-3. Inverse square law conceptualization.

Collimated radiation, however, has an asymmetrical or directional spatial radiation pattern. Automobile headlights are a good example of a somewhat collimated source, with the visible light directed forward toward the road ahead. Lasers are highly collimated sources and exhibit a very narrow beam of radiation for long distances; they have a very narrow, or tight, divergence.

Interference

The principle of superposition maintains that amplitudes of intersecting waves will combine to produce a resultant wave. Therefore, the net effect of two waves of the same frequency will be either constructive (the resultant amplitude is larger than either two of the input waveforms) or destructive (the resultant amplitude is smaller than either of the two input waveforms; the two waves cancel each other out). Constructive interference occurs when two waves of equal amplitude are in phase (their crests/troughs overlap); the result is a single wave with twice the amplitude. Destructive interference occurs when the two waves are out of phase, for example, 180° (a peak overlaps a trough), where the result is no wave, since the energies cancel each other out point by point. A common physics experiment demonstrating interference is described along with the diffraction phenomenon in the Interaction with Matter section below.

Coherence

Coherence is the measure of the degree of phase correlation within the electromagnetic radiating field from the transmitting source (either a light source or radio antenna) at different times and places along the propagating wave. Coherence is further described in two main forms: temporal coherence and spatial coherence. Temporal coherence, the time in which radiation remains in phase after emission, is essentially a measure of how monochromatic (consisting of a single wavelength) the radiation is. Spatial coherence, on the other hand, is a measure of the radiation’s phase with respect to a given wave plane, and dictates the uniformity of the radiation over a unit in space.[2] Lasers emit nonionizing radiation in both temporal and spatial coherence. The radiation emitted by lasers is near monochromatic in nature, and all photons are in phase with one another across the radiation beam.

Polarization

Polarization refers to the orientation in space of the oscillating fields of the electromagnetic wave, usually given as the direction of the electric field vector. For example, a wave traveling in the z-direction may have an electric field oscillating along the x-direction, in which case it could be referred to as an x-polarized wave; this could also be considered horizontal or vertical polarization depending on how the coordinate frame is defined. More generally, waves polarized in this way (along one particular spatial dimension) are said to be linearly polarized. Waves may also be elliptically or circularly polarized, which means that the direction of polarization changes (rotates) as the wave propagates.

Interaction with Matter

The polarization or orientation of the electromagnetic field components can greatly affect the radiation’s interaction with matter, and can in turn be affected by that interaction. These effects are most evident in matter that exhibits a preferred direction of some kind on a spatial scale comparable to the incoming radiation’s wavelength. For example, the physical orientation of a monopole antenna (like those on portable radios), whether vertical, horizontal, or any position in between, will correspond with the polarization it transmits and receives. Another example is ordered matter such as a crystal lattice, through which polarized light will propagate at different speeds depending on the direction of the polarization. Most sources of electromagnetic radiation do not exhibit a preferred orientation, and are therefore unpolarized. Electromagnetic radiation may gain a preferred direction of oscillation by reflection or transmission through a material, or through a transmitting antenna or radiation-producing aperture. For example, sunglasses with polarizing filters prevent glare by blocking the horizontally polarized light that reflects off glossy surfaces such as car hoods and windshields.

When electromagnetic radiation contacts matter, it interacts directly with the atoms and molecular structure of the medium. Behaviors of the incident energy may take the form of scattering, reflection, absorption, refraction, transmission, or diffraction. The resulting effect of the electromagnetic radiation on matter depends on numerous factors including the wavelength, transmission, and reception media; polarization of the radiation; and the angle of incidence.

Reflection, Refraction, and Scatter

Reflection of an incident electromagnetic wave depends on the surface’s roughness relative to the wavelength of the radiation. The smoother the surface relative to wavelength of the radiation, the better it will reflect the incident wave. If the relative roughness of the medium interface is larger than the incident wavelength, scattering of the electromagnetic radiation occurs. If the reflection image of the incident radiation is scattered in all directions upon interacting with the surface, the image is described as a diffuse reflection. An example of a diffuse reflection is lighting up a room by shining a light at the ceiling or wall. If, however, the reflected image of the incident radiation is maintained with little or no distortion, the image is described as a specular reflection. An example of a specular surface for visible light is the ubiquitous silvered mirror. Figure 23-4 shows diffuse versus specular reflections of laser beams.

Figure 23-4. Diffuse versus specular reflections. The laser line to the left indicates a scattered diffuse reflection; incident beam qualities are lost upon interaction with the surface. The laser line to the right indicates a specular reflection where the incident beam reflects at the same angle of incidence with little distortion.

The speed of electromagnetic radiation in any medium depends on (a) its wavelength and (b) the medium’s physical properties of transmission. It is always slower than the speed of light in a vacuum. The change in velocity for a given material has the nonintuitive result that light changes direction when it passes into a material, a phenomenon known as refraction. This can be seen when light passes from air into another medium (such as acrylic or water) in which it slows down, as seen in Figure 23-5. Eyeglasses and other lenses also exploit refraction in order to direct the image (onto the back of the retina, in the case of eyeglasses).

Scattering mechanisms depend on the size of the particle composing the medium and the wavelength of the incident radiation. The radiation exhibits Rayleigh scattering when the size of the particle is on the same order as the incident wavelength. A good example of Rayleigh scattering is the reddening of the sky during a sunset on a clear evening. The scattering of light by larger-sized particles with respect to wavelength is referred to as Mie scattering. Mie scattering is not as dependent on the incident wavelength and may produce scattering both forward and backward with respect to the direction of radiation travel (Figure 23-6).

Figure 23-5. Refraction of laser light through a clear acrylic block. Although the acrylic is clear, a slight specular reflection occurs at each of the surfaces where the refraction occurs.

Transmission

Figure 23-6. Mie scattering in acrylic showing the beam of a green helium neon laser. Small impurities or air bubbles in the block scatter the laser light both forward and backward to enable viewing of the beam path.

The interactions of a given medium with electromagnetic radiation may be highly selective based on wavelength of the incident radiation. The material may transmit all energy at one wavelength while completely absorbing another wavelength. For example, redcolored glass transmits light around the wavelength of 650 nm but absorbs the wavelengths of green (550 nm) and blue (450 nm). If the medium is not capable of transmitting energy at a given wavelength, it scatters or absorbs and dissipates the energy by other means, typically as heat.

Absorption

When electromagnetic radiation interacts with matter and is absorbed, its energy is transferred to the medium. According to the particle model, an atom absorbs the incident photon and excites an orbiting electron to a higher energy state; the excited electron eventually decays back to its ground state either by giving off another photon or by nonradiative (mechanical, thermal, or photochemical) means. The wave-model description of absorption is that atoms and molecules are immersed in the oscillating field of a passing wave, and the electrons respond mechanically to the oscillation (by rotating or vibrating); this energy is then either re-radiated in the form of another electromagnetic wave, siphoned off as frictional heat, or stored via photochemical reaction. Each description uses different language and mathematical formalisms, but the observed physics (heating, photochemistry, and photon exchange) is the same.

The main effect of electromagnetic radiation on a medium is ultimately dictated by the radiation’s wavelength, intensity, and duration of the exposure. By changing or increasing the intensity of the radiation, or the duration of exposure, the total energy absorbed in the matter will increase. At IR, visible light, and other short wavelength radiation regions, the photons have enough energy to excite electrons to high states, or molecules to high-energy vibrational modes, whereas longer wavelength photons are capable of inducing only the lower energy rotational modes of molecules. A common example of heating matter through molecule rotation is the microwave oven, which uses radio frequency radiation (2.45 GHz) to “flip” the polar water molecules in the food or drink being heated.

Figure 23-7. Single slit diffraction physics experiment showing the interference pattern of spatially coherent light.

Diffraction

Electromagnetic radiation will diffract when it encounters obstacles—that is, it will bend or move around particles, corners, edges, or apertures. The closer in size the obstacle is to the wavelength of the radiation, the more pronounced the effect. A classic physics example of this is single slit diffraction (Figure 23-7). In this example, monochromatic light from a helium-neon laser is incident upon a narrow slit, in this case the gap between two razors. Because the gap is on the same order as the wavelength of light, the laser light “bends” or diffracts around the razor edges and spreads out into the line seen in the figure. Also evident in the photograph is an interference pattern: light starting at different positions along the slit, but reaching the same point on the wall, will interfere either constructively or destructively in a periodic pattern as the differences in path length change by multiples of the wavelength. The nodes (locations at which the light is cancelled out) are seen in the dark regions. The antinodes (locations where the light adds together) are seen in the bright regions.

RADIO FREQUENCY RADIATION

In 1864 James Clerk Maxwell proposed mathematically that energy could be transferred through electric and magnetic fields travelling together at a finite speed. Over 20 years later, in 1886, Heinrich Hertz constructed the first basic oscillator transmitter and receiver. Hertz’s experiment consisted of two metal spheres connected to a high-voltage power supply to create a simple spark gap transmitter. The receiver consisted of a loop of wire with a miniature gap constructed in it to “tune” it to a desired frequency. With this basic equipment, Hertz conducted experiments that demonstrated the similarities between radio and light-based waves, along with the polarization, refraction, and reflection of electromagnetic waves. Although Hertz’s experiments utilized relatively short wavelengths (50–450 MHz), later developments in radio made use of longer and more tunable wavelengths.[3]

Radio Communication and Radar Technology

Guglielmo Marconi used Maxwell’s equations for electromagnetic waves and Hertz’s experiment to put theories into practical use for communication systems. In 1901 Marconi successfully demonstrated radiotelegraphy across the Atlantic Ocean. By 1907 wireless communication services had been established between North America and Europe through the telegraph. Marconi not only successfully demonstrated wireless communication between continents, but also conceptualized the use of radio waves for radio detection and ranging (radar). At the time, however, he was unsuccessful in attracting support for this application.

Later, Marconi’s suggestions stimulated experimental work at the US Naval Research Laboratory, which resulted in the first radio detection of a wooden ship in 1922, and the first radio detection of an aircraft in 1930. In 1932, radio detection systems operating at 33 MHz were capable of detecting the presence of an aircraft at distances up to 50 miles. At the time, however, specific target position information such as range and bearing could not be determined.4(p856)

After the primitive radio detection equipment was developed in the 1930s, research and development efforts continued at a rapid pace. The US Army Signal Corps successfully tested its first radio detection assembly in 1936. Two years later, the Army introduced the first operational radio detection and ranging (radar) system for aiming anti-aircraft fire, the SCR-268. This radar was used in conjunction with searchlights due to the radar’s poor angular position accuracy, although its range information was superior to comparable optical methods used at the time. Also used in the pre-World War II era was the SCR-270, a radar developed in 1939 for the Army as a long-range early warning radar for aircraft. This radar system detected the first signs of the Japanese attack on Pearl Harbor, Hawaii, in 1941, but unfortunately, they were ignored until after the bombing began. The SCR-268 was the standard fire control radar until early 1944, when it was replaced by the SCR-584, developed though research conducted at the Massachusetts Institute of Technology’s radiation laboratory.4–6

Microwave Radar

In 1936 the first efforts to develop radar in the microwave frequency range were published in two research papers that discussed replacing the conventional wire transmission line with a tubular waveguide.[7] The waveguide resulted in less transmission line loss than the wire-based transmission line. Secondly, a successful cavity magnetron was developed in Great Britain in 1940, which made it possible to generate substantial magnitudes of microwave radio frequency energy. In partnership with the Massachusetts Institute of Technology’s radiation laboratory, magnetron units were shipped to the United States to promote research in the field of microwave frequencies for radar applications. Most of this early work was directed toward the use of the newly invented magnetron in aircraft microwave radar applications, namely due to the smaller antenna aperture needed to transmit and receive the RF signals.

The term “radar” was applied to microwave RF-producing equipment, with which objects can be electronically “seen” by means of a transmitted electromagnetic radio wave. The targeted object reflects a percentage of the wave back to the receiver of the radar equipment, which then translates the input to range and position (azimuth and elevation). The use of microwave radar equipment revolutionized the older very high frequency (VHF) radio detection systems. By using higher frequencies, and thus, much smaller wavelengths, newer radar systems could be much smaller and have greater range and versatility.

Radar During World War II

Although the radar used in the Battle of Britain operated at VHF, it provided accurate range and tracking data, and was able to function in spite of fog, clouds, and darkness, thus reducing the threat from Hitler’s bombers. The introduction of microwave techniques not only sharpened these abilities, but also reduced the size and weight of the equipment and extended the applications of radar. Many radar systems at this time could now be installed on mobile platforms, without needing the support infrastructure of a base station to operate the radar system.

Until 1942, allied airborne antisubmarine radar, operating at a frequency of approximately 200 MHz, had neutralized the effectiveness of German submarines in the North Atlantic. At that time, many German submarines were equipped with listening receivers operating at VHF to detect the allies’ operation of the radio detection units. A German submarine with a directional antenna could determine the direction of allied antisubmarine aircraft and estimate their range from the strength of the signal received. The effectiveness of allied antisubmarine aircraft decreased greatly because German submarines, warned of impending attack, were able to dive before the aircraft were positioned to drop depth charges.

However, allied aircraft then countered the effect of the submarines’ receivers by using an attenuator inserted between the radar transmitter and the transmitting antenna. During the final phase of attack, the radar operator adjusted the attenuator to reduce the radiated signal level. The operator of the listening receiver in the submarine would then note a decrease in the signal strength and conclude that the aircraft was moving away, when in fact the aircraft was approaching for attack.

When the allied forces introduced microwave radar, the German forces mistakenly believed that some sort of IR equipment sensing heat from the submarines had replaced the VHF radio detection systems. Because the German military made no attempt to develop microwave listening receivers, allied antisubmarine operations increased in effectiveness. By 1943, microwave equipment operating at a wavelength of approximately 10 cm had replaced most of the VHF airborne detection systems.

During the next 2 years, new types of radar were developed, including airborne targeting radar and ground-controlled approach radar. Airborne targeting radar allowed bombers to accurately locate targets on the ground in overcast conditions. Ground-controlled approach equipment permitted operators on the ground to direct an aircraft to a safe landing under zero visibility conditions. Neither of these technologies had been practicable before the advent of microwave radar because the required antenna directivity was not possible using small VHF antennas.

Since World War II, microwave equipment has been used for various types of communication systems, including microwave relay installations that handle telegraph, telephone, and television signals. The wide microwave band affords significant data-handling capacity, offers flexible antenna gain due to a much smaller wavelength, and requires relatively low-power transmitting equipment.

Physical Properties That Determine Energy Transfer

RF energy is typically transferred to the body through conduction, coupling, and absorption mechanisms, which are dependent on both the wavelength and the body’s distance from the radiating source. Distances from the source in wavelengths and their corresponding mechanisms are:

- 0 λ = conduction (contact)

- 0 – λ/2π = coupling (currents induced by nonradiating fields)

- > λ/2π = absorption (conversion to heat)

Conduction

Conduction occurs when the body makes contact with an RF source (for example, when an individual touches an antenna element or an exposed transmission line). This is no different than sticking a fork in an electrical outlet, although the frequencies involved are generally orders of magnitude higher. The detrimental effects associated with conducted energy are electrical shock and burn, which comprise the most serious injuries associated with RF energy. As frequency increases, the conductivity of (and penetration into) human tissue decreases: at 60 Hz, the frequency associated with the US power grid, the threshold for a painful shock is 9 mA, whereas the threshold at 10,000 Hz is 55 mA. The threshold for shock and burn also increases with increasing surface area—a grasping contact with the entire hand reduces the energy density in tissue compared to single-finger (touching) contact, thereby reducing adverse effects.

Even if the induced thermal current from RF conduction is not sufficient to create a thermal injury, it can stimulate the nervous system and cause a response similar to that invoked by an electrical shock. The individual may jerk involuntarily or reflexively, and the resulting movement could cause an injury to the victim or to someone nearby.[8]

Maximum permissible exposures (MPEs), quantified in standards, are intended to limit induced and contact RF-current flow through the body for frequencies less than 110 MHz and reduce RF shocks and burns.[9] From 100 kHz to 110 MHz, the MPE limits the RF current through each foot, and at the point of a grasping contact, to 100 mA. The current limit through both feet is simply double, 200 mA. These limits are conservative enough that even if currents at these levels were to enter through a single fingertip, it would not be enough to produce RF shock or burn. The RF current limits in mA per foot below 100 kHz are equivalent to the frequency in kHz; for example, at 40 kHz the limit is 40 mA for one foot, or 80 mA for both feet.

The MPE drops with frequency to accommodate the increased penetration depth of the current and correspondingly higher probability of interaction with the heart and central nervous system. At frequencies lower than approximately 3 kHz, the biological effects associated with RF current flow in the body are clearly discernable and the physiological effects are well understood. They include (in addition to shock and thermal injury) electronarcosis, ventricular fibrillation, and involuntary movement. However, allegations of low-level effects (below the respective MPEs) have been made regarding the frequency region lower than 3 kHz with the largest cluster of questions presently concerning the 60 Hz power-line frequency.9–11

Coupling

During transmission, energy is stored around the antenna in nonradiating electric and magnetic fields in the region known as the reactive near field, which spans from the source to a distance of λ/2π (approximately 0.159 λ). A second conductor introduced into this region (for example, another antenna or a human) will “couple” with the source conductor through either the magnetic or electric field. This is referred to as inductive and capacitive coupling, respectively, and the effect in either case is the penetration of an electric field into the introduced conductor. Exposure levels resulting from electromagnetic coupling are difficult to calculate using field strength probes alone because the probes themselves will couple with the antenna, significantly affecting the results. Similarly, electrical properties of the transmitting antenna (such as impedance) will also be altered by the presence of a second conductor in the reactive near field. Therefore, instead of a direct external field measurement, induced currents and electric fields in realistic models of humans (in both shape and electrical properties) are measured.[12]

The reactive near field of an antenna transmitting at a frequency of 1 GHz ends within 2 in. of the radiating surface, meaning that coupling effects are usually associated with transmission on the lower frequency end of the spectrum, especially when considering human-sized conductors. Specifically, coupling with reactive near fields below 5 MHz can, like direct RF conduction, result in nonthermal electrostimulation effects more serious than thermal effects, including involuntary movement, pain stimulation, and ventricular fibrillation. It is important to protect against induced currents with frequencies up to about 110 MHz.

Absorption

At distances greater than λ/2π, radiated electromagnetic fields dominate over reactive (nonradiating) fields, so the primary means of energy transfer of this radiation is absorption. Just as coupling is associated with low frequencies, radiation absorption becomes a concern as frequency increases, when reactive fields have retreated close enough to the antenna to no longer be practically accessible. Measurements of radiated fields beyond the reactive near field are relatively easy to measure, and conductors immersed in them have no impact on the transmission properties of the antenna being measured. Heating of tissue is the only direct effect potentially hazardous to people from absorption of radiation.

Direct Biological Effects

The common theme in all the previously discussed energy transfer mechanisms is the transformation of energy from electric and magnetic fields into one or more types of energy modes in the target material. When translational modes (movement) are excited, the ambient cell temperature rises due to the heat generated by friction. If the temperature rise is sufficient, proteins denature and a burn results.

Depositing RF radiation energy into the body increases its overall thermal load. The thermoregulatory system responds to the increased thermal load by the usual means: transfer of energy to the surrounding environment through convection, evaporation of body water, and radiation (primarily IR). When RF radiation causes localized heating of certain organs, such as the eyes, prolonged exposure can directly damage that organ. However, short-duration exposure to RF-induced thermal load will usually not cause damage and the heat will be dissipated. For this reason, RF radiation exposure is not cumulative, unlike ionizing radiation exposure. The biological effects of RF radiation are thoroughly treated in textbooks such as the Handbook of Biological Effects of Electromagnetic Fields.13,14

Burns caused by exposure to nonionizing radiation are different from conventional and electrical burns in that contiguous tissues are not necessarily affected; which tissue will be affected depends on the frequency of the incident radiation. For example, microwaves tend to excite thermal modes in water molecules, and tissues with high water content, such as skin and muscle, are affected more severely than tissues with low water content, such as fat. Therefore, microwave-induced burns tend to damage skin and muscle preferentially, and (relatively) spare the subcutaneous fat layer that separates these two structures. In addition, tissue interfaces such as organ capsules and fascial planes tend to be more susceptible to microwave damage. Also, with electrical burns, charring is minimal and usually localized to the site of the current’s entry. Nuclear streaming (when cellular nuclei align along the direction of current flow) is characteristic of electrical burns but not radiation burns.[15]

The lens of the eye is recognized as the most sensitive site for thermal damage. Studies on rabbits show that cataracts can be induced above a certain time-power threshold, down to a minimum power density, by frequencies from the low MHz to several GHz.[16] Attempts to establish a similar relationship in other nonhuman models (including rats, dogs, and monkeys) have been less successful. Several epidemiological studies of military and industrial workers have yielded no evidence of increased risk to these populations. One of the only known potentially credible cases of human exposure to RF resulting in cataract formation, analyzed by Hirsch,[17] involved an electronics technician under nearly continuous occupational exposure to power densities from 1,000 to 9,000 W/m^2.

Low-Level Effects of Radio Frequency Electromagnetic Radiation

Popular controversy surrounds the possibility that electromagnetic radiation may cause harmful biological changes in the absence of demonstrable thermal effects. Thermal effects occur following measurable increases in temperature and at energy levels at least 10-fold greater than the officially mandated MPEs.[18] RF environments in the US Army are relatively safe, but medical officers must realize that thermal effects can range from nuisance, to minor discomfort, to serious injury, to death. Serious effects such as extensive burns are obvious, but low-level effects may not be so clear cut.

Effects of low-level RF radiation, actual or alleged, have involved temperature increases that are (a) too small to measure, (b) transient, or (c) too localized to distinguish.[19] The significance of these effects on health is a subject of much debate among scientists, public health officials, and various special interest groups. The relatively recent proliferation of cell phones and local area wireless networks has made these technologies the target of the most common allegations of low-level exposure effects, but less ubiquitous sources such as “smart” utility meters and radiofrequency identification readers have also triggered concern. Earlier, power grid transmission lines and cathode ray tube video display terminals were cited as examples of chronic low-level exposure.

Although thermal effects are the basis of the current RF radiation exposure standards, scientific investigations during the last 20 to 30 years have focused on effects of low-level exposure. Cancer, birth defects, behavioral changes, and other detrimental effects have been investigated using low-level (below current MPEs) RF energy. These investigations include epidemiological studies, animal studies, and other research efforts. No conclusive evidence substantiates claims of low-level RF radiation effects.[9]

Indirect Biological Effects

Although most manufacturers carefully design sensitive healthcare devices (intended to be used in a fixed setting such as a hospital) to operate satisfactorily in conventional RF environments, RF radiation indirectly poses a threat to health through electromagnetic interference (EMI) with electronic devices by disrupting their normal operation. EMI affects medical personnel by causing interference with sensitive healthcare devices (such as electrocardiograph equipment, operating-room monitors, or cardiac pacemakers), and affects military personnel by causing electronic weapons platforms (such as helicopters) to fail.

Currently, the US Army Medical Department is only addressing concerns associated with the interference of medical devices, specifically from EMI sources produced and operated by the DoD. These evaluations determine system characteristics such as rise time (the time required for the RF pulse to reach peak intensity), modulation, duration, and peak amplitude of the RF radiation. The US Army Public Health Center (USAPHC) is tasked with studying EMI problems with healthcare devices at Army hospitals. The USAPHC maintains special measuring equipment capable of detecting very low EMI threat levels. Typical EMI threat levels may be 7 to 10 orders of magnitude below the MPE associated with direct biological effects.

Implantable electronic devices such as cardiac pacemakers may be subject to EMI-related failure in certain RF radiation environments, such as near electromagnetic pulse (EMP) generators. Most implanted pacemakers provide a stimulating pulse to the heart only when the heart’s own pacemaker fails to do so. The implanted pacemaker monitors the biological pacemaker, but the artificial pacemaker is sometimes susceptible to EMI. Fortunately, the device’s shielding and the surrounding tissue act to reduce the threat of EMI.

During 1987 to 1989, a citizen group protested the use of an EMP generator that supposedly posed an EMI threat to implanted cardiac pacemakers.[20] The Army and other military services used this generator to test the susceptibility of electronic weapons platforms to the effects of EMPs. A thorough study of the alleged threat was conducted in response to the protest, and the results showed that EMPs could indeed interact with modern implanted cardiac pacemakers. Individuals who work close to the EMP source are at risk and require radiation protection controls; however, the EMP levels actually encountered by the public will not produce EMI interactions.

Presently, although the Army’s RF environments pose no known uncontrolled EMI threats to pacemakers or similar medical devices, pacemaker wearers are denied access to controlled areas that might pose an undetermined threat. Such devices and sources of EMI are continually evaluated through the US Army Radiation Protection Control Program.21–24

Radio Frequency Radiation Protection

Protection of personnel from RF electromagnetic fields is mandated and implemented through Department of Defense Instruction (DoDI) 6055.11, Protecting Personnel from Electromagnetic Fields.[25] DoDI 6055.11 adopts the Institute of Electrical and Electronics Engineers (IEEE) C95 series standard for applicable MPE and localized exposure limits (IEEE C95.1-2005).[9] The IEEE C95.7-2005 standard provides recommended practices for developing an RF radiation safety program (discussed later in this chapter). DoDI 6055.11 also established a DoD hotline for electromagnetic field injuries (Exhibit 23-1), as well as the Transmitted Electromagnetic Field Radiation Protection Working Group, which provides technical guidance and recommended policy for RF electromagnetic field safety.

Within the Army, several regulations and pamphlets provide information for the protection of personnel from RF radiation (Table 23-1). Army Regulation (AR) 40-5, Public Health, outlines overall public health policies and their use within the Army, from chemical, biological, and ionizing radiation hazards to nonionizing radiation (RF and laser/optical radiation). AR 385-10, The Army Safety Program, implements requirements of the Occupational Safety and Health Act of 1970 and provides policy on Army safety management procedures with emphasis on responsibility hierarchy and organizational concepts. Department of the Army Pamphlet (DA PAM) 385-24, The Army Radiation Safety Program, focuses specifically on implementation of the radiation safety program established by AR 385-10. Included in the DA PAM are sections for both ionizing and nonionizing radiation, from RF to visible light and near UV. The pamphlet also provides guidance for implementing RF radiation protection measures outlined in DoDI 6055.11.

Exposure Limits

MPEs (formerly known as permissible exposure limits) have greatly changed in the past 50 years since the creation of a standard for RF control. After the dawn of mainstream RF sources in the 1960s, permissible exposure limits were initially published through the American National Standards Institute (ANSI) and the IEEE (before the creation of the C95 series documents). The exposure limit was a constant 10 mW/cm^2, applicable to the public and military alike. Since then, as a result of studies and research papers, the standards began to account for the effects of frequency and temporal characteristics (pulsing) of the incident energy. Current RF limits set forth in the IEEE C95.1-2005 adopt an MPE and localized exposure limit that is frequency dependent, based on the diverse studies on the effects of RF radiation to the human body. Additionally, a two-tier approach to the limits are implemented for the action level (general public) and upper tier (controlled environment) settings depending on how the RF system is used.

EXHIBIT 23-1

MILITARY SAFETY PROGRAM AND EMERGENCY CONTACT INFORMATION

Department of Defense Laser Injury Hotline:

1-800-473-3549

The US Army Public Health Center Nonionizing Radiation Division can provide assistance in the identification of and protection against radiofrequency and laser/optical radiation hazards.

5158 Blackhawk Road

ATTN: MCHB-PH-NIR

Aberdeen Proving Ground, MD 21010-5403

Radio Frequency Radiation phone: 410-436-3353;

DSN: 584-3353

Laser/Optical Radiation phone: (410) 436-3932;

DSN 584-3932

fax: (410) 436-5411; DSN 584-5411

email: usarmy.apg.medcom-phc.mbx.nonionizing@mail.mil

The US Air Force School of Aerospace Medicine Occupational/Environmental Health Division manages the Tri-service Laser Incident Hotline and provides assistance in the identification of and the protection against laser hazards from lasers used by the Air Force.

USAF School of Aerospace Medicine

2947 Fifth Street

Wright-Patterson Air Force Base, OH 45433

phone: 1-888-232-ESOH (3764) or (937) 938-3764;

DSN: 798-3764

email: esoh.service.center@wpafb.af.mil

The US Air Force Research Lab Optical Radiation Branch can also provide assistance in the identification of and the protection against laser hazards in the Air Force.

Chief, Optical Radiation Safety Team

Air Force Research Laboratory

Optical Radiation Branch (RHDO)

4141 Petroleum Road

Joint-Base San Antonio, TX 78234-2644

phone: (210) 539-8205

email: usaf.jbsa.711-hpw.mbx.usaf-laser-safety@mail.mil

The US Navy Naval Surface Warfare Center Code G71 Lead Navy Technical Laboratory for Navy and Marine Corps Laser Safety can provide assistance in the identification of and the protection against laser hazards in the Navy and Marine Corps.

NSWCDD

Code G71

Dahlgren, VA 22448

phone: (540) 653-1060/1149/2442; DSN: 249-1060

email: lasers@nswc.navy.mil

TABLE 23-1

US ARMY GUIDANCE ON RADIO FREQUENCY RADIATION PROTECTION

Regulation

Title

Purpose

AR 40-5

Army Public Health Program

Regulation to establish the Army Radiation Safety Program

DA PAM 40-11

Army Public Health Program

Department of the Army Pamphlet to give guidance on execution of the regulation

AR 385-10

The Army Safety Program

Regulation to provide guidance on radiation safety within the Army

DA PAM 385-24

The Army Radiation Safety Program

Provides guidance on execution and initializing a working radiation safety program from Army-wide to installation and commands

DoDI 6055.11

Protecting Personnel from Electromagnetic Fields

Establishes protection standards for radio frequency electromagnetic fields, and instructs personnel to use MPE limits and practices from the IEEE C95 series standard

IEEE C95.1

IEEE Standard for Safety Levels with Respect to Human Exposure to Radio Frequency Electromagnetic Fields, 3 kHz to 300 GHz

Provides the frequency-dependent MPE limits and guidelines on protecting personnel from overexposure, contact and induced currents, and discharge contact voltages

IEEE C95.6

IEEE Standard for Safety Levels with Respect to Human Exposure to Electromagnetic Fields, 0–3 kHz

Provides MPE limits and guidelines on protecting personnel for sub-radio frequency fields in the range of 0–3 kHz. Main protection is from electrostimulation, contact voltages, contact and induced currents, and magnetic field strength

IEEE C95.7

IEEE Recommended Practice for Radio Frequency Safety Programs, 3 kHz to 300 GHz

A useful tool for radiation safety officers and safety personnel on development and implementation of a radio frequency safety program

IEEE: Institute of Electrical and Electronics Engineers

MPE: maximum permissible exposure

Current MPEs are derived from specific absorption rate limits, known as the basic restrictions (BRs), which are defined as the maximum allowable RF (or electromagnetic) power deposited per unit mass of biological tissue, in units of watts per kilogram (W/kg). Often, for low frequencies, exposure is best directly compared to the BR using dosimetric methods. As the frequency of the radiation increases, the energy is deposited closer to the surface, and comparison to the derived MPE values via measurements of external fields becomes more practical. External field power densities are given in the units of watts per square meter (W/m^2), or milliwatts per square centimeter (mW/cm^2) in older versions of the IEEE C95 standard. Electric and magnetic field components of any incident RF radiation are given in units of either volts per meter (V/m) for the electric field, or amps per meter (A/m) for the magnetic field. In all frequency ranges, the BRs are the most fundamental restriction: the MPE may be exceeded provided the BR is not, but the reverse is never true.

Radiation Control

When assessing the hazard severity of an RF-producing source, certain operating parameters must be known: transmit frequency, transmit power (and possibly duty cycle), and antenna gain. The transmit frequency of the source is used to look up the proper MPE limit in the IEEE C95.1 standard tables. Transmitter power is then used (along with the antenna geometry) to determine the near field power density for comparison with the MPE. If a given RF source exceeds the MPE in the near field, the (far field) antenna gain can be used along with the transmitter power to calculate a standoff distance for personnel to maintain while the system is transmitting. The standoff distance, typically given in meters or feet, is the distance from the antenna beyond which the calculated or measured power density falls below the MPE. Engineering-based controls and administrative procedures may be used to restrict access to areas where the MPE is exceeded.

Emission of Radio Frequency Radiation

A typical RF system has three basic components to convert electrical power and a modulated signal into the electromagnetic waves that propagate from an antenna. First, the RF oscillator generates the necessary waveform within the RF spectrum. The intensity of the waveform is then increased to the required level by an amplifier. These two components are collectively referred to, in this context, as the transmitter. The transmission line then “guides” the energy from the transmitter to an antenna for propagation. A transmission line, which may take on many forms, must be able to transfer energy effectively to the antenna. Third and last is the antenna. The function of the antenna is to match electrical parameters from the transmission line to free space, effectively coupling the energy to a free-space radiating wave.

The Transmitter

The RF oscillator is a means to convert electrical power in a circuit to a time-varying waveform. Typically, the oscillator is the fundamental component of an RF transmitter. Included within the transmitter is an amplifier, which amplifies the RF-generating source and provides an output matching the impedance of the transmission line or the antenna itself. There are many types of oscillators and amplifiers, the details of which are outside the scope of this publication, but amplifiers may be broadly divided into two categories: solid-state and vacuum tube based. Solid-state amplifiers are common among radio communication systems and some radar assemblies, while vacuum tube-based designs are still ubiquitous in high power applications such as long-range search radars and radio/television broadcast towers. RF safety concerns for personnel at the transmitter are usually minimal and, as before, are dictated by transmitter power and frequency. When hazards do manifest, the connection point between the transmitter and the rest of the system (ie, transmission line or antenna) is the most likely culprit.

The Transmission Line

The purpose of the transmission line is to guide the RF energy from the transmitter to the antenna. Some systems couple the transmitter directly to the antenna, omitting a transmission line completely. The many types of RF transmission lines may be divided into two main categories: conductor-based lines and waveguides.

The more familiar of the two, conductor-based transmission lines, are so called because the energy is primarily stored as electrical current within conducting wires (strands of metal or metal alloys) during transit. Examples include single wire conductors, parallel or ladder lines, and coaxial cables; applications include commercial power transmission lines (cross-country transmission wires), older “rabbit ears” and “bow tie” type television antenna hookups, and modern cable television coaxial hookups (Figure 23-8). The diameters of a coaxial cable typically denote the operating power, with larger diameters able to handle more power. As frequency increases, the losses in conductor-based transmission lines also increase. Coaxial cable can be used at frequencies well into the millimeter wave band, but if efficiency is important, waveguides should be used.

Waveguides become practical at a frequency around 1 GHz. Waveguides make use of a single conductor in the shape of a hollow metal tube and, instead of RF power being transferred through voltages and currents on conductors, a propagating wave develops on the interior walls of the tube. Waveguides are rectangular for linear polarization modes and circular for circular polarization modes. Most modern microwave RF systems make use of waveguides to transfer energy from the transmitter to the antenna; however, coaxial cables may still be used in specific circumstances. The cross section dimensions of the waveguide (length and width or radius of the interior) determine the operation frequency. Therefore, as the frequency increases, the dimensions of the waveguide decrease. Figure 23-8 shows various waveguide sizes.

Figure 23-8. Assortment of conductor and waveguide transmission lines. The brown two-wire transmission line was salvaged from an old television set-top antenna. The light green cable handles the smallest amount of power transmission, while the coaxial cable section on the far left handles the most power. The waveguides increase in frequency from left to right.

Potential hazards for the transmission line of an RF system may be either overexposure or electric shock or burn. An RF shock or burn can occur on a conductor-based transmission line where the voltages and currents exceed limits set forth in the current IEEE C95.1 standard. This includes both a contact voltage and contact current along any conductor of the transmission line. Waveguides pose a problem of potential overexposure if the transmitted power is high enough because the RF energy propagates as a coupled electromagnetic wave down the waveguide. RF radiation may leak out into the surrounding area if the transmitter waveguide is cracked or open during transmission.

The Antenna

The antenna is the final constituent of an RF free space-radiating system. The antenna’s purpose is to couple the energy from the transmission line to free space. Like transmitters and transmission lines, antenna design and safety concerns are a function of frequency and power, but the antenna introduces a third factor: beam shape. When transmitting, the antenna does not radiate electromagnetic waves in a sphere of perfectly uniform intensity (isotropic radiation), but instead concentrates the radiation in certain areas. The degree to which an antenna’s radiation pattern (or beam shape) departs from that of an isotropic radiator is known as its directivity; the more concentrated the beam is, the higher its directivity. Directivity is frequently combined with other antenna efficiency factors and compared to a lossless isotropic antenna—the resulting quantity is referred to as the gain of the antenna.

Antennas take on many forms, from conductor-based designs (like the set-top antennas found on over the air broadcast televisions) to high-gain aperture horn antennas used when high directivity is desired. An example of a typical low-gain antenna is the monopole whip antenna on many vehicles. The RF radiation emitted from these antennas is omnidirectional; the energy is radiated from all directions broadside to the antenna. An example of a high-gain antenna is a parabolic dish antenna. An electrically conductive parabolic dish typically has a waveguide horn aperture positioned at the dish’s focal point to yield a high gain.

Military Applications

The subtopics below provide some examples of common US Army RF radiation-producing systems and the potential hazards to operating them. For a more complete list of systems and their respective technical parameters, consult the Communications-Electronics Command technical bulletin 43-0133.[24]

VHF/UHF Radio Communications Systems

VHF and ultra-high frequency (UHF) radio systems are ubiquitous in the Army for voice and data communication and coordinating operations. Radios take on numerous forms but are essentially grouped into three main categories: handheld or manpack systems, vehicular radio systems (Figure 23-9), and systems used in a base station or tactical operations center. Many radios are also capable of operating within some or all of these categories, depending on their configuration. For example, the AN/PRC-154 Rifleman radio is a handheld radio that can be mounted into a docking station in a vehicle. The docking station may also provide additional amplification to the initial 5-W power output to cover a greater distance. Another example is the AN/PRC-155 radio transceiver. The radio itself may be used in all three configurations, and depending on the antenna configuration. Handheld and manpack radios typically do not pose a hazard from RF radiation emitted by the antenna; however, they may pose a risk of shock or burn if the antenna or transmission line is bare wire or has metal surfaces. Vehicular radio and base station radio sets generally transmit more power than portable radio systems, and therefore may require additional precautions against radiation hazards, shock, and burn. A common single-channel ground and airborne radio system transmits about 50 W into its antennas, and may require standoff distances during transmission.

Figure 23-9. A mine-resistant, ambush-protected (MRAP) vehicle provides a variety of radio frequency communication systems. The most prevalent are the omnidirectional very high frequency (VHF) and ultra-high frequency (UHF) antennas. US Army photo by Specialist Elisebet Freeburg, Joint Sustainment Command–Afghanistan, PAO.
Reproduced from: https://www.army.mil/e2/-images/2009/10/23/53959/index.html

Very Small Aperture Terminal Communication Systems

Very small aperture terminal (VSAT) communication systems are ubiquitous in the US Army today for maintaining communications in the field. The main goal of a VSAT is to communicate with a geosynchronous satellite network, providing ground connections to the secure and nonsecure internet protocol routing networks (SIPR/NIPR) and other networks. Transmit power of a typical VSAT can range from a few watts to systems capable of 200 to 300 W, as in the AN/TSC-208, pictured as the trailer-mounted VSAT in Figure 23-10a. As technology has progressed and microwave electronic devices have become more affordable, smaller VSAT configurations have become available in a manpack form for greater portability. The VSAT pictured in Figure 23-10b is part of the AN/TSC-203 Global Response Intelligence Terminal.

These two different forms provide similar communications, but may pose different hazards. Specific equipment may differ, but when the transmit power is greater than approximately 20 W, personnel should avoid the region between the antenna feed and reflector. This recommendation typically applies to the bigger VSATs such as the AN/TSC-208 trailer-mounted system. Also, although VSAT systems are capable of a maximum specified transmit power, in most cases they will use only enough power to establish reliable communication with the satellite. Therefore, transmit power may be a fraction of the full rated power of the system while in operation on the satellite network. Additionally, VSAT systems are directed to the sky toward satellites in geosynchronous orbit.

Microwave Radars

The main purpose of microwave radar systems is to acquire and track targets, either on the ground or in the air. The radar system transmits high-energy pulses of RF radiation using the antenna to direct the energy in a specified pattern. Range is computed by the time it takes for the transmitted pulse to reach the target, reflect, and be received back at the radar. The antenna is typically mounted on an electromechanical positioner to direct it to potential points of interest. It may scan 360°, or only oscillate in a given direction, depending on application. Common transmitter peak power for microwave radars ranges from a few hundred watts to several hundreds of kilowatts. Despite the high peak power of a radar transmitter, the average power may be quite low, due to the duty cycle (on/off time) of the transmitter when operating.

Figure 23-10. Two common very small aperture terminal (VSAT) deployments for portable operations: (a) a trailer-mounted AN/TSC-208; (b) a part of the AN/TSC-203 Global Response Intelligence Terminal.

Areas of concern with microwave radar assemblies include the main beam of the antenna, the region between the antenna feed and reflector, and the waveguides that supply the transmitter power to the antenna. Additionally, if the radar transmitter uses a vacuum tube-based amplifier, special consideration must be taken to guard against high voltage and potential x-ray generation. Most if not all systems today have interlocks built into the enclosure and critical components to prevent hazard to individuals. Figure 23-11 shows a typical acquisition and tracking radar for aerial applications. When the radar is in operation, personnel should be advised not to occupy the platform via administrative procedures (signs, warning lights), or prevented from accessing the platform through engineering controls (fences and barriers).

Figure 23-11. A microwave radar system installed at an Army depot. The waveguides feed the radio frequency power through the arm at the top of the antenna.

Phased Array Antenna Systems

Phased array antenna systems operate in a similar fashion to parabolic reflector microwave antennas; however, the main radiating beam is not geometrically dependent on the antenna. Rather, in a phased array system, the antenna plane consists of many antenna elements that essentially work together to create a desired radiating pattern. By altering the phase of the RF signal at each antenna element, the radiation is electrically steered (in contrast to mechanical steering, used in traditional microwave systems). This allows the radiating beam to transmit from the antenna at oblique angles to the phased array plane and change the radiation pattern at an extremely fast rate. Phased array radars can track targets by scanning the radiation beam in a two-dimensional pattern. If a target of interest is designated, the phased array antenna may dwell, or “stare” at the target, to acquire more precise location information than is possible with a quick sweep of the scanning beam. Phased array systems are typically stationary or mounted on a slow-moving positioner.

For high power phased array systems, the potential hazard area is broader because of the electrical steering of the beam; the antenna plane does not necessarily denote where the radiation comes from. Additionally, personnel working around the system may not know the radiation pattern of the antenna. The hazard zone of a high power phased array system may be a semicircle or hemisphere on the front of the antenna. Figure 23-12 depicts a phased array antenna radar system.

Exposure Incidents

The severity of any suspected personnel overexposure to RF radiation determines the extent of both the medical and technical investigations. When a suspected RF overexposure occurs, the local medical department activity must examine the patient and complete a Special Telegraphic Report of Selected Condition (Requirement Control Symbol MED-16), as required by AR 40-5, Army Public Health Program, Section 3-20, Public Health Information Systems, 3-21: Records Management. The report must be sent to the Office of The Surgeon General’s Preventive Medicine Division. The medical evaluation initiates a technical evaluation to analyze the following RF radiation parameters and incident data:

- operating (transmit) frequency,

- antenna gain,

- average and peak power output of the transmitter,

- transmission line losses between the antenna and transmitter,

- distance from the antenna or waveguide to the location of the suspected overexposure, and

- duration of the exposure.

Figure 23-12. A trailer-mounted phased array radar system. Note that there is no defined parabola dish on the antenna. There is a red covering on the antenna for absorbing radio frequency radiation that attenuates the output power during maintenance or repair work; it is removed during operation.

The initial technical evaluation of the suspected overexposure permits investigators to determine the exposure level an individual may have encountered. However, an incident is not classified as an overexposure only if the power density level exceeded the MPE. According to current IEEE standards, in most frequency ranges, a 6-minute timer period is used to average the exposure. A safety factor of 10 is also incorporated into the MPEs for further protection. If the technical evaluation indicates that an individual may have been exposed to RF radiation greater than 5 times the MPE, the following procedures must be followed: (1) medical personnel will administer a complete medical evaluation (however, the only manifestation of overexposure that the evaluation will diagnose is thermal injury); (2) the USAPHC will conduct an investigation; and (3) an investigation report will be published. The investigation report includes:

- on-site interviews,

- evaluation of the RF radiation source,

- measurements at the incident site from the source,

- consideration of other evidence to establish the extent of the overexposure, and

- recommendations for improving potential deficiencies in the nonionizing radiation safety program.

Below are two case studies of exposure investigations.

Case Study 23-1

One RF radiation exposure incident involved a soldier working near a high power illuminator radar (HIPIR) unit that was tracking aircraft (Figure 23-13). The soldier was dismantling a tent 35 to 40 m from the HIPIR when he reported feeling localized heating on his back. As the soldier turned around to discern the heat source, he noticed the HIPIR directed toward him. Immediately, he entered a nearby equipment shelter, which put the HIPIR out of sight (thus making the soldier feel safe). The soldier soon began to notice sunburn-like reddening on the backs of his arms and on his upper back.

Although the soldier’s commanding officers did not direct him to a medical facility, he later visited the installation hospital for treatment of the burned areas and the general uncomfortable feeling he was experiencing. The burned areas, described as superficial burns, were 1 cm^2 on the arm and 3 cm^2 on the upper back. There was no generalized erythema. All vital signs were normal and the soldier was released after being treated with Silvadine (Monarch Pharmaceuticals, Bristol, TN) ointment (a 1% suspension of silver sulfadiazine in a hydrophilic base).

The hospital created a MED-16 report of the occupational injury because RF radiation was a possible cause. [The actual medical records, which would have told exactly what physical signs were present, were not available for this case report. Medical officers might ask (a) if the burns were first, second, or third degree, or (b) whether localized, rather than generalized, erythema were present. The use of Silvadine suggests that bullae characteristic of second-degree burns were present, but if so, the lack of erythema would be unusual.—Eds.]

Figure 23-13. The high power illuminator radar (HIPIR) is an acquisition radar of the Hawk air-defense system.

In addition to the initial medical examinations, the Office of The Surgeon General requested that the US Army Environmental Hygiene Agency (now the US Army Public Health Center) conduct an investigation of the circumstances surrounding the incident. This investigation, which was performed within several weeks of the incident, included determinations of (a) the actual RF radiation levels to which the soldier may have been exposed, (b) the duration of exposure, and (c) the possible biological effects resulting from the exposure. The initial evaluation was conducted via telephone interviews. The preliminary findings indicated that the maximum RF radiation levels that the soldier may have experienced were between 110 and 150 mW/cm^2. However, the actual exposure duration could not be determined. Because the RF radiation levels exceeded the MPE by more than 5-fold, the Environmental Hygiene Agency initiated a full investigation of the incident, including a visit to the incident location to obtain the actual power density measurements.

The investigation team dispatched to the incident site consisted of medical and engineering personnel. The team conducted extensive interviews with personnel associated with the operation of the HIPIR at the time of the incident, the soldier who allegedly was injured by radiation from the HIPIR, personnel who were working with the soldier at the time of the incident, and hospital personnel who examined the soldier. The interviews were used in an attempt to create an overall picture of the events surrounding the incident.

In addition, the team engineers conducted measurements of the actual RF radiation levels at 35 to 40 m from the HIPIR source. The measured values agreed with those predicted in the initial evaluation. The team also determined that the HIPIR was in a tracking mode at the time of the incident. When a HIPIR loses its target, the radar will coast (continue in the same direction with the same velocity) in an attempt to reacquire the target. If the HIPIR does not reacquire the target within a few seconds, the radar will return to its primary target (the direction is preset by the operator), which, in this instance, was away from the tent. It is likely that the soldier was exposed to the main beam of the HIPIR during this coasting function.

The investigation team determined that no RF radiation overexposure had occurred. The MPE in the frequency range of the HIPIR is 10 mW/cm^2 when averaged over 6 minutes. The duration of the exposure could not have exceeded a few seconds. Therefore, the soldier was not exposed to RF radiation in excess of the MPE. The burn may have been caused by another heat source such as the sun. The sensation of heat from the RF energy may have exacerbated the soldier’s injury, but RF energy did not cause it. Nevertheless, unauthorized personnel will not be permitted within the RF radiation control range established for the HIPIR.

The soldier continued to report fatigue and chest pains. A series of examinations including liver function tests, blood counts, pulmonary function tests, and ophthalmic examinations were conducted over the next 6 months. All these examinations found no abnormalities. Later examinations included an electroencephalogram and a computed tomography scan. These examinations also found no abnormalities. The attending internist recommended regular neurological evaluations, which also found no abnormalities.

Case Study 23-2

Another RF radiation exposure incident involved two soldiers performing maintenance operations on a HIPIR. They were attempting to determine why the antenna’s arc detector crystal, located inside the transmitter housing, repeatedly burned out. While the radar was transmitting, the two soldiers removed the transmitter housing cover and visually examined the inside. After having examined the inside for 10 minutes, they noticed that a rigid waveguide was positioned incorrectly. They shut off the radar to remove the antenna pedestal head assembly. Upon further inspection after removing the assembly, they found the source of the repeated crystal burnout: a section of flexible waveguide that transfers high-power RF radiation to the antenna had been severed (Figure 23-14).

Within hours of discovering the severed waveguide, the two soldiers independently reported nausea and general malaise, and they reported the incident to the radiation safety officer (RSO). The RSO used an RF radiation meter to attempt to determine the actual power density levels to which the soldiers may have been exposed. The measured levels exceeded the 100 mW/cm^2 limit of the meter, and therefore the RSO requested the services of the US Army Environmental Hygiene Agency.

On the day after the incident, before the US Army Environmental Hygiene Agency investigation team arrived, the soldiers received ophthalmic examinations. The examinations included tests for visual acuity, a slit lamp evaluation of the crystalline lens, ophthalmoscopy, and an intraocular pressure test. The examinations revealed no abnormalities in either of the soldiers’ eyes. The soldiers also reported that their initial nausea had subsided.

The US Army Environmental Hygiene Agency medical and engineering investigation team conducted an investigation. They interviewed the two soldiers, the RSO, and medical personnel at the installation. In addition, they measured the actual power density levels in the regions where the soldiers were trouble-shooting. The RF radiation levels ranged from 50 to 250 mW/cm^2. Assuming that at least the minimum exposure level was experienced for a maximum of 6 minutes, there is no question that the soldiers were exposed to RF radiation more than 5-fold greater than the MPE (10 mW/cm^2).

The primary recommendation of the investigation team was to test the HIPIR to determine why the flexible waveguide section had broken (this was apparently not the first time the waveguide had broken in this manner). The investigation team also recommended that maintenance personnel should always perform visual inspections around the transmitter housing with the power to the transmitter turned off.

Figure 23-14. A broken radio frequency (RF) transmitter waveguide may leak RF energy into the surrounding environment during transmit modes. It is important to periodically check the waveguides and flanges for breaks and to replace them before transmitting with an RF device.

The Radio Frequency Radiation Safety Program

The installation or activity RSO is responsible for ensuring that a comprehensive nonionizing radiation safety program is in place and implemented in accordance with Army regulations (see Table 23-1). The safety program should include information on nonionizing radiation-producing sources, environments, control procedures, and points of contact in case of emergencies. No personal protective equipment is used by the DoD for RF radiation protection.[25] The USAPHC Nonionizing Radiation Program can provide assistance in the identification of and protection against RF radiation hazards (contact information is provided in Exhibit 23-1).

Inventory of Radio Frequency-Producing Sources

The installation or activity RSO must maintain an inventory list of all nonionizing radiation sources that exceed the respective MPEs. The threat classification of the source should be included on the inventory. Using the inventory, the RSO can recommend appropriate engineering controls or administrative procedures to further protect personnel from exposure.

Radio Frequency Controls and Administrative Procedures

Engineering controls include any device or subsystem that modifies the design, construction, or operation of the RF system to prevent undesired radiation or hazards. Examples include safety interlocks on cabinets and couplings, and termination (dummy) loads to dissipate power instead of radiating the power through the antenna. Azimuth and elevation sector blanking switches, couplers, or attenuators provide additional interlocks to prevent antenna radiation in unintentional locations. Engineering controls may also restrict access to locations that exceed the MPE by the placement of fences or structures to limit or mitigate exposures. For example, the placement of an aircraft scanning radar may be put on a tower (with restriction to the tower itself) to mitigate the exposure of personnel on the ground. Secondly, the door to access the radar platform may also be installed with an interlock to disable the antenna rotation and transmission once the door is opened.

When physical barriers and other engineering controls are not feasible to integrate into the radiation safety program for the system, administrative procedures provide alternative methods to protect personnel. RF signage, caution tape (or simple ropes or chains), flashing lights, and warning sirens are some examples of administrative procedures that warn personnel of the potential hazards for a given system or location, but do not necessarily prevent an exposure from occurring (unlike an engineering control, which turns off the transmitter or shuts down the system). Administrative procedures rely on individuals to ensure their own radiation protection through observing the environment (signs, lights, etc) and documents such as standard operating procedures. RF signage signal words such as “caution,” “warning,” and “danger” convey the severity of the hazard, along with the coloring of the sign. The IEEE C95.7 standard includes a recommended practice for sign signal words based on the severity of the potential RF exposure in terms of the MPE.

Training Programs

Personnel who should receive radiation safety training include those responsible for operating, maintaining, and repairing RF sources capable of exceeding the MPE. This training should be conducted when the individual is first employed and annually thereafter. It is the RSO’s responsibility to maintain records containing an outline of the training material (or material itself) and a list of personnel who received the training. Training material should include:

- exposure potential associated with specific equipment used;

- biological effects associated with overexposure to power density levels exceeding the MPE;

- proper use of protective equipment and tools such as signs, indicators, barriers, and cones;

- accident-reporting procedures and points of contact in the event of an emergency;

- routine radiation safety program surveys; and

- procedures for maintaining an operational and maintenance log for recording radiation safety-related events (such as radiation hazard zone violations, overrides of warning lights or safety interlocks, failure to post signs during testing).

LASER AND OPTICAL RADIATION

In 1913 Niels Bohr published his model of the hydrogen atom, proposing that atoms could (a) only exist in discrete energy states, and (b) radiate light of well-defined wavelengths in transitions between these energy states. In 1917, while studying the theory of black body radiation, Albert Einstein theoretically proved that emission of monochromatic light (light consisting of a single wavelength) was possible by showing that a process of stimulated emission of radiation was necessary to account for the black body’s radiation spectrum. However, it was not until 1958 that Charles Townes first demonstrated microwave amplification by stimulated emission of radiation (maser). In 1960 Theodore Maiman experimentally constructed the first laser using chromium-doped aluminum oxide (synthetic ruby crystal) as the solid-state laser gain medium.[26] It was first called an “optical maser” because the ruby transitioned at a wavelength of 694 nm (red light); the name changed to “laser” soon after optical masers became common.

The current inventory of fielded laser systems in the Army consists primarily of two types: solid-state and semiconductor-based. In the wider world of physics and engineering, semiconductor devices would be considered a subset of solid-state devices, but semiconductor-based lasers are different enough from other solid-state lasers (as well as all other lasers), in both design and beam properties, that the two domains are commonly redefined into non-overlapping categories. Solid-state lasers use solid-phase materials, usually crystals or glasses, such as neodymium doped yttrium aluminum garnet (Nd:YAG), and erbium doped glass (Er:Glass). Semiconductor-based laser diodes are similar to light-emitting diodes, and are typically referred to by their elemental composition; for example, two common semiconductor lasers in use by the Army are gallium arsenide and indium gallium arsenide.

Prototype ruby laser range finders were introduced in the late 1960s. The first vehicles to utilize the ruby laser range finder in the early 1970s were the M55A1 Sheridan vehicle and the M60A2 missile-firing tank shortly after. During the 1980s, a transition was made to Nd:YAG in infantry, armor, aviation, and artillery units, due to the increased lasing efficiency of Nd:YAG versus ruby laser technologies. Further development occurred in the late 1980s, and use of semiconductors for light emitting diodes and laser diodes became widespread. Semiconductor laser diodes are able to achieve higher efficiencies than Nd:YAG and produce comparable laser power output in a much smaller package. Today, semiconductor lasers have become the default choice for many of the most common laser roles (such as pointing and illuminating) and are not uncommon as rangefinders or light detection and ranging (LIDAR). Nd:YAG remains the laser of choice in high power, low divergence applications such as laser designation for the precision guidance of smart munitions, as well as for the production of high intensity green light. Figure 23-15 shows three stages of laser technology.

Specific Properties of Lasers and Optical Sources

Stimulated emission, in theory, can be used to generate electromagnetic radiation of any frequency. In practice, stimulated emission sources cover a spectral range from x-rays to kilohertz frequencies, with various gaps along the way. Stimulated emission devices emitting at radio and microwave frequencies are known as masers, and although masers are considered the predecessor of the laser, they are not any different from lasers in principle. Masers have a more limited scope of application than lasers because radio frequencies are more easily produced by traditional means. Stimulated emission on the short wavelength extreme of the spectrum, ionizing x-rays and extreme UV, is generated by devices that are still considered lasers but, like masers, are found only in highly specialized environments. Hence, current laser safety standards address devices operating in a spectral range of 180 nm to 1 mm, also known as the optical radiation range.

Figure 23-15. Three examples of laser technology: the ruby laser (left), the Nd:YAG laser (center), and a common red laser pointer diode (right, on the white box). Note the size of each laser core and how technology has progressed in the development of more powerful and efficient laser designs.

Lasers operating in this spectral range generally share three features: a lasing medium, a pumping system, and a resonant cavity. The lasing medium (also known as the gain medium) is the material in which the beam initially forms, and can be a solid, liquid, gas, or plasma. One special class of lasers uses an electron beam to generate the radiation (Exhibit 23-2). Lasers are typically referred to by the kind of lasing medium they use, for example, Nd:YAG and ruby. The pumping system (or pump) is the means by which energy is transferred into the lasing medium. Electric currents, flash lamps, and secondary lasers are all common types of pumping systems. The resonant cavity, while not technically required to create a laser, is what makes most laser designs practical. The simplest kind of resonant cavity consists of two mirrors, each facing the lasing medium at either end. In this way, the medium can be reused to amplify the beam repeatedly as it bounces between the two mirrors.

The specific properties of laser radiation are a direct result of the physics of stimulated emission. A simple way of understanding this process is to say the photons in a laser are “cloning” themselves. An initial photon, in most lasers the product of spontaneous emission in the laser medium, encounters an atom or molecule within the medium that has been excited by the pump system, and stimulates it to emit a photon that is its exact match in direction, frequency, phase, and polarization, with some wiggle room for quantum randomness. On the macro scale, these properties correspond (respectively) to a highly directional, monochromatic, coherent, and polarized radiation beam. The two photons then continue onward, encountering more atoms or molecules and creating more copies of themselves, until they have exhausted the laser medium. Mirrors then reflect the beam back to the gain medium to be further amplified after the medium has been re-excited by the pump system. Note that stimulated emission merely lends itself to these properties, and some lasers may violate any one of them. For example, some lasers are designed to emit a broad range of wavelengths comparable to traditional light sources.

EXHIBIT 23-2

THE FREE ELECTRON LASER

The stable, monochromatic nature of laser light is perhaps its most well-exploited feature, but it also makes individual lasers inflexible. Because of this, broadband, tunable laser sources have been an important area of laser research. Impressive strides have been made by taking advantage of vibronic electron energy states in crystal lasers and other state-dense gain media, but ultimately these solutions are limited by the physical structures containing the electrons. The free electron laser (FEL) addresses this limitation by using a beam of free electrons, traveling through a vacuum, as the emission source. Free from the electromagnetic background of atoms and molecules, the electron beam can be manipulated by artificially produced electromagnetic fields to emit wavelengths over a huge, continuous spectrum ranging from a 10th of a nanometer to several millimeters. FELs have already been used in some surgeries, where their tunable output enabled precision ablation with minimal collateral damage. The Office of Naval Research has an FEL program, with the hopes of eventually producing a megawatt class weapon.

Other optical sources rely entirely on spontaneous emission to generate radiation, and are in general much less complicated than lasers and other stimulated emission devices. They can be divided into two categories: incandescent and luminescent. Incandescent light is the result of spontaneous emission from electrons that have been excited by an increase in temperature. Glowing hot metal, filament light bulbs, and stars all emit incandescent light. Luminescence is a catch-all term that simply means “not incandescence,” and therefore contains the other two familiar modern light sources: fluorescent lamps and light-emitting diodes. Regardless of category, spontaneous emission optical sources emit with random direction, phase, and polarization. Spontaneous emission spectra are, like lasers, dependent on the emission medium, but because the photons are not “clones,” their spectra are much broader.

Direct Biological Effects

Biological effects associated with exposure to the optical region of the electromagnetic radiation spectrum involve the skin and the retina, lens, cornea, and conjunctiva of the eye. The mechanism of injury for most effects is either photochemical or thermal. Thermal (heating) effects continue to dominate through the IR part of the optical spectrum, as they do in the microwave region. Photochemical (causing a direct chemical change) effects become important starting in the visible spectrum and continue to dominate throughout the UV range.

Because the nature and degree of injuries vary with wavelength, it is useful to consider the effects in the seven optical spectral bands that the International Commission on Illumination (Commission Internationale de l’Eclairage) has adopted (Figure 23-16). Actinic UV radiation (UV-C, 100–280 nm, and UV-B, 280–315 nm, which produce photochemical changes) characteristically produces erythema and photokeratitis (welder’s flash). UV-A, 315–400 nm, can also produce these effects, but to a far lesser extent. Unless the exposed individual is also being treated with photosensitizers, which make people more sensitive to UV-A, exposure to UV-A (for example, UV-A black lights such as those used in industry) seldom produces an adverse effect. The recent identification of the injurious wavelengths (the action spectrum) associated with UV cataracts concluded that only radiation of 295 to 325 nm was effective in producing a temporary or permanent lenticular opacity for acute exposures.[27]

Lasers energetic enough to damage skin thermally have become much more common in Army applications over the last 2 decades, but gross thermal damage is still only possible with special lasers. One relatively common fielded laser that emits in excess of the skin MPE is the Green Laser Interdiction System, or GLIS, which has a skin hazard distance of around 2 m. Blocking the GLIS beam near the exit port with a finger or hand has been likened to the sensation of a pinprick.

Figure 23-16. International Commission on Illumination (CIE) spectral bands with corresponding adverse effects. The direct biological effects of optical radiation are frequency dependent. In the visible and infrared (IR) regions, the interaction mechanism is primarily thermal. In the ultraviolet (UV) region, the interaction mechanism is predominantly photochemical, although thermal injury is also present. The biological effects for IR radiation are corneal burns and cataracts. The biological effects for visible radiation are retinal burns, cataracts, and degradation of color and/or night vision. The biological effects for UV radiation are photokeratitis, cataracts, and erythema. UV-A and UV-B are also known causes of skin cancer.

For hazard analysis, effects on the eye are the greatest concern. There is an obvious interest in defining the sites of principle absorption, such as the retina, lens, or cornea. Another consideration is not only how much energy is absorbed in tissue, but also its relative biological effectiveness once absorbed. This is particularly important outside the spectral region where thermal effects predominate, at wavelengths shorter than 400 nm in the ultraviolet spectrum.

Mechanisms of Injury

Distinguishing the category of injury mechanism is of paramount importance in proposing exposure limits and in predicting the potential long-term, delayed, or chronic effects of exposure.

Photochemical injury. UV effects and blue-light retinal injury are considered photochemical in origin. Photochemical processes involve breaking or forming molecular bonds, or both, and result from stimulation of electronic energy modes. One property that aids in understanding photochemical injuries is reciprocity (the product of irradiance, or exposure rate, and the time necessary to produce an effect), which is constant over a wide range of exposure durations. The property of reciprocity is important in understanding photochemical processes: they obey the reciprocity rule for exposure duration from microseconds to hours. For example, 20 mJ/cm^2 of UV radiation produces the same degree of erythema whether it is delivered as 20 kW/cm^2 for 1 microsecond, or as 20 μW/cm^2 for 1,000 seconds, provided the same wavelengths are employed. Exposure reciprocity is assumed to hold for up to 8 hours (one workday), and there appears to be very little (although measurable) additivity for multiple exposures if carried over one day. Exposure guidelines, such as the threshold limit values defined by the American Conference of Governmental Industrial Hygienists (ACGIH) or the MPEs for eye or skin exposure to UV radiation, are therefore expressed as radiant exposure durations.

Thermal injury. Reciprocity does not hold for thermal injury; therefore, it is always necessary to specify the exposure duration when studying a thermal injury. For thermal injury of the skin or eye from a pulsed source, it is the duration of the pulse that determines the threshold irradiance, threshold limit value, or MPE for a given wavelength and effect. The rate-process nature of thermal injury suggests that for exposure durations of less than approximately 10 to 100 microseconds, the rate of delivery of thermal energy to the tissue plays only a minor role because heat conduction cannot occur in so short a time.

Even the MPEs established for lasers tend to reflect this fact. For example, for ultrashort laser exposures of picoseconds, the biological effect is nonlinear and does not appear to be thermal. For the body to sustain thermal injury, exposure to a higher-intensity laser for durations greater than 100 microseconds is required. However, because the body’s blood flow and heat conduction away from the exposed site tend to provide some protection, if thermal injury has not occurred within a few seconds, it is unlikely to occur because a minimal critical temperature (perhaps 45°C) would not be reached through further exposure.

Laser beams may be capable of forming shock waves within tissue. The shock wave is believed to result from the rapid expansion of a plasma, which has been caused by the near-instantaneous heating of a tiny volume of tissue to approximately 10,000°F. Lasers are used in this manner to perform posterior capsulotomies in the treatment of cataracts, and to pulverize gallstones during laparoscopic surgery. Perhaps the clicking or popping sound anecdotally reported by people who have inadvertently gazed into a laser’s beam can be attributed to such a shock wave.28,29

Recent Research on the Injury Process

Until recently, the thermal-injury mechanism was thought to be associated with retinal injury sustained when individuals view bright light sources such as the sun. Researchers were puzzled that the calculated retinal temperature rise for an individual who stares at the sun was only 2° to 3°C for a 2-mm pupillary diameter. Laboratory studies of thermal retinal injury also showed that a 10° to 20°C temperature elevation in the 160-μm solar image was required to produce retinal injury within a few seconds. At this duration, short-wavelength light proved to be far more damaging than longer wavelengths, and reciprocity was maintained over a period of hours. Research thus concluded that the actual mechanism of retinal injury was photochemical, not thermal.[30]

The discovery of the blue-light retinal injury process and the theory of photochemical injury answered unexplained questions about solar retinitis (eclipse blindness). Researchers had not understood why individuals who gazed at the sun for 2 to 3 minutes during a solar eclipse at midday developed eclipse scotoma, but individuals who gazed for several minutes at the sun while it was low in the sky—and lacking in blue light—did not even sustain solar retinitis.[30]

UV light interacts with a number of different molecules in the skin and initiates several different signaling cascades that are still an area of active research. Consequently, the physiology behind UV erythema, photokeratitis, and blue-light retinal injuries is multifactored and multistaged, with the manifestation of injury delayed anywhere from hours to days.

Indirect Biological Effects

Many laser systems used in both research and development and industry contain or are associated with potential ancillary sources of adverse biological effects such as chemical burns, loss of hearing, exposure to airborne contaminants, and electric shock.[31] These sources include chemical reactants and byproducts, target-generated contaminants, cryogenic fluids, dyes and solvents, ionizing radiation, noise, and high voltage. Consensus standards (such as those from the ACGIH, local and state agencies, and the Occupational Safety and Health Administration) govern many of these sources to limit exposure to contaminants with laser operation (Table 23-2). Potentially hazardous ancillary sources are listed below.

Voltage or Radiation During Maintenance

Lethal voltage levels often are generated inside the laser-system enclosure. Personnel can be exposed to these voltages if the system covers are removed or if the electrical interlocks are defeated. Standard electrical safety precautions can reduce risk of electrocution. A potential for exposure to lethal voltages or other harmful radiation hazards might exist when protective covers are removed for service or maintenance. Safety precautions are provided in the appropriate technical manuals.

Fuels and Exhaust

Many chemical fuels and exhaust products are associated with the operation of some laser systems (see Table 23-2). For example, the use of high-energy hydrogen fluoride or deuterium fluoride chemical lasers can cause atmospheric discharges of helium, oxides of nitrogen and sulfur, and several fluorinated compounds (including hydrogen fluoride and deuterium fluoride, which are corrosive and environmentally toxic). Normal ventilation techniques, such as dilution and local exhaust, and other engineering and administrative controls can reduce the concentrations of chemical reactants and their byproducts.

Targets

The target of a laser operation can itself generate airborne contaminants during laser material processing, beam termination, and interactions with metal surfaces (such as arc welding). The ACGIH has recommended limits for welding fumes to provide protection from arc-welding contaminants. Control of airborne contaminants can also be achieved through local and dilution exhaust ventilation, and other engineering and administrative controls.

TABLE 23-2

LASER-GENERATED AIR CONTAMINANTS

Contaminant

Probable Source

OSHA Allowable TWA

OSHA Ceiling Value

Asbestos

Target backstop

0.1 F*/cc

—

Beryllium

Firebrick target

0.002 mg/m^3

0.025 mg/m^3

Cadmium oxide fume Metal target

0.1 mg/m^3

0.3 mg/m^3 (0.05 mg/m^3)

Carbon monoxide

Laser gas

5 ppm

200 ppm

Carbon dioxide

Active laser medium

10,000 ppm

30,000 ppm†

Chromium metal

Metal target

1.0 mg/m^3 (0.5 mg/m^3)

—

Cobalt, metal fume, and dust

Metal target

0.05 mg/m^3

—

Copper fume

Metal target

0.1 mg/m^3(0.2 mg/m^3)

—

Fluorine

HF chemical laser

0.1 ppm

(2 ppm)†

Hydrogen fluoride

Active medium of laser

3 ppm

6 ppm† (3 ppm)

Iron oxide fume

Metal target

10 mg/m^3 (5 mg/m^3)

—

Manganese fume

Metal target

1 mg/m^3 (1 mg/m^3)

3 mg/m3†

Nickel and insoluble compounds

Metal target

1 mg/m^3 (0.05 mg/m^3)

1 mg/m3†

Nitrogen dioxide

GDL discharge

(3 ppm)

1 ppm† (5 ppm)†

Ozone

Target and Marx generators

0.1 ppm

0.3 ppm† (0.1 ppm)

Sulfur dioxide

Laser exhaust

2 ppm (2 ppm)

5 ppm† (5 ppm)†

Sulfur hexafluoride

Saturable absorber

1,000 ppm

—

Uranium (soluble/insoluble)

Target

0.05/0.2 mg/m^3 (0.2 mg/m^3)

0.6 mg/m3† (0.6 mg/m^3)†

Vanadium fume

Target

0.05 mg/m^3 (0.05 mg/m^3)

—

Zinc oxide fume

Target

5 mg/m^3 (5 mg/m3)

10 mg/m3† (10 mg/m^3)†

Values in parentheses denote level recommended by American Conference of Governmental Industrial Hygienists.

*fibers > 5 μm in length; †short-term exposure limits; —: no OSHA ceiling value

GDL: ground designator laser; HF: hydrogen fluoride; OSHA: Occupational Safety and Health Administration; TWA: time-weighted average

Cryogenic Fluids

Cryogenic fluids such as liquid nitrogen are utilized to cool some lasers and many high-sensitivity photodetectors. When cryogenic fluids evaporate, they displace breathable oxygen and thus should be used only in areas of good ventilation. Another safety hazard associated with the use of cryogenic fluids is the possibility of explosion from ice collecting on a valve or a connector. Both protective clothing and face shields should be used when handling large quantities of liquid nitrogen. Workers using gas canisters and cryogenic Dewar flasks are required to follow numerous safety procedures (which are beyond the scope of this chapter) to prevent serious accidents.

Dyes and Solvents

Organic dyes and solvents are used in older laser technology that is being replaced by safer alternatives, but they may still exist in some inventories. Solvents usually compose 99% of the dye solution by weight and are commonly flammable and toxic by inhalation or percutaneous absorption. Control measures for dyes and solvents include exhaust ventilation and proper storage and handling of flammable chemicals.

X-Rays

Ionizing radiation (x-rays) are generated from some high-voltage power tubes and electron-beam lasers. This radiation can be controlled through proper monitoring and shielding procedures. Manufacturers can successfully shield lasers to prevent x-radiation leakage if the lasers are operated with the shields in place.

Noise

Certain high-energy lasers generate noise levels that exceed acceptable standards, although most lasers operate silently. However, hazardous noise levels occur only near the laser or its target, where personnel are not permitted. Other safety considerations thus obviate the need for noise-control measures.

Laser Protection Standards

Until 1973, when the first ANSI standard (Z136.1)[32] pertaining to lasers was published, only general standards for the use of lasers existed. ANSI Standard Z136.1 laid the groundwork for a multitude of laser standards, including standards pertaining to laser use in industry and the military, performance standards, and environmental and international laws. The standard was originally updated triennially, but since 1980 updates have been done about every 7 years. There are eight additional ANSI standards encompassing other laser uses, such as lasers in healthcare and military settings. Although the US Army uses ANSI Standard Z136.1 directly, the US Air Force and Navy maintain their own standards: Air Force Occupational Safety and Health Standard 161-10[33] and Office of the Chief of Naval Operations (OPNAV) Instruction 5100.27.[34] The Army also maintains several regulations and technical bulletins pertaining to laser use (Table 23-3).

Title 21 CFR, Part 1040, dictates performance standards for all laser devices manufactured after 1976.[35] In July 2001, the Food and Drug Administration (FDA) issued guidance stating that some parts of the International Electrotechnical Commission 60825-1 standard may be substituted.36,37 Additionally, some exemptions have been made for the military.[35] Soon after the FDA regulation was promulgated, the DoD obtained exemptions for tactical systems, outdoor training lasers, and lasers classified as in the interest of national defense. In addition, alternative design criteria were developed for the Army, Navy, and Air Force, which were published in Military Standard 1425A.[38] Military Standard 882E addresses safeguards from other, related potential hazards.[39]

Even certain environmental laws affect the use of lasers and laser facilities. Congress passed the National Environmental Policy Act of 1969 to minimize adverse environmental consequences of federal actions. Certain provisions of the act are incorporated into other federal regulations, including the National Historic Preservation Act of 1966 and the Endangered Species Act of 1973. Army Regulation 200-1, Environmental Protection and Enhancement, contains Army policy pertaining to these matters.[40] Because lasers can be used outdoors on a range, the effect of laser radiation on endangered species and other wildlife must be considered.

Lasers are also subject to state and international regulation. The United States is part of the North Atlantic Treaty Organization, which maintains a standardization agreement on laser radiation, Standardization Agreement 3606.[41] New York and Texas have also set restrictions for laser use.

Official standards do not yet address the use of high-intensity optical sources other than lasers. Safety guidelines for these sources are provided in the ACGIH publication, Threshold Limit Values and Biological Exposure Indices.[42] This document provides guidelines for the use of intense visible sources, which can produce retinal thermal injury; sources of intense blue light, which can produce retinal photochemical injury; and IR radiation, which can adversely affect the lens. These guidelines will probably provide a basis for future Army standards regarding these sources.

Laser Hazard Classification

Lasers and laser systems are evaluated to determine the severity of hazard they are capable of posing. Each laser or laser system is classified in one of four basic hazard categories; class 1 is the least hazardous and class 4 is the most.[35] Class 1 lasers do not pose a hazard to personnel, even if all the energy emitted were focused into a person’s eye. Most range finders, as well as the training mode on many military systems, fall into this category. If a laser system falls below the class 1 limit for unaided viewing, but would be classified as class 3R or 3B when optics such as binoculars are used, then it is considered a class 1M laser, with an associated hazard distance during the use of optics.

Class 2 lasers, which must be visible wavelength lasers, only pose a hazard if an individual overcomes the normal aversion response and stares into the laser for more than 0.25 seconds. Lasers less than 1 mW are categorized as class 2. If a laser system falls below the class 2 limit for unaided viewing, but would be classified as class 3R or 3B when optics such as binoculars are used, then it is considered a class 2M laser, with an associated hazard distance during the use of optics.

Class 3 is divided into two subclasses, 3R and 3B. Class 3R is the boundary category, in which lasers are considered to pose a remote hazard, but are given a hazard distance and some controls. The class 3R limit is five times the class 1 limit for lasers outside the visible spectrum, and five times the class 2 limit for lasers within that spectrum. Class 3B lasers are capable of producing a permanent injury to the retina from even a momentary exposure, and therefore the Army requires 3B lasers to be inventoried and their operators trained in laser safety. The class 3B limit is 0.5 W.

TABLE 23-3

US ARMY GUIDANCE ON LASER USE

Regulation

Title

Purpose

AR 40-5

Army Public Health Program

Regulation to establish the Army Radiation Safety Program

DA PAM 40-11

Army Public Health Program

Department of the Army Pamphlet to give guidance on execution of the regulation

AR 385-63

Policies and Procedures for Firing Ammunition for Training, Target Practice, and Combat

Regulation to provide procedures for operating lasers outdoors on a US Army range

TB MED 524

Control of Hazards to Health from Laser Radiation

Technical bulletin provides exposure limits and guidance, establishes responsibilities for personnel protection from optical radiation; applies to active US Army, National Guard, Army Reserve, and Corps of Engineers facilities

21 CFR 1040

Food and Drug Administration, Center for Devices and Radiological Health, Performance Standards for Light Emitting Products

Over-arching standard that the Army cites for standard implementation; states that ANSI/IEC standards may also be used for determining the MPEs and safety constraints of lasers and high intensity optical sources

ANSI Z136.1

Safe Use of Lasers

Provides the main information for setting the standard the Army uses for determining user hazards, based on accessible emission limit to personnel, of lasers and high intensity optical sources

ANSI Z136.6

Safe Use of Lasers Outdoors

Utilizes ANSI Z136.1 and expands upon guidance for using lasers outdoors and in a range environment

IEC 60825-1

International Standard for Safety of Laser Products

Provides guidance for manufacturers of lasers on safe emission limits from laser devices based on an international consensus and standard

ANSI: American Nationals Standards Institute; IEC: International Electrotechnical Commission; MPE: maximum permissible exposure

Class 4 lasers are those with an average output power exceeding 0.5 W. Some are capable of producing thermal injuries on the skin; others pose hazards from combustion or diffuse reflections.

Many lasers may contain dangerous or powerful laser radiation within an enclosure of some kind, but only emit class 1 or 2 radiation into accessible areas. A laser system is classified based upon its accessible radiation, and therefore the classification of the device contained within an appropriately interlocked enclosure is not considered in the overall classification. For example, a laser etching system may employ a class 3B or 4 laser, but that laser is within an opaque box with an interlocked lid that only allows radiation not exceeding the class 1 limit to escape. Therefore, this laser etcher is considered a class 1 system.

Military Applications

Using light for long-range, line-of-sight communications is not new. Paul Revere received a coded message in light before his ride in 1775. Morse code utilizing light was widely used during World War II. Current military uses of laser systems (both hand-held and mounted on vehicles and aircraft) include range-finding and distance measurement, tactical target designation, and simulation of ballistic characteristics for training purposes. Lasers can also be used as part of fire-control systems and in conjunction with night-vision and IR-sensing technologies. Many devices combine some or all of these lasers into a single device.

Laser Range Finders

Laser range finders emit a single pulse or series of pulses toward a target. A counter is activated when the pulse is emitted. When light contacts the target, a diffuse reflector, it is scattered in all directions. Optical sensors receive the light reflected back to the range finder and deactivate the counter. Thus, the distance from the range finder to the target can be calculated from the time of travel between the laser and target and the speed of light using the formula

r = (c•t)/2

where r is the range, c is the speed of light, and t is the time at which the counter is stopped (ie, the round-trip time of the laser pulse).

Most modern range finders have moved to wavelengths beyond 1,500 nm, where MPEs are more relaxed due to the eye’s inability to focus light at that wavelength. The AN/PVS-6 Mini Eyesafe Laser Infrared Observation Set is a hand-held laser range finder first introduced in the 1980s, making it one of the first range finders to emit outside of the retinal hazard region. Laser target locators, including Vector 21 and Mark VII variants, are newer handheld or tripod-mounted range finders. The AN/PED-1 Lightweight Laser Designator Rangefinder is a larger, tripod-mounted system that incorporates a class 4 designator along with the range finder module. The AN/PSQ-23 Small Tactical Optical Rifle-Mounted Micro-Laser Rangefinder is, as the name suggests, a small-arms-mounted laser for target ranging and location. All of the range finders in these systems are class 1 and emit beyond 1,500 nm.

A related technology is LIDAR (light detection and ranging, also known as LADAR), which uses a rapidly scanning laser to create a picture of the scanned object or environment. While generally more powerful than typical range finders, LIDAR systems are usually rendered safe by the scanning motors. A scan failure, which causes the beam to “stare” at a single point, can result in potentially hazardous exposure. Special-purpose LIDAR systems, such as airborne terrain-mapping or water-penetrating LIDAR, may pose a hazard even after accounting for scan rate.

Designators and Markers

Designators and markers (the terms are sometimes used interchangeably) include some of the most potentially hazardous lasers in military use, with both direct and indirect hazards. These devices continuously emit a coded laser pulse toward the target, and the scattered radiation is then picked up by the receiver on a missile, bomb, or artillery projectile. Guidance systems then maneuver the munitions toward the source of the scattered radiation. To achieve precision marking at long ranges, the laser beam must be both high power and low divergence, making it a potential personnel hazard over long distances. Ocular hazard distances for laser markers frequently extend into the tens of kilometers.

Because of the performance requirements of laser designation, Nd:YAG, emitting at 1,064 nm, is still the lasing medium of choice for these systems. Systems currently in use include the aforementioned Lightweight Laser Designator Rangefinder, as well as the AN/PEQ-1 Special Operations Forces Laser Marker, another tripod-mounted designator. The Apache helicopter’s target acquisition designation sight is a long-serving airborne designator. The handheld laser marker is a system designed for close-range target marking, with the intent that users will hand off the target to a longer-range marker before munitions are released. All of these lasers are class 4 and emit at 1,064 nm.

Pointers and Illuminators

Some of the most commonly produced and issued lasers in the military today are small-arms-mounted pointing and illuminating devices. Most of these emit in the near IR, within the detectable range of night vision systems. Generally, a pointer is considered an elevation- and windage-adjustable laser with a narrow beam, while an illuminator is essentially a flashlight that illuminates only for those using night vision optics. Pointers are typically class 3R or 3B, whereas illuminators span from class 1 to class 4. Stationary illuminators meant to expose large areas (eg, over ranges) are generally classified as more hazardous than personal, rifle-mounted illuminators, but there are exceptions.

The multifunction aiming light family of lasers includes some of the most ubiquitous pointer/illuminator devices, such as the AN/PEQ-15 Advanced Target Pointer Illuminator Aiming Light (ATPIAL). The ATPIAL, which may be hand-held or weapon-mounted, integrates a visible aim pointer for daylight use, an IR aim pointer for use with night vision, and an IR illuminator. The AN/PEQ-15A Dual Beam Aiming Laser Advanced is similar in function; both devices are class 3B.

Directed Fire Simulator

Lasers are used extensively in military training to simulate ballistic characteristics of live-fire weapons. The most frequently used laser training system is the Multiple Integrated Laser Engagement System, which uses laser diode technology. In most cases, the diode used is gallium arsenide, which emits a wavelength of about 905 nm. The laser diode is programmed to emit a code of pulses that lets the receiver, attached to the trainee’s target, determine which weapon is being simulated. Lasers developed for the program are required to be class 3R or below.

Countermeasures and Escalation of Force

The increased interaction between the US military and foreign civilian populations brought about by the conflicts in Iraq and Afghanistan has spurred development of crowd control and escalation of force technologies. Ocular disruption lasers, such as the GLIS, are among those that have been fielded. These green beam devices are meant to flash-blind or startle targets without causing permanent injury. This gives soldiers the ability, for example, to determine the intent of a vehicle approaching a checkpoint by blooming its windshield with bright green light. These systems are almost all class 3B.

A conceptually related (but practically and technologically very different) technology is the laser countermeasure system. Primarily airborne, these lasers seek and track incoming guided munitions and send a beam directly into the munitions’ sensors, blinding them. Because ocular safety is a minor concern in this scenario, these lasers are made as powerful as practical in order to maximize the blinding effect.

New Applications

Research and development in laser technology has expanded rapidly within the military in the last 2 decades. Niche applications have prompted the creation of highly specialized lasers with limited production runs; maturing technology is allowing old ideas to finally become reality; and some laser technologies are being commercialized for the first time.

A recent trend has been toward longer wavelength lasers and optics. Night vision technology is being expanded to include so called “thermal” wavelengths, the parts of the spectrum in which warm objects, including people, radiate. New types of semiconductor diode lasers have enabled the creation of laser beams in this part of the spectrum as well. Looking even further into the future, novel high-efficiency solid-state masers hold the promise of closing the terahertz gap, a region of the electromagnetic spectrum in which few devices are capable of emitting.

The recent publicized success of naval laser weapons research hints at a future in which lasers take on an even more active role in warfare. Less celebrated, but just as significant, are the relatively portable high-powered lasers that have become practical solutions to in-the-field materials processing and ground-based directed energy weaponry. Such powerful systems were formerly restricted to experimental setups in laboratories, where hazard control is much simpler.

Another formerly laboratory-confined technology that has recently seen advances in commercialization is the mode-locked laser. Although laser mode locking has existed since the 1960s, its implementation has been too complicated and delicate for use outside of the laboratory, and certainly for military applications, until recently. The key attributes distinguishing mode locking from other laser technologies are an extremely high pulse repetition frequency, extremely short-lived pulses, and broad frequency bandwidth. There is currently little experimental data on the biological effects of these ultrashort pulses.

There are no doubt many other novel laser applications to come over the next decades, unforeseen by the authors. Despite over 50 years of intense research and development in academia and industry, laser applications, and optical technology generally, continue along a kind of Moore’s law trajectory, creating new challenges in clinical practice and injury prevention.

Laser and Optical Radiation Exposure Incidents

Unlike RF radiation overexposures, few incidents of potential laser and optical radiation overexposures have been reported since 1981, when the Army Environmental Hygiene Agency (now USAPHC) began investigating them. In 1988, a formal procedure was established for the investigation of laser and RF radiation exposure incidents. This procedure may involve a formal investigation followed by an official report, but only when directed by the Office of The Surgeon General.

The following four case studies of laser and optical radiation exposures have been selected to illustrate the range of incidents that the USAPHC investigates. The first two concern serious retinal injuries, while the third and fourth describe incidents in which the reported ocular effects were inconsistent with the potential laser exposure.

Case Study 23-3

On March 3, 1987, a civilian employee at Aberdeen Proving Ground, Maryland, was adjusting an Nd:YAG-pumped dye laser when he reported seeing a single orange flash. The laser was operating at a wavelength of 620 nm with a pulse-repetition frequency of 10 Hz. The individual was not wearing laser eye protection at the time because it inhibited his view, and viewing the beam is essential for performing adjustments.

During the eye examination conducted after the exposure, the individual reported seeing a central reddish scotoma approximately 2 ft in radius in his right eye when observing a large object 20 ft away. The examination showed visual acuity of 20/x (not measurable) for the right eye, and 20/20 for the left eye. A funduscopic examination showed a macular hemorrhage approximately 1.5 disc diameters wide in the right eye and a normal left eye. Retinal photographs were taken on the day of the injury and on follow-up eye examinations (Figure 23-17).

Figure 23-17. (a) The retinal photograph of an accident victim’s right eye shows macular hemorrhage. (b) The retinal photograph of the patient’s right eye, taken 3 months after the accident, shows recovery to 20/20 vision.

The examinations and investigation believe that the individual probably received a total intraocular exposure of approximately 550 μJ, which is 3,000-fold greater than the occupational exposure limit of 0.19 μJ. The injury was consistent with the exposure parameters. The individual did regain 20/20 vision in the injured eye, but continues to experience a slight visual degradation in his visual field when using the affected eye for monocular vision.

Case Study 23-4

On July 18, 1989, a US Army soldier stationed in the Federal Republic of Germany reported two laser exposures induced by an MX-9838 AN/GVS-5 laser IR observation set. The soldier claimed that he was exposed to the direct beam at 10 to 12 in. from the source. With each exposure, the soldier reported seeing a whitish flash, hearing a click, and then immediately seeing a dark spot in his visual field. Later, he reported seeing what appeared to be dark jellyfish tendrils in his field of view, which appeared red in high-level ambient illumination.

Because the GVS-5 is a single-shot laser range finder, a maximum of one injury is expected per exposure. The retinal examination, however, showed four separate lesions in and around the macula. The ophthalmologist, who examined the soldier the day following the injury, found the right eye to demonstrate poor visual acuity (20/400), and the left eye to demonstrate 20/20 visual acuity (Figure 23-18). Although the ophthalmologist found the left eye to be normal, the right eye had sustained multiple macular and perimacular laser burns with edema, subretinal hemorrhages, rupture of the internal limiting membrane, and vitreal hemorrhage.

The eye examination and the Army Environmental Hygiene Agency investigation concluded that the maximum intraocular exposure for each pulse could be 15 mJ at 1,064 nm, if the exposed eye collected all the radiant energy emitted. The occupational exposure limit for a pulse less than 50 microseconds at 1,064 nm is 1.9 μJ. The potential exposure was therefore approximately 8,000-fold greater than this limit. Although the severity of the injuries was consistent with the exposure, the number of injuries was not consistent with the incident as reported.

Case Study 23-5

On October 4, 1984, an individual at Jefferson Proving Ground, Indiana, reported being exposed to a helium-neon laser for 1 to 2 minutes. The individual reported seeing a dark afterimage in a uniform circle, approximately the size of a golf ball. The afterimage gradually disappeared, and it had completely disappeared within 1 hour after the alleged exposure.

The individual had two eye examinations after the alleged incident. An examination performed 6 hours after the incident showed visual acuity of 20/30 for the right eye, and 20/20 for the left eye. The individual reported no visual disturbances. Six days later, a follow-up examination demonstrated 20/20 visual acuity in both eyes. Neither of the two examinations revealed any ophthalmoscopically visible retinal changes.

Figure 23-18. (a) This retinal photograph of the patient’s right eye was taken three weeks after the incident. Little change is noted and vision has not improved beyond 20/400. (b) This retinal photograph of the patient’s right eye was taken approximately 1 month after exposure to an AN/GVS-5 laser.

Like the eye examination, the Army Environmental Hygiene Agency investigation of the incident failed to prove that an overexposure had occurred. The investigation showed that at the time of the alleged exposure, the individual was located approximately 8.1 m from the transmitter. The laser was rigidly mounted and the direct beam’s height was too far above the ground to expose the individual’s eyes. If the individual had been exposed to the direct beam at this distance, he would have received a corneal irradiance of 170 μW/cm^2. Approximately 1 minute of exposure to 170 μW/cm^2 is permitted, and similarly, 8 hours of exposure is permitted for 17 μW/cm^2. The actual exposure was probably approximately 1.7 μW/cm^2, which is far below the 8-hour limit. Therefore, the individual was not exposed beyond the occupational limit, and the persistence of the afterimage was not consistent with the exposure level.

Case Study 23-6

On July 2, 1986, while inside the turret of an M60A3 tank at Fort Indiantown Gap, Pennsylvania, an individual performed a self-test on a ruby laser range finder operating at 694.3 nm. Within one-half hour of performing the self-test, the individual complained of an irritation in his left eye. Inflammation increased, becoming more intense over the next 4 days. When the individual returned to work after a holiday, he was sent for an examination. The civilian ophthalmologist’s examination proved normal, except for a preexisting nevus on the fundus of the left eye, and episcleritis and keratitis of the left eye. The ophthalmologist did not attribute the nevus to laser exposure, but did attribute the episcleritis and keratitis to accidental laser exposure because the individual had been working with lasers at the onset of these conditions.

US Army ophthalmologists examined the individual’s eyes and disagreed with the findings of the civilian ophthalmologist. The patient was then flown to Walter Reed Army Medical Center for examination 4 days after the initial eye examination. Army ophthalmologists there agreed with the clinical findings of the civilian ophthalmologist, but were more guarded about attributing the other two findings to laser exposure. Contrary to the civilian ophthalmologist’s conclusion, episcleritis is a relatively common inflammation of the anterior segment of the eye and its cause is usually unknown. Similarly, the civilian ophthalmologist’s conclusion that a ruby laser induced the keratitis is inconsistent with scientific and clinical evidence suggesting that red light at 694.3 nm cannot damage the cornea unless it is of sufficient intensity to cause catastrophic injury to postcorneal ocular tissue. The onset of the episcleritis and keratitis after the laser self-test was coincidental. In addition, radiometric measurements verified that no laser radiation was present inside the turret during the self-test.

The Laser Safety Program

The laser safety program adopts many aspects of the RF safety program. The installation or activity RSO is responsible for control of laser radiation sources within their organization. Lasers that are classified as class 3B or 4 need to be controlled and included in a comprehensive nonionizing radiation safety program. A typical laser safety program includes elements such as an inventory of all lasers within the organization that are classified as class 3B or 4, engineering controls and administrative procedures, laser safety training, and laser eye protection. Outdoor laser ranges must be in an approved setting designated by the organization RSO, with additional controls. See Exhibit 23-1 for the DoD laser injury hotline and service-specific safety program contact information.

Inventory of Laser and High Intensity Optical Sources

A complete list of laser radiation sources should be available to the RSO. Included in the list should be laser specifics such as laser wavelength, output power or energy, nominal ocular hazard distance (if necessary), laser eye protection optical density, location of the laser source, and the classification of the laser. Laser sources with classifications of 3B and 4 should be included in the inventory because they are capable of causing injury. Classes 1, 2, and 3R do not need to be listed because they do not require safety controls for operation.

Engineering Controls and Administrative Procedures

When dealing with the higher power class 3B and class 4 laser sources, care must be taken to ensure safe use of the device and prevent potential overexposures. The laser system must use engineering controls, such as remote interlocks, key control, emission indicators, and shudders/beam stops to prevent undesired laser radiation emission. CFR 1040.10 outlines specific engineering controls based on the laser classification. These controls are designed to prevent unintentional use or exposure by turning the laser off or placing it into a known safe state (not emitting radiation). Administrative procedures protect personnel through placement of signage (entry doors to laboratories, entering the laser approved range, etc) to alert personnel of the potential for laser radiation in a given zone. For lasers with relatively long nominal ocular hazard distance, the RSO should establish a nominal hazard zone.

If a laser system cannot meet all criteria for engineering controls set forth CFR 1040.10 or ANSI Z136.1, an exemption may be filed with the FDA. Typical exemptions are for signage, emission indicators, and key controls, or allowing a class 3B or 4 laser to omit a specific safety feature. For example, placing a standard laser aperture sign on the device may compromise camouflage and affect mission performance. FDA exemptions for lasers are only applicable to DoD laser systems, and the laser must be used in combat or combat training situations for the exemption to apply. Exempt military lasers, regardless of hazard class, must be included in the laser safety program and inventoried to satisfy the requirements of the DoD exemption.

Training Programs

Laser safety training is necessary for all personnel who operate potentially hazardous lasers and high intensity optical sources. This training should include instruction concerning the specific equipment, protection methods for prevention of overexposure, and emergency procedures if an incident does occur. Instructors involved in the training should receive further instruction on basic optics, biological effects of lasers, laser safety standards, laser eye protection and protective garments, and preparation of laser range areas. Additionally, instructors or RSOs must familiarize themselves with the approved reporting channels in the event of a suspected laser incident or injury.

Laser Eye Protection

Laser eye protection is the last line of defense when operating class 3B or 4 lasers and protecting the eyes from potential overexposures. Laser eye protection provides attenuation to the incoming laser light, and dissipates the energy or power, dropping the exposure to below the applicable MPE. A note of caution: laser eye protection is wavelength specific, including certain dyes and materials within the lenses to attenuate the laser yet provide vision in wavelengths not emitted by the laser source. It is important to match laser emission to the wavelength and the relative stopping power (optical density) of the laser eye protection. For example, if using an Nd:YAG designator at 1,064 nm (near IR), make sure the laser eye protection has a significant optical density protection for a wavelength of 1,064 nm.

Currently, the only approved brand of laser eye protection is Revision Sawfly (Revision Military, Essex Junction, VT). Previous versions of laser eye protection, such as the ballistic/laser protective spectacles, are aging technology and are no longer procured by the DoD. The two current Revision Sawfly lens options offer two- and three-wavelength laser protection, and are interchangeable with regular safety glasses and sunglass lenses.

Outdoor Ranges and Laser Range Controls

General range control philosophy, and a general laser safety concept, is to prevent direct and collateral injury or damage to personnel or equipment resulting from laser use. Key elements to an outdoor laser safety range program include: (a) the use of backstops, both natural and manmade; (b) buffer zones defined by the pointing accuracy of the laser; (c) a limited line of sight to occupied areas; (d) maintenance of communication if down-range of the laser firing point; (e) avoidance of specular surfaces that may reflect the laser beam, such as water or metallic surfaces; and (f) appropriate warning signs and lights or sirens during the laser’s operation. Individuals down range within the laser hazard danger zone are also required to wear laser eye protection when working with or observing targets. The ultimate goal of the laser range RSO is to follow the standard operating procedure for safe operation of the laser on the range. He or she must also ensure that the danger zone is controlled so personnel are not exposed to laser radiation above the MPE limits (class 1). Control of the danger zone may be mitigated by terrain (firing the laser into a mountain or hill backstop) or delineated out to the nominal ocular hazard distance.

SUMMARY

Electromagnetic radiation may be ionizing or nonionizing. Nonionizing radiation includes electromagnetic radiation with wavelengths greater than around 100 nm, which is divided into the categories of UV radiation, visible light, IR radiation, terahertz radiation, microwave radiation, and RF radiation. Nonionizing radiation possesses a variety of physical characteristics, such as divergence, interference, coherence, and polarization, which, together with the media with which the radiation interacts, determines how the radiation is scattered, absorbed, reflected, transmitted, refracted, or diffracted. It can interact with tissue in a variety of ways, the most medically important being absorption in tissue and photochemical reactions in the blue light and UV wavelength regions. Optical radiation effects occur to the eyes and the skin. RF radiation can affect all organs of the body; however, the eyes and skin are generally the most sensitive.

The protection of Army personnel from overexposure to nonionizing radiation is accomplished through a comprehensive radiation protection program. The implementation of the program is the responsibility of the installation or activity commander. To this end, consensus standards for occupational exposure to nonionizing radiation have been developed and are enforced through Amy regulations. Procedures have been established for the investigation of alleged overexposure incidents. The incidence of accidental exposure to nonionizing radiation in excess of established limits has been rare, especially considering the number and variety of sources in use today and the types of environments where they are used. The best medicine is preventive. In the event of an accidental overexposure, it is the responsibility of the attending physician to determine if an injury has occurred and to prescribe the treatment. An eye examination should be performed at the minimum.

REFERENCES

1.   DeFrank JJ, Bryan PK, Hicks CW Jr, Sliney DH. Nonionizing radiation. In: Deeter DP, Gaydos JC, eds. Occupational Health: The Soldier and the Industrial Base. Washington, DC: Borden Institute; 1993: Chap 15.

2.   Pedrotti LS, Frank L. Optics and Vision. Upper Saddle River, NJ: Prentice Hall; 1998.

3.   Santo B. Making waves at 100. IEEE Spectrum. 1988;(May):58–60.

4.   Encyclopedia Britannica. Vol 14. Chicago, IL: William Benton; 1972.

5.   Adams JA. Electrotechnology in World War II: Detecting the enemy. IEEE Spectrum. 1987;(Aug):37–41.

6.   Fitzgerald K. Electrotechnology in World War II: Targeting the enemy. IEEE Spectrum. 1987;(Aug):42–48.

7.   Southworth GC. Principles and Applications of Waveguide Transmission. Princeton, NJ: Van Nostrand; 1950.

8.   Chatterjee I, Wu D, Gandhi P. Human body impedance and threshold currents for perception and pain for contact hazard analysis in the VLF-MF band. IEEE Trans Biomed Eng. 1986;33(5):486–494.

9.   Institute of Electrical and Electronics Engineers. IEEE Standard for Safety Levels with Respect to Human Exposure to Radio Frequency Electromagnetic Fields, 3 kHz to 300 GHz. New York, NY: IEEE; 2006.

10.   Bernhardt JH. Evaluation of human exposures to low frequency fields. In: The Impact of Proposed Radio-Frequency Radiation Standards on Military Operations. Neuilly Sur Seine, France: NATO Advisory Group for Aerospace Research and Development; 1985. AGARD Lecture Series No. 138.

11.   Gandhi OP, Chen JY, Riazi A. Currents induced in a human being for plane-wave exposure conditions 0-50 MHz and for RF sealers. IEEE Trans Biomed Eng. 1986;33:757–767.

12.   Chatterjee I, Gandhi OP, Hagmann MJ. Numerical and experimental results for near-field electromagnetic absorption in man. IEEE Trans Microw Theory Techniques. 1982;33(5):1000–1005.

13.   Polk, C, Postow, E. Handbook of Biological Effects of Electromagnetic Fields. 2nd ed. Boca Raton, FL: CRC Press; 1996

14.   DeLorge JO. Disruption of behavior in mammals of three different sizes exposed to microwaves: Extrapolation to larger mammals. In: Stuchly SS, ed. Symposium on Electromagnetic Fields in Biological Systems. Edmonton, Canada: International Microwave Power Institute; 1979: 215–228.

15.   Alexander RC, Surrel JA, Cohle SD. Microwave oven burns to children: An unusual manifestation of child abuse. Pediatrics. 1988;79(2):255–260.

16.   Barnes F, Greenebaum B. Biological and Medical Aspects of Electromagnetic Fields. 3rd ed. Boca Raton, FL: CRC Press; 2007.

17.   Hirsch F. Microwave cataracts: a case report reevaluated. Electronic Prod Radiat Health Physicist. 1970;(Oct):110–140.

18.   Sagan LA. Epidemiological and laboratory studies of power frequency electric and magnetic fields. JAMA. 1992;268(5):625–629.

19.   Stuchly MA. Interaction of radiofrequency and microwave radiation with living systems, a review of mechanisms. Rad Environ Biophys. 1979;16:1–14.

20.   Craig G. Central location for pulse tests urged by EPA officials. Potomac News. March 7, 1989.

21.   Ruggera PS, Elder RL. Electromagnetic Radiation Interference with Cardiac Pacemakers. Rockville, Md: US Department of Health, Education, and Welfare; 1971.

22.   World Health Organization. Extremely Low Frequency (ELF) Fields. Geneva, Switzerland: WHO; 1984. Environmental Health Criteria 35.

23.   Duchene AS, Lakey JRA, Repacholi MH. IRPA Guidelines on Protection Against Nonionizing Radiation. Highstown, NY: McGraw-Hill; 1992.

24.   US Department of the Army. Hazard Criteria for CECOM Radiofrequency and Optical Radiation Producing Equipment. Washington, DC: DA; 1991. Technical Bulletin 43-0133.

25.   US Department of Defense. Protecting Personnel from Electromagnetic Fields. Washington, DC: DoD; August 19, 2009. DoD Instruction 6055.11.

26.   Ulaby FT, Michielssen E, Ravaioli U. Fundamentals of Applied Electromagnetics. 6th ed. Upper Saddle River, NJ; Prentice Hall: 2007.

27.   Pitts DG, Cullen AP, Hacker PD. Ocular effects of ultraviolet radiation from 295 to 365 nm. Inv Ophthal Vis Sc. 1977;16910:932–939.

28.   Keller J. Lasers for tomorrow’s battlefield. Milit Intell Magazine. 1981;7(2):39–43.

29.   Decker CD. Accident victim’s view. Laser Focus. 1977;13(8):6.

30.   Sliney DH. Eye protective techniques for bright light. Ophthalmology. 1983;90(8):938–944.

31.   Sliney DH, Wolbarsht M. Safety with Lasers and Other Optical Sources. New York; NY: Plenum Press; 1980.

32.   American National Standards Institute. American National Standard for the Safe Use of Lasers. Toledo, OH: Laser Institute of America; 1986. ANSI Standard Z136.1.

33.   US Department of the Air Force. Health Hazards Control for Laser Radiation. Washington, DC: DAF; 1980. AFOSH Standard 161-10.

34.   US Department of the Navy. Navy Laser Hazards Control Program. Washington, DC: DN; May 2, 2008. OPNAV Instruction 5100.27B

35.   21 CFR, Parts 1000 and 1040.

36.   US Food and Drug Administration. Laser products – conformance with IEC 60825-1 and IEC 60601-2-22 (laser notice no. 50). Published June 24, 2007. https://www.fda.gov/MedicalDevices/DeviceRegulationandGuidance/GuidanceD-ocuments/ucm094361.htm. Accessed July 12, 2017.

37.   International Electrotechnical Commission. IEC 60825-1, Safety of Laser Products, Part 1: Equipment Classification, Requirements and Users Guide. 3rd ed. Geneva, Switzerland; IEC; 2014.

38.   US Department of Defense. Safety Design Requirements for Military Lasers and Associated Support Equipment. Washington, DC: DoD; 1991. Military Standard 1425A.

39.   US Department of Defense. Systems Safety Program Requirements. Washington, DC: DoD; May 11, 2012. Military Standard 882E.

40.   US Department of the Army. Environmental Protection and Enhancement. Washington, DC: DA; 2007. AR 200-1.

41.   North Atlantic Treaty Organization. Laser Safety Evaluation for Outdoor Military Environments. 6th ed. Brussels, Belgium: NATO; 2012. STANAG 3606.

42.   American Conference of Governmental Industrial Hygienists. Threshold Limit Values and Biological Exposure Indices for 1990–1991. Cincinnati, OH: ACGIH; 2011.

Chapter 24

CARBON MONOXIDE

STEVEN R. SMITH, MD, MPH*; JOHN W. DOWNS, MD†; THOMAS D. LOUWERS, MD, MPH‡; GREGORY J. MARTIN, MD, MPH§; TIMOTHY B. WEYANDT, MD, MPH¥; AND CHARLES DAVID RIDGELEY JR, MD, MS¶

INTRODUCTION

NONMILITARY SOURCES OF EXPOSURE

MILITARY EXPOSURES

PATHOPHYSIOLOGY

CLINICAL PRESENTATION

DIAGNOSIS

TREATMENT

HEALTH STANDARDS AND GUIDELINES

MEDICAL SURVEILLANCE

SUMMARY

ATTACHMENT: EXAMPLE OF MODELING PERCENT OF CARBOXYHEMOGLOBIN WITH TIME USING MICROSOFT EXCEL

*Colonel (Retired), Medical Corps, US Army; formerly, Chief, Occupational Medicine, Department of Preventive Medicine, Madigan Army Medical Center, Joint Base Lewis-McChord, Washington 98433

† Major, Medical Corps, US Army; Chief, Department of Preventive Medicine, Blanchfield Army Community Hospital, Fort Campbell, Kentucky 42223

‡ Lieutenant Commander, US Navy; Physician, Department of Occupational Medicine, Naval Hospital Bremerton, Bremerton, Washington 98337

§ Colonel, Medical Corps, US Army; Chief, Occupational Medicine, Madigan Army Medical Center, 9925 5th Street, Building 9025, Tacoma, Washington 984319

¥ Director, Occupational Health Program, Pennsylvania State University, University Park, Pennsylvania 16802; Lieutenant Colonel, US Army (Retired); formerly, Medical Advisor for Clinical, Occupational, and Environmental Health; US Army Biomedical Research and Development Laboratory, Fort Detrick, Maryland

¶ Lieutenant Colonel, US Army; Occupational Medicine Physician, Occupational and Environmental Medicine Division, US Army Environmental Hygiene Agency, Aberdeen Proving Ground, Maryland 21010-5422

INTRODUCTION

This chapter is being published as an update to Chapter 11, Carbon Monoxide, in the previous edition of this textbook.[1] Much of the chapter has been revised to reflect carbon monoxide (CO) exposure in the military occupational setting and health regulations for service members. CO is a colorless, odorless, tasteless, and nonirritating gas that forms during the incomplete combustion of carbon-containing materials.2,3 CO has high inherent toxicity and extensive exposure potential; it is the most significant and widespread toxic gas in the workplace.4,5

The Centers for Disease Control and Prevention (CDC) estimates that CO poisoning accounts for 15,000 visits to the emergency department and 500 deaths each year.[6] Over 68,000 CO exposures were reported to poison control centers between 2000 and 2009. Of these exposures, 45% were treated on site and 55% were treated in healthcare facilities.[6] Estimates of annual US incidents of confirmed CO poisoning has ranged from 1.4 to 2.3 cases per 100,000 people.2,6 Recent natural disasters (eg, hurricanes, floods, and snowstorms) have led to CO poisoning events because people are unfamiliar with the risks of operating emergency generators and cooking indoors without proper ventilation.6–8

The CDC found that 12% of the CO exposures reported to poison control centers between 2000 and 2009 and 7% of unintentional CO poisoning deaths occurred in the workplace.5,6 In 2000, CO poisoning was the top cause of poisonings and one of the ten most frequent occupational exposures in the US Army.[9]

NONMILITARY SOURCES OF EXPOSURE

Exposures in the General Population

Endogenous Sources

CO is endogenously produced in the body through breakdown of heme at a rate of approximately 10 mL/day2,4 and elevates baseline carboxyhemoglobin (Hbco) levels by 0.3% to 0.7%.4,10–12 Medical conditions that involve red blood cell breakdown (hemolytic anemia, polycythemia), blood transfusions, and sepsis all increase Hbco levels, though rarely reaching clinically concerning levels.2,5 Hbco levels increase by 0.4% to 2.6% during pregnancy in nonsmoking mothers.[12]

Outdoor Air Pollution

Approximately 56% of all atmospheric CO emissions come from motor vehicles, while another 22% comes from construction equipment and boat engines. Metal processing, chemical manufacturing, residential wood burning, forest fires, volcanic eruptions, and lightning strikes also contribute to atmospheric CO levels.

Tobacco Smoke

In the 1920s, tobacco smoke was identified as a source of CO that produces an elevation in human Hbco levels.[4] Interestingly, smoke exhaled by a smoker contains only about 5% CO by volume, while smoke produced from burning cigarettes and other tobacco products produces 70% to 90% of the CO generated.[5] Designated smoking areas may have CO levels that exceed 11 ppm, while CO in nonsmoking areas is less than 2 ppm.[5]

Nonsmokers have Hbco levels between 0% and 2%, while smokers have Hbco levels that range from 4% to 20%, based on the number of cigarettes smoked per day. One-pack-a-day smokers can see elevations of 5% to 6% Hbco, two-pack-a-day smokers see a 7% to 9% rise in Hbco levels, and three-pack-a-day smokers can see rises in Hbco levels of 20%.13,14 On average, Hbco levels rise 2.5% for each pack of cigarettes smoked per day.[15]

Cooking and Heating Appliances

Cooking and heating appliances that burn fuel and are unvented, inadequately vented, or improperly maintained have caused numerous CO poisonings and deaths.7,13,16 Thousands of fatal and nonfatal human CO poisonings occur in the United States each year because of inadequately vented or malfunctioning water heaters, furnaces, and kerosene heaters. The use of grills for heating or cooking indoors and the misuse of gas stoves and ovens to heat houses contributes to the problem of CO poisonings.7,13,16,17

Industrial Exposures

CO exposure can occur in mines after blasting or when fires occur; in petroleum refineries near the catalytic cracking units; and in pulp mills near lime kilns and kraft recovery furnaces. In general industry, CO exposure occurs in boiler rooms and wherever internal combustion engines are used or repaired.[5] CO is used in industrial processes to reduce the oxygen content of iron and other metals, so gas and blast-furnace effluent can contain upwards of 25% to 30% CO.[5] In the chemical industry, CO is the feedstock for acrylate, aldehyde, ethylene, isocyanate, methanol, and phosgene production.[5]

Internal Combustion Engines

When internal combustion engines are run indoors without adequate ventilation, CO exposures occur.[17] Military vehicle crewmembers, law enforcement officers, taxi drivers, ambulance operators, and bus and truck drivers are all at risk of CO exposure. Mechanics in military motor pools, toll takers, garage attendants, and installation security guards are also routinely exposed to CO.17,18 Workers inside buildings may be exposed to CO when vehicle exhaust enters through improperly placed air intakes.[5] The use of propane-powered forklifts indoors may expose the operator to CO.[5] Pickup truck campers can fill with CO and cause serious CO intoxication, particularly among children.[5] Also, numerous CO poisonings and deaths have occurred when residents slept in their homes with vehicles left running in attached garages.6,17

Mines

Blasting operations and fires during mining operations produced some of the worst CO occupational exposures in the late 19th and early 20th century,[5] and recent mine accidents have highlighted the dangers of CO in the workplace.

Structural Fires

CO remains a particular concern for firefighters who must enter enclosed, poorly ventilated spaces and encounter lethal CO concentrations during the “knockdown” (when materials are actively burning) and “overhaul” (searching for “hot spots”) phases of firefighting.[5] The most common cause of death in fires is smoke inhalation, and CO is a major contributing factor for individuals who succumb.[18]

Methylene Chloride

Methylene chloride is an unusual industrial hazard that is metabolized into CO. Methylene chloride is widely used in industry for paint stripping and as an aerosol propellant and degreaser.[16]

Methylene chloride is highly volatile, lipid soluble, and readily absorbed, which makes the exposure potential high. An 8-hour exposure of 50 ppm will produce about 3% Hbco.16,17

MILITARY EXPOSURES

Exposure to CO has long been recognized as a potential hazard associated with incomplete combustion of carbon fuels, including during combat mining operations in World War I.1,18 Military personnel face unique and deadly sources of significant CO exposure not found in the private sector. Military crewmembers of armored vehicles (eg, tanks and howitzers) and aircraft (eg, armed helicopters) involved in weapons firing can be exposed to CO.1,18 Firing of missiles can also result in CO exposure. Exposures to CO may also occur in small arms indoor firing ranges and shoot houses, and exposures have also occurred indoors during the testing of howitzer tubes and during explosive detonation.1,18

Historical Exposures

World War I Combat Mining Operations

Defensive mining operations were conducted early in World War I where mines were used to guard important trenches or sectors of the line. After late 1915, mines were also used in offensive operations. This required personnel to dig more tunnels and use larger quantities of high-explosive munitions, resulting in more soldiers being poisoned by CO due to the detonations. Hydrogen, methane, and oxides of nitrogen were also generated, but CO was the most toxic.1,3

Mine detonations promoted forward movement of the troops. An exploded mine would create a crater 60 to 90 feet in diameter that could be occupied by infantry troops to advance and establish their position. The CO generated by detonations usually dissipated rapidly, and compressor engines were used to ventilate the area following detonation, but soldiers were frequently overcome as a result of incomplete detonation, subsequent gas collection, and entrapment.1,3 Burning gas was frequently seen following an incomplete detonation as a blue flame that persisted for hours.1,3 CO poisoning also occurred when the compressor engine was turned off in order to listen, when fuel or engine lubricants were not available, or when an unexpected breakdown occurred.1,3 Because CO is odorless, colorless, and non-irritating, an exposed individual often failed to recognize the danger until it was too late, which also increased the incidence of exposures. CO was never used as an offensive chemical warfare agent.1,3

World War I Tank Warfare

In the early days of tank warfare, crews spent prolonged time inside their tanks and complained of headache and faintness, and they often lost consciousness. Their symptoms were aggravated when they fired the Hotchkiss and 6-pounder guns.1,3 Symptoms were caused by the poor design of early tanks, which permitted heat accumulation and exposure to toxic gases of combustion. CO exposure occurred because of leakage from exhaust lines that ran inside of the tank and back drafts from other tanks. In one 1918 incident, both tank drivers and the tank commander became unconscious. This demonstrated that improved tank ventilation was needed, so fresh outside air was infiltrated around gun ports and other openings to help dissipate the CO accumulation.1,3

World War II Tank Warfare

In World War II, CO was a problem for large numbers of soldiers who operated in armored fighting vehicles (AFVs). In response, scientists at the Armored Medical Research Laboratory at Fort Knox, Kentucky, developed a reliable, transportable infrared gas analyzer to measure CO in AFVs. High levels of CO were detected in the M3A4 tank after bursts were fired.[19] After five rounds were fired from the 75-mm gun, CO levels increased rapidly to 0.718% (7,180 ppm) in less than a minute, then decreased back to baseline in 4 minutes. The CO levels generated when the 37-mm was fired were substantially lower than when the 75-mm gun was fired.[1]

CO exposures were measured in a medium tank, the M4A1,1,20 and in a tank-towing vehicle, the M32B1, on a flat surface and at a 4% grade, for each crew position. Hazardous levels of CO were found in the M4A1 tank and the M32B1 towing vehicle, both of which had engine exhausts directed rearward.[20] Riders in the tank were exposed to levels of CO in excess of 0.2% (2,000 ppm), and the exposures were affected by changes in wind direction, surface grade, monitoring position, and whether the towing cable or towing bar was used. The M4A1 tank and the M32B1 towing vehicle were retrofitted with an exhaust deflector shield to direct exhaust toward the ground.1,20

Modern Era Exposures

During World War II, only 3% of soldiers in the US Army used AFVs. In contrast, nearly all US soldiers used armored vehicles, such as the mine-resistant ambush protected vehicle, in operations in Iraq and Afghanistan. Furthermore, electronic networks and systems on the battlefield have significantly increased the use of internal combustion generators for electricity production. Today’s service members are more likely than those in earlier conflicts to be exposed to CO, and at significantly higher levels if control measures fail. Even more effective ventilation systems and cleaner burning propellants have not reduced the risk of CO exposure in today’s AFVs.[1]

M1E1 Tank

In 1984, an exposure to CO was reported during the operational test of the M1E1 tank. A firing exercise was run in accordance with a test plan that called for the hatches to be closed, the primary nuclear, biological, and chemical (NBC) system to be off, and backup system (M13A1) to be on. Also, the breech was open, and the engine was off during most of the exercise, although it was started periodically to recharge the batteries. The crew was dressed in mission-oriented protective posture (MOPP) gear. Breathing air was supplied to the protective masks through the M13A1 gas particulate filter unit, although the masks were not worn for most of the exercise. The tank fired 26 main gun and approximately 100 machine gun rounds. At the end of the exercise, the loader slumped forward in his seat. A short time later, the tank commander aroused the loader and assisted him out of the turret. The tank commander was also dizzy and lay down on the tank. The loader and tank commander were taken to the hospital and later admitted.1,21 During the medical evaluation of the crew, Hbco levels were obtained. The loader had a level of 33% Hbco and the tank commander had a level of 27.8%. It should be noted that these Hbco measurements underestimate the true Hbco levels because of the short biological half-life of Hbco in the blood.

In March 1984, the US Army Human Engineering Laboratory Liaison Office, at Fort Hood, Texas, made the following recommendations to improve the M1E1 tank:[21]

- Reroute the air intake for the M13A1 gas particulate filter unit away from the turret area.

- Advise individuals at all test sites about the CO hazard when the main gun and/or coaxial machine gun is fired with the hatches closed and NBC system off.

- Advise personnel that the M13A1 gas particulate filter provides no CO protection.

- Include a warning in the operators manual about the CO hazard when the weapon is fired and the inability of the M13A1 system to remove the CO, and describe the ventilation steps needed.[21]

Bradley Fighting Vehicle

The Bradley fighting vehicle (BFV) is a tracked, light-armored vehicle. The BFV has an M242 turret-mounted 25-mm chain gun and an M240 7.62-mm coaxial machine gun, and a TOW (tube-launched, optically tracked, wire-guided) anti-tank missile launcher. In 1980 the US Army Environmental Hygiene Agency conducted toxic gases testing on the BFV.[22] Real-time monitoring was done inside the vehicle during a worst-case firing scenario to determine peak and total CO exposure concentrations.

Two hundred rounds of 25-mm and 75 rounds of 7.62-mm ammunition were fired over 20- and 60-minute periods. Peak exposures in the turret were measured at above 600 ppm; the average exposure concentration was 190 ppm. The total exposure concentration was 11,400 ppm-minutes based on the cumulative exposure being the product of the average airborne concentration and total exposure time. The firing-exposure scenario was repeated, and peak measures in the turret were found to exceed 800 ppm; total exposure measured 24,730 ppm-minutes. In the driver’s compartment, CO peaks measured in excess of 400 ppm, and total exposure concentrations were 10,600 ppm-minutes. In the crew compartment, peak exposures were detected above 400 ppm, and total exposure concentrations of approximately 8,200 ppm-minutes were measured.[22]

Total concentration exposures in the BFV exceeded the acceptable limit of 6,000 ppm-minutes established in Military Standard 800.[23] The study concluded that under firing conditions, exposures could result in Hbco levels of about 15% in 15 minutes. These exposure levels were considered a health risk that caused significant signs and symptoms of impairment of combat effectiveness.[22]

In a study of the BFV performed in 1984, real-time CO measurements were obtained using an infrared CO analyzer.[24] The study found that firing conditions in the BFV affected CO concentrations. The type of weapon fired, the position of the hatches (open or closed), the crew position, and the position of the turret with respect to the hull all affected the measured CO levels. Wind speed also affected firing conditions. Closed-hatch firing was not permitted at wind speeds above 10 mph, and open-hatch firing was not permitted at wind speeds above 5 mph. Hull fans were turned off, and gas particulate filter units were turned on during firing of both the 7.62-mm and 25-mm rounds.[24]

The 1984 study concluded that firing BFV weapons generated Hbco levels above 5%, and in three conditions, Hbco levels ranged between 11.0% and 13.4%. The maximum peak concentration, 1,462 ppm, was measured at the driver position, and levels of 1,087 ppm and 1,200 ppm were detected in the crew compartment.24,25 The M13A1 filter unit had no ability to remove CO and contributed to high levels of CO exposure within the driver’s and crew’s compartments.[24]

M109 155-mm Self-Propelled Howitzer

The M109 self-propelled howitzer is an armored and air-transportable field artillery weapons system, generally operated by a crew of four. It was designed to provide support to armored and mechanized infantry units. The system has been improved several times, including the addition of NBC protection for the crew and increased projectile range with rocket-assisted projectiles. The M109 carries conventional rounds and two oversized projectiles on board.[26] The main armament is a modified 155-mm M185 cannon assembly (the M284) and an M178 gun mount. The modified muzzle break deflects propellant gases back along the gun tube.

A 1988 Environmental Hygiene Agency health hazard assessment found that many variables affect the measured level of propellant combustion gases generated by the M109 howitzer.[26] Tube-firing elevation, wind speed, wind direction, hatch configuration, ventilator mode, propellant type and quantity, system failure, fire rate, and industrial hygiene sampling practices all influenced the results. The bore evacuator is a pressure-responsive tube evacuation system designed to promote the movement of post-fire combustion gases from the breech toward the muzzle. Compromised bore evacuator function and wind direction are critical variables associated with exposure concentrations after firing. Exposures were highest when the vehicle fired with the hatches closed. The crew compartment had a slight negative pressure, which caused combustion gases to enter the crew compartment from the breech when it was opened. A head wind significantly increased exposure to combustion gases, and reconfiguring the muzzle break did not reduce the exposure.[26]

The M109A6 Paladin weapon system was used from 1993 to 2000. Over its lifespan, the system received a new gun assembly, bore evacuator, and muzzle brake, along with improvements to the breach and recoil system. The Paladin had a range of 20 miles with a rocket-assisted projectile, and fired four rounds a minute. The Paladin’s advanced bore evacuator was much more efficient than the standard bore evacuator, which reduced CO concentrations in the crew compartment.[27]

On December 9, 1999, a CO exposure occurred at Fort Carson, Colorado, involving the crew of an M109A6 Paladin that resulted in the gunner and loader experiencing symptoms of CO poisoning. The Paladin crew took part in a routine training exercise in which the main gun was fired with hatches closed to simulate operating in an NBC environment.[27] The intake ventilation system was not used while the rounds were fired, and the exhaust ventilation system was not used afterward.[27] Following the exercise, the gunner and loader who experienced CO poisoning symptoms were air-evacuated to a hospital with a hyperbaric chamber for treatment.[27] Their Hbco blood levels were 29% and 16%, respectively, upon arrival at the hospital. Their symptoms resolved after 2 hours of hyperbaric oxygen treatment.[27]

On January 13, 2000, another CO poisoning event occurred at Fort Carson during a training exercise with an M109A6 Paladin, when three solders (section chief, gunner, and loader) experienced symptoms.[28] During the exercise, the crew was engaged in direct fire, and the rear hatch was open, the tank commander’s hatch was opened briefly after the firing of at least some of the rounds, and the driver’s hatch was closed.[28] The intake ventilation system was used during firing, but the exhaust ventilation system was not used at the end of mission.[28] The section chief had the highest Hbco level (20%). The chief and another crew member were treated in a hyperbaric chamber.[28] The other two crewmembers had much lower Hbco levels (8% each).[28]

Following the January 2000 incident, the Fort Carson 223rd Preventive Medicine Medical Detachment conducted four different tests on three different M109A6 Paladins at the National Training Center (NTC) on Fort Irwin, California, from February 11 to 21, 2000.[29] The testing did not detect high concentrations of CO, nor were Hbco levels found in the blood of Fort Carson crews. Hbco levels were well below the American Conference of Governmental Industrial Hygienists (ACGIH) biological exposure index (BEI) Hbco level of 3.5%.[29]

The 223rd did a separate test in February 2000 of nonsmoking crewmembers exposed to CO concentrations ranging from 50 to 83 ppm over 275 minutes that resulted in Hbco levels between 6.4% and 11.4%, assuming an initial Hbco level of 1%. In the same Paladin, 1 week later, average CO exposures over a 155-minute exposure interval were significantly less, ranging from 18 to 22 ppm, and predicted Hbco levels were much less than the ACGIH BEI of 3.5% Hbco.[29] Differences in exposure concentrations between the two tests may possibly be explained by any of the following: differences in the amount of rounds fired and type of powder used; weapons fire dynamics; or wind velocity and direction. It should be noted that the Hbco levels estimated above are likely to be underestimates because CO measurements did not adequately capture the large fluctuations in CO concentrations expected during weapons firing.[29]

The US Army Center for Health Promotion and Preventive Medicine (USACHPPM) was contacted to help review Fort Carson’s local board actions and opinions, confirm CO measurements, determine why CO levels were elevated, and recommend corrective actions.[30] USACHPPM provided several explanations as to why the measured Hbco levels did not mirror the signs and symptoms experienced by the crew members.[27] First, the measured Hbco levels would have been lower than the actual Hbco level at the completion of firing, given the biological half-life of Hbco and delay in obtaining blood samples for an hour to several hours after the exposure. Second, blood was drawn from the patients who had been given oxygen therapy. Altitude may have also contributed somewhat to the effects of CO poisoning, but the Paladin crews had been at the altitude for well over 4 weeks, and should have been physiologically acclimatized. So even though altitude increased the crew risk of hypoxia, it was not considered a significant explanation for the observed signs and symptoms. Also, some crewmembers were smokers, which confounded the investigation somewhat. Other noxious gases (eg, nitric oxide) were ruled out as a significant confounder by USACHPPM toxic gas testing; measured nitric oxide concentrations were low.

Testing was done on March 10, 2000, to re-create the situation. Crewmembers wore supplied-air respirators. Paramedics were present outside the Paladin during the tests.[27] One Paladin was tested in two configurations: (1) with the rear and side hatch open and (2) with the side hatch closed and the rear hatch open. In both instances, the tank commander’s and driver’s hatches were closed. The NBC scenario with all hatches closed was not re-created, but measured CO concentrations would likely have been much higher than the concentrations found during the tests with open hatches.

When the January 2000 scenario was re-created (rear hatch open, side hatch closed, tank commander’s hatch closed, driver’s hatch closed), CO concentrations were found to be substantially elevated inside the crew compartment.[27] The CO dosimeters worn by the crew did not record the actual concentrations because they did not read above 1,000 ppm, which was exceeded for about 10 minutes. The average concentrations recorded by the dosimeters for the crewmembers were about 500 ppm for 30 minutes, with 15-minute average concentrations as high as 851 ppm. The 15-minute average concentrations are more representative of the concentrations while firing rounds than the average concentration, which includes lead time and exhaust period at mission end.[27]

The CO concentrations measured during the test in the crew compartment underestimate the actual concentrations. Concentrations may have been as much as double the measured concentrations. Given this uncertainty and the varying CO concentrations measured at different positions in the crew compartment, Hbco levels of about 15% to 30% were predicted over the 30-minute interval for crewmembers.

After the first test, an investigation revealed that the rear bore evacuator seal/O-ring was missing, which reduced the efficiency of the bore evacuator and contributed to the increase in CO inside the crew compartment. Once discovered, the missing bore evacuator seal/O-ring was replaced.[27] This was felt to be the main reason for the elevated CO levels inside the crew compartment, though headwinds and the intake ventilation may have also contributed to the problem.

Testing was repeated once the missing rear bore evacuator seal/O-ring was replaced.[27] This time, the average CO concentrations inside the crew compartment ranged from 4 ppm to 10 ppm, which is well below the level of a health hazard. The highest 15-minute average concentrations ranged from 5 ppm to 12 ppm, which was thought to be more representative of the concentrations seen when rounds were fired. Predicted Hbco levels during the 27 minutes were well below the ACGIH BEI of 3.5%.

USACHPPM made a number of recommendations to avoid repeated CO exposures with Paladins, including the following[27]:

1. Take any Paladins missing the bore evacuator seals/O-rings required by manufacturer out of service, and require each vehicle to carry spare seal/O-ring sets.

2. Ensure preventive maintenance is performed on all Paladins, including a bore evacuator system check.

3. Avoid firing in the presence of headwinds that increase CO exposures in crew compartments.

4. Ensure that the intake ventilation is on during round firing and for 2 minutes after firing; after that the exhaust ventilation should be on for 10 minutes.

5. Request USACHPPM support through Forces Command to study soldier occupational exposures.

6. Have the Paladin program manager examine whether there is sufficient intake ventilation make-up air for the bore evacuator to work efficiently with hatches closed.

7. Consult with Army NBC safety and preventive medicine personnel about whether the ventilation intake should be turned on during firing in an NBC environment (or when training for such an environment), when all hatches are closed.

8. Because CO is readily introduced through the ventilation intake and climate conditioning system intake, consider moving these systems to the rear of the vehicle.

9. Install a CO monitor with an audible and visual alarm in every Paladin that activates at concentrations equivalent to an Hbco level of less than or equal to 10%.

Although 10% Hbco was adopted as an operational limit by the Army,[31] values less than 15% Hbco do not affect performance but may cause a mild headache.[32] Values exceeding 25% Hbco are considered dangerous and require aggressive treatment in addition to removal from exposure.[32]

Military Aviation

Unsafe levels of CO were generated in military aircraft by early piston-driven engines, which caused the deaths of many pilots. Later, CO exposures from engines were eliminated, but high levels of toxic gases were generated when weapons systems were fired aboard aircraft. In 1988, CO levels were tested when an M134 mini-gun mounted in the UH-60A Black Hawk helicopter was fired. In the tests, 2,700 rounds were fired, and the average CO concentration was 79.4 ppm during the 4 minutes of firing. The maximum predicted Hbco level was 4.90%, so firing restrictions were not recommended.

More recently, CO poisonings have been reported in the fixed-wing fighter community in the US Air Force and Navy. F-22 Raptors were grounded in 2011 for several months due to suspected CO poisoning at Elmendorf Air Force Base, Alaska, when planes were started inside hangars.[33] Air Force investigators thought exhaust gases containing CO accumulated inside the hangar and were subsequently taken back up into the engines and entered the On-Board Oxygen Generation System (OBOGS). The Navy has reported similar problems with the F/A-18 Hornet OBOGS,[34] which prompted flight surgeons to look for evidence of hypoxia in pilots in planes equipped with the system.

Other Recent Exposure Incidents

Fort Hood, Texas

In early November 1997, two active duty soldiers, a married couple, woke up at 0200 in their off-base apartment and felt nauseated and dizzy.[35] They felt better when they went outside, but decided to go to the local emergency room for evaluation. The soldiers did not smoke, and their Hbco levels were 31.6% and 28.3%, respectively for the husband and wife. They were diagnosed with CO poisoning, given 100% oxygen with a non-rebreather mask, and sent for hyperbaric oxygen therapy (HBOT). Their residence did not have a CO detector, and the furnace that was turned on the night before had malfunctioned, causing high levels of CO.

Fort Campbell, Kentucky

In November 1997, the wife of a soldier woke up with a headache, fatigue, and difficulty standing.[35] She went to the emergency room and was tested for CO poisoning. She was a nonsmoker and her Hbco level was 33%. She was treated with 100% oxygen and sent home. She lived off-post in a trailer equipped with a CO detector, which had gone off the day before the incident. The trailer owner told her the CO detector was installed too close to the furnace, so she moved it. The alarm continued to go off but she ignored it the day of the incident. The day after the incident, an inspector checked the furnace and discovered it had a clogged flue.[35]

Olsbrucken, Germany

On November 7, 2000, two children of an Air Force retiree living in Germany awoke at 0330 disoriented and vomiting, with diarrhea and abdominal cramps.[36] Both the father and mother were also affected, with sudden onset of headache, vomiting, and nausea. The German ambulance put the family on oxygen and took them to the Landstuhl Regional Medical Center emergency department. All family members improved after leaving the house. Their history and clinical presentations and improvement after leaving the house were highly suggestive of CO poisoning.

The emergency room staff found that the concentration of Hbco in the family’s blood ranged from 19.6% to 26.5%. The family members were all placed on 100% oxygen and observed in the emergency department for several hours, and the emergency room physician reported the CO poisoning to the US Army Public Health Center–Europe.[36] After laboratory results confirmed CO poisoning, industrial hygienists interviewed the family and surveyed their home, finding CO concentrations of 200 ppm at the house’s entrance. Based on the reading, the industrial hygienists alerted the German fire department, who sent personnel equipped with a self-contained breathing apparatus to survey the inside of the house. They found the CO concentration in the boiler room was over 500 ppm.[36] It was later determined that ash in the chimney caused the buildup of CO and prevented proper ventilation of the heating system.

Fort Irwin National Training Center, California

On January 12, 2001, two soldiers died at Fort Irwin NTC from CO poisoning and anoxia after purchasing a Coleman Powermate 15,000-BTU unvented propane gas heater to warm up their tent.[37] Testing confirmed that the tent was airtight,[37] that oxygen had been depleted by the soldiers’ breathing, and that CO had accumulated from the unvented heater in the tent.[37] Because of these deaths, safety bulletins, alerts, and guidelines have been issued to prevent a recurrence.38–43

Poisoning Events, 1998–2008

The Armed Forces Health Surveillance Center recorded 227 CO poisonings over a 10-year period from July 1998 to June 2008, which averaged 23 poisonings per year. These numbers reflect a decrease from 1,000 CO poisoning in the previous 10-year reporting period in the US military.[44] However, the more recent case definition limited cases to those involving hospitalizations or lost duty time, while prior reporting included cases that were not clinically significant. Among the 227 reported cases, 53% required hospitalization, and 9 cases (4%) were fatal.[9] CO poisonings peaked during winter months. Most cases were in the 20 to 29 age group (66%); 56% involved US Army personnel; and two installations, Fort Hood, Texas, and Fort Lewis, Washington, each accounted for 10% of the identified cases.[9]

PATHOPHYSIOLOGY

In the body, CO is produced by heme destruction and excreted by exhalation.[10] CO impairs the oxygen-carrying capacity of hemoglobin in two ways. First, CO competitively binds to hemoglobin with an affinity 200 to 250 times greater than that of oxygen. CO also causes changes in the conformation of the hemoglobin molecule, which shifts the hemoglobin dissociation curve to the left and decreases the amount of oxygen released.[15] In addition, CO interferes with cellular respiration by binding to cytochrome oxidase, which causes neurological and myocardial injury.[44]

Until recently, the primary mechanism of CO toxicity was thought to be the formation of Hbco and subsequent tissue hypoxia. However, the results of recent scientific studies have challenged this principle.15,45 The clinical presentation of a patient with CO poisoning does not always correlate with blood Hbco level, nor does clinical improvement correlate with the clearance of Hbco.2,15,45 Clinical CO toxicity is now thought to result from a combination of hypoxia and inflammatory mechanisms. These mechanisms include the CO’s binding to intracellular proteins such as myoglobin and cytochrome a, lipid peroxidation affecting myelin proteins and apoptosis in neurons, increased nitrous oxide production and oxidative stress within the vasculature, and increased amino acid levels.45,46

The local and systemic inflammation combined with anoxia leads to neurologic and cardiac injury. Recent studies suggest that myocardial injury following moderate to severe CO poisoning increases mortality. In a prospective study of 230 CO poisoning cases, 37% had acute myocardial injury, and an additional 38% died within 7.6 years of follow-up. Among the relatively young, healthy cohort, the observed death rate was 300% higher than the expected death rate.[43] Studies of CO poisoning cases note that a third of patients have persistent headaches and memory problems for 4 weeks following the exposure, and half had neuropsychological symptoms up to 6 weeks later.[45]

CLINICAL PRESENTATION

The signs and symptoms of CO poisoning were described in 1923.[47] Table 24-1 describes acute health effects in healthy adults, based on information in Patty’s Toxicology[4] and other sources.5,17,18,48,49 CO targets metabolically active tissue that has a good supply of oxygen-rich blood.18,50–53

Signs and Symptoms

Headache, dizziness, and nausea are the most common symptoms. If CO poisoning continues and Hbco levels rise, additional symptoms may include fatigue, dyspnea, chest and abdominal pain, impaired judgment and memory, visual disturbances, drowsiness, and agitation. Common clinical signs include vomiting, ataxia, confusion, syncope, coma, seizures, tachypnea, and cardiac dysrhythmias. The symptoms and degree of impairment with CO exposure are worse with higher concentrations and prolonged exposure. The symptoms of CO exposure are exacerbated by muscular activity that increases oxygen demand, while individuals at rest may experience no symptoms before becoming unconscious.[46]

Providers must have a suspicion about CO poisoning because the symptoms are nonspecific, and CO poisoning is commonly confused with other conditions such as influenza or gastroenteritis.2,54 The classic sign of “cherry-red” skin or lip color is actually uncommon, and it is a late finding in lethal or near-lethal CO poisoning cases.2,13,15

The medical history for CO poisoning cases usually involves an exposure from gas-burning appliances, fireplaces, or gasoline engines being operated in poorly ventilated areas. People who have survived a fire and those who work in enclosed spaces may have elevated Hbco levels. Also, mechanics and others who work with paint strippers and solvent degreasers containing methylene chloride may have delayed onset of symptoms because the methylene chloride is metabolized to CO and can cause a rise in Hbco levels.16,54

Severe toxicity occurs through metabolic acidosis due to lactate formation from hypoxia, as well as renal failure due to rhabdomyolysis. Bullae may form from direct toxic effects of CO or from pressure necrosis. CO poisoning affects the basal ganglia in the brain and causes tremor, slowed reaction time, decreased manual dexterity, poor eye-hand coordination, and inability to process complex movements.[50] The ocular signs of CO poisoning occur early and persist for some time; they include retinal vessel congestion and optic disc hyperemia. In 1921 Wilmer noted that amblyopia and complete blindness are common sequelae of CO poisoning.[55]

In combat, soldiers who experienced CO poisoning during World War I had anoxia and first experienced extremity weakness, followed by giddiness, confusion, breathlessness, and palpitations as the CO concentrations increased. At higher CO concentrations, mental confusion caused soldiers to appear drunk. Mental confusion and extremity weakness reduced both the desire and ability to escape, and consequently many individuals went into a coma and died.[3]

In contrast to acute CO poisoning cases at high CO concentrations, individuals with mild cases of CO poisoning develop symptoms more slowly and experience nonspecific clinical signs of headache and nausea, which is often confused with mountain sickness.[3] Mechanics, heavy equipment drivers, armored vehicle crews, and aviators who are chronically exposed to low levels of CO have not developed health problems, but providers must remain vigilant.[54]

Central Nervous System Effects

Individuals with CO poisoning exhibit signs and symptoms of hypoxia, but these symptoms can be caused by any neurological condition. People with acute CO intoxication have been reported to have signs of multiple sclerosis, parkinsonism, bipolar disorder, schizophrenia, and conversion disorder.[50] The neurologic sequelae of CO poisoning, which can occur immediately or be delayed, include headache, myalgia, weakness, memory loss, paralysis, cortical blindness, and peripheral neuropathy and convulsions.56,57 These signs usually resolve within days, but can persist for months to years.[47] Permanent memory loss and personality changes occur in between 0.3% and 10% of CO poisoning cases.[58]

TABLE 24-1

ACUTE HEALTH EFFECTS OF CARBON MONOXIDE EXPOSURE*

Blood Saturation Hbco (%)

Range Notes

Response of Healthy Adults

Response of Patients with Severe Coronary Artery Disease

0.4–0.7, increasing up to 2.6 during pregnancy

Normal range due to endogenous CO production

No known detrimental effect

No known detrimental effect

1–2

Background levels in urban population due to combination of endogenous CO and environmental exposure

No known detrimental effect

No known detrimental effect

2–5

Range found in commuters on urban highways

Possible slight decrements in psychomotor function (eg, reduced video game performance)

Less exertion required to induce chest pain

5–10

Range found in cigarette smokers

- Compensatory increase in CNS and coronary blood flow

- Slight decrease in capacity for strenuous exercise

- Prolonged levels may affect the performance of tasks requiring a high degree of vigilance (eg, flying an aircraft or monitoring a control panel)

Greater frequency and complexity of ventricular ectopic beats during exercise

10–20

Note: triservice laboratory diagnosis for CO poisoning: >10% in nonsmokers, >15% in smokers†

Range found in cigar smokers

Slight headache, fatigue, lightheadedness

Exertion may precipitate myocardial infarction

20–30

Moderate headache, nausea, fine manual dexterity impaired, visual evoked response abnormal, flushing and tachycardia

No difference

30–40

Severe headache, nausea and vomiting, hypotension and ataxia

No difference

40–50

Syncope

No difference

50–65

Coma and convulsions

No difference

>65–70

Lethal if not treated

No difference

*Exposure to CO at high concentrations (>50,000 ppm or 5% CO) can result in a fatal cardiac arrhythmia and death before the Hbco is significantly elevated.

† Defense Health Agency. Revised Armed Forces Reportable Medical Events Guidelines and Case Definitions. Washington, DC: DHA: June 30; 2017. Memorandum. https://health.mil/Policies/2017/07/17/Revised-Armed-Forces-Reportable-Medical-Events-Guidelines-and-Case-Definitions. Accessed September 12, 2017.

CO: carbon monoxide

CNS: central nervous system

Hbco: carboxyhemoglobin

Data sources: (1) Apfelbach G. Carbon monoxide poisoning. In: Kober G, Hayhurst E, eds. Industrial Health. Philadelphia, PA: P. Blakiston’s Son & Co; 1924. (2) Goldstein M. Carbon monoxide poisoning. J Emerg Nurs. 2007;34(6):538-542. (3) American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. Cincinnati, OH: ACGIH; 2001. (4) National Research Council, Committee on Toxicology. Emergency and Continuous Exposure Guidance Levels for Selected Airborne Contaminants. Vol 4. Washington, DC: National Academy Press; 2007. (5) American Industrial Hygiene Association. Carbon Monoxide Documentation for Emergency Response Planning Guidelines. Fairfax, VA: AIHA; 1999.

Acute CO poisoning can cause neurobehavioral effects including compromised dark adaptation and impaired visual tracking, which can reduce performance in aircraft handling and target acquisition. Military-specific Hbco limits and equipment-design specifications[31] were developed because visual acuity becomes impaired at Hbco levels between 3% and 5%.[52]

Cardiovascular Effects

The heart is highly sensitive to CO poisoning because it depends almost exclusively on aerobic metabolism. Normally the heart consumes pyruvate and lactate in metabolic oxidation, but this does not occur when Hbco levels rise above 8.7%.[48] Individuals with cardiopulmonary conditions including coronary artery disease, anemia, and lung disease are more likely to have problems with CO-induced tissue hypoxia.[50] At low Hbco levels, people with ischemia have experienced angina. Recent studies suggest that young, otherwise healthy individuals who experience moderate to severe CO poisoning develop myocardial injury and are at increased risk of mortality over time.44,59

The crews of armored vehicles are routinely exposed to CO levels that induce ischemic responses in animals and humans.60,61 It is possible that soldiers with early cardiovascular disease could suffer an adverse myocardial event when the vehicle operates and generates high concentrations of CO. A study conducted by the US Army Biomedical Research and Development Laboratory showed that individuals with 10% to 20% Hbco levels who performed work at 35% of the maximal work rate demonstrated only minimal increases in heart rate after working a period of 3.5 hours; however, individuals with Hbco levels of 40% to 45% had physical work capacity that was dramatically compromised.[18] CO poisoning decreases maximum work capacity (as defined by Vo_2 max) when Hbco levels rise above 5%, and both fatigue and angina develop sooner with CO exposure.[53]

Chronic Effects

Most patients recover completely after being removed from CO exposure, but some patients develop central nervous system (CNS) or cardiovascular sequelae days to weeks after poisoning.50,57 Prior to 2001, the prognosis for recovery was thought to be related to the degree of asphyxia, and men exposed to CO in mines were thought to develop a permanent weakness of the heart.[4] Vision loss, speech problems, and CNS defects were also reported. However, recent reports show that only long-term mortality due to myocardial injury is correlated with Hbco levels.45,51

Magnetic resonance imaging studies taken several days following the event (but not earlier) show low-density lesions in the area of the globus pallidus that are associated with CO-induced encephalopathy, which occurs in 50% of severe CO poisoning cases.[57] Lesions in the basal ganglia gray matter may resolve, but lesions in the white matter that are associated with neuropathy are usually permanent.[50]

CO-induced neuropsychiatric illness may occur up to 6 weeks after the event in between 2% and 30% of CO poisoning cases.[62] Delayed sequelae occur in both young and old, but elderly patients are more at risk. Clinical signs of delayed sequelae may include urinary or fecal incontinence, weakness, gait disturbances, tremor, mutism, speech abnormalities, and mental deterioration. Complete recovery occurs in about 75% of individuals within a year.[62]

Autopsy Findings

Anatomic autopsy findings are helpful in determining cause of death. The skin color of a CO-poisoned person differs from the skin color of other deceased individuals.[48] The face may be bright red and there may be rose-red spots on the face, neck, breast, and limbs. The color of the skin between the red areas is likely to be discolored and may be cyanotic. Blood ranges in color from bright red to black. Ecchymoses, effusions, or hemorrhages may occur even with no change in blood coagulation. The respiratory tract is generally unchanged, although mucus or digestive contents have been found in the upper respiratory tract. The brain swells and the intraventricular fluids become blood tinged. Hemorrhagic lesions ranging in size from microscopic to “apple sized” have been seen.[47] Other common pathologic findings of CO poisoning include bronchopneumonia, blood vessel deterioration, necrosis in the lenticular nucleus, thrombosis, and encephalitis.[4]

DIAGNOSIS

The differential diagnosis for CO poisoning includes influenza, gastroenteritis, food poisoning, cerebrovascular events, myocardial infarction, asphyxia, delayed parkinsonism, ethanol intoxication, sedative-hypnotic overdose, hypothermia, and myxedema coma.13,16,54 Headache and dizziness are common symptoms of many of the conditions in the differential diagnosis, which increases the likelihood of misdiagnosis, especially with winter visits to the emergency department.[46] Mental status changes and ataxia associated with ethanol intoxication or medication overdose may confuse the provider’s neurological assessment. Other gas exposures may cause the altered mental status often seen with CO poisoning. Physical asphyxiants (eg, natural gas, carbon dioxide, acetylene, helium) may lead to temporary unconsciousness. Irritant gases (eg, formaldehyde, hydrogen chloride, nitrogen dioxide) are more likely to be associated with coughing and bronchospasm due to pulmonary and mucous membrane irritation. Cellular asphyxiants that bind cytochrome oxidase (eg, hydrogen cyanide, hydrogen sulfide) cause more abrupt loss of consciousness than does CO.[54] The clinician should consider coexisting cyanide toxicity if the patient suffered from smoke inhalation.[2]

Because the signs and symptoms of CO poisoning are variable depending on the severity and duration of exposure, headaches, dizziness, nausea and vomiting, blurred vision, impaired cognition, and seizures can all occur to some degree and severity.[63] Physicians must be alert to the possibility of CO poisoning when a patient presents with this constellation of signs and symptoms. The diagnosis can only be made when the Hbco test confirms toxicity due to CO poisoning.

When ordering confirmatory laboratory tests, other causes of mental status changes should be considered (eg, hypoglycemia, hypoxemia, metabolic changes, systemic infection, drug/alcohol intoxication, toxins, adverse drug reactions). The laboratory tests should include complete blood count, metabolic profile, urinalysis, urine drug screen, and serum ethanol. Creatine kinase may be useful for detecting rhabdomyolysis. In suspected CO poisoning cases, the patient’s blood should be sampled and analyzed to determine Hbco levels.4,13,16 The diagnosis of CO poisoning is confirmed when the Hbco level is greater than 3.5% in nonsmokers, or greater than 10% in smokers.2,15 (However, as previously stated, Hbco level does not predict long-term outcomes well, nor is it a good measure for monitoring clinical progress.)

Hampson et al[15] proposed three criteria for diagnosing CO poisoning: (1) history of exposure to CO, (2) elevation in blood Hbco, and (3) signs or symptoms of CO toxicity. Clinicians should consider initiating treatment with oxygen therapy if they suspect CO poisoning until the Hbco test results are made available.

It is important to note that pulse oximetry is a poor test to use when CO poisoning is suspected because the standard pulse oximeter uses two wavelengths (660 and 990 nm) and cannot discern between oxyhemoglobin and Hbco.[15]

The DoD no longer requires providers to report CO poisoning since it has been removed from the list of reportable medical events.[64] However, many local jurisdictions still consider CO poisoning a reportable event, and healthcare providers are still encouraged to report any patient diagnosed with CO poisoning to their local preventive medicine service or public health detachments. Case definitions for a CO poisoning event vary by state, so clinicians are encouraged to report any suspected case.

TREATMENT

Any patient suspected of CO poisoning must first be removed from the contaminated environment to prevent further poisoning. The basic “CABD” (circulation, airway, breathing, disability) approach should be followed in CO poisoning cases. Once the patient is safely removed from the exposure, the following interventions should be considered:

- Place an advanced airway if mental status or upper airway is compromised.

- Mechanically ventilate if the gas exchange is poor during respiration.

- Obtain intravenous access to infuse resuscitative fluids and vasoactive drugs if necessary.

The patient should get 100% supplemental oxygen as soon as possible. If the patient is not intubated, a tight-fitting facemask will be required to deliver the oxygen. Oxygen should be continued for 6 to 12 hours to permit shifting the oxygen hemoglobin saturation curve to the right and displacing the CO.[46]

Electrocardiogram and cardiac monitoring should be used to evaluate for cardiac ischemia. Patients with Hbco levels greater than 25% often get ST-segment depression, which is one of the criteria for instituting HBOT.[48] The goal of treatment is to increase the partial pressure of oxygen in the lungs to displace CO from the Hbco. While delivering 100% oxygen at 1 atmosphere absolute (ata) is effective, the displacement can be accelerated by using hyperbaric oxygen. The half-life of Hbco is 4 to 6 hours at room air, 1 hour at 100% oxygen, and 20 minutes with hyperbaric oxygen at 3 ata.[46]

Hyperbaric oxygen may help reduce cerebral and myocardial hypoxia and cerebral edema, and also may enhance CO elimination sooner than other treatment options.[56] HBOT supports metabolic oxygen requirements by rapidly providing dissolved plasma oxygen and enhancing Hbco dissociation and CO clearance.48,50 HBOT is thought to benefit patients with cerebral edema by reducing secondary intracranial pressure by 50% within 1 minute of its administration.[48]

EXHIBIT 24-1

CONSULTATION AND ASSISTANCE WITH LOCATING HYPERBARIC OXYGEN TREATMENT FACILITIES

Unit Name

Availability

Phone Contact

*Navy Experimental Diving Unit, Panama City, Fl

Normal hours (0730–1600)
After 1600

850-230-3100
850-234-4351

*Navy Dive School, Panama City, FL

Normal hours (0730–1600)

850-234-4651

*Army Hyperbaric Medicine Service, Eisenhower Army Community Hospital, Augusta, GA

Normal hours (0730–1600)
After 1600

706-787-3110
706-787-9284

US Divers Alert Network (offers emergency phone consult)

Available 24 hours a day

919-684-9111

___________________

*Hyperbaric chamber on site

Despite this relatively simple concept of decreasing the elimination time for Hbco, as well as its physiologic benefits, HBOT remains controversial in practice. Controlled trials of HBOT in CO poisonings have not consistently found benefit. Consequently, HBOT remains controversial both in terms of indications for use and in treatment protocols. According to expert opinion, HBOT should be attempted for individuals with no other risk factors if Hbco levels are over 25%.[2] In patients with Hbco levels over 15% and under 25%, HBOT is generally indicated when the patient has altered mental status or loss of consciousness, abnormal neurologic findings, seizures, hypotension, cardiac ischemia, or pregnancy. Other indications may include persistent metabolic acidosis, concurrent burns, or pregnancy with any history of CO exposure.11,15 No superior hyperbaric treatment protocol has been identified. An initial treatment at 2.5 to 3.0 ata is recommended; more treatment sessions can be added if symptoms persist.[46] Hyperbaric oxygen facilities range in size from large walk-in chambers to much smaller chambers that can only accommodate one person.

The fetus is more susceptible to CO poisoning than the mother. The fetal oxyhemoglobin dissociation curve is to the left of the adult dissociation curve. CO reacts to form fetal Hbco, which accentuates the left shift. While the Hbco levels in the fetus lag behind those in the mother, the final fetal Hbco level may be 10% to 15% higher than the maternal level.[14] Most importantly, the half-life of fetal Hbco is 15 hours, so it takes substantially (5 times) longer to regenerate oxyhemoglobin in the fetus than in the mother.[50] Exhibit 24-1 contains information on locating HBOT centers in the United States.

HEALTH STANDARDS AND GUIDELINES

Developing consistent exposure standards has been problematic because it is difficult to determine the exposure levels at which CO causes health effects; a large number of variables affect exposure levels, many of which fluxuate widely. Therefore, the guidelines below should not be substituted for sound clinical judgment in determining what constitutes a safe or dangerous exposure.

When deciding which standard or guideline to apply, the following factors must be considered:

- whether a healthy or susceptible population is exposed;

- whether exposures are to the general public or to a smaller subset of the population;

- whether or not operations are military-specific;

- whether exposures are occupational or residential; and

- whether exposures are chronic and relatively low-level or acute and high-level.

Tools are provided below to help investigators estimate Hbco and CO concentrations at the time and place of exposure.

On occasion, signs and symptoms may not correspond with what is expected based upon the measured Hbco in blood or CO concentrations measured or predicted at the incident site. The presence of confounders may provide a partial explanation for the observed signs and symptoms that may not be satisfactorily explained by Hbco levels.

Military Occupational Exposures

The Army has established CO standards for military-unique workplaces, operations,[31] equipment, and systems.[65] These include combat and operations, as well as testing and maintenance of military weapons, aircraft, ships, submarines, missiles, early warning systems, military space systems, ordnance, and tactical vehicles. Also included are peacekeeping missions; field maneuvers; combat training; naval operations; flight and missile operations; military research, development, test, and evaluation activities; and national defense contingency conditions.

Work performed in some DoD workplaces and operations is similar to work performed in private sector businesses. These operations are not considered militarily-unique operations and can include work performed in weapon, vessel, aircraft, or vehicle maintenance; construction; supply; engineering; public works; medical services; and administrative office work.[65]

Military-Unique Standards

Where occupational exposures occur in military-unique settings, the CO concentration has to be reduced to the lowest level feasible,[31] and less than the OSHA permissible exposure limit (PEL) where practicable.[65] The Army, Navy, and NASA apply a CO exposure standard for military-unique workplaces and operations.[31] The ACGIH threshold limit value (TLV) may also be applied in military-unique situations.[65]

The Department of Defense design standard for human engineering (MIL-STD-1472G) requires that “Personnel shall not be exposed to concentrations of CO that will result in COHb [Hbco] levels in their blood greater than 5.0 percent for all system design objectives and aviation system performance limits and 10 percent for all other system performance limits.”[31] The DoD handbook for human engineering design (MIL-HDBK-759C), paragraph 5.13.7.4.5, specifies use of the following empirical formula to predict Hbco blood content as a result of exposure to CO, and is based upon the Coburn, Foster, and Kane equation (CFKE)66,67:

Hbcot = %(Hbco_0 (e(-t/A)) + 218(1-e(-t/A)) • (1/B + ppm CO/1,403)

In this formula, Hbcot is the predicted Hbco in the exposed individual; Hbco_0 is the amount of Hbco usually found in nonsmoking adults; t is the exposure duration in minutes; and ppm CO is the CO concentration in ppm in the contaminated environment. The value of e, a numerical constant, is equal to 2.71828, and variables A and B are constants that depend on the physical activity level of the individual during the exposure, obtained from Table 24-2.

TABLE 24-2

WORK-EFFORT CONSTANTS FOR PREDICTING CARBOXYHEMOGLOBIN BLOOD CONTENT

Work-Effort Scale

Work-Effort Description

Alveolar Ventilation Rate (L/min)

A Value*

B Value*

1

Sedentary

6

425

806

2

Light work
(eg, cooking, truck driving)

12

241

1,421

3†

Moderate work
(eg, light walking, cycling)

18

175

1,958

4†

Heavy work
(eg, loading, shoveling)

24

134

2,553

5

Very heavy work
(eg, jogging, hill climbing)

30

109

3,144

*A and B values for each work-effort level is described in paragraph 5.13.7.4.5 of US Department of Defense. Handbook for Human Engineering Design Guidelines. Washington, DC: DoD; 1995: 302–303. MIL-HDBK-759C: 302-–03.

† A work-effort level of 4 should be chosen for periods of weapons fire, and a work-effort level of 3 should be chosen for periods of pause, when no weapons are fired.

Data sources: (1) Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. Coburn equation calculator. https://www.cdc.gov/niosh/topics/co-comp/default.html. Accessed August 28, 2017. (2) US Department of Defense. Design Criteria Standard (Human Engineering). Washington, DC: DoD; 2012. MIL-STD-1472G. (3) Smith SR, Steinberg S, Gaydos JC. Errors in derivations of the Coburn-Forster-Kane equation for predicting carboxyhemoglobin. Am Ind Hyg Assoc J. 1996;57(7):621–625.

This equation allows the calculation of a predicted %Hbcot from a CO exposure (in ppm CO) over a time interval and with respect to a particular work-effort level, and is very useful in situations where CO concentrations are episodic and fluctuate significantly over time, such as during the firing of a main tank gun or machine gun. During firing, the levels often rise steeply; during pauses in firing, levels fall. Because of the dynamic nature of such exposures, the use of this equation is a more accurate means of assessing exposure risk than by measuring and averaging CO exposures over an 8-hour time-weighted average (TWA) and comparing the result to an 8-hour PEL for CO. The equation accounts for the minute respiratory volume of contaminated atmosphere actually inhaled by an exposed individual based on the level of physical activity (either estimated or specified). The equation also accounts for the elimination of CO by the body. The equation is applicable to short-duration high-level exposures as well as low-level exposures of long duration.66,67

A value of 1% Hbco_0 must be chosen as the initial value before exposure begins.[67] The %Hbcot predicted for one time interval becomes the %Hbco_0 for the next time interval, and the process is repeated to predict %Hbco with time.[67] This model can be programmed into a National Institute of Occupational Safety and Health (NIOSH) computer model[68] and Microsoft Excel (see the attachment at the end of the chapter for an example).

Some studies show that nonsmoking, healthy personnel do not experience any significant effects of CO exposures with Hbco levels less than 5%.17,66 However, other studies suggest that visual acuity may degrade at or below Hbco levels of 15%.[69] Because of the uncertainties evident in the research and the critical nature of crew tasks involving visual perception (night flight operations), the DoD limited CO exposures in aviation systems to keep Hbco levels below 5%. The system design objectives for CO exposures in all other systems was set to keep Hbco levels below 10% (paragraph 5.7.9.4.2 of MIL-STD-1472G).[31]

Other available computer models predict %Hbco. Tikuisis developed a computer program for the Canadian Department of National Defense in 1996 that allows the user to predict %Hbco over time based upon work-effort level (1–5), exposure concentration, and exposure duration.[32] Compared to the model described in MIL-HDBK-759C, the Tikuisis model is more flexible in allowing the user to select more variables that could affect the %Hbco level in a particular individual. For instance, the Tikuisis model allows entry of barometric pressure, and demographic variables (eg, height and weight, nonsmoker, light smoker, and heavy smoker).[32]

The Navy has set a separate standard for submarine environments. At the Navy’s request, the National Research Council’s Committee on Toxicology (NRC COT) developed and recommended a continuous exposure guideline level (CEGL) for CO. A CEGL is recommended for specific situations in which exposure to a chemical may occur continuously for up to 90 days.[18] It is defined as a ceiling limit designed to prevent adverse health effects, either immediate or delayed, and to avoid degradation in crew performance that might endanger the objectives of a particular mission. The 90-day CEGL for CO is 20 ppm and should not result in blood Hbco above 3.3%.[18] The CEGL is intended to be applied to a young, healthy military population; it is not intended to be applied to other occupational groups or the general public.[18]

Nonmilitary-Unique Standards

Where exposures are occupational in nature and where the workplace or operation is not considered military-unique, the Army applies either the ACGIH TLV or the OSHA PEL, whichever is more stringent.[70] Currently, the 8-hour ACGIH TLV-TWA of 25 ppm is more stringent than the OSHA 8-hour PEL-TWA, which is 50 ppm.71,72 However, in maritime operations, workers must be removed from exposure if the CO concentration exceeds 100 ppm for any duration, even if the 8-hour TWA of 50 ppm has not been exceeded.

Permissible exposure limits. The OSHA 8-hour PEL-TWA for CO of 50 ppm produces an Hbco level of 8% to 10% in most workers. Generally workers free of cardiovascular conditions do not exhibit signs or symptoms of health impairment when exposed at this level in nonstressful conditions.[73] The 8-hour PEL-TWA for CO in maritime operations is set at 50 ppm; workers must be removed from exposure if the CO concentration exceeds 100 ppm.[73] This exposure level corresponds to a predicted Hbco level of 1.4% based on the predictive equation in MIL-HDBK-759C, assuming moderate work effort (level 3), an exposure duration of 5 minutes, an initial Hbco level of 1%, and no other CO exposures. A 200-ppm peak CO level was set for employees engaged in roll-on, roll-off operations during cargo loading and unloading. This concentration results in an Hbco level of 1.8% using the equation in MIL-HDBK-759C, with the same assumptions as noted above.

Threshold limit values. The ACGIH set the 8-hour TLV-TWA for CO at 25 ppm.14,72 This was done to maintain blood Hbco levels below 3.5% in order to minimize adverse neurobehavioral and cardiovascular effects and maintain work capacity.14,72 The ACGIH adopted this CO level to maintain a margin of safety for susceptible individuals, including pregnant workers and their fetuses and those with cardiopulmonary conditions.14,72 The ACGIH recommends that CO exposures be kept below 5 times the TLV-TWA, or 125 ppm, at all times, and kept at 75 ppm for no more than 30 minutes a day.14,72

Nonetheless, it must be understood that some exposures less than the 25-ppm TLV-TWA may result in Hbco levels that exceed 3.5%. Variation in exposures during the day may produce higher Hbco levels. For example, a 60-minute exposure to 200 ppm would result in an 8-hour TWA of 25 ppm, but the Hbco level could be as high as 10%. It is likely that the Hbco level would be less than 1% to 2% at the end of the shift in the absence of CO exposure for the remainder of the 8-hour shift.

CO is eliminated through the lungs.[14] The NIOSH established a BEI for CO of 3.5% Hbco and a CO level of 20 ppm in end-exhaled breath at the end of the work shift.[14] This exhaled breath concentration corresponds to a Hbco level of 3.5%.[14] The BEI is not applicable to tobacco smokers or people who drive on congested roadways,[14] nor is it applicable in emergency situations, during the first 3 hours of the shift, later than 15 minutes after the end of the work shift, or when there are large fluctuations in exposure concentrations.[14] It should be noted that when analyzing end-exhaled breath, false positives can occur in workers with lactose intolerance, those with intestinal malabsorption,[5] and anyone who has been drinking alcohol.[54]

Army Housing and Tents

Family Housing

To avoid CO poisoning in housing, occupants should follow the guidelines developed by the Consumer Product Safety Commission and the CDC, which describe the sources of CO in the home and what steps are needed to prevent CO poisoning. These steps include regular inspection and routine maintenances of fuel-burning appliances and use of CO detectors or alarms.[74]

CO alarms are highly recommended by the CDC. The US Army Corps of Engineers is required to install CO alarms in new and renovated family housing units with fuel-burning appliances, fireplaces, or an attached garage.[75] Generally, one CO alarm should be located on each level of the housing unit in or near the bedroom. The alarms should be hardwired and wall-mounted 50 inches off the floor. They should also be audible and have a continuous digital display, peak level memory, test button, and test reset button and be approved by Underwriters Laboratory (UL) as meeting UL standard 2034. Housing unit occupants can check the UL website to ensure their CO alarm is a UL-certified product.

CO detectors and alarms are important as a secondary defense; their use does not preclude the responsibility for proper use, regular inspection, or preventive maintenance of fuel-burning appliances. The intent of using such devices is to warn occupants of CO concentrations well before they have reached levels that may result in death or the incapacity to take action or exit. It is conceivable that there may be low-level CO exposures within the living area that do not activate the alarm but may be harmful to persons with cardiovascular disease.

Army policy prohibits military family housing residents from using portable gas or liquid fuel space heaters in family quarters or in tents.[76] Exceptions for interim emergency heating can only be granted by the installation commander, and only when CO alarms are present and working properly.[76]

Troop Tents

The deaths in Fort Irwin described above demonstrate the dangers of gas heaters. Commanders should only allow the use of vented tent heaters that meet military field heating requirements and are proven safe and effective, such as those listed in the Natick Soldier Center’s Commanders’ Smart Book Equipment Catalogue.[43] Only trained and licensed personnel are allowed to set up and operate heaters.[43] Individually owned heaters and commercial propane or natural gas heaters must not be used under any circumstances.[43] Unvented kerosene heater use should be restricted to areas where people do not sleep, such as guard houses, ranges, or training areas (or when approved by the commander as interim emergency heating with CO alarms in place).[5]

Acquisition of commercial nonstandard heaters is justifiable only in mission-critical circumstances; if nonstandard heaters are needed, the first general officer in the unit’s chain of command must approve their purchase and use, based on the recommendations of safety, health, and fire protection personnel.[43] A complete risk assessment should be done if the commander decides that operational necessity requires use of an unvented kerosene heater in tents or other enclosed shelters. The risk of cold stress must be balanced against the risks of using the heater.[43] Precautions must be followed when using these heaters, and personnel must be trained on the health and safety issues related to heater use, including identifying heaters as a potential source of CO and teaching people about the symptoms of CO poisoning.[43]

Environmental Exposure Standards for the General Population

The Environmental Protection Agency (EPA) set the US national ambient air quality standards for CO at 9 ppm for 8 hours and 35 ppm for 1 hour.74,77 These outdoor limits are intended to protect the general population and most sensitive subpopulations, including those with heart disease, by maintaining Hbco in nonsmokers below 2.0%.[4] Studies have noted that Hbco levels between 2.4% and 2.9% have aggravated angina and other cardiac conditons72,77 and decreased exercise capacity.[77] Continuous exposure at 9 ppm would result in an Hbco level of about 1.5% when using the equation in MIL-HDBK-759C.

The EPA uses air monitoring stations to measure CO levels around the country, and the measurements are then compared to these standards. The EPA maintains a list of US areas not meeting these standards; these places are required to develop and carry out plans to reduce CO emissions. In 1995, 80% of CO emissions were generated by transportation (highway and off-road vehicles) and construction sources.[5]

Emergency and Accidental Exposures

NIOSH set the IDLH level for CO at 1,200 ppm based on acute toxicity data in humans.[72] OSHA requires employers to consider whether the range of exposures anticipated includes the NIOSH IDLH when selecting respiratory protection.[78] Per NIOSH, the IDLH value was set to the airborne concentration from which a worker could escape without injury or health effects in the event of the failure of respiratory protection equipment. The IDLH is considered a maximum concentration above which only SCBA should be permitted. In determining IDLH values, NIOSH considered the ability of a worker to escape without loss of life or irreversible health effects along with certain transient effects, such as severe eye or respiratory irritation, disorientation, and lack of coordination, which could prevent escape. IDLH values incorporate a margin of safety based on effects that might occur as a consequence of a 30-minute exposure.[72]

A 1,200-ppm exposure to CO would result in a Hbco level of about 30% when using the formula in MILHDBK-759C, using the standard set of assumptions with a work-effort level of 3. At a work-effort level of 4 (heavy work), a 1,200-ppm CO exposure for 30 minutes would result in a Hbco level of 38%.

The NRC COT developed emergency exposure guidance levels (EEGLs) for a healthy military population,[18] as well as submarine escape action levels (SEALs) for the Navy to protect crewmembers from toxic gases in disabled submarines.[79] Additionally, the American Industrial Hygiene Association established emergency response planning guidelines (ERPGs) to protect the general public and workers from exposures.[80]

Committee on Toxicology Emergency Exposure Guidance Levels

The NRC COT EEGLs were established for a military population of healthy soldiers and are not intended for other occupational groups or the general public.[18] The EEGLs and the predicted %Hbco levels associated with these EEGLs are provided in Table 24-3. The EEGLs were developed using air concentrations that do not exceed Hbco levels of 10%.[18]

TABLE 24-3

NATIONAL RESEARCH COUNCIL EMERGENCY EXPOSURE GUIDANCE LEVELS

Exposure Duration

EEGL*

Maximum %Hbco, Sedentary, 6 L/min, Work-Effort Level 1

Maximum %Hbco, Moderate Work, 18 L/min, Work-Effort Level 3

Maximum %Hbco, Heavy Work, 24 L/min, Work-Effort Level 4

10 min

1,500 ppm

6.4%

14%

18%

30 min

750 ppm

8.9%

19%

24%

60 min

400 ppm

9.1%

19%

23%

24 h

50 ppm

7.8%

7.9%

7.8%

*National Research Council, Committee on Toxicology. Emergency and Continuous Exposure Guidance Levels for Selected Airborne Contaminants. Vol 4. Washington, DC: National Academy Press; 2007.

EEGL: emergency exposure guidance level

Hbco: carboxyhemoglobin

EEGLs represent the ceiling limit for a single exposure (rare in a lifetime) of 60 minutes or less.[18] They consider the statistical likelihood that a non-incapacitating, reversible health effect may occur in the exposed population.[18] EEGLS are designed to prevent substantial performance impairment during emergencies.[18] EEGLs must not be used for routine, predictable, and controllable operations such as in firing the main gun in a tank or howitzer.

Navy Submarine Escape Action Levels

SEALS were established to protect crew members in disabled submarines from the effects of exposure to high concentrations of toxic gases[79]; CO is one of eight gases of concern. A collision or explosion that causes onboard fires can expose crewmembers to high concentrations of toxic combustion products. Exposures to any of the eight gases can damage the respiratory system and CNS, which could result in death, either directly or by impeding crew members’ ability to escape after a serious incident. The Navy developed two SEALS for each of the eight gases and requested that the COT independently review the available toxicological and epidemiologic data and evaluate the scientific validity of the two SEAL levels. The NRC reviewed the data and recommended that the Navy adopt a SEAL 1 (the maximum concentration of CO in a disabled submarine to which healthy submariners can be exposed for up to 10 days without irreversible health effects) of 80 ppm. The COT recommended the Navy adopt a SEAL 2 (the maximum concentration of CO in a disabled submarine to which submariners can be exposed for up to 24 hours without experiencing irreversible health effects) of 96 ppm.[79]

Emergency Response Planning Guidelines

The American Industrial Hygiene Association developed ERPGs to assist emergency responders in planning for chemical releases into the community with a goal of protecting the general public.[80] The predicted %Hbco levels presented in Table 24-4 were calculated using the equation in MIL-HDBK-759C using the same assumptions as stated previously.

Confounders

Many confounders alter the effects of CO poisoning, which may explain why the expected signs and symptoms do not always correlate to measured Hbco levels. There is a greater risk of CO toxicity in a population with decreased oxygen-carrying capacity or reduced oxygen availability.[14] Respiratory disease can impair oxygen exchange, and increased oxygen-hemoglobin affinity in the fetus may also increase the risk of CO poisoning.[14] Reduced atmospheric pressure at high altitudes, as well as increased work, can put workers at increased risk when exposed to CO.[14] In addition to CO, chemicals such as hydrogen cyanide and nitric oxide are products of combustion that may cause chemical asphyxiation, albeit by different mechanisms. Other chemicals such as methylene chloride are metabolized to CO.

Altitude

Oxygen deficiency generally causes no physiologic effects in healthy adults when the partial pressure of oxygen (Po_2) is greater than 132 mm Hg.[72] However, people living at elevations of 5,000 ft or above, where the Po_2 of the atmosphere may be less than 120 mm Hg, are more sensitive to CO and other asphyxiants.[72]

The effects of CO and of hypoxia from altitude are additive and similar, though the decreased Po_2 at high altitudes and increased Hbco produce different physiological responses.74,81 The Po_2 in the atmosphere decreases as a function of increased altitude, though the %O_2 remains the same.74,76 For example, at sea level the Po_2 is about 159 mm Hg (ie, 0.21 × 760 mm Hg), whereas at an altitude of 7,000 ft above sea level, the Po_2 is about 121 mm Hg (ie, 0.21 × 580 mm Hg).[72] An ambient level of 121 mm Hg corresponds to an alveolar Po_2 level of 60 mm Hg due to dead space, carbon dioxide, and water vapor. Hemoglobin will be 90% saturated and normal levels of oxygen transport will occur in healthy adults provided the alveolar Po_2 stays above 60 Po_2.[72] An altitude of 6,000 ft (about 128 mm Hg Po_2) is the approximate physiologic equivalent to a CO exposure of 25 ppm CO at equilibrium (ie, at equilibrium, the Hbco level does not rise or decrease upon subsequent exposure to CO).[82]

The effects of altitude are more likely to be a contributing factor for someone who is not acclimatized. The body acclimatizes over about 4 weeks[83] through five mechanisms: (1) increased pulmonary ventilation, (2) increased red blood cells, (3) marked increase in diffusing capacity of the lungs, (4) increased blood vessels in the tissue, and (5) increased cell ability to use oxygen at low Po_2.[83] At an elevation of 17,000 ft, unacclimated and acclimated work capacities are 50% and 68% respectively.[83] Some workers in the Peruvian Andes live at an altitude of 17,500 ft and work in a mine at 19,000 ft.[83] The work capacity of these workers is 87%.[83]

CO exposure limits may be multiplied by an adjustment factor (AF) to account for the approximate effects of altitude on persons unacclimated to high altitudes. For instance, at an altitude of 6,000 ft and where the ACGIH TLV-TWA is applicable, an 80% AF might be applied to the 8-hour TWA exposure limit to get 20 ppm (ie, 0.8 AF × 25 ppm) until the person is acclimatized.1(p49)

TABLE 24-4

EMERGENCY RESPONSE PLANNING GUIDELINES*

*The values in the table are intended for planning purposes only and not intended for use in routine operations or to distinguish between safe and unsafe exposure levels. The work-effort level used in developing the ERPGs is between sedentary (level 1) and light work (level 2).

ERPG: emergency response planning guideline

Hbco: carboxyhemoglobin

Studies of laboratory animals and humans show that Hbco levels are elevated at altitude.[74] Also, higher Hbco levels have been observed in individuals breathing CO (9 ppm) at rest at altitude compared to those Hbco levels observed at sea level.[74] Exercise in a CO atmosphere (50–150 ppm) at altitude produced lower Hbco levels than those found under similar conditions at sea level, which may be due to either suppressed Hbco formation or a shift in the CO storage.[74]

Hypoxic hypoxia caused by high altitude (25,000 ft) seems to be better tolerated by smokers than nonsmokers, who tend to experience more severe symptoms and have less work capacity.[74] This may be due to the fact that smokers have chronic hypoxemia and develop a partial tolerance to hypoxic hypoxia.[74]

Heat Stress/High Temperature

Heat stress and high temperature when combined with CO exposure produced a decrement in the exercise performance at concentrations of 50 ppm CO.14,74

Tobacco Smoking

Tobacco smokers have an elevated Hbco level, ranging from 4% to 20%, and subsequent exposures to other sources of CO will further raise their Hbco. The Hbco level rises with the amount of smoking, with a mean of 5% to 6% Hbco for one pack of cigarettes per day; a mean of 7% to 9% Hbco for two to three packs of cigarettes per day; and up to 20% Hbco for cigars.[14] An empirical formula in MIL-HDBK-759C (paragraph 5.13.7.4.5)[66] based upon the CFKE predicts Hbco blood content as a result of exposure to CO and can be used to roughly estimate the impact of tobacco smoking by entering an initial Hbco expected for a smoker.

Nitric Oxide

Additive toxicity can be anticipated upon simultaneous exposure to nitric oxide and CO.14,17 Nitric oxide exposure results in the formation of nitrosyl hemoglobin, a compound that is incapable of oxygen transport.14,17 Following inhalation of very high nitric oxide concentrations (eg, 80 ppm), circulating methemoglobin concentrations of up to 15% can be reached.14,17

Hydrogen Cyanide

There seems to be a slight additive interaction between CO and cyanide, reducing the lethal concentration for 50% of test animals by about 10% when rats have been exposed simultaneously to high concentrations of CO and cyanide.14,17 Cyanide easily diffuses into all parts of the body and inhibits the metabolic enzyme cytochrome oxidase, which is involved in the transfer of electrons to molecular oxygen.[84] As a result, cyanide quickly halts practically all cellular aerobic respiration.[85]

Methylene Chloride

Methylene chloride is a solvent and paint stripper that is metabolized in the body to CO.14,17 Exposure at the ACGIH TLV-TWA of 50 ppm produces a 3% Hbco level.14,17

Additive Effects Formula for Chemical Mixtures

When individuals are exposed to chemical mixtures involving CO and other substances such as nitric oxide and methylene chloride, the following formula should be applied to determine the exposure concentration and time limit:

C_1/T_1 + C_2/T_2 + … Cn/Tn

The combined exposure is determined by adding the concentrations divided by time interval of the exposure for each chemical encountered, where C_1 indicates the observed atmospheric exposure concentration and T_1 is the corresponding exposure time limit.[72]

Health Status

Individuals with cardiopulmonary conditions including chronic obstructive pulmonary disease, coronary artery disease, and congestive heart failure have reduced blood oxygen content and are at greater risk from CO exposure because the additional reduction in blood oxygen-carrying capacity resulting from Hbco formation increases the relative hypoxemia.[74] Individuals with medical conditions affecting the blood including anemia and polycythemia are also at increased risk from CO poisoning.[74]

Ototoxicity

In 2003, USACHPPM published a fact sheet listing occupational ototoxins that contribute to hearing loss.[86] CO is on the list; it contributes to noise-induced hearing loss when CO exposure is combined with hazardous noise exposure.85,87–92 The mechanism of ototoxicity for CO poisoning is thought to be free radical formation, which potentiates the effects of hazardous noise exposure on the hair cell.[90]

For workers enrolled in a hearing program due to excessive noise exposure, clinicians must be aware of the possible potentiating effects of CO exposure. They may need to initiate actions to reduce exposure to both noise and CO.[86] USACHPPM recommends that workers’ exposures be kept below 50% of the occupational exposure limit for ototoxic substances, regardless of the actual noise level. Thus, audiograms should be performed when exposures are at one-half the 8-hour TLV-TWA of 25 ppm, or when the CO exposure exceeds 12 ppm and hazardous noise is present in the workplace.

Exposures should be documented in the comments section of DD 2215, Reference Audiogram, and DD 2216, Hearing Conservation Report, noting the ototoxins present in the workplace and the exposure levels of each. For CO exposures, the following should be included: CO exposure concentrations over the course of the day; predicted Hbco levels over the course of the day; noise exposure levels over the course of the day with respect to CO concentrations throughout the day; and other activities conducted outside of work that may have combined CO and noise exposures (eg, volunteer firefighting, playing in a rock band). Also, if the worker is a smoker, the number of packs of cigarettes or number cigars smoked per day should be noted.[86]

MEDICAL SURVEILLANCE

Workers routinely exposed to CO must receive hazardous communications training on the potential hazards of CO, as well as the role of engineering controls and use of personal protective equipment in controlling the risk of exposure. Pregnant workers and others considering pregnancy should be encouraged to quit smoking, advised about CO toxicity risks to the fetus, and trained on the ways to minimize the exposure potential. The employer must provide and properly maintain personal protective equipment. The criteria for enrolling workers into periodic medical surveillance for CO is if exposures exceed the action level for 30 days a year. An industrial hygienist should provide the occupational health clinic with documentation of CO exposures for placement in the medical records of all affected employees.

Workers must also undergo a preplacement physical examination, including a complete history, to identify medical conditions that put them at increased risk from CO toxicity, including smoking, chronic obstructive pulmonary disease, coronary artery disease, cardiovascular disease, CNS disorders, and anemia. In addition, workers must receive periodic and termination examinations. All three exams should emphasize the cardiovascular system, the pulmonary system, and the CNS. A complete blood count baseline should be obtained in the preplacement exam, and subsequent counts should be obtained when clinically indicated. A complete blood count should also be obtained immediately following acute exposure, and the worker should be examined for evidence of CO toxicity. After exposure, a venous blood sample should be obtained and examined for Hbco level.[93]

An occupational medicine physician can perform and document evaluations of the patient’s mental, baseline neurological, and visual or ophthalmological status. A useful tool is the CO neuropsychological screening battery, which tests short-term memory, concentration, visual spatial ability, agnosia, and aphasia.[94]

SUMMARY

Exposure to CO can cause acute clinical illness. Military exposures to CO may occur outdoors; inside homes, vehicles, and workplaces; and while using military vehicles and weapons systems. Soldiers exposed while operating vehicles or weapons systems may experience a cyclic exposure, in which high peak exposures are followed by periods of minimal exposure, followed by successive peaks and troughs.

Cellular enzyme systems are adversely affected by CO poisoning due to hypoxia produced by formation of Hbco. Individuals with coronary artery disease appear to be at higher risk of ischemia following CO poisoning, but there have been reports of ophthalmologic and neurologic problems as well. Timely diagnosis and early oxygen therapy will help reduce Hbco levels and facilitate tissue oxygenation, which can reduce both the morbidity and mortality in CO poisoning cases.

ACKNOWLEDGMENTS

The authors thank Christopher H. Carroll, MSES, for his work preparing the chapter for publication.

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30.   Paladin Carbon Monoxide Incidents. Fort Carson, CO: 7th Infantry Division and Fort Carson Headquarters; February 11, 2000. Memorandum for Commander, USACHPPM.

31.   US Department of Defense. Design Criteria Standard (Human Engineering). Washington, DC: DoD; 2012: 194. MIL-STD-1472G.

32.   Tikuisis P, Keefe A. COHb Prediction Model for PC Application. North York, Ontario, Canada: Defense and Civil Institute of Environmental Medicine; July 26, 1996. Technical Memorandum.

33.   Majumdar D. Sources: USAF suspects carbon monoxide in F-22 grounding. Defense News. July 21, 2011.

34.   Naval Safety Center Aeromedical Division. Medical investigation of suspected hypoxic events. Approach: The Navy & Marine Corps Aviation Safety Magazine. 2010;55(4):2.

35.   US Army Medical Surveillance Activity. Carbon monoxide intoxication, Fort Hood, Texas, and Fort Campbell, Kentucky. MSMR. 1997;3(9):14–16.

36.   US Army Medical Surveillance Activity. Carbon monoxide poisoning in a family, Olsbrucken, Germany. MSMR. 2001;7(2):10.

37.   US Army Soldier and Biological Chemical Command. Soldier Crew Tent Air Quality Testing. Aberdeen Proving Ground, MD: SBCCOM; 2001.

38.   Safety Alert: Soldier Deaths at Fort Irwin. Fort Rucker, AL: US Army Safety Center; 2001.

39.   2 soldiers found unconscious die. Los Angeles Times. January 16, 2001. http://articles.latimes.com/2001/jan/16/news/mn-12888. Accessed September 3, 2017.

40.   US Army Forces Command. Safety Alert Message: Soldier Deaths From Asphyxiation While Sleeping in a Soldier Crew Tent. Ft Bragg, NC: FORSCOM; 2001.

41.   Army Safety Center. Silent killer claims two lives. Countermeasure. 2001;22(9):2–3.

42.   Army Safety Center. Seconds count … to save lives. Countermeasure. 2002;23(10):9.

43.   Army Public Health Command. Just the facts: guidance on the use of heaters inside tents and other enclosed shelters. Published 2005. http://www.wsmr.army.mil/PDF/heaters.PDF. Accessed September 3, 2017.

44.   Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA. 2006;295(4):398–402.

45.   Weaver LK. Clinical practice. Carbon monoxide poisoning. New Engl J Med. 2009;360(12):1217–1225.

46.   Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. 2006;26(1):99–125.

47.   Sayers R, Yant W. Dangers of and Treatment for Carbon Monoxide Poisoning. Reports of Investigations. Washington, DC: US Department of the Interior, Bureau of Mines; 1923.

48.   Kindwall E. Carbon monoxide. In: Zenz C, ed. Occupational Medicine: Principles and Practical Applications. 2nd ed. Chicago, IL: Year Book Medical Publishers; 1988: 503–508.

49.   American Industrial Hygiene Association. Carbon Monoxide Documentation for Emergency Response Planning Guidelines. Fairfax, VA: AIHA; 1999.

50.   Seger D. Carbon monoxide. In: Sullivan J, Krieger G, eds. Hazardous Materials Toxicology: Clinical Principles of Environmental Health. Baltimore, MD: Williams & Wilkins; 1992: 1160–1164.

51.   US Department of Health Education and Welfare. Criteria for a Recommended Standard: Occupational Exposure to Carbon Monoxide. Washington, DC: National Institute for Occupational Safety and Health and US Government Printing Office; 1972.

52.   Turino GM. Effect of carbon monoxide on the cardiorespiratory system. Carbon monoxide toxicity: physiology and biochemistry. Circulation. 1981;63(1):253A–259A.

53.   Nightingale T. Biological Effects of Short, High-level Exposure to Gases: Carbon Monoxide. Rockville, MD: US Army Biomedical Research and Development Laboratory; 1980.

54.   Tomaszewski C. Carbon monoxide. In: Clinical Toxicology. 1st ed. Philadelphia, PA: WB Saunders Company; 2001: 657–667.

55.   Wilmer W. Effects of carbon monoxide upon the eye. Am J Ophthalmol. 1921;4:73-90.

56.   Kim JK, Coe CJ. Clinical study on carbon monoxide intoxication in children. Yonsei Med J. 1987;28(4):266–273.

57.   Quinn DK, McGahee SM, Politte LC, et al. Complications of carbon monoxide poisoning: a case discussion and review of the literature. Prim Care Companion J Clinical Psychiatry. 2009;11(2):74–79.

58.   Crocker PJ. Carbon monoxide poisoning, the clinical entity and its treatment: a review. Milit Med. 1984;149(5):257–259.

59.   Satran D, Henry CR, Adkinson C, Nicholson CI, Bracha Y, Henry TD. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Coll Cardiol. 2005;45(9):1513–1516.

60.   Penney DG. Hemodynamic response to carbon monoxide. Environ Health Perspect. 1988;77:121–130.

61.   Turnbull TL, Hart RG, Strange GR, et al. Emergency department screening for unsuspected carbon monoxide exposure. Ann Emerg Med. 1988;17(5):478–483.

62.   Davies DM, Smith DJ. Electrocardiographic changes in healthy men during continuous low-level carbon monoxide exposure. Environ Res. 1980;21(1):197–06.

63.   Rubenstein E. Carbon monoxide poisoning and smoke inhalation. In: Rubenstein E, Federman DD, eds. Scientific American Medicine. New York, NY: Scientific American; 1990: Chap 8.

64.   Armed Forces Health Surveillance Center. Tri-Service Reportable Events: Guidelines and Case Definitions. Silver Spring, MD: AFHSC; 2007: 23–28.

65.   US Department of Defense. DoD Safety and Occupational Health (SOH) Program. Washington, DC: DoD; 1998. DoD Instruction 6055.1.

66.   US Department of Defense. Handbook for Human Engineering Design Guidelines. Washington, DC: DoD; 1995: 302–303. MIL-HDBK-759C.

67.   Smith SR, Steinberg S, Gaydos JC. Errors in derivations of the Coburn-Forster-Kane equation for predicting carboxyhemoglobin. Am Ind Hyg Assoc J. 1996;57(7):621–625.

68.   Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. Coburn equation calculator. https://www.cdc.gov/niosh/topics/co-comp/default.html. Accessed August 28, 2017.

69.   Peabody T, Furr A, Ditmetaroj N. Carbon monoxide and the eye: a teaching case report. Optom Educ. 2013;38(3):114–124. http://journal.opted.org/articles/Volume38_Number3_CarbonMonoxide.pdf. Accessed September 11, 2017.

70.   US Department of the Army. Preventive Medicine. Washington, DC: DA; 2009. DA PAM 40-11.

71.   US Department of Health and Human Services. NIOSH Pocket Guide to Chemical Hazards. Cincinnati, OH: National Institute for Occupational Safety and Health; 2007.

72.   American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 7th ed. Cincinnati, OH: ACGIH; 2010.

73.   Occupational Safety and Health Administration. OSHA Fact Sheet: Carbon Monoxide Poisoning. Washington, DC: OSHA: 2002.

74.   US Environmental Protection Agency. Carbon monoxide’s impact on indoor air quality. https://www.epa.gov/indoor-air-quality-iaq/carbon-monoxides-impact-indoor-air-quality. Accessed September 2, 2017.

75.   US Army Corps of Engineers. Family Housing. Washington, DC: USACE; 2002. Technical Instruction TI 801-02.

76.   US Department of the Army. Facilities Engineering: Army Facilities Management. Washington, DC: DA; 2012. Army Regulation 420–1.

77.   US Environmental Protection Agency. National Ambient Air Quality Standards (NAAQS). Published 2012. http://www.epa.gov/air/criteria.html. Accessed May 24, 2014.

78.   29 CFR, Part 1910.134. Respiratory protection. http://www.osha.gov/SLTC/respiratoryprotection/standards.html. Accessed August 23, 2017.

79.   National Research Council. Review of Submarine Escape Action Levels for Selected Chemicals. Washington, DC: National Academy Press; 2002.

80.   American Industrial Hygiene Association. Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Handbook. Fairfax, VA: AIHA; 2008.

81.   World Health Organization. Environmental Health Criteria 213: Carbon Monoxide. 2nd ed. Geneva, Switzerland; WHO; 1999. http://www.inchem.org/documents/ehc/ehc/ehc213.htm. Accessed May 24, 2014.

82.   National Research Council. Carbon Monoxide. Medical and Biological Effects of Environmental Pollutants. Washington, DC: National Academy Press; 1977.

83.   Guyton A. Textbook of Medical Physiology. 8th ed. Philadelphia, PA: WB Saunders Company; 1991.

84.   Hathaway G. Chemical Hazards of the Workplace, Procter and Hughes’. 4th ed. Indianapolis, IN: John Wiley & Sons; 1996.

85.   Fechter LD, Chen GD, Rao D, Larabee J. Predicting exposure conditions that facilitate the potentiation of noise-induced hearing loss by carbon monoxide. Toxicol Sci. 2000;58(2):315–323.

86.   US Army Public Health Command. Occupational Ototoxins (Ear Poisons) and Hearing Loss. Aberdeen Proving Ground; MD: APHC; 2012. Fact sheet 51-002-0713. http://phc.amedd.army.mil/PHC%20Resource%20Library/Ototoxin_FS_51-002-0713.pdf. Accessed May 24, 2014.

87.   Chen GD, Fechter LD. Potentiation of octave-band noise induced auditory impairment by carbon monoxide. Hear Res. 1999;132(1-2):149–159.

88.   Chen GD, McWilliams ML, Fechter LD. Intermittent noise-induced hearing loss and the influence of carbon monoxide. Hear Res. 1999;138(1-2):181–191.

89.   Fechter L. Combined effects of noise and chemicals. Occup Med. 1995;10(3):609–621.

90.   Morata TC. Chemical exposure as a risk factor for hearing loss. J Occup Environ Med. 2003;45(7):676–682.

91.   Rao DB, Fechter LD. Increased noise severity limits potentiation of noise induced hearing loss by carbon monoxide. Hear Res. 2000;150(1-2):206–214.

92.   Young JS, Upchurch MB, Kaufman MJ, Fechter LD. Carbon monoxide exposure potentiates high-frequency auditory threshold shifts induced by noise. Hear Res. 1987;26(1):37–43.

93.   Stewart RD, Stewart RS, Stamm W, Seelen RP. Rapid estimation of carboxyhemoglobin level in ire fighters. JAMA. 1976;235(4):390–392.

94.   Messier LD, Myers RA. A neuropsychological screening battery for emergency assessment of carbon-monoxidepoisoned patients. J Clin Psychol. 1991;47(5):675–684.

ATTACHMENT: EXAMPLE OF MODELING PERCENT OF CARBOXYHEMOGLOBIN WITH TIME USING MICROSOFT EXCEL

CO: carbon monoxide

Hbco: carboxyhemoglobin

%Hbco_0: initial percent carboxyhemoglobin

%Hbcot: final percent carboxyhemoglobin

ppm: parts per million

Chapter 25

BERYLLIUM

DALE HARMAN, MD, MPH*; NICOLE S. CHAVIS, MPH†; AND TIMOTHY M. MALLON, MD, MPH‡

INTRODUCTION

INDUSTRIAL USE

ENVIRONMENTAL EXPOSURE

OCCUPATIONAL EXPOSURE

REGULATION AND LEGISLATION

HEALTH EFFECTS

Pathophysiology of Chronic Beryllium Disease

Acute Beryllium Disease

Beryllium Sensitization

Symptoms and Effects of Chronic Beryllium Disease

Carcinogenesis

Dermatologic Effects

Biomarkers of Exposure and Effect

OCCUPATIONAL SURVEILLANCE

GENETIC PREDISPOSITION

DIAGNOSIS AND TREATMENT OF CHRONIC BERYLLIUM DISEASE

Diagnosis

Treatment

PREVENTION AND CONTROL

SUMMARY

* Captain (Retired), Medical Corps, US Navy; Occupational and Environmental Medicine Physician, Independent Contractor, Portsmouth, New Hampshire 03870

† Research Associate, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

‡ Colonel (Retired), Medical Corps, US Army; Adjunct Assistant Professor, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

INTRODUCTION

Beryllium is a naturally occurring element found on the earth’s surface in rocks at concentrations of 1 to 15 mg/kg. In the periodic table, beryllium appears in group IIA, alkaline earth elements. It has an atomic weight of 9.012, with two common oxidation states, Be(0) and Be(+2).[1] It has a melting point of 1,287°C and a boiling point that ranges from 2,469° to 2,970°C.[2] Beryllium is not naturally found as a free metal because of its high reactivity. The important beryllium minerals in the world are beryl (Be_3Al_2(SiO_3)6) and bertrandite (Be_4Si_2O_7(OH)2).3,4 Beryllium is a light-weight, grey metal that is relatively transparent to x-rays and has nonmagnetic properties, along with low density, high tensile strength, and good corrosion resistance.3,4 It is widely used in manufactured products, ranging from nuclear weapons to golf clubs and helicopter rotor and airplane parts, due to its light weight and high tensile strength. Beryllium has chemical properties like aluminum, but is only two-thirds the weight of aluminum, and it has six times the tensile strength of steel.5,6

The chemical and physical properties of beryllium make it important for military applications, including nuclear bomb casings, non-sparking tools for the ammunition industry, and aircraft applications in helicopters and airplanes. At the same time, beryllium’s unique properties make it potentially extremely toxic for people who come in contact with either its metal or alloy form.[7]

This chapter will discuss in detail the production and industrial uses of beryllium, with a focus on how beryllium is used in military applications. The environmental and occupational sources of exposure will be highlighted. The chapter will review the health effects of beryllium exposure and the supporting medical evidence, including sensitization, chronic beryllium lung disease, genotoxicity, and lung cancer. The legal and regulatory requirements, as well as exposure prevention and treatment strategies, will be outlined. Beryllium’s toxicological properties will be examined, with a focus on pulmonary and renal changes. The basis for the genetic predisposition for beryllium-exposed workers to develop sensitization and chronic beryllium lung disease will be explored.

Additionally, the chapter will discuss elements of a medical surveillance program for beryllium, including a review of available biomarkers of exposure and effect, such as the beryllium lymphocyte proliferation test (BeLPT). However, medical surveillance for beryllium exposure is complicated because x-ray changes do not always appear right away, and pulmonary function tests do not change rapidly in response to exposure. New studies report improved sensitivity and specificity for the BeLPT, which requires that split samples be drawn for confirmatory testing at one or more laboratories.

INDUSTRIAL USE

The United States is one of only three countries that produce beryllium products. It is the leading manufacturer of beryllium metals, alloys, and oxides.[8] US production of beryllium was reported as 180, 235, 200, 216, and 270 metric tons in 2010, 2011, 2012, 2013, 2014, respectively.[8] Beryllium-copper-nickel alloy was first used in the United States in 1926 in the manufacture of fluorescent lighting. In the 1940s, a small cluster of chronic beryllium disease (CBD) was identified in fluorescent lighting plant workers.[9]

The US Geological Survey estimated that consumer electronics uses 42% of the available beryllium, telecommunications uses 11%, the Department of Defense uses 11%, commercial aerospace and energy applications both use 8%, and the remailing 28% is used in appliances, automotive electronics, and medical devices.[8] The three primary beryllium-containing materials used today in the electronics, aerospace, defense, and automotive industries are beryllium metal; beryllium alloys including copper, aluminum, magnesium, or nickel; and beryllium oxide. Beryllium is found in the vital sensing equipment of fire suppression systems and automobile airbags. Its use in automobile ignition control systems improves gas mileage and decreases emissions. Additionally, it is critical to the functioning of such medical equipment as laser bores, mammography x-ray windows, and pacemakers. Because of its magnetic transparency, strength, and corrosion resistance, beryllium is utilized in satellites, weather forecasting equipment, and aircraft landing gear bearings. Beryllium’s light weight and conductivity make it ideal for use in mobile phones and computer systems. Compounds and alloys containing 40% to 100% beryllium are used in the defense industry in targeting systems, lasers, high-speed circuitry, missile production, radar systems, and infrared countermeasure equipment.[9] In the nuclear industry, beryllium is used to absorb and reflect neutrons and to produce neutron sources.[10] Exhibit 25-1 lists jobs with potential exposure to beryllium, and Exhibit 25-2 lists manufactured products that include beryllium.

ENVIRONMENTAL EXPOSURE

Beryllium is naturally occurring in rocks, coal, oil, soil, and volcanic dust, and it is taken up by plants. The average US soil concentration of beryllium is 0.6 mg/kg[3]. Beryllium will dissolve in water and can be toxic to fish at high levels.[11] Exposure to beryllium in the general population varies by geographic location; drinking water concentrations average 190 ng/L but range from 10 to 1,220 ng/L.[12] The Geological Survey’s National Water-Quality Assessment Program, a comprehensive study of trace elements detected in groundwater across the United States from 1992 to 2003, collected data from 5,183 monitoring and drinking-water wells and found that beryllium levels did not exceed 4 μg/L.[13]

The average US air concentration of beryllium is 0.3 × 10-4 μg/m^3; however, in metropolitan areas, the concentration is markedly higher, with a mean of 0.2 × 10-3 μg/m^3.[14] Atmospheric beryllium comes from three primary sources: anthropogenic sources account for 45.3% of atmospheric beryllium, windblown dust accounts for 52%, and volcanic activity accounts for 2%.[14] Inhalation of beryllium-containing fumes and dust originating from processing plants poses the most serious hazard to people.[11] In 2008, eight CBD cases were diagnosed in the community surrounding a beryllium manufacturing plant in Reading, Pennsylvania.[15] Between 1974 and 2010, environmental air sampling was conducted at the Lawrence Livermore National Laboratory in California, where beryllium is manufactured, machined, and stored. The beryllium airborne concentrations at the sites ranged from 0.2 to 490 pg/m^3, with a median concentration of 11.8 pg/m^3.[16] Monthly sampling showed seasonal variation in beryllium levels, with the highest levels in late summer/early fall, when temperatures and wind speed are elevated and precipitation is low. Lower levels of beryllium were observed in the winter months, when precipitation is higher.[16]

EXHIBIT 25-1

WORKERS WITH POTENTIAL OCCUPATIONAL EXPOSURE TO BERYLLIUM

- Primary beryllium production workers

- Workers processing beryllium metal/alloys/composites

- foundry workers

- furnace tenders

- machine operators

- machinists

- metal fabricators

- welders

- dental technicians

- Secondary smelting/refining (recycling electronics, metals)

- Abrasive blasters (slags)*

___________________

*Certain types of slags (coal, copper) used in abrasive blasting operations may contain trace amounts of beryllium (< 0.1 % by weight). Due to high dust conditions in abrasive blasting, workers may be exposed to dangerous levels of beryllium.
Reproduced from: US Department of Labor, Occupational Safety and Health Administration. Safety and health topics: beryllium. https://www.osha.gov/SLTC/beryllium. Accessed October 10, 2017.

EXHIBIT 25-2

MANUFACTURED PRODUCTS THAT USE BERYLLIUM

- Aerospace (aircraft braking systems, engines, satellites, space telescopes)

- Automotive (antilock brake systems, ignitions)

- Ceramic manufacturing (rocket covers, semiconductor chips)

- Defense (components for nuclear weapons, missile parts, guidance systems, optical systems)

- Dental labs (alloys in crowns, bridges, and dental plates)

- Electronics (x-rays, computer parts, telecommunication parts, automotive parts)

- Energy (microwave devices, relays)

- Medicine (laser devices, electro-medical devices, x-ray windows)

- Nuclear energy (heat shields, reactors)

- Sporting goods (golf clubs, bicycles)

- Telecommunications (optical systems, wireless base stations)

___________________

Reproduced from: US Department of Labor, Occupational Safety and Health Administration. Safety and health topics: beryllium. https://www.osha.gov/SLTC/beryllium. Accessed October 10, 2017.

Among individuals who are not employed in the beryllium industry, exposure occurs primarily through smoking, food, and water. While the nonoccupational intake of beryllium is unknown, estimates have ranged from 0.12 to 100 μg/day.[12] The average whole-body burden of beryllium in individuals who are not occupationally exposed is less than 0.08 mg/kg, although it is slightly higher in lung tissue, which averages 0.20 mg/kg.[17] A smoker who smokes 20 cigarettes per day is exposed to 1.5 μg of beryllium per day.[18]

OCCUPATIONAL EXPOSURE

In 1943, Dr Van Ordstrand of the Cleveland Clinic published the first reported cases of beryllium-related disease in workers at two beryllium production plants in Cleveland.[19] In 1946, when doctors Irving Tabershaw and Harriet Hardy attributed previously diagnosed sarcoidosis cases to exposure to beryllium, the notion of beryllium-related lung disease began to gain acceptance.[20] These findings raised concern about the health of the general public and for workers in the lighting industry. As a result, use of phosphors of beryllium was discontinued in the manufacture of fluorescent lights after 1949.[9]

The utilization of beryllium in the atomic weapons industry has decreased over the last 4 decades due to the worldwide downsizing of nuclear arsenals. However, beryllium is now used in a variety of other industries. Prior to 2000, CBD was reported to affect between 2% and 6% of exposed workers, with rates as high as 16% for those in beryllium manufacturing and maintenance jobs. With aggressive exposure controls in modern worksites, the prevalence of beryllium sensitization (discussed below) was decreased from 18% to 1% in one company’s plant over 24 months.[21]

The total number of workers with beryllium exposure has been as high as 800,000, but the numbers have declined over the last 2 decades. In 2004, the estimated total of federal and private beryllium workers was 134,000.21,22 The Occupational Safety and Health Administration (OSHA) estimates that in 2017, approximately 62,000 workers were potentially being exposed to beryllium in approximately 7,300 establishments in the United States.23,24 In addition, family members of beryllium workers also have potential exposure from contaminated work clothing and vehicles. Presently, beryllium workers in primary beryllium manufacturing and alloy production, and workers in recycling, have the highest average exposures to beryllium.23,24

The number of workers in the Department of Defense exposed to beryllium remains steady. Exposures to Air Force personnel mostly occur during installation and repair of aircraft systems that include bushings, bearings, and washers made of beryllium copper alloy, as well as braking systems on the Lockheed C-5 Galaxy built before 1980. Aircraft panel removal generates dust from the wear of alloy materials. Forward-looking infrared systems, low-altitude navigation-targeting infrared for nighttime operations, and field instruments for detecting low-energy radiation all contain beryllium. Service of equipment by maintenance personnel has the potential to expose workers to 61 different work processes that pose a likely inhalational hazard.

The National Academy of Sciences Committee on Toxicology reviewed Air Force personnel exposures to beryllium and recommended several steps the Air Force should take to protect its personnel. First, skin and respiratory exposures should be minimized by maintaining effective controls for processes that generate dust and fumes. Next, the committee recommended screening personnel and putting the resulting information into a centralized surveillance database. Further, the Air Force should do a comprehensive exposure assessment by characterizing each job task and identifying the beryllium in all materials in the workplace, then remove products containing beryllium as soon as feasible. Lastly, the Air Force should train personnel on the health hazards of beryllium and steps necessary to prevent exposure.[25]

The Navy has discontinued the use of beryllium in fabricating dental prosthetics for patients. However, beryllium continues to be used in commercial dental bridges and prosthetics and fabrication facilities. Significant numbers of Army workers and contractors are exposed to beryllium in the maintenance shops at ammunition plants around the country where non-sparking tools are necessary to prevent explosion. The grinding and reconditioning of these tools puts maintenance workers and others in the immediate vicinity at risk of exposure. Further, rotary-wing aircraft mechanics are routinely exposed when maintenance work for Army and Navy helicopters is performed on the main and tail rotor assemblies, which contain beryllium in component parts.

Known occupational risk factors include work in ceramics production, machining of various types of beryllium, beryllium metal production, copper-beryllium alloy melting and casting, processing of alloy rod and wire products, and work in analytic laboratories.[26] Workers at highest risk for developing CBD are those who work in industries that generate airborne beryllium particles, and those involved in machining beryllium usually have the highest levels of exposure among beryllium workers. This group is at an increased risk of becoming sensitized to beryllium and developing CBD.[26] Machining, either by grinding, deburring, lathing, milling, or other processes, produces beryllium particles that are highly respirable and easily deposited in the alveoli. When beryllium is machined, 50% of the particles generated are larger than 0.6 μm in diameter. The remaining 50%, which are smaller than 0.6 μm, tend to be dispersed throughout the work area, exposing others not involved in the machining process to beryllium and CBD risk.[27]

At the Lawrence Livermore site, beryllium was found in the carpets after vacuuming, at a concentration ranging from 0.002 to 0.480 μg/cm^2. Beryllium was also detected in surface dust at the front offices and wire annealing areas of a copper-beryllium alloy facility at Lawrence Livermore at concentrations of 0.05 to 13.6 μg/cm^2. At an industrial facility located in Schenectady, New York, beryllium concentrations in overhead dust were reported to range from 19.4 to 151 μg/cm^2.[16]

REGULATION AND LEGISLATION

The first steps toward the establishment of an occupational exposure limit (OEL) for workers came in 1947 when the Atomic Energy Commission’s Health and Safety Laboratory, under the direction of Merrill Eisenbud, began to investigate the health impacts of beryllium exposure.28,29 Based on this work, a permissible maximum peak exposure limit of 26 μg/m^3 over a period of 30 minutes was recommended for workers in the beryllium industry. A community ambient air standard of 0.01 μg/m^3 averaged over a 1-month time interval was also proposed to protect the public living near beryllium manufacturing facilities.[22] The establishment of this recommended ambient air standard was driven by a cluster of CBD cases in nonoccupationally exposed individuals within a 0.75-mile radius of a beryllium plant in Lorain, Ohio. In 1948 the average beryllium concentration in the air within 0.25 miles of this plant was 1 μg/m^3, 100 times the proposed standard.[30]

Eisenbud proposed an 8-hour time-weighted average (TWA) of 2.0 μg/m^3 as the OEL, based on the known toxicity of other heavy metals and their atomic weights,[31] which was implemented by the Atomic Energy Commission in 1949.[22] The OEL of 2.0 μg/m^3 was subsequently adopted by the American Industrial Hygiene Association in 1956, and by the American Conference of Governmental Industrial Hygienists in 1959 as a threshold limit value (TLV). The American National Standards Institute (ANSI) incorporated this value as a consensus standard in 1970, and in 1972 OSHA adopted the ANSI standard as the permissible exposure limit (PEL).[22]

In January 2017, OSHA published a new beryllium final rule that lowered the PEL for beryllium to 0.2 μg/m^3 of air, averaged over 8 hours. OSHA also lowered the short-term exposure limit for beryllium to 2.0 μg/m^3 of air over a 15-minute sampling period.23,24 This rule provides staggered compliance dates to give employers time to meet the requirements and ensure the needed protections are put in place. One year after the effective date of the rule, most provisions must be adopted. Employers must put change rooms and showers in place 2 years after the rule was published, and they must install engineering controls no later than 3 years after the rule was published.23,24

The rule also requires employers to limit access to areas with high levels of beryllium and provide respiratory and dermal protection in the form of personal protective clothing to workers who must enter these areas. They must also develop a written exposure control plan and train workers on the plan. Lastly, employers are required to offer workers medical surveillance when their exposure exceeds the action level for beryllium (discussed below).23,24

HEALTH EFFECTS

The most common health effects associated with overexposure to beryllium in the workplace include acute beryllium disease (ABD), beryllium sensitization, CBD, and lung cancer.23,24

Pathophysiology of Chronic Beryllium Disease

CBD is an immune-related disease. This categorization is based on observations of CBD in individuals exposed to low airborne concentrations of beryllium. Further, the tissue burden of beryllium did not correspond to the severity of the disease. In addition, several cases of CBD were known to occur months to years after the termination of exposure. Finally, beryllium causes a delayed skin test response as well as a granulomatous response in the lungs and skin.[32]

A mechanism has been proposed for the development of lung inflammation and granuloma formation in CBD, which occurs during and after beryllium exposure.[33] Beryllium particles, acting as haptens, bind to proteins in lung tissue. The protein-bound beryllium particles are ingested by alveolar macrophages, which act as antigen-presenting cells to CD4+ T lymphocytes. Beryllium alone also causes activation of T cells. T lymphocytes proliferate in response and, combined with macrophages, release inflammatory cytokines (IFN-γ, TNF-α, IL-2, and IL-6) that promote the accumulation, activation, and aggregation of macrophages, resulting in the development of granulomatous inflammation through a cell-mediated, type IV mechanism. Beryllium also induces macrophage apoptosis, which reduces clearance from the lung, causing continual reexposure.34–36

Acute Beryllium Disease

ABD is a rapid onset form of chemical pneumonia that results from breathing high airborne concentrations of beryllium.23,24 ABD is generally associated with exposure to beryllium levels at or above 100 μg/m^3 and may be fatal in 10% of cases. ABD is extremely rare in the workplace today due to more stringent exposure controls implemented following occupational and environmental standards set in the 1970s.23,24

In 1997 two cases of ABD were detected in workers exposed to beryllium fluoride in a metal production department that was part of a reduction furnace operation in Korea.[37] Exposure levels to beryllium were low, with most of the facility’s air concentrations under 10 μg/m^3. After working for several months, the workers complained of shortness of breath, chest pain, and a dry cough. Chest x-rays were normal, but pulmonary function tests showed decreases in forced vital capacity and carbon monoxide diffusing capacity. With continued exposure, the respiratory symptoms worsened, as did both pulmonary function tests, but the chest radiographs remained unchanged. After removal from exposure, the respiratory symptoms and pulmonary function test results were improved. One of the workers returned to working with soluble beryllium, and his respiratory symptoms returned; he had impaired lung function within several months. The second worker went to work in another area of the facility, which involved less exposure to beryllium compounds. Eighteen months later, both workers were asymptomatic, but chest radiographs and biopsies revealed non-caseating granulomas. Because of these cases, it was hypothesized that ABD may be part of the continuum from acute to chronic beryllium disease, and that ABD was likely due to an immunological response to beryllium rather than an irritant response.[37]

Beryllium Sensitization

Beryllium sensitization is the activation of the body’s immune response to beryllium. Beryllium sensitization can result from inhalation or skin exposure to beryllium dust, fume, mist, or solutions.38,39 Two positive BeLPT tests over any time period define sensitization.40,41 While no clinical symptoms are associated with sensitization, a sensitized worker is at risk of developing CBD when inhalation exposure to beryllium has occurred.42–44

Several studies have evaluated the prevalence of beryllium sensitization among workers at different types of facilities, but most of the studies lacked exposure monitoring data. The prevalence of beryllium sensitization in workers has varied from a low of 1.3% in a nuclear weapons facility to a high of 7% to 19% in a beryllium production facility.45–47

Symptoms and Effects of Chronic Beryllium Disease

CBD is a chronic granulomatous lung disease caused by inhaling airborne beryllium after becoming sensitized to beryllium. The currently accepted diagnostic criteria for CBD in patients with known exposure to beryllium are sensitization to beryllium and pulmonary epithelioid granulomas identified on lung biopsy.[48]

Common symptoms of CBD are shortness of breath, unexplained coughing, fatigue, weight loss, fever, and night sweats. CBD can result from inhalation exposure to beryllium at levels below the current OSHA PEL (0.2 μg/m^3).23,24 Progression from sensitization to CBD can vary among individuals, and not all sensitized individuals go on to develop CBD.49,50 After initial exposure to beryllium, some workers may quickly develop signs and severe symptoms of CBD. Others may not experience signs and symptoms until months or years after initial exposure. Symptoms can sometimes worsen even after the worker has been removed from exposure.51–53 CBD can progress to a chronic obstructive lung disorder, resulting in loss of quality of life and the potential for decreased life expectancy. CBD shares many signs and symptoms with pulmonary sarcoidosis, a granulomatous lung disease of unknown cause or origin.48,54

Individuals who have been exposed to beryllium do not respond uniformly. Most people show no evidence of sensitization (immune response) or of CBD. Some individuals become sensitized but have no evidence of CBD.51,53 Some individuals demonstrate evidence of interstitial lung disease that may or may not be characterized by microscopic granulomas, but macroscopic granulomas are usually seen on x-ray as the disease progresses.[48] It is thought that only sensitized individuals progress to develop CBD.[48] To date, it is unknown if cessation of exposure to beryllium in sensitized workers reduces the progression rate to CBD.[53]

Latency (length of time from exposure to CBD development) ranges from zero to more than 25 years.48,53 One study followed beryllium-sensitized workers over 5 years, with 30 of 79 workers still employed at the end of the study. During the 5-year period, 30% of the original group of 79 workers developed CBD. The rate of progression from sensitization to CBD was examined: approximately 13% of workers developed CBD at year 2, 19% had developed CBD at year 4, and 37% of workers had developed CBD by year 6.55,56

The study also evaluated the connection between beryllium particulate size and CBD risk. Because CBD is a granulomatous disease found primarily in the alveolar regions of the lung, it was thought that only respirable beryllium particles less than 10 μm in diameter were responsible for CBD, and this was confirmed. Another study showed that more CBD cases occur in areas when particle size is less than 5 μm in diameter, and fewer cases occur in areas where particle size is larger than 5 μm.[26] These findings support the notion that the size of respirable particles may be a good indicator of CBD risk.

In addition, beryllium can damage the liver by producing granuloma formation adjacent to or within the portal tracts. Dot necrosis, acidophilic degeneration, white blood cell infiltration, fibrosis, portal cirrhosis, and Kupffer cell proliferation have been reported.[57] Similarly, beryllium can induce granuloma formation and fibrosis in the kidney. However, renal findings are rarely noted in the absence of significant pulmonary disease. Hypercalcemia, hypercalciuria, and calcium kidney stones may occur.[58]

Carcinogenesis

Based on numerous studies in occupational settings, OSHA has determined that occupational exposure to beryllium causes lung cancer in humans. In addition, the International Agency for Research on Cancer classified beryllium as a group 1 lung carcinogen in humans in 1993, 2009, and 2015.[59] The Environmental Protection Agency and the National Toxicology Program also consider beryllium to be a carcinogen.60,61 One large study examined lung cancer and urinary tract cancer mortality in 9,199 workers at seven beryllium facilities in the United States. Beryllium exposure was assessed by estimating maximum and daily average exposure and time spent at specific jobs to create a job-exposure matrix. The study found elevated risk of lung cancer risk of 20% and 45% at two of the facilities, an overall combined increased risk of 17% across all facilities, and a 3-fold increase risk of uterine cancer also across all facilities.[62] Another study reported a latency of 20 years for cancer associated with beryllium exposure.[62]

Dermatologic Effects

Nonpulmonary forms of CBD can present as a granulomatous disorder that affects the lymphatics and skin. Skin exposure to beryllium in sensitized individuals manifests initially as a dermatitis. Skin or pulmonary exposure (unrelated to dermatitis or beryllium implantation in the skin) may lead to subcutaneous granulomas. Implanted beryllium particles may result in skin ulceration that requires removal of the particles for resolution.57,58

Skin exposure to beryllium results in mild to moderate changes in the skin. Initially, spongiosis involving the lower layers of the epidermis and focal edema of the papillary epidermis were observed on skin biopsy obtained 96 hours postexposure.[63] A skin biopsy obtained 2 to 5 weeks postexposure in the same patient showed granuloma formation, with spongiosis and edema resolved.[63] Skin patch testing in individuals with CBD have resulted in strongly positive reactions that were characterized by erythema, induration, and vesicles.[64]

Biomarkers of Exposure and Effect

Blood Beryllium Levels

A 2008 study of ten subjects in Montreal, Canada, showed beryllium can be detected in the blood and serum using graphite furnace atomic absorption spectrometry. The average concentration of beryllium detected was 0.63 μg/L in the blood and 0.43 μg/L in serum. Smokers had slightly higher levels than nonsmokers.[65]

Urine Beryllium Biomarkers

A 2011 study conducted in the United Kingdom examined beryllium levels in the urine of a group of workers at an aluminum smelting facility and in a group of non-exposed individuals.[66] The mean and 90th percentiles of beryllium in the urine for workers at the aluminum smelter were 19.5 and 42.0 ng/L, respectively, while the mean and 90th percentile of the control group were 11.6 and 20.0 ng/L, respectively.[66]

Beryllium Lymphocyte Proliferation Test

The BeLPT is an immune-based test that measures the reaction of lymphocytes in body fluid, usually venous blood or broncho-alveolar lavage (BAL), to beryllium.[67] Lymphocytes previously sensitized to beryllium respond with higher rates of proliferation and radioactive thymidine uptake.[68] Although the test is ingenious, the nuances and difficulties of cell culture and measuring thymidine uptake have made its standardization across laboratories, and even within laboratories, challenging.69,70

The sensitivity and specificity of the BeLPT test has improved over the past 10 years. One recent study involved over 25,000 BeLPT tests done on 12,194 workers employed at 18 Department of Energy sites. The workers were exposed to beryllium or beryllium oxide and beryllium-copper alloy. A false positive result was defined as an abnormal test result that could not be confirmed by additional BeLPT retests conducted within 2 months of the original sample. The false positive rates ranged from 0.0 to 3.4%, with an average false positive rate of 1.1%. False negative results were assessed among workers with two or more abnormal results and were defined as a normal result occurring within 2 years of the initial abnormal result. Overall, the false negative rate was 31.7%. Inter-laboratory agreement of abnormal results ranged from 26.2% to 61.8%. Test sensitivity, the probability that a patient with CBD will have an abnormal BeLPT result, was 68.3%. Test specificity, the proportion of normal tests in all patients who do not have CBD, was 96.9%.[71]

Another analysis of the BeLPT sensitivity and specificity employed different testing algorithms, one with testing performed at one lab followed by analysis at two different labs, and a second algorithm that employed split samples analyzed at two different laboratories. The second algorithm yielded the highest sensitivity and specificity for the BeLPT test, with a sensitivity of 86.0% and a specificity of 99.8%.[72]

The positive predictive value (the likelihood that a person who meets the criteria is truly sensitized to beryllium) varies with the beryllium sensitization prevalence in the population. If the prevalence in the test population is low (1%), then the positive predictive value is low at 37%. At a 10% prevalence, the positive predictive values was 99.7%.

Another test has been developed to assess beryllium sensitization using a cytokine-based assay of CD4+ T cells.[73] An enzyme-linked immune spot (ELIS) analysis was performed to measure interferon (IFN-γ) gamma-secreting CD4+ T cells. In former beryllium workers, similar rates of sensitization were found using BeLPT (8.1%) and an IFN-γ ELIS test (10%). Among current workers, the BeLPT identified only 1.3% of workers as sensitized, compared to 9.9% identified using the IFN-γ ELIS test. The difference in the test results was thought to be due to poor proliferation of beryllium-specific CD4+ T cells. The IFN-γ ELIS test had a sensitivity of 85% and a specificity of 100%. The IFN-γ ELIS test was also able to differentiate between beryllium sensitization and CBD. More than 93% of the beryllium-sensitized subjects had less than 10 spot-forming units, and subjects with over 40 spot-forming units had an 81% probability of progressing to CBD.[73]

Whether all workers with a positive BeLPT or IFN-γ ELIS should undergo bronchoscopy and lung biopsy is questionable. Induced sputum cytology, using a CD4 to CD8 ratio of greater than 2.5 as a cut-off, has been shown to compare with bronchoscopy and biopsy in diagnosing CBD when each are combined with a positive BeLPT.[74] However, sputum cytology has yet to become a widely accepted alternative to bronchoscopy and biopsy. OSHA regulations now permit the employee to decide whether to take advantage of medical removal based on a positive BeLPT or IFN-γ ELIS sensitization test result.23,24

OCCUPATIONAL SURVEILLANCE

The purpose of medical surveillance is to educate workers about potential health effects, detect early signs and symptoms of disease to eliminate ongoing exposures, and prevent short- and long-term adverse health effects. Medical surveillance programs can contribute to the success of workplace health and safety programs by identifying potential problem areas and verifying the effectiveness of existing control and prevention programs.

The beryllium standard (29 CFR 1910.1024) requires employers to offer medical surveillance to workers who are exposed above the action level of 0.1 μg/m^3 for 30 days in a year, when workers show signs or symptoms of CBD, and when workers are exposed to beryllium in an emergency or their physician or other licensed healthcare professional (PLHCP) recommends continued surveillance.23,24 Employees may opt out of the medical surveillance program if they so choose.

The medical surveillance requirements for beryllium-exposed workers include obtaining a medical and work history with emphasis on past and present airborne exposure to or dermal contact with beryllium.23,24 The PLHCP must also ascertain if there is a history of smoking or any respiratory conditions. The provider must examine the lungs for difficulties breathing and examine the skin for rashes.23,24 A pulmonary function test and BeLPT are required, and the PLHCP may order other tests such as a high-resolution computed tomography (CT) scan when they feel it is necessary for the diagnostic work-up.23,24

The employer must provide the PLHCP with a copy of the OSHA beryllium standard, the job description that details the employee’s duties involving airborne and dermal exposure potential, and available air sampling data that shows actual beryllium exposure levels.23,24 The employer must also give the PLHCP a description of personal protective equipment used by the employee and any abnormal results from prior physical examinations.23,24

The PLHCP must provide the employee with a written medical opinion that details the results of the medical examination and listing any condition that puts the employee at increased risk of injury from exposure to beryllium, as well as any newly developed medical conditions that require further evaluation or treatment.23,24 The PLHCP must advise both the employee and employer regarding recommendations for use of personal protective equipment, and they must say whether the employee was referred to a CBD diagnostic center and whether medical removal is recommended. The PLHCP must notify the employer in writing of the date of the examination, and certify that the results of the exam were explained to the worker and that the exam met the requirements of the beryllium standard.23,24

GENETIC PREDISPOSITION

Genetic susceptibility contributes to the development of beryllium sensitization and progression of sensitization to CBD.[75] CBD is characterized by an accumulation of beryllium-specific CD4- T-cells in the lung. In 1993, researchers studying genetic markers noted that alleles of the major histocompatibility complex class II gene HLA-DPB1 glutamate 69 (Glu69) appears to increase the probability of CBD developing in exposed people.76,77 The marker has been found to be expressed in 84% to 97% of CBD cases.[78] A further study found HLA-DRPhe47 to be associated with beryllium sensitization in Glu69-negative subjects.[79] An 8-fold increased rate of CBD has been demonstrated in workers who have the Glu69 marker and are exposed to elevated levels of beryllium in the workplace.80,81

Genetic screening holds promise for identifying individuals who have an increased susceptibility for development of beryllium sensitization or CBD. However, because of the low prevalence of beryllium sensitization and CBD in the exposed population and the limited understanding of the genetic role in beryllium-induced pathology, these markers are not useful as clinical screening tools for beryllium-related disease.[20] Further, genetic testing in the worker population has been prohibited by the Genetic Information Nondiscrimination Act of 2008.[82]

DIAGNOSIS AND TREATMENT OF CHRONIC BERYLLIUM DISEASE

Diagnosis

Beryllium disease may mimic sarcoidosis. Individuals with CBD usually present with the slow onset of exertional dyspnea, decreased exercise tolerance, fatigue, and a nonproductive cough.[35]

Criteria for diagnosing CBD include the following: (1) evidence of beryllium exposure; (2) evidence of an immune response to beryllium (ie, positive responses in blood or BAL fluid beryllium lymphocyte proliferation tests); and (3) histopathological (biopsy) evidence consistent with CBD.[25] With more advanced disease, the patient may experience progressive declines in lung volumes and diffusing capacity, eventually resulting in pulmonary fibrosis, respiratory failure, and cor pulmonale.[35] Further, the patient will exhibit anorexia, weight loss, cough, chest pain, or arthralgias. Physical exam findings may be absent except in advanced disease, when rales, tachycardia, fever, cyanosis, edema, and clubbing of fingers may be present.[52] Patients suspected of having CBD should be offered medical removal from further beryllium exposure.

Radiographic findings are those of a pneumoconiosis. They include ill-defined nodular pulmonary opacities and, with advanced parenchymal changes, hilar adenopathy may be present (though this is less common than in sarcoidosis patients). The nodular opacities are more commonly seen in the apical regions and may coalesce into large masses. A high-resolution CT scan is more sensitive in detecting granulomatous disease in its early stages. CT evaluation generally reveals small parenchymal nodules (57%) along with interlobular septal thickening (50%). Ground glass opacities (32%) and bronchial wall thickening (46%) are also common.[83]

Pulmonary function test results may be normal in the early stages of clinical disease but deteriorate with the increase in granuloma formation. The later stages of CBD may demonstrate either a restrictive or obstructive pattern, but in most cases the pattern is mixed. With advanced disease the diffusion capacity of the lung for carbon monoxide is reduced due to pulmonary epithelial damage.[51] KL-6, a known marker of epithelial cell injury, is elevated in both the serum and BAL fluid of CBD patients and has been proposed as a means of quantifying the severity of disease.[67]

Treatment

Patients suspected of having CBD should immediately be removed from beryllium exposure because improvement in lung function has been seen after cessation of beryllium exposure. A trial of corticosteroids should be initiated as soon as possible unless contraindicated for health reasons.[84] The response to corticosteroid therapy, as measured by forced vital capacity and diffusing capacity, is short-lived but significant.[85] One study showed early treatment with steroids led to significant improvement in pulmonary function initially, but pulmonary function subsequently declined.[85] Another study noted sustained improvement in lung function following long-term corticosteroid treatment.[86] It should be noted that once pulmonary fibrosis has developed, steroid therapy will not reverse the damage.[86] Individuals started on corticosteroid therapy should be followed by regular chest radiographs and pulmonary function testing to monitor the clinical response and guide adjustments in the dose and duration of treatment.[85]

Chelating agents may prove useful in reducing the beryllium burden in exposed workers. Several chelating agents, including glutathione, 2,3-dimercapto propane sulfonic acid with sodium selenite, and D-penicillamine, were successfully used to reduce beryllium levels in the liver, kidneys, lungs, and uterus of rats.[87] D-penicillamine was the most effective chelating agent. However, more work will be necessary before the Food and Drug Administration can approve the use of these chelating agents.[87]

PREVENTION AND CONTROL

The goals of a prevention program are to limit inhalation and dermal exposures and reduce the number of employees who are directly exposed. This may be achieved by elimination or substitution of beryllium, engineering controls such as local exhaust ventilation, use of personal protective equipment, and administrative changes such as exclusion of workers from specific areas to prevent contact with beryllium.[48] The nonoccupationally exposed population encounters beryllium in food, drinking water, and the ambient air daily. There have been cases of CBD due to this type of exposure. Routine use of beryllium-containing consumer products does not pose an exposure risk because most consumer product applications do not generate particulate matter by remaining intact during normal use; performing maintenance on these products would increase the likelihood of exposure.[88]

SUMMARY

Beryllium, though extremely useful in industry, poses a threat to those involved in its manufacture and processing. Some workers exposed to beryllium develop sensitivity to it, which may lead to CBD, a disabling, irreversible pulmonary disease. There is evidence that those who have had significant exposure to beryllium may be at increased risk for respiratory cancers. Current exposure limits do not appear to adequately control the health effects of beryllium on exposed workers. Biological monitoring of beryllium exposure is challenging because there is no test specific to beryllium disease that meets all the criteria for an acceptable screening test. The BeLPT is useful in the diagnosis of CBD, but this test is not mandated in routine military beryllium occupational medical surveillance. An exposure limit of 0.2 μg/m^3 has been adopted by some government and private industries, and will be proposed by a new OSHA standard.

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63.   Toledo F, Silvestre JF, Cuesta L, et al. Contact allergy to beryllium chloride: Report of 12 cases. Contact Dermatitis. 2011;64(2):104–109.

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65.   Stephan CH, Fournier M, Brousseau P, et al. Graphite furnace atomic absorption spectrometry as a routine method for the quantification of beryllium in blood and serum. Chem Cent J. 2008;2:14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2459166/. Accessed September 30, 2017.

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Chapter 26

SHIPBOARD MEDICINE

TERRANCE RILEY, MD*; TIMOTHY J. BERGAN, DO, MPH†; ROBERT N. UNISKIEWICZ, MD, MPH‡; AND LOUIS KROOT, MD§

INTRODUCTION

OVERVIEW OF SHIPBOARD CONDITIONS

SHIPBOARD OPERATIONAL MEDICINE DURING WARTIME

THE MEDICAL DEPARTMENT ABOARD SHIP

PREDEPLOYMENT PLANNING

ENVIRONMENT IN THE SHIPYARDS, UNDERWAY, AND AT PORT CALLS

MEDICAL CARE AT SEA

SUMMARY

*Formerly, Captain (Retired), Medical Corps, US Navy; Professor of Neurology, Department of Neurology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030; Deceased

† Lieutenant Commander, Medical Corps, US Navy; Force Medical Officer, Military Sealift Command, Medical Department (Code: N13X), Bldg SP-64, 471 C Street, Norfolk, Virginia 23511-2419

‡ Lieutenant Commander, Medical Corps, US Navy; Occupational Medicine Department Head, Naval Medical Center Portsmouth, 620 John Paul Jones Circle, Portsmouth, Virginia 23708

§ Commander (Retired), Medical Corps, US Navy; Surface Medical Department Officer; currently, Department of Emergency Medicine, University of Kentucky Chandler Medical School, Lexington, Kentucky 40536-0298

INTRODUCTION

This chapter is being published as an update to Chapter 29, Shipboard Medicine, in Medical Aspects of Harsh Environments, Volume 2.[1] Many of the operational environments described in this chapter have been updated to reflect new and emerging technology and medical equipment. The references and figures have been updated as well.

The shipboard environment influences how medicine is practiced at sea. Even at sea, medicine is still medicine: diagnosis still requires a medical history and examination, diagnostic adjuncts are weighed against resources, and treatment is based on the universal principles of surgery and medication. And yet, being at sea is different. Short of space travel, the stress of close living quarters, isolation, and a hazardous environment is unequaled. The prolonged absence from home, community, and normal environment creates profound emotional stress. Shipboard isolation also precludes normal exposure to minor infections, rendering an entire crew not only immunologically isolated but also immunologically naïve, compared with shore populations. The cramped living and working spaces create complicated and unnatural challenges for hygiene, nutrition, and infection control. The ship is also a unique industrial environment, which carries additional occupational medicine concerns.

Although there are no diseases unique to ships, several factors make shipboard medicine unique.

- Medical personnel are fully integrated with their patients (ie, the crew) and the life of the ship.

- The medical officer (MO) must not only plan for every medical eventuality, but also fully interact with all other departments for all battle group events.

- Medical operations vary widely with the different phases of the ship’s cycle.

- Roles that customarily belong to public health departments, industrial hygienists, and hospitals belong to the ship’s medical department.

There are few books on shipboard medicine,2,3 and this chapter adds to the topic area by focusing on military medicine on surface ships; medical problems aboard submarines are substantially similar[4] and will not be addressed here.

OVERVIEW OF SHIPBOARD CONDITIONS

Organization Aboard Ship

The ship as an organization has many of the same departments and key positions seen in other large military units. However, sea service traditions and unique seafaring features have evolved into special roles and titles, so that terminology sometimes differs from other services. For example, in the US Army a quartermaster is a storekeeper; on a ship, a quartermaster is a navigational expert. “First lieutenant” is not the rank but rather the title of the officer who runs the deck department, which takes care of all the lines (ropes), deck appliances, boats, and the architectural concerns of the ship. Similarly, the captain, also known as the commanding officer (CO) of a small ship, may hold a lower rank, such as commander.

The survival of a ship and its crew depends on watch stander vigilance. Watch standing is a system that divides duties and responsibilities among qualified personnel on a rotational basis in order to operate a ship continuously. The ship has a special document, the Watch Quarter and Station Bill, which assigns every crew member to watch standing rotations and specific positions and duties for military action or emergencies at sea. The bill for each department is posted where everyone can see, and crew members are expected to memorize their own assignments and those of their shipmates. Watch standers may be alone for long periods and fatigued from their ordinary work; staying awake on watch can be difficult, and staying alert may be even more so. Therefore, the watch standing culture and responsibility are immeasurably important, both for the safety and health of the crew and because medical watch standers are the first line of treatment in an emergency.

Ships and Missions

While ultimate responsibility on a ship rests with the CO, it is the MO’s responsibility to thoroughly assess the medical needs of a ship’s crew and keep the CO informed of the department’s status. A coastal freighter with a crew of 15 has less need, fewer resources, and an entirely different class of medical threats than an aircraft carrier with 100 jet aircraft and several thousand crew members. Only through a thorough understanding of the ship, the ship’s cycle, and its specific missions can the MO give the CO necessary information regarding requirements to provide optimal care for the crew.

There are many classes of US Navy ships; several of these ship classes and their medical department assets are described in Table 26-1. Warships are unique for their complex surveillance programs, training requirements, and dangerous environments. The aircraft carrier is one of the largest ships in the fleet, with a complement of 5,000 crew members and a very large medical department. The aircraft carrier operates one of the most complex and hazardous environments afloat. Figure 26-1 shows the USS Ronald Reagan (CVN 76), underway in the South China Sea with vessels from the Japanese Defense Force.

In many cases, the medical department’s responsibility is not limited to the ship’s company. An amphibious attack ship may start with a crew of 1,000, but when it embarks there are an additional 2,000 Marines aboard along with 70 helicopters and jet aircraft. A large medical department is required simply to care for all the people. Furthermore, when the ship enters amphibious operations, it becomes a hospital for ground troops, many of whom will be transported from other ships, so even more medical personnel are needed.

Life Aboard

From the time a ship is commissioned until it is decommissioned, it is never “turned off” or left unmanned. Ships at sea are large factories performing inherently dangerous operations that pose hazards for assigned crew members at all times as they work, eat, and sleep. Work hazards on the flight deck include helicopter and jet landings. During helicopter operations, personnel are exposed to noise, prop wash, flying debris, fuel, and fuel combustion products. Figure 26-2 shows an MH-60S Sea Hawk maritime helicopter during resupply operations on the deck of the guided-missile destroyer, USS Barry (DDG 52). Aircraft landings and takeoffs involving jets like the fighter attack F/A-18E/F Super Hornet can be particularly hazardous on the flight deck because of the catapult cable movement and danger due to snapping during landing operations with the arresting cable. Steam catapults with their rapidly shutting transoms are further injury sources. Figure 26-3 shows an F/A-18E/F Super Hornet landing on a carrier deck.

Ship personnel direct aircraft movement on the flight deck, and these operations present unique hazards. In the crowded on-deck environment, tractors that tow aircraft pose a significant collision hazard to deck personnel. Figure 26-4 shows an aviation boatswain’s mate directing a C-2A Greyhound aircraft on the flight deck. Sailors who haul fueling lines on deck face wet and windy environments and slippery deck surfaces, both of which increase the risk of falling overboard. In addition, sailors are exposed to lifting hazards and skin contact when working with jet fuels. Figure 26-5 shows a sailor carrying a refueling hose on the flight deck.

The tension on the lines that hold two ships together during underway replenishment can be extremely hazardous for nearby sailors on deck, particularly if the lines break or snap back, which could cause severe injuries such as amputation or decapitation. Figure 26-6 shows underway replenishment operations between the nuclear aircraft carrier USS Ronald Reagan and Military Sealift Command fleet replenishment oiler USNS Guadalupe (T-AO 200).

Excessive heat and noise pervade the engineering spaces, boiler rooms, and machinery compartments. Steam pipe insulation poses an asbestosis threat to crew members and the steam itself is dangerous if the pipes break. All kinds of equipment constitute electrical hazards. Toxic fumes and materials from welding, paints, batteries, and the amalgams and epoxies the dental department uses for fillings are ubiquitous.

In addition to those hazards, shipboard life presents challenges simply because of confined space; even with the very largest ships, space is always critical. Although habitability on military ships has improved over the last 50 years, life aboard is still more arduous than living ashore or in barracks. Enlisted crew racks (ie, beds) typically have only 20 to 36 in. of vertical clearance between them, and usually are stacked three to five racks high. On amphibious ships, the embarked troops may have racks with even less clearance stacked up to six high.

A rack is a sailor’s only private place; most ships have curtains that can close off each rack for further privacy and darkness. Racks are usually arranged in rows that form small, room-like enclaves to permit a sense of community and some privacy. Berthing assignments customarily place people with members of their own department in similar pay grades. The inclusion of women in crews requires more ingenuity to maintain departmental and rank-based berthing that separates men and women. Since the ship operates around the clock, invariably some crew member is beginning a watch or regular work duties in the middle of an adjacent sailor’s sleeping period. This traffic adds to the already difficult challenge of sleep hygiene and schedule accommodation.

Ventilation is critical in the confined berthing compartments, so many vents are located in the overhead (ie, the ceiling). Many other projections dangle from the overhead and intrude into the space above the top rack. The berthing areas are crowded with racks, lockers, ship fittings, and other sailors. Simple daily events, such as dressing, are difficult when the six to twelve people in a cubicle try to accomplish it at the same time in a deck space that may be only 3 or 4 ft by 8 or 10 ft.

TABLE 26-1

CLASSES OF SHIPS AND THEIR MEDICAL DEPARTMENTS

Ship

Function

Total Personnel

Medical Department Personnel

Destroyers, DD class; Frigates, FF class; 4,500–8,000 tons

Surface patrol and combat, ASW

200–300

2–3 corpsmen, at least one an IDC. Small sick bay with 1 operating table and ≤3 infirmary beds. 2–3 BDSs.

Cruiser, CG class; 8,000–10,000 tons

Anti-air warfare, surface patrol and combat, missile warfare

450–600

1 IDC, 2–3 corpsmen, 4 ward beds. Sick bay slightly larger than on DD or FF. 3 BDSs. No full OR or ICU

Auxiliary (service) ships, AD, AGF, AOE, AOR, AR, AS classes; 10,000–20,000 tons

Logistics, supply: general replenishment, ordnance, fuels

300–500

1 GMO, 1 PA or nurse practitioner; often a dental officer (DO). 5–10 corpsmen. Larger sick bay with 1 operating table and 1–2 examining tables, 1 dental operatory. Usually 5–13 infirmary beds. 2–3 BDSs.

Aircraft carrier, CVN (nuclear power); 75,000–92,000 tons

Tactical aircraft, ASW helicopters, power projection and joint operations

> 5,300

6 MOs (including 1 general surgeon, 1 family physician or internal medicine physician and a senior medical officer who has completed a residency in aerospace medicine); 2 or 3 flight surgeons from embarked airwing. 1 RN, 1 CRNA or anesthesiologist, 1 PA, 4 dentists (1 an oral surgeon), 30 corpsmen, 13–14 dental technicians. 1 OR; audiology booth; endoscopy, pharmacy, and X-ray facilities; and laboratory. 4–6 BDS.

Command Control ship, LCC class; 19,000 tons

Command and Control of fleet, theater, and Amphibious Task Force Operations

720–900

1 MO and 1 dentist (plus a senior MO on the embarked flag staff for staff planning), 12 corpsmen (at least 1 IDC), and often a PA, 3 dental techs. 20 ward beds, and 4 “quiet beds” that can be more intensive.

Tank Landing ships, LST class; 8,450 tons

Transport and land amphibious vehicles, tanks, and combat vehicles and equipment

> 700

5 corpsmen, 1 IDC. Embarked Marines may bring 12–20 corpsmen. Occasionally, embarked Marines may also have 1 GMO. Med Dept has lab and X-ray capability. 9 ward beds.

Amphibious Assault ships, LHA, LHD, and LPD classes; 40,000 tons

Primary landing ships, and sea control, large troop carrying helicopters and VSTOL jets (Harriers)

> 3,000 (ship’s company and troops)

Ship’s company has 1 MO, 1 dentist, 15–17 corpsmen. Embarked troops have 1–2 flight surgeons, 2 GMOs, and 12–20 corpsmen. Embarked surgical team to operate the large operating and ward suites: 3 MOs, including at least 1 surgeon, 1 anesthesia provider, 2 RNs (1 a perioperative specialist), 1 medical regulator, 10–12 corpsmen. Medical suite 4–6 ORs, 17 ICU beds, 40–50 ward beds, and 300–500 overflow beds.

Hospital ships, T-AH class; 69,400 tons

Mobile, flexible, surgical and intensive full hospital for combat and other operations

≥1,300 patient census

12 ORs, 80 ICU beds, 20 recovery beds, 280 intermediate beds, 120 light care, 500 limited care. Lab, X ray, pharmacy, and blood bank facilities. 55 MOs, 6 dentists, 172 nurses, 20 MSCs, 674 corpsmen, 16 dental techs.

ASW, antisubmarine warfare; BDS, battle dressing station; CRNA, certified registered nurse anesthetist; GMO, general medical officer; ICU, intensive care unit; IDC, independent duty corpsman; MO, medical officer; MSC, Medical Service Corps; OR, operating room; PA, physician assistant; RN, registered nurse; SMO, senior medical officer. Adapted from: Riley, T. Shipboard Medicine. In: Pandolf KB, Burr RE, eds. Medical Aspects of Harsh Environments Volume 2. Washington, DC: Borden Institute; 2002: 882.

Figure 26-1. USS Ronald Reagan (CVN 76) steams alongside JS Hamagiri (DD 155), JS Myōkō (DDG 175), JS Haruna (DDH 141), and JS Yūgiri (DD 153) of the Japan Maritime Self Defense Force in preparation for a refueling at sea evolution March 17, 2007. The Ronald Reagan Carrier Strike Group is underway on a deployment in support of US military operations in the Western Pacific.
US Navy photo by Chief Mass Communication Specialist Spike Call. (Released).
Reproduced from: http://www.defenseimagery.mil/imageRetrieve.action?guid=6719ec3648fa2930775e795d84832f7d81befc74&t=2.

Figure 26-2. Two seaman attach cargo pendants to an MH-60S Sea Hawk helicopter, assigned to Helicopter Sea Combat Squadron 25 (HSC-25), on the flight deck of guided-missile destroyer USS Barry (DDG 52).
US Navy photo by Petty Officer 2nd Class Kevin V. Cunningham.
Reproduced from: http://www.navy.mil/management/photodb/photos/161006-N-UF697-396.JPG.

Showers, sinks, and commodes are called “heads” on a ship and are usually distributed among berthing departments. With several dozen sailors per shower and commode, heavy use can overwhelm the ventilation in those compartments. If showers do not dry between uses, fungi, soapy residue, and bad odors accumulate. Sailors then avoid the bad shower and use one in a different area, so that it, too, is overwhelmed.

Figure 26-3. An F/A-18E/F Super Hornet prepares to catch the arresting cable on the aircraft carrier USS Dwight D. Eisenhower (CVN 69).
US Navy photo by Mass Communication Specialist 3rd Class Chad R. Erdmann. Reproduced from: http://www.navy.mil/view_image.asp?id=86449.

Figure 26-4. An aviation boatswain’s mate directs a C-2A Greyhound high-wing cargo aircraft assigned to Carrier Airborne Early Warning Squadron 120 (VAW-120) onto a catapult as it prepares for takeoff on flight deck of the aircraft carrier USS Harry S. Truman (CVN 75).
US Navy photo by Mass Communication Specialist Seaman Lorenzo J. Burleson. Reproduced from: http://www.navy.mil/gallery_search_results.asp?terms=air+craft+carriers&page=9&r=4.

Tight living and working conditions have obvious health implications. Many jobs on ship cause crew members to sweat and expose them to petroleum products and dirt. Lice and other parasites are a constant threat. To prevent eczema and contact dermatitis, crew members must have clean, dry garments, yet clothing and boots do not dry well in crowded spaces, so access to clean garments and laundry service are more important at sea than under other circumstances.

Figure 26-5. A sailor brings a refueling hose on the flight deck of aircraft carrier USS Dwight D. Eisenhower.
US Navy photo by Seaman Joshua Murray.
Reproduced from: http://www.navy.mil/management/photodb/photos/161006-N-WC455-093.JPG.

Primary prevention is critical for diseases spread by respiratory routes or personal contact, which can infect dozens of sailors within a few hours. An influenza outbreak could rapidly devastate a crew, so vaccinations are administered annually. Secondary prevention is no less important once index cases of respiratory illness are detected. A crew member with respiratory symptoms may require a barrier-to-droplet transmission, such as a surgical mask.

Sea sickness is a major problem for new crew members and in high seas, and is aggravated in berthing or working spaces where sailors lose sight of the horizon. Whether a ship pitches or rolls, in cramped living spaces some of the racks will unavoidably orient in the axis of motion most conducive to sea sickness.

The loss of privacy aboard ship is terribly stressful to many people. The feeling of being only one of a multitude can threaten a young person’s self-esteem and cause a paradoxical sense of loneliness. The psychological consequences of this kind of living are all the more threatening to immature sailors and those with personality or anxiety disorders.

The Ship’s Cycle

A ship has a recurring cycle much like a living organism. The cycle’s components include the following:

Figure 26-6. Supply pallets are sent from the Military Sealift Command fleet replenishment oiler USNS Guadalupe (TAO 200) to the aircraft carrier USS Ronald Reagan during a replenishment at sea.
US Navy photo by Mass Communication Specialist 3rd Class Alexander Tidd.
Reproduced from: http://www.navy.mil/gallery_search_results.asp?terms=supply+underway&page=3&r=4.

- Pre-deployment testing and training. Months before a ship departs on extended deployment, the crew runs a series of tests and training sessions to prepare for increasingly complex demands during underway periods. The first short outings teach the crew to work the ship’s power and navigational systems. Longer cruises follow to test maneuvers, weapons, communications, and tactics. Finally, periods at sea are spent coordinating with other ships in the task force, embarked amphibious forces, or other branches of the armed forces. Evaluations and inspections are held at each step to certify the ship’s readiness to advance to the next phase.

- Deployment. The ship’s mission or patrol (deployment) involves many months away from home. Because emergencies during deployment invariably entail cooperation among the ships traveling in a task force, medical aspects of mass casualty and damage control drills must be inserted into group deployment training plans and executed during the deployment.

- Postdeployment maintenance. On the ship’s return from deployment, maintenance and minor upgrades are performed in the shipyard. This work may require only a few weeks for a small ship or 6 months for a large, complex ship such as an aircraft carrier.

- Major overhaul. After two to five complete cycles, the ship needs a major overhaul to implement technological advances and repair accumulated wear and tear. Large ships may require more than a year in the shipyard.

The crew also has a cycle. Because military crew members are assigned to a ship for periods of only 2 to 5 years, at least one-third of the crew turns over annually. After a long deployment and time in the shipyard, new crew members and incumbents must undergo extensive training; the entire crew may require new skills or training on new technology and tactics for a planned deployment.

The ship is an entirely different organism in each phase of its cycle. The medical problems of each phase differ too. In the shipyard, the ship becomes an intense, crowded, dangerous industrial plant. Ordinary ventilation, plumbing, and electrical systems are compromised. Passageways are crowded and cramped with people and equipment. Sandblasting, other respiratory hazards, paint, and solvents are everywhere. Welding aboard a ship causes fire risks and vision hazards. Grinding equipment creates hearing and ocular hazards. Workers are vulnerable to falling tools and metal objects; common injuries include head trauma, burns, crushed extremities, and lacerations. Workers unfamiliar with the ship can wander into unventilated spaces and die of asphyxia.

When the ship is underway, the safety of all systems must be checked, certified, and treated with great respect. New crew members are likely to trip over unfamiliar projections on decks and are vulnerable to falls down ladder wells and holds. Burns and lacerations are common; puncture wounds and wrist and ankle fractures occur too. New crew members encounter sea sickness, loneliness, cramped spaces, unprecedented stress, and long working hours. Depression, acting out, and suicidal gestures emerge as significant clinical problems. In addition, the medical department must implement a major teaching program to train all crew members in ship hygiene, first aid, cardiopulmonary resuscitation, locations of first aid boxes, and how to respond to a mass casualty, including the role of each crew member.

During the cruise, the ship is almost always deployed outside its home waters, away from families and domestic ports for several months. The medical department manages all of the ship’s routine medical care, pursues required preventive medicine programs, maintains its own working and berthing spaces, and prepares to care for mass casualties even if major portions of the ship—possibly including the main medical department—are destroyed in battle. The medical department also manages the details of any necessary medical evacuations (MEDEVAC). Depending on the type of ship and its mission, port calls are often made to foreign nations, where the crew carries the home nation’s culture and image to other peoples and is in turn exposed to the local culture—and its endemic diseases. Morale and readiness are usually at their highest at the early part of the cruise and before port calls.

SHIPBOARD OPERATIONAL MEDICINE DURING WARTIME

In naval warfare, medical care is limited to resources aboard the ship. If the decision is made that one ship has to assist another, its primary mission must be subordinated to transporting medical assets to assist another vessel. Assisting a disabled vessel during wartime effectively doubles the number of unavailable vessels to the operational commander.

Medical Care During Battle

As Captain Richard R. Cooper wrote in his article, “Medical Support for the Fleet,”[5] medical support during battle at sea assumes the following:

- Casualties are injured or wounded rather than killed.

- A ship that has been hit stays afloat long enough for the casualties to be medically managed.

- Medical personnel and equipment in the damaged ship remain functional.

- Treatment is focused on supporting those who are able to return to the battle.

- Transfer to another unit is feasible despite isolation of the ship, bad weather, or an ongoing battle.

- The receiving unit has medical capabilities, a place to hold the wounded, and the ability to treat or transfer them out of the battle area.

The delivery of medical care during battle is completely different from care during peacetime because saving the ship is the first priority. The two main threats to a ship’s survival during combat are fire and flooding. More ships have been lost to fire and flooding than have been sunk by weapons. During general quarters (the ship’s maximum readiness battle condition), ship compartments and air shafts are sealed to control fire and flooding. Damage control central coordinates and clears all movement to ensure air and watertight integrity and to minimize and control damage from enemy missiles, torpedoes, shells, and mines. When enemy action or accidents damage the ship, repair parties (which are preassigned and trained) for specific areas of the ship respond to control the threat. Fire and flood threats are so great to the ship that the repair party will only move casualties to permit work in the damaged space. The injured are transported for medical assistance only after the threat is contained. A key factor that optimizes shipboard medicine performance during war is how well the ship’s medical officers and enlisted personnel train the ship’s crew to assist with first aid, litter carrying, and evacuation.

Shipboard battle casualties are unique in that they happen suddenly and in large numbers. Naval history teems with examples of what happens to a crew when a warship sustains sudden catastrophic damage. For example, on May 24, 1941, early in the Battle of the Denmark Strait, the Royal Navy battlecruiser HMS Hood was struck by several German shells, the magazine exploded, and the ship broke into two parts and sank within 3 minutes; only 3 crew members of 1,400 survived.[6]

In March 1945, the flight deck of the US Navy aircraft carrier USS Franklin (CV 13) was struck by two bombs, which exploded in the ship’s hanger and detonated the Franklin’s aircraft ordinance and fuel. The resultant secondary explosions and fires destroyed the aft portion of the ship, killing 724 personnel and wounding 264. The main battle dressing station (BDS) was destroyed, and only one ship’s doctor was able to care for the wounded (he later wrote an article on the realities of shipboard medicine during war).[7]

Figure 26-7. Crewmen fight to extinguish the fierce blaze from airplanes burning on the deck of USS Forrestal (CVA-59) operating in the Gulf of Tonkin, July 29, 1967.
Reproduced from: https://www.history.navy.mil/our-collections/photography/numerical-list-of-images/nhhc-series/nh-series/USN-1124000/USN-1124780.html.

Figure 26-8. USS Forrestal crewmen direct a fire hose on burning aircraft on the carrier’s deck while operating in Gulf of Tonkin, July 29, 1967.
Reproduced from: https://www.history.navy.mil/our-collections/photography/numerical-list-of-images/nhhc-series/nh-series/USN-1124000/USN-1124772.html.

On July 29, 1967, the aircraft carrier USS Forrestal (CV 59) was off the coast of Vietnam, preparing to launch aircraft, when a Zuni rocket malfunctioned and set an A-4 Skyhawk aircraft afire on the flight deck. Within minutes several other armed aircraft caught fire and exploded (Figure 26-7). Dozens of flight crew and workers on the flight deck were instantly killed or severely burned. The fires and explosions extended down many decks, trapping and wounding more sailors in the messdecks and berthing areas. In all, 134 Forrestal sailors died, and several hundred others suffered severe burns, inhalation injury, and fractures. Figure 26-8 shows sailors on the Forrestal flight deck during firefighting operations. To handle the casualties, a staging and triage area was set up in the forward hangar bay and forward messdecks. The first casualties arrived in the main medical area within 10 minutes, and the operating room was in constant use for several days. The 53 beds in the medical ward quickly filled, so patients were treated in makeshift holding beds in the messdecks and berthing compartment. Major treatment areas also had to be set up in the forward battle dressing stations on the 0-3 deck just below the flight deck and in the forward messdecks. Most treated casualties were able to return to duty to fight the fires and perform damage control. The severely injured were forced to wait 5 days after the fire started for evacuation, which was when the tactical firefighting situation allowed flight operations. This event illustrates the importance of planning for and evacuating the wounded from a damaged ship[7] as early as possible.

TABLE 26-2

SHIPBOARD REQUIREMENTS FOR SPECIFIC MEDICAL EQUIPMENT

Medical Equipment per No. of Personnel

No. of Personnel

First Aid Boxes

4/100

< 500

5/100

500

8/100

1,500–3,000

10/100

> 3,000

Stokes Litters

1.5/100

< 1,500

3/100

1,500–3,000

4.5/100

> 3,000

Neil Robertson litters*

N/A

0

Portable medical lockers

1/250

N/A†

Battle dressing stations‡

N/A

0

* One located adjacent to each vertical trunk, machine room, and shop space. The quantity is determined by the number of personnel occupying the space or compartment.

† Located adjacent to each repair party station.

‡ Quantity determined by class of ship; minimum: 2 (frigates) to 6 (aircraft carriers).

Adapted from: Riley, T. Shipboard medicine. In: Pandolf KB, Burr RE, eds. Medical Aspects of Harsh Environments Volume 2. Washington, DC: Borden Institute; 2002: 911.

The medical department places staff in BDSs throughout the ship in order to protect medical assets during a single hit. Moving medical supplies and litters from sick bay to the injured is not realistic; therefore, medical staff scatter portable medical lockers (also called “BDS in a box”), decontamination boxes, and litters throughout the ship as prescribed by Navy regulations shown in Table 26-2. Each BDS is equipped with a 50-gallon gravity-fed water tank, multiple battery-powered lanterns, emergency power backup, and communication lines. All communications and evacuations are cleared through damage control central first; the safety of the ship must take priority over individual medical care or everyone may perish. Maintaining watertight integrity and fire boundaries may require four litter bearers 20 to 30 minutes to move a single casualty 500 ft and the same amount of time to return.

Sinking, Immersion, and Survival

Despite the horrific nature of immediate, direct damage to ships in naval warfare, according to data from experiences of the Royal Navy[8] and US Navy,[9] 66% of deaths have occurred after the crew successfully abandoned a sinking ship. The main threat to a sailor’s survival is the environment. The hazards associated with immersion are listed in Exhibit 26-1. If sailors are in lifeboats, the most critical survival items are food, water, and blankets. If sailors remain in the water, extra clothing may counteract hypothermia. However, water conducts heat 25-fold faster than air; and sudden immersion and exposure to cold induces a sympathetic reflex, which causes tachycardia, hypertension, tetany, and hyperventilation. At the same time hypothermia causes sailors to become lethargic and lose the ability to protect their airway and turn their backs to a choppy sea. A sailor’s survival after abandoning a ship is dependent on the water temperature, sea state, swimming ability, and physical conditioning. According to Royal Navy data, most deaths from hypothermia occurred within the first 24 hours after immersion. But if a sailor survives the first 24 hours of immersion, the chances for survival improve dramatically.[8]

EXHIBIT 26-1

HAZARDS OF BEING SUNK AT SEA

Hypothermia

Drowning

Entanglement in or traumatic contact with a sinking ship

Inhalation of and contamination with fuel oil

Trauma from surfacing objects

Underwater explosions

___________________

Source: Handbook for Royal Naval Officers. London, England: Ministry of Defense, Medical Directorate General (Naval); July 1981. BR 2193.

The next greatest survival threat occurs shortly after survivors of a sinking ship are rescued. Sudden collapse and death have been observed, usually within the first 15 minutes of rescue, but occasionally up to several hours later. When the Argentinean cruiser General BelGrano was torpedoed and sunk during the Falkland War (1982), 71 survivors were rescued from life rafts; of those, 69 had hypothermia and 18 died of exposure. Both the Royal Navy and the US Navy have made recommendations for maximizing the survival of sailors who suffer from immersion. Exhibit 26-2 lists the Royal Navy’s detailed recommendations.

After hypothermia, the next greatest survival threat at sea is the lack of potable water. The human body needs water for survival and the record for survival without water is 11 days. The Royal Navy found that water consumption of 150 mL per day was associated with a 22% mortality over a 6-day period. However, when water consumption was between 150 mL and 450 mL/day, the mortality was 0.6% for the same period.[8] The US Navy recently started putting reverse osmosis units like the Katadyn (Katadyn Group, Zürich, Switzerland) MROD-06-LL and the MROD-35-LL desalinators in liftrafts.[10] These reverse osmosis units squeeze salt water through a semi-permeable membrane fine enough to remove salt and other contaminants. The MROD-06-LL is an extremely small, hand-operated desalinator that provides one liter of fresh drinking water from seawater per hour. The larger MROD-35-LL is a 9-pound hand-operated pump that produces over 4 liters per hour.[10] In order to minimize evaporative loss from sweating in high temperatures, work should only be done during the coolest part of the day (in the early morning and late evening). A full moon may allow work parties to safely work at night. Clothing soaked in seawater can decrease sweating by 83%,[8] but clothing must dry before sunset to avoid heat loss at night.

Body fluids contain approximately 1% saline. The maximum concentration of salts in urine is 2%, half of which is sodium chloride and half urea. Drinking seawater increases the salt concentration in the body fluid, further aggravating dehydration. The only way to get rid of the excess salt is by sacrificing internal water. Additionally, mixing salt water with freshwater does not help because of the obligatory shift from intracellular to extracellular water. Both these scenarios hasten death.[8] Therefore, sailors are advised not to drink seawater or mix it with freshwater. Survivor mortality associated with seawater consumption is given in Table 26-3.

Amphibious Operations

EXHIBIT 26-2

CARE OF SURVIVORS OF VESSELS SUNK AT SEA

Assist survivors out of the water into the rescuing vessel*

- Conscious:

Never leave unsupervised for first 72 h

Prevent postural hypotension

Avoid alcohol consumption

Minimize ambulating to rewarming area

Rewarm survivors by seating them, clothed, under a hot shower, and gradually remove clothing†

- Unconscious:

Maintain the airway

Place under warm blankets after wet garments have been removed

Notes on near-drowning:

60% vomit during resuscitation

Pulmonary edema may occur between 15 min to 72 h after rescue from water

___________________

*During World War II, many sailors were lost when they attempted to climb up the net on the side of the rescue ship. The effort was too great; they fell back into the sea and were lost. Later, lifeboats were lowered and sailors were pulled into them and then hoisted aboard ship.

† There is currently no other accepted therapy for treating hypothermia.

Adapted from: Handbook for Royal Naval Officers. London, England: Ministry of Defense, Medical Directorate General (Naval); July 1981. BR 2193.

Amphibious operations against a defended beachhead are the most arduous and dangerous type of military campaign. On the first day of an amphibious assault, the wounded in action rate can average 62.5 per 1,000 personnel.[9] Amphibious ships have more medical assets and space than other ships to care for the high numbers of expected casualties from marine combat operations. The problem of caring for wounded patients aboard ships is that wounds require surgery, best handled by trained surgeons during the “golden hour” (first hour after injury). When one considers the facilities and personnel required to care for 50 seriously wounded patients, as well as for 100 patients with minor wounds, it becomes apparent that three medical officers with limited equipment, regardless of their talent, will be challenged to provide sufficient care for the high numbers of expected casualties.[11] With time for adequate planning, and support, medical resources can be re-programmed at the fleet headquarters surgeon level to augment an amphibious ship’s medical department to handle the expected number of casualties.9,11

TABLE 26-3

MORTALITY ASSOCIATED WITH DRINKING SEAWATER

Seawater

No. of Life Craft Voyages

No. of Men

No. of Deaths

Died (%)

Drank

29

997

387

38.8

Did Not Drink

134

3,994

133

3.3

Adapted from: Handbook for Royal Naval Officers. London, England: Ministry of Defense, Medical Directorate General (Naval); July 1981. BR 2193.

Casualty management requires advanced planning so mistakes, such as concentrating medical resources in one location, are not repeated. It is critical to consult with medical personnel before casualties are evacuated to ensure adequate medical assets are available at the arrival location. Casualties are triaged so that only those patients who are medically cleared8,9,11 and deemed stable enough to make the trip are evacuated.

Today’s Navy does not have sufficient medical resources dedicated to support amphibious operations. Additionally, with improvements in satellite communication and surveillance, the time it takes to recognize and respond to a threat has decreased dramatically, and the distance at which the US military can successfully intervene has correspondingly increased. Amphibious operations can commence suddenly with little time for the medical department to deploy wartime resources. The capability to launch amphibious operations beyond visual and radar range of the shoreline, also known as “over the horizon,” brings new vulnerabilities. The accelerated pace and depth of modern military capabilities has increased demands on medical support to sustain military operations and to care for casualties from both military and civilian victims of a conflict.[12]

THE MEDICAL DEPARTMENT ABOARD SHIP

The term “medical department” may apply to one person and equipment on a small ship or as many as 70 people staffing a virtual hospital on a large amphibious ship. Regardless of size, the department is obliged to look after its own spaces, the personal needs of its members, and its budget. Every department also has to take a role in ship-wide business, which includes berthing arrangements, watch standing, cleaning passageways and common areas, scheduling meetings, and interacting with all other departments (eg, supply, deck, weapons, and navigation). On some ships, departments also share housekeeping chores such as preparing food, loading supplies, and painting.

Medical department spaces on virtually all ships are confined and constrained. Even on large ships, pipes, valves, and overhead structures intrude into the working spaces of every BDS, creating nooks and corners that are used to brace and store medical equipment. The medical team must familiarize itself with the layout and location of supplies and equipment. A ship overhaul sometimes results in improved medical spaces. Conversely, another department or a naval architect may suggest using medical space for nonmedical purposes. Although the change may benefit the ship’s functionality, the MO must protect the ship’s medical capability and ensure that the CO and executive officer (XO) clearly understand the consequences of any such change.

The Medical Officer’s Line and Staff Roles

As in any military organization, the ship has both line and staff functions. Most department heads are line officers and usually report to the XO, who is second in command, is responsible for the ship’s daily activities, and reports to the CO. Staff officers, such as the lawyer and chaplain, report directly to the CO to provide expert advice in matters that broadly affect the crew across department boundaries. The aggregate volume of directives and policies from higher authority is large, and the topics are frequently so technical that the CO, who is ultimately responsible for compliance, must rely on the department heads and staff officers to implement policy and advise of any shortcomings.

The head of the medical department fulfills both line and staff functions. This chapter refers to this person as the MO; however, an independent duty corpsman may fill the role on small ships. The MO on any large ship serves as the chief of the medical staff, a position that requires medical training beyond residency as well as several years of practice, including hospital experience. The ability to interface with senior officers and other ship commands requires several years in the Navy and at least one prior tour at sea. In this role, the MO serves as a department head, a line officer role who reports to the XO. Although the MO’s daily job is to run the medical department, the role of staff officer and advisor to the CO is often paramount because planning and preventive medicine are more important to the overall health of the command than medical treatment after the fact. The MO serves as the CO’s eyes and conscience in medical matters and can deviate from medical directives when necessary and with the CO’s knowledge. When medical resources fall short of the required standard of care, the MO must convince the CO or higher military authority to take corrective measures. An effective MO develops confidence and mutual trust with the CO and XO.

All actions aboard a ship have medical ramifications, which the MO understands only in the context of (1) the physical threats and stresses involved in naval operations and (2) a thorough knowledge of the ship. The MO must recognize when proposed operations might affect crew health, require extra medical attention, or threaten to exceed medical capabilities, and inform other department heads of these situations. A representative of the medical department is included in all interdepartmental conferences and planning sessions. Although many operational topics are classified or confidential, the MO always has a “need to know.”

Medical staff must interact with their department counterparts for meals, casual conversation, and off-duty activities in order to build trusting relationships. MOs and chief petty officers should visit the bridge and all the ship’s working spaces and observe how others do their jobs. The word “shipmate” denotes an abiding relationship unlike any other. Trust, esteem, reliance, compatibility—ingredients for the deepest kind of teamwork—are necessary to build a place for the medical department among all ship personnel. This process may be especially challenging on a small ship where the head of the medical department is a corpsman and other department heads are officers. In such cases, the corpsman must develop strong relationships with the CO and the XO to gain acceptance by other department heads.

Medical Staffing

The size and composition of the medical staff depends on the number of the crew and the ship’s mission. As a rule of thumb, there should be one independent provider per 800 to 1,000 crew members, but at least one on every ship. On small ships, the sole provider is usually an independent duty corpsman, who is a senior petty officer with a minimum of 6 years of experience as a corpsman followed by a year of intensive medical training. On larger ships with several providers, three-fourths should be physicians. A ship with women onboard needs at least one provider with special skills in gynecological diagnosis.

Every shipboard medical provider needs to be proficient and certified in both Advanced Trauma Life Support[13] and Advanced Cardiac Life Support.[14] Falls, burns, and lacerations are frequent aboard ship and can require endotracheal intubation, emergency cricothyrotomy, insertion of chest tubes, diagnostic peritoneal lavage, and venous cut downs. Smaller ships do not have operating rooms, but larger ships like aircraft carriers and amphibious assault ships are fitted with a full operating room that is staffed by a general surgeon, an oral surgeon, and an anesthesiologist or a nurse anesthetist, as well as a qualified operating room nurse and at least two fully trained surgical technicians.[11]

Ships with continuous air operations and embarked aviation groups of squadron size or larger need a flight surgeon and at least one aeromedical technician. On aircraft carriers and amphibious attack ships, embarked aviation units bring their own flight surgeons. On an aircraft carrier, the senior MO is also an experienced flight surgeon. Destroyer, frigate, cruiser, and auxiliary ships with a one- or two-helicopter detachment rarely have a flight surgeon aboard; aviation personnel must obtain aeromedical services from other elements of the battle group.

An example of the complex organizational relationships aboard ship is the surgical team that usually embarks with an amphibious ready group. Although the surgical team reports operationally to the commander of the amphibious task force, it is administratively assigned to the ship’s medical department. The team’s credentials and privileges are managed by higher military medical authority, but they must also be reviewed and certified for the CO by the ship’s MO.

The hospital ships USNS Comfort (T-AH-20) and USNS Mercy (T-AH-19) have the largest medical capacity of all US Navy ships[15] that can deploy to a theater of operations (Figures 26-9 and 26-10). These hospital ships are as tall as a 10-story building and as long as three football fields. Their primary purpose is to serve as a floating hospital that travels with the fleet; their secondary mission is humanitarian. These ships have a full complement of medical staff including surgeons, anesthetists, operating room nurses, technicians, and preventive medicine and environmental health specialists.[15] In as little as 5 days, these ships can be converted from a skeleton crew into up to a 1,000-bed mobile hospital with a medical and support staff of 1,200.

Figure 26-9. Surgeons operate on a patient aboard the hospital ship USNS Comfort (T-AH 20).
US Navy photo by Photographer’s Mate 1st Class Shane T. McCoy.
Reproduced from: http://www.navy.mil/gallery_search_results.asp?terms=comfort+operating+room&page=3&r=4.

Figure 26-10. Corpsmen monitor heart rates of patients in the intensive care unit aboard the USNS Comfort.
US Navy photo by Photographer’s Mate 1st Class Shane T. McCoy.
Reproduced from: http://www.navy.mil/management/photodb/photos/030423-N-6967M-090.jpg.

Standards of Care

It was once acceptable to expect a lower standard of medical care in arduous, isolated environments such as military deployments or ships at sea than in fixed facilities. Throughout the 1980s, deployable medical systems in the US military were held to a standard called “austere but adequate,” which meant the care was sufficient to preserve life and limb but implied “not quite as in civilian settings but good enough.” Today, state-of-the-art medical care is the only standard acceptable to military patients, the Department of Defense, and the US Congress. The expectation is that injured personnel who survive to reach medical attention will be healed, and that medical or surgical outcomes at sea will match the standards of civilian facilities. However, experienced military medical officers know that this not always possible in the austere environment of a ship at sea.

The ship’s medical department must be able to handle all contingencies that could foreseeably occur during the mission, either by providing definitive care aboard or managing expeditious patient transport to more capable facilities. The medical department must ensure that the training of all medical personnel as well as sanitation and equipment in the medical department meet the standards of any medical facility of similar size at home. The department must be able to treat any illnesses or injuries or expeditiously and safely transport the patient to definitive medical care. If the medical department cannot meet the foregoing conditions, the MO must either take steps to remedy the situation or notify the CO. Although the CO has the authority to decide that military necessity overrides medical care, the MO must be sure the CO understands the potential consequences.

Credentials, Inspections, and Higher Military Medical Authority

The procedures for establishing credentials and delineating privileges for independent providers are the same as onshore and are usually managed by the fleet commander’s medical staff.[11] Although shipboard medical departments do not require accreditation by civilian agencies such as the Joint Commission for Accreditation of Healthcare Organizations, naval inspections at every phase of the ship’s cycle resemble their civilian equivalents and are, in many regards, more stringent.

During shipyard periods, the Navy safety officer at the shipyard conducts frequent surveys of the ship’s working conditions and environmental surveillance programs. Before beginning predeployment readiness exercises, the squadron medical officer and the ship’s medical staff perform medical readiness assessments, which include checking the ship’s medical equipment, storerooms, pharmacy, and condition of the medical spaces, as well as inspecting the crew’s health records and the medical department’s logs and training records. Medical providers on naval vessels must maintain and provide evidence of active state licensure as well as participation in continuing medical education to include basic and advanced life support. During the predeployment period, the fleet training group conducts a specific battery of evaluations and inspections called refresher training. For the medical department, this focuses particularly on how well the crew at large performs in first aid and mass casualty drills, the medical department’s response to medical emergencies, and how well individual members of the medical department know the functions of all of the ship’s other departments. At the end of the predeployment period, after preparation of the entire battle group, the fleet commander’s medical staff conducts a thorough evaluation of all the ships in the battle group, rating the ships medical departments collectively in medical communication, patient transport and evacuation, and emergency preparedness.

Each administrative and operational command has its own medical staff, which periodically sends direction, guidance, and inquiries to the ship. Higher medical authority is expected to route communications through the ship’s command channels. When direct communication occurs by phone or email between the MO and the fleet medical officer, the MO must inform both the XO and the CO of contact with higher medical authority. On those rare occasions when there is disagreement between the ship’s command and guidance from higher medical authority, the MO must explain to their XO and CO the medical rationale for the decision-making. Nonetheless, if the MO cannot persuade the CO to adopt the medical viewpoint, the CO’s decision prevails.

Education and Training for the Ship’s Crew

The fleet or squadron medical officer inspects and evaluates the ship’s medical department on crew performance in first aid and in mass casualty and MEDEVAC drills. Therefore the ship’s MO must ensure that all crew members get training in CPR (cardiopulmonary resuscitation) and the resuscitation of an unconscious victim of electrocution. In addition, all crew members must know how to treat casualties for the “GITMO 8,” a training series which covers treatment of the most common wounds and injuries likely to occur in a major explosion or fire.[16] Victims of these injuries can be saved by fast action; Personnel can use the skills they learn from the GITMO 8 to treat other traumatic injuries. The eight wounds are:

1. sucking chest wound (chest puncture with pneumothorax),

2. traumatic amputation of the hand,

3. maxillofacial trauma with compound fracture of the mandible,

4. abdominal wound with penetration of viscera,

5. compound fracture of the lower leg,

6. smoke inhalation,

7. burns; and

8. electrical shock.

Most ships have a closed-circuit television system, an invaluable way to spread medical and safety information. Many entertaining and understandable videos on medical topics are available. In addition, the MO should frequently have “call in” sessions to discuss current health topics such as the annual influenza vaccinations, illness outbreaks, or health issues in upcoming port calls. Notwithstanding the frenetic work schedule in all ship departments, medical staff should schedule frequent classes with small groups on subjects such as diet, hearing protection, responsible sex practices, prevention of unwanted pregnancy and sexually transmitted diseases (STDs), smoking cessation, substance abuse, and the importance of water consumption while at sea. The medical staff also provides health training for special occupational groups on the ship such as barbers, food handlers, and laundry workers.

PREDEPLOYMENT PLANNING

When a ship leaves the pier, it must have aboard all the medical resources the staff could possibly need throughout the deployment because operations or weather can prevent replenishment efforts. The MO and medical department must train, gather information, and plan well in advance because once the ship is underway, the entire crew works 12- to 16-hour days, with full attention to the daily workload and operational events. General guidance to plan a medical inventory can be found in the International Medical Guide for Ships[2] and the Handbook of Nautical Medicine.[3] In the US Navy, the medical supplies each type of ship requires are listed in the Authorized Medical Allowance List. The minimum required stocks of medical equipment, medicines, and other consumable supplies is large; even for small ships, the list is dozens of pages long and contains thousands of items.

Nearly every action onboard ship carries health and medical consequences, yet line officers who are discussing tactics, weapons systems, or sailing plans may not realize the medical implications of those actions. For instance, certain operations may expose the crew to physiological hazards such as hypothermia and exhaustion, or the ship’s route may impact MEDEVAC. The MO must recognize such problems and insist that other department heads consider this information in military and operational planning phases. The MO must also inform the CO when operational plans exceed the medical department’s capabilities and the consequences of such situations. The CO may either adapt operational plans to reduce medical risks or accept the risks when they are balanced against other considerations. Such difficult decisions can only be made correctly with the MO’s full counsel.

Many deployments involve a number of ships traveling in company. Destroyers or other ships with limited medical departments may be part of a task force that includes larger ships with extensive facilities. Under these conditions, potential interaction among the ships in the group must be carefully planned. Systems for medical consultation and communication should be exercised, as well as methods of patient transfer between ships.

Medical Intelligence

Medical intelligence can be used for both medical and military planning.[17] For medical planning, the MO gathers data about ports or countries the ship will visit. The MO interprets immunization campaign or disease outbreak information to help the operations and intelligence departments understand a nation’s condition and its preparedness for war. This must be done well enough in advance to procure and administer immunizations and plan for such prophylactic measures as antimalarial medications and gamma globulin for protection from hepatitis. Intuitively, it seems that crew members should encounter infectious diseases only during port calls when they are ashore. However, the risk of disease has increased with the frequent use of aircraft for logistics, mail flights, and transport of visitors and replacement personnel. All new arrivals are potential infection carriers because they will have traveled through intermediate countries. In addition, crates and bags of vegetables brought aboard may carry rodents and insects. To take the necessary precautions, the MO must be familiar with endemic conditions in all areas of planned operation.

The main sources of medical intelligence for the Navy are the National Center for Medical Intelligence at Ft Detrick, Maryland, which is oriented toward biological and medical intelligence sources, and the Navy environmental and preventive medicine units, which focus on medical threats and health concerns for naval ships in a specific region. The two sources provide slightly different information. Early in the planning cycle and again immediately before departure, the MO must communicate directly with the Navy environmental and preventive medicine unit nearest the ship’s planned area of operations and ask the theater or fleet medical staffs for information about recent disease outbreaks and epidemiology. Finally, the MO should seek information from medical representatives at embassies and consulates in nations where the ship expects port calls and near passage, although information from State Department sources is often less authoritative than from military sources.

Planning for Medical Evacuation

Every aspect of MEDEVAC must be planned and written into operating procedures before the cruise begins.[12] To begin with, the ship’s medical staff must assess their capabilities and limitations and describe the patients that will need a MEDEVAC in their operating procedures. The MO should review MEDEVAC plans and notify the theater or fleet medical staffs of the ship’s medical capabilities, so they know when to expect a MEDEVAC. All of these issues are then briefed to the CO and strike group commander. The CO must have a clear understanding of the potential risks to patients who may die because a ship’s planned movements will take it beyond the reach of air transportation or shore hospitals so that MEDEVAC is not possible.

Crew Preparation and Screening

The first step in deployment preparation is to medically screen assigned personnel. Ships are hazardous and some people do not belong aboard: in an emergency at sea, one person’s limitations or illness can put many crew members at risk. The Manual of the Medical Department[18] establishes physical and medical standards for sea duty. Vision and hearing are critical to hazard awareness; although hearing aids and eyeglasses may be acceptable, crew members must be able to see well enough under poor lighting conditions to avoid injury while moving about and must be able to hear alarms even while asleep. Crew members must be agile enough to use the narrow passageways and steep ladders that typify military ships. A person with a chronic medical condition can be accepted for a cruise only if the medical department and its staff can manage the condition and its consequences.

Some classes of ships, such as aircraft carriers and amphibious assault ships, carry large numbers of embarked troops. Although they require the same immunizations and preparation as the ship’s company, such troops are seldom available to the ship’s medical department in advance. The MO must therefore arrange details early by communicating with the medical staffs of all commands that will embark troops. It is imperative that the XO or CO participate in this discussion because the ship could be at risk later if the command fails to insist on medical clearance before deployment.

Most military ships today embark numbers of nonmilitary personnel, including dignitaries and journalists on familiarization visits, technical representatives from industry, law enforcement agents, and educators under contract to teach college or vocational courses to crew members. These people, usually civilians, are easily overlooked by the medical department. Although they may not have the same physical requirements as sailors, they should be evaluated for mobility limitations and screened for chronic medical conditions that could lead to emergencies. Coronary artery disease is the most commonly encountered medical condition in this group of civilians.

The medical department must inform the command and entire crew of the need to acquire certain types of personal items well before going to sea. Most important are corrective lenses, medications not in the ship’s formulary, and special clothing items such as shoe inserts or orthotics. These and other items that may be taken for granted at home may be difficult or impossible to obtain once deployed.

Contact lenses are not recommended for use at sea. Dust and fumes aggravate contact lens wearers, and crew members with long duty hours often forget to change contacts as advised, especially the long-wear and soft varieties. Crew members who use contact lenses must bring several pairs of them and sufficient supplies of cleaning and lubricant solutions for the duration of the cruise. Moreover, all crew members who require refraction, even if they use contact lenses, must bring at least two pairs of shatterproof, current prescription eyeglasses. Personnel who are required to wear safety glasses on the job must also bring two pairs. Eye injury treatment can be very limited depending on the size of the ship and medical department staffing.

Personality disorders are a serious cause of problems at sea.19–21 Sailors with antisocial, narcissistic, and borderline type personalities who have acted out or required disciplinary action should be detached from the ship before deployment, because the incidence of suicidal gestures and disruptive behavior is so high among people with significant personality disorders. Unfortunately, these personality disorders are often not recognized until the combination of sleep deprivation, demanding work, and congested living cause enough stress to precipitate calamitous behavior. When such problems occur, the MO must persuade the command that although a personality disorder is not a medical illness, it is evidence of unsuitability for sea duty and that the sailor must be reassigned as soon as possible. A sailor with any prior suicide attempt should not go to sea except with the strongest supportive endorsement by a qualified military psychiatrist, preferably one familiar with sea duty stresses and limitations. Aircraft carriers have psychologists who will take the lead on these cases.

ENVIRONMENT IN THE SHIPYARDS, UNDERWAY, AND AT PORT CALLS

The environment aboard changes in significant ways during the various phases of the ship’s cycle. Although the close spaces, noise, and high trauma risk remain constant, the training, work tempo, maintenance, industrial activities, and food service requirements differ. Predeployment operations allow for training and fine tuning of shipboard systems. In the deployment period, readiness and operations tempo put pressure on the crew and shipboard systems to perform at peak efficiency. This puts pressure on maintenance and operations departments to continue at this high operations tempo for long periods. During the postdeployment yard periods, the crew faces pressure to complete all required maintenance during the scheduled yard period. Crew exposures to heat, noise, dust, asbestos, chemicals, and radiation are markedly increased, which adds to the stress of being in the shipyard.

Traditional occupational and preventive medicine concerns are intertwined on a ship, because the crew lives in the workspace and because the same medical personnel are responsible for both preventive and occupational medicine programs.[22] The medical and safety departments are responsible for most prevention and surveillance programs. For example, a ship may carry an industrial hygienist who is assigned to the safety officer but works closely with both occupational medicine and engineering personnel. The supply and preventive medicine departments share food service responsibilities; the engineering department oversees heat illness prevention, ventilation, and hearing conservation, while preventive and occupational medicine provides monitoring and related equipment, treats illnesses and injuries, and performs record keeping for occupational injuries and illnesses.

Heat and Noise

Engineers are primarily responsible for protecting the crew from heat stress and excessive noise; the medical department treats and monitors these conditions. It is easier to prevent both heat stress and hearing loss than it is to treat them after they have progressed. For instance, acoustical injury can be both cumulative and permanent—and heat stroke can be fatal. Thermal stress is a special problem on ships.[22]

Flight and weather decks may be exposed to severe heat and cold as the ship moves through different climatic zones. Heat, sun, and black painted metal decks often cause problems, which are amplified because all crew members on deck are required to wear protective headgear, long-sleeved jerseys, and flotation vests. The combination of intense work, high temperature, and protective garments causes overheating and dehydration. In addition, the work pace is so high that crew members must be reminded to hydrate; supervisors and corpsmen must frequently monitor flight deck workers to encourage fluid intake and watch for fatigue and signs of overheating.

The most common heat concern is excessive temperature and humidity below decks. Although modern ships have complex ventilation and air conditioning systems that reach most spaces, it is not possible to completely control the climate in engine rooms, galleys, sculleries, and laundries. Galleys are areas of insidious heat stress, with hot appliances and heavy workloads, and sailors work long hours in sculleries with high humidity and heat from hot water and dishwashers. Laundries also require special attention; dryers and pressing machines generate large amounts of heat, and ventilation may be inadequate, especially when equipment has been upgraded or the laundries occupy spaces originally designed for other uses. The operation of large equipment can create high heat loads in adjacent spaces where the work would not otherwise be stressful. For example, the steam catapults on aircraft carriers can raise the temperature and humidity in the layer of spaces immediately below the flight deck, which are occupied by offices, living spaces, and ready rooms.

The first steps in heat injury prevention are appropriate engineering design and insulation, but they can only be accomplished during ship construction or a major overhaul. Ventilation is more tractable and depends not only on fans and ducts but also on open doors, hatches, and scuttles. Under high heat threat conditions, when watertight integrity is required, doors, hatches, and scuttles must be secured, and the resulting decline in air flow can raise thermal stress to dangerous levels. The medical department can help prevent heat illness by visiting all shipboard spaces and seeing that sailors hydrate and avoid physical exhaustion.

Many medical emergencies are the result of heat-related injuries. The medical department is responsible for educating the crew about adequate hydration and heat stress prevention. In the engine spaces and flight decks, water loss can exceed 6 to 8 qt per day, so the importance of water intake must be constantly reinforced to the crew. The final step of heat stress prevention is to restrict exposure. The wet bulb globe temperature index is a measure of heat stress in direct sunlight. Corpsmen use wet bulb globe temperature readings to regulate work in hot environments and protect troops from heat injuries until they acclimate to the temperatures.[23]

Navy crew members can incur cumulative acoustical trauma that leads to hearing loss over many years. Individual hearing protection must prevent hearing loss or prevent the worsening of the condition. Audiograms should be obtained when the sailor first reports to the ship and performed annually thereafter. If the ship does have a sound booth and a hearing technician, then the medical department must schedule the crew for audiograms elsewhere.

Standards for required hearing protection are outlined in the many directives available to medical and engineering departments. Hearing protection is always required in engine spaces, flight decks, hangar decks, and machine shops; both internal and external devices may be necessary in the loudest environments. Crew members are especially at risk of hazardous noise exposure near aircraft platforms.

Isolation and Confinement

The ship environment at sea is, paradoxically, both crowded and isolated. The crew is packed close together without much privacy in living quarters, and they see the same faces during meals and at work. At the same time, people feel isolated because there are few opportunities to communicate with family or friends back home. Time at sea means being away from land, vegetation, and most ordinary diversions. This is especially stressful for young people, many of whom are away from their families and homes for the first time. Common stress reactions include shortness of breath, insomnia, anxiety, depression, panic attacks, and prolonged sea sickness. Bedwetting is less common and headaches usually have other causes. Bedwetting and sleep parasomnias (ie, sleepwalking) are particular conditions that are not conducive to sea duty; materials on psychiatric symptoms and emergencies are useful when dealing with such conditions at sea.20,21

The ship’s command must take measures to minimize psychological problems and to ensure that crew members will recognize stress symptoms in themselves and others. Otherwise, a young sailor who reports to sick call with symptoms and is told that the cause is stress may interpret this response as dismissive. The CO should address the psychological effects of confinement and isolation at captain’s calls and in talks to the crew early in each cruise. Division officers and chief petty officers should bring up the topic early and often at daily muster in quarters.

Recreation and distraction are other ways to fight isolation and confinement. The command must make special efforts to promote vigorous exercise and recreational programs that focus on getting the sailors out of their berthing and working spaces. Most ships, other than submarines or mine sweepers, have decks or flight decks that permit jogging, basketball, and calisthenics. Group sports are valuable and provide vigorous interaction with crew members other than bunk mates or workers from the same shop, although injuries from such activities also cause a significant proportion of lost duty time.[24] Diverse interactions reduce the sensation of being trapped with only a small circle of friends. Movies and television provide views of land, communities, and automobiles, as well as diversion, but they are passive and can keep a sailor in the berthing area when it would be better to get away.

Historically, sailors looked forward to a daily tot of rum or grog, and some navies still allow small amounts of alcohol at mealtime. The US Navy strictly prohibits alcohol, and sneaking it on naval vessels is now quite rare. However, drinking on liberty (shore leave) can be a problem, and alcohol withdrawal can become a medical concern from the second day underway. Alcohol withdrawal must be suspected in sailors with new tremors, autonomic symptoms, insomnia, or seizures in the first few weeks at sea. All ships have an alcohol abuse counselor assigned with special training in recognizing and helping sailors with substance abuse problems. The counselor will identify sailors with potential substance abuse problems and request the MO to rule out other medical conditions including neurologic, endocrine, or psychiatric problems that might explain the sailor’s symptoms.

Epidemiology and Epidemics

Information on epidemiology and methods to track disease outbreaks may be found in the Manual of Naval Preventive Medicine.[22] The CDC Health Information for International Travel[25] is also a useful resource. Military Preventive Medicine: Mobilization and Deployment, Volume 1, is also an excellent resource.[26] The most common outbreaks on ships are food-borne illnesses, respiratory diseases, and skin conditions. Waterborne illness outbreaks are less common and are more likely caused by chemicals than by infectious agents. Any infectious disease outbreak must be reported immediately to the surgeon of the fleet commander and the nearest Navy environmental and preventive medicine unit. Tracking outbreaks begins with a clear diagnosis or at least a detailed description of the symptoms and time course of the index case or cases. It is imperative to confirm that the problem represents physical illness, since in close environments, outbreaks of hysterical somatic complaints can spread rapidly and be just as devastating as physical illness.

Most food-borne outbreaks can be traced to food storage problems, mixing of foods that should be kept apart, and poor hygiene among crew members.[22] The main defenses are good personal hygiene among food workers, clean work spaces and equipment, and proper practices in the storage and serving of foodstuffs. Many ships have hand sanitizer stations, especially at or around the galley and heads. The most common food-borne outbreak symptoms are acute gastroenteritis with cramps and diarrhea. Medical personnel should be able to identify the food items, meal shift, and galley common to affected members by taking a careful dietary history from each crew member. Patients must be adequately hydrated; oral rehydration salts are preferable to intravenous fluids. Antispasmodic medications may help severe cases. It is usually impractical to identify specific bacterial or viral agents aboard ship; if bacterial culturing is available, it may be useful to identify the genera Shigella, Salmonella, or Vibrio, which can require antibiotics for effective treatment. Widespread use of antibiotics among the crew is seldom warranted.

The rapid spread of respiratory illnesses is fostered by closely confined quarters and compromised ventilation aboard ship; respiratory symptoms are among the most common reasons for sick call visits. Harsh contrast zones between cool–dry and hot–humid spaces cause cough and local mucosal irritability, which can be so widespread as to both mimic infectious outbreaks and increase the crew’s vulnerability to them. Although respiratory infections are usually mild and self-limited, influenza and tuberculosis are much feared at sea.[21] Despite the youth of a ship’s crew, it is critical to vigorously enforce annual influenza vaccinations to avoid an epidemic. Secondary prevention of respiratory diseases is relatively ineffective because crew members are usually infectious before symptoms develop. There are often requests for cough suppressants and decongestants or antihistamines, none of which reliably hasten recovery and all of which may have side effects that can be dangerous on a ship. The most important measures are to provide bed rest for as many of the affected crew as possible, encourage high fluid intake, control air conditioning, and prevent cigarette smoke. Medical staff must resist the temptation to prescribe antibiotics to everyone with a cough unless there is good evidence of a susceptible pathogen. An antibiotic-resistant organism in a crew who will work together for the next several months can be more hazardous than delaying diagnosis and antibiotic treatment.

Pests and Vectors

External parasites, insects, and rodents are recurrent problems aboard ships, and their control is addressed in the US Navy Shipboard Pest Control Manual.[27] Scabies, lice, and other external parasites are best prevented by crew education and hygiene. Bathing and laundry standards are most important. Skilled preventive medicine technicians should frequently inspect berthing areas, with special attention to bed linens. There must be a high level of suspicion during sick call; any sailor who complains of itching or other skin symptoms must be disrobed and examined with particular attention to hairy areas and spaces between digits. Whenever a case is detected, the affected individual must be treated immediately and berthed in an isolated area such as the medical ward, if possible. All linen in the berthing compartment must be laundered immediately, and mattresses may need to be discarded.

Cockroaches thrive in the warm, damp areas of a ship and where nutrients are available. Cockroaches are controlled by detection and prevention measures. Traps are used for detection rather than eradication and should be placed and maintained in most heads and all food preparation areas. Storing and eating food in berthing compartments is prohibited and strictly enforced. Standing water and moisture should be eliminated by vigorous cleaning and by venting heads, galleys, and sculleries. Insecticide sprays add a margin of control, but are still only secondary to cleanliness and prevention.

Rodents are a serious problem aboard ships. Rats usually enter a ship in port areas where hiding spaces and litter are abundant. Preventative measures include vigilance at brow walkways and the installation of rat cones on ship’s lines. Since rats can swim, preventive medicine technicians need to work with the deck department and local authorities to inspect the hull at the water line at least daily and preferably several times per day. Both rats and mice live in storerooms. Mice usually enter the ship in store crates, especially those of grain and flour products. All new stores should be inspected for breaks in containers and the presence of droppings. Stores should be stacked and arranged so that inspectors can see all areas where rodents might enter or hide. As with roaches, the main control measure is to deprive rodents of food by careful storage and by confining food and eating to mess decks. Rodents and other vermin are usually eliminated by traps and careful use of poisons. A severe or resistant infestation requires that certified technicians fumigate the area.

Hypoxic Spaces

A ship has many sealed or unventilated spaces that can become hypoxic or can accumulate toxic or explosive gases. For example, stored vegetables consume oxygen, so that whenever a worker goes into a food storeroom, someone must be on watch outside with oxygen breathing apparatus nearby. Crew members are trained to be aware of such hypoxic hazards, but civilian workers in the shipyards may open doors or bolted covers in the course of their work with fatal consequences.

Welding is a hazard that arises during the shipyard phase of the ship’s cycle because it consumes oxygen at a high rate, and compartments where welding is done are often closed to forestall interruptions. Because welding requires a watcher in adjacent compartments in case a fire starts when heat is conducted through a metal bulkhead, the “firewatcher” should also be trained to monitor the welder for signs of hypoxia.

Flight Operations at Sea

Although aircraft carriers and large amphibious ships are well known for their flight operations, many other ships also have flight decks and carry one or two helicopters at sea. All the hazards inherent in military flight operations pertain at sea, including windblast, collisions, fires, and explosions. However, the naval environment aggravates some of these risks.[28] For the flight crew, a failed landing—which runs an aircraft into the grass on land—produces a rapidly sinking metal coffin at sea, since jet canopies are difficult to open and helicopters that land in water invert and sink immediately, owing to the weight of their overhead engines. Jet blast can blow a sailor over the ship’s side, and the fall from the flight deck—30 to 40 ft—can be incapacitating. Pneumothorax from impact, abdominal injuries, and hypothermia should be anticipated from any accident that puts a person in the water. Therefore, the ship’s flight deck personnel must wear survival vests or jackets with a self-inflating mechanism, as well as locator beacons, sea dye markers, and shark repellant.

Although major mishaps with mass trauma and severe burns are a constant concern during flight operations, less dramatic injuries are more common and still dangerous. They include musculoskeletal injuries and fractures, eye trauma, contusions, lacerations, crush injuries, dehydration, and severe sunburn. Chronic fatigue and sleep deprivation can lead to absentmindedness. Medical crews need to be on the deck during flight operations to assist in rescue, and the main medical department assumes a high level of alert. On aircraft carriers and large amphibious assault ships, closed-circuit television allows the main medical department to monitor flight operations for immediate medical response to mishaps.

MEDICAL CARE AT SEA

Sick Call

Sick call is the daily period when the clinic is open for routine visits and treatment. Sick call is far more important on a ship than in other military settings, because minor problems must be treated early to keep them from worsening beyond the ship’s treatment capacity. In addition, sick call provides over-the-counter medications, band aids, and other items a drugstore carries.

Sick call provides the most fundamental means for monitoring the crew’s health. Complaint and injury rates vary with the ship’s type and mission, the climate, the phase of the ship’s cycle, and the time of year. During high operational tempo, sailors are less likely to frequent sick call for minor problems. At these times, members of the medical staff must walk through all work spaces to assess fatigue levels and target those who need treatment. Special efforts to encourage fluid intake are also necessary. The “sick list” is a daily report to the CO and XO that includes the number of sailors treated and their diagnoses. One of the most common sick call “prescriptions” is a note or “chit” recommending light duty or rest. Although the sailor’s division officer or chief petty officer often honors such a chit, it is only a recommendation.

On most ships, sick call is open two or three times each day to accommodate working and sleeping schedules. Patients are usually seen first by junior corpsmen; a standard operating procedure details treatment for specific problems and lists those complaints that require a physician’s or senior corpsman’s attention. The MO must train the medical staff to appropriately triage the sick patients for conditions that need a higher level of care and to avoid turning away truly sick crew members. On large ships, many sailors gather at the clinic door for sick call and form a line that extends down the passageway. Medical department corpsmen should quickly screen complaints and see the most sick patients first, while others are given appointment times to return to the clinic. Crew members who need follow-up visits are asked to return after the second group. This allows crew members to stay at work and avoids long lines of patients outside the clinic.

Privacy is hard to provide on a ship but is essential in sick call. It is necessary to have a sign-in method that allows sailors to state their medical complaints where others cannot hear, and the sign-in log must not be visible to other patients. Because most sailors are reluctant to discuss medical history or emotional topics if they can be overheard, there must be a consultation room with a door that can be closed. Sick call is a haven for sailors who need sympathy or respite; they should feel that they can trust “the docs”—a term used for corpsmen as well as physicians—to provide a sympathetic ear as well as prompt treatment. Knowing that even minor aches and pains will be taken seriously and treated in a private, dignified manner is important to young people who have few distractions aboard ship and can be prone to worry about physical problems.

Some sailors come to sick call so often that they win a reputation as slackers or “sick bay commandos,” and it is important for the medical staff to avoid becoming cynical or hardened to these sailors. When a large number of hypochondriacal complaints appear, it may well be the sign of a morale problem that is as important to the command as a physical illness outbreak. A physical illness may cause subtle symptoms for some time before it is evident on physical examination or laboratory tests. A patient who is dismissed or becomes discouraged at the first visit to sick call may not return until the illness worsens. Most importantly, crew members must trust the medical department if they are to be forthcoming about medical histories and feel confident at times of emergency or personal crisis. While the medical department’s goal is to return sailors to work and discourage hypochondriasis, it is far better to tolerate “sick bay commandos” than to build a reputation for skepticism or insensitivity.

Disposition of the Sick Sailor

The MO at sea must consider proper patient treatment in the context of both occupational and military requirements. To determine whether a sick or injured sailor can return to duty, the MO often visits the sailor’s work area to better understand the nature of the job and workspace. Additionally, the MO considers the long work hours that accompany sea duty along with sleep deprivation and fatigue, which impair recovery. Bed rest, or “sick in quarters,” is the oldest and most reliable treatment for many ills. The value of rest and repeat examination cannot be overemphasized for cases of nonspecific illness. Crew members with fever or general weakness, or who require intravenous fluid for any reason, should be berthed in the medical ward when possible. On some ships, the sick bay does not have ward beds or the number of patients exceeds berthing. Any sailor who is confined to sick in quarters status should have an attendant from the same department and berthing area. Medical personnel should visit the patient several times a day to record vital signs.

The maximum period a sick sailor can be kept on the ship is established by the theater evacuation policy and the ship’s own predeployment plan. Even the most sophisticated medical department lacks the diagnostic capability of a hospital ashore, and an illness that eludes diagnosis or a sailor who cannot return to duty can be demoralizing to the crew, deprives the crew of a useful member, and consumes important resources. Medical staff must not allow indecision to tempt them into keeping a sick sailor beyond the predetermined time limit.

Telemedicine

Experience shows that corpsmen and young physicians do not seek consultation as often as they should, and they should be taught that consultation not only improves treatment but can also prevent unnecessary patient transfers and evacuations.29,30 Voice communication is the first level of consultation among medical departments in a battle group. Even when a ship is steaming independently, satellite communication often allows consultation with physicians or specialists on distant ships or at major shore facilities. Procedures for medical communication may be specified in predeployment plans or arranged at need.

Satellite television transmission for medical use is available on an increasing number of ships. While the consultant cannot touch or palpate patients, the ability to interview them and see facial expressions adds great value. These medical systems can transmit electrocardiograms and include appliances for auscultation as well as otoscopic and ophthalmoscopic examinations. The image allows very good dermatological diagnosis and visualization of endoscopy. Also, many medical departments have an issued digital camera and can email jpeg images to specialists for review. These diagnostic steps can take place in real time to assist the isolated medical provider, even in emergencies.

Medical Evacuation

The best way to transfer a patient is from a pier. Because all forms of transportation at sea incur risk, and most are rough compared to land transportation, evacuation at sea is viable only when predetermined medical criteria are met, consultation and telemedicine have been fully exploited, and the transport risks are outweighed by the patient’s needs.

In years past, transfer at sea was by Stokes litter or boatswain’s chair on high-tension cable strung between ships. While Stokes are still ubiquitous on ships, the present stretcher of choice is the Reeves Sleeve (HDT Expeditionary Systems, Fairfield, VA). Today, patient transport at sea is usually by helicopter. Most military ships have landing areas; if not, the helicopter can hover over the deck and winch the patient aboard in a litter cage. However, the latter process is terrifying for most patients and can be a rough ride, so it should be used only when no other transport is available. When the patient can wait long enough for evacuation, the medical department contacts the fleet’s medical regulating officer, who arranges for the best treatment facility, transportation, and itinerary. The possibility of a long stay, further transport, or even reassignment is predictable, so all medical and personnel records accompany the patient at the time of transfer.

Safety is the first consideration in preparing a patient for transport. A medical escort who is adequately trained in water survival must accompany the patient to provide in-flight care. The patient must wear a survival vest, preferably one that does not require inflation. An ambulatory patient should walk aboard the aircraft and strap in like any other passenger. Litter patients must be secured with straps that permit quick release in an emergency. Tubes for fluids or oxygen must not dangle where they can become entangled, and intravenous fluids and blood must be contained in plastic bags without air pockets. If the patient could not survive a crash or water landing at sea, then the transfer should be reconsidered.

Most patients sick enough to warrant evacuation should have supplemental oxygen, since even a low-altitude helicopter flight can drop the partial pressure of oxygen too low for a patient with blood loss or compromised pulmonary function. The medical escort should watch the patient wearing an oxygen mask for vomiting and aspiration. A pneumothorax must be vented through a chest tube attached to a flutter valve or other mechanism to prevent backflow. Neither inflatable casts nor military antishock trousers can be used because they will expand in flight.

Port Calls

The MO reviews local disease surveillance reports long before the ship approaches any port of call.[13] An advance party usually visits the port to handle diplomatic issues and arrange docking and replenishment. The advance party should include a medical representative; if that is not possible, the MO must consult with members of the advance party to ensure they gather the necessary information. General epidemiological information must be updated with particular attention to the following:

- current outbreaks of disease;

- incidence of tuberculosis, arthropod-borne diseases, malaria, hepatitis, and STDs;

- occurrence of any disease with antibiotic-resistant organisms;

- the capabilities and standards of local hospitals;

- local water purification standards;

- food and restaurant sanitation standards; and

- incidence of recreational drug use in the area.

Before allowing sailors to go ashore, the chief petty officer or division officers of every department brief their members. These briefings must include persuasive remarks about malaria prophylaxis, warnings about food and waterborne illnesses, and safe sex practices. Unless the MO is satisfied with food safety and potable water supplies, the crew is advised to avoid eating or drinking in the local economy and to take bottled water from the ship.

In areas with significant malaria risk, the MO should persuade the CO to either select an alternate port for rest and recreation or keep the crew aboard the ship. Crew members who are required to go ashore for operational reasons must follow strict measures to prevent malaria, including the use of insect repellant, long-sleeved garments treated with permethrin, mosquito nets when it is necessary to sleep ashore, and rigorous adherence to malaria chemoprophylaxis.[31] Because chloroquine-resistant malarial strains are spreading over the world, it is essential that the MO review current information.

On arrival in port, the MO must visit the nearest hospital to which crew members will be referred, if necessary. In this visit, the MO can assess the standards and capabilities of local medical practice and establish the method of payment for medical treatment ashore. The MO must also explain the ship’s requirements and limitations to local providers so they will not overestimate the medical facilities and return sailors to the ship who should have been treated at the hospital.

Most STDs are contracted on shore. Sexual relations among crew members are forbidden. Educational programs that encourage abstinence, monogamous relations, and barrier (condom) protective measures are still the best ways to prevent STDs.

Special Medical Concerns Aboard Ship

Conditions aboard ship place many medical issues in a special context. The increasing numbers of women stationed aboard ships mean that medical departments must provide advice and care in areas of gynecology and obstetrics. The availability of highly capable, fully staffed operating rooms aboard large warships not only improves the level of available care, but also obligates staffs to provide colposcopy and other services for women. As shipboard medical environments adapt, there may be reason to reevaluate the propriety of performing elective surgery aboard instead of transferring patients to onshore hospitals. Other concerns include the implementation of a “walking blood bank” to support emergency transfusions at sea and the proper disposal of medical waste in an era of concern over protecting ocean ecology.

Medical Care of Women

Women have served on auxiliary US Navy ships as integrated members of the crew since 1978 and began serving aboard combat ships in 1994. The ability of a ship’s medical staff to provide obstetrical and gynecological care must be consistent with the general level of medical and surgical care. The sole provider or corpsman should have knowledge regarding differential diagnosis, the effects of hormonal cycles, pregnancy hazards, diagnosis of pelvic pain and pelvic infections, and when consultation and transport are necessary. Larger ships with at least one physician—especially if more than 200 women are on the ship—should also have a provider such as a nurse practitioner who has specialized training in the care of women. Ships with personnel capable of performing abdominal operations must have at least one provider aboard who is trained in colposcopy and vaginal ultrasound.

From the medical planner’s standpoint, the primary issues concerning women’s healthcare are:

- the availability of personal hygiene items (a supply department issue with health implications) and direction on how to properly dispose of them at sea;

- privacy for medical history taking, screening programs, and examinations;

- staff competence and proficiency in reproductive and routine gynecological care;

- equipment for appropriate gynecological examinations and procedures; and

- contraception and pregnancy.

Contraception should always be a concern for male crew members, but the personal significance and medical consequences of contraception are much greater for women.

Present US Navy policy permits women to remain assigned to sea duty for the first 20 weeks of pregnancy, as long as they remain within 6 hours of definitive gynecological, surgical, and obstetrical care. This limitation reflects the risks of spontaneous abortion and hemorrhage from ectopic pregnancy during the first 20 weeks.32,33 The rule permits pregnant women to remain aboard on deployments in the Mediterranean and Caribbean, within several hundred miles of most coasts, and worldwide when assigned to a hospital ship. During the first 20 weeks, a pregnant woman should be able to perform her ordinary job, although women who do considerable bending and heavy lifting may need some duty modifications because they are at increased risk of musculoskeletal strain. A pregnancy more advanced than 20 weeks requires the sailor to be transferred ashore.

Babies should not be delivered on naval ships; however, women have been able to conceal pregnancy for many months, and some have gone into labor at sea. Therefore, on any ship that has women aboard, at least one member of the medical department should be competent to perform a vaginal delivery, including a low-forceps delivery, if necessary. Ships with an operating room should have a physician who is able to perform a cesarean section. Neonates cannot be properly managed on a military ship, so if a baby is delivered, the ship must return to port as soon as possible to disembark the mother and child at the pier. Evacuation by helicopter is a distant second choice, owing to difficulties with keeping an infant warm, performing resuscitation en route, and ensuring survival at sea in case of an aircraft mishap.

Elective Surgery

Many surgical operations are well within a large ship’s capabilities, which carries a competent operating room, a qualified surgical staff, and modern anesthesia. Emergency operations that can be performed include appendectomy, repair of an acute or strangulated inguinal hernia, resection of perforated bowel, and a number of other urgent procedures. However, performing elective surgery is not recommended, particularly when the ship is within reach of a hospital.[34] This is because even the best medical department at sea lacks the capability of a hospital to deal with complications. On the other hand, the surgeon must practice to maintain skills through exercises. The debate over elective surgery continues because both sides have strong arguments; however, a fatality during elective surgery aboard ship is intolerable. Despite the great challenge to maintain surgical skills aboard ship, elective procedures should be delayed until they can be scheduled in a hospital on shore.

Competence for Duty Examinations

Sometimes a supervisor observes unusual clumsiness or poor work performance and suspects the sailor is physically impaired because of some form of misconduct or dereliction such as alcohol consumption, drug use, or late night activity. The supervisor may bring the sailor to the medical department for a formal examination to determine competence for duty. The formal examination is not a medical diagnosis and treatment, but rather a legal requirement for disciplinary or personnel action. Such an examination should be performed only on written order of the CO or a duly designated officer in the sailor’s chain of command. The MO is expected to perform a clinical examination and state whether the crew member is physically able to perform duties. The MO will obtain blood and urine tests to check for alcohol intoxication, presence of drugs, and other incapacitating substances.

Depending on the ship’s operating tempo, sleep deprivation may be another explanation for poor duty performance. The MO should order only those laboratory tests that are necessary to formulate a clinical conclusion. For example, if the sailor appears to be drunk and smells of alcohol, then a diagnosis of intoxication can be made without ordering a blood alcohol test. The MO may ethically provide a professional opinion as legal evidence, but the medical department does not perform legally binding blood alcohol or drug screens, and medical staff must not be placed in the role of investigators or enforcement agents.

Mass Casualty Situations

A mass casualty event is one in which the number and severity of injuries exceeds the medical department’s capacity to care for them, so that response requires coordination throughout the ship and rationed care for the injured.[7] Although civilian triage is performed to preserve as many lives and limbs as possible, on a military ship the overarching goal must be to save the mission or perhaps the ship itself. Therefore, the priority is to return the greatest possible number of injured to their duties in order to keep the ship afloat and in action. All crew members assigned to moving or treating patients must thoroughly understand this rationale.

A mass casualty situation requires immediate removal of the injured from the scene to a clear area where they can be laid out for quick evaluation and triage. At the triage station, casualties receive initial first aid measures such as intravenous lines, pain medication, and dressings. Some of the injured who receive adequate first aid may be released directly from triage for return to duty. However, it is imperative that all patients are tracked and accounted for at all times.

Coordination is critical in any mass casualty situation. A senior member of the medical department must move immediately to damage control central (the station center where damage control is coordinated) to determine the best locations for triage, a staging area if required, and the main medical treatment site or BDS. These decisions must be coordinated from damage control central because it has the best information about the state of the ship; areas that have been damaged; and routes for moving patients when many doors, passageways, and hatches are secured for general quarters. Members of the medical department must know how to use sound-powered telephones, which use wire strung during the emergency, to bypass damaged communications and power systems. In addition, runners must be designated in advance from among the litter bearers; in case of complete communications failure, they carry messages, questions, and information among the triage, staging, and treatment sites and to damage control central.

Corpses

The disposition of human remains aboard ship is frequently misunderstood. Planning and a firm understanding of issues regarding human remains is important; if a death does occur, responsibilities and processes should be clear. The medical specialists complete the death certificate, ensure medical records are maintained properly, and ensure autopsy reports are completed accurately in a timely fashion. In operational and doctrinal terms, however, a human body is no longer a patient at the time of death. The management and transport of corpses is the responsibility of the supply officer who will arrange for the disposition of the body. The MO should direct all questions regarding body disposition procedures and inventory of coffins, refrigerators for corpses, transport boxes, and body bags to the supply officer.

The Blood Bank

A modern blood bank is simply not available at sea except on hospital ships and sometimes on large amphibious attack ships. Even carrying supplies of Type O, Rh negative blood is impractical for technical and logistical reasons. Artificial blood products that rely on human hemoglobin show progress but have not yet been approved by the US Food and Drug Administration for clinical applications. Severe blood loss at sea can only be treated by using blood donated by crew members. The term “blood bank” refers to a group of prescreened, registered crew members who volunteer that have a known blood type and Rh status and agree to give blood for emergency blood transfusions at sea.

Personnel in the blood bank are screened annually for syphilis, hepatitis B and C, HIV (human immunodeficiency virus), and tuberculosis. In addition to the blood testing, a medical history should be taken to exclude crew members who had malaria, leishmaniasis, or other blood-borne disease. A blood smear and complete blood count with differential should be obtained to exclude personnel with blood dyscrasias and hemoglobin variants such as sickle cell trait, thalassemia minor, or glucose-6-phosphate dehydrogenase deficiency.

Blood collected from crew member donations does not meet the standards of safe blood found in modern medical centers. For example, there is always a risk that a donor has acquired a pathogen such as hepatitis or HIV between the last set of tests and donation. While these risks may be unacceptable in any hospital in the United States, the situation is different underway. Blood donated by crew members is the only immediate source of large quantities of replacement blood when it is essential to preserve life and limb. Blood collection procedures must be rehearsed periodically while at sea.

Disposal of Medical Waste

In the past, ships disposed of all trash and refuse at sea; currently, only that which is biologically degradable and harmless to ocean ecology and the sea floor is thrown over the ship’s side. No plastic is disposed at sea and great efforts are made to limit the amount of plastic that is even allowed aboard. The Navy is concerned with how to limit the amount of, and how to handle, the seven classes of waste aboard ships:

1. human elimination products, which pass through commodes and sinks into the ocean at sea or into holding tanks in port;

2. garbage and food waste, which are thrown into the sea and can be safely devoured by marine life;

3. degradable trash, such as some paper, which is incinerated or dissipated safely into the ocean;

4. metal and other recyclable material, which must be stored and brought to shore for proper disposition;

5. hazardous materials, such as paint, chemicals, batteries, some plastics, and expired medications, which are stored and disposed of ashore by authorities or certified agents;

6. medical waste that contains specific medical and biological material, certain medicines, spent needles and scalpels, and all tissues, which are held in designated medical spaces until released to capable disposal agencies; and

7. infectious waste or material, which requires special handling by the medical department.

SUMMARY

A ship’s organization, physical structure, and specific mission form its working environment. In turn, a ship’s medical department is configured and staffed to meet the needs of a specific ship and its mission. Life at sea is demanding, and the ship environment often leads to preventable injuries and illnesses. A ship’s MO works with other department heads to emphasize injury prevention and precautions. The MO serves dual line and staff roles. The line function involves running the medical department; the staff function involves informing and advising the CO and XO concerning medical aspects of military planning and the crew’s overall health and morale.

Medical care aboard ship should meet the highest standards of practice. The MO is frequently inspected by higher medical authority within the Navy. When planning for deployment, the MO must know the medical capabilities of each deploying ship and its staff. The MO should also have familiarity with and access to deployment planning resources. Before departure, the crew is screened for acute and chronic medical conditions and receives necessary immunizations. Common medical problems that occur while underway include fatigue, psychological stress, food-borne illness, respiratory disease, and skin conditions. The MO can use sick call rates to monitor the health and well-being of the crew. Medical personnel may recommend light duty or bed rest for sick sailors, or these patients may be admitted to sick bay. Anyone who remains ill beyond a predetermined time limit must be transferred to a more capable medical facility.

Shipboard medicine has adapted to recent changes such as the inclusion of women on combatant ships. Basic gynecological care and the capability to deliver a baby, if required, is available on most ships. Large ships have true operating rooms and carry surgical staffs and intensive care facilities. Telemedicine has made it easier for the MO to consult with subject matter experts in the field when the patient has difficult-to-diagnose conditions. The surgical staff remain medically active through humanitarian missions, during port calls, and through coordination with other ships to address surgical needs. The medical department must take the lead in preparing the ship’s crew for drills and mass casualty exercises. Other issues include the proper handling and disposition of corpses, the organization of blood donations, and arrangements for the proper disposal of medical waste.

ACKNOWLEDGMENTS

The author thanks Timothy Mallon, MD, Professor, Uniformed Services University of the Health Sciences, Bethesda, Maryland, for assembling the tables and providing the figures and legends in this chapter.

REFERENCES

1.   Riley T. Shipboard medicine. In: Pandolf KB, Burr RE, eds. Medical Aspects of Harsh Environments, Volume 2. Washington, DC: Borden Institute; 2002: Chap 29.

2.   World Health Organization. International Medical Guide for Ships, Including the Ship’s Medicine Chest. 3rd ed. Geneva, Switzerland: World Health Organization; 2007.

3.   Goethe WHG, Watson EN, Jones DT, eds. Handbook of Nautical Medicine. New York, NY: Springer-Verlag; 1984.

4.   DiGiovanna T, Rosen T, Forsett R, Sivertson K, Kelen GD. Shipboard medicine: A new niche for emergency medicine. Ann Emerg Med. 1992;21(12):1476–1479.

5.   Cooper RR. Medical support for the fleet. Nav War Coll Rev. 1990;43(3):43–54.

6.   Smith AM. Any navy can go to war alone, but staying there is another thing. Navy Med. 1990;81:9–15.

7.   Sherman SR; Herman JK, interviewer. Flight surgeon on the spot: Aboard USS Franklin 19 March 1945. Navy Med. 1993;84(4)4–10.

8.   Handbook for Royal Naval Officers. London, England: Ministry of Defense, Medical Directorate General (Naval); July 1981. BR 2193.

9.   Blood CG. Shipboard and Ground Troop Casualty Rates Among Navy and Marine Corps Personnel During World War II Operations. Washington, DC: Naval Medical Research and Development Command, DoN; 1990. Report 9016.

10.   Sparks M. Abandon ship! Prepare to die!: How the US Navy lives in denial and is not ready for combat. Life Support International, Inc website. http://www.combatreform.org/USNAVYINDANGER/abandonshippreparetodie.htm. Published 2005. Accessed September 30, 2017.

11.   Surface Warfare Medicine Institute. Fleet Medicine Pocket Reference, 2010. Falls Church, VA: Bureau of Medicine and Surgery, Department of the Navy; 2010. http://www.med.navy.mil/sites/nmotc/swmi/documents/fleetmedicinepocketreference2010.pdf. Accessed October 5, 2017.

12.   Llewellyn CH, Smith AM. Tactical and logistical compromise in the management of combat casualties: There is no free lunch! Nav War Coll Rev. 1990;43(1):53–66.

13.   Committee on Trauma, American College of Surgeons. Advanced Trauma Life Support Program for Physicians: Instructor Manual. 9th ed. Chicago, IL: ACS; 2013.

14.   Cummins RO, ed. ACLS Provider Manual. Dallas, TX: American Heart Association; 2001.

15.   Hospital Ships–T-AH. US Navy fact file. http://www.navy.mil/navydata/fact_display.asp?cid=4625&tid=200&ct=4. Updated March 15, 2017. Accessed January 8, 2018.

16.   Department of the Navy. Standard First Aid Course. Washington, DC: DoN; NAVEDTRA 13119. 2003. https://www.scribd.com/document/7822299/US-Navy-Course-NAVEDTRA-13119-Standard-First-Aid-Course. Accessed October 6, 2017.

17.   Beebe GW, DeBakey ME. Battle Casualties: Incidence, Mortality, and Logistic Considerations. Springfield, IL: Charles C Thomas; 1952:20–22.

18.   US Navy Bureau of Medicine and Surgery. Manual of the Medical Department. Church Falls, VA: BUMED; 2012. NAVMED P-117.

19.   Hourani L, Warrack G, Coben PA. A Demographic Analysis of Suicide Among US Navy Personnel. San Diego, CA: Naval Health Research Center; 1997. NHRC-97-30. http://www.dtic.mil/dtic/tr/fulltext/u2/a335283.pdf. Accessed September 30, 2017.

20.   Clancy G; adapted and revised by Bakalar NL. Emergency Psychiatry Service Handbook. Washington, DC: Department of the Navy; 1998.

21.   US Navy Bureau of Medicine and Surgery. General Medical Officer Manual. Falls Church, VA: BUMED; 2000. NAVMED P-5134.

22.   US Navy Bureau of Medicine and Surgery. Manual of Naval Preventive Medicine. Falls Church, VA: BUMED; 2004. NAVMED P-5010.

23.   Pandolf K, Burr RE, Wenger BC, Pozos RS, eds. Medical Aspects of Harsh Environments, Volume 1. In: Zajtchuk R, Bellamy RF, eds. Textbook of Military Medicine. Washington, DC: Borden Institute; 2001.

24.   Krentz MJ, Li G, Baker SP. At work and play in a hazardous environment: injuries aboard a deployed US Navy aircraft carrier. Aviat Space Environ Med. 1997;68(1):51–55.

25.   Centers for Disease Control and Prevention. US Public Health Service. Health Information for International Travel 1999–2000. Atlanta, GA: CDC; 1999.

26.   Kelley PW, ed. Military Preventive Medicine: Mobilization and Deployment, Volume 1. In: Zajtchuk R, Bellamy RF, eds. Textbook of Military Medicine. Washington, DC: Borden Institute; 2003.

27.   Department of the Navy. US Navy Shipboard Pest Control Manual. Washington, DC: Navy Disease Vector Ecology and Control Center. Bureau of Medicine and Surgery, DoN; 2000.

28.   Society of US Naval Flight Surgeons. US Naval Flight Surgeon’s Handbook. 2nd ed. Pensacola, FL: SUSNFS; 1998. http://www.operationalmedicine.org/Library/Manuals/Flight%20Surgeon%20Handbook/FSH97.html. Accessed September 30, 2017.

29.   Nice DS. US Navy medical communications and evacuations at sea. Mil Med. 1987;152(9):446–451.

30.   Stoloff PH, Garcia FE, Thomason JE, Shia DS. Cost effectiveness analysis of shipboard telemedicine. Telemed J. 1998;4(4):293–204.

31.   US Navy Bureau of Medicine and Surgery. Navy Medical Department Pocket Guide to Malaria Prevention and Control. Church Falls, VA: BUMED; 2007. Technical Manual NEHC- TM 6250.1. http://www.public.navy.mil/surfor/Documents/6250_1.pdf.

32.   Means-Markwell M, Hawkins R, Reichow K, et al. A survey of women’s health care needs on US Navy ships. Mil Med. 1998;163(7):439–443.

33.   Garland FC, Garland CF, Gorham ED. A model of the expected occurrence of adverse pregnancy outcomes aboard US Navy ships. Mil Med. 2000;165(9):691–697.

34.   Fontana M, Lucha P, Snyder M, Liston W. Surgery aboard ship: Is it safe? Mil Med. 1999;164(9):613–615.

Chapter 27

DEPLOYMENT SURVEILLANCE

RAÚL ALEXANDER MIRZA, DO, MPH*; ELISABETH M. HESSE, MD, MTM&H†; AND COLEEN BAIRD, MD, MPH‡

INTRODUCTION

CONSEQUENCES OF THE PERSIAN GULF WAR

DEPLOYMENT SURVEILLANCE TODAY

Documenting Exposures

The Periodic Occupational and Environmental Monitoring Summary

DATA REPOSITORIES

The Defense Occupational and Environmental Health Readiness System

Department of Defense Serum Repository

Defense Medical Surveillance System

PASSIVE DEPLOYMENT MEDICAL SURVEILLANCE: MEDICAL SITUATIONAL AWARENESS IN THE THEATER

ACTIVE DEPLOYMENT MEDICAL SURVEILLANCE

Disease Reporting System-internet

Postdeployment Health Surveys

Theater Medical Information Program

Deployment Environmental Surveillance Program

Modeling

DEPLOYMENT SURVEILLANCE DURING A UNIQUE MISSION: THE EBOLA OUTBREAK

CHALLENGES IN DEPLOYMENT SURVEILLANCE

SUMMARY

*Major, Medical Corps, US Army; Division Chief, Occupational Medicine Division, US Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010-5403

† Major, Medical Corps, US Army; Division Chief, Disease Epidemiology Division, US Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010-5403

‡ Division Chief, Department of Environmental Medicine, US Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010-5403

INTRODUCTION

The Persian Gulf military campaigns of the early 1990s, Operations Desert Storm and Desert Shield, shined a spotlight onto the Department of Defense (DoD) public health programs dedicated to addressing deployment exposures and associated health outcomes of deployed service members and veterans. Media reports and personal testimonies of syndromic illnesses and disease conditions rose throughout the decade. However, the impacts of deployment exposures and related illnesses were not unique to the Persian Gulf War. Ongoing health effects, physical and nonphysical, are a poignant legacy of any military campaign. In this regard, the public health toll of military conflict is not truly known at the time each deployment ends.

CONSEQUENCES OF THE PERSIAN GULF WAR

Historically, the DoD placed general public health and preventive medicine emphasis on food and water safety, arthropod-borne diseases, endemic infections, and other communicable diseases with the potential to negatively impact deployed forces. Emphasis included providing and managing resources and capabilities needed to support base and expeditionary forces. For example, deployment preventive medicine personnel assessed and provided recommendations for exposures to heat and cold. If such recommendations were not taken, heat injuries (eg, heat stroke or heat exhaustion) or cold injuries (eg, frostbite or chilblains) may predictably have occurred. As another example, water evaluation and treatment in deployed settings mostly focused on chlorine disinfection. Without such preventive measures, diarrheal and infectious diseases such as dysentery and salmonella caused significant disease outbreaks. In the past, soldiers were trained to conduct industrial operations so that hazards were minimized and appropriate personal protective equipment was worn. However, after the Persian Gulf War, with its many potential environmental exposures, such as oil well fire smoke, pesticides, chemical warfare agents, and particulate matter, as well as reports of veterans experiencing various health issues, the DoD increased its focus on capturing environmental exposure data for service members both during and after deployments.[1]

Health symptoms are commonly reported following armed conflicts. Symptoms have included fatigue, shortness of breath, headache, sleep disturbances, forgetfulness, and impaired concentration,2,3 and the etiologies of these problems have remained largely undefined. Concerns over potential wartime exposures have risen as well. The US military deployed Agent Orange, a blend of tactical herbicides sprayed in the jungles of Vietnam in the 1960s, to remove trees, mangroves, and dense tropical foliage that provided enemy cover.[4] In subsequent years and in the decades that followed the Vietnam conflict, veterans suffered cancerous diseases and other health problems.[5] It wasn’t until 1991 that the US Department of Veterans Affairs (VA) began linking certain illnesses to Agent Orange.[4]

The National Academy of Sciences conducted a review of the scientific and medical literature concerning Agent Orange and other herbicides exposure and possible health effects as required by Public Law (PL) 102-4, the Agent Orange Act of 1991.3,6 The academy sought to demonstrate a statistical association between health outcomes and herbicide exposure, identify the risk of developing adverse health outcomes following herbicide exposure, and identify mechanisms of action or evidence of a causal relationship between health outcomes and herbicide exposures. The National Academy of Sciences committee faced great difficulty in their epidemiological review, given the scarcity of quantifiable exposure information. Hence, cohort reconstruction, dose estimation, and the ability to address causality were not fully achieved from substantiated data.[3]

Today, the VA maintains a presumptive policy that postulates an association between specific symptoms and conditions with exposure to Agent Orange if the veteran meets legitimizing criteria.[6] Yet, even considering the costs and problems associated with Agent Orange exposure in Vietnam, it was not until after the Persian Gulf War that the DoD heightened efforts to identify potential environmental exposures to service members and the adverse health outcomes they may cause.

By June 13, 1991, the ground war was considered a victory and the last US service members who supported the Persian Gulf War returned home.[7] Disease and injury rates were very low in comparison with other conflicts, and the low rates were attributed to successful preventive medicine efforts. Nonetheless, over 60,000 service members, veterans, and their families eventually sought medical evaluation as part of medical registry programs developed after the Persian Gulf War.8–10

In December 1991, PL 102-190, the National Defense Authorization Act for Fiscal Year 1992, as amended, served as the first of many congressional forays into the area of assessing deployment-related exposures and their potential health consequences. PL 102-190, section 734, required the secretary of defense to establish and maintain a registry of service members who were exposed to the fumes of burning oil in Operation Desert Storm.[11]

In response to PL 102-190, the US Army Environmental Hygiene Agency developed a database and public website where Persian Gulf War veterans could request or look up potential exposures to and health risks from oil well fire emissions. This was the first time a service member could estimate his or her individual exposure based on environmental sample data and modeled exposure data.[1]

In November 1992, Congress recognized that other potential hazards and environmental factors may have led to the medical problems of some Persian Gulf War participants. In response, PL 102-585, section 704, directed the DoD Persian Gulf Registry to expand and include any other member who served in Operation Desert Storm.[11] The Office of the Secretary of Defense, Office of the Special Assistant for Gulf War Illnesses, stood up GulfLINK, established in August 1995, to provide online access to Persian Gulf War medical, operational, and intelligence documents from 1990–1991. Its purpose was to provide service members, veterans, and interested persons with information regarding health effects of those who served in the Persian Gulf War.[12]

In the years following the Persian Gulf War, multiple expert boards and committees studied veterans of the war and the health consequences of their service.8,10,11,13–17 The Institute of Medicine and the Presidential Advisory Committee on Gulf War Veterans’ Illnesses noted that the formalized registries established by the DoD and the VA served an important purpose but were not designed to answer epidemiological questions.9,10,13,14 The Presidential Advisory Committee noted that the current scientific evidence did not support a causal link between the symptoms and illnesses reported by Persian Gulf War veterans and known environmental exposures.[9] It was noted that very little personalized exposure information was available. Defining relevant control groups and obtaining data for them were very difficult, and the lack of exposure data limited even the most expert and well-funded investigations to identify health outcomes linked to specific environmental exposures or risk factors.[9] The Government Accounting Office noted that without accurate exposure information, further epidemiological research on the risk factors or potential causes for veterans’ illnesses may result in little return.[15] Even now, in the many years following Operation Desert Shield and Operation Desert Storm, uncertainty remains regarding the link between potential exposures, health risks, and adverse outcomes in the 697,000 deployed US troops.

DEPLOYMENT SURVEILLANCE TODAY

Documenting Exposures

A major limitation of all epidemiological studies to date has been the lack of detailed exposure data. Every committee reviewing the Persian Gulf War has recommended that broad-based exposure and outcome data be collected on all future deployments. Health surveillance is the ongoing, systematic collection, analysis, and interpretation of data derived from instances of medical care or medical evaluation, and the reporting of population-based information for characterizing and countering threats to a population’s health, well-being, and performance.[16] Deployment encompasses all activities from origin or home station through destination, specifically including the continental United States, inter-theater, and intra-theater movement legs, staging, and holding areas.[17] The Institute of Medicine recommended “a single, uniform, continuous and retrievable electronic medical record for each service person. The uniform record should include each relevant health item (including baseline personal risk factors, every inpatient and outpatient medical contact and all health-related interventions).”[14] Although this system does not yet exist, progress has been made to move this vision forward.

The history of compensating veterans for health issues emanating from military occupational exposures is extensive. Obtaining and understanding individual exposures through objective sampling and analysis during operational conditions such as contingency and expeditionary missions has been logistically difficult for the military. Making the association between a deployment exposure and a health outcome is not straightforward. This was certainly true in the case of personnel who served in the Persian Gulf War. The absence of data for Persian Gulf War exposures believed to have resulted in veterans’ health problems prompted the DoD, following the Persian Gulf War, to expand its efforts to collect and document battlefield exposures, track operational movement, and periodically survey service members’ health status. A first attempt was implemented in Bosnia during Operations Joint Endeavor and Joint Forge. Efforts matured in the wake of policies and investments in equipment, training, software, and skilled personnel.

In the years following Operations Joint Endeavor and Joint Forge, occupational and environmental health deployment exposure data were documented in various reports and stored in multiple databases, many of which were restricted or included limited content. Exposure data was summarized in various documents by deployment location and through proprietary formats depending on the DoD service collecting the exposure data and preparing the reports. Further, some of the limited exposure reports were used for inclusion into the service member’s medical record using an overlay of Standard Form 600, Chronological Record of Medical Care. However, there was no standardization among these documents when considering format, content, analysis, and conclusions. Eventually, the Army and Navy determined that inclusion of exposure documents in individual medical records was inappropriate because the information only broadly estimated population-based exposures and potentially associated health risks. The deputy assistant secretary of defense (force health protection and readiness), the proponent for DoD Instruction 6490.03, Deployment Health (2006),[18] directed the development of a multiservice exposure monitoring summary as a solution to these problems.

The Periodic Occupational and Environmental Monitoring Summary

The Periodic Occupational and Environmental Monitoring Summary (POEMS) became the multiservice document to implement DoD’s interpretation of occupational and environmental health exposure information for deployment sites. Deployment sites include, but are not limited to, regions of combat operations, peacekeeping, deterrence operations, disaster relief, and humanitarian assistance. The POEMS describes conditions at base camps, airports or airbases, seaports, forward operating vicinities, forward operating bases, and so on. The POEMS yields a broad assessment of potential short-term (acute) and long-term health effects that may be experienced by personnel at a particular deployment site, based on the hazards known to exist at that site.[1]

The POEMS addressed the requirements within DoD Instruction 6490.3, Implementation and Application of Joint Medical Surveillance for Deployments (1997); DoD Instruction 6055.05, Occupational and Environmental Health (2008); and Joint Chiefs of Staff Memorandum MCM 0028-07, Procedures for Deployment Health Surveillance (2007).17–19 The DoD Joint Environmental Surveillance Work Group developed a standard template for the POEMS. The work group included representation from the offices of the deputy under secretary of defense, the deputy assistant secretary of defense, the Joint Staff, the US Central Command, and the service surgeons’ offices.

The POEMS is the responsibility of the combatant commander but is authored and edited by technical specialists from the service-specific surveillance centers (specialized deployable teams and units, the Army Public Health Center, the Navy and Marine Corps Public Health Center, the US Air Force School of Aerospace Medicine) who assess data and attribute the potential health risks. These analysts comb through information from field observations, reports, sampling results, and known geographic and endemic conditions. The information within the report is typically unclassified.

Service members, veterans, and the doctors who care for them are the primary audience of the POEMS. The environmental surveillance data and the summaries of associated health risks contained in the POEMS are population-based assessments. Occupational and environmental health surveillance data do not reflect individual exposures, and the resultant risk assessments are not predictive of any future health outcomes for an individual within the population at the site. Rather, the POEMS is a tool to assist clinicians in addressing patient concerns and in developing differential diagnoses or identifying diagnostic procedures for observed health outcomes that they believe may be related to prior or current environmental exposures.

Service members also have access to the POEMS to help them understand any health risks from potential occupational and environmental exposures. The exposures may be listed on their predeployment and postdeployment screening questionnaires. The POEMS may also be used to address various congressional inquiries. The POEMS are posted on a publicly accessible (login and password required) DoD database, the Deployment Occupational and Environmental Health Surveillance (DOEHS) data portal.[20]

DATA REPOSITORIES

While the POEMS captures population-based assessments of deployment sites, it does not provide individual-level data. Data are collected at every step of the deployment process, from the first predeployment medical examinations through each movement and medical encounter in theater, until after the final postdeployment medical assessments are completed. While these encounters are not primarily designed for medical surveillance, the data that they generate can be used to provide a more complete picture of an individual’s exposures and outcomes. These data are collected in the repositories described below.

The Defense Occupational and Environmental Health Readiness System

The Defense Occupational and Environmental Health Readiness System–Industrial Hygiene (DOEHRS-IH) is a comprehensive, automated information system that provides a single point for assembling, comparing, using, evaluating, and storing occupational personal exposure information, workplace environmental monitoring data, personal protective equipment usage data, observation of work practices data, and employee health hazard educational data. DOEHRS-IH provides a definition, collection, and analysis platform to generate and maintain a service member’s Individual Longitudinal Exposure Record, a joint DoD/VA initiative to create a complete record of service members’ exposures over the course of their careers. DOEHRS-IH describes the exposure assessment, identifies similar exposure groups, establishes a longitudinal exposure record baseline to facilitate postdeployment follow-up, and provides information to enable exposure-based medical surveillance and risk reduction. Stakeholders include the following:

- the Navy, Air Force, Army, and Marine Corps;

- the Military Health System;

- line components;

- DoD functional community working groups, the DoD Industrial Hygiene Work Group, and the Joint Environmental Surveillance Work Group;

- service chief information officers and functional representatives;

- the Defense Logistics Agency;

- the US Army Veterinary Command; and

- the National Nuclear Security Agency.

The DoD recognizes the importance of linking environmental hazard data with unit locations and works closely with the VA to provide exposure data to adjudicate disability claims as required. Since 1991 the DoD has implemented programs and policies to better address the health protection of deployed service members for both acute and latent or chronic health conditions that may result from environmental health hazard exposures. Occupational and environmental health assessments are conducted at base camps soon after they are established to document baseline monitoring of the air, water, and soil for hazardous agents. In addition, annual (or periodic) occupational and environmental monitoring summaries are completed at major deployment locations to identify any changes in occupational and environmental health exposure risks and associated health implications. Exposures of concern are promptly investigated, and if there is a likelihood of latent or chronic health effects, special medical surveillance programs are established, such as in response to the chromium exposures at the Qarmat Ali Industrial Water Treatment Plant in Iraq. When appropriate, exposure registries are created for a specific event, as conducted in response to the Operation Tomodachi, Fukushima Nuclear Power Station, Japan, accident in spring 2011.

The Individual Longitudinal Exposure Record will create exposure registries based on location, date, time, and exposure agent, supporting contemporary benefits claims as well as retrospective studies. This concept will assist service members and veterans in verifying whether their disabilities were caused by their military service. Exposure alone does not always lead to illness or injury; the VA relies on scientific evidence to determine when there is a link between exposure to environmental hazards and specific illnesses or injuries that would make service members or veterans eligible for VA disability benefits.

Department of Defense Serum Repository

The DoD Serum Repository was established in 1989 to store serum that remained following mandatory HIV testing in the Army, Navy, and Marine Corps. Air Force samples were added in 1996. In 1997, the DoD began mandating an HIV test and the associated collection of a serum sample both within 1 year before deployment, and within 30 days after redeployment. These paired sera samples can be queried for seroconversions to infectious diseases encountered during deployment, as well as biomarkers and signs of environmental exposures. In addition, the serum samples are tied to relevant demographic, occupational, operational, and medical information, which are useful for epidemiologic analysis.

Defense Medical Surveillance System

The Defense Medical Surveillance System, operated by the Armed Forces Health Surveillance Branch, is a relational database including data on service members throughout their careers in the military since 1990. The system receives and integrates standardized data from multiple service and DoD sources worldwide, including medical events such as hospitalizations, outpatient visits, reportable diseases, HIV results, and health risk appraisals; personal demographic characteristics; and military and operational experiences of all Army, Navy, Air Force, and Marine personnel over their military careers. There are now more than 200 million rows of data regarding more than 6.5 million service members in the online database.

PASSIVE DEPLOYMENT MEDICAL SURVEILLANCE: MEDICAL SITUATIONAL AWARENESS IN THE THEATER

Surveillance of any type, including medical surveillance, can be defined as either active or passive. Active surveillance involves asking someone to provide specific information, such as filling out reportable disease reports or special surveys. Active surveillance is time and labor intensive because it requires someone to do something they would not otherwise do in the course of their regular duties. Passive surveillance is much more common. It is less time and labor intensive than active surveillance because it is simply the gathering of data that were collected for other purposes. The tradeoff is that because the data were not collected specifically for surveillance, it is more likely to be incomplete or not able to fully answer all of the questions that need to be answered.

Medical Situational Awareness in the Theater (MSAT) is an example of passive surveillance. It is a web-based application available through the DoD Secret Internet Protocol Router Network (SIPRnet), which in 2010 replaced a legacy product, the Joint Medical Workstation. MSAT provides medical decision support and a common operating picture by combining information from multiple sources, such as the electronic health record, personnel movement and location records, medical logistics, and biosurveillance systems. While none of these systems were set up for the specific purpose of providing overall medical situation awareness to Joint Task Force commanders’ medical staff, their integration provides a more complete picture in a more timely and less labor intensive manner than requiring individuals at each location to provide separate medical situation reports.

ACTIVE DEPLOYMENT MEDICAL SURVEILLANCE

Disease Reporting System-internet

After the H1N1 influenza pandemic, the disease epidemiology program of the then-US Army Public Health Command determined that the Reportable Medical Events System, in use at the time, lacked the flexibility, completeness, and timeliness to effectively monitor and report disease information. Therefore, the web-based Disease Reporting System-internet (DRSi) was designed to be web-based, be more cost-effective, and employ joint-service technology solutions. All preventive medicine assets within fixed medical treatment facilities transitioned to DRSi by the beginning of fiscal year 2011. By policy, all medical treatment facilities must enter all armed forces reportable medical events into DRSi within 24 hours. Armed forces reportable medical events, selected and defined by the consensus of a tri-service panel, are those determined to represent an inherent and significant threat to public health and military operations. Although most armed forces reportable medical events are infectious diseases and match those required by the Centers for Disease Control and Prevention and the Council of State and Territorial Epidemiologists for reporting at state and national levels, there are a few, such as cold and heat injuries, that are more specific for military populations.[21]

Postdeployment Health Surveys

In fiscal year 2000, the Armed Forces Health Surveillance Branch assumed the DoD mission of receiving, tabulating, and archiving all completed predeployment and postdeployment survey forms. The Pre-Deployment Health Assessment is primarily a medical screening tool ensuring that the deploying service member is medically fit for that particular deployment and has been prescribed all needed medications and vaccinations. The Post-Deployment Health Assessment is completed by redeploying service members within the first week of redeployment. The Post-Deployment Health Reassessment is completed between 90 and 180 days following redeployment. Both of these post-deployment surveys include general questions about symptoms and exposures that may have been encountered during deployment. They are primarily tools to be used to connect redeploying service members to medical services. Unfortunately, they are unsuitable as passive surveillance tools because their design was determined to be inadequate for supporting epidemiological research; data has demonstrated that recall bias and misclassification occur frequently.[22]

Theater Medical Information Program

The Theater Medical Information Program was included in PL 105-85, the National Defense Authorization Act for Fiscal Year 1998, which identified the requirement for a system that assesses the medical condition of active, reserve, and Guard members of the armed forces during deployment outside the United States. The requirements included accurate records of service members’ medical conditions before deployment, as well as any changes in their medical condition during deployment. The Theater Medical Information Program is also designed to address many functional areas, including medical logistics, blood management, and medical threat and intelligence.

Deployment Environmental Surveillance Program

In July 1996, the then-US Army Center for Health Promotion and Preventive Medicine established the Deployment Environmental Surveillance Program to serve as a single point of contact for deployed occupational and environmental health surveillance. The goal of the program is to meet continuing requirements and recommendations regarding exposure information during deployment, a necessity following the concerns about unknown exposures during the Persian Gulf War.7,9,13,14,23,24 Its mission is to develop a system capable of providing pertinent information needed by commanders and other decision-makers to detect, assess, and counter environmental and occupational hazards. Today, the Deployment Environmental Surveillance Program is staffed by environmental scientists, engineers, health risk assessors, and geographers, and it is provided additional support from occupational medicine physicians, industrial hygienists, entomologists, health physicists, chemists, and epidemiologists assigned to the technical programs throughout the current Army Public Health Center (Provisional).

The current primary functions of the Deployment Environmental Surveillance Program are analyzing deployment occupational and environmental health surveillance data and producing information on ways of detecting, assessing, and countering environmental health risks during deployments. The program provides consultative assistance, laboratory analyses, and on-site environmental surveillance to deployed preventive medicine assets to identify, prevent, and reduce potential environmental health risks. Program staff also perform spatial and temporal analysis of potential environmental and occupational exposures and health risks using geographic information systems. This information is integrated with health outcome data to identify necessary changes in medical threat assessment and countermeasures. Finally, archives of environmental and occupational hazard data collected by deployed units allow investigations of any future adverse health outcomes following a deployment.

Modeling

The National Center for Medical Intelligence and the Armed Forces Health Surveillance Branch use sophisticated modeling software and predictive algorithms to identify and analyze disease threats and exposure-related health risks, accounting for geographic region, climate, seasonality, and vector presence. This type of modeling is supported by service-specific public health organizations to plan strategies, for example, clinical predeployment prophylaxis measures for preventing and mitigating expeditionary and deployment-related communicable and endemic diseases. Results from these analyses are used to assist military public health officers, military commanders, and medical personnel to plan deployment medical packages. Additionally, the results enable these personnel to focus on interim deployment medical surveillance for syndromic illnesses and conditions that are not captured through straightforward reportable medical event reports. Reliable exposure modeling requires adequate and pertinent data; highly trained and experienced people; sophisticated computer hardware and software; and time.[25]

DEPLOYMENT SURVEILLANCE DURING A UNIQUE MISSION: THE EBOLA OUTBREAK

The Ebola virus disease (EVD) outbreak in western Africa between 2013 and 2016 was one of the most expansive and deadliest epidemics in the modern era. As of June 2016, the epidemic resulted in 28,616 confirmed, probable, and suspected EVD cases.[26] An EVD case was characterized by fever and malaise and included nonspecific symptoms such as myalgia, headache, vomiting, and diarrhea. Of those with EVD, 30% to 50% developed the hemorrhagic form resulting in multiorgan failure and subsequent shock or death.[27] EVD was widespread, impacting large parts of Guinea, Liberia, and Sierra Leone, among other countries. It resulted in unprecedented modern social disruption, humanitarian needs, and death. As of June 10, 2016, there were 11,300 fatalities.[26]

The DoD, in support of the US Agency for International Development, made critical contributions against EVD, including the deployment of uniformed personnel to Monrovia and Liberia as part of Operation United Assistance (OUA).[28] The DoD joined a global initiative including local and regional ministries of health, the World Health Organization, the Centers for Disease Control and Prevention, and others collaborating to conduct investigations, coordinate contact tracings, implement controls, administer and manage treatment, and promote prevention measures. In addition to those deployed as part of OUA, the DoD successfully trained 1,539 healthcare workers and support staff, formed 30-member medical support teams for short-term assistance to medical professionals, erected 10 DoD EVD treatment units, stood up a 25-bed Monrovian medical unit, operated 7 mobile laboratories, and contracted the procurement of 1.4 million sets of personal protective equipment.[28] As of 2016, OUA cost $402.8 million, including direct support, research and development (eg, vaccine development), and cooperative threat reduction (eg, biosurveillance and biosecurity).[28] Nearly 3,000 personnel were deployed to western Africa at the peak of the epidemic.[29]

The DoD established predeployment training requirements for personnel in OUA. The predeployment training, an example of occupational health primary prevention, was developed as a tiered approach based on exposure risk assessments of the probable conditions to be encountered by personnel supporting OUA.[30] Tier I consisted of universal training required for all deployers and included education on the basic EVD process, transmission, symptomology, avoidance awareness, donning and removal of personal protective equipment, and daily symptom and temperature screening. Tier II outlined requirements for personnel expected to interact with the local populace. Tier III was for personnel assigned to medical units or expected to handle remains. Lastly, Tier IV training was required for personnel supporting laboratory testing.[30]

On the ground, commanders, leaders, and troops were required to conduct daily surveillance for specific symptoms experienced by their personnel over the interim 24-hour period and refer those with symptoms to sick call.[31] Further, onsite clinical operational personnel conducted routine drills for the management and aeroevacuation of EVD casualties. Ground personnel were responsible for performing logistical activities in accordance with published guidance on protocols to prevent transmission of infectious disease during the decontamination of equipment, decontamination of personnel transport vehicles, and execution of site waste management.32–34

DoD clinical and aeromedical support to OUA included contingency operation plans for EVD exposure casualties, with guidance for the screening, management, and evacuation of individuals presenting at or having been transferred to their facilities or vehicles following travel to a country with widespread Ebola virus transmission. Further, the guidance included procedures for environmental cleaning, waste management, and updated infection control protocols. For example, the US Military Hospital–Kuwait developed an occupational health screening program that was risk stratified according to Centers for Disease Control and Prevention definitions of EVD exposure risk. The surveillance program included twice daily temperature checks, as well as symptom screening over 21 days following the last day of potential exposure. Positive screens warranted removing personnel from the hospital’s direct patient care and communal work environment, isolation for further evaluation, and as needed, clinical management. Furthermore, the hospital updated infectious control policies for percutaneous or mucocutaneous exposure to blood or body fluids.

Active surveillance for confirmed, probable, and suspected EVD cases was conducted through the DRSi, by telephone to the US Army Public Health Command, and through procedures stipulated by local public health departments. Clinical Ebola specimen submission and testing on patients was coordinated with the medical treatment facility laboratory, the preventive medicine department, and the appropriate state or local public health departments. Surveillance for changes to soldier health continued even after the mission concluded in western Africa. In the 30 days before or after returning to the United States (the redeployment period), troops were required to complete the Post-Deployment Health Assessment and undergo debriefings and training for the recognition and reporting of clinical symptoms. Troops were also required to complete the Post-Deployment Health Reassessment 90 to 180 days after return to their home duty station.

CHALLENGES IN DEPLOYMENT SURVEILLANCE

Deployment surveillance efforts continue to mature and provide better information regarding deployment exposures and outcomes. This data-driven approach is broadening the concept of operational health support from the recognition and treatment of injury and disease as it occurs to analyses that take place after samples have been collected, analyzed, archived, and evaluated for association with measured outcomes. Ideally, the results of samples and measurements taken on deployments are available in a timely fashion so that preventive measures to reduce exposure can be taken when warranted; however, this is not always possible.

The ability to measure exposures and ultimately evaluate them with respect to delayed health effects raises questions, such as what should be sampled, how frequently, and to what limit of detection. Many of these questions can be reasonably resolved utilizing a combination of intelligence, professional judgment, and common sense, but there are still numerous unknowns in terms of exposures, outcomes, and dose and temporal responses.

Complicating matters in military populations, it is necessary to account for competing exposure risks and mission requirements. What is considered an acceptable exposure may be debated and is sometimes adjusted based on the requirements and details of each mission. For the commander on the ground, environmental exposures add complexity to the process of managing competing risks. Army commanders are currently trained to manage risk in accordance with Field Manual 100-14, Risk Management, which applies a probability and severity of health outcome matrix to specific hazards.35,36 Obvious catastrophic events such as a release of highly toxic materials have severe health risks, although the probability of such a release may be estimated as very low. The commander can mitigate risk by selecting troop locations with regard to proximity and plume direction from industrial facilities. However, exposure to low ambient levels of chemicals may cause delayed health effects or produce little obvious and measurable impact on the immediate mission, although the probability of occurrence is likely higher. Even with immediate monitoring information, uncertainties relating to actual health impact make decision-making difficult.[37]

For some hazards, guidance for acceptable levels of occupational exposure exist but may not be applicable for extended work shifts or the continuous exposures possible in deployed settings. Screening levels derived for application in risk assessment to represent “no adverse effect levels” for the general population are not suitable because they are meant to protect sensitive members of the population for lifetime exposures and utilize very conservative assumptions at each step of the derivation. These screening levels may be suitable as a basis for determining whether or not a remedial action should be considered, but do not serve as a useful threshold to predict the frequency or magnitude of a health effect. There may be no health effects, or they might be subtle and not discernable without specific, tailored, outcome-based medical surveillance. Without such surveillance, specific outcomes might be identified only after weeks, months, or years. A time lag between measurement and available results has affected the usefulness of monitoring on recent deployments. Because of the time lag, monitoring data may not be utilized in a preventive sense to reduce exposure but may still raise questions with respect to significance and prognostic interpretation for those exposed once the reports are written. This raises questions regarding the value of such information for any purpose other than after-the-fact epidemiological analysis.2,10,23,38

In 1997, the Government Accounting Office reviewed Gulf War illness analytic efforts and emphasized the need for accurate, dose-specific information beyond simply measuring the presence or absence of exposure when low-level or intermittent exposure is possible.[15] With current technology, this would require continuous monitoring of a broad range of low-level hazards during deployments, as well as a large enough population with frequent enough outcomes to identify a trend in dose-response. Further, adequate information on confounding variables would need to be collected. Identifying such confounding variables prior to deployment may be difficult without knowledge of which exposures or outcomes will be a concern and subject to analysis. Specific information would also be required at the individual level. Adequate predeployment baselines on conditions or symptoms would be necessary to establish the critical chronological relationship. Current predeployment questionnaires are too simple to capture these data, although the proposed seamless medical record may alleviate this problem.

In May 2015 the US Government Accountability Office published a report following the examination of

(1) the extent to which the military Services centrally store occupational and environmental health surveillance (OEHS) data and verify its reliability; (2) how, if at all, the DOD identifies potential occupational and environmental health risks for sites in Iraq and Afghanistan, and to what extent these risks are mitigated; and (3) the extent to which DOD and VA use occupational and environmental health surveillance data to address post-deployment health conditions.[35]

For the report, the Government Accountability Office reviewed and analyzed DoD and military service policies and interviewed DoD, military service, and VA officials, as well as groups representing service members and veterans. The Government Accountability Office found inconsistencies between the DoD and service-specific policies regarding occupational and environmental health surveillance data storage. This conclusion is supported by the fragmentation and duplication of exposure data held within the DOEHRS and the military exposure surveillance library. Further, DoD’s policy did not address quality assurance of occupational and environmental health data. The assessments stored in the DOEHRS and the military exposure surveillance library include recommended countermeasures; however, the extent to which they are being implemented is unclear because combatant commands do not require forward-deployed base commanders to document their decisions and actions on implementing them. Another limitation underpinning the limited usefulness of the occupational and environmental health surveillance data is the inability to capture deployment exposure data at the individual level. This has rendered it difficult to establish a causal link among deployment exposures and health outcomes.[39]

SUMMARY

The Institute of Medicine has determined that military deployments, especially in Vietnam and the Persian Gulf, demonstrate that health consequences of participation in military action arise and continue long after the deployment ends. Evaluating these concerns and providing healthcare to those who have been affected is challenging to both epidemiologists and medical caregivers. Although the DoD and the military services have developed policies resulting in occupational and environmental health surveillance data capturing and reporting systems, much work needs to be done to improve data quality and usability. However, no system can be expected to address every unanticipated research issue. Even in the face of these challenges, the DoD takes seriously the recommendations of objective panels and reviews, and accepts the challenge of implementing them. The military proactively assesses potential deployment-related exposure threats to the health and safety of its service members. This is done amid a broadening spectrum of occupational and environmental health concerns, ranging from acute injury as a result of combat operations to possible influences of low-level chemical and physical exposures on chronic diseases that might manifest years later, perhaps long after cessation of military service. This is especially true as forces are increasingly used for worldwide operations other than war, including humanitarian assistance and nation-building missions. While debate is ongoing regarding the scope and appropriate level of concern for deployment exposures as a basis for decision-making, current monitoring affords US troops more varied and sensitive sampling of their environment than any working population in the world.

ACKNOWLEDGMENT

The authors thank Dr. Joel C. Gaydos, MD, MPH, FACOEM, for his extensive knowledge on the history of deployment medical surveillance and for all of his reviews and edits.

REFERENCES

1.   US Army Public Health Command (Provisional). The Periodic Occupational and Environmental Monitoring Summary (POEMS)—History, Intent, and Relationship to Individual Exposures in Health Outcomes. Aberdeen Proving Ground, MD: DA; 2009. Technical Information Paper 64-002-1110.

2.   Hyams KC, Wignall FS, Roswell R. War syndromes and their evaluation: from the US Civil War to the Persian Gulf War. Ann of Intern Med. 1996;125(5):398-405.

3.   Weese CB. Gulf War Syndrome: questions, some answers, and the future of deployment surveillance. In: Somani SM, Romano JA Jr, eds. Chemical Warfare Agents: Toxicity at Low Levels. Boca Raton, FL: CRC Press; 2001: Chap 9.

4.   Stellman JM, Stellman SD, Christian R, Weber T, Tomasallo C. The extent and patterns of usage of Agent Orange and other herbicides in Vietnam. Nature. 2003;422(6933):681-687.

5.   Frumkin H. Agent Orange and cancer: an overview for clinicians. CA Cancer J Clin. 2003;53(4):245-255.

6.   Compensation, Veterans Exposed to Agent Orange. US Department of Veterans Affairs Website. http://www.benefits.va.gov/compensation/claims-postservice-agent_orange.asp. Updated July 13, 2017. Accessed July 27, 2017.

7.   Presidential Advisory Committee on Gulf War Veterans’ Illnesses, Special Report. Washington, DC: US Government Printing Office; 1997. http://www.gulflink.osd.mil/gwvi/. Updated November 17, 1997. Accessed July 28, 2017.

8.   Gray GC, Hawksworth AW, Smith TC, Kang HK, Knoke JD, Gackstetter GD. Gulf War veterans” health registries. Who is most likely to seek evaluation? Am J Epidemiol. 1998;148(4):343-349.

9.   Presidential Advisory Committee on Gulf War Veterans’ Illnesses: Final Report. Washington, DC: US Government Printing Office; 1996.

10.   Institute of Medicine, Committee on the Department of Defense Persian Gulf Syndrome Comprehensive Clinical Evaluation Program. Evaluation of the U.S. Department of Defense Persian Gulf Sydrome Comprehensive Clinical Evaluation Program. Washington, DC: National Academy Press; 1996.

11.   Gulf War Rev. 2001;9(4):1–8. https://www.publichealth.va.gov/docs/gulfwar/gw_newsletter_aug01.pdf. Accessed September 22, 2017.

12.   GulfLINK. Office of the Special Assistant for Gulf War Illnesses. http://gulflink.fhpr.osd.mil/. Accessed August 3, 2017.

13.   Institute of Medicine, Committee to Review the Health Consequences of Service During the Persian Gulf War–Medical Follow up Agency. Health Consequences of Service During the Persian Gulf War: Initial Findings and Recommendations for Immediate Action. Washington, DC: The National Academies Press; 1995.

14.   Institute of Medicine, Committee to Review the Health Consequences of Service During the Persian Gulf War–Medical Follow up Agency. Health Consequences of Service During the Persian Gulf War: Recommendations for Research and Information Systems. Washington, DC: The National Academies Press; 1996.

15.   US General Accounting Office. Gulf War Illnesses: Improved Monitoring of Clinical Progress and Reexamination of Research Emphasis Are Needed. Washington, DC: National Academy Press; 1997. GAO/NSIAD-97-163 Gulf War Illnesses.

16.   US Department of Defense. Comprehensive Health Surveillance. Washington, DC: DoD; 2012. DOD Directive 6490.02E.

17.   Goldfein S. Procedures for Deployment Health Surveillance. Washington, DC: Joint Chiefs of Staff, Office of the Chairman; 2007.

18.   US Department of Defense, Under Secretary of Defense for Personnel and Readiness. Deployment Health. Washington, DC: DoD; 2006. DoD Instruction 6490.03.

19.   US Department of Defense. Occupational and Environmental Health (OE). Washington, DC: DoD; 2008. DoD Directive 6055.05.

20.   US Army Public Health Center. Military Exposure Surveillance Library [database online]. Washington, DC: USAPHC; 2017. https://phc.amedd.army.mil/TOPICS/ENVIROHEALTH/HRASM/Pages/MESL.aspx. Accessed September 22, 2017.

21.   Armed Forces Health Surveillance Center. Armed Forces Reportable Medical Events Guidelines and Case Definitions. Falls Church, VA: Defense Health Agency; 2017.

22.   Brix K, O’Donnell FL. Panel 1: medical surveillance prior to, during, and following potential environmental exposures. Mil Med. 2011;176(7 Suppl):91-96.

23.   Defense Science Board. Report of the Defense Science Board Task Force on Persian Gulf War Health Effects. Washington, DC: Office of the Under Secretary of Defense for Acquisition and Technology; 1994.

24.   Green GM, Gordis L, Bingham E, et al. The Persian Gulf experience and health. JAMA. 1994;272(5):391-396.

25.   Gaydos J, Kreiss K. Discussion summary: exposure characterization—questionnaires and other tools. In: Baird CP, Harkins DK, eds. Airborne Hazards Related to Deployment. Fort Sam Houston, TX: Borden Institute; 2015: Chap 29.

26.   World Health Organization. Situation report: Ebola virus disease. http://apps.who.int/iris/bitstream/10665/208883/1/ebolasitrep_10Jun2016_eng.pdf?ua=1. Published June 10, 2016. Accessed August 21, 2016.

27.   Dixon MG, Schafer IJ. Ebola viral disease outbreak—West Africa, 2014. MMWR. 2014;63(25):548-551.

28.   US Department of Defense. DOD Helps Fight Ebola in Liberia and West Africa. http://archive.defense.gov/home/features/2014/1014_ebola/. Accessed August 4, 2017.

29.   Bray R, Pemberton M, Hourani L, et al. 2008 Department of Defense Survey of Health Related Behaviors Among Active Duty Military Personnel. Research Triangle Park, NC: Research Triangle Institute; 2009.

30.   Chairman of the Joint Chiefs of Staff. Ebola Virus Disease Pre-Deployment Training. Washington, DC; 2014. CJCS Notice 4210.

31.   US Army Pubic Health Command. Daily health checklist for leaders, West Africa. https://phc.amedd.army.mil/PHC Resource Library/DailyHealthChecklist.pdf. Published September 26, 2014. Accessed August 4, 2017.

32.   US Army Public Health Command. Decontamination of Equipment Used in the Area of Operations (AO) Impacted by Ebola Virus Disease (EVD). Aberdeen Proving Ground, MD: USAPHC (Provisional); 2014. Technical Information Paper No. 13-032-1014.

33.   US Army Public Health Command. Decontamination of Vehicles Used for Transportation of Potential Ebola Virus Disease (EVD) Patients or Related Equipment. Aberdeen Proving Ground, MD: USAPHC (Provisional); 2014. Technical Information Paper No. 13-031-10142014.

34.   US Army Public Health Command. Controlled Monitoring Site Waste Management. Aberdeen Proving Ground, MD: USAPHC (Provisional); 2014. Technical Information Paper No. 13-035-1114.

35.   US Department of Army. Risk Management. Washington, DC: DA; 1998. Field Manual 100-14.

36.   Hill AB. The environment and disease: association or causation? Proc R Soc Med. 1965;58(5):295.

37.   National Research Council, Board of Environmental Studies and Toxicology, Commission on Life Sciences. Strategies to Protect the Health of Deployed U.S. Forces, Assessing Health Risk to Deployed U.S. Forces, Workshop Proceedings. Washington, DC: National Academy Press; 2000.

38.   Institute of Medicine, Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides. Veterans and Agent Orange: Update 2002. Washington, DC: National Academies Press; 2003. https://www.nap.edu/catalog/10603/veterans-and-agent-orange-update-2002. Accessed 27 July, 2017.

39.   Draper DA, Anderson B, Andresen A, et al. Defense Health Care: DOD Needs to Clarify Policies Related to Occupational and Environmental Health Surveillance and Monitor Risk Mitigation Activities. Washington, DC: US Government Accounting Office; 2015. GAO-15-487.

Chapter 28

EXPLOSIVES AND PROPELLANTS

TIMOTHY M. MALLON, MD, MPH*; PETER G. MATOS, MD, MPH†; W. SCOTT MONKS, PA-C, MPAS‡; RAÚL A. MIRZA, MD, MPH§; AND DONALD T. BODEAU, MD, MPH¥

INTRODUCTION

HISTORY

ENERGETIC MATERIALS

EXPOSURE

GENERAL MEDICAL CONSIDERATIONS

COMMON MANIFESTATIONS OF EXPOSURE

THE ALIPHATIC NITRATE ESTERS

THE NITROAROMATICS

THE NITRAMINES

THE INITIATING EXPLOSIVES

COMPOSITE PROPELLANTS AND EXPLOSIVES

LIQUID PROPELLANTS

SUMMARY

* Colonel (Retired), Medical Corps, US Army; Adjunct Assistant Professor, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland

† Formerly, Major, US Army; Command Surgeon, US Army Joint Munitions Command, Rock Island Arsenal, Illinois 61259-5000

‡ Army Public Health Center, Directorate of Clinical Public Health & Epidemiology, Division of Occupational Medicine, Aberdeen Proving Ground, Maryland 21010

§ Major, Medical Corps, US Army; Division Chief, Occupational Medicine Division, US Army Public Health Center (Provisional), Aberdeen Proving Ground, Maryland 21010-5403

¥ Department of Occupational Medicine, Midelfort Clinic, 733 West Clairemont Avenue, Eau Claire, Wisconsin 54701

INTRODUCTION

This chapter is an update to Chapter 9, Military Energetic Materials, Explosives, and Propellants, in the previous edition of this book.[1] Much of the chapter has been revised to reflect new policies related to workplace exposure limits, and the references have been updated as well. The US military is both a producer and consumer of explosives and propellants. Although the toxic effects of most of these compounds have been recognized for many years, and data on their effects on human health have been published since World War I and World War II, many gaps remain in the understanding of their human and ecological toxicity. The database on the health effects (especially human) is evolving as research continues. Newly discovered carcinogenic and reproductive effects are especially concerning. However, lack of exposure data in human occupational epidemiology studies, and lack of route-specific toxicity data (especially inhalation and dermal absorption) in animal studies, hampers the ability to make dose-response estimates for most explosives. Therefore, judgments about human exposures to these chemicals must err on the side of safety, and data on structurally similar chemicals must be included in assessments of the health hazards of explosives.

The production of most of these explosives parallels US military activity. Peacetime production is usually sufficient only for research and training needs. During wartime, the manufacture of these compounds increases; the workforce increases (thereby increasing the number of inexperienced workers who are unfamiliar with these compounds); and providers who are inexperienced with the unique hazards posed by these chemicals are suddenly charged with the care of explosives workers. The rapid increase in production during wartime has tended to result in far higher exposures, with correspondingly more numerous and more severe adverse effects, than the few mild adverse reactions that occur during peacetime.[1]-[4] Furthermore, the regulatory environment that surrounds these and other industrial exposures to hazardous substances is constantly evolving.

This chapter focuses exclusively on military explosives and propellants, and is structured according to the chemical family of the compounds: (a) aliphatic nitrate esters, (b) nitroaromatics, (c) nitramines, (d) initiating explosives, (e) composite propellants, and (f) liquid propellants. Most munitions, however, are mixtures of chemicals. Medical professionals need to learn about these propellants and explosives and understand the steps in the manufacturing process to identify where chemical exposures are likely to occur. Occupational health clinic personnel need to expect, in addition to exposures among plant workers, sporadic exposures among ammunition quality-assurance specialists, explosive ordnance-disposal specialists, and personnel who test or use explosives in enclosed spaces.

HISTORY

The Chinese are generally credited with inventing explosives—in the form of fireworks—before 1,000 ce. Black powder was not introduced to the Western world until approximately 1225. Roger Bacon, an English monk, conducted and described some of the first scientific experiments with this explosive mixture of saltpeter, charcoal, and sulfur in 1249. The age of gunpowder began nearly simultaneously in Europe and China with the invention of cannons early in the 14th century. However, the development of explosives was limited mainly to improvements in the manufacture and application of black powder until 1800. Modern explosive technology was developed during the 19th century with increased research on and development of propellants, high explosives, and weapons technology.[5]

Because of their ready natural availability, inorganic nitrate-based explosives were the first to gain importance. (Today, the most important inorganic nitrate explosive is ammonium nitrate, which is used in demolition and construction.) Inorganic nitrates formed the basis of black powder, which was the predominant explosive used in the United States before 1900.[5] Its last major military use was during the Spanish-American War of 1898. Black powder is an easily produced physical mixture of sulfur, charcoal, and potassium nitrate, but it is not well suited for most modern military uses: it produces excessive smoke and flash (which could alert the enemy to the position of the gun) and has a dangerous tendency to cake and misfire. However, it is still used in primers, safety fuses, flares, grenades, practice munitions, blanks, fireworks, signals, and specialized quarry work.[5]

During the opening years of the 20th century, faster, cheaper, and higher-volume methods for producing explosives were developed. Numerous compounds were synthesized and used as detonators, boosters, and flash suppressors; dynamite almost completely supplanted black powder in commercial use, and trinitrotoluene (TNT) became the most commonly used military explosive.[5]

With these developments, attention became focused on organic nitrate explosives. The aliphatic nitrates were the first group to achieve importance because cellulose, glycerol, sugars, and coal-tar derivatives were readily available for use as raw materials. Later, as cost-effective bulk synthesis of ammonia and formaldehyde became possible, the aromatic nitrates became important militarily. The most recent group to achieve prominence is the nitramines.[5]

In the early years of World War II, low production capacity for most explosives and propellants plagued the United States, and numerous changes in manufacturing processes were made in attempts to increase production. Adaptation to the shortages of raw materials, in addition to the unique requirements of each type of weapon, led to the increasing complexity of munitions design. Inadequate resources in rocket propellants led to the addition of nitroguanidine to nitrocellulose to form nitroglycerin-based propellants, which increased production capability and met exacting requirements for new weapons systems.[5] Additional weapons research after World War II has further expanded the uses of these compounds. The plethora of explosives and propellants currently in use and under development has resulted from continued research into the properties, cost, safety, stability, and reliability of explosives.

The British were the first to respond to the threat posed by the manufacture of explosive materials. In 1875, they passed the Explosives Act after an industrial explosion killed 53 people.[5] This law established “inspectors of explosives,” who were authorized to inspect all magazines and factories to ensure that operations were accomplished safely.

At the beginning of World War I, TNT was generally believed to be nontoxic in all its stages of production, but this belief changed.[4] During the course of the war, the major powers used approximately 5 billion pounds of high explosives, primarily TNT, resulting in millions of battlefield casualties.[5] In the United States, at least 17,000 cases of TNT poisoning occurred during the war, resulting in more than 475 deaths.4,6,7 Efforts to reduce the burden of disease included job rotation, medical examinations, and workplace ventilation and hygiene. These efforts were only marginally effective. Successful control of worker exposure was finally achieved through the automation of many operations during shell loading, and the application of strict standards of workplace hygiene.5,8

The World War I experience demonstrated that ammunition-loading plants were among the most dangerous industrial operations, due to the open handling of dusty and fuming compounds. Beginning in 1938, the Ordnance Department and the US Public Health Service coordinated an intensive effort to forge an integrated health and hygiene program in ordnance plants to reduce the burden of worker death and disability.[4] This effort was the first large-scale demonstration of what can be accomplished in a large industry with many serious health hazards by a vigorous medical and engineering program.[2] Consequently, the successes of and lessons learned from this effort led to the establishment of the occupational medicine field in the Army, in which providers monitor the health of over 100,000 civilian employees at depots, arsenals, and ammunition plants.

ENERGETIC MATERIALS

An energetic material is a compound that can undergo rapid, self-sustaining, exothermic reduction-oxidation reactions. Energetic materials may be categorized according to their intended uses: (a) explosives, (b) propellants, and (c) pyrotechnics. Explosives and propellants evolve large volumes of hot gas when burned; they differ primarily in their rates of reaction.[5] Pyrotechnics (powder or ammunition used for igniting a rocket or producing an explosion; the term is also used in the military to designate flares and signals) generate large amounts of heat but much less gas than explosives or propellants.[5] Energetic materials may also be grouped according to their rate of reaction. Both propellants and pyrotechnics are considered to be low explosives. The velocity at which the combustion proceeds through these materials is usually 400 m/sec or slower. In comparison, high explosives are detonated by a process in which the very rapid rate of the combustion reaction itself produces a shock wave, capable of shattering objects, in the surrounding medium.[5] The shock wave moving through the explosive material causes further explosive decomposition of that material, and the reaction rate is determined by the speed of the shock wave. The shock wave’s velocity ranges from 1,000 to 9,000 m/sec.[5] In addition to being used as explosive charges, many high explosives are also used in propellant formulations.[5] For purposes of this discussion, the term “explosive” is used generically to indicate any energetic material.

Explosives

Modern explosive devices employ an explosive train that takes advantage of the specific explosive properties of its components: the initiator, the detonator, the booster charge, and the main charge.[5] The initiator, or primary explosive, consists of a small quantity of material that is very sensitive to heat, spark, impact, or friction. Primary explosives may intensify the energy up to 10 million times that of the initiating stimulus.[5] Geometric arrangement of the explosive device directs either the flame or the detonation wave of the initiator toward the detonator charge. The detonator, a larger amount of less sensitive but more powerful explosive material, then detonates either the booster charge or the main charge. The booster charge is an optional component that further magnifies the explosive impulse. The main explosive (or bursting) charge contains the largest amount of an insensitive but powerful explosive. Explosives used as booster and main charges are usually not capable of being initiated by impact, friction, or the brief application of heat, and are known as secondary explosives.[5]

The secondary explosives used currently in most military explosive devices are physical mixtures of one or more high explosives with various additives. The use of mixtures provides for greater flexibility in explosive design, and additives extend the range of performance. Melt-loading, commonly used with TNT mixtures, is a process in which a molten explosive mixture is introduced into an empty shell casing and allowed to cool and harden. Secondary explosive mixtures are used to facilitate the melt-loading process to optimize oxygen balance, explosive characteristics of blast and fragmentation, and metal properties of malleability and strength.[5]

Explosives and explosive-actuated devices are used widely in both industry and the military. Explosives are used in construction, mining, quarrying, demolition, welding, and cladding. Explosive-actuated devices are used to drive turbines, move pistons, operate rocket vanes, start aircraft engines, eject pilots, and provide heat. Between 1972 and 2016, domestic industrial explosive consumption has fluctuated with the US involvement in the wars in Vietnam, Iraq, and Afghanistan. For example, TNT consumption was 500,000 pounds in 1972, increased to 1 million pounds in 1985, and rose to 10 million pounds in the Persian Gulf War, remaining at that level until the Operation Iraqi Freedom surge ended in 2010. Since then consumption has fallen off considerably.5–7 The specific military uses of explosives are numerous and include the production of fragments, air blasts, and underwater shock; armor penetration; demolition; the ejection of personnel from aircraft; and components of nuclear weapons.5–7

Propellants

Propellants are explosive materials formulated and engineered to react at carefully controlled rates, producing a sustained pressure effect over a longer period of time than high explosives. In contrast to the detonation of high explosives, the process of propellant burning is referred to as deflagration, wherein the rate of heat transfer determines the rate of the reaction, which proceeds at subsonic speeds.5–7

Like explosives, propellants utilize a series of materials in an ignition train. An electrical or mechanical impulse impinges on the sensitive primer material. This ignites the igniter, a pyrotechnic, which in turn ignites the main propellant grain. Propellants may be formulated either as solids or as liquids. Solid propellants are used more frequently in guns, cannons, and smaller rockets, while liquid propellants are used in high-performance missile systems and certain other applications.

Solid propellants may be classified by their chemical composition. Each class has unique properties that render it useful in certain applications. All solid propellants may contain additives similar to those used in explosive mixtures. The additives can be more toxic than the principal components of the propellant and must be considered in occupational hazard analysis. Regardless of the composition class, the chief advantages of solid propellants include their compactness, safety, ease of storage, tolerance of temperature extremes, and ease of handling. In comparison, liquid propellant systems permit greater thrust control and deliver higher specific impulses.5–7 Liquid propellants have been limited to use in high-performance missile systems until recently, when research focused on using liquid gun propellants for howitzers. Several liquid gun propellants are discussed later in this chapter.

Pyrotechnics

Pyrotechnic materials are relatively slow-burning, nonexplosive powders such as metals, alloys, and hydrocarbon mixtures.[5] The only pyrotechnic compounds discussed in this chapter are those used in initiating compositions and propellants. However, pyrotechnics are also widely used in the military as flares, signals, relays, delays, and fuses.

EXPOSURE

Ammunition plants operated by the US Army for the Department of Defense are the primary sites of occupational exposure to military explosives.5–8 The types of ammunition plants include (a) propellant- and explosive-manufacturing plants, (b) metal-parts plants, (c) small-arms plants, and (d) shell loading, assembly, and packing (LAP) plants. Private companies have operated most of these ammunition plants under government contracts since the late 1950s.

In addition to the work at ammunition plants, workplace exposures occur at other types of facilities: munitions are manufactured (in limited quantities), tested, and stored at arsenals; munitions are tested at proving grounds; and munitions are maintained, stored, and demilitarized at depots. Unique operations are conducted at each type of facility. Workers may perform duties that expose them to toxic hazards, and occupational medicine providers must be aware of these potential exposures.

Furthermore, propellant and explosive manufacturing plants produce a limited number of specialized products, but workers can be exposed to feedstock and process chemicals as well as the finished explosives. Feedstock chemicals include toluene and nitric acid used in the synthesis of TNT, and chemical salts and acids in the synthesis of nitrocellulose. Exposures are usually controlled by enclosing the manufacturing process and the feedstock chemicals.

LAP plants pose the greatest exposure potential for employees, due to their use of a wide variety of explosive compounds during labor-intensive loading operations.5–8 Comparatively few employees are exposed to explosives at small-arms plants, arsenals, or depots. Workers at metal-parts plants can be exposed to a variety of industrial chemicals including carbon monoxide, lead, nitrogen oxides, solvents, paints, and cutting oils.[2] Metal-parts plant workers manufacture the hardware in which explosives are loaded and used, such as rocket tubes, shell casings, bomb casings, and trigger assemblies. Cutting oils (usually mineral oil) are used to lubricate and cool the saws and machining tools used to shape the metal parts. Cutting oils have been found to be contaminated with nitrosamines, a class of potent carcinogens. Machinists exposed to these contaminated oils via the dermal and inhalational routes may be at high risk for cancer.7,9

Exposure Controls

Several types of workplace standards have been established to regulate employee exposure. Army policy follows the most stringent of the Occupational Safety and Health Administration (OSHA) permissible exposure limit (PEL)[10] or the American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value (TLV).[11] In addition, because dermal absorption is a significant route of exposure for explosives, OSHA has given a skin designation to these chemicals. Skin exposure to chemicals with significant dermal absorption should be avoided. However, where published limits from OSHA and the ACGIH are either unavailable or inadequate to meet Army requirements, the US Army Public Health Command established military exposure guidelines to protect service members (published in Technical Guide 230[12]).

General Safety Practices

Safety is of paramount importance when personnel handle explosives and propellants. The accidental detonation or deflagration of these materials poses serious hazards to employees, other people nearby, and property, including blast overpressure, fragmentation, and burns. Creating a safe workplace around explosives demands that cardinal principles of safety be followed:

- Separate each handling operation to prevent fires, blasts, or fragmentation.

- Use the minimum number of personnel necessary for each operation.

- Stockpile only the minimum amount of explosive or hazardous material necessary for efficient operation.

The Department of Defense has established uniform safety standards applicable to ammunition and explosives,[13] which the Army implemented in Army Regulation 385-64.[14] Most of these address factors such as the sensitivity of explosive materials to accidental initiation; the quantity of material available to be detonated or deflagrated; the heat that would be generated; the rate of burning; the potential sources of accidental ignition and initiation; and the protection capabilities of shields, clothing, and fire-protection systems. Other health-focused standards address the potential toxicity of the explosive materials and control measures that must be in place to ensure that worker exposure is within acceptable limits.

Industrial Hygiene Principles

Applying industrial hygiene principles such as (a) engineering controls, (b) administrative controls, and (c) personal protective equipment (PPE) in the workplace will further limit potential worker exposures.

Engineering Controls

The preferred method of control for industrial hazards is through design changes or product substitution involving a safer or less toxic process or material. However, substitution as a long-term solution is not always possible. For example, finding a substitute for dinitrotoluene (DNT), which is toxic to humans, mutagenic in animal systems, and classified as suspect carcinogen,[15] has been difficult. Qualified industrial hygiene and safety personnel should work closely together during any workplace modification. Some controls have endured the test of time. Methods in use today include

- enclosure of processes (eg, the melt unit used in TNT melt-loading operations);

- general exhaust ventilation (eg, the type used in rooms where poured TNT munitions are cooled);

- local exhaust ventilation (eg, the type used in dusty operations such as screening flaked DNT or TNT);

- temperature control to reduce vapor generation (used in rolling operations with propellants containing nitroglycerin); and

- remote-controlled operations (eg, the modern continuous-flow nitrator used to produce nitroglycerin).16,17

Administrative Controls

Administrative controls have consistently emphasized work and sanitation practices that involve more than just rotating employees in and out of areas with high-exposure potential. These controls include essential measures such as (a) educating workers about the safety hazards of the materials; (b) enforcing strict work practice guidelines to minimize dust and vapor production and prevent dermal contact; (c) adhering to sanitation practices with strict attention paid to preventing explosive contamination of workers’ bodies or clothing; and (d) providing changing and shower rooms with separate locker facilities to segregate street and work clothing. Contaminated clothing must be removed immediately and placed in closed containers until laundered or discarded. Contaminated skin should be washed promptly with soap and water. Furthermore, workers must wash their face, hands, and forearms thoroughly with soap and water before eating, drinking, smoking, or using toilet facilities.16–18 In work areas, employees must also be prohibited from storing, preparing, dispensing, or consuming food or beverages; storing or applying cosmetics; using tobacco products; and storing or using chewing gum.

Personal Protective Equipment

PPE to control exposure should be used only when engineering and administrative controls are inadequate. Using changing rooms and wearing coveralls continue to be widespread practices. Respiratory protection and gloves must be used where indicated; the National Institute for Occupational Safety and Health (NIOSH) has published guidance on the types available.15–19 Some respirators, especially those with air supplied (by a tank or compressor and hose), can create sparks and therefore pose an unacceptable risk of igniting an explosion.[10]

GENERAL MEDICAL CONSIDERATIONS

The challenge facing a provider beginning work in an industrial environment is to understand the hazards faced by employees. Military ammunition plants are no exception: each type of projectile and munition contains a unique combination of explosives. A careful occupational history might reveal exposures. The provider must be able to interpret this information in terms of specific chemical exposures, just as he or she would interpret chemical trade names in civilian practice. Those who work with composition C4 should be assessed for RDX (hexahydro-1,3,5-trinitro-1,3,5-triazine) toxicity, or given medical surveillance for RDX; cyclotol workers should be assessed for both TNT and RDX toxicity; amatol workers should be assessed for both TNT and ammonium nitrate toxicity; and base propellant workers should be assessed for both nitroglycerin and nitrocellulose toxicity. Sources of information include Material Safety Data Sheets and military specifications of ammunition products. Often the best information is available from a safety officer, industrial hygienist, or plant commander.

Preplacement Considerations

Preplacement examinations establish work ability and baselines for hearing, vision, pulmonary function, and various blood indices for comparisons over time. The 1990 Americans with Disabilities Act, as amended in 2008,[20] precludes preemployment examinations from being applied as discriminatory tools and requires that they be used only to assess critical aspects of job performance.

Preplacement medical examinations remain part of the foundation of a medical surveillance program for workers exposed to hazardous agents. They are done to (a) identify preexisting conditions, (b) identify hypersusceptible individuals, and (c) establish preexposure baseline values. Preplacement examinations must identify preexisting conditions to ensure the worker’s safe performance of critical job tasks (eg, blindness would preclude a worker’s being assigned as a forklift operator, and certain neurobehavioral conditions such as epilepsy and severe psychiatric disorders may not be appropriate among explosives workers).[21] In addition, susceptible individuals must be identified because they may be at higher risk for developing diseases related to specific occupational exposures. For example, individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency may have a hemolytic crisis when exposed to methemoglobin-inducing agents.

Examples of preexposure baseline values include erythrocyte counts and liver-function tests for workers who are exposed to agents capable of inducing anemia or hepatotoxicity. Thorough details of prior occupational exposure should be documented. In addition, recreational activities or hobbies that could expose an individual to chemicals should be documented.

Acute Exposure Decontamination

First aid measures and treatment procedures for individuals who have been exposed to explosives and propellants are similar to those for exposure to other toxic substances. Rescue procedures follow those dictated for most emergencies, but personnel must guard against additional exposures among would-be rescuers. The main goals of initial treatment are to prevent further absorption and enhance excretion, which may be achieved by first removing the victim from exposure and then removing contaminated clothing. Rescuers should thoroughly cleanse victims’ skin with soap and copious quantities of water, paying attention to hair and nails. Contaminated clothing should be either laundered carefully or discarded. Eyewash fountains should be placed throughout the workplace to provide copious irrigation of the eyes in the event of a splash. The treatment of mild, asymptomatic cases may require nothing more than removal from exposure and decontamination.

COMMON MANIFESTATIONS OF EXPOSURE

Commonly, organic nitrates share these major toxic effects: allergic contact dermatitis (ACD), methemoglobinemia, vasodilation, and carcinogenesis. Nitrates used in explosives are no exception. Each of these effects can occur separately or in combination; however, not every organic nitrate causes all four effects. The prevalence of each effect varies with the specific chemical. For example, tetryl causes ACD almost exclusively, nitroglycerin causes vasodilation, and DNT is a mutagen and probable carcinogen. The International Agency for Research on Cancer classifies 2,4- and 2,6-DNT as Group 2B carcinogens (possibly carcinogenic to humans).[21] Many organic nitrates are potent vasodilators, but few have found therapeutic uses in clinical medicine.

Dermatitis

ACD is a type IV delayed hypersensitivity reaction mediated by the immune system and caused by cutaneous exposure to a chemical. The other major occupational dermatitis is irritant contact dermatitis, which is a nonallergic reaction of skin exposed to a chemical. The immune system is not involved in irritant contact dermatitis, but is involved in the allergic form. Dermatitis caused by exposure to organonitrates has no characteristics to distinguish it from other irritant or allergic reactions.

Both allergic and irritant contact dermatitis have been seen in explosives workers.[22] The agents most responsible are tetryl, TNT, amatol, ammonium pic-rate, picric acid, and mercury fulminate. However, the role of other ingredients and exposures must not be overlooked: industrial exposures to solvents, cutting oils, and degreasers all occur in the munitions industry and can also induce dermatitis.

Occupationally induced dermatitis is considered to be the most prevalent occupational disease in workers.[23] During World War I and World War II, morbidity from TNT exposure was a major cause of time lost from work. Fortunately, these effects resolve after the worker has been removed from exposure, and they generally do not sensitize the individual to other chemicals.

Methemoglobinemia

Methemoglobinemia has been recognized as an adverse occupational effect. Many drugs and chemicals exert an oxidant stress on hemoglobin, which oxidizes the iron in the heme portion of the molecule from the ferrous to the ferric form, thus rendering the hemoglobin molecule incapable of binding oxygen. The body spontaneously produces small amounts of methemoglobin, but enzymatic reducing systems within the erythrocyte normally maintain that concentration below 1% of the total hemoglobin. Clinical effects of methemoglobinemia may develop when more than 10% to 15% of the total hemoglobin is converted to methemoglobin. The acute signs and symptoms of methemoglobinemia include persistent, slate-gray cyanosis; fatigue; malaise; headache; and reddish-brown discoloration of the peripheral blood, which does not become bright red when exposed to oxygen. Massive exposure may cause 60% to 70% of the hemoglobin to convert to methemoglobin, which can produce collapse, coma, and death.

Chemicals that induce methemoglobinemia tend to cause chronic anemia, which may develop even in the absence of cyanosis.[24] This anemia usually occurs when erythrocytes that contain methemoglobin hemolyze. Patients with mild chronic methemoglobinemia due to enzyme deficiencies may be treated with oral medications in an attempt to decrease cyanosis. These medications include methylene blue, ascorbic acid, and riboflavin. The methylene blue dosage in this situation is 100 to 300 mg/day, which may turn the urine blue in color. The ascorbic acid dosage is 200 to 500 mg/day; however, long-term oral ascorbic acid therapy can cause the formation of sodium oxalate stones. The riboflavin dosage is 20 mg/day.[24]

As with many toxic exposures, individuals have a wide range of sensitivity to methemoglobin-inducing chemicals. For example, individuals with G6PD deficiency and other hemoglobinopathies are uniquely sensitive to the hemolytic effects of exposure to these agents. Preemployment screening should identify individuals with G6PD deficiency and sickle-cell trait. Aggressive medical surveillance of workers at high risk has effectively reduced such exposures and health effects. Methemoglobin can be measured directly, but this must occur within just a few hours of sample collection because methemoglobin in erythrocytes reduces rapidly to hemoglobin. All cases of cyanosis and abnormal blood findings should trigger exposure-control action.[22]

Individuals with mild to moderate cases of methemoglobinemia will recover spontaneously within 2 to 3 days. In more severe symptomatic cases, methylene blue (administered intravenously as a 1% solution in saline at 1–2 mg/kg over 10 min) is an effective therapy. A second dose may be administered after 1 hour, if necessary.24,25 The US Food and Drug Administration warns against using methylene blue concurrently with serotonergic psychiatric drugs, unless such usage is indicated for life-threatening or urgent conditions.24,25

Hyperbaric oxygen treatment is another option for situations in which methylene blue therapy is ineffective or contraindicated. This approach permits tissue oxygenation to occur through oxygen dissolved in plasma, rather than through hemoglobin-bound oxygen.[25]

Vasodilation and Carcinogenesis

Although organic nitrates as a class cause both dermatological and hematological effects, specific explosives such as nitroglycerin and DNT are vasodilatory and mutagenic, respectively. These substance-unique effects are discussed below.

THE ALIPHATIC NITRATE ESTERS

The aliphatic nitrate ester class of compounds includes many members with explosive properties, some of which are militarily significant. With the exception of nitrocellulose, members of this class are manufactured similarly and are similarly toxic. The physical properties and uses of the individual compounds vary, as does the amount of toxicological data available.

Nitroglycerin

Nitroglycerin was the first organic nitrate to be used as an explosive. Although Ascanio Sobrero, an Italian chemist, first synthesized nitroglycerin in 1847, it was not widely appreciated until 1863, when Alfred Nobel began to use it as a blasting compound.[26] To make nitroglycerin safer to work with, Nobel began using solid materials to adsorb liquid nitroglycerin, from which dynamite was formed.

In 1888, Nobel demonstrated that, by using nitroglycerin to gelatinize nitrocellulose, the explosive properties of nitroglycerin could be converted to propellant uses; as a result, he developed not only the earliest of the smokeless powders, but also the first double-base propellant. Until then, all propellants had nitrocellulose alone as the explosive component—now called single-base propellants. Double-base propellants are those with nitroglycerin in addition to nitrocellulose. Triple-base propellants have nitroguanidine as the third explosive component.[5] Military use of nitroglycerin is almost exclusively in combination with nitrocellulose in double- and triple-base propellants.

The freezing point of nitroglycerin (55.4°F) caused a major safety problem with early dynamite.[27] Explosions were not uncommon when munitions or dynamite were accidentally frozen during winter. Nitroglycerin in the solid state is much less sensitive than in the liquid. But while thawing, nitroglycerin is much more sensitive to detonation than while either a solid or a liquid. Decomposed nitroglycerin is especially dangerous. Not only is it more sensitive to accidental detonation than when pure, but the formation of nitrogen oxides may also constitute a separate toxicity hazard.[6] However, because military use of nitroglycerin is limited to the double- and triple-base propellants, which are stable colloidal mixtures with lower freezing points, the instability of nitroglycerin at its freezing point is no longer a problem.

Other aliphatic nitrate esters have limited, specialized uses. In 1905, ethylene glycol dinitrate (EGDN; freezing point -8°F) was introduced as an additive to lower the freezing point of nitroglycerin, and since 1920 EGDN has been a major component of most civilian dynamite formulations.[27] EGDN has little current military use. However, another aliphatic nitrate ester, propylene glycol dinitrate (PGDN), is used as a torpedo propellant.[5]

Manufacture and Exposure Hazards

Nitroglycerin is manufactured by one of three closed, continuous-flow processes known as the Biazzi, Schmid-Meissner, and Nobel nitrator processes, in which glycerin is mixed with concentrated nitric acid.[5] A closed process is one in which liquid chemicals are piped from one closed container to another—from the beginning of the process, where feedstock is introduced, to the end, where finished product is packed for shipping or storage. A continuous-flow process is one in which the reactions occur constantly, not in batches. The product is subjected to a series of purifying washes and then transported by gravity flow to storage tanks. The nitration and purification processes—controlled remotely via closed-circuit television—are conducted in small, heavily revetted buildings. Other liquid aliphatic nitrates may be prepared by similar methods using other aliphatic polyols instead of glycerin.

Liquid nitroglycerin, together with nitrocellulose and other ingredients, is manufactured into double- and triple-base propellants by two methods.[5] In general, the solvent process is used for propellants that contain less than 40% nitroglycerin, and the solventless process is used for compositions that contain more than 40% nitroglycerin. The solvent process begins with the addition of a solvent such as ether or acetone to water-wet nitrocellulose in a dough-type mixer. Nitroglycerin and other ingredients are added and mixed until a dry colloid forms. The mixture is then subjected to a series of presses to remove the solvent and complete the colloiding process. Finally, the mixture is extruded through a die, cut to length, and dried in an oven to form the finished propellant. The solventless process begins with mixing a slurry of nitrocellulose and nitroglycerin in a tank of water. Other ingredients are added, and the excess water is removed by centrifugation. The process is completed by extruding the dried colloid through a die and drying it in an oven.

Occupational exposure to nitroglycerin can occur during any of these operations. In the solventless process, dermal exposure is especially significant among roller-press operators, and can be detected in blood samples that have concentrations of nitroglycerin in blood. Due to the widespread use of engineering controls, exposure to vapors is minor during nitration, but inhalational exposure can be significant for press operators and drying-room attendants. During World War II, nitroglycerin toxicity caused at least 78 reported cases of lost time among propellant workers, several of whom required transfers to different worksites.[2] Almost certainly, other cases of nitroglycerin toxicity occurred during World War II, but they either went unreported, were unrecognized, or did not result in time lost from work.

Human Exposure and Health Effects

The effects on human health from exposure to nitroglycerin have been observed since its discovery. Because of its vasodilating properties, nitroglycerin has been a mainstay of antianginal therapy since it was introduced to medicine in 1879. Reports of effects that appeared in nitroglycerin workers and their families were described in the literature as early as 1890.28–31

Toxicokinetics. The toxicokinetics of nitroglycerin have been studied and reviewed intensively.32–37 Nitroglycerin is readily absorbed through intact skin, as well as via the respiratory and gastrointestinal tracts. Vascular-tissue uptake and local metabolism are extensive, thus explaining the rapid systemic clearance of nitroglycerin. Once nitroglycerin is absorbed, it is rapidly metabolized by hydrolysis and glutathione-dependent organic nitrate ester reductase.

Because of their rapid hydrolyses, nitroglycerin and the other aliphatic nitrates have shorter biological half-lives than other classes of explosives.[36] Variations among individuals in sensitivity, plasma levels, time of onset of symptoms, and duration of effects are extremely wide. Metabolites may alter the toxicokinetics of the parent compound during chronic dosing.[37]

Acute effects. Acute or intermittent exposure to nitroglycerin may cause a constellation of symptoms in sensitive individuals. Vasodilatory effects can occur with inhalation of airborne concentrations as low as 0.1 mg/m^3. Symptoms due to vasodilation include headache, dizziness, nausea, palpitations, hypotension, flushing, and abdominal pain. Most of these symptoms are due to direct vasodilation of the meningeal, cutaneous, and systemic blood vessels. Other effects of acute exposure appear to be mediated by other mechanisms and include methemoglobinemia, reflex tachycardia, and increased respiratory rate. Hyperthyroidism has been reported to potentiate the acute toxicity of the organic nitrates.[30] Inhalation exposure at levels as low as 14 mg/m^3 have led to more severe effects such as electrocardiogram (ECG) changes, chest pain, and palpitation. Massive acute exposure may cause cyanosis, coma, and death.

Other acute effects have been described but are less well documented. Central nervous system (CNS) symptoms, such as confusion and hallucinations, and psychotic episodes, including homicidal violence, have been reported in patients after they handled nitroglycerin. Peripheral nervous system effects such as paresthesias have also been reported.

Ingestion of nitroglycerin is an industrial hygiene problem. It can occur via contamination of food or smoking materials in the workplace. However, the use of sublingual nitrates is a common form of therapy for coronary artery disease, taking advantage of the transdermal and transmucosal absorption and the vasodilatory effect of some nitrates.

Chronic effects. Most workers become tolerant to the vasodilatory effects of nitroglycerin within 1 week after their exposure has begun and develop compensatory vasoconstriction. This effect has also been described in patients who receive therapeutic nitroglycerin.[37] The tolerance persists for approximately 1 week after the worker is removed from the exposure.

Evidence of a withdrawal syndrome or sudden death in chronic users has been controversial, and more study of the long-term effects is needed. Withdrawal may precipitate angina pectoris, myocardial infarction, and sudden death. The condition has been called “Monday morning angina” because the symptoms appear after a 48- to 72-hour absence from work. Anecdotal reports of these effects have appeared since the early 1900s, but the first medical case series was reported in 1952.[38] Some evidence of withdrawal has been found in a small cohort of patients taking nitroglycerine,[39] and a recent epidemiological study found evidence of sudden death in long-term nitroglycerine users.[40]

The mechanism associated with angina and sudden death appears to be a series of events starting with habituation to the hypotensive effects of chronic nitrate exposure. When removed from exposure, the employee develops rebound hypertension, which may be followed by coronary insufficiency.[22] Coronary insufficiency is, therefore, a secondary effect due to rebound coronary vasoconstriction, making the heart less able to compensate for the additional strain caused by systemic hypertension. Studies done with animals have shown that nitroglycerin-tolerant subjects become more sensitive to vasoconstrictors after they are withdrawn from nitroglycerin. Some have shown electrocardiographic ST segment changes and ventricular arrhythmias suggestive of coronary artery spasm.[31] Evidence shows that withdrawal from nitroglycerin increases the sensitivity of α_1 adrenergic receptors in the coronary arteries to endogenous and exogenous vasoconstrictive agents.[31]

The chronic cardiac effects of nitroglycerin withdrawal appear to be latent for 6 to 10 years before the onset of symptoms.[40] Several studies of Swedish dynamite workers have demonstrated excess mortality from cardiovascular and cerebrovascular disease. This excess mortality was only significant for workers with long-term employment and had a latency of 20 years.[37] A more recent retrospective cohort-mortality study of workers at a US Army ammunition plant showed an excess of mortality from ischemic heart disease among workers younger than 35 years of age.[31] Pathological examinations of nitroglycerin workers who experienced cardiac events have failed to reveal coronary artery disease, strengthening the conclusion that rebound vasospasm is responsible.31,41

A 1965 review of earlier case reports revealed complaints of digestive troubles, tremors, neuralgia, and, in rare cases, ACD among nitroglycerin workers.[42] Decreased alcohol tolerance is common and may be caused by nitroglycerin’s interference with liver alcohol dehydrogenase. Simultaneous exposure to ethanol and nitroglycerin can cause manic behavior.[43]

Numerous other chronic effects of nitroglycerin exposure have been reported but, as with some acute effects, are poorly documented. Research has been conducted on other chronic effects in mammals, but the results have not been substantiated in humans. Chronic oral administration of nitroglycerin in rats has produced liver cancer. Other research with mammals has indicated the possibility of male reproductive, fetotoxic, and teratogenic effects.29,44 Recent evidence has shown that nitroglycerin does not increase intraocular pressure to cause glaucoma.[36]

Medical Surveillance

Early identification of cardiovascular disease is the primary goal of medical surveillance of nitroglycerin workers. A preplacement examination must be administered to all new employees, and should consist of both medical and occupational histories, a physical examination, and indicated laboratory tests. When their employment begins, nitroglycerin workers should maintain a daily record of their pulse rates. Periodic examinations should be conducted semiannually, with the same focus as the preplacement examination. During the periodic examination, the provider should be aware that headaches occurring during work shifts can indicate skin absorption of nitroglycerin, even if air concentrations of nitroglycerin are below the PEL. Similar examinations are necessary when exposure to nitroglycerin has been terminated, although surveillance should perhaps extend beyond employment due to the latency of the withdrawal effects.[18]

In addition to performing medical surveillance examinations, the plant provider should follow these procedures to safeguard the workers’ health:

1. The provider should alert the worker’s private provider to the effects of exposure to and withdrawal from nitroglycerin.

2. Workers who leave the plant due to any kind of illness should be cleared through the medical department.

3. Workers should also be examined before they return to work after lengthy absences.

This procedure, common in all types of industries, is a management tool used as an administrative control measure. When workers leave the plant with any illness, a medical examination can help determine if that illness is due to an acute overexposure to nitroglycerin (or any other toxic agent). By early detection of a sentinel event, plant managers can intervene at the worksite and thus protect other workers in the area, as well as the ill individual on his or her return to work. An examination is necessary whenever a nitroglycerin worker returns from an illness to ensure that the worker’s health status has not changed in such a way that he or she will be placed at risk. Specifically, the occupational provider should look for changes in cardiovascular status, such as a recent myocardial infarction or new-onset hypertension.

A biological marker of exposure would be a useful aid to the occupational health provider, but none are reliable. Blood methemoglobin levels increase after high exposures, but these are not sufficiently sensitive to monitor exposure to nitroglycerin.45,46 Nitroglycerin can be detected in blood, but because cubital venous blood samples reflect almost exclusively the locally absorbed compound from the distal part of the arm, they are unreliable indicators of systemic exposure.45–47

Primary Prevention

The most efficacious method to control occupational nitroglycerin toxicity is to prevent exposure using engineering controls and hygienic work practices. This is especially true because adverse effects occur at exposure levels below the odor and eye-irritation thresholds that could warn workers of potentially hazardous environments.29,48

Several types of engineering controls have proven to be effective in reducing inhalational exposure, including automation, closed-circuit television, and ample work-area ventilation. Volatilization of the aliphatic nitrates can be minimized by processing these materials at the lowest practicable temperatures. Operations that require heating should be controlled remotely.16,22 Maintaining a water seal over liquid nitroglycerin will prevent its evaporation and reduce its concentration in air.

When necessary, PPE should be worn to prevent dermal contact and to reduce airborne levels to an acceptable range. Particular attention must be devoted to the type of gloves worn. Polyethylene gloves may be the best choice, because nitroglycerin easily penetrates neoprene, leather, and rubber. Cotton or canvas gloves, frequently changed, are also preferable to rubber gloves. A face shield or splash-proof safety goggles may also be necessary to protect the eyes. An organic vapor respirator may also be required to prevent headache, especially at concentrations higher than 0.02 ppm.[15]

The selection of a respirator should be consistent with NIOSH guidance and be approved for use in explosives manufacture to avoid potential safety hazards.10,15 To date, the only respirators that have been demonstrated to provide a sufficiently high protection factor are full-face, supplied-air respirators. However, even these are yet to be proven safe in the potentially explosive atmospheres that may exist in nitroglycerin manufacturing operations. Therefore, the only way to ensure that workers are protected is to lower the airborne level through engineering controls. However, this is not feasible in all cases. Both the government and industry are aggressively pursuing a resolution to this problem to comply with the lower OSHA PEL for nitroglycerin.[10]

Careful attention to personal hygiene is necessary to prevent workers from contaminating their street apparel and, as a result, possibly poisoning their family members. At a minimum, manufacturing plants should provide changing facilities that contain an adequate number of coveralls, gloves, and caps for use during the shift and shower facilities for use at the end of the shift.[48] Indicator soaps are available that turn red in the presence of residual nitroglycerin not removed from the skin (sodium sulfite in the soap reacts with nitrate groups in nitroglycerin to form sodium sulfonate).[48]

The treatment for nitroglycerin poisoning consists of removing the patient from the source of exposure, thoroughly cleansing the skin and mucous membranes of nitroglycerin contamination, and providing cardiovascular support. Washing the skin with aqueous sodium thiosulfate will assist in neutralizing any nitroglycerin that remains. The use of oral nitrates and calcium channel-blocking agents has been somewhat efficacious in the treatment of nitroglycerin withdrawal. Both reduce reflex vasospasm; oral nitrates work by drug replacement (analogous to using nicotine gum in tobacco cessation to overcome the physiological effects of withdrawal), and calcium channel blockers relax and widen blood vessels by affecting the muscle cells in the arterial walls.[49]

Nitrocellulose

Nitrocellulose is a nonvolatile, fibrous white solid consisting of chains of glucoside units in which the hydroxyl groups have reacted to form nitrate esters. The molecular weight depends on the chain length and the degree of polymerization, which in turn depend on the source of the cellulose. Many sources of cellulose are used, including paper rolls, cotton linters, wood pulp, and waste cotton.[5]

Manufacture and Exposure Hazards

Nitrocellulose was first produced in 1838, but practical difficulties in manufacturing and using the material were not overcome until 1865. Since that time, it has become the basic component of single-base solid propellants. Nitrocellulose is the principal ingredient in gun and mortar propellants, smokeless powder, and ball powder. The military’s production of nitrocellulose is second only to its production of TNT. Nitrocellulose is also a component of combustible cartridge cases, and in the civilian sector is used in manufacturing blasting fuses and mining charges.

In explosive applications, nitrocellulose requires a higher degree of nitration than that produced for its nonexplosive uses (such as lacquers, medical collodion, ink bases, or filter membranes). Military-grade nitrocellulose is produced at various Army ammunition plants in a process wherein cellulose is nitrated with concentrated nitric and sulfuric acids. The only significant byproducts of manufacture are the spent acids, which are concentrated and then reused.

Human Exposure and Health Effects

Insoluble in water and resistant to biological degradation, nitrocellulose per se has a very low potential as a hazard to human health. As an insoluble polymer, nitrocellulose is not absorbed in the gut, and in fact does not appear to be absorbed by any route. The only effects of ingestion are due to the bulk of fiber, which may occlude the intestinal lumen, and are no different than effects of non-nitrated cellulose. Nitrocellulose is not irritating to the skin, and no mutagenic activity has been detected.[50]

Other exposures during the manufacture of nitrocellulose are of greater significance to workers. These include exposures to acids and acid vapors during the initial nitration process, which may lead to dental erosion and chemical burns. Uncontrolled exposure to raw cotton dust from the linters before nitration can cause byssinosis, an allergic, occupational respiratory disease of cotton, flax, and hemp workers characterized by symptoms—especially wheezing—that are most severe at the beginning of each work week (because the lack of exposure over the weekend allows large quantities of the mediators of allergy, such as histamine, to accumulate).

The potential hazards encountered during the manufacturing process necessitate that precautions be taken. Adequate ventilation during both preparation of linters and nitration is essential. It is recommended that PPE be worn by employees who work near the acids. No special medical surveillance for exposure to nitrocellulose is necessary, and treatment for the sequelae of acid contact is not unique. No exposure limits have been established for nitrocellulose.

THE NITROAROMATICS

The nitroaromatics were the second class of organic nitrates to become important as explosive compounds, and they continue to be represented prominently in the world’s arsenals. These chemicals are well absorbed by all routes and tend to rapidly penetrate the dermis. The major effects of these chemicals include methemoglobinemia, cancers of the urinary tract, anemia, and ACD.51,52

Trinitrotoluene

The best known of the aromatic nitrate explosives, TNT was first prepared in Germany in 1863. It was manufactured industrially starting in 1891 and rapidly became the premier high explosive.[27] Major military powers adopted TNT as their major high explosive in 1901, and the first significant military use of TNT was during the Russo-Japanese War of 1905. Many factors, including its low cost, safety in handling, compatibility with other explosives, low melting point, moderate toxicity, and low sensitivity, made TNT the most widely used military explosive. Before 1940, its manufacture was limited by the availability of toluene, but advances in petroleum chemistry during World War II permitted the synthesis of large quantities of inexpensive toluene, which greatly enhanced TNT production capacity in the United States.[27]

TNT can be found in virtually all military applications and is frequently mixed with aluminum and other high explosives to form binary or ternary explosives. Its easy availability during World War II made TNT a perfect suspension agent for more powerful explosives such as RDX, and made melt-loading methods feasible.[51]

Manufacture and Exposure Hazard

TNT manufacturing methods are based on continuous stepwise nitration of toluene, with a mixture of concentrated nitric and sulfuric acids flowing counter-current to the toluene. Anhydrous sodium carbonate and sodium sulfite are used in the washing and crystallization processes to purify the crude TNT solution. The purified TNT is then dried in a steam-jacketed pan before being flaked and packed. Occupational exposure to acids, toluene, and impure TNT have been reduced during the continuous-manufacture process.53,54

The most significant risk of exposure to TNT occurs during shell-loading operations. Exposure can occur during several of the steps, most of which involve the melt-loading process. In this process, dry flakes of TNT are poured into a steam-heated melting kettle and heated to approximately 212°F. Other high-temperature melting, nonmetallic additives such as RDX are added at this point. Continued heating drives off the water, and flaked aluminum may be added at this point. The mixture is then cooled until the established pouring consistency is reached. After the mixture is poured, the loaded shells are cooled under controlled conditions.

Exposure to TNT dust, fumes, and vapor can occur during any of these operations. TNT exposure is considered high when the levels are above the OSHA PEL of 1.5 mg/m^3, which is based on an 8-hour time-weighted average (TWA).[55] Moderate levels of exposure occur below the OSHA PEL and above the ACGIH TLV of 0.1 mg/m^3 (also based on an 8-hour TWA).[56] Exposure levels below the ACGIH TLV are considered low, but even low exposure levels cause hemolytic anemia in workers.

Exposure to TNT can occur during numerous work processes in addition to shell loading. Some of the highest TNT dust levels occur during screening operations (passing TNT flakes through a sieve), where concentrations up to 75 mg/m^3 have been measured in breathing zones.16,57 Workers can also be exposed to TNT fumes and vapors during demilitarization, when munitions may be steam-cleaned to melt and remove the high-explosive charge.

Significant amounts of TNT and its manufacturing byproducts have been released into the environment in huge volumes of liquid waste from factories and LAP plants, and as a result, people living near these facilities have been exposed to TNT. The liquid wastes (known as “pink water”) contain TNT isomers, DNT isomers, and mononitrotoluenes. Due to the difficulty and expense of disposing of this waste, the United States currently imports most of the TNT it uses.[53]

Human Exposure and Health Effects

TNT’s toxicity to animals and humans has been recognized for at least 75 years.58–63 Most of this knowledge results directly from work performed during the two world wars. From 1914 to 1918, approximately 24,000 people were poisoned with TNT in the United States, fatally in 580 instances. Similar experiences were described in other combatant nations. In Great Britain, 475 cases of TNT poisoning were reported between 1916 and 1941, of which 125 were fatal.[64] During World War II, TNT poisoning was a factor at US manufacturing and loading plants and arsenals, although the case rates at arsenals and manufacturing plants were less than half that at loading plants. Of the 21 deaths that occurred, 18 were at loading plants, 2 at arsenals, and 1 at a TNT-manufacturing facility.[2] Progressively more people were exposed to more chemicals as the war continued, yet the morbidity was much lower. Case rates for all locations fell dramatically despite the marked increase in TNT production, demonstrating the effectiveness of occupational health and industrial hygiene interventions.

Researchers have analyzed the 21 TNT fatalities of World War II, together with a later death of a former TNT worker. Of this series, 8 died of toxic hepatitis and 13 of aplastic anemia. The late death occurred in a worker who apparently had recovered from hepatitis but later succumbed to aplastic anemia. Only one-third of these fatalities had been exposed to average airborne concentrations higher than the maximum allowable concentration of 1.5 mg/m^3, which reflects the contribution of dermal absorption. Workers who died of toxic hepatitis were younger than those who died of aplastic anemia (the median ages were 35 and 45 years, respectively). In both conditions, the median period of exposure was quite short: 63 days for hepatitis, and 216 days for anemia.[8]

Other cohort studies of TNT workers have shown that virtually all cases of toxic hepatitis have occurred within the first 3 months of exposure; however, cross-sectional studies have not shown significant signs of hepatotoxicity.[65] This may indicate that a sensitive subgroup of individuals is at risk for this effect.

Another World War II–era study evaluated the effects of TNT intoxication in 250 male and 103 female workers in a bomb- and shell-loading facility.[66] No cases of severe TNT intoxication were seen; however, adverse effects of TNT exposure were found in 32 workers (30 of whom were males), of whom 21 had either gastritis or hepatitis; 14 had anemia; and 3 had systemic manifestations of intoxication.[66]

More recent workplace occupational exposures involving TNT have been substantially lower than levels seen in World War I and II. 67–69 Several researchers who examined workplace medical surveillance results observed workplace anemias and altered liver function tests in workers exposed at levels below the PEL and, to some extent, below the TLV.

Toxicokinetics. TNT is readily absorbed by all routes of exposure. Approximately 60% to 70% of oral doses are absorbed; inhaled TNT appears not only to be absorbed faster than oral doses, but it also reaches higher concentrations in the blood. Dermal absorption is less efficient, but its significance must not be underestimated. TNT dissolved in water is particularly well absorbed through the dermis. This effect is greater in hot weather when workers wear cotton coveralls that become saturated with sweat, which increases TNT skin absorption. Workers’ coincident exposure to hygroscopic chemicals such as ammonium nitrate further promotes dermal absorption by keeping the skin moist.[26] Consequently, measuring only airborne levels may significantly underestimate the workers’ total systemic exposure.62,65

TNT is metabolized primarily by a two-step process: the reduction of the nitro group and its conjugation to glucuronide. Some enterohepatic recycling occurs, but urinary clearance of the glucuronides occurs fairly rapidly, preventing bioaccumulation. The urine of humans who have been exposed to TNT becomes discolored with a red metabolite.

Dermatitis and systemic effects do not correlate well.[62] Hematological effects appear to occur at lower doses than hepatic effects, but susceptible individuals will develop hepatotoxicity sooner after initiation of exposure.

Acute effects. Acute exposure to airborne TNT can cause irritation of the upper respiratory tract and skin; symptoms include sneezing, coughing, rhinitis, and erythematous dermatitis. The onset of acute systemic toxicity is frequently heralded by gastrointestinal symptoms such as nausea, anorexia, and epigastric pain.[64] Systemic symptoms may progress to include headache, fatigue, malaise, palpitations, loss of memory, and cyanosis.[65]

Chronic effects. The most serious chronic manifestations of TNT toxicity are (a) anemia and other hematological changes and (b) hepatitis; chronic effects may also include dermatitis, ocular effects, neurological effects, and cancer.

Hematological effects result from the action of TNT on both the bone marrow and mature erythrocytes. Although virtually every cell series in the marrow is affected, the most significant hematological effects occur in the erythrocytic series, and may result in anemia with both aplastic and hemolytic components. TNT depresses erythropoiesis and induces aplastic anemia by suppressing two enzymes that catalyze heme synthesis: δ-aminolevulinic acid synthase and heme synthase. This suppression has been demonstrated even in the clinical absence of anemia.

Hemolysis in TNT toxicity occurs as a result of methemoglobinemia. This is a dose-related effect, with low-grade anemia and compensatory reticulocytosis noted at airborne TNT concentrations lower than 0.5 mg/m^3. Exposures of 0.2 to 0.5 mg/m^3 appear to have minimal and well-compensated effects on erythrocytes. Poikilocytosis may occur, as well as hepatic and splenic congestion related to hemolysis. Early signs and symptoms of fatal anemia—even in the absence of G6PD deficiency—include weakness, anorexia, weight loss, cough, epistaxis, elevated bilirubin, decreased hemoglobin, and decreased leukocyte counts. Survival in the case reports of fatal anemia varied from 6 to 185 days, but the median was only 40 days.[6] Hemolytic crisis has been seen in G6PD deficiency within the first few days after exposure.

Other hematological effects include both leukocytosis and leukopenia. Transitory leukocytosis and moderate eosinophilia have been described at airborne levels lower than 2.5 mg/m^3. Leukopenia develops late, well after the hemoglobin level and erythrocyte count fall, in contrast to other chemically induced aplastic anemias. Exposure to TNT causes the monocyte count to increase, regardless of the presence of symptoms, and neither the extent of dermal contact nor the length of inhalational exposure influences the intensity of the hematological response.[59]

TNT poisoning can induce both massive hepatic necrosis and cirrhosis. As with most hepatotoxic agents, the hepatitis manifests with increases in the concentrations of serum transaminases and lactate dehydrogenase (LDH). Researchers found no liver function abnormalities at a TWA lower than 0.5 mg/m^3, but they found elevated aspartate aminotransferase (AST) and LDH at airborne concentrations of 0.8 mg/m^3, which persisted even at 0.6 mg/m^3.[67] Early symptoms of TNT-induced hepatitis include nausea, vomiting, malaise, and hepatic tenderness. Jaundice, although a late symptom of TNT hepatitis, develops rapidly as the liver atrophies and indicates a poor prognosis. In a study of TNT-induced hepatitis fatalities from World War II, the average elapsed time from the first definite symptom to death was 34 days, with a range of 12 to 53 days.[6]

Dermatitis is the most common chronic effect of exposure to TNT. Yellow-orange staining of the skin, hair, and nails is a common sign, and irritant contact dermatitis may occur. Dermatitis requires at least 5 days of exposure to develop, and most patients become tolerant to mild cases.20,70 Palmar lesions with deep vesicles are characteristic. Allergic contact dermatitis with classic eczematous lesions have been reported, and may rarely appear as an erythema-multiformelike eruption. ACD usually affects the upper limb, but the skin at friction points such as the collar line, belt line, and ankles may also be involved.[18] Workers exposed to high levels of TNT dust are especially at risk for dermatitis, although it may occur in workers throughout the manufacturing process.

Several studies performed in Europe noted that exposure to TNT was associated with cataracts, but at undefined levels of exposure. TNT workers in Finland developed equatorial cataracts at concentrations of airborne TNT of 0.14 to 0.5 mg/m^3. These characteristic cataracts are insidious in their development and are present only at the lens periphery; consequently, they do not affect vision. They may not be noted on a routine ophthalmological examination, although they are easily observed when the affected eyes are dilated and examined with a slitlamp.[71] Most affected subjects in these studies had normal liver function tests. The duration of exposure to TNT was 1.2 to 17.0 years, with a mean of nearly 7 years. Older workers were more commonly affected, and the lens changes appear to be irreversible. Cataract formation may result from direct action of TNT on the lens via lipid peroxidation and production of superoxide anions.[72]

Research into whether neurological signs develop from TNT exposure has yielded controversial results. Some studies of TNT exposure report neurasthenia and polyneuritis.[5] While some accounts of TNT exposure in the United States support these findings, at least one investigator has concluded that symptoms of peripheral neuritis among workers were not solely due to TNT exposure.[73] This study found that, when present, symptoms were limited to mild sensory disturbances, with no objective evidence of the disease.

TNT has been implicated in carcinogenesis in studies done with laboratory animals. The results of studies performed on rodents have shown increased incidence of bladder papilloma and carcinoma, and statistically insignificant increases in leukemia and lymphoma. In 1996 the International Agency for the Review of Cancer found little evidence in humans and animals and concluded that the carcinogenicity of TNT was not classifiable.[60] However, the German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area classified TNT as a class 2 carcinogen in 1991.[61] TNT might be genotoxic; it has given positive results in Ames assays both with and without metabolic activation.62,63 Many studies published on TNT since 1996 have found an association between TNT and cancer. In 2008 both the US and California environmental protection agencies reviewed the carcinogenicity of TNT. The US Environmental Protection Agency classified TNT as a possible human carcinogen.[62] The California Environmental Protection Agency ruled that through scientifically valid testing according to generally accepted principles, TNT causes cancer.[63]

Numerous other manifestations that have been attributed to TNT exposure include myalgia, cardiac dysrhythmia, nephritis, increased vascular permeability, cardiotoxicity, pancreatic exocrine abnormalities, increased capillary fragility, menstrual disorders, and testicular atrophy and hyperplasia.[64]

Primary Prevention and Medical Surveillance

Historically, control of TNT exposure has been accomplished through general safety and hygiene measures, yet specific additional measures are necessary. For example, hazard communication programs at each facility should instruct workers about the need for strict personal and shop hygiene, and about the hazards of particular operations conducted in that plant. In addition, soap that contains 5% to 10% potassium sulfite not only helps remove TNT dust from the skin, but suds that turn red also indicate any remaining contamination.[54] Furthermore, respiratory protective equipment, selected according to NIOSH guidance, should be worn during operations that release dust, vapor, or fumes.

Because TNT interacts with certain medications, including those that cause intrahepatic cholestasis, hepatocellular necrosis, and bone marrow depression, patients taking medications such as isoniazid, halothane, phenylbutazone, phenytoin, and methotrexate, and whose exposures to TNT cannot be prevented, should be closely followed by an occupational health provider.

The US Army currently recommends preplacement and periodic (semiannual) examinations of TNT workers. The occupational health provider should determine on a case-by-case basis the elements of examinations to use in periodic surveillance. However, to identify workers with higher than normal sensitivity to TNT toxicity, workers should undergo monthly hemoglobin, LDH, and AST determinations during the first 3 months of exposure to TNT.[65] One study demonstrated that assaying for AST, LDH, and hemoglobin in combination detected all abnormal cases, whereas if the assays were performed alone or in pairs, many cases were missed.67,73 Periodic examinations provide inadequate warning of impending aplastic anemia.[74] Workers who have abnormal results should be removed from exposure and evaluated further.73,75

Bioassays for TNT exposure began during World War II with the use of the Webster test for urinary TNT.[76] This qualitative test was based on the reaction of alcoholic potassium hydroxide with an ether extract of acidified urine, wherein colors are produced when TNT and other polynitro compounds are present in urine.[77] In comparison to the qualitative Webster test, a quantitative test for urinary aminodinitrotoluene (ADNT), a metabolite, can be related to TNT absorption within 24 hours of exposure. Urinary ADNT is measured via gas chromatography with electron-capture detection.[77] Most individuals excrete the highest concentrations of ADNT within a few hours after exposure, but some continue excreting significant amounts many hours later. This prolonged excretion time may indicate that TNT or a metabolite has been retained, or may indicate delayed skin absorption. Prolonged dermal absorption has been indicated in a group of explosives workers whose urinary concentrations of ADNT indicated higher total exposures than were predicted from the concentrations in ambient air.58,78

Dinitrotoluene

Toluene is converted to DNT, which is widely used in military applications. DNT is used in the synthesis of toluene diamine, an intermediate in the production of toluene diisocyanate. DNT may comprise up to 10% of commercial dynamite formulations as well. Military uses of DNT are similarly broad; it is most often used as an additive to modify the properties of other explosives. For example, DNT may function as a combustion modifier in propellants, as a gelatinizer, or as a waterproofing agent in explosives.[5]

Manufacture and Exposure Hazard

Due to the serious safety and health hazards inherent in the manufacture of DNT (it is a carcinogen and even more hazardous than TNT), current practices for technical-grade DNT production uses continuous, closed systems that are highly automated and remotely controlled. Technical-grade DNT is a greasy liquid comprised of approximately 80% 2,4-DNT and 20% 2,6-DNT, but military-grade DNT requires highly purified 2,4-DNT flakes. Significant occupational exposure is possible during purification and flaking, as well as during mixing and shell-loading operations. Because DNT is also present in the waste water of TNT manufacturing and shell-loading plants, significant environmental contamination and environmental exposure can also occur.

Human Exposure and Health Effects

DNT is readily absorbed via all routes of exposure, but absorption through the dermis is probably the most significant. In rats, both the 2,4- and 2,6-isomers are extensively metabolized by the liver and then excreted in bile.[79] Intestinal nitroreductase-active bacteria further metabolize the product, which is resorbed and metabolized in the liver to a genotoxin.[80] The excretion of 2,4-DNT metabolites in humans is qualitatively similar to that in rats; however, humans do not excrete the reduced metabolite of 2,6-DNT. This qualitative difference in metabolism makes interspecies extrapolation of the carcinogenic risks difficult.81,82

Acute effects. The most characteristic sign of acute DNT toxicity is methemoglobinemia. Associated symptoms include headache, fatigue, cyanosis, irritability, and nausea. Moderate exposures may cause ataxia, respiratory depression, and arthralgias, while severe exposure may lead to progressive CNS depression and death.80,81

Chronic effects. Anemia and ischemic heart disease are the most commonly recognized chronic effects of exposure to DNT.[80] The anemia, which occurs when erythrocytes that contain methemoglobin hemolyze, is typically low grade and partially compensated.[81] Increased mortality from ischemic heart disease has been seen in munitions workers who were exposed to DNT during the 1940s and 1950s.83,84 Unfortunately, a lack of adequate exposure data prevents making accurate dose-response estimates for these effects.

Concerns about DNT’s carcinogenicity have been expressed for several years, and have recently focused on incompletely burned DNT in propellant residue at waste propellant disposal sites. Anyone exposed is at risk for carcinogenesis, including workers at the disposal sites and all who are environmentally exposed via dust, groundwater, or direct contact with contaminated soil. DNT isomers exhibited only weak mutagenic activity in Ames assays[81] and no activity in various mammalian cell culture genotoxicity assays. However, studies in rats using technical-grade 2,4-DNT and 2,6-DNT showed a high incidence of hepatocellular carcinomas produced by 2,6-DNT, with a lower incidence in females compared to males. Enterohepatic recirculation with hepatic and intestinal microfloral metabolism are necessary for the production of the carcinogen. Three major mammalian carcinogenicity studies have indicated that 2,6-DNT is both an initiator and a promoter, while 2,4-DNT is only a promoter.24,81 Evidence of carcinogenicity in humans is lacking, however. Two occupational cohort studies have been completed on workers exposed to DNT. Neither study showed any excessive incidence of cancer, but both demonstrated elevated cardiovascular and cerebrovascular mortality.[83]

Deleterious effects on the reproductive system have been reported in rats given large doses of DNT (≥ 34.5 mg/kg/d), but such effects were not seen in a NIOSH study of workers at a DNT-toluene diamine plant.[85] Testicular atrophy, decreased spermatogenesis, and nonfunctioning ovaries have been seen in rats, mice, and dogs in feeding studies performed to assess chronic exposures. Results of multigenerational reproductive studies in animals have been negative. Only one of three epidemiological studies has shown effects on the human reproductive system, and these were limited to decreased sperm counts, minor morphologic changes in sperm, and a small increase in spontaneous abortions among wives of exposed workers.80,81 Studies done on animals and humans have failed to identify teratogenic effects.

Other chronic effects noted in animal studies include neurotoxicity and hepatotoxicity, with histological changes in both organs noted at autopsy. ACD may also occur, but not as frequently as with exposure to TNT. Friction sites are frequently affected by DNT dermatitis.

Primary Prevention and Medical Surveillance

As with all potential carcinogens, prevention of exposure is essential with DNT. Workers who could potentially be exposed to DNT should be informed of its deleterious health effects, including the possible reproductive system effects. In addition to the safety and hygiene measures previously mentioned, occupational health personnel should monitor for residual buildup of DNT on clothing, boot linings, and hardhat liners. Respiratory protection is usually unnecessary because DNT has low vapor pressure.

Medical surveillance should consist of the same protocol as that for TNT, with the addition of a reproductive history and measurement of urinary DNT. The preplacement evaluation should include a baseline sperm count and morphology assessment for workers who intend to have children. Semen analysis is not necessary during routine periodic medical surveillance of exposed workers.

THE NITRAMINES

The nitramines are the most recently introduced class of organic nitrate explosives. The most prominent member of this class is RDX (hexahydro-1,3,5-trinitro-1,3,5-triazine, known as research department explosive); HMX (octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine, known as high-melting explosive); nitroguanidine; tetryl; and IMX, or insensitive munitions explosive.

Hexahydro-1,3,5-trinitro-1,3,5-triazine

Although RDX was first prepared in 1899, its explosive properties were not appreciated until 1920. RDX was used widely during World War II because, unlike other explosives, petroleum was not needed as a raw ingredient.[27] After World War II, RDX became the second most widely used high explosive in the military, exceeded only by TNT. As with most military explosives, RDX is rarely used alone; it is widely used as a component of plastic explosives, detonators, high explosives in artillery rounds, Claymore mines, and demolition kits. RDX has limited civilian use as a rat poison.

Manufacture and Exposure Hazard

RDX is manufactured using the continuous Bachman process, in which hexamine is nitrated with ammonium nitrate and nitric acid in a solvent mixture of acetic acid and acetic anhydride. The byproducts of RDX manufacture include nitrogen oxides, sulfur oxides, acid mists, and unreacted ingredients. In 1964, during mobilization for the Vietnam War, the Holston Army Ammunition Plant alone produced approximately 750,000 pounds per day of RDX and HMX combined.[86]

Soldiers and other workers have been exposed to RDX during its manufacture, in the field, and through environmental contamination. The main occupational exposure to RDX during its manufacture is through the inhalation of fine dust particles. Ingestion is possible, but it is poorly absorbed through the skin.[87]

The greatest potential for occupational exposure to RDX occurs at ammunition plants with LAP operations, among workers involved with melt-loading and maintenance operations.[87] During World War II, there were no fatalities and little morbidity at RDX manufacturing plants. Small numbers of Italian and German workers, who handled powdered RDX in the drying, cooling, screening, and packing processes, were reported to have experienced RDX toxicity, but all recovered completely.[88]

In 1962, five cases of convulsions, unconsciousness, or both occurred at a US RDX manufacturing plant. In four of these cases, exposure was from inhaled dust during cleanup of a mixing area. The fifth employee screened and blended dried RDX from different batches; gross skin and air contamination occurred because no mechanical ventilation was used and the individual did not follow hand-washing and hygiene precautions. All five employees had convulsions during their work shifts or within a few hours after their shifts were over. These patients exhibited little or no prodrome, and the postictal phase lasted up to 24 hours. No abnormal laboratory or physical findings were noted.[88]

Troops have also become intoxicated during field operations from exposure to composition C4 plastic explosive, which contains 91% RDX. These field exposures occurred because the C4 was either chewed as an intoxicant or used as a fuel for cooking; thus, the route of exposure was ingestion or inhalation. At least 40 American soldiers experienced convulsions due to RDX ingestion during the Vietnam War.89,90

RDX in waste water from manufacturing and loading operations has also contaminated the environment. Although contamination has appeared in soil and groundwater near some ammunition plants, RDX’s low solubility in water has limited its migration in most cases.

Human Exposure and Health Effects

The mainstay of treatment for RDX exposure is removal from exposure. Patients who are experiencing seizure activity should be given phenobarbital. Phenytoin is ineffective in controlling RDX-induced seizures.[89]

Toxicokinetics. Gastrointestinal absorption of RDX in humans is slow but complete; serum levels peak approximately 12 hours after ingestion. Clearance of RDX from the serum occurs in approximately 15 hours. The highest tissue levels of RDX occur in the kidneys, with slightly lower levels in the liver, brain, and heart. RDX is metabolized by the liver, and the metabolites are excreted primarily in the urine.[90] Unlike most other nitrated explosives, RDX does not metabolize to form nitrite in the blood.

Acute effects. RDX has relatively low acute toxicity. After acute exposure by inhalation or ingestion, there is a latent period of a few hours, followed by a general sequence of intoxication that begins with a prodromal period of irritability. Neurological symptoms predominate and include restlessness and hyperirritability; headache; weakness; dizziness; hyperactive reflexes; nausea and vomiting; prolonged and recurrent generalized convulsions; muscle twitching and soreness; and stupor, delirium, and disorientation.[91]

Clinical findings in acute exposures may also include fever, tachycardia, hematuria, proteinuria, azotemia, mild anemia, neutrophilic leukocytosis, elevated AST, and electroencephalogram abnormalities.[5] These abnormal effects, transient and unreliable for diagnostic purposes, last at most a few days. In fact, all physical and laboratory tests may remain normal, even in the presence of seizures.5,88,90 Electroencephalograms made at the time of convulsions may show bilateral synchronous spike and wave complexes (2–3/sec) in the frontal areas with diffuse slow wave activity; normalization occurs within 1 to 3 months.[89] Patients will recover from acute RDX exposure within days to months, gradually but completely, and they may experience amnesia early in the process.

Several case reports of RDX ingestion have been documented. In one instance, a 3-year-old child ingested plasticized RDX that had adhered to the boots and clothing of the child’s mother, who worked in a munitions plant. The child presented with status epilepticus, but recovered without sequelae. Laboratory tests were essentially normal, and the dose of RDX ingested by the child was estimated to be 84 mg/kg.[92] In the instances of convulsions that occurred among American soldiers in Vietnam, signs and symptoms usually began 8 to 12 hours after ingestion. Renal toxicity was observed in 3 of 18 patients (16%) in one series.[89] The sequence of symptoms was similar to that which occurs after occupational exposures, proceeding from confusion and hyperirritability to myoclonic contractions, severe prolonged generalized seizures, prolonged postictal confusion, and amnesia.5,89,90

The effects of acute exposure to RDX have also been studied in animals. In rats, the median lethal dose of orally administered RDX was approximately 200 mg/kg. Groups of 20 rats at each dose level were administered 25 mg/kg, 50 mg/kg, or 100 mg/kg; all doses produced hyperirritability, convulsions, and mortality up to 86.6%.[91]

Chronic effects. Although intensive research with animals has revealed some effects, few effects of chronic human exposure to RDX have been reported. One study reported that occupational exposure to TWAs of 0.28 mg/m^3 to 1.57 mg/m^3 did not cause hematological, hepatic, or renal abnormalities. This study also failed to substantiate a suspected association of RDX exposure with systemic lupus erythematosus. Moderate reductions of the erythrocyte count and hemoglobin occur during the first month of exposure, but these values return to normal by the end of the second month.[90]

Tests done on animals have supplemented the knowledge of the chronic effects of RDX in humans. Dogs fed 50 mg/kg of RDX daily for 90 days developed hyperirritability, convulsions, and weight loss, with no alterations of their blood chemistries or cytology. No histological lesions have been found in animals that have had RDX-induced seizures. In addition to the effects noted in humans, several others have been seen in animal tests: cancer, weight loss, anemia, hepatotoxicity, testicular degeneration, and suppurative inflammation of the prostate.[90]

Investigations into the mutagenicity and carcinogenicity of RDX have yielded conflicting results. RDX does not appear to be a mutagen, based on negative results in the Ames test, the dominant lethal test, and the unscheduled deoxyribonucleic acid synthesis assay. RDX has not been found to be carcinogenic in gavage studies performed on rats, but increased hepatocellular carcinoma and adenoma were noted in females of one strain of mice. Due to this finding, the US Environmental Protection Agency has classified RDX as a possible human carcinogen.[90]

Reproductive effects have been noted in rabbits and rats. A study performed on rabbits showed teratogenic effects at 2 mg/kg/day (10% of the dose that caused maternal toxicity).[90] Similarly, a teratology study performed on pregnant rats exposed to RDX resulted in offspring with lower body weights and shorter body lengths than were found in the control group. These researchers therefore recommended that workers desiring children be protected from exposure to RDX.

Primary Prevention and Medical Surveillance

Despite the low toxicity of RDX, exposure should be maintained at the lowest levels possible due to its possible carcinogenicity and reproductive effects. Sound industrial hygiene and preventive medicine measures, such as those used in the handling of TNT, should suffice to protect workers.

General medical surveillance examinations may be conducted, but specific testing for the effects of low-level occupational exposure does not appear warranted, given the absence of abnormal results even in patients with RDX-induced seizures. Surveillance for both males and females should also include a screening questionnaire for reproductive history.

Octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine

HMX is the highest energy solid explosive produced on a large scale in the United States. It is used exclusively for military purposes to implode fissionable material in nuclear devices, as a component of plastic-bonded explosives, as a component of rocket propellant, and as a high-explosive burster charge.[5]

Manufacture and Exposure Hazards

Exposure to HMX can occur during the manufacture and filling of munitions or through the environmental contamination of groundwater and soil. HMX, like RDX, is manufactured using the continuous Bachman process. Although its solubility in water is very low, HMX can be present in particulate form in water effluent from manufacturing, LAP, and demilitarization operations.

Human Exposure and Health Effects

Data on the effects on human health of exposure to HMX are very limited. HMX causes CNS effects similar to those of RDX, but at considerably higher doses.[93] In one study, volunteers submitted to patch testing, which produced skin irritation. Another study of a cohort of 93 workers at an ammunition plant found no hematological, hepatic, autoimmune, or renal diseases. However, the study did not quantify the levels of exposure to HMX.

HMX exposure has been investigated in several studies on animals. Overall, its toxicity appears quite low. HMX is poorly absorbed by ingestion. When applied to the dermis, it induces mild skin irritation but not ACD. Various acute and subchronic neurobehavioral effects have been reported in rabbits and rodents, including ataxia, sedation, hyperkinesia, and convulsions. Chronic effects of HMX documented in animal studies include decreased hemoglobin, increased serum alkaline phosphatase, and decreased albumin. Pathological changes were also observed in the animals’ livers and kidneys.[94] No data are available concerning the possible reproductive, developmental, or carcinogenic effects of HMX.

Primary Prevention and Medical Surveillance

Both primary prevention and medical surveillance for HMX exposure should be conducted as they would be for exposure to RDX.

Nitroguanidine

Nitroguanidine was first prepared in 1877, but was not used as an explosive until World War II. Today, it is a major component of triple-base solid propellants. The properties that give nitroguanidine an advantage over nitrocellulose or nitroglycerin include cooler burning, greater production of gas, less flash, less smoke, and less corrosion in gun barrels.

Manufacture and Exposure Hazards

Nitroguanidine is produced using the British aqueous fusion process, which does not depend on either coal or petroleum for raw ingredients. The ingredients and process chemicals used in nitroguanidine production include calcium carbide, nitrogen, calcium cyanamide, ammonium nitrate, guanidine nitrate, ammonia, and sulfuric acid.[5]

Workers can be exposed to nitroguanidine during the manufacturing process or during its incorporation into propellants. Nitroguanidine is moderately soluble in water and is rapidly absorbed in the gastrointestinal tract. It is only negligibly metabolized, however, and the body rapidly excretes unaltered nitroguanidine in the urine.

Human Exposure and Health Effects

Although no studies of the effects of nitroguanidine on humans have been done, studies performed on animals have indicated generally low toxicity. The oral median lethal dose (LD_50) is 3.9 g/kg in mice and 10.2 g/kg in rats. Direct contact with nitroguanidine may burn the skin and eyes. Single sublethal doses of nitroguanidine in rodents have caused respiratory effects (epistaxis and dyspnea), gastrointestinal effects (diarrhea and hemorrhage), and CNS effects (depression, hyperactivity, ataxia, and tremors). Chronic exposure to nitroguanidine may result in osmotic diuresis and modest hematological and liver function changes.[95] Results of studies of the reproductive and teratogenic effects of nitroguanidine appear to be negative, as do results of testing for mutagenicity.[96]

Primary Prevention and Medical Surveillance

Employees who work with nitroguanidine should avoid exposing skin, eyes, and the respiratory tract, and should wear PPE (safety glasses and respiratory protective equipment) when exposure to nitroguanidine exceeds the permissible exposure limit. Preplacement examinations should focus on the kidneys, liver, and blood and include renal and liver function tests and complete blood counts (CBCs). Because the toxic effects are subtle and the long-term implication of alterations in these clinical tests results is unclear, occupational health providers should use an interim medical history to determine the contents of periodic examinations on a case-by-case basis. Abnormal test results may indicate the need for improved exposure control in the workplace and additional medical follow-up.

Insensitive Munitions

Since explosives were first used by the military, accidental fires and munitions explosions have led to death of service members and destruction of military equipment. In July 1967, a rocket accidentally discharged on the flight deck of the aircraft carrier USS Forrestal. The chain reaction of exploding bombs and ordnance resulted in 134 fatalities, and the aircraft carrier was out of commission for several years. A similar incident occurred at US Army Camp Doha in Kuwait, where fire led to a chain reaction of explosions from stored artillery. These incidents underscore the need for insensitive munitions. The munition IMX is harder to explode in thermal, mechanical, and electrical tests than conventional military energetics such as TNT.[97] IMX is more stable and less reactive to shocks from gunfire, fire, and bombs. Although IMX is a high explosive, it cannot be detonated unintentionally, and IMX-filled rounds, mortar, projectiles, shells, and rockets are designed to be safer for soldiers to handle and transport.

Manufacture and Exposure Hazard

IMX is a high-performance insensitive energetic compound developed as a direct replacement for TNT in 155-mm M795 and M122 rounds.[97] IMX is composed of three compounds: 2,4-dinitoanisole (DNAN), nitrotriazolone (NTO), and nitroguanidine.[97]

IMX-101 is manufactured by a stepwise melt-pour manufacturing process. During manufacturing, DNAN is added to the nitroguanidine in a large stainless, steel steam-jacketed melt kettle. The kettle’s temperature is increased to a point above DNAN’s melting point, allowing it to melt (known as “charging” the melt kettle) and the residual moisture to evaporate. When this is complete, the temperature is adjusted https://frederick.craigslist.org/zip/d/free-chairs/6743884097.html to allow the nitroguanidine to melt. Once all the residual moisture of the DNAN-nitroguanidine mixture is removed, NTO is slowly added to the melt kettle and charged as well. Strips of the molten explosive mixture are then transferred from the melt kettle onto a flaker belt, where they are cooled and solidified while traveling along the belt. At the end of the flaker belt, the IMX-101 flakes are packaged.[98] The flakes are then shipped to a “load and pack” facility, re-melted, and poured into the explosive cavities of ammunition rounds.

Workers are exposed to IMX-101 during several of the steps in the manufacturing process, mostly during the melt-pour and shell loading operations. During these operations, exposure to IMX-101 dust, fumes, and vapor can occur. Exposure to IMX-101 can also occur through environmental contamination of the ground and surface water.

Human Exposure and Health Effects

There is limited information in the literature regarding human toxicity and adverse health effects of IMX-101. Nitroguanidine animal studies show no toxic effects. The US Army Public Health Center (USAPHC) conducted several studies to examine the health effects of the other two components of IMX-101. A study of oral toxicity was conducted in rats that noted several health effects including testicular atrophy, low sperm count, decreased sperm density and motility, splenomegaly, tubular degeneration, and lethality at high doses of DNAN (> 500 mg/kg/d). The LD_50 in male and female rats was 1,237 mg/kg and 924 mg/kg, respectively, and the combined LD_50 value was 1,100 mg/kg.[99]

The lethality and splenomegaly are suspected to be due to the DNAN because these effects are observed at similar concentrations of DNAN alone. The reproductive effects of the IMX-101 are likely due to NTO, which has a similar effect. However, in the IMX-101 mixture, the effect is seen at much lower levels, indicating there may be some synergistic effects. In a 2012 study, a 14-day oral administration of IMX-101 caused reductions in testicular mass at a daily dose of 100 mg/kg. This is a 10-fold lower concentration than the concentration when similar reproductive effects are seen in NTO alone, which caused a reduction in testicular mass at a daily dose of 1,000 mg/kg per day.[99]

The USAPHC studies on IMX-101 components showed that IMX-101 can affect blood, liver, eyes, skin, and endocrine function. DNAN is a nitroaromatic, and one of the main health concerns are hematopoietic effects. DNAN causes a reduction in red blood cell count, hematocrit, and hemoglobin levels. It also causes increased spleen mass and extramedullary hematopoiesis in rats, according to a 90-day oral gavage USAPHC toxicology study.[99] DNAN seems to have some dermal effects as well. Rabbits exposed to DNAN exhibited slight dermal irritation that was reversible within 24 to 48 hours. However, studies in guinea pigs indicated otherwise, showing that DNAN was not a sensitizer.[99] Other researchers have observed ophthalmologic effects after exposure in multiple species that is thought to be due to the DNAN metabolite, DNP.[100]

In a 2012 USAPHC study,[101] rodents given oral doses of DNAN had increased liver mass, which was observed at lower dose levels in male rodents compared to females. In addition, alanine transaminase and bilirubin became elevated in rats given DNAN at 50 and 100 mg/kg per day due to hepatocellular injury.[102]

A 2010 USAPHC study investigating oral exposure to NTO showed elevated AST levels and hepatocellular hyperplasia in male rodents at high doses. However, the main health effect of NTO is on the reproductive system. NTO is associated with decreased sperm count, testicular atrophy, and decreased epididymis mass in rats. These effects suggest that NTO might be an endocrine disruptor, but NTO does not appear to affect testosterone or estrogen-mediated signaling pathways. NTO targeting of reproductive organs was also tested in vivo using Hershberger bioassays, which provided no evidence that NTO acts as an estrogenic or antiandrogenic endocrine disruptor. Biologically significant effects on organ mass were limited to reductions in testes and epididymis mass. The study also noted that NTO does not act as an estrogen- or thyroid-active compound.[101] NTO may cause mild dermal irritation according to the safety data sheet produced by the IMX-101 manufacturer.

Primary Prevention and Medical Surveillance

In September 2011, the Joint Munitions Command surgeon, in conjunction with USAPHC, convened an expert panel to provide recommendations regarding medical surveillance of IMX-101. The panel included experts from academia and the surgeon general’s consultants for occupational medicine, endocrinology, hematology, and oncology. The panel’s recommendations were adopted for worker medical surveillance for IMX-101 (Exhibit 28-1).

In 2013, the Joint Munitions Command surgeon reviewed the medical surveillance data obtained from clinics performing IMX surveillance. Hemolytic anemia was the most prevalent health effect observed in IMX workers.[102] DNAN has similar effects on hemoglobin levels as other nitrogen-based explosives, such as TNT. Monitoring hemoglobin levels has been standard practice for the medical surveillance of workers exposed to TNT, and the same monitoring is required for IMX-101 workers. The primary laboratory test for the hematopoietic effects of IMX-101 is a CBC. Diagnosis of hemolytic anemia includes obtaining a health history, family history, occupational history, clinical presentation, and special laboratory testing including electrophoresis. Work-up of IMX-101 workers for hemolytic anemia should rule out other causes of hemolytic anemia, including blood loss, intravascular hemolysis, metabolic defects, membrane abnormalities, hemoglobinopathy, autoimmune defects, and fragmentation hemolysis.

Preliminary Exposure Level

The USAPHC established a preliminary occupational exposure limit (OEL) for two of the compounds in IMX-101 using the data from the multiple USAPHC animal studies. The OEL for DNAN was established at 0.10 mg/m^3. An OEL for NTO was established at 1.6 mg/m.[3] An OEL for nitroguanidine has not yet been established because the only observed health effects with IMX-101 are attributed to DNAN (hematopoietic effects) and NTO (reproductive effects in males).[100]

EXHIBIT 28-1

IMX MEDICAL SURVEILLANCE RECOMMENDATIONS

Preplacement Examination

- Complete history using DD Form 2807-1, Report of Medical History: a review of systems with emphasis on the eyes, gastrointestinal tract, skin, and the hematologic, reproductive, central nervous, cardiovascular, and respiratory systems.

- Medical examination should be recorded on DD Form 2808, Report of Medical Examination, and include vital signs, and a focused exam of the eyes, gastrointestinal tract, skin, and the hematologic, reproductive, central nervous, cardiovascular, and respiratory systems.

- Laboratory tests should include the complete blood count (CBC), compete metabolic panel (CMP), dipstick urinalysis, γ-glutamyltransferase (GGT), alkaline phosphatase (ALP), and glucose-6-phosphate dehydrogenase.

90-Day Assessment

- Repeat the history and physical elements of the preplacement examination with a focus on the male reproductive system and hematopoietic changes.

- Repeat CBC, CMP, GGT, ALP, and dipstick urinalysis.

- Abnormal labs require follow-up by the occupational health clinic provider or personal physician. If there are no health status changes, a 6-month evaluation cycle starts.

Semiannual Examination

- Repeat the history and physical elements of the preplacement examination with a focus on the male reproductive system and hematopoietic changes.

- Repeat CBC, CMP, GGT, ALP, and dipstick urinalysis, and add a haptoglobin (Hp) and serum lactic acid dehydrogenase (LDH). The occupational health provider should consider adding a peripheral blood smear, a reticulocyte count, and other testing as indicated.

Termination Examination

- Perform the examination within 30 days of the end of employment.

- The termination exam contains the same evaluations as the semiannual evaluation.

Temporary Removal From Work

- The healthcare provider should consider medical removal when lab test abnormalities exist compared to the baseline or periodic laboratory exam, AND one confirmatory lab finding is abnormal.

- Primary lab test abnormalities include a fall in hemoglobin of 2.0 g/dL or more from the initial or periodic test, and a level for a male below 14.0 g/dL or for a female below 12.0 g/dL.

- Confirmatory lab abnormalities include a decreased Hp, increased reticulocyte count, increased LDH, or abnormal peripheral blood smear.

- The worker’s supervisor must be notified of the recommendation for medical removal, including the duration of the removal and the indicators for return to work that will be tracked.

Return to Work

- Any worker who is medically removed should be examined by a medical provider and cleared to work after follow-up lab testing confirms a return to baseline primary or confirmatory lab values.

- The employee may be tested at the occupational health clinic, or they may see their own provider for testing.

- Once testing is completed, the employee should be cleared by the occupational health clinic provider to return to work.

___________________

Data source: Monks WS, Mirza RA. Medical surveillance examinations for workers exposed to IMX-101 and its components. Army Med Dep J. In press.

At the same time, the Occupational Alliance for Risk Science produced workplace environmental exposure levels (WEELs) for DNAN, NTO, and nitroguanidine. The WEELs for DNAN (8-h TWA: 0.1 mg/m^3) and NTO (8-h TWA: 2 mg/m^3) were published in 2014,101,103 and the WEEL for NQ (8-h TWA: 7 mg/m^3) was published in 2016.[104]

THE INITIATING EXPLOSIVES

The initiating explosives, which are used in combination with more powerful explosive charges, are a heterogeneous group of chemicals that are prepared and used in very small quantities (thus limiting their potential for exposure). The most frequently used initiating explosives are lead azide and lead styphnate. A less common initiator is diazodinitrophenol (DDNP), an ingredient in primers and commercial blasting caps.

Lead Azide

Lead azide, first prepared in 1890, is produced when lead nitrate reacts with sodium azide; sodium nitrate is a byproduct.[27] Because it is quite stable, lead azide is one of the best initiators for sensitive explosives such as tetryl and RDX. Lead azide is usually used in combination with lead styphnate and DDNP. In the civilian sector, it is used in cartridge primers, primer cords, and blasting caps.

Lead azide is composed of 70% lead by weight, and it releases poisonous lead and nitrogen oxide fumes when heated. However, due to safety constraints, there is little opportunity for exposure to lead azide itself. During its manufacture, lead azide is screened in barricaded rooms to avoid continuously exposing the workers. Workers can be exposed intermittently while entering the screening rooms, but they should only do so when wearing respiratory protective equipment. Some exposure can occur while primers are loaded, but this can be prevented by local exhaust ventilation.

The acute effects of exposure include vasodilation and headache, and the chronic effects are those of lead intoxication. Due to these health effects, silver azide has been investigated as a substitute for lead azide. Regulations and medical surveillance associated with exposure to lead azide should be based on the lead content. These specific requirements are dictated by 29 CFR, Part 1910.1025.[105]

Lead Styphnate

Lead styphnate was first prepared in 1914 by von Hertz in Germany, and it was used as an explosive by Russia in World War I. Although lead styphnate is easily ignited, it is a relatively poor initiator, and thus is often used in combination with other primary explosives. Manufactured from 2,4,6-trinitroresorcinol, magnesium oxide, and lead nitrate, lead styphnate may be used as a covering charge (ie, the booster) for lead azide, as an ingredient of priming compositions, as a component in blasting caps, and as a component in small-arms primers (eg, M16 primer uses 4 mg of lead styphnate).

The effects on human health have not been well studied, but acute effects appear to be limited to dermatitis and yellow staining of the hair and skin.[20] Chronic exposure may result in lead toxicity, and the lead content of this explosive should form the basis of monitoring and medical surveillance for exposure.

COMPOSITE PROPELLANTS AND EXPLOSIVES

Composite propellants are solid rocket fuels that are being used in an increasing number of applications. As with all explosives and propellants, they consist of an oxygen donor—the oxidizer—and a hydrocarbon fuel. The oxidizer is usually an inorganic salt, and the fuel is a polymeric binder (essentially a plastic). The composites have a wide range of performance characteristics, are tremendously stable, and are inexpensive. However, they are so reactive that they corrode the metal in gun barrels.

The vast number of alternatives available for use as oxidizers and binders preclude discussion of them all. Information about the toxicity of the inorganic salts is widely available in the toxicology and occupational medicine literature. Therefore, this discussion focuses on ammonium perchlorate, the most widely used oxidizer in composite propellants due probably to its cost, stability, ease of manufacture, and versatility. Ammonium perchlorate is used in the Multiple Launch Rocket System and in rocket-assisted howitzer projectiles. Workers can be exposed via the dermal and inhalational routes during all stages of propellant production.

Before it can be used in munitions, an oxidizer must be ground and screened by particle size to ensure it will burn uniformly. Both grinding and screening raise significant levels of dust, some of which is respirable and must be controlled. The process of mixing the oxidizer with the binder can also be quite dusty.

Numerous polymeric binders are currently in use. After the binder is mixed with the oxidizer, the resultant propellant can either be cast or pressed into a mold. Cast materials are melted, then poured as a liquid into a mold, while pressed materials are kept in their solid state and shaped by simply molding or extruding. A high-temperature curing process then effects polymerization, a process that releases toxic vapors, to which the workers can be exposed. The propellant core is then removed from the mold and machined or trimmed as needed. Workers can be exposed to dust during these operations.[106]

Plastic-bonded explosives are similar in concept to the composite propellants, but are designed to function as high explosives rather than as propellants. Several major groups are the PBX, PBXN, and LX-10 series. These explosives represent a variety of mixtures combining high mechanical strength, excellent stability, and a wide range of explosive properties. They contain a high percentage of basic explosive (RDX, HMX, hexanitrostilbene, or penta-erythritol-tetranitrate), which is mixed with a polymeric binder (polyester, polyurethane, nylon, polystyrene, rubbers, nitrocellulose, or Teflon [DuPont, Wilmington, DE]); plasticizer (dioctylphthalate or butyldinitrophenylamine); and metallic fuel (powdered aluminum or iron). A major advantage of using plastic-bonded explosives is that the final product can be injection- or press-loaded at ambient temperatures, or even loaded in the field. The binders are thermally degradable, so that in demilitarization operations the ingredients can be completely recovered.[5]

Specific medical information regarding composite propellants and explosives is difficult to provide. For all practical purposes, the polymers are medically inert. The other components, which are heterogeneous and from different chemical families, have vastly different effects, many of which are not yet characterized.

LIQUID PROPELLANTS

The two types of liquid propellants are liquid rocket propellants and liquid gun propellants. Both the National Aeronautics and Space Administration and the US Air Force use liquid rocket propellants in high-performance missile systems. The armed services have developed liquid gun propellants for use in large-caliber weapons such as the 120-mm main tank cannon, 105-mm howitzer, 155-mm howitzer, and 8-in. howitzer.

Rocket Propellants

Many chemicals have been used as components of liquid rocket propellants. Most of them have only limited military use and therefore will not be discussed in this chapter. The liquid rocket propellants that do have military applications include (a) hydrazine, (b) nitrogen tetroxide, and (c) boranes.

Hydrazine is widely used in the chemical industry, where most of the studies of its effects on human health have been conducted. Studies on humans and animals have demonstrated deleterious health effects. The effects on humans have been limited to irritation of the skin and mucosa and hepatic disorders, but the effects found in animal studies have been more severe. Mice have developed hepatomas after being fed hydrazine, rats exposed to hydrazine vapor have developed nasal tumors, and hamsters have developed lung adenomas. Urinary levels of hydrazine have shown some utility in monitoring exposure. At a minimum, medical surveillance should periodically assess erythrocyte indices, hypoglycemia, kidney and liver disease, hemorrhagic diathesis, and allergies to phenylhydrazine and isoniazid.[107]

Nitrogen tetroxide has also been used widely in the space program, with potential health effects. The vapors can cause immediate or delayed swelling and blistering of the adnexa oculi and severe burns of the dermis. When nitrogen tetroxide is inhaled, it can react with moisture in lung tissue to form nitric acid and cause delayed pulmonary edema.[5]

During the past 60 years, the fuel boron hydride and its derivatives, also known as boranes, have become widely used in rocketry as rubber vulcanizers, corrosion inhibitors, and components in other chemical processes. The reactivity of the boranes has led to a proliferation of uses, but has also contributed to their significant toxicity. Regardless of their use, boranes are toxic to the respiratory system, cardiovascular system, CNS, skin, kidneys, and liver.

Carboranes—boranes that contain carbon in addition to boron and hydrogen—have been developed and investigated for use in solid-fuel systems. The carboranes are skin irritants, but they do not sensitize. They appear to have relatively low acute toxicity. Subchronic inhalation exposure in dogs resulted in interstitial pneumonitis and early emphysematous changes, but no developmental effects were noted.[108]

Gun Propellants

Liquid gun propellants have several advantages over solid propellants for use in self-propelled howitzers and naval vessels: they are less expensive to produce and transport, less vulnerable to secondary ignition, and easier to store in combat vehicles; they can also be demilitarized more safely and easily than solid propellants.[109] However, more workers can be exposed to the chemical components during the manufacture, transport, and use of liquid propellants compared to solid propellants.[110]

Liquid gun propellants consist of aqueous solutions of hydroxyl ammonium nitrate (HAN) mixed with either trimethanol ammonium nitrate or triethanol ammonium nitrate. No studies on the effects on human health have been reported on either of the mixtures or the individual components. However, the aqueous solutions and pure HAN have been evaluated for mammalian toxicity.111–116 The mixtures were found to be moderately toxic to both rats and rabbits: for male rats, the oral LD_50 was 822 mg/kg, and for female rats, 520 mg/kg; for rabbits, the oral LD_50 was 101 mg/kg.[113] Oral exposure to the mixtures induces cyanosis, respiratory distress, and, at high doses, death.[111] A single intragastric dose of 400 mg/kg produced no ECG changes in dogs. Treatment with methylene blue rapidly reversed the acute toxic effects. The mixtures were also found to be ocular irritants, but were not corrosive to the cornea.[110] However, exposure to mixtures induced hematological changes: methemoglobinemia occurred; oxygen tension decreased; free nitrites, Heinz bodies, and crenated erythrocytes formed; and, at lower doses, serum potassium decreased.[111]

The rabbit studies also found that HAN applied to the dermis caused chronic and ulcerative dermatitis, and at higher doses, hemolytic anemia in addition to the systemic effects described previously for exposure to the mixture. However, no blood chemistry changes were noted.[112] When administered orally to three groups of rabbits (1, 5, and 25 mg/kg/d) for 21 days, HAN induced splenic congestion and hyperplasia of the reticuloendothelial system at all doses.[113] At 25 mg/kg/day, HAN caused anemia and myeloid hyperplasia of the bone marrow.[113] Inhalation of aerosolized HAN has been found to induce Heinz-body formation and upper respiratory irritation.[114] Several other liquid gun propellants have also been investigated as aerosols, and the effects they elicited were qualitatively similar to those of HAN.[115]

The Occupational Medicine Division of the USAPHC has established preliminary guidelines for medical surveillance, and a provisional military exposure guideline of 3 mg/m^3 has been proposed for liquid gun propellants.116,117 Testing for methemoglobinemia or examining the peripheral blood for Heinz bodies should be considered part of the medical monitoring for exposed employees. Reasonable occupational precautions include restricting employees from eating, drinking, and smoking in areas where these chemicals are handled or stored; ensuring adequate ventilation; preventing spills and splashes; and using PPE such as splash goggles and gloves.

SUMMARY

In defending the United States, military and civilian personnel must necessarily produce, store, and handle a variety of munitions. In the Army, these operations occur around the country at various arsenals, proving grounds, depots, and ammunition plants, which together employ more than 100,000 workers. Despite incomplete laboratory studies and imperfect data, information has been gathered during the last 50 years on the effects of workplace exposures to these chemicals, much of it recorded during wartime while large quantities were being produced.

The chemical families represented among energetic materials (explosives, propellants, and pyrotechnics) include aliphatic nitrate esters (such as nitroglycerin), nitroaromatics (such as TNT), and nitramines (such as RDX). Considering the properties of the energetic materials—explosives, propellants, and pyrotechnics—it was inevitable that they would be utilized in military weapons. Explosives create a shock wave that progresses rapidly, while propellants release large amounts of hot gas in a more controlled manner. Pyrotechnics burn slowly, emitting tremendous heat or light. Most modern weapons utilize energetic compounds in combination, capitalizing on their individual properties.

As these energetic materials are synthesized and assembled into munitions, workers can be exposed to the raw materials, the finished product, or any number of chemical intermediates along the way. These chemicals are usually absorbed via the dermal, inhalational, and, less importantly, the ingestional routes; as a class they can produce dermatitis, methemoglobinemia, vasodilation, and cancer. The standard industrial hygiene principles of engineering and administrative controls and PPE can minimize exposures. Obviously, the explosive properties of these chemicals necessitate strict compliance with safety guidelines. Preplacement screening and periodic surveillance must be tailored to the specific hazards in each industrial operation and at each site. Generalized medical guidance regarding these mixtures has little practical significance.

Individuals exposed to mixtures of chemicals such as TNT and IMX must be enrolled in medical surveillance programs for each chemical. Where the laboratory tests overlap, redundant labs should be eliminated. The effects of exposure to multiple chemicals cannot be predicted with certainty because the response may be additive or synergistic, or the exposure may have no effect at all. Thus, a thorough baseline medical examination done prior to exposure is important; the provider should review of the occupational history and capture previous exposures and work-related injuries and illnesses. Depending on the exposure, an endocrinology consult may help in developing medical surveillance recommendations for these individuals.

The above approach should also be followed for individuals in other unique populations, such as those who work in research and development of chemical munitions; those with hormone abnormalities; those undergoing active chemotherapy or biologic therapy; and those with blood disorders. A thorough medical evaluation of these individuals and a conversation with their providers may be necessary for a coordinated care approach to ensuring worker safety.

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80.   US Department of Health and Human Services, National Institute for Occupational Safety and Health. Dinitrotoluenes (DNT). Washington, DC: USDHHS; 1985. NIOSH Current Intelligence Bulletin 44, DHHS (NIOSH) Publication 85-109.

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82.   Rickert DE, Chism JP, Kedderis GL. Metabolism and carcinogenicity of nitrotoluenes. Adv Exp Med Biol. 1986;197:563–571. https://www.ncbi.nlm.nih.gov/pubmed/3766281. Accessed October 31, 2017.

83.   Levine RJ. Dinitrotoluene: Human Atherogen Carcinogen, Neither or Both? Research Triangle Park, NC: Chemical Industry Institute of Toxicology Activities, Centers for Health Research; 1987:1–5.

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85.   Hamill PVV, Steinberger E, Levine RJ, Rodriguez-Rigau LJ, Lemeshow S, Avrunin JS. The epidemiologic assessment of male reproductive hazard from occupational exposure to TDA and DNT. J Occup Med. 1982;24(12):985–993.

86.   Mura WR, Small MJ, Rosenblatt DH, Dacre JC. Munitions-Related Substances of Potential Concern as Airborne Pollutants. Fort Detrick, MD: US Army Medical Bioengineering Research and Development Laboratory; 1974. USAMBRDL Technical Report 7409.

87.   Small MJ. The Hazard Ranking and Allocation Methodology: Evaluation of TNT Wastewaters for Continuing Research Efforts. Fort Detrick, MD: US Army Medical Bioengineering Research and Development Laboratory; 1978. USAMBRDL Technical Report 7808.

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93.   Burrows EP, Rosenblatt DH, Mitchell WR, Parmer DL. Organic Explosives and Related Compounds: Environmental and Health Considerations. Fort Detrick, MD: US Army Medical Bioengineering Research and Development Laboratory; 1989. USAMBRDL Technical Report 8901.

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95.   Frost DG, Morgen EW, Letellier Y, et al. Ninety-day Subchronic Oral Toxicity Study of Nitroguanidine in Mice. San Francisco, CA: Letterman Army Institute of Research; 1988. Final Report, Technical Report No. 319.

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Chapter 29

BIOLOGICAL MONITORING

TIMOTHY M. MALLON, MD, MPH*; RICHARD P. PHIPPS, PHD†; JUILEE THAKAR, PHD‡; COLLYN WOELLER, PHD¥; DEAN P. JONES, PHD§; DOUGLAS I. WALKER, PHD¶; KARAN UPPAL, PHD**; MARK UTELL, MD††; AND THOMAS THATCHER, PHD‡‡

INTRODUCTION

DEFINITION AND TYPES OF BIOMARKERS

DEPARTMENT OF DEFENSE NEEDS FOR EXPOSURE ASSESSMENT AND BIOMARKERS

BIOMARKER DISCOVERY AND APPLICATIONS

PHYSIOLOGICAL TEST MATRICES

NEW DEVELOPMENTS IN BIOMARKERS

GENETIC AND EPIGENETIC BIOMARKERS

BIG DATA ANALYSIS

SUMMARY

*Colonel (Retired), US Army; Adjunct Assistant Professor, Department of Preventive Medicine & Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

† Professor, Departments of Medicine and Environmental Medicine, University of Rochester Medical Center, Rochester, New York 14618

‡ Professor, Departments of Microbiology & Immunology and Biostatistics & Computational Biology, University of Rochester Medical Center, Rochester, New York 14618

¥ Professor, Department of Environmental Medicine, University of Rochester Medical Center, Rochester, New York 14618

§ Professor, Clinical Biomarkers Laboratory, Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University, Atlanta, Georgia 30322

¶ Assistant Professor, Clinical Biomarkers Laboratory, Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University, Atlanta, Georgia 30322

**Assistant Professor, Clinical Biomarkers Laboratory, Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University, Atlanta, Georgia 30322

†† Professor, Departments of Medicine and Environmental Medicine, University of Rochester Medical Center, Rochester, New York 14618

‡‡ Research Associate Professor, Department of Medicine/Pulmonary and Critical Care, University of Rochester Medical Center, Rochester, New York 14618

INTRODUCTION

Biological monitoring, also termed biomonitoring, is the use of blood, urine, or other human samples to assess an individual’s state of health, responses to therapeutics, and exposure to chemicals, or other environmental agents of concern.[1] Biomonitoring is of considerable potential value to assess military exposures and possible contributions to health outcomes.2,3 This chapter provides a review of biomonitoring for military purposes and a perspective for research and surveillance opportunities for biomonitoring both within and outside the military. It also addresses the potential to develop partnerships to examine deployment health-related questions. Further, the chapter will define the exposome; describe several types of currently available biomonitoring; discuss biomonitoring detection methods, sample media, and “omics” technologies available to examine biomarkers; and address the considerable range of information provided by these tools. The chapter’s last section discusses new directions in biomonitoring and big data analysis.

The chapter also addresses how the Department of Defense (DoD) Serum Repository (DoDSR) can continue providing data for biomonitoring and ultimately improve health protection of service members while also contributing to advancing research in the field. Through the adoption of improved quality assurance practices and the addition of capabilities to handle varied sample types, the repository will be able to maintain state-of-the-art capabilities to support biomonitoring in the future.4,5

DEFINITION AND TYPES OF BIOMARKERS

What Are Biomarkers?

The National Institutes of Health defines a biomarker as “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacological responses to a therapeutic intervention.”[6] A biomarker could be any chemical produced by the body, an environmental chemical or its metabolites, or a measurement of physiological or cognitive function that reflects the effect of chemicals on the body. In all cases, the measured biomarker reflects the unique genetic interaction of the host with the environmental chemical and the metabolism of the chemical in the body. Everyone’s susceptibility to environmental chemicals is affected by their nutritional status and how well the body metabolizes and excretes the metabolic breakdown products.[7] Figure 29-1 diagrams a completed pathway of exposure from external dose to potential health outcome.

Certain biomarkers can be used to assess internal dose of exposure, while others can be used to assess physiological effects, such as pulmonary function test results. Biomarkers must be stable in the blood or body fluid in which the chemical or metabolite is found. The biomarker is useless if it is metabolized and excreted before the sample media can be collected.[8] Biomarkers for military use must be reliably measured; sample collection must be minimally invasive or noninvasive and the sample feasible to collect while deployed; and the test must be economical and logistically feasible to analyze in the deployed environment.[9]

Figure 29-1. Pathway from exposure to disease.

Types of Biomarkers

Biomarkers of Exposure

Chemicals that enter the body can be measured directly as the unchanged compound; they also can be measured as the metabolic breakdown product of the chemical; or they can be measured as the product of their interaction with tissues in the body.[10] The identification and quantification of chemicals, or their metabolites, in biological sample media can provide accurate assessments of systemic exposures and total dose. Baseline and periodic assessments of chemical substances in the blood or urine of deployed service members may support health risk assessments related to deployment exposures.

In recent decades civilian and military scientists have been enhancing medical surveillance programs with biomonitoring applications. Since the 1990s, the Centers for Disease Control and Prevention have measured biomarkers of exposure for more than 300 environmental chemicals and nutritional indicators in non-occupationally exposed populations in the United States as part of the National Health and Nutrition Evaluation Survey (NHANES).[11] The chemicals selected for measurement are found in air pollution, pesticides, plastics (such as bisphenol A), and flame retardants. Trends observed over time allow for assessment of regional differences and demographic differences. NHANES measured 308 chemicals in a cross-section of the US population, but it is estimated there are between 25,000 and 85,000 chemicals in production today.[11] Thus, the ability to assess biologically relevant dose may not be possible for most chemicals in production today. However, with newly advanced chemical profiling techniques, it is possible to identify and monitor environmental exposures in deployed troops.

In 2001, as part of the Military Deployment Human Exposure Assessment Study, researchers obtained air and personal monitoring samples for a variety of chemicals commonly encountered during deployments.12,13 The air and personal monitoring was done during and after deployment. Predeployment serum was collected but the serum was not analyzed. The capabilities exist to retrospectively examine serum for specific biomarkers of chemical exposure, but this is not routinely done because the costs are prohibitive. After exposure, a retrospective look-back at the predeployment serum is possible for selected hazards in small numbers of troops to monitor changes in internal dose over time after consideration of other confounders that affect exposure.

The use of biomarkers of exposure in deployed military populations has been recommended in the past when personal breathing zone air sampling data was not available. This data is necessary to gain an understanding of the complex exposure situations that exist during deployment, for example, when personnel encounter smoke from open-pit burning of trash.14,15 The biological specimen must be collected soon after exposure, before the chemical is metabolized or excreted. Understanding the toxicokinetics of the chemical in the body will permit selection of the most appropriate exposure biomarker so that problems of specificity can be minimized. Information on smoking status is also helpful to control for metal and volatile organic chemical exposures found in cigarettes. It is also important to note that any biomarker detected may have little to no relationship with recorded health outcomes.[8] Exposure biomarkers approved for use by the DoD currently include blood lead and the 24-hour urine-depleted uranium bioassay for troops who report exposures on the Post Deployment Health Risk Assessment.[16] Additionally, red blood cell cholinesterase is used to monitor occupational exposure to nerve agents in explosive ordinance handlers and pesticide applicators.

In the occupational setting, exposure biomonitoring is most frequently done as part of established medical surveillance programs. Workplace chemicals are sampled in the blood or urine to evaluate whether exposures have exceeded acceptable limits.[17] DoD Instruction 6055.05M, Occupational Medical Examinations and Surveillance Manual, recommends sampling for a few specific hazards.[18] DoD pesticide applicators and technical escort personnel who handle explosive ordinance have medical monitoring requirements.

At least two highly publicized incidents of specific chemical exposures have occurred after which the individuals involved were offered biological monitoring. In one incident, National Guard members providing security around a water treatment plant in Iraq were exposed to sodium dichromate powder that was dispersed when thieves stole drums storing the powder. In another incident, at Camp War Eagle in Iraq, off-camp burning by local nationals exposed troops to high lead concentrations.19,20

Surrogate biomarkers can be considered a type of exposure biomarker when the biomarker is used to substitute for a clinical endpoint. For example, cotinine levels are elevated in smokers.21,22 Methemoglobin levels have been used as a marker of cyanide exposure, but clinicians should be aware that other chemical exposures will also raise methemoglobin levels.[23]

Biomarkers of Effect

When the chemical agent or its metabolite causes a measurable change in a biochemical process or an alteration in a structure or body function, the biomarker reflecting the measurable change is a biomarker of effect. The change may be due to a specific airborne hazard in the deployed environment; for example, pulmonary function testing results may be altered when service personnel experience high silica exposures during sand storms in Iraq and Afghanistan. Exposure to these inhalation hazards may impact pulmonary function as much as, if not more than, personal habits such as smoking.24,25 Workers exposed to nerve agents will show a drop in their red blood cell cholinesterase immediately after exposure.

Biomarkers of Susceptibility

Biomarkers of susceptibility reflect an individual potential risk of developing disease, genotypic and phenotypic changes, or physiological changes in response to environmental exposures. Asthma and other respiratory conditions, cardiorespiratory disease, and other diseases produce changes in metabolomic, immunologic, and genetic and epigenetic biomarkers that are clues to changes in disease susceptibility. Although several molecules, including proteins and ribonucleic acid (RNA), can serve as susceptibility markers, genome polymorphisms are particularly well suited as indicators of susceptibility. Genetic susceptibility to air pollution has been studied in asthma patients. Genetic variation has been shown to increase susceptibility to environmental tobacco smoke and diesel exhaust; variation in metabolizing genes may also increase susceptibility to pollutant-related cellular damage.26,27 Toxicology studies have led to new genetic screening tests for susceptibility to specific exposures. For example, a mutation on the HLA-B69 increases workers’ risk of becoming sensitized to beryllium and developing chronic beryllium lung disease, and coal workers who developed silicosis were found to have a polymorphism in tumor necrosis factor that increases their risk of developing silicosis.[28]

Comparison of Biomarker Types

An environmental chemical is taken into the body through inhalation, ingestion, or skin absorption. When dose response information is known for a given chemical, it may be possible to predict health effects if the internal dose is known. Exposure biomarkers detect the agent or its metabolic breakdown products, which is considered to be a measure of internal dose closer to the targeted site of action than the external dose.[14] Biological markers of effect may identify subclinical changes caused by various exposures. More recently, biomarkers in the pathophysiology of tissue injury or inflammation, including chemokines, cytokines, and immunoglobulins, are being used to examine specific tissue injuries.

Limitations on Use of Biomarkers

Advancements in analytical chemistry have permitted the identification of biomarkers of exposure at extremely low levels, so it is imperative that detection of these biomarkers in a given sample be sensitive and specific. Low detection limits for these biomarkers make correlation with clinical findings very difficult, and only subclinical effects are expected. In order for the biomarker to be used, there must be a population reference value that defines the background levels in the unexposed general population, so that sample results can be compared to the reference population values. Further, the toxicology of the chemical should be worked out so that at a given exposure level, the biomarker sample results should correspond to the degree of severity of the response based on pathology studies.[9] Pre-validation and validation studies are also necessary prior to clinical or biomonitoring use so that reference values can be provided and the results can be explained to the affected individuals.

Lastly, use of biomarkers to study associations between environmental exposure and health outcomes is difficult to do in a scientifically rigorous way because of the lack of breathing zone sampling data, often poorly understood toxicodynamics, variability in nutritional status, and genetic variability among individuals.

DEPARTMENT OF DEFENSE NEEDS FOR EXPOSURE ASSESSMENT AND BIOMARKERS

The Exposome

The “exposome” is the cumulative measure of environmental influences and biological responses throughout a lifespan.29,30 The exposome includes all environmental, dietary, microbiome, behavioral, therapeutic, and endogenous processes experienced cumulatively throughout life. Military personnel experience a broad array of exposures, and advances in this area will enhance the interpretation and utility of biomonitoring for military exposures.[31] New developments in this area are also helping to drive advances in personalized, or precision, medicine.[32]

Airborne Hazards and Military Deployment

This section briefly presents an overview of prior deployment exposures and associated studies to illustrate the need for real-time breathing zone sampling and expansion of the DoDSR to increase the specimen types that are collected and stored there. Service members who fought in Vietnam were potentially exposed to the dioxin-containing herbicide Agent Orange; many filed compensation claims because they believed Agent Orange exposure caused their health problems.33,34 No area sampling data or breathing zone sampling data was performed documenting exposure to Agent Orange. Research on Agent Orange exposure showed few differences in health outcomes between the exposed and unexposed groups and supported the conclusion that most troops were not heavily exposed to Agent Orange.[34]

However, because uncertainty regarding actual exposure levels remained, the US Department of Veterans Affairs (VA) presumptively awarded compensation to veterans who deployed to Vietnam, regardless of exposure status, if they developed any health conditions linked to Agent Orange exposure.33,34 Unfortunately, no predeployment serum samples were drawn that could be used to assess baseline dioxin levels for comparison with the postdeployment laboratory analysis of serum dioxin levels. If DoD had collected predeployment and postdeployment serum dioxin levels, and collected blood for monitoring changes in deoxyribonucleic acid (DNA) to identify genetic susceptibility for the conditions linked to Agent Orange exposure, the health risks and disability compensation determinations may have been more evidence based.

Similarly, many service members who fought in the first Gulf War developed Gulf War illness. They reported poorly characterized symptoms following exposure to smoke from oil well fires, pesticides, depleted uranium, mustard and nerve chemical warfare agents, vaccinations for anthrax and smallpox, and the nerve agent antidote pyridostigmine bromine. Again, there was no breathing zone sampling data to document exposures. Over a third of Gulf War veterans still report nonspecific symptoms. Deployment exposures were thought to be the cause of several conditions that were collectively referred to as “Gulf War syndrome,” but no exposures were definitively established as the cause.[35]

In response to public concerns and congressional direction to obtain better deployment exposure information, DoD Instruction 6490.03, Deployment Health,[36] was revised in 2006 to require the military services to perform deployment health risk assessments that included baseline, routine, and incident-related exposure monitoring and to document any deployment-related exposures in the individual medical record.[1] Routine exposure monitoring was recommended for chronic low-level exposures.

During the early years of Operation Enduring Freedom and Operation Iraqi Freedom, service members were exposed to high levels of silica-containing particulate matter that exceeded the US Environmental Protection Agency’s national ambient air quality standard by a factor of six during dust storms.[37] Some personnel were also exposed to smoke from open-pit burning operations, other personnel were exposed to hexavalent chromium dust at a water treatment plant, and still others were exposed to sulfur dioxide while fighting a sulfur mine fire.[37]

Personnel who deployed to Iraq were potentially exposed to smoke from burn pits that were used to destroy plastics, metals, rubber, paints, solvents, munitions, wood, and medical waste.38–45 Very high levels of particulate matter were recorded in the vicinity of the burn pits, in addition to low levels of volatile organic compounds, polycyclic aromatic hydrocarbons (PAHs), and heavy metals.38–41 Burn pit operations were conducted at Joint Base Balad, Iraq, until incinerators were installed in 2010. During the peak of burn pit operations in 2007, the base housed 25,000 troops, who generated 250 tons of waste that was burned daily.39–42 Ambient air monitoring stations were set up to monitor particulate levels that year.39–41

In 2010, the Institute of Medicine, part of the National Research Council (NRC), was asked to examine health effects of exposure to open-pit burning during deployments.[43] The resulting 2011 report, “Long Term Health Consequence of Exposure to Burn Pits in Iraq and Afghanistan,” noted that DoD did not collect breathing zone exposure data on individual service members.[43] Further, it observed that linking ambient air pollution measurements to individuals and their health outcomes was not possible because the air sampling was not carefully designed, nor was it representative of an individual’s exposure. The report recommended that DoD collect breathing zone samples, conduct long-term studies to examine the health outcomes of deployed troops, and address service members’ concerns about perceived health risks.[42] The NRC recommended identification of a cohort who had deployed and a control cohort whose serum could be obtained from the DoDSR and compared. However, as the NRC recognized, this comparison had considerable uncertainty because the time the service members had actually spent at Joint Base Balad, their proximity to the burn pits, and other variables were unknown. Individual breathing zone sampling and bio-specimens taken at known intervals before, during, and after deployment would have supported a more rigorous, scientifically based health outcome study.[42]

Assessing deployment-related health outcomes with little or no breathing zone sampling data has challenged military epidemiologists.43–46 Recent epidemiologic studies have investigated the association between deployment environmental exposures and postdeployment chronic illness, including chronic respiratory conditions, among service members and veterans.43–46 These studies compared deployed with nondeployed personnel and produced a range of findings, from no association to evidence of increased symptoms and specific lung conditions.43–46 Sharkey et al reported that deployment to Afghanistan was associated with an elevated risk of postdeployment respiratory symptoms and new onset asthma.[46]

Environmental sampling can capture the external dose using real-time breathing zone sampling, which is the gold standard for exposure assessment, but this is often difficult to achieve in the deployed setting.42,47 Operational commanders give their attention to managing the greatest risks first, such as protecting the troops from enemy fire. In this scenario, the logistics involved in conducting breathing zone sampling could hinder other force health protection measures needed by deployed service members to survive in combat. A careful balance must be struck between methods designed to monitor for possible exposures that could lead to long-term health effects and the immediate risks of combat.

Efforts that rely upon traditional exposure assessment, such as breathing zone sampling collectors and pumps worn by the individual, limit mobility, have short battery lives, and require oversight by an individual trained in their operation. Further, the specimen collected must be analyzed in a laboratory equipped with gas chromatography and mass spectrometry. Ideally, the results should be reviewed by a healthcare provider and explained to the service member before being placed in the medical record. Unfortunately, the analyses may take weeks to months to complete, and often the service member has moved or redeployed out of theater, so the results do not make it into the medical record.

For these reasons, breathing zone sampling in combat situations with the available equipment was thought to be impractical.42,47 However, breathing zone sampling was conducted by the US Air Force at Bagram Air Field, Afghanistan, from November 2011 until March 2012, to assess potential exposures from open-pit burning. Blasch et al collected breathing zone sampling data (without interfering with combat readiness) and noted several PAHs and metals in low concentrations in the breathing zone of a cohort of deployers that often exceeded concentrations in ambient sampling data.[48]

The DoD has focused efforts on the areas of health risk assessment and identification, analysis, and prevention of exposures since the start of Operation Enduring Freedom and Operation Iraqi Freedom.1–3,49,50 However, lack of data as well as conflicting data indicates a need for alternative ways to characterize exposures that are both valid and reliable. In the absence of breathing zone air sampling data, exposure biomarkers may provide measures of internal doses that allow the DoD to demonstrate exposures to health hazards and any associations between exposure and health outcomes that require further investigation and research.

In 2012, the NRC published a report called “Exposure Science in the 21st Century: A Vision and Strategy,” which was developed to guide research on developing exposure information for large segments of the population to relate human health and the environment.[14] The authors noted that a key research need is to develop advanced analytic tools for measuring internal dose, identifying bio-signatures of exposure, and measuring biochemical modifiers of internal dose to complement the individualized biomedical profiles available from genotyping.[14] The use of “omics” technologies, including metabolomics, proteomics, metallomics, transcriptomics, immunomics, genomics, and methylomics, provides many of the measures recommended by the NRC, including use of exposure susceptibility and biological response biomarkers, biomarkers of effective dose, and markers of health outcomes.

The emergence of new laboratory omics technologies offers a potential means of dealing with exposures to assess internal dose. Integration of metabolomics with traditional exposure assessments and a central platform that links exposure to internal dose, biological response, and health outcomes may yield useful measures for the study of long-term adverse health consequences in the future. Many of these platforms are now sufficiently developed to support analyses of stored biological specimens. Applying this approach to DoDSR samples can greatly improve an individual’s exposure characterization. The large number of samples, diversity of the population, and extensive demographic and health information in the DoDSR-associated Defense Medical Surveillance System (DMSS) makes the DoDSR an invaluable resource for DoD exposure assessment and precision medicine research.[3]

The US military has been unsuccessful in identifying and assessing potentially hazardous exposures in deployed service members in real time or near real time to give commanders recommendations for preventing environmental exposures. Many area environmental samples have been collected, but few efforts have been made to collect individual breathing zone samples, nor has there been much effort to link results of the sample analysis to the health record of a particular person or group deployed to a specific location at a specific point in time. Among many reasons for this gap are limitations in the training of personnel collecting the samples, limitations in sampling equipment, and limitations in the information technology that prevent sample results from being linked to an individual’s medical record.

The DoD is engaged in a significant effort to improve training of personnel to oversee the proper collection of airborne sampling data. DoD efforts are also directed at decreasing the size of sample collection equipment so it does not add weight to service members’ equipment or interfere with warfighting capabilities. Improvements are needed so that service members’ laboratory results are linked to their medical records, and to ensure results are reviewed by healthcare providers and discussed with the service members.

Department of Defense Serum Repository

The DoDSR was established in 1989 to store serum collected when mandatory HIV testing was performed on active, Guard, and reserve service members,51,52 and samples have been collected from military personnel every 2 years since. The registry currently contains 61 million serum samples that are linked to individual service members and their health data.51,52 Service members provide predeployment and postdeployment serum samples, which may be used to address questions related to deployment exposures. DoDSR studies of specimens have usually addressed biological exposures for which antibodies could be measured.51,52 The associated DMSS database includes service member medical outcome data and predeployment and postdeployment health questionnaire information, which is linked to the DoDSR by Social Security numbers.51,52

To ensure future pre-event and post-event evaluation of exposure biomarkers, the Armed Forces Health Surveillance Center (AFHSC) asked, “What could be done better with the serum?” and “What other biospecimens should be collected?” AFHSC identified gaps in current capabilities along with areas for improvement to ensure that serum quality was maintained. Adoption of a quality assurance program that involved testing of the serum against quality control standards was one advance.[4] Other enhancements, including expanding the types of specimens stored and lowering the temperature from -30°C to -80°C, would allow the DoDSR to remain a state-of-the-art bio-repository.[5]

The serum samples stored in the DoDSR have been used for a variety of studies.[53] These studies range from analyses of antibody levels against various infectious agents to analyses for biomarkers possibly associated with physiological changes that could be linked to combat, such as posttraumatic stress disorder. However, serum has not been found useful for whole genome sequencing or RNA analysis. Serum samples are linked to demographic, medical encounter, military occupation, and deployment data. This data provides a powerful epidemiologic resource to investigate deployment burn pit exposures, serum biomarkers, and potential for specific health outcomes.[54] Further, a large cohort of deployers to Iraq and Afghanistan who provided security around burn pits had their predeployment and postdeployment serum examined for PAHs, dioxins, cotinine levels, microRNA (miRNA) levels, metabolic breakdown products, and inflammatory biomarkers. The study noted that the serum was of excellent quality and all those biomarkers could be detected in it. Thus, the DoDSR should be considered a resource for future studies of biomarkers of exposure.54–61

Recent studies using new laboratory technologies have confirmed optimism about the quality of serum specimens currently in the DoDSR. The serum specimens were consistently found to contain glucose and amino acids in the normal physiological range.[61] The current DoDSR has considerable utility, but its utility could be expanded if the latest technological advances and laboratory management practices were incorporated into daily operations. Serious consideration must be given to upgrading the capabilities of the DoDSR to allow for the collection and storage of state-of-the-art bio-repository specimens that are not currently collected, including urine, fecal, and whole blood samples or blood spots.3–5

To expand the DoDSR’s capabilities, its storage equipment must be upgraded to permit colder storage, at -80°C. In addition, standardized procedures should be put in place to ensure specimens are collected, processed, shipped, received, and stored properly, with routine quality assurance procedures to allow a statement of assurance to be issued to specimen users. Presently there is variability in sample collection and processing. Use of state-of-the-art collection tubes may minimize threats to specimen quality.[3]

Although possibly of little value in general health surveillance, the new laboratory technologies could be of great value for examining individual exposures. Military leaders and preventive medicine personnel must be informed of the need to rapidly identify and respond to actual or possible exposures, and to be prepared to collect the specimens and data needed to meaningfully assess the health risk.

BIOMARKER DISCOVERY AND APPLICATIONS

Many different molecular methods are available to study exposure biomarkers. Potentially useful applications of each method are being identified and evaluated.62,63 For example, a recent study of ultrafine particulate levels and inflammatory biomarkers, including C-reactive protein, demonstrated cardiovascular effects in a group of exposed individuals compared with controls.[62] The different omics techniques (Exhibit 29-1) have been recognized for their potential power in precision medicine, epidemiology, and exposome research.64–66 The following is a brief description of what each of these techniques analyzes and the benefit that they might provide to military medicine.

EXHIBIT 29-1

“OMICS” TECHNOLOGIES

Metabolomics. High-resolution metabolomics studies provide evidence of thousands of unidentified chemicals in human plasma. The human metabolome is defined as the chemical profile of all low-molecular-weight compounds in a biological specimen and includes endogenous metabolites, chemicals from human-environment interaction, and reactants arising from interaction of these compounds with enzymatic and bacterial processes occurring within the body.

Genomics. Genomics is the analysis of DNA sequencing and requires high-quality DNA. Studies of service members are underway to look for single nucleotide polymorphisms that identify genetic predispositions to diseases caused by environmental exposures and induced mutations caused by mutagenic agents.

Transcriptomics. Transcriptomics is the analysis of messenger RNA (mRNA) transcription as expressed genes in cells. It requires high-quality RNA, which is difficult to obtain because it degrades easily. Transcription analysis can detect metabolic changes due to exposure to infectious agents or toxins that are controlled at the mRNA level.

Serum cytokines and proteins. Biomarkers of inflammation and cardiovascular risk are measured in serum using bead-based multiplex technology from Luminex Corporation (Austin, TX). Immunologic and cardiovascular changes can be detected. The cytokine panel includes 22 cytokines and chemokines associated with inflammation. The cardiovascular panel includes 10 markers including β_2-microglobulin, C-reactive protein, and a number of other serum markers. Serum microRNA. MicroRNAs (miRNAs) are a class of small, endogenous regulatory RNA molecules that are essential in physiologic processes and regulating stress responses, inflammation, and immunity. Unlike RNAs, miRNA are stable, exist at high levels in serum, and can serve as biomarkers of exposure.

Serum IgE. A sentinel of allergy and asthma, serum IgE is increased by exposure to environmental chemicals, including diesel exhaust and other hydrocarbon pollutants that promote allergic sensitization. Serum IgE levels can be measured using a commercial enzyme-linked immunosorbent assay (ELISA) kit.

Serum cotinine. Cotinine is a metabolic product of nicotine and a sensitive indicator of tobacco smoking status. Tobacco smoke contains polyaromatic hydrocarbons (PAHs) and is a potential confounder in exposure assessments. Cotinine can be measured in serum by testing using a commercial ELISA kit.

Polyaromatic hydrocarbons and dioxin. PAHs and dioxins can be measured in serum by cloud-point extraction. The resulting nonpolar core micelles are isolated, extracted with hexane, and analyzed by gas chromatography and mass spectrometry. Benzo[a]pyrene is converted by cellular enzymes to benzo[a]pyrene diol epoxide (BDPE), which forms adducts with DNA and proteins. BDPE-protein adducts can be detected in serum using a commercial ELISA.

Proteomics. Proteomics is the study of proteins in the host examining molecular events after transcription has occurred. The Department of Defense force health protection program uses proteomics to identify biomarkers and metabolic changes associated with diseases. Environmental chemicals may bind to serum proteins when reactive electrophiles bind to protein carriers in the blood and serum, forming protein adducts.

Epigenomics. Epigenomics is the study of heritable changes not directly encoded in DNA sequences. These changes do not alter the genome and are reversible. The most common epigenetic effects are histone modification and DNA methylation. These DNA modifications are involved in gene regulation and affect gene transcription and expression. Epigenomic analysis allows for the study of pre-transcriptional changes that effect gene regulation before mRNA is produced.

Genomics

Genomics is the analysis of data derived from DNA sequencing. It requires high-quality DNA material. The DoD has invested in genomics as a force health protection tool.[3] The DoD and VA have undertaken genomics studies of service members to look for single nucleotide polymorphisms that may identify individuals with genetic predispositions to diseases caused by various environmental exposures. Also, DNA sequence analyses in exposed personnel might identify induced mutations related to mutagenic agent exposures.67–69 Additionally, genome-wide association studies, coupled with epidemiologic analysis, may help identify specific alleles and their associated risk of disease.

Transcriptomics

Transcriptomics is the analysis of messenger RNA (mRNA) transcription levels as expressed genes in the cell. This technique requires high-quality RNA, which is much more difficult to generate experimentally than DNA because RNA is prone to degradation. Transcription analysis can be used to detect metabolic changes resulting from exposure to infectious agents or toxins that might be controlled at the mRNA level.70–72 Transcriptomics has also been used to predict health outcomes following influenza exposure in clinical studies.[73]

Proteomics

Proteomics is the study of proteins in the host to examine molecular events after transcription has occurred.[3] Proteomics techniques require non-degraded protein, and recent studies have noted that serum samples in the current DoDSR are suitable for analyzing circulating protein, but not cellular or cell-associated protein. The DoD force health protection program could use proteomics to identify biomarkers associated with specific disease states and to detect metabolic changes associated with these diseases.[3] Proteomics may also detect specific biomarkers that represent changes in serum and cellular proteins.72,74,75 Environmental chemicals may bind to serum proteins when reactive electrophiles bind to protein carriers in the blood and serum to form protein adducts.[76] Quantification of DNA adducts in humans is challenging, even with the use of targeted methods.[77] Protein adducts have been detected by targeting the sulfhydryl group of human serum albumin using high-resolution mass spectrometry up to 30 days after exposure.[78] Redox proteomics, which aims to measure redox-based changes in the proteome, has also been used to identify exposure-response changes.[79]

Metabolomics

Metabolomics has been extensively developed but not yet extensively used for biomonitoring of military exposures. Importantly, high-resolution metabolomics studies have provided evidence of thousands of unidentified chemicals in human plasma. Low-level exposures present a challenge for reliably measuring chemical residues. The human metabolome is defined as the chemical profile of all low-molecular-weight compounds in a biological specimen and includes endogenous metabolites, chemicals from human-environment interaction, and reactants arising from the interaction of these compounds with enzymatic and bacterial processes occurring within the body.[80] Biomarkers in human specimens can therefore provide measures of metabolites from core biochemical processes, lipids, microbiome-related metabolites, dietary chemicals, pharmaceuticals, and chemicals from environmental sources and commercial products.[81]

Various platforms are in use to measure the metabolome, including nuclear magnetic resonance and mass spectrometry. Due to recent advances in instrumentation and computational techniques, applications using liquid chromatography with ultra-high resolution mass spectrometers provide the greatest capabilities for exposome and precision medicine research.[82] Feasibility studies suggest it is possible to measure nearly a million mass-to-charge (m/z) signals. This analytical framework has been successfully applied to identify the metabolic phenotype of chronic diseases,83–90 aging,[91] infectious diseases,[92] and inflammation[93]; it has also been used as a central platform linking exposure to internal dose and biological response through a metabolome-wide association study framework.[94]

Recent studies have shown DoDSR serum samples are of suitable quality for profiling by high-resolution metabolomics. Initial characterization of 30 samples obtained from the DoDSR showed these samples provided measures of common metabolites consistent with expected ranges, and a detectable biological response to benzo[a]pyrene (a PAH and ubiquitous environmental pollutant) exposure was present.[61] Additional characterization by Liu et al using complementary analytical strategies for high-resolution metabolomics could routinely detect over 20,000 m/z features, including over 7,000 matches to metabolites present in the Kyoto Encyclopedia of Genes and Genomes.[95]

Another study examined cotinine levels, tobacco use, and common health indicators. Its results provided further evidence of DoDSR sample quality and suitability for metabolomic profiling.[96] Based on these results and the available technology, high-resolution metabolomics is sufficiently developed to allow implementation on a test basis for ongoing deployment surveillance.[55] The measures available from this platform include metabolic indicators of nutrition, renal function, and liver function, as well as other indicators. If adapted, chemical profiling of samples obtained before and after deployment, and over the course of service, can be evaluated for exposure biomarkers, effects, and health outcomes. This may improve identification of individuals with risk for environment-associated disease. Implementation is cost effective, and including these capabilities into the DoDSR structure may facilitate hazard identification and improved management of health risks associated with troop deployments.

New methods of monitoring exposure such as silicone wrist bracelets and badges, which are inexpensive and require no external power source, show promise.97,98 Coupled with untargeted chemical profiling by high-resolution mass spectrometry, these monitors have the potential to improve characterization of exposure to both known and unknown chemical agents. However, there are still challenges with linking external exposure to internal dose, measuring biological relevance, and developing a system for widespread distribution to troops. Thus, biological samples collected for the DoDSR represent a key resource for monitoring troop exposures.[52]

Metallomics

Heavy metal exposure and its associated health effects are an ongoing concern in the military. Chemical profiling by metabolomics can measure organic metal compounds. Metallomics, which uses inductively coupled plasma mass spectrometry (ICP-MS), can be applied to measure the total and speciated metal levels in biological specimens.[3] Biomonitoring studies have shown that the sensitivity of the ICP-MS method is superior to other analytical methods and is more cost effective than graphite furnace atomic absorption spectroscopy. Some recent studies have assessed the micronutrient status and background levels of exposure to toxic metals, but there are limitations with this approach, including contamination during sample collection and suitability of a matrix for metal species.[3]

Epigenomics

Epigenomics is the study of heritable changes that are not directly encoded in the cell’s DNA sequences.[3] Epigenetic changes do not modify the sequence of the genome and are reversible. The two most common epigenetic effects are histone modification and DNA methylation. These two DNA modifications are involved in gene regulation in that they affect gene transcription and gene expression.[3] Epigenomic analysis allows for the study of pretranscriptional processes that effect gene regulation before the production of mRNA. The bio-sample most suitable to support this technique is high-quality genomic DNA, although methylation studies have been done on DNA recovered from dried blood spots. Epigenomic analysis has been used to predict disease outcome, especially in the areas of cancer and neurological disorders.85,87,89 One preliminary study suggests that DNA methylation states may be associated with posttraumatic stress disorder.[88]

Immunomics

Immunomics is the analysis of information pertaining to the immune system, particularly associated with adaptive immunity.[3] This includes the study of the immune response to pathogens as well as to environmental chemicals. To do a full and complete immunomic analysis, white blood cells must be stored and analyzed for immunological markers. Analysis of host immune cells can provide information about the vaccination status and the health of the person’s immune system following potential toxic exposures. Immunomic technology has been used to analyze physiological processes, such as autoantibody response, and to develop personalized medical treatments.[3]

MicroRNA

In contrast to the above categories, miRNAs (see below for more detail) are encoded by the genome and are strong regulators of gene expression, but they are not translated into protein and thus do not fit in the transcriptomic or epigenomic categories. However, they provide an important measure of responses to environmental exposures and have been associated with a number of human diseases including Alzheimer disease.89,91 Recent studies have shown that miRNAs are both upregulated and downregulated in response to environmental chemical exposures.[1] Environmental exposures may interfere with miRNA-regulated translation of proteins; for example, PAHs were found to alter circulating levels of miRNAs in the serum.[63]

Serum IgE

Serum IgE, a sentinel of allergy and asthma, is increased during exposure to environmental toxicants, including diesel exhaust and other hydrocarbon pollutants that promote allergic sensitization. Serum IgE levels can be measured in small volumes of serum using a commercial enzyme-linked immunosorbent assay (ELISA) kit. An analysis of predeployment and postdeployment serum noted that deployment exposures contributed to allergic sensitization and pulmonary symptoms.[1]

Serum Cotinine

Cotinine is a metabolic product of nicotine and a sensitive indicator of tobacco smoking. Tobacco smoke contains PAHs, and tobacco smoke PAHs must be accounted for when examining individuals for exposure to PAHs in the deployed environment. The DoD examined cotinine levels to control for smoking by testing serum using a commercially available ELISA kit in a cohort of deployed individuals who were exposed to PAHs from open-pit burning of trash.[1]

PHYSIOLOGICAL TEST MATRICES

Historically, patients have been monitored with conventional physiological measurements such as height, weight, blood pressure, pulse, oxygen saturation, audiometric testing, and pulmonary function testing. With the advancement of biological monitoring, whole blood, serum, plasma, urine, saliva, and cerebrospinal fluid began to be used to measure the body’s changes in response to internal and external stimuli.[99] Of these, blood and urine are the most commonly collected media to study biomarkers. Biomarkers of internal dose, either the chemical itself or its breakdown product in blood, may indicate recent chemical exposure or mobilization from stores from prior exposure. Urinary biomarkers can also indicate recent exposure, but there is a slight lag time compared to when chemicals show up in the blood. Some chemicals may be sequestered in fat, bone, or other tissue and not show up in blood or urine. Operational commanders and service members prefer the least invasive way of assessing troops for exposure, including sample media collections, if the required quality of information can be obtained.

Nasal Lavage Analysis

Nasal lavage is increasingly gaining attention in allergen testing and as a test matrix for lung injury biomarkers.[93] Nasal lavage has been found to be a useful, noninvasive method in biomarker studies of asthma patients to examine eosinophil-derived neurotoxin for evidence of eosinophilic inflammation.[86]

Exhaled Breath Condensate

Exhaled breath contains microscopic droplets of lung lining fluid that contain biomolecules present in the lung. Exhaled breath can be condensed and collected, and the resulting fluid, exhaled breath condensate (EBC), can be assayed for biomarkers of interest. Portable EBC collecting units have been developed that consist of a collection tube with mouthpiece and integrated sample vial. The collecting tube is placed in a metal sleeve that has been pre-chilled in a freezer, and the donor breathes through the mouthpiece for 10 minutes to collect 1 to 2 mL of EBC. The sample vial is capped and stored for later analysis, the sleeve is returned to the freezer for subsequent collections, and the remainder of the unit is disposable. The process is fast, simple, and noninvasive.100,101

EBC samples the lung lining fluid, and numerous analytes have been found in EBC, including proteins, fatty acids, byproducts of metabolism, and host- and pathogen-derived DNA and RNA.[102] Analytical methods include ELISA and similar multiplex methods, polymerase chain reaction (PCR), and mass spectrometry, depending on the analytes to be measured. EBC has been used to investigate DNA mutations in lung cancer, surfactant proteins in chronic obstructive pulmonary disease, and proinflammatory cytokines in asthma.[103] In the field of occupational and environmental medicine, EBC has been used to study exposures to traffic air pollution, ozone, foundry dust, metal nanoparticles, welding fumes, and industrial chemical exposures. EBC has been evaluated as a screening tool for asthma in military recruits, and used to demonstrate increased proinflammatory markers in sailors after an 8-hour duty period on board small diesel-powered coast guard patrol boats.104,105 As analytical techniques grow ever faster, more sensitive, and less expensive, EBC is poised to become a major sampling site for biomonitoring of pulmonary and systemic health, disease, and occupational exposures.

Saliva

Saliva is an excellent medium, better than urine or blood, for exposure biomonitoring. It can be quickly collected by noninvasive methods, which makes the collection process easy and acceptable in deploying troops. Saliva biomarkers can be used to monitor health and conduct disease surveillance.[92] Biomarkers for therapeutic interventions, hormonal and immunological changes, and toxic chemicals and their metabolic intermediates can be detected in saliva. For example, thiocyanate can be detected in the saliva of smokers.[106]

NEW DEVELOPMENTS IN BIOMARKERS

Exposure Memory

Although still an evolving concept, evidence suggests multiple exposure memory systems exist with the potential to provide long-term markers of underlying injury arising from exposure.55,107 These systems can be used as nonspecific indicators of exposure, and comparing predeployment and postdeployment indicators provides a means of identifying changes in these systems. Current approaches to measure exposure memory include redox-proteomics, epigenomics, and metabolomics. In one study, metabolic changes were observed in individuals exposed to an extremely high dose of dioxin. The study, conducted in 2011, examined biomarkers that were obtained from healthy controls and eleven workers exposed to dioxin residues during the 1960s. The data showed these metabolic alterations were still present in the workers relative to the healthy controls, and included changes in expression of cytochrome P-450, hepatotoxicity, bile acid biosynthesis, and oxidative stress.[108] The data showed that changes in the metabolome due to a recent, acute dioxin exposure could still be detected in exposed individuals 40 years later. Exposure memory is a key component of the exposome, and continued characterization of multiple systems is ongoing through efforts integrating different omics platforms and health outcomes.[109]

Serum Cytokines and Protein Biomarkers

Biomarkers of inflammation and cardiovascular risk can be measured in serum using bead-based multiplex technology from Luminex Corporation (Austin, TX), which allows detection of 42 different molecules in a single 0.025-mL sample. The cytokine panel includes 22 cytokines and chemokines associated with inflammation. The cardiovascular panel includes 10 markers including β_2-microglobulin, C-reactive protein, and a number of other serum markers that can be assayed in 0.05 mL of serum to simultaneously measure 32 biomarkers. A recent study utilized two panels of biomarkers to detect immunologic and cardiovascular changes associated with service-related exposures.56,60

Biomarkers of Pulmonary Injury

The goal in the study of pulmonary injury is to develop omics technologies that can provide molecular signatures indicative of lung injury.[110] Recent studies demonstrate the potential utility of several types of biomarker molecules in different media.[111] Many new biomarkers of volatile organic compounds have been detected and quantified in EBC.[112] These biomarkers provide a measure of airway inflammation and offer a complementary tool to assess airway disease and asthma.[113]

Development of new analytical platforms, including GC Orbitrap (Thermo Scientific, Carlsbad, CA) high-resolution mass spectrometers, has greatly improved the capability to measure low-molecular-weight volatile organic compounds in small volumes of biological samples.[114] The use of high-resolution mass spectrometry greatly improved the detection of ethyl-thiocyanate generated from thiocyanate present in EBC, resulting in low nanomolar detection limits. The improved detection limits were a direct result of the ability to extract accurate mass ion chromatograms, which is not possible using traditional instrumentation due to noise at low m/z levels.

Additionally, biomarkers of oxidative stress and inflammation including proteins have been measured in bronchoalveolar lavage fluid. The study of chronic obstructive pulmonary disease and lung function impairment has led to discoveries through transcriptomic analyses of gene expression in the bronchial airway epithelium and lung parenchyma cells. Condition-specific genes and altered molecular pathways were noted to be associated with cigarette smoking.115,116 Further, RNA expression studies were used to identify gene expression signatures for particular types of pulmonary injury or disease. In addition, recent findings in asthma transcriptomics studies noted that T-cell type 2–mediated inflammation symptoms correlated well with biomarker levels of interleukin 13 and interleukin 14–induced genes.[117] While noninvasive testing is preferred, bronchial lavage and brushing can provide researchers with biomarkers that may one day enhance the understanding of molecular disease mechanisms caused by the inhalation of airborne hazards.

GENETIC AND EPIGENETIC BIOMARKERS

In the past 10 years, epigenetics has expanded through technological advancements in the laboratory including the use of high-throughput multiplex methodologies.[118] For environmental exposures, research has focused on how these exposures affect posttranslational modification of proteins.[119] Researchers continue to focus on how exposures and other environmental factors (eg, demographic, exercise, diet) alter the normal epigenetic processing of proteins and other molecules.[120] Recent research has suggested that environmentally induced epigenomics changes may alter gene expression in such a way that specific pathway alterations may become permanent.121–123 More research is needed to confirm that the observed epigenetic changes are causally related and not just correlated with long-term changes.

Non-Coding RNAs

Non-coding RNAs (RNAs that do not encode for protein) have recently emerged as powerful candidates for biomarker discovery. The most widely described are the miRNAs, a class of small, endogenous regulatory RNAs (20–25 nucleotides in length) that are essential in normal physiology and disease processes, as well as the regulation of stress responses, inflammation, and immunity. A single miRNA can regulate expression in literally hundreds of distinct target genes, and thus one miRNA can have a profound impact on gene expression and physiology. Changes in miRNA levels lead to altered gene expression and the development or promotion of disease states. To date, about 1,500 different miRNA species are encoded in the human genome.

Emerging evidence supports miRNA expression profiling as a crucial diagnostic tool. Highly abundant in human serum and plasma samples, miRNAs are much more stable than other classes of RNAs due to their small size, sequestration into small particles called exosomes, and binding proteins that shield them from the abundant RNA-degrading enzymes found in most biological fluids.[123] The remarkable stability of some miRNAs has been revealed by several studies of miRNA levels in stored serum and other biofluids over extended time periods.124,125 For example, one study showed that even at -20°C, many serum miRNAs are stable for up to 8 years, with minimal impact on detection. Interestingly, differential miRNA levels have been detected in blood (serum, plasma), urine, EBC, and tissue biopsies from patients with disease compared to unaffected individuals.

Another advantage of utilizing miRNAs as biomarkers is the relative ease and universal method of their detection. Levels of miRNAs can be accurately quantified from biological fluids using PCR, a laboratory technique that uses selective amplification steps to reliably measure the level of nucleic acids (in this case specific miRNA). The ability of PCR to dramatically amplify the level of the analyte means many miRNAs can be detected in small biological samples (up to 120–150 different miRNAs can readily be detected in only 0.1–0.2 mL of human serum). Specific miRNA levels can also be used to determine biological sample quality. For example, miRNA expression by quantitative PCR can be used to determine if certain serum samples are affected by hemolysis (red blood cell lysis) due to the presence or absence of specific miRNAs found almost exclusively in red blood cells.[126]

In addition to being utilized as biomarkers of disease state, miRNAs are being tested as markers of exposure. Recent work has linked environmental PAH exposures with altered plasma miRNA levels.[63] Serum samples from the DoDSR were used to identify specific miRNAs that show a strong correlation with smoking status and serum markers including inflammatory cytokines.[56] Another study used DoDSR serum samples to show that certain miRNAs change expression after personnel deployment to military bases with active open-air burn pits.[60] Thus, miRNAs may provide an ideal biomarker for exposure, disease, or pathological state.

While miRNAs are currently the most widely used non-coding RNA class for biomarkers, other RNA species are increasingly being investigated as novel biomarkers. Long non-coding RNAs (lncRNAs) are typically over 200 nucleotides in length and have been related to multiple functions, including activating or repressing gene expression, recruiting various protein cofactors, and inducing methylation-dependent epigenetics,[127] and they are also involved in gene imprinting and X-chromosome inactivation. Recently, differences in certain lncRNAs have been detected in atherosclerosis and certain cancers. However, given the lower stability of lncRNAs compared to miRNAs, and the current lack of studies on lncRNAs in various biological fluids readily obtainable for biomarker analyses, the usefulness of lncRNAs in biomarker discovery requires more study.

Another class of non-coding RNA is the piwi-interacting RNAs (piRNAs), which form RNA-protein complexes with the piwi proteins. Like miRNAs, piRNAs regulate gene expression through epigenetic and posttranscriptional gene silencing. Compared to miRNAs, piRNAs are slightly larger and less stable, and piRNAs are unique in that they are abundantly expressed in germ line cells (sex cells), and thus can be directly inherited by offspring. Recently, piRNAs have been measured in human blood samples, and differences in piRNA expression were observed in certain cancers, suggesting they may be potential biomarkers.[128] Whether piRNAs are altered by various environmental exposures is currently unknown and future studies are needed.

Genetics in Pulmonary Injury Research

Genome-wide association studies have permitted the discovery of gene mutations associated with increased susceptibility to environmental hazards. Currently, whole genome sequencing studies in large military cohorts are planned that will link alterations in DNA sequences to health outcomes and exposures (phenotypes).129,130 Genetic research may also yield information on biomarkers and specific pathways altered due to specific environmental exposures and dosages. Lung disease studies of gene–environment interactions have identified a number of genes that predispose people to higher injury risk.[131]

Polymorphisms caused by oxidative stress have been found to make individuals more susceptible to environmental exposures to particulate matter and ozone.[132] Research in nutrition and gene interaction in the presence of pollution has shown that ϖ-3 fatty acids, antioxidants, and methyl nutrients are protective.27,133,134 Susceptibility studies in silicosis patients have noted a cellular DNA polymorphism associated with increased risk.[135] Researchers also examined biomarkers of susceptibility in animals following exposure to inhaled silicon dioxide nanoparticles, noting that toxicity varied with age and suggesting that there may be different biomarkers of susceptibility at different stages of development.[29]

Gene–environment interactions is another area of ongoing research. In one study, individuals were exposed to airborne endotoxins and genotype signatures were examined. Carriers of three single nucleotide polymorphisms in the CD14 gene and one in the MD2 gene were associated with increased risk of asthma symptoms following endotoxin exposure, compared with the allele homozygotes.[136] Genetic research in the military is helpful in understanding lung injury under specific conditions. However, its use for susceptibility screening may be of limited value. The test will only be cost effective when the prevalence of the genetic mutation is moderately high and susceptibility cannot be determined. In the end, change in the genotype linked to a health decrement caused by exposures is the gold standard for proving causation. Once the evidence is established, exposure prevention countermeasures become necessary to avoid adverse health outcomes.

The military has an ongoing screening program for personnel who are at risk for a genetically linked glucose-6-phosphate dehydrogenase (G6PD) deficiency.[137] The services screen for G6PD deficiency prior to deployment to regions of the world where malaria is endemic. Personnel who have the G6PD deficiency can have adverse blood reactions to the antimalaria drug primaquine. The G6PD deficiency occurs in 6% of individuals worldwide, but the prevalence is lower in US military personnel, where 2.5% of males and 1.6% of females have the deficiency, usually African American, Asian, and Hispanic individuals.

BIG DATA ANALYSIS

Informed and appropriate “big data” collection and storage, with support from experienced analysts, will allow public health practitioners and researchers to integrate results from a multitude of diverse laboratory tests with clinical, demographic, and exposure data. Presently, big data is used mainly for susceptibility studies.[137] In the future, big data will have increased use in support of environment-wide associated studies, which provide a hypothesis-free approach that examines associations among multiple variables. This approach links biomarker discovery studies by specifically integrating metabolomics data with results of studies in many other areas, such as gene expression, microbiomics, and redox proteomics. Most current efforts to monitor and minimize exposures to toxic chemicals and other hazards use a public health approach. This has been the most cost-effective way to provide maximum benefit to populations because it prioritizes risks according to those with the greatest hazard and likelihood of exposure. The public health approach has also yielded precise analytical measurement and extensive population data on a relatively small number of known hazards. However, existing exposure surveillance methods to monitor and protect against hazardous exposures in civilian life differ from military exposure surveillance because the range, intensity, and complexity of hazardous exposures in the deployed environment exceed those encountered by civilians and cannot be fully anticipated.

Recent analytical developments have created an opportunity for a different approach to exposure surveillance based on ultra-high resolution mass spectrometry and new strategies in biomonitoring.[138] Application of either liquid chromatography or gas chromatography with ultra-high resolution mass spectrometry and advanced data extraction techniques now routinely provide relative quantification of up to 20,000 chemicals. These approaches provide for the measurement of environmental chemicals in human samples at five to seven orders of magnitude lower than many endogenous metabolites, and hundreds of environmental chemicals have been detected at low levels using these methods without prior knowledge of the chemicals’ existence.[139]

Development of computational metabolomics has mirrored advances in analytical chemistry.[2] An important advance is the use of multiple technical replicates to enhance reliability of detection of low-abundance chemicals. Bioinformatics methods are now available to link multiple metabolic byproducts derived from a single chemical precursor.[139]

Additionally, advances in high-throughput technologies have enabled large-scale and high-resolution measurements of various molecular signatures of exposure (eg, in the genome, transcriptome, proteome, and metabolome) to assess the health status of military personnel. Figure 29-2 is an overview of how big data analytic methods are used to integrate omics results with clinical symptoms. The observed health status and clinical symptoms are related to exposures to chemicals measured by environmental profiling techniques described above. The observed clinical symptoms are an outcome of a complex interplay between the exposure, the genotype, and alterations in structure or function noted by omics technologies. Indeed, medicine must rely on information captured at increasingly greater depth. This requires new tools to enable the use of big data for presymptomatic detection of disease and clinical decision-making.

The goal of big data analysis is to identify molecular signatures using data generated from omics analysis that results from environmental exposures and correlates with observed clinical symptoms. Statistical distributions of the data generated by omics analysis is the first step, followed by data processing and normalization.140–142 Data processing evaluates signal-to-noise ratios so that low signal fields can be thrown out. Data normalization is done to reduce systematic biases prior to any downstream quantitative analysis. Several technology-specific parametric and nonparametric statistical methods are currently available for this analysis.[143] Graphical representation of sample results and variables facilitates interpretation and identification of the most informative data features. Principal component analysis and other methods permit visualization of data where there is considerable noise. To identify molecular signatures that correlate with clinical symptoms, group machine learning approaches can be used with International Classification of Diseases, Ninth Revision codes to find variables and integrate the data.144,145 Thus, molecular signatures associated with the clinical symptoms of military service members can be investigated for use as new biomarkers. These can then be experimentally tested in animal models or clinical studies in humans.[146] Bioinformatic tools such as gene set analysis methods, also called pathway analysis methods, allow contextualization of high-throughput data with a priori biological knowledge about interaction and coexpression of genes, which maximizes use of big data.147–150 For example, the miRNAs and metabolic pathways associated with deployment exposure may be used to develop interventions to reduce service member exposures.151,152

Figure 29-2. “Big data” analytic methods to integrate “omics” results with clinical symptoms.

Finally, clinical decision-making enabled by data-intensive technologies will test the limits of the current information technology infrastructure in terms of physical storage, database management, data processing, and data mining. Complex data management systems like the US Army Medical Research and Materiel Command’s SysBioCube and data integration tools are needed to offer scalable and collaborative solutions to explore and contextualize data.153,154 Beyond technological developments, concerns about information privacy and security must be addressed.

SUMMARY

Although the DoD has made great progress in using the DoDSR to address questions related to infectious agent and other environmental exposures of military service members, there are opportunities to do more by studying the serum of deploying service members using available omics technologies. Most of the medical information gained from omics-based studies is research oriented, but the search for specific associations with disease will facilitate acceptance of this new technology. The most advanced of these technologies is genomics and genome-wide association studies coupled with mass spectrometry-based proteomic analysis.[155] However, these technologies are only part of a complicated systems biology approach that likely will pay benefits in the future. As more scientific information is gained, it may become possible to screen service members for the propensity to develop specific medical outcomes in response to environmental exposures. Future research may provide information that supports the notion that service members’ medical conditions are associated with specific exposures such as fires, dust, or aerial spraying, to name a few. These are critical questions that DoD must address.

Improvements in exposure science are needed to better understand the effects of deployment exposures on service member health.42,156 Exposure information that can be linked to an individual is needed for conducting rigorous epidemiologic studies designed to compare health outcomes in the exposed and non-exposed populations,[4] leading to better force health protection measures such as troop relocation and use of personal protective equipment.[19] Biological monitoring will add to the DoD’s tools for assessing the internal dose of exposure. Refinements in biomarker science may permit the linkage of exposure with health outcomes to identify populations at higher risk from exposures. High-throughput omics technologies are driving analyses of the exposome and enabling analyses of the entire internal biochemical environment. Omics in the future may identify the absorbed dose of chemicals and provide insight into how the metabolic pathways and gene and protein expressions are altered.

The DoD must develop the infrastructure needed to appropriately and effectively use available modern technologies. Considerable work has been done to identify bio-repository needs for the future and the options available.3–5 However, this information has not yet been put into a plan to secure funding. The large quantity of data generated from omics studies will require big data analysis capabilities that do not currently exist. Improvements could be achieved by developing in-house capability; forming civilian partnerships, possibly with universities already doing this work; or a combination of both. Lastly, the DoD must consider all new and emerging technological capabilities and decide which suites of tools will be employed in various scenarios to assess actual or possible exposures. Clearly defined protocols for exposure assessment using biological monitoring and analysis of the results is critical to achieving informative and cost-effective health risk assessments.

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Chapter 30

COLD STRESS

ANDY CHERN, MD, MPH,* AND DAVID W. DEGROOT, PHD†

INTRODUCTION

PHYSIOLOGY

TEMPERATURE MEASUREMENTS

EXPOSURE GUIDELINES

General

Body Protection and Insulation

Hand Protection and Insulation

External Equipment

Other Safety Considerations

COLD INJURIES

Freezing Cold Injuries

Nonfreezing Cold Injuries

Accidental Hypothermia

MEDICAL SURVEILLANCE

PREVENTION

SUMMARY

*Captain, Medical Corps, US Army; Associate Program Director and Assistant Professor, Occupational & Environmental Medicine Residency Program, Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

† Major, Medical Service Corps, US Army; Deputy Chief, Department of Clinical Investigation, Tripler Army Medical Center, Honolulu, Hawaii 96859

INTRODUCTION

Cold is a physical hazard that has historically caused significant morbidity and mortality among military personnel. Since the ancient times of Xenophon and Hannibal, soldiers have succumbed to the effects of cold-related injuries, resulting in thousands of deaths during war.[1] Cold weather injuries (CWIs), however, are not exclusive to military operations during wartime but affect peacetime training as well. One study over a 52-month period at a hospital in Wurzburg, Germany, found that a majority of cold injuries occurred during general field training, and another study of the Israeli military found rates of CWI from routine training and duties to be twice that of combat.2,3

With advances in education, training, and equipment, rates of CWI have been significantly reduced. During World War I, rates of CWI from British soldiers declined from 33.9 to 3.8 cases per 1,000 person-years after the implementation of educational programs.[4] Similar findings of significant reductions in total CWI rates were observed in US Army personnel between 1980 and 1999.[5]

Cold injuries can be classified into three main categories:

1. freezing cold injuries,

2. nonfreezing cold injuries (NFCIs), and

3. hypothermia.

Freezing cold injuries and NFCIs are generally localized to the extremities of exposed skin. Freezing cold injuries may also be referred to as cold/dry or frostbite injuries, and NFCIs may be referred as cold/wet injuries. In contrast, hypothermia refers specifically to an abnormally low core body temperature. Figure 30-1 diagrams the different types of CWI.

PHYSIOLOGY

Body core temperature is the summation of heat production internally and heat gains and losses from the external environment. While heat can be gained from the environment via radiation, conduction, and convection, exposure to cold environments results in heat loss. Body core temperature is controlled by the preoptic area of the anterior hypothalamus, which regulates two core functions in regard to cold exposure, namely, peripheral vasoconstriction and shivering. Peripheral vasoconstriction, initiated in response to reduced skin temperatures, concentrates the blood in the internal organ structures, away from the surface of the body, thereby increasing tissue insulation and conserving heat. Shivering helps increase heat production through involuntary muscle contraction, resulting in increased metabolic heat production. Shivering can increase the metabolic rate 2- to 5-fold.[6] There is also an initial associated increase in the respiratory and heart rates. However, if the body core temperature continues to decrease, the metabolic, respiratory, and heart rates will decrease.

Although peripheral vasoconstriction occurs initially, continued cold exposure will lead to alternating cold-induced vasodilation (CIVD) in order to intermittently conserve dexterity and function in the extremities through periodic rewarming.[7] Furthermore, prolonged cold exposure results in cold diuresis and decreased fluid volume as blood is shunted centrally.

Minor physiologic acclimatization to the cold can occur, and generally manifests in three patterns: habituation, metabolic acclimatization, and insulative acclimatization, depending on the nature of the cold exposure.[8] Unfortunately, the physiological adjustments to chronic cold exposures are slower to develop, less pronounced, and less practical in relieving thermal strain and preventing cold injury compared to heat acclimatization. Due to the increased metabolic demand to maintain body core temperature homeostasis, work in cold environments requires an additional 10% to 15% more calories.[9]

Figure 30-1. Types of cold injuries.
Reproduced from: US Department of the Army. Prevention and Management of Cold-Weather Injuries. Washington, DC: DA; 2005: 41. Technical Bulletin MED 508.

Also, a unique phenomenon occurs during immersion in cold water, which triggers the diving reflex, involving an acute bradycardic response.[10] With colder water, the bradycardia becomes more pronounced.[11]

TEMPERATURE MEASUREMENTS

Several key components are important for evaluating cold exposures, including body core temperature and wind chill temperature (WCT) index. Generally, body core temperature is measured by a low-reading rectal thermometer. Measuring body core temperature at other sites, including sublingual, temporal, and axillary, results in inaccurate readings and is not recommended.[12] However, in the hospital, an esophageal temperature probe is the preferred instrument to monitor core temperatures.[13]

Ambient temperatures should be measured by thermometers capable of measuring temperatures down to at least -40°C (-40°F). Furthermore, the WCT index helps determine the risk of cold injury by estimating the relative cooling ability from the combination of air temperature and wind velocity. Additionally, although natural winds may be low, riding in open vehicles or standing near propeller- or rotor-generated winds can expose individuals to dangerous wind chill and should be taken into consideration. However, there is no risk of frostbite when the ambient air temperature is above 0°C (32°F), even if the WCT is below freezing. Similarly, wet skin will not freeze when the air temperature is above 0°C (32°F).[9] However, wet skin exposed to temperatures below 0°C (32°F) will freeze faster than dry skin.

Altitude must also be considered when planning operations. At higher elevations, winds are usually stronger, and the air temperature is usually lower. In general, with every 1,000 feet above the site at which the temperature is measured, the air temperature is 2°C (3.6°F) cooler.[9]

EXPOSURE GUIDELINES

General

In general, suitable thermometry should be available when environmental temperatures reach below 16°C (60.8°F). When air temperature falls below -1°C (30.2°F), the dry bulb temperature should be measured and recorded at least every 4 hours. Warning and safety briefings should also be provided, especially when temperatures drop below -7°C (19.4°F).

For a single, occasional cold exposure, a decrease in body core temperature no lower than 35°C (95°F) is permissible. Although clinical signs and symptoms of hypothermia may manifest even above this temperature, continuous, vigorous shivering should be taken as a dangerous sign, and removal from the cold exposure or recovery measures should be implemented immediately.

Body Protection and Insulation

When air temperature is below 4°C (39.2°F), whole-body protection, including adequate insulated dry clothing, should be provided. Furthermore, continuous cold exposure to unprotected skin such as the ears and face should not be permitted without adequate protection when the equivalent WCT is below -32°C (-26.5°F). Work should be modified or suspended if adequate dry clothing is not available. When clothing becomes wet, it should be changed immediately. Sweating is an important consideration because clothing appropriate for resting cold exposure may lead to wet skin and subsequent increased heat loss during physical work.

Hand Protection and Insulation

Protective measures should be established for the hands, particularly if manual dexterity is needed for work. At air temperatures of -17.5°C (0°F) or less, the hands should be protected by insulated gloves or mittens. If fine work with bare hands is required for more than 10 to 20 minutes in an environment below 16°C (60.8°F), adequate measures to maintain the warmth of extremities should be implemented. Additionally, tools should have appropriate protection. For instance, metal handles should be covered by thermal insulating material at temperatures below -1°C (30.2°F). Anti-contact gloves should also be employed to prevent contact frostbite.

Special precautions should be taken for workers dealing with evaporative liquids (eg, gasoline, alcohol, cleaning fluids) or liquefied gases (eg, liquid natural gas, liquid oxygen, liquid nitrogen). In the event of a spill, appropriate protective equipment from both the cold and the spilled agent must be employed.

External Equipment

External equipment, such as shielding material for the work area, can limit effects of wind and rain that can contribute to cold-induced injuries. If work is performed in outdoor environments below 4°C (39.2°F), external equipment should be utilized. Moreover, heated warming shelters (eg, tents, cabins) should be available nearby for periodic use at regular intervals if work is to be performed continuously when the equivalent WCT is below -7°C (19.4°F). Progressive signs or symptoms of cold injury should prompt immediate return to warming shelters.

Other Safety Considerations

Workers should be instructed in proper safety techniques prior to working in cold environments. This includes knowledge of first aid rewarming measures, appropriate personal protective equipment and clothing, adequate nutrition and hydration, signs and symptoms of cold injuries, and safe working practices. At temperatures below -12°C (10.4°F) equivalent chill temperature, constant supervision should be maintained, such as employing a “buddy” system. In addition, work intensity and exertion should be controlled to prevent workers from sweating heavily, which can accelerate heat loss.

Depending on factors in the cold environment such as precipitation, wind, and sunlight, eye protection should also be worn to protect the eyes not only from physical debris (eg, blowing snow and ice crystals) but also from ultraviolet (UV) light. Prolonged work in a snowy environment without eye protection can lead to photokeratitis, also known as snow blindness, caused by UV rays directly from the sun or indirectly from reflected rays of sunlight off the snow and ice, which can cause eye pain, blurred vision, headache, and temporary vision loss. Treatments for photokeratitis are listed in Exhibit 30-1.

EXHIBIT 30-1

TREATMENT FOR PHOTOKERATITIS (SNOW BLINDNESS)

Topical cycloplegic drops

- 1% cyclopentolate

- 2–5% homatropine

- 0.25% scopolamine

Ophthalmic antibiotics

- erythromycin

- bacitracin

- polymyxin B/bacitracin

Topical ophthalmic nonsteroidal anti-inflammatory drugs

- diclofenac

- ketorolac

- 0.5% tromethamine

Oral analgesics

- ibuprofen

- oxycodone

___________________

Data sources: (1) Jacobs DS. Photokeratitis. UpToDate. Sep 30, 2016. http://www.uptodate.com/contents/photokeratitis?source=machineLearning&search=snowblindness&selectedTitle=1~11&sectionRank=1&anchor=H7#H7. Accessed May 8, 2017. (2) Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: do ophthalmic nonsteroidal anti-inflammatory drugs reduce the pain associated with simple corneal abrasion without delaying healing? Ann Emerg Med. 2003;41(1):134–140.

COLD INJURIES

Freezing Cold Injuries

Freezing injuries generally encompass damage to localized tissue when the local skin or tissue temperature falls below 0°C (32°F). Prolonged exposure to subzero temperatures and the resulting peripheral vasoconstriction can directly and indirectly lead to reversible and potentially irreversible damage. Multiple studies indicate that tissue damage can result from the following effects: intracellular and extracellular ice formation, cell dehydration and shrinkage, abnormal intracellular electrolyte concentrations, thermal shock, denaturation of lipid-protein complexes, production of inflammatory markers, and capillary structure damage.9,14 As with other cold injuries, wind velocity can play a significant role in the development of freezing injuries, particularly when the ambient air temperature is already below zero. (As previously mentioned, there is no risk of freezing injuries when the ambient air temperature is above 0°C [32°F] even if the WCT is below freezing.[9]) Peripheral vasoconstrictive medications as well as nicotine use can increase susceptibility to freezing injuries. There is a 30% higher incidence of peripheral cold injuries in heavy smokers (two to three packs per day), likely secondary to reduction in the CIVD response from nicotine.[9]

Epidemiology

In the United States, no formal reporting system exists for freezing injuries. However, analysis of subgroup populations including the military have been analyzed. In the US military, of the 19 cases of CWI of service members serving in Operation Enduring Freedom and Operation Iraqi Freedom between 2001 and 2009, only two were from freezing injuries, one of which required surgical intervention.[15] A review of CWI among soldiers in Alaska revealed that the majority of freezing injuries were either first- or second-degree frostbite or superficial freezing injuries.[16] In the study of Israeli Defense Forces, of the 136 CWIs reported between 1994 and 2001, less than 5% were from freezing injuries.[3]

Classification and Clinical Features

Freezing injuries have traditionally been categorized into a four-tiered system, but some researchers and organizations (eg, the Wilderness Medicine Society) have proposed a two-tiered approach for simplicity, especially for field use. Both systems are described below. Most freezing injuries are described in the context of frostbite. Frostnip, another associated term, refers to the mildest form of freezing injury to the skin, sometimes categorized in conjunction with first-degree frostbite.

Four-tiered system. The traditional four-tiered approach ranges from first-degree frostbite (the least severe) to fourth-degree frostbite (the most severe).

Figure 30-2. Second-degree frostbite of the left foot. Full recovery will take weeks to months.
Reproduced from: Burr RE. Environmental medicine: heat, cold, and altitude. In: Kelley PW, ed. Military Preventive Medicine. Mobilization and Deployment. Vol 1. Washington, DC: Borden Institute; 2003: Figure 19-11.

1. First-degree frostbite is caused by a relatively short-duration exposure to cold air or direct physical contact with a cold object resulting in a partial thickness skin injury that spares deep structures. First-degree frostbite presents with mild erythema, edema, and hyperemia at the site of injury. Although mild pain and desquamation may accompany first-degree injuries, recovery is complete without scarring.

2. Second-degree frostbite produces a complete thickness skin injury sparing subcutaneous structures (Figure 30-2). However, with a full thickness injury, vesicles and bullae may form within 12 to 24 hours. Similar to first-degree frostbite, there is no permanent tissue loss; however, pain, numbness, cold sensitivity, and hyperhidrosis may occur.

3. Third-degree frostbite includes injuries produced by second-degree frostbite but also damages subcutaneous structures. Skin may appear black and hard. Generalized edema is common, and care should be taken to observe for potential compartment syndrome. Vesicles and bullae are similarly formed as in second-degree frostbite, but may be hemorrhagic versus filled with clear fluid. Once healing begins, ulcerations are produced with resulting scarring. Pain may be burning, aching, throbbing, or shooting and last up to a month.

4. Fourth-degree frostbite further damages deeper subcutaneous structures, potentially including muscles, tendons, or bones. Due to this extensive damage, mobility in the region is unlikely. Even with rewarming, mobility may be limited by the damage. Although some damage may be reversible, dry gangrene can occur, resulting in mummification within 5 to 10 days and possibly auto-amputation. To evaluate the severity of frostbite injuries if there is a concern for subcutaneous tissue damage, technetium 99m bone scan is the preferred diagnostic modality and can help guide surgical intervention.[17]

Two-tiered system. The two-tiered approach is divided into superficial and deep freezing injuries. Superficial freezing injuries will not result in tissue loss, whereas deep freezing injuries will result in tissue loss. Superficial freezing injuries essentially comprise the first-degree and second-degree frostbite injuries, and deep freezing injuries encompass the third-degree and fourth-degree frostbite injuries (Table 30-1).

TABLE 30-1

CLASSIFICATION OF FREEZING COLD INJURIES AND ASSOCIATED SIGNS

Superficial

Deep

First degree

Third degree

- Partial thickness freezing

- Mild erythema, edema, hyperemia

- No scarring

- Full thickness and subcutaneous freezing

- Potential compartment syndrome

- Scarring may occur

Second degree

Fourth degree

- Complete thickness freezing

- No subcutaneous structures involved

- Vesicles and bullae

- Full thickness and subcutaneous freezing

- Involves muscles, tendons, or bones

- Gangrene and mummification possible

Treatment

Regardless of the severity of the freezing injury, initial management should include removing the patient from the cold environment. Once rewarming is initiated, the patient should not be reexposed to the cold because thawing and refreezing can lead to more tissue damage. For mild frostbite cases, thawing can occur at room temperature. However, for more severe cases and when in the field, the decision about whether to rewarm or not may be difficult. A general guideline is that if the transport time to a medical facility is within 2 hours, the risks posed by thawing and refreezing are greater than the risk of delaying field treatment.[9]

The definitive treatment for frostbite is rapid rewarming in water. The ideal water temperature is between 36° and 42.2°C (96.8°–108°F).18,19 Because the risk of infection is increased with more severe freezing injuries, an antiseptic solution (eg, hexachlorophene, povidone-iodine) may be added to the rewarming bath. In addition, analgesics and sedatives should be considered because rewarming can be extremely painful.[20] After thawing is complete, the injured site should be kept clean, dry, and protected from additional trauma. Furthermore, a tetanus booster should be provided if the patient is not currently up to date, and prophylactic antibiotics (eg, penicillin) should be considered if severe skin edema occurs (edema has been associated with inhibition of the skin’s own strep-tococcicidal properties).[21] Early surgical intervention is not recommended, even with severe fourth-degree frostbite injuries, because some recovery may still occur without surgery.[9]

Adjuvant therapies have been shown to have efficacy in treating freezing injuries. Nonsteroidal anti-inflammatory drugs such as ibuprofen inhibit inflammatory reactions and pain, and have been shown to decrease tissue loss.[14] Prostaglandin E_1, which has been shown to reduce digital amputation rates, has several functions, including dilation of arterioles and venules, reduction in capillary permeability, suppression of platelet aggregation, and activation of fibrinolysis.[22] Other vasodilators including reserpine, pentoxifylline, and buflomedil have shown evidence of decreasing tissue loss as well.23–25 Low-molecular-weight dextran has also been shown to reduce tissue damage in animal models.[26] Use of adjuvant therapies should be guided by a medical professional trained in their uses.

Nonfreezing Cold Injuries

NFCIs occur from prolonged exposures (12 hours to 4 days) to near freezing temperatures, generally between 0° and 15°C (32°–59°F).27–29 Maximal peripheral vasoconstriction occurs at 15°C (59°F), and a further decrease in temperature to 10°C (50°F) results in CIVD, where periods of vasodilation interrupt the vasoconstriction that occurs at cold temperatures to help maintain some degree of perfusion to local tissue.[14] Despite the periods of CIVD, tissue damage occurs from the prolonged periods of vasoconstriction, resulting in damage to the endothelium and surrounding tissue from oxygen deprivation. In one study involving cold-water immersion of the fingers, subjects with weaker CIVD had higher risk of local cold injuries.[30]

Epidemiology

Accurate incidence rates of NFCI even among the military are difficult to determine because the condition often goes unrecognized. The clinical manifestations of NFCI are also often less dramatic than with freezing injuries. However, because NFCIs occur under milder environmental conditions, they likely occur more frequently than frostbite.[3] Among the Israeli Defense Forces in an 8-year period, the majority of 66 peripheral cold injuries were NFCI, specifically trench foot.[3] At the same time, reports in the US military have documented frostbite as the most common cold injury, possibly reflecting underdiagnosed NFCI.[31]

Classification

NFCI consists of two main categories, trench foot and chilblains (also called pernio or kibe). Trench foot occurs when tissue, most commonly of the feet, is exposed to cold temperatures for more than 12 hours. Chilblains, on the other hand, can occur within a few hours of exposure to the bare skin. Generally, these NFCIs occur in conjunction with wet environments.

Clinical Features

The initial clinical presentation of NFCI is similar for chilblains and trench foot. However, chilblains refers only to superficial damage, and it resolve without sequelae after rewarming (Figure 30-3). Clinically, there are four stages in the injury and recovery process for NFCI9,14,32,33:

1. Stage 1 occurs during the cold exposure, when local anesthesia and loss of proprioception occur. Due to intense vasoconstriction, tissue will initially be erythematous, then change to a paler color, and eventually turn white. If the NFCI is milder, as in cases of chilblains, pruritus can be present as well.

2. Stage 2, the prehyperemic phase, follows the removal of the cold exposure and immediate rewarming. Lasting anywhere from a few hours to a few days, this stage presents with tissue color change from white to mottled pale blue. Edema may also set in; however, if intermittent rewarming occurs, the edema is less severe. Peripheral pulses may also be absent, and capillary refill may be sluggish. Generally, pain is uncommon at this stage.

3. Stage 3, the hyperemic phase, is characterized by the body’s attempt to increase perfusion to the affected region. Lasting anywhere from a few days to a few months, this stage is characterized by hot, erythematous, and flushed skin.[34] Peripheral pulses become bounding; however, capillary refill may remain prolonged. The anesthesia from prior stages begins to resolve, and significant pain ensues. In addition, the affected region may become hyperalgesic, and edema with potential vesicles and bullae may form, which can be blood-filled. Muscle weakness may also be apparent.

4. Stage 4, the posthyperemic phase, lacks obvious physical signs, but may last anywhere from a few weeks to years.32,35 The inflammatory response with increased reperfusion observed in stage 3 diminishes, and due to the tissue damage, temperature regulatory mechanisms of the skin may be disrupted. The skin can experience temperature sensitivity, particularly to the cold. Furthermore, pain typically transitions to dull aches, and numbness may persist at more distal sites. Hyperhidrosis is also observed, which may contribute to recurrent fungal infections. More severe findings include contractures from deposition of fibrous scarring as well as gangrene from necrotic tissue and secondary infections.

Figure 30-3. Chilblains of the feet can be pruritic and painful.
Reproduced from: Burr RE. Environmental medicine: heat, cold, and altitude. In: Kelley PW, ed. Military Preventive Medicine. Mobilization and Deployment. Vol 1. Washington, DC: Borden Institute; 2003: Figure 19-14.

Treatment

Removal of the cold exposure and wet, constrictive clothing is the primary management goal. For immediate field management of NFCI, covering the affected area with loose, warm, dry clothing during evacuation is also important. Specific protocols for treating more severe NFCI are not well defined in the literature, but continued monitoring of peripheral perfusion, providing analgesics for pain control, and potentially using calcium channel blockers (eg, nifedipine) or tricyclic antidepressants (eg, amitriptyline hydrochloride) may provide a degree of benefit.[9]

TABLE 30-2

ESTIMATED SURVIVAL TIME IN COLD WATER

Water Temperature

Approximate Survival Time

°C

°F

20

68

10 h

15

59

3–6 h

10

50

2–5 h

5

41

1–3 h

0

32

< 90 min

Data sources: (1) Hayward JS, Eckerson JD, Collis ML. Thermal balance and survival time prediction of man in cold water. Can J Physiol Pharmacol. 1975;53(1):21–32. (2) Molnar GW. Survival of hypothermia by men immersed in the ocean. J Am Med Assoc. 1946;131(13):1046–1050.

Accidental Hypothermia

Accidental hypothermia is defined as an involuntary drop in the core body temperature below 35°C (95°F). It develops when the sustained heat loss to the environment exceeds heat production. Although hypothermia can occur in extremely cold environments, below-freezing temperatures are not necessary to develop the condition. Effects from factors including wind chill, water immersion, rain, and sweating may significantly contribute to hypothermia, even in milder temperatures. Particularly when the skin is exposed to water for prolonged periods, such as in the case of water immersion (Table 30-2) or wet clothing from rain or sweating, hypothermia can occur rapidly. Heat loss secondary to conduction can occur up to 5 times faster with wet clothing and up to 25 times faster with water immersion.[36] In addition, effects of alcohol, certain medications, and medical conditions can further predispose individuals to hypothermia.[37]

Epidemiology

The burden of accidental hypothermia, a preventable condition, is demonstrated by the mortality among the US civilian population. Between 1979 and 2002, an average of 689 persons per year died from hypothermia-related causes.[38] The incidence of hypothermia-related deaths increased between 1999 and 2011, averaging 1,301 deaths per year.[39]

Historically, the military has also suffered significant fatalities due to hypothermia, as mentioned previously. However, even within the last 30 years, the military remained susceptible to hypothermia-related casualties and deaths both in training and combat. For instance, in 1995, a class of US soldiers in Ranger School training in the swamps of Florida suffered from hypothermia, eventually resulting in four fatalities.[40] In the study of cold-weather injuries in military service members during Operation Enduring Freedom and Operation Iraqi Freedom from 2001 to 2009, 17 hypothermia cases were identified without any fatalities.[15] The Israeli study identifying CWIs in the Israeli Defense Forces between 1994 and 2001 revealed that 10% of cold injuries from combat were hypothermia-related, whereas 71% of cold injuries from training activities were hypothermia-related, compared to peripheral injuries.[3]

Classification

Accidental hypothermia is classified in several ways. Hypothermia can be classified by how it is induced and the relative time frame of induction. These categories include acute (immersion), submersion, subacute, and subchronic.[9]

- Acute (immersion) hypothermia: induced by partial or full immersion when conductive heat losses far exceed heat production (eg, falling through ice into cold water). Initially, the cold induces an initial hyperventilation (with risk of water aspiration) as well as a sudden fall in blood pressure. Heat loss can be minimized by limiting movement and huddling. Self-rescue is possible, but the longer the duration of immersion, the more difficult self-rescue will be.

- Submersion hypothermia: total submersion of the body in ice-cold water. This is more prevalent when young children fall through ice; water aspiration is more likely in this situation than with acute immersion. However, successful resuscitation has been achieved even after 45 to 60 minutes of submersion.

- Subacute hypothermia: exposures less severe than cold water immersion. Examples include prolonged exposure to cold air with wind, rain, and physical exertion. Subacute hypothermia develops over hours or several days.

- Subchronic hypothermia: prolonged exposure to cold temperatures, occurring over days to weeks. Examples include isolated soldiers in survival situations and the malnourished elderly in the civilian population.

Hypothermia can also be classified based on the corresponding body core temperature. Most staging categories include mild, moderate, and severe, while others further include a profound category. Table 30-3 delineates the staging of hypothermia and associated physiologic changes.

TABLE 30-3

HYPOTHERMIA STAGING WITH PHYSIOLOGIC CHANGES ASSOCIATED WITH CORE TEMPERATURE

Stage

Core Temperature

Description

°C

°F

Mild

35.0

95.0

Maximal shivering, increased blood pressure

34.0

93.2

Amnesia, dysarthria, poor judgment, behavior change

33.3

91.4

Ataxia, apathy, cold diuresis

Moderate

32.0

89.6

Stupor

31.0

87.8

Shivering ceases

30.0

86.0

Cardiac arrhythmias, decreased cardiac output, insulin ineffective

29.0

84.2

Unconsciousness, pupils dilate

Severe

28.0

82.4

Ventricular fibrillation likely, hypoventilation, paradoxical undressing^1

27.0

80.6

Loss of reflexes and voluntary motion

26.0

78.8

Acid-based disturbances, no response to pain

25.0

77.0

Reduced cerebral blood flow, loss of cerebrovascular autoregulation

24.0

75.2

Hypotension, bradycardia, pulmonary edema

23.0

73.4

No corneal reflexes, areflexia

19.0

66.2

Electroencephalographic silence

18.0

64.4

Asystole

15.2

59.3

Lowest infant survival from accidental hypothermia^2

13.7

56.7

Lowest adult survival from accidental hypothermia^3

1. Brandstrom H, Eriksson A, Giesbrecht G, Angquist KA, Haney M. Fatal hypothermia: an analysis from a sub-arctic region. Int J Circumpolar Health. 2012;71:1–7.

2. Nozaki R, Ishibashi K, Adachi N, Nishihara S, Adachi S. Accidental profound hypothermia. N Engl J Med. 1986;315(26):1680.

3. Gilbert M, Busund R, Skagseth A, Nilsen PA, Solbo JP. Resuscitation from accidental hypothermia of 13.7 degrees C with circulatory arrest. Lancet (London, England). 2000;355(9201):375–376.

Lastly, a clinical staging system is increasingly utilized based on the Swiss staging system, particularly when accurate measurements of core body temperature are not feasible. The staging system ranges from HT I to HT IV. In HT I, the individual is both conscious and shivering; in HT II, the individual has impaired consciousness and is no longer shivering; in HT III, the individual is unconscious, not shivering, but has vital signs; and in HT IV, the individual no longer has vital signs.

Clinical Features

Hypothermia is insidious in onset and early identification may be difficult. Accidental hypothermia must be suspected and recognized to administer appropriate therapy. Evaluating suspected hypothermia-related cases should include a clinical history, physical examination, and obtaining the rectal temperature.

Although hypothermia is defined as a core body temperature below 35°C (95°F), signs and symptoms may begin to appear at body temperatures of 36.0°C (96.8°F), including increased metabolic rate, elevated blood pressure, and increased muscle tension. Additional signs and symptoms are increasingly apparent as the core body temperature declines. Between 25°C (77°F) and 32.2°C (90°F), shivering diminishes and peripheral vasoconstriction is lost. Below 25°C (77°F), coordinated heat regulatory and heat conservation mechanisms are nonfunctional (see Table 30-3).[14]

Treatment

Hypothermia is a medical emergency, and rewarming is the goal of hypothermia management. In general, rewarming someone with suspected hypothermia should not be delayed either to find a low-reading thermometer or to run a clinical laboratory test. Rewarming can be active or passive and will depend on the available resources and current atmospheric environment. In passive rewarming (also called spontaneous rewarming), normal physiologic heat production is maximized through insulating the affected individual (including the head) and sheltering them from atmospheric conditions.[41] Since passive rewarming depends on an intact thermoregulatory system, it should only be employed as the sole source of rewarming with mild hypothermia cases, when core temperature exceeds 32.2°C (90°F).[42] In previously healthy and conscious individuals suffering mild hypothermia, voluntary physical activity and warm, nonalcoholic and decaffeinated beverages may be considered in addition to insulation. Moreover, if an individual with mild hypothermia is wearing wet clothing, it should only be removed after the individual has reached a warm, dry, sheltered environment because removing the clothing in the field can produce more rapid heat loss.[43] To maximize rewarming, distal extremities should be kept cool because warm hands and feet can reduce the stimulus for heat production and increase vascular dilation, thereby increasing heat loss.[43]

With core temperatures below 32.2°C (90°F), active rewarming is generally required. Active rewarming involves a source to conduct heat directly to the individual. This includes a variety of methods, ranging from noninvasive sources including heated garments, water immersion at 40°C (104°F), and heated and humidified air, to more invasive techniques involving heated dialysate (40°C [104°F]) in peritoneal dialysis and blood rewarming procedures (eg, cardiopulmonary bypass, arteriovenous rewarming, venovenous rewarming, hemodialysis).[44] Ideally, when core temperatures are significantly below 32.2°C (90°F), individuals should be transported to definitive medical care for careful monitoring and rewarming; core temperatures this low can cause cardiac arrhythmias, pulmonary edema, fluid imbalances, coagulopathies, acid-base imbalance, electrolyte disturbances, and blood glucose variations. Figure 30-4 displays a basic decision algorithm for initial hypothermia management.

Figure 30-4. Initial treatment algorithm for hypothermia.
Data sources: (1) Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia. N Engl J Med. 2012;367(20):1930–1938. (2) Durrer B, Brugger H, Syme D. The medical on-site treatment of hypothermia: ICAR-MEDCOM recommendation. High Alt Med Biol. 2003;4(1):99–103.

MEDICAL SURVEILLANCE

Three vital components to identify before work begins in cold environments include (1) determination of the physical and mental qualifications appropriate to the specific job, (2) medical evaluation of the worker’s physical and psychological ability to work in the cold, and (3) identification of specific medical conditions that may disqualify the individual from work in cold environments.[45] Even with appropriate protective equipment, cold stress can still place significant demands on the body, and inappropriately qualifying individuals to work in the cold can risk the safety of the individual as well as those he or she supports.

Medical history should be screened carefully to determine potential risk factors for suffering a cold-related injury. For instance, conditions that may preclude work in certain cold environments (below -1°C [30.2°F]) include exertional angina, previous cold injury, asthma, peripheral vascular disease, coronary artery disease, drug and alcohol abuse, and thermoregulatory disorders.[46] Other risk factors identified in the literature include gender and race (women and African Americans are at higher risk), poor physical conditioning, fatigue, and inadequate caloric intake.5,31,38 Also, because cold exposure encompasses a wide range of atmospheric conditions, much colder conditions (below -24°C [-11.2°F]) with wind speeds less than 5 miles per hour, or air temperature below -18°C (0°F) with wind speeds above 5 miles per hour, should warrant medical clearance.

Since cold injuries are preventable, there should be a strong focus on appropriate prevention measures and early identification and treatment, especially during deployments in the field. Medical providers and supporting staff should communicate closely with commanders and supervisors to ensure proper recommendations are disseminated and practiced, particularly in the training environment.

PREVENTION

For all work required in cold environments, adequate protective barriers, insulated clothing, safe work cycles, and early identification of cold injuries will significantly decrease morbidity from the cold. As mentioned previously, protective shielding from the wind and rain will reduce additional heat loss. Furthermore, proper cold weather clothing can maximize body temperature homeostasis. The degree of insulation will depend on clothing factors such as fabric material, thickness, and amount of dead-space air trapped within a garment or between garments.[47] Clothing can be assigned a value known as a clo unit. This unit expresses the relative resistance to heat transfer by clothing. Specifically, a clo unit is the amount of thermal insulation that allows a person at rest (whose metabolic rate is 58 W/m^2) to maintain thermal equilibrium in an environment at 21°C (69.8°F) in a normally ventilated room (0.1 m/s air movement) with relative humidity less than 50%.[48] The approximate amount of clothing insulation needed at different air temperatures and physical activity levels measured by metabolic equivalents is depicted in Figure 30-5. Table 30-4 provides examples of various articles of clothing and associated insulator factor.

Figure 30-5. Approximate clothing insulation needed at different air temperatures and physical activity level. Wind speed is assumed to be less than 5 mph. At higher wind speeds, a windproof layer may be needed. One MET refers to energy expenditure at rest.
MET: metabolic equivalent
Adapted from: US Department of the Army. Prevention and Management of Cold-Weather Injuries. Washington, DC: DA; 2005: 22. Technical Bulletin MED 508.

In extremely cold environments, where multiple layers of clothing are required, clothing layers should maximize the ability to wick moisture away from the body and limit cooling effects from wind and rain. For example, inner layers could consist of materials such as polypropylene, which help wick moisture to outer layers; intermediate layers of wool or Thinsulate (3M, St Paul, MN) provide added insulation; and outer layers should be wind-resistant and water-repellant (eg, Gore-Tex; WL Gore & Associates, Newark, DE), allowing moisture generated from perspiration to evaporate. Similar laying should occur with the hands, feet, and head. When wearing cold weather clothing, a helpful mnemonic (“COLD”) can be used[9]:

TABLE 30-4.

INSULATION VALUE OF VARIOUS CLOTHING

Clothing Item

Insulation Value (Clo)*

Short sleeve shirt

0.18–0.25

Long sleeve shirt

0.22–0.29

Long sleeve sweater

0.20–0.37

Long underwear

0.20–0.30

Long pants

0.26–0.35

Socks (knee high)

0.08–0.13

Army improved physical fitness uniform

0.30

Army PT uniform with nylon pants and jacket

0.70

Battle dress uniform (BDU)

1.15

Expedition-weight polypropylene underwear

1.35

ECWCS (US Army) field coat and trouser liners

1.93

Gore-Tex† parka and trousers

1.95

Fleece jacket, bib overall

2.37

Total ECWCS (US Army)

3.4

*Ranges of clo values depend on clothing thickness and material.

† WL Gore & Associates, Newark, DE

ECWCS: Extended Cold Weather Clothing System

PT: physical training

Data sources: (1) US Department of the Army. Prevention and Management of Cold-Weather Injuries. Washington, DC: DA; 2005. Technical Bulletin MED 508. (2) Goldman R, Kampmann B. Handbook on Clothing. Biomedical Effects of Military Clothing and Equipment Systems. 2nd ed. Brussels, Belgium: NATO Research Study Group 7; 2007.

- C: Keep clothing Clean

- O: Avoid Overheating

- L: Wear Loose and in Layers

- D: Keep clothing Dry

Depending on the environment and work duties, insulation of exposed skin may not necessarily be needed; however, outdoor work with exposure to UV radiation should prompt use of sunscreen products as well. Additionally, proper eye protection can mitigate corneal abrasions and photokeratitis from a combination of wind, snow, ice, and UV radiation.

Table 30-5 provides recommended guidance on administrative controls and work cycles in cold environments, based on environmental conditions. However, when progressive signs and symptoms of cold injury become apparent, regardless of the environmental temperature, it is paramount to evaluate and appropriately treat the person prior to returning the individual to his or her duties. Prolonged cold exposure can inhibit the sensation of cold, which highlights the importance of supervision and having a buddy system.

Due to the increased metabolic demand of working in cold environments and the potential for cold diuresis, adequate nutrition and hydration should be stressed. Food is the fuel that helps generate and maintain the body core temperature, and a deficiency in critical fuel sources (carbohydrates, proteins, fats) may impact survival. Furthermore, dehydration can reduce appetite, further compounding cold environmental hazards. In general, and depending on activity level, military personnel need to increase their caloric consumption by 10% to 40% when operating in cold environments.[49] Specific rations have been developed with higher caloric content for cold weather operations such as the Meal, Cold Weather/Food Packet, Long Range Patrol (MCW/LRP) and the Ration, Cold Weather (RCW).

Leaders and supervisors should also establish a program for regular hydration. Actual fluid requirements depend upon the level of physical activity; however, urine that is dark yellow may signify inadequate fluid intake. Hot drinks may also be beneficial because the additional warmth can elevated mood.[50] Caution, however, should be taken to limit excessive caffeine consumption, which can lead to difficulty sleeping, and withdrawal can also cause headaches and nausea. Fluids such as alcohol are discouraged not only because they can impair judgment, but also because they can provide a false sense of feeling warm. Cold acclimatization programs should be considered if training allows; however, since their benefits are significantly less effective compared to heat acclimatization programs, the other preventive modalities should receive significantly more attention.

TABLE 30-5

WORK CYCLE RECOMMENDATIONS DURING COLD ENVIRONMENTAL CONDITIONS

The work cycle schedule applies to a 4-hour period of moderate to heavy intensity work. Normal breaks are assumed to take place once every 2 hours.

Table courtesy of the Canadian Centre for Occupational Health and Safety—Occupational Health and Safety Division of the Government of Saskatchewan.

Other data sources: (1) American Conference of Governmental Industrial Hygienists. 2013 TLVs and BEIs—Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, OH: ACGIH; 2013: 2-2. (2) Occupational Safety and Health Administration. Cold stress. https://www.osha.gov/dts/weather/winter_weather/windchill.html. Accessed May 8, 2017.

SUMMARY

The cold environment is unforgiving and has accounted for countless deaths in civilian and military operations. Although the weather and external environment cannot be altered, CWIs can be prevented with proper training and equipment. Early identification of CWIs should be addressed promptly before irreversible damage is done. With increased awareness among all military personnel, from senior supervisors to front line operators, cold weather casualties can be reduced significantly.

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ABBREVIATIONS AND ACRONYMS

A

AAP: Army ammunition plant

ABD: acute beryllium disease

ACD: allergic contact dermatitis

ACGIH: American Conference of Governmental Industrial Hygienists

AD: Army depot

ADA: Americans with Disabilities Act

ADC: Army Dosimetry Center

ADHD: attention deficit hyperactivity disorder

ADLs: activities of daily living

ADNT: aminodinitrotoluene

AF: adjustment factor

AFHSC: Armed Forces Health Surveillance Center

AFI: Air Force instruction

AFMAN: Air Force manual

AFMSA: Air Force Medical Support Agency

AFPD: Air Force policy directive

AFV: armored fighting vehicle

AG: antigen

AGE: arterial gas embolism

AGSM: anti-G straining maneuver

AIHA: American Industrial Hygiene Association

ALARA: as low as reasonably achievable

ALP: alkaline phosphatase

ALT: alanine aminotransferase

AMC: Army Materiel Command

AMCOM: Aviation and Missile Life Cycle Management Command

AMEDD: Army Medical Department

AMSP: asbestos medical surveillance program

ANSI: American National Standards Institute

AOEHP: Army Occupational and Environmental Health Program

APHC: Army Public Health Center

AR: Army regulation

ASD HA: Assistant Secretary of Defense for Health Affairs

AST: aspartate aminotransferase

ASW: antisubmarine warfare

ata: absolute atmosphere

atm: atmosphere

ATPIAL: Advanced Target Pointer Illuminator Aiming Light

AV: antivibration

B

BAL: broncho-alveolar lavage

BBP-SPM: blood-borne pathogen surveillance program manager

BDPE: benzo[a]pyrene diol epoxide

BDS: battle dressing station

BE: bioenvironmental engineering

BEI: biological exposure index

BeLPT: beryllium lymphocyte proliferation test

BFV: Bradley fighting vehicle

BLL: blood lead level

BOMC: base operational medicine clinic

BOS: base operating support

BR: basic restriction

BSI: biological surveillance initiative

BUMED: Navy Bureau of Medicine and Surgery

C

C4ISR: communications, computers, intelligence, surveillance, and reconnaissance

CAD: chemical agent detector CAM: chemical agent monitor

CAMS: Central Atmosphere Monitoring System

CAP: Computer/Electronic Accommodations Program

CARC: chemical agent-resistant coating

CB: constrictive bronchiolitis

CBC: complete blood count

CBD: chronic beryllium disease

CBLI: cumulative blood lead index

CBRN: chemical, biological, radiological, and nuclear

CD: chemical depot

CDC: Centers for Disease Control and Prevention

CEGL: continuous exposure guideline level

CEMR: civilian employee medical record

CEU: continuing education unit

CFKE: Coburn, Foster, and Kane equation

CFR: US Code of Federal Regulations

CHCS: Center for Healthcare Services

CHPPM: US Army Center for Health Promotion and Preventive Medicine

CHRA: Civilian Human Resources Agency

CIA: Central Intelligence Agency

CIE: International Commission on Illumination

CITE: center of industrial and technical excellence

CIVD: cold-induced vasodilation

CMC: commandant of the Marine Corps

CME: continuing medical education

CMP: complete metabolic panel

CNO: chief of naval operations

CNS: central nervous system

CO: commanding officer

COCO: contractor-owned, contractor-operated

COT: Committee on Toxicology

CPP/DCPAS: Civilian Personnel Policy/Defense Civilian Personnel Advisory Services

Cr VI: hexavalent chromium

CRNA: certified registered nurse anesthetist

CS: compensation specialist

CSP: Chemical Surety Program

CT: computed tomography

CURR: US Armed Services Center for Unit Records Research

CV: cardiovascular

CWA: chemical warfare agent

CWIs: cold weather injuries

D

DA: Department of the Army

DAF: Department of the Air Force

DBNP: 2,6-di-tert-butyl-4-nitrophenol

DBP: 2,6-di-tert-butylphenol

DCPAS: Defense Civilian Personnel Advisory Service

DCS: decompression sickness

DCS PH: deputy chief of staff for public health

DDC: deck decompression chamber

DEET: N,N-diethyl-meta-toluamide

DHA: Defense Health Agency

DISSUB: disabled submarine

DMDC: Defense Manpower Data Center

DMED: Defense Medical Epidemiologic Database

DMO: diving medical officer

DMSA: 2,3-dimercaptosuccinic acid

DMSS: Defense Medical Surveillance System

DNA: deoxyribonucleic acid

DNAN: 2,4-dinitoanisole

DNIF: duty not involving flying

DNT: dinitrotoluene

DO: dental officer

DoD: Department of Defense

DoDI: Department of Defense instruction

DoDSR: Department of Defense Serum Repository

DOEHRS: Defense Occupational and Environmental Health Readiness System

DOEHS: Deployment Occupational and Environmental Health Surveillance

DoN: Department of the Navy

DoT: Department of Transportation

dps: disintegration per second

DR: digital radiography

DRSi: Disease Reporting System-internet

DSOC: Defense Safety Oversight Council

DTPA: diethylenetriamine pentaacetic acid

DU: depleted uranium

DVCC: disease vector control center

DVECC: disease vector ecology control center

E

EAB: emergency air breathing

EAD: equivalent air depth

EBC: exhaled breath condensate

ECG: electrocardiogram

ECWCS: Extended Cold Weather Clothing System

ED: emergency department

EDTA: ethylenediaminetetraacetatic acid

EEGL: emergency exposure guidance levels

EGDN: ethylene glycol dinitrate

EKG: electrocardiogram

ELIS: enzyme-linked immune spot

ELISA: enzyme-linked immunosorbent assay

EMI: electromagnetic interference

EMP: electromagnetic pulse

EOD: explosive ordnance disposal

EPA: Environmental Protection Agency

Er:Glass: erbium doped glass

ERPG: emergency response planning guidelines

ESAMS: Enterprise Safety Applications Management System

ESIP: Environmental Surveillance Integration Program

ESOH: environment, safety, and occupational health

EST: exercise stress test

EVD: Ebola virus disease

F

FAA: Federal Aviation Administration

FBR: fast-burst reactor

FDA: Food and Drug Administration

FDPMU: forward deployable preventive medicine units

FECA: Federal Employees’ Compensation Act

FEDCU: fleet epidemic disease control units

FEL: free electron laser

FEP: free erythrocyte protoporphyrin

FEV: forced expiratory volume

FMCSA: Federal Motor Carrier Safety Agency

FOM: flight and operational medicine

FORSCOM: Forces Command

FRC: Federal Radiation Council

fsw: feet of seawater

FVC: forced vital capacity

G

G6PD: glucose-6-phosphate dehydrogenase

G-LOC: G-induced loss of consciousness

GA: tabun

GAO: Government Accountability Office

GB: sarin

GDL: ground designator laser

GF: cyclosarin

GFR: glomular filtration rate

GGT: γ-glutamyltransferase

GINA: Genetic Information Nondiscrimination Act

GMO: general medical officer

GOCO: government-owned, contractor-operated

GOGO: government-owned, government-operated

GS: general service

GWI: Gulf War illness

H

HAN: hydroxyl ammonium nitrate

Hbco: carboxyhemoglobin

HBIG: hepatitis B immune globulin

HBOT: hyperbaric oxygen therapy

HBsAg: hepatitis B surface antigen

HBV: hepatitis B virus

HCE: Hearing Center of Excellence

HCV: hepatitis C virus

Hep B sAB: hepatitis B surface antigen

Hep C AB: hepatitis C antibody

HEPA: high efficiency particulate air

HF: hydrogen fluoride

HIPAA: Health Insurance Portability and Accountability Act

HIPIR: high power illuminator radar

HIV: human immunodeficiency virus

HMX: octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine

Hp: haptoglobin

HPD: hearing protection device

HPNS: high pressure nervous syndrome

HRA: health risk assessment

HRM: human resource management

I

IARC: International Agency for Research on Cancer

ICP-MS: inductively coupled plasma mass spectrometry

ICRP: International Commission on Radiation Protection

ICU: intensive care unit

ID: infectious disease

IDC: independent duty corpsman

IDLH: immediately dangerous to life or health

IED: improvised explosive device

IEEE: Institute of Electrical and Electronics Engineers

IFN-γ: interferon

IH: industrial hygiene

IHC: inner hair cell

IHO: industrial hygiene officer

IME: independent medical exam

IMX: insensitive munitions explosive

INST: instruction

IOM: Institute of Medicine

IR: infrared

J

JMC: Joint Munitions Command

L

LAP: loading, assembly, and packing

LASIK: laser in situ keratomileusis

LD_50: median lethal dose

LDH: lactate dehydrogenase

LEP: laser eye protection

LFT: liver function test

LIDAR: light detection and ranging

LINAC: linear accelerator

lncRNA: long non-coding RNA

LV: lung volume

M

MAJCOM: major command

MCL: maximum contaminant level

MCT: mask confidence training

MCW/LRP: meal, cold weather/food packet, long range patrol

MDRO: multi-drug resistant organisms

MEA: monoethanolamine

MEB: medical evaluation board

MEDCEN: medical center

MEDCOM: Army Medical Command

MEDDAC: Medical Department activity

MEDEVAC: medical evacuation

MEDPROS: Medical Protection System

MERS-Cov: Middle East respiratory syndrome coronavirus

MESL: Military Exposure Surveillance Library

MHS: Military Health System

miRNA: microRNA

MIS: management information system

MMWR: Morbidity and Mortality Weekly Report

MO: medical officer

MOPP: mission-oriented protective posture

MOUT: mission operations on urban terrain

MPE: maximum permissible exposure

MRAP: mine-resistant, ambush-protected

mRNA: messenger RNA

MRSA: methicillin-resistant S aureus

MSAT: Medical Situational Awareness in the Theater

MSC: Medical Service Corps

msw: meters of seawater

MTF: medical treatment facilities

N

NAF: non-appropriated funds

NAS-COT: National Academy of Science’s Committee on Toxicology

NATO: North Atlantic Treaty Organization

NBC: nuclear, biological, and chemical

NCRP: National Council on Radiation Protection

NDI: nondestructive inspection

NDSTC: Naval Diving and Salvage Training Center

Nd:YAG: neodymium doped yttrium aluminum garnet

NECE: Navy Entomology Center of Excellence

NEDU: Navy Experimental Diving Unit

NEHC: Navy Environmental Health Center

NEPMU: Navy environmental and preventive medicine unit

NFCI: nonfreezing cold injury

NFPA: National Fire Protection Association

NGIC: National Ground Intelligence Center

NHANES: National Health and Nutrition Evaluation Survey

NIEHC: Navy Industrial Environmental Health Center

NIHI: noise-induced hearing injury

NIHL: noise-induced hearing loss

NIOSH: National Institute for Occupational Safety and Health

NITROX: nitrogen-oxygen mixture

NMC: Naval Medical Center

NMCPHC: Navy and Marine Corps Public Health Center

NMCPHC-TM: Navy and Marine Corps Public Health Center Technical Manual

NOHIMS: Navy Occupational Health Information Management System

NRC: National Research Council

NRC COT: National Research Council’s Committee on Toxicology

NSMRL: Naval Submarine Medical Research Laboratory

NTC: National Training Center

NTO: nitrotriazolone

NTP: National Toxicology Program

NU: natural uranium

NVGs: night vision goggles

O

OASD: office of the assistant secretary of defense

OBOGS: On-Board Oxygen Generation System

OEF: Operation Enduring Freedom

OEH: occupational and environmental health

OEHS: occupational and environmental health surveillance

OEHSA: OEH site assessment

OEHWG: OEH working group

OEL: occupational exposure limit

OEM: occupational and environmental medicine

OHC: occupational health center

OHC: outer hair cell

OHP: Occupational Health Program

OHPSR: OHP status report

OIF: Operation Iraqi Freedom

OMPA: Occupational Medicine Program Assessment

OND: Operation New Dawn

OPM: Office of Personnel Management

OPNAV: Office of the Chief of Naval Operations

OR: operating room

OSAGWI: Office of the Special Assistant for Gulf War Illnesses

OSHA: Occupational Safety and Health Administration

OTR: Operation Tomodachi Registry

OTSG: Office of the Surgeon General

OUA: Operation United Assistance

OWCP: Office of Workers’ Compensation Programs

P

PA: physician assistant

PAH: polycyclic aromatic hydrocarbons

PAM: pamphlet

PCR: polymerase chain reaction

PDHRA: Post Deployment Health Reassessment

PEF: peak expiratory flow

PEL: permissible exposure level

PEO: Program Executive Officer

PEPline: Postexposure Prophylaxis Hotline

PET: positron emission tomography

PFO: patent foramen ovale

PFT: pulmonary function test

PGDN: propylene glycol dinitrate

PH: public health

PHA: preventative health assessment

piRNA: piwi-interacting RNA

PL: public law

PLHCP: physician or other licensed healthcare professional

PMU: preventive medicine unit

POC: point of contact

POEMS: Periodic Occupational and Environmental Monitoring Summary

POWER: Protecting Our Workers and Ensuring Reemployment

PPE: personal protective equipment

PRK: photorefractive keratectomy

PT: physical training

PTC: personnel transfer capsule

PTS: permanent threshold shift

PWO: physician’s written opinion

Q

QA WTP: Qarmat Ali Water Treatment Plant

QWE: quality of the work environment

R

RBCs: red blood cells

RCW: ration, cold weather

RDD: radiation dispersal device

RDECOM: Research, Development and Engineering Command

RDX: hexahydro-1,3,5-trinitro-1,3,5-triazine

REL: radiation exposure limit

RF: radio frequency

RHC: regional health command

RN: registered nurse

RNA: ribonucleic acid

RSC: Radiation Safety Committee

RSO: radiation safety officer

RTD: return to duty

RV: residual lung volume

S

SCBA: self-contained breathing apparatus

SCUBA: self-contained underwater breathing apparatus

SDV: SEAL delivery vehicle

SEAL: sea, air, land

SEAL: Submarine Escape Action Level

SEG: similar exposure group

SEIE: submarine escape immersion equipment

SHARE: Safety, Health and Return to Employment

SIPRnet: Secret Internet Protocol Router Network,

SMART-PM: Special Medical Augmentation and Response Team–Preventive Medicine

SME: subject matter expert

SMO: senior medical officer

SNHL: sensorineural hearing loss

SOF: Special Operations Forces

SOH: safety and occupational health

SOP: standard operating procedure

SPECT: single photon emission computerized tomography

SPOD/E: sea port of debarkation/embarkation

SRDRS: submarine rescue diving and recompression system

STD: sexually transmitted disease

STS: significant threshold shift

SUBEX: submarine exercise

T

Tdap: tetanus, diphtheria, and acellular pertussis vaccine

TEH: Total Exposure Health

TLC: total lung capacity

TLD: thermoluminescent dosimeter

TLV: threshold limit value

TNT: trinitrotoluene

TRADOC: Training and Doctrine Command

TRANSCOM: Transportation Command

TTS: temporary threshold shift

TWA: time-weighted average

U

UBA: underwater breathing apparatus

UHF: ultra-high frequency

UHMS: Undersea and Hyperbaric Medical Society

UIC: unit identification code

UL: Underwriters Laboratory

UPTD: unit pulmonary toxicity dose

USAHEA: US Army Environmental Hygiene Agency

USAPHC: US Army Public Health Center

USD (AT&L): Office of the Under Secretary of Defense for Acquisition, Technology, and Logistics

USD (P&R): Office of the Under Secretary of Defense for Personnel and Readiness

USMC: US Marine Corps

USN: US Navy

USPHS: US Public Health Service

UV: ultraviolet

V

VA: Department of Veterans Affairs

VA: Veterans Administration

VC: vital capacity

VHA: Veterans Health Administration

VHF: very high frequency

VSAT: very small aperture terminal

W

WAG: waste anesthetic gas

WCT: wind chill temperature

WEEL: workplace environmental exposure level

WESS: Web-Enabled Safety System

WG: wage grade

WMSD: work-related musculoskeletal disorders

WRNMMC: Walter Reed National Military Medical Center

WTC: World Trade Center

X

XO: executive officer

Z

ZPP: zinc protoporphyrin

INDEX

A

Abbreviations, xix–xxii

Aberdeen Proving Ground, 9

Acceleration injury, 268

Accreditation Council for Graduate Medical Education, 122

ACGIH. See American Conference of Governmental Industrial Hygienist

Acquisition, Technology, and Logistics, Under Secretary of Defense for, 115–116

Acronyms, xix–xxii

ADA. See Americans with Disabilities Act

Adams, John, 42

Administrative medical examinations, 63–64

Advanced Very High Resolution Radiometer, 76

Aerospace medicine

acceleration injury, 268

altitude-induced hypoxia, 264–265

barotrauma, 265–266

circadian rhythm disturbance, 273–275

color vision, 279–281

counter fatigue programs, 278–279

decompression sickness, 266–267

ejection injury, 268

environmental risk factors, 276–277

ergonomics, 275

fatigue, 273–275

fitness testing programs, 278

hazards, illness and injury, 264–276

heat stress, 268

hypothermic injury, 268

industrial hazards, 275–276

laser eye protection, 281

loss of consciousness, 268

military aviation administration, 283–286

modified duty programs, 278

motion sickness, 271–272

new accession exams, 277–278

night vision goggles, 281–282

noise-induced hearing loss, 272–273

personal protective equipment, 279

pressure illness, 265–268

readiness and deployment, 277–279

refractive surgery, 282–283

sleep deprivation, 273–275

spatial disorientation, 270–271

structure of atmosphere, 264

sustained acceleration, 269–270

thermal stress, 268

three-dimensional motion, 268–272

transient acceleration, 269

travel health hazards, 275

visual performance and protection, 279–283

weaponry and injury, 275

Afghanistan, Operation Enduring Freedom, 86–100

AFMSA. See Air Force Medical Support Agency

Agency Query System, 146

Agent Orange, 72

Ahmadi Oil Fields, Kuwait, 73

Air evacuation, 285–286

Air Force Medical Support Agency, 13

Air Force occupational and environmental health program

critical elements of, 17

emerging developments in Air Force Occupational Medicine, 19

employee role and responsibilities, 16

execution of, 17–18

exposure assessment model, 17–18

headquarters level role and responsibilities, 12–13

installation level role and responsibilities, 13–16

major command roles and responsibilities, 13

management review, 19

overview, 12

planning process, 16–17

role and responsibilities, 12–16

supervisor role and responsibilities, 16

Air pollution, 478

Air-purifying respirators, 220–222

Air sampling, 84–85

Airborne hazards, 596–599

Al Tuwaitha Nuclear Research Center, 92

Aliphatic nitrate esters

nitrocellulose, 572

nitroglycerin, 568–572

Altitude-induced hypoxia, 264–265

Ambient air regulations, 392

AMC. See Army Materiel Command

AMCOM. See Aviation and Missile Life Cycle Management Command

American Conference of Governmental Industrial Hygienist, 156, 236, 239, 368

American Industrial Hygiene Association, 236, 368

Americans with Disabilities Act, 129

Ammunition plants, 5–7

Amsden, Sergeant 1st Class Lance, vi

Anesthetic gases, 175–176

Anniston Army Depot, 4

Anniston Defense Munitions Center, 5

Anthrax attacks, 88–89

Anti-G straining maneuver, 270

Antineoplastic agents, 176–177

AOEHP. See Army Occupational and Environmental Health Program

APHC. See Army Public Health Center

Armed Forces Health Longitudinal Technology Application, 100

Army Center for Health Promotion and Preventive Medicine, 74

Army Chemical Materials Activity, 8

Army Contracting Command, 7

Army ergonomics program, 244–245

Army Health Promotion Program, 65–66

Army Hearing Conservation Program, 200–213

Army industrial hygiene program, 239–240

Army Materiel Command

Army Materiel Systems Analysis Activity, 8

The Logistics Support Activity, 8

mission of, 3

motto, 2

quality of work environment, 8–9

US Army Aviation and Missile Life Cycle Management Command, 5

US Army Chemical Materials Activity, 8

US Army Communications-Electronics Command, 5

US Army Contracting Command, 7

US Army Joint Munitions Command, 5–7

US Army Military Surface Deployment and Distribution Command, 7–8

US Army Security Assistance Command, 8

US Army Sustainment Command, 7

Army Materiel Systems Analysis Activity, 8

Army Medical Command, 117

Army Military Surface Deployment and Distribution Command, 7–8

Army Occupational and Environmental Health Program

budgeting, 123–124

contracting for occupational health services, 124

DoD program structure and management, 115–117

expanding service delivery, 124

funding, 123–124

management of, 117–118

overview, 114–115

personnel, 120–123

quality measures, 118–120

Army Occupational Health Programs

administrative medical examinations, 63–64

Army Occupational and Environmental Health Program, 115–124

in Bosnia, Herzegovina, and Kosovo, 83–86

credentialing and privileging, 60–61

disability retirement examinations, 64

emergency treatment, 66

employee health clinics, 60

employees, 62

epidemiological investigations, 65

evaluation of, 59

fitness-for-duty examinations, 64

health hazard education, 64

health promotion, 65–66

health providers, 61

immunizations, 65

industrial hygienists, 61

informatics, 100–103

laws, regulations, and guidance, 56–59

marketing, 58–59

medical centers, 59–60

medical directives, 58

medical records management, 62–63

medical surveillance, 63

monitoring absences due to illness, 64–65

nurses, 61

occupational health business plan, 58

occupational health clinics, 59–60

Operation Enduring Freedom, 86–100

Operation Iraqi Freedom, 86–100

organization of, 59–62

during Persian Gulf War, 72–83

program document, 57–58

safety personnel, 61–62

staffing, 60–62

standard operating procedures, 58

status report, 57–58

supervisors, 62

worksite evaluations, 64

Army Public Health Center, 117–118

Army Public Health Command, 117

Army Security Assistance Command, 8

Army surgeon general, 117

Army Sustainment Command, 7

Arsenals, 7

Arsenic, 369–370

Arterial gas embolism, 266–267, 323, 328, 335–338

Asbestos

asbestos medical surveillance program, 162, 163

forms of, 380

health effects, 161–162

medical surveillance, 381

routes of exposure, 380

toxicology, 380–381

uses, 380

Asbestosis, 380

Aseptic bone necrosis, 332

Assistant Secretary of Defense for Health Affairs, Office of, 116

Atmosphere-supplying respirators, 223–224

Atmospheric structure, 264

Atomic Energy Commission, 424

Atomic fission, 401

Attack submarines, 355

Audiograms, 134–135

Audiology, 33

Audiometry, 208

Aviation and Missile Life Cycle Management Command, 5

Aviation and Missile Research, Development, and Engineering Center, 3

Aviation medicine, 46–47. See also Aerospace medicine

B

Back injuries, 252–256

Baggage inspection systems radiation, 415

Ballast handling, 390

Ballistic missile submarines, 356

Barotrauma, 265–266, 319–323

Base operational medicine clinic, 19

Basic Program Elements for Federal Employee Occupational Safety and Health Programs, 56

Beaver, Hull Technician Fireman R., 35

Benton, Thomas Hart, 46

Beryllium

acute beryllium disease, 510

biomarkers of exposure, 511–512

carcinogenesis of, 511

dermatologic effects, 511

diagnosis of chronic beryllium disease, 513

environmental exposure, 507–508

exposure prevention and control, 514

genetic predisposition, 513

health effects, 509–512

industrial use, 506

manufactured products that use beryllium, 507

occupational exposure, 508–509

occupational surveillance, 512–513

pathophysiology of chronic beryllium disease, 509–510

regulation and legislation, 509

sensitization, 510

symptoms of chronic beryllium disease, 510–511

treatment of chronic beryllium disease, 513–514

workers with potential occupational exposure to, 507

Bioenvironmental engineering, 14–15

Biological exposure indices, 239

Biological hazards, 178–181

Biological monitoring

airborne hazards, 596–599

big data analysis, 606–607

biomarker discovery and applications, 599–602

biomarkers definition, 594

biomarkers of pulmonary injury, 604

DoD needs for exposure assessment and biomarkers, 596–599

epigenetic biomarkers, 604–606

exhaled breath condensate, 603

exposure memory, 603–604

genetic biomarkers, 604–606

genetics in pulmonary injury research, 605–606

nasal lavage analysis, 603

physiological test matrices, 602–603

protein biomarkers, 604

saliva, 603

serum cytokines, 604

types of biomarkers, 594–596

Biological surveillance initiative, 74, 75

Biomarkers

applications, 599–602

comparison of, 596

definition, 594

discovery of, 599–602

DoD needs for, 596–599

of effect, 595

epigenetic, 604–606

of exposure, 594–595

genetic, 604–606

limitations on use of, 596

protein biomarkers, 603–604

of pulmonary injury, 604

of susceptibility, 595–596

Blane, Sir Gilbert, 43

Blood-borne pathogen exposure control plan, 193–198

Blue Grass Army Depot, 7

BOMC. See Base operational medicine clinic

Borden, Captain William C., 403

Bosnia and Herzegovina

air sampling, 84–85

environmental concerns, 83–84

Operation Joint Guardian, 86

Operations Joint Endeavor, Joint Guard, and Joint Forge, 84–85

pesticide wipe sampling, 86

soil sampling, 86

water sampling, 85–86

Boyle’s law, 315–316

Brachytherapy, 410

Bradley fighting vehicles, 480–481

Breath-hold diving

compression of descent, 339–340

decompression sickness, 340

diving reflex, 338–339

hypercapnia, 340

hypoxia, 340

Brown, Dr. Ernest, 48

Brown, Tarnisha, 33

BSI. See Biological surveillance initiative

Buchan, Dr. William, 42

BUMED. see Bureau of Medicine and Surgery

Buoyancy, 306–307, 317

Bureau of Medicine and Surgery, 24, 30

Burn pits, 98–100

Bush, George W., 87, 143

C

Cadmium, 370–371

Camp Freedom, Kuwait, 72

CAP. See Computer/Electronic Accommodations Program

Capstone Report, 77

Carbon dioxide retention, 297–298

Carbon dioxide toxicity, 325–326

Carbon monoxide exposure

altitude and, 494–495

appliances, 478

Army housing and tents, 492

autopsy findings, 487

cardiovascular effects, 487

central nervous system effects, 485–487

chronic effects, 487

clinical presentation, 485–487

Committee on Toxicology Emergency Exposure Guidance Levels, 493–494

confounders, 494–496

diagnosis of, 487–488

emergency and accidental exposures, 493–495

emergency response planning guidelines, 494–495

environmental exposure standards, 493

exposure incidents, 483–484

health standards and guidelines, 489–496

health status and, 496

heat stress and, 495

high temperature and, 495

historical exposures, 479–480

hydrogen cyanide and, 496

hyperbaric oxygen treatment location, 489

industrial exposures, 478–479

internal combustion engines, 479

medical surveillance, 497

methylene chloride, 479, 496

military occupational exposures, 490–492

military sources of exposure, 479–484

mines, 479

modern era exposures, 480–483

Navy submarine escape action levels, 494

nitric oxide and, 496

nonmilitary sources of exposure, 478–479

ototoxicity, 496

outdoor air pollution, 478

pathophysiology, 484–485

structural fires, 479

symptoms, 485

tobacco smoke, 478, 495–496

toxicity, 326–327

treatment for, 488–489

work-effort constants for predicting carboxyhemoglobin blood content, 490, 503

Carboxyhemoglobin, 490, 503

Cardiovascular disease

carbon monoxide exposure effects, 487

risk assessment for respirator wearers, 229

Cargo inspection systems radiation, 415–416

CEMR. See Civilian employee medical records

Center for Health Promotion and Preventive Medicine, 74, 76, 79, 84, 86–91, 93–95

Center for Unit Records Research, 75, 80

Central Intelligence Agency, 79, 81

Central nervous system

carbon monoxide exposure effects, 485–487

oxygen toxicity in divers, 293, 324–325

Central Technical Support Facility, 5

Certification exams, 34–35, 157–158

Champion, Hospital Corpsman 3rd Class James, 33

Charles’s law, 316

Chelation, 395

Chemical agent monitor, 413

Chemical agent-resistant coatings, 373

Chemical hazards, 175–178

Chemical Materials Activity, 8

Chemical Volatile Organic Compound Unit, 28

Chemical warfare agents, 8, 78–81, 96–98

Chest radiographs, 135

Chiarelli, General Peter, 8

CHPPM. See Center for Health Promotion and Preventive Medicine

Chrome holes, 90, 91

Chromium, 371–372

Chromium exposure, 89–92

Chronic diseases surveillance, 165

CIA. See Central Intelligence Agency

Circadian rhythm disturbance, 273–275

Civilian employee medical records, 62–63

Civilian employees medical care, 47–48

Civilian Personnel Advisory Centers, 128

Civilian Personnel Policy/Defense Civilian Personnel Advisory Services, 128

Claim management process, 144–145

Clean Air Act, 76, 392

Clinton, Bill, 128

Closed-circuit mixed-gas scuba, 296

Closed-circuit oxygen scuba, 294–296

COCOs. See Contractor-owned, contractor-operated plants

Cold stress

accidental hypothermia, 624–627

body protection and insulation, 619

cold injuries, 620–627

estimated survival time in cold water, 624

exposure guidelines, 619–620

external equipment, 620

freezing cold injuries, 620–622

hand protection and insulation, 619

insulation value of clothing, 628

medical surveillance, 627

nonfreezing cold injuries, 622–624

photokeratitis treatment, 620

physiology of, 618–619

prevention, 627–630

temperature measurements, 619

work cycle recommendations during cold environmental conditions, 629

Cold temperature risks, 246, 252

Color vision, 279–281

Commercial driver medical examinations, 159

Commission on Illumination, 463

Committee on Toxicology Emergency Exposure Guidance Levels, 493–494

Communications-Electronics Command, 5

Compensation. See Federal workers’ compensation

Compensation specialist, 140–143

Comprehensive Environmental Response, Compensation, and Liability Act, 391

Computed tomography, 405–406, 410

Computer/Electronic Accommodations Program, 140

Consciousness loss, 268

Constrictive bronchiolitis, 95

Consultative support, 33–34

Consumer Product Safety Improvement Act, 392

Contact lenses, 282

Contaminated diving, 352–354

Continuing education units, 123

Continuing medical education, 123

Contracting Command, 7

Contractor-owned, contractor-operated plants, 3

Corrosion control, 36

Cotinine, 602

Counter fatigue programs, 278–279

CPACs. See Civilian Personnel Advisory Centers

Crane Army Ammunition Activity, 5–6

Crane operators examination, 159

Credentialing, 60–61

Cryogenic fluids, 465

Crystalline silica, 381–382

CS. See Compensation specialist

CURR. See Center for Unit Records Research

Cutbush, Dr. Edward, 44–45

CWAs. See Chemical warfare agents

CWM. See Chemical warfare materiel

Cyanide, 372–373

Cyclosarin, 80

Cytokines, 604

D

Dalton’s law, 317

Data quality, 119

DBNP. See 2,6-Di-tert-butyl-4-nitrophenol

DCPAS. See Defense Civilian Personnel Advisory Service

Decompression procedures

decompression sickness, 266–267, 299, 328–338

dive computers, 301

diving at altitude, 303, 332–333

flying after diving, 303, 332–333

helium-oxygen diving, 302

in-water decompression stops, 300

multilevel diving, 301

nitrogen-oxygen diving, 301–302

no-stop dives, 299–300

omitted decompression, 302–303

repetitive diving, 300, 301

safety of decompression practices, 303

surface decompression, 301

trimix diving, 302

Decompression sickness

altitude exposure after diving, 303, 332–333

arterial gas embolism, 266–267, 328

aseptic bone necrosis, 332

bubble formation, 329

clinical presentation, 330–332

decompression tables, 334

diving at altitude, 303, 332–333

factors affecting individual susceptibility, 333–334

of free diving, 340

inert gas exchange, 329

oxygen treatment for table, 267

patent foramen ovale as risk factor, 334

pathophysiology of, 329–330

prevention of, 299, 334

probability of, 334

in saturation diving, 337–338

symptoms of, 331

treatment of, 266, 335–338

types of, 266

US Navy treatment tables, 335–337

Defense Ammunition Center, 5

Defense Civilian Personnel Advisory Service, 141, 143

Defense Health Agency, 116–117

Defense Health Board, 91

Defense Manpower Data Center, 75, 80–81

Defense Medical Surveillance System, 553

Defense Occupational and Environmental Health Readiness System, 12, 100–101, 240, 553

Defense Occupational and Environmental Health Readiness System-Hearing Conservation, 36, 100–101

Defense Occupational and Environmental Health Readiness System-Industrial Hygiene, 9, 86, 100–102

Defense Safety Oversight Council, 115

Department of Defense

Federal Employees Compensation Act program, 141–143, 146

Hearing Center of Excellence, 210

industrial hygiene exposure assessment model, 237–239

Laser Injury Hotline, 452

military workers’ compensation cost and rates, 143–144

needs for exposure assessment and biomarkers, 596–599

occupational health regulations and guidance, 57–58

policy for handling exposures to depleted uranium, 434–435

program structure and management, 115–117

Protecting Our Workers and Ensuring Reemployment, 143, 146–148

radiation safety program, 429–434

reviews of military compensation programs, 144–146

Serum Repository, 553, 599

Department of Labor

compensation program management efforts, 146–148

Department of the Navy

organization of, 24–26

safety and occupational health programs, 26–37

Department of Transportation

commercial driver medical examination, 159

Depleted uranium, 76–78, 414, 434–436

Deployment assessment, 277–279

Deployment Environmental Surveillance Program, 100, 101, 555

Deployment surveillance

active deployment medical surveillance, 554–555

challenges, 556–557

consequences of the Persian Gulf War, 550–551

data repositories, 552–553

Deployment Environmental Surveillance Program, 555

Disease Reporting System-internet, 554

documenting exposures, 551–552

during the Ebola outbreak, 555–556

medical situational awareness in the theater, 554

modeling, 555

passive deployment medical surveillance, 554

Periodic Occupational and Environmental Monitoring Summary, 552

postdeployment health surveys, 554

Theater Medical Information Program, 554–555

Depots, 7

Dermatitis, 567

DHA. See Defense Health Agency

2,6-Di-tert-butyl-4-nitrophenol, 357–358

Diesel exhaust, 373

Digital radiography, 408

Dignified Burial and Other Veterans’ Benefits Improvement Act, 99

Diisocyanates, 373–374

Dinitrotoluene, 576–577

Disabilities. See Employees with disabilities

Disability retirement examinations, 64

Disabled submarines, 359–361

Disease Reporting System-internet, 554

Disease vector control centers, 27, 28

Disinfectants hazards, 174

Dive computers, 301

Dive medicine, 46–47

Diving. See also Undersea medicine

barotrauma, 319–323

breath-hold diving, 338–340

buoyancy, 306–307, 317

carbon dioxide retention, 297–298

carbon dioxide toxicity, 325–326

carbon monoxide toxicity, 326–327

central nervous system oxygen toxicity in divers, 293, 324–325

contraindications to diving, 308–309

decompression procedures, 299–303

decompression sickness, 299, 328–338

dyspnea, 297–298

gas laws, 315–317

hearing underwater effects, 318–319

helium effects, 327–328

hydrogen effects, 328

hyperbaric oxygen therapy, 309–310

individual susceptibility to impaired consciousness, 299

inert gas effects, 328

interactions between gases and impaired consciousness, 298–299

medical standards for diving, 307–309

nitrogen narcosis, 327, 351

ocular oxygen toxicity, 325

overview, 292

oxygen toxicity, 324–325, 350–351

pathophysiological effects of common diving gases, 323–328

physical principles, 314–317

pulmonary oxygen toxicity, 324

recompression chambers, 309–310

role of respiration in diving injuries, 297–299

saturation diving, 303–306

thermal protection, 306–307

underwater breathing apparatuses, 293–296

vision underwater effects, 317–318

Diving medical officers, 307

Diving reflex, 338–339

DMDC. See Defense Manpower Data Center

DoD. See Department of Defense

DOEHRS. See Defense Occupational and Environmental Health Readiness System

DOEHRS-IH. See Defense Occupational and Environmental Health Readiness System-Industrial Hygiene

DoN. See Department of the Navy

Dosimetry, 422

Drinking water regulations, 392

Drugs, hazardous, 176–177

DSOC. See Defense Safety Oversight Council

DVCCs. See Disease vector control centers

Dysbaric osteonecrosis, 332

Dyspnea, 297–298, 354

E

Ear. See also Hearing conservation programs

anatomy and physiology, 200–202

inner ear barotrauma, 321

Ebola outbreak, 555–556

Edison, Thomas, 419

Ejection injury, 268

Electrical soldering hazards, 390

Electrocardiograms, 135

Electromagnetic radiation, 402

Electronic Data Interchange system, 141

Elemental exposures, 380–383

Emergency contact information, 452

Emergency Exposure Guidance Levels, 493–494

Emergency Fleet Corporation, 48

Emergency treatment, 66

Emotional stress, 183

Employees. See Federal workers’ compensation; Personnel

Employees with disabilities, 129–131, 165

Energy Research and Development Administration, 424

Environment, safety, and occupational health, 12

Environmental exposures, 391

Environmental extremes, 182

Environmental health. See Occupational and environmental health program

Environmental monitoring, 84–86

Environmental Protection Agency, 73, 76, 84–86, 273, 423–424

Environmental regulations, 391–392

Environmental Surveillance Integration Program, 101–102

EPA. See Environmental Protection Agency

Epidemiological investigations, 65

Epigenetic biomarkers, 604–606

Epigenomics, 602

Ergonomics

active surveillance, 246–247

aviation risks, 275

basic ergonomics assessment survey form, 260–261

cold temperature assessment, 252

duration assessment, 251

forceful exertion assessment, 251

health contribution, 249

manual material handling, 252–256

mechanical compression assessment, 251

passive surveillance, 247

personal protective equipment, 249–250

posture assessment, 250

program organization, 244–245

program regulations, 244

recognizing hazards, 246–247

repetition assessment, 251

risk factor management, 247–249

risk factors, 245–246

US Army ergonomics program, 244–245

vibration assessment, 252

wellness contribution, 248–249

worksite task analyses, 250–252

ESIP. See Environmental Surveillance Integration Program

ESOH. See Environment, safety, and occupational health

Exercise stress test, 135

Exhaled breath condensate, 603

Experimental Diving Unit, 47

Explosive ordinance handlers examination, 159–160

Explosives

acute exposure decontamination, 567

administrative controls, 566

aliphatic nitrate esters, 568–572

carcinogenesis, 568

composites, 583–584

dermatitis and, 567

energetic materials, 563–564

engineering controls, 565–566

exposure, 564–566

history of, 562–563

industrial hygiene principles, 565–566

initiating explosives, 583

methemoglobinemia and, 567–568

nitramines, 577–583

nitroaromatics, 572–577

personal protective equipment, 566

preplacement considerations, 566–567

safety practices, 565

vasodilation and, 568

Explosives vehicle operators examination, 159–160

Exposome, 596

Exposure assessment model, 237–239

Eye tests, 134

F

FAA. See Federal Aviation Administration

Facilities maintenance, 182–183

Fatigue risks, 273–275, 278–279

FDPMUs. See Forward deployable preventive medicine units

FECA. See Federal Employees Compensation Act

FEDCUs. See Fleet epidemic disease control units

Federal Aviation Administration, 133

Federal Employees Compensation Act, 48, 57, 140–143, 146

Federal Motor Carrier Safety Agency, 128, 133

Federal Radiation Council, 423

Federal workers. See Personnel

Federal workers’ compensation

Computer/Electronic Accommodations Program, 140

Department of Labor program management efforts, 146–148

DoD FECA program, 141–143

FECA management challenges, 146

Federal Employees Compensation Act program, 140–141

military workers’ compensation cost and rates, 143–144

Office of Workers’ Compensation Programs, 140–141

reviews of military compensation programs, 144–146

Felloney, Landing Signal Officer Brian, 33

Firefighters examination, 160

Firefighting operations, 93–96

Firing ranges hazards, 389–390

Fit test records, 233

Fitness-for-duty examinations, 64, 278, 284–285

Fitness standards, 128–131

Fleet epidemic disease control units, 26

Flight and operational medicine, 16

Flight medicine, 46–47, 284–286

FMCSA. See Federal Motor Carrier Safety Agency

FOM. See Flight and operational medicine

Food and Drug Administration, 392

Food contamination, 392

Forceful exertion risks, 246, 251

Forklift operators examination, 160

Formaldehyde, 177

Fort Campbell, Kentucky, 484

Fort Hood, Texas, 483–484

Fort Irwin National Training Center, California, 484

Forward deployable preventive medicine units, 28

Free diving, 338–340

Free electron laser, 462

Fukushima, Japan, 429

Full-face respirators, 221, 223

Functional health status, 119

G

G-induced loss of consciousness, 269–270

GAO. See Government Accountability Office

Gas laws, 315–317

Gas removing respirators, 222

Genetic biomarkers, 604–606

Genetic Information Nondiscrimination Act, 130–131

Genomics, 600

Gilmer, Thomas, 45, 46

GINA. See Genetic Information Nondiscrimination Act

Glutaraldehyde, 177

GOCOs. See Government-owned, contractor-operated plants

GOGOs. See Government-owned, government-operated plants

Goiânia, Brazil, 411–412

Gordon, Dr. Maurice Bear, 42

Government Accountability Office, 102, 144, 146

Government-owned, contractor-operated plants, 3

Government-owned, government-operated plants, 3

Green, Dr. Ezra, 42

Ground System Enterprise, 4

Guided missile submarines, 356

Gulf War illness, 72–73, 83

Gun propellants, 585

GWI. See Gulf War illness

H

Half-face respirators, 221

Hawthorne Army Depot, 7

Hazardous substances. See also specific substances

arsenic, 369–370

asbestos, 380–381

cadmium, 370–371

chromium, 371–372

crystalline silica, 381–382

cyanide, 372–373

diesel exhaust, 373

diisocyanates, 373–374

elemental exposures, 380–383

inorganic exposures, 380–383

lead, 388–395

metals, 369–372

methyl ethyl ketone, 375–376

methylene chloride, 374–375

mustard agents, 376–377

occupational exposure limits, 238–239, 368

organic exposures, 372–380

organophosphate nerve agents, 377–378

pentachlorophenol, 378–379

trichloroethylene, 379–380

tritium, 382–383

white phosphorus, 383

Hazards. See Health hazards

HCV exposure, 195

Health Advisory Program, 85

Health Affairs, Assistant Secretary of Defense for, 116

Health hazard education, 64

Health Hazard Information Management, 100

Health hazards

abatement strategies, 183–185

anesthetic gases, 175–176

antineoplastic agents, 176–177

biological hazards, 178–181

blood-borne pathogen exposure control plan, 193–198

chemical hazards, 175–178

emotional stress, 183

environmental extremes, 182

facilities maintenance, 182–183

formaldehyde, 177

glutaraldehyde, 177

hazardous drugs, 176–177

hepatitis B, 178–179

hepatitis C, 178–179

human immunodeficiency virus, 179

latex, 180–181

medical maintenance, 182–183

mercury, 178

methicillin-resistant Staphylococcus aureus, 181

methyl methacrylate, 178

in military healthcare facilities, 172, 173

musculoskeletal strain, 182

noise hazards, 181–182

overview, 172–174

personnel and population screening, 174–175

physical hazards, 181–183

psychosocial hazards, 183

radiation hazards, 181

of selected solvents, reagents, and disinfectants, 174

shift work, 183

tuberculosis, 179–180

types of, 175–183

workplace violence, 185

Health Insurance Portability and Accountability Act, 62, 130–131, 158

Health Program business plan, 58

Health promotion, 65–66

Health risk assessment, 74, 75

Health Services Command, 56

Health status measurement, 119

Healthcare workers health hazards. See Health hazards

Hearing, underwater effects, 318–319

Hearing Center of Excellence, 210

Hearing conservation programs

Army program, 200–213

DoD Hearing Center of Excellence, 210

engineering controls, 208

expanded program components, 211

garrison-based hearing conservation programs, 207

health education, 208–209

hearing anatomy and physiology, 200–202

hearing conservation on the battlefield, 211–213

hearing protection, 208

improving hearing loss prevention efforts, 209–211

incidence of hearing loss in the Army, 205–206

medical surveillance, 165–166

mission-critical hearing studies, 210–211

monitoring audiometry, 208

Navy program, 35–36

noise hazard evaluation, 207–208

noise-induced hearing loss, 202–204

preventing noise-induced hearing loss, 207–209

program evaluation, 209

sound identification, 212–213

sound localization, 212

tinnitus, 205

Hearing Evaluation Automated Registry System, 100

Hearing loss, 35

Hearing protection devices, 208

Heat stress, 268

Helium-oxygen diving, 302, 327–328

Henry’s law, 317

Hepatitis B, 178–179, 196

Hepatitis C, 178–179

Hexahydro-1,3,5-trinitro-1,3,5-triazine, 577–579

High frequency exposures, 203

High power illuminator radar, 458

High pressure nervous syndrome, 305–306

HIPAA. See Health Insurance Portability and Accountability Act

HIV. See Human immunodeficiency virus

Holston Army Ammunition Activity, 6

Horner, Dr. G.R.B., 45

Hot-particle trauma, 426

HRA. See Health risk assessment

HRM. See Human resource management

Human Capital Distribution Plan, 120

Human immunodeficiency virus, 179, 195

Human resource management, 128

Hybrid Single-Particle Lagrangian Integrated Trajectories, 76

Hydrogen cyanide, 496

Hydrogen diving, 328

Hyperbaric arthralgia, 305

Hyperbaric oxygen therapy, 309–310, 489

Hypercapnia, 340, 354

Hyperthermia, 307, 352

Hypothermia, 306–307, 351–352, 624–627

Hypothermic injury, 268

Hypoxia, 340, 354

Hypoxia, altitude-induced, 264–265

I

Imaging radiation, 414–416

Immunizations, 65

Immunomics, 602

Improvised explosive devices, 202

IMX, 580–583

In-water decompression stops, 300

Industrial hygiene, 28, 31–32, 61, 75

Industrial hygiene program management

Army-specific requirements, 239–240

Defense Occupational and Environmental Health Readiness System, 240

DoD exposure assessment model, 237–239

metrics, 240

organization of program, 236–237

overview, 236

practicing Army industrial hygiene, 237–240

Inert gas diving, 328, 329

Informatics, 100–103

Initiating explosives, 583

Injury statistics, 143

Inner ear barotrauma, 321

Inorganic exposures, 380–383

Insensitive munitions, 580–583

Installation occupational health regulations, 57

Institute of Medicine, 78, 99–100

Ionizing radiation

Army personnel exposure standards, 425

biological effects of radiation, 417–421

categories of effects, 420

combined internal and external exposures, 426

controlling contamination in the medical treatment facility, 428–429

depleted uranium, 414

development of dosimetry, 422

development of standards, 422–423

developments in atomic fission, 401

discovery and applications of X-rays, 402–408

discovery and uses of radioisotopes, 408–413

DoD radiation safety program, 429–434

electromagnetic radiation, 402

external irradiation, 426

the Fukushima incident, 429

high-dose exposures, 427–428

hot-particle trauma, 426

imaging techniques, 414–416

intermediate-dose exposures, 427

internal deposition, 425–426

low-dose exposures, 427

mass casualties, 426–427

mechanisms of effects, 420

medical examination, 162–164

medical response to depleted uranium exposure, 434–436

medical response to incidents, 425–429

in military operations, 413–417

non-occupational dose limits, 424–425

nuclear reactors, 413–414

occupational dose limits, 424

occupational radiation risks, 420–421

particulate radiation, 400, 402

personnel security screening systems, 416

physical security systems, 414

procedures for whole-body exposures, 427–428

properties of, 400–402

protecting the medical team, 428

protection against radiation, 421–425

radiation dispersal devices, 416

radiation produced by nuclear weapons, 414

radiological base camp assessments, 416–417

recognition of effects, 417–420

regulatory agencies, 423–424

types of exposures, 425–427

Iowa Army Ammunition Activity, 6

Iraq, Operation Iraqi Freedom, 86–100

Isocyanates, 373–374

J

Jet propellants JP-5 and JP-8, 82

JMC. See Joint Munitions Command

Joint Munitions Command, 5–7

Jones, Captain John Paul, 42

Jones, Dr. John, 42

Jones, Dr. Robert, 48

K

Kellogg Brown and Root, 89

Kennon, Captain Beverly, 45, 46

Kerst, Donald, 407

Khamisiyah Ammunition Supply Point, 78–81

Kleghorn, Dr. James, 45

Kosovo

air sampling, 84–85

environmental concerns, 83–84

Operation Joint Guardian, 86

Operations Joint Endeavor, Joint Guard, and Joint Forge, 84–85

pesticide wipe sampling, 86

soil sampling, 86

water sampling, 85–86

Kuwait

Ash Shuaiba Port, 92–93

oil well fires, 72–76

L

Laboratory tests, 134

Lake City Army Ammunition Activity, 6

Laser eye protection, 281

Laser Injury Hotline, 452

Lasers

direct biological effects, 462–464

exposure incidents, 469–471

indirect biological effects, 464–466

laser-generated air contaminants, 465

military applications, 467–469

overview, 460–461

properties of, 461–462

protection standards, 466–467

safety program, 471–473

LASIK, 282–283

Latex, 180–181

Lead

air exposures, 391

ambient air regulations, 392

from ballast handling, 390

blood lead level, 393

bone lead measurement, 393

cardiovascular effects, 395

chelation, 395

clinical implications of lead exposure, 394–395

cumulative blood lead index, 393

drinking water regulations, 392

effects in adults, 394–395

effects in children, 394

from electrical soldering, 390

endocrine effects, 394

environmental exposures, 391

environmental regulations, 391–392

exposure tests, 393

from firing ranges, 389–390

food contamination, 392

gastrointestinal effects, 395

hematological effects, 394

history of lead toxicity, 388

military occupational exposures, 389–390

neurological effects, 394

occupational surveillance, 392

in paint, 392

from paint stripping, 389

pregnancy effects, 394

renal effects, 394

soil exposures, 391

water exposures, 391

from welding, 389

zinc protoporphyrin test, 393

Lead azide, 583

Lead styphnate, 583

Letterkenny Munitions Center, 6

Life Cycle Management Command, 4–5

Lightfoot, Hull Maintenance Technician 2nd Class A., 35

Lind, Dr. James, 43

Linear accelerator, 407

Liquid propellants, 584–585

Livingston, Stanley, 409

Log of Federal Occupational Injuries and Illnesses, 59

Logistics and Readiness Center, 5

Logistics Support Activity, 8

Longshore and Harbor Workers’ Compensation Act of 1927, 48

Lukavac Base, 84

M

Maiello, Commander Richard, 28

Mail inspection systems radiation, 415

MAJCOM. See Major command

Major command roles, 13

Malaria and Epidemic Control Organization, 26

Management information system, 12, 13

Manpower Review Program, 120

Manual material handling

administrative control, 253–254

engineering control, 253

frequency factors, 256

individual risk factors, 254–255

lifting, 252–254

objects distribution, 255–256

weight distribution, 255–256

Marine Corps

Marine Corps War Memorial, 26

Navy and Marine Corps Public Health Center, 24, 26, 30, 34, 49–50

Marine Corps safety and occupational health program

components of, 34–37

organization of, 30, 31

Public Health Center technical manuals, 34

resources, 34–37

staffing, 30

Marine life risks, 354–355

Marshall, General George E., 274

Mass casualties, 426–427, 544

Materiel Systems Analysis Activity, 8

Maximum contaminant levels, 85

McAlester Army Ammunition Activity, 6

McCann rescue chamber, 47

MCLs. See Maximum contaminant levels

M1E1 tanks, 480

Mechanical compression, 246, 251

MEDCOM. See Medical Command

MEDEVAC, 285

Mediastinal emphysema, 322

Medical Command, 117, 120–121

Medical Department of the Army Coat of Arms, iii

Medical directives, 58

Medical evaluation records, 232–233

Medical Information Module, 100

Medical intelligence, 535

Medical maintenance, 182–183

Medical Matrix, 50

Medical Matrix Committee, 50

Medical Matrix Validation Committee, 34–35, 50

Medical records management, 62–63

Medical standards of fitness, 128–131, 307–309

Medical surveillance

Army program, 63

asbestos, 161–162, 163

assessing need for programs, 154–155

certification examinations, 157–158

crane operators, 159

Department of Transportation commercial driver medical examination, 159

documenting physical exam and managing results, 158–159

employees with chronic diseases, 165

employees with physical disabilities, 165

examinations, 132–133

explosive ordinance handler, 159–160

explosives vehicle operator, 159–160

firefighter, 160

forklift operator, 160

hearing conservation, 165–166

Navy program, 34–35

police, 160–161

program design, 155–157

radiation, 162–164

reproductive hazards, 164–165

security guards, 160–161

specific occupations, 159–161

Medical Surveillance Procedures Manual, 50

Medical treatment facilities, 24–25

Mercury, 178

MESL. See Military Exposure Surveillance Library

Metabolomics, 601

Metallomics, 602

Metals toxicology, 369–372

Methemoglobinemia, 567–568

Methicillin-resistant Staphylococcus aureus, 181

Methyl ethyl ketone, 375–376

Methyl methacrylate, 178

Methylene chloride, 374–375, 496

MicroRNA, 602

Microwave radar, 448, 456–457

Middle ear barotrauma, 319–321

Milan Army Ammunition Activity, 6

Military aviation administration

air evacuation, 285–286

aviation fitness evaluation, 284–285

determining flight status, 285

determining work relatedness, 285

facility and equipment design, 283

flight medicine, 284–286

health hazard evaluations, 284

inspections, 284

management commitment, 283

mishap investigation, 284

safety and health, 283–284

training and education, 283–284

Military diving operations. See Diving

Military Exposure Guidelines, 86

Military Exposure Surveillance Library, 86, 101–102

Military Surface Deployment and Distribution Command, 7–8

MIS. See Management information system

Mishap investigation, 284

Mishraq State Sulfur Mine, 93–96

Modified duty programs, 278

Motion sickness, 271–272

Mouth bit respirators, 221

MRSA. See Methicillin-resistant Staphylococcus aureus

MTFs. See Medical treatment facilities

Multilevel diving, 301

Musculoskeletal strain, 182

Mustard agents, 376–377

N

NAS-CT. See National Academy of Science’s Committee on Toxicology

Nasal lavage analysis, 603

National Academy of Science’s Committee on Toxicology, 77

National Ambient Air Quality Standards, 76, 84

National Defense Authorization Act for Fiscal Years 1992 and 1993, 73

National Fire Protection Association, 160

National Institute for Occupational Safety and Health, 368, 493

National Research Council, 390, 493

National Safety Council, 115

National Toxicology Program, 389–390

Natural uranium, 76

Naval Armament Act of 1797, 43

Naval Diving and Salvage Training Center, 292

Naval Health Research Center, 50

Naval Medical Center, 24–25, 28

Naval Ordnance Systems Command Environmental Health Center, 49

Naval Safety Center, 29

Navy and Marine Corps Public Health Center, 24, 26, 30, 34, 49–50

Navy Bureau of Medicine and Surgery, 24

Navy Entomology Center of Excellence, 28

Navy Environmental and Preventative Medicine Units, 28

Navy Environmental Health Center, 28

Navy Industrial Environmental Health Center, 49–50

Navy Medical Department organization, 27

Navy Medical Service Corps, 28

Navy Medicine

the colonial Navy, 42–43

establishment of flight and dive medicine, 46–47

evolution of occupational medicine practice, 42–50

the new Navy, 43–46

occupational and environmental health programs, 24–37, 50

organization of, 24–26

preventive medicine, 26–28

role of, 30

Navy Occupational Health Information Management System, 50

Navy safety and occupational health program

audiology, 33

certification exams, 34–35

components of, 34–37

consultative support and oversight, 33–34

current strategic-level responsibilities, 29

history of, 26–28

industrial hygiene, 31–32

laws, regulations, and guidance, 30

Medical Matrix Validation Committee, 34–35

medical surveillance, 34–35

occupational and environmental medicine, 32–33, 50

organization of, 30–34

process improvement, 37

program self-assessment, 37

Public Health Center technical manuals, 34

resources, 34–37

safety officers, 30–31

staffing, 30–34

worksite visits, 36

NECE. See Navy Entomology Center of Excellence

Negative pressure respirators, 230–231

NEHC. See Navy Environmental Health Center

NEPMUs. See Navy Environmental and Preventative Medicine Units

New accession exams, 277–278

NIEHC. See Navy Industrial Environmental Health Center

Night vision goggles, 281–282

Nightingale, Florence, 172

NIHL. See Noise-induced hearing loss

9/11 terrorism attacks, 87–88

NIOSH. See National Institute for Occupational Safety and Health

Nitramines

hexahydro-1,3,5-trinitro-1,3,5-triazine, 577–579

insensitive munitions, 580–583

nitroguanidine, 579–580

octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine, 579

Nitric oxide, 496

Nitroaromatics

dinitrotoluene, 576–577

trinitrotoluene, 572–576

Nitrocellulose, 572

Nitrogen narcosis, 327, 351

Nitrogen-oxygen diving, 301–302

Nitroglycerin

freezing point of, 568

health effects, 569–570

manufacture and exposure hazards, 569

medical surveillance, 570–571

primary prevention, 571–572

Nitroguanidine, 579–580

NITROX, 301–302

NMC. See Naval Medical Center

NMCPHC. See Navy and Marine Corps Public Health Center

No-stop dives, 299–300

NOHIMS. See Navy Occupational Health Information Management System

Noise Control Act of 1972, 273

Noise hazards, 181–182

Noise-induced hearing loss

aviation hazards, 272–273

high frequency exposures, 203

mechanisms of, 202–203

ototoxins, 203–204

preventing, 207–209, 273

susceptibility to, 203

ultrasonic exposures, 203

Non-coding RNAs, 604–605

Nonionizing radiation

absorption, 447

characteristics of electromagnetic radiation, 443–447

coherence, 445

diffraction, 447

divergence, 444–445

electromagnetic spectrum, 442

emergency contact information, 452

interaction with matter, 445–447

interference, 445

lasers, 460–473

optical radiation, 460–473

overview, 442–443

physical properties, 444–445

polarization, 445

radio frequency radiation, 447–460

reflection, refraction, and scatter, 445–446

transmission, 446–447

Nonneutral postures, 245, 250

Nuclear medicine, 49

Nuclear reactors, 413–414

Nuclear Regulatory Commission, 423–424

Nuclear weapons radiation, 414

Nurses, occupational health, 61

O

Obama, Barack, 143

Occupational and Environmental Health Data Portal, 101–102

Occupational and environmental health programs. See also Army Occupational Health Programs

Air Force, 12–19

Navy, 24–37, 50

Occupational and Environmental Health Site Assessment, 102–103

Occupational and environmental medicine, 32–33

Occupational exposure limits, 238–239, 368

Occupational hazards. See Health hazards

Occupational health business plan, 58

Occupational health clinicians, 142–143

Occupational Health Management Information System, 101

Occupational Health Program Evaluation Guide, 37

Occupational Medicine Program Assessment, 37

Occupational Safety and Health Act of 1970, 30, 50, 101

Occupational Safety and Health Administration

ionizing radiation regulation, 423–424

lead standard, 389–390

occupational exposure limits, 368

Occupational Safety and Health Administration Act, 12, 56–57

required medical surveillance examinations, 132–133

respiratory protection, 220–233

standards, 30

Occupational Safety and Health Administration Act, 12, 56–57

Octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine, 579

Ocular oxygen toxicity, 325

OEH. See Occupational and environmental health programs

OEHSA. See Occupational and Environmental Health Site Assessment

Office of Personnel Management

general schedule occupations with medical or physical requirements, 130

role of, 128

Office of the Special Assistant for Gulf War Illnesses, 77, 79–81

Office of the Surgeon, 2

Office of Workers’ Compensation Programs, 140–141, 146

OHP. See Occupational Health Program

OHPEG. See Occupational Health Program Evaluation Guide

Oil well fires, 72–76

Olsbrucken, Germany, 484

“OMICS” technologies, 600

Omitted decompression, 302–303

OMPA. See Occupational Medicine Program Assessment

Open-circuit, self-contained underwater breathing apparatus, 293

Operation Enduring Freedom, 86–100

Operation Iraqi Freedom, 86–100

Operation Joint Guardian, 86

Operation New Dawn, 87

Operation Vigilant Warrior, 92–93

Operations Joint Endeavor/Joint Guard/Joint Forge, 84–85

OPM. See Office of Personnel Management

Optical radiation

direct biological effects, 462–464

exposure incidents, 469–471

indirect biological effects, 464–466

overview, 460–461

properties of, 461–462

Organ of Corti, 202–203

Organic exposures, 372–380

Organophosphate nerve agents, 377–378

OSAGWI. See Office of the Special Assistant for Gulf War Illnesses

OSHA. See Occupational Safety and Health Administration

OSHA 300 Log of Federal Occupational Injuries and Illnesses, 59

Ototoxicity, 496

Ototoxins, 203–204

OWCP. See Office of Workers’ Compensation Programs

Oxygen toxicity, 293, 324–325, 350–351

P

Paint

lead from paint stripping, 389

lead in, 392

Particulate matter, 84–85, 94

Particulate radiation, 400, 402

Particulate respirators, 222

Pascal’s law, 317

Patent foramen ovale, 334

Pathogens, blood-borne, 193–198

“Peacemaker,” 45–46

Pentachlorophenol, 378–379

Pentagon terrorism attacks, 86–88

Performance measurement systems, 119

Periodic evaluations, 131–135

Periodic Occupational and Environmental Monitoring Summary, 102–103, 552

Permissible exposure levels, 156, 239

Perry, Commodore Matthew, 45

Persian Gulf War

chemical weapons use, 78–81

depleted uranium exposure, 76–78

deployment surveillance consequences, 550–551

Gulf War illness, 72–73, 83

jet propellants JP-5 and JP-8, 82

Khamisiyah storage facility, 78–81

Kuwaiti oil well fires, 72–76

Personal protective equipment, 155, 237–238, 248–250, 279, 566

Personnel. See also Federal workers’ compensation

Army staffing assessment model for civilian occupational health providers, 121–122

documentation requirements, 135

employees with disabilities, 129–131

Human Capital Distribution Plan, 120

making the case for more personnel, 122

managing authorizations and requirements, 120–121

medical standards of fitness, 128–131

medical tests and procedures, 134–135

OSHA-mandated medical surveillance examinations, 132–133

periodic evaluations, 131–135

physical requirements, 129

physician professional development, 122–123

policy enforcement examinations, 135–136

preplacement evaluations, 131–135

provider-patient relationship, 128–129

recruitment and retention, 122

role of providers, 121

role of surgeon general’s consultant, 120–121

special surveillance programs and examinations, 133

surveillance examination content, 133–134

termination medical examinations, 137

training and competencies, 122

Personnel and Readiness, Under Secretary of Defense for, 115–116

Personnel Proponency Directorate, 121

Personnel security screening systems, 416

Pesticide wipe sampling, 86

Phased array antenna systems, 457

Phillips, Dr. Ralph, 406

Photokeratitis, 620

Photorefractive keratectomy, 282–283

Physical examinations

documenting, 158–159

managing results, 158–159

pre-employment, 43

Physical hazards, 181–183

Pine Bluff Arsenal, 7

Pleural plaques, 380

PMUs. See Preventive medicine units

Pneumothorax, 322–323

POEMS. See Periodic Occupational and Environmental Monitoring Summary

Police examination, 160–161

Policy enforcement examinations, 135–136

Position risks, 245–246

Positive pressure respirators, 230–231

Postdeployment health surveys, 554

Postexposure prophylaxis, hepatitis B, 196

Posture risks, 245, 250

POWER. See Protecting Our Workers and Ensuring Reemployment

Powered air-purifying respirators, 221–222

Pre-employment physicals, 43

Preplacement evaluations, 131–135

Pressure equivalents, 316

Pressure illness, 265–268

Preventative health assessment, 277

Preventive medicine, 26–28

Primary prevention, 154

Privileging, 60–61

Process improvement, 37

Program assessment tools, 119–120

Program Objective Memorandum, 9

Program self-assessment, 37

Propellants

acute exposure decontamination, 567

administrative controls, 566

aliphatic nitrate esters, 568–572

carcinogenesis, 568

composites, 583–584

dermatitis and, 567

energetic materials, 564

exposure, 564–566

history of, 562–563

industrial hygiene principles, 565–566

initiating explosives, 583

liquid, 584–585

methemoglobinemia and, 567–568

nitramines, 577–583

nitroaromatics, 572–577

personal protective equipment, 566

preplacement considerations, 566–567

safety practices, 565

vasodilation and, 568

Protecting Our Workers and Ensuring Reemployment, 143, 146–148

Protein biomarkers, 604

Proteomics, 601

Provider-patient relationships, 128–129

Psychosocial hazards, 183

Public health

Air Force, 15–16

Navy and Marine Corps Public Health Center, 24, 26, 30, 34, 49–50

Public Health Center technical manuals, 34

Public Law 79-658, 56

Puget Sound Naval Shipyard and Intermediate Maintenance Facility, 36

Pulmonary barotrauma, 321–322

Pulmonary function tests, 90–91, 94–95, 135, 156, 229

Pulmonary oxygen toxicity, 324

Pyrotechnics, 564

Q

Qarmat Ali Water Treatment Plant, 89–92

Quality improvement, 119–120

Quality measures, 118–120

Quality of life measurement, 119

Quality of work environment, 8–9

Quiet Communities Act of 1978, 273

QWE. See Quality of work environment

R

Radar technology, 447–448

Radford Army Ammunition Activity, 7

Radiation. See also Ionizing radiation; Nonionizing radiation

classification of, 162–163

regulations, 163

Radiation Control for Health and Safety Act, 423

Radiation dispersal devices, 416

Radiation hazards, 181

Radiation safety program

administrative controls, 431–432

designation of restricted areas, 432

elements of, 431–434

engineering controls, 432

goals of, 429–430

medical surveillance, 433

personnel monitoring, 433–434

radiation safety committee, 430

radiation safety officer, 430–431

recordkeeping, 434

respiratory protection, 434

responsibilities, 430–431

standard operating procedures, 431

training, 431–432

Radio communication, 447–448

Radio communications systems, 455

Radio frequency radiation

absorption, 450

administrative procedures, 460

conduction, 449

controls, 460

coupling, 449–450

direct biological effect, 450–451

emergency contact information, 452

emission of, 454–455

exposure incidents, 457–459

exposure limits, 452

indirect biological effects, 451

inventory of radio frequency-producing sources, 460

low-level effects, 451

microwave radar, 448

military applications, 455–458

physical properties that determine energy transfer, 449–450

radar during World War II, 448–449

radar technology, 447–448

radiation control, 453

radiation protection, 451–453

radio communication, 447–448

safety program, 459–460

training programs, 460

Radioisotopes

accident at Goiânia, Brazil, 411–412

brachytherapy, 410

diagnostic uses, 409–410

industrial uses, 411–413

medical uses, 408–411

nondestructive inspection, 411

radioactive commodities, 411–413

radiopharmaceutical therapy, 410

teletherapy, 410–411

therapeutic uses, 410

Radiological base camp assessments, 416–417

Radiopharmaceutical therapy, 410

RDECOM. See Research, Development and Engineering Command

Readiness assessment, 277–279

Reagents hazards, 174

Recompression chambers, 309–310

Recording and Reporting Occupational Injuries and Illnesses, 57

Recruit screening, 45

Red River Army Depot, 4

Redstone Arsenal, 7, 8

Refractive surgery, 282–283

Rehabilitation Act of 1973, 129

Repetition risks, 245–246, 251

Repetitive diving, 300, 301

Reproductive hazards, 164–165

Research, Development and Engineering Command, 3–4

Resource Conservation Recovery Act, 391

Respiration, diving injuries and, 297–299

Respiratory protection

air-purifying respirators, 220–222

atmosphere-supplying respirators, 223–224

breathing air for supplied-air respirators, 232

cardiovascular risk assessment and evaluation procedures, 229

cleaning and storage, 231

color coding, 231

disqualifying conditions for respirator use, 227

filtration mechanisms and classification, 222–223

fit test records, 233

function checks, 231

inspection, 231

maintenance, 231–232

medical considerations and evaluation, 226–229

medical evaluation records, 232–233

physiological effects of respirator wear, 226

physiological problems, 226–228

program evaluation, 232

psychological problems, 226–228

pulmonary function testing, 229

purpose of medical evaluation, 228

record keeping, 232–233

respirator classification, 220–224

respirator selection guidelines, 225–226

respirator service life, 224

respirator tests and checks, 230–231

respiratory protection programs, 224–225

training, 232

training records, 233

Risk adjustment, 119

Risk categorization, 15

Risk management process, 12, 14

Rock Island Arsenal, 5, 7

Rock Island Arsenal Joint Manufacturing and Technology Center, 4

Rocket propellants, 584

Roentgen-ray tubes, 403

S

Safe Drinking Water Act, 85, 391

Safety, Health, and Return to Employment, 143

Safety and occupational health programs

Air Force, 12–19

Marine Corps, 30, 31

Navy, 24–37

Safety officers, 30–31

Saliva analysis, 603

Sarin, 80

Saturation diving

atmospheric control, 304–305

decompression, 306

decompression sickness, 337–338

fire risk, 305

high pressure nervous syndrome, 305–306

hyperbaric arthralgia, 305

infection risk, 305

overview, 303–304

temperature control, 306

Scott Air Force Base, 7

Scranton Army Ammunition Activity, 7

Scuba diving. See Diving

Scurvy prevention, 43

Sea port of debarkation/embarkation, 92–93

SEAL delivery vehicles, 292

Seaman’s Sickness and Disability Act of 1798, 45

Secondary prevention, 154

Secret Internet Protocol Router Network, 102

Secretary of Defense, Office of, 115–116

Security Assistance Command, 8

Security guards examination, 160–161

Self-contained breathing apparatus, 223–224

Self-propelled howitzers, 481–483

Semmelweis, Dr. Philipp Ignaz, 172

Serum cotinine, 602

Serum cytokines, 604

Serum IgE, 602

Serum Repository, 553, 599

SHARE. See Safety, Health, and Return to Employment

Shift work hazards, 183

Shipboard medicine

amphibious operations, 530–531

blood bank, 544

classes of ships, 524

competence for duty examinations, 543

corpses, 544

crew preparation and screening, 535–536

disposal of medical waste, 544–545

disposition of the sick sailor, 541

elective surgery, 543

environment in shipyards, underway, and at port calls, 536–540

epidemiology and epidemics, 538–539

flight operations, 539–540

heat issues, 537

hypoxic spaces, 539

isolation and confinement, 537–538

life aboard, 523, 525–526

mass casualties, 544

medical care of women, 542–543

medical departments, 524, 531–534

medical evacuation, 541–542

medical intelligence, 535

mortality associated with drinking seawater, 531

noise issues, 537

operational medicine during wartime, 527–531

organization aboard ship, 522

pests and vectors, 539

planning for medical evacuation, 535

port calls, 542

predeployment planning, 534–536

requirements for specific medical equipment, 529

ships and missions, 522–523

the ship’s cycle, 526–527

sick call, 540–541

sinking, immersion, and survival, 529–530

telemedicine, 541

Sick call, 540–541

Sierra River Army Depot, 4–5

Silicosis, 381–382

Similar exposure groups, 238

Sinus barotrauma, 321

SIPRNet, 102

Sleep deprivation risks, 273–275

SMART-PM. See Special Medical Augmentation and Response Team-Preventive Medicine

Smith, Lieutenant Linwood, 48

Snow blindness, 620

Software Engineering Center, 5

SOH. See Safety and occupational health programs

Soil sampling, 86

Solvents hazards, 174

Sound navigation, 355

Spatial disorientation, 270–271

Special Medical Augmentation and Response Team-Preventive Medicine, 87, 89–91

SPOD/E. See Sea port of debarkation/embarkation

SRDRS. See Submarine rescue diving and recompression system

St. Medard, Dr. Peter, 44

Standard operating procedures, 58

Standards of fitness, 128–131

Staphylococcus aureus, methicillin-resistant, 181

Status report, 57–58

Steam-powered ships, 45–46

Stephenson, Rear Admiral Charles, 49

Stockton, Captain Robert F., 46

Stoddert, Benjamin, 44

Stress, emotional, 183

Submarine rescue diving and recompression system, 360–361

Submarines

2,6-di-tert-butyl-4-nitrophenol, 357–358

atmosphere management and control, 358–359

attack submarines, 355

ballistic missile submarines, 356

carbon monoxide exposure, 494

central atmosphere monitoring system, 357

disabled submarines, 359–361

environment, 357

escape and rescue, 360–361, 494

guided missile submarines, 356

oxygen depletion, 359–360

sleep, 361–362

toxic gases, 359–360

types and classes, 355–356

working schedule, 361–362

Sulfur mine fire, 93–96

Supplied-air respirators, 232

Surface decompression, 301

Surface-supplied diving, 293–294

Surveillance programs. See Medical surveillance

Sustained acceleration, 269–270

Sustainment Command, 7

T

Tank-Automotive and Armaments Command Life Cycle Management Command, 4–5

Team Aerospace

bioenvironmental engineering, 14–15

flight and operational medicine, 16

public health, 15–16

TEH. See Total Exposure Health

Telemedicine, 541

Teletherapy, 410–411

Termination medical examinations, 137

Terrorism attacks, 9/11, 87–88

Tertiary prevention, 154

The Gulf War Oil Spill, 73

The Logistics Support Activity, 8

Theater Medical Information Program, 554–555

Thermal stress, 268

Three-dimensional motion, 268–272

Threshold limit values, 156, 239

Tinnitus, 35, 205

Tobacco smoke, 478, 495–496

Tobyhanna Army Depot, 5

Tooele Army Depot, 7

Total Exposure Health, 19

TRANSCOM. See US Transportation Command

Transcriptomics, 600–601

Transient acceleration, 269

Transmission imaging, 414–415

Travel health hazards, 275

Treadway, Lieutenant Commander Paul, 32

Tri-service industrial base, 3–9

TRICARE Management Agency, 116

Trichloroethylene, 379–380

Trimix diving, 302

Trinitrotoluene, 572–576

Troop Movement Database, 75, 80

Tuberculosis, 179–180, 382

Tuzla Air Base, 84

Tyler, John, 45

U

UHF radio communications systems, 455

Ultrasonic exposures, 203

Under Secretary of Defense for Personnel and Readiness, 115–116

Undersea medicine

contaminated diving, 352–354

dyspnea, 297–298, 354

hypercapnia, 340, 354

hyperthermia, 307, 352

hypothermia, 306–307, 351–352

hypoxia, 340, 354

illness or injury resulting from diving, 349–350

marine life risks, 354–355

nitrogen narcosis, 327, 351

oxygen toxicity, 293, 324–325, 350–351

physical properties, 350

pressure, 350

problems with underwater breathing equipment, 354

protective gear, 352–354

sound, 351

sound navigation and ranging, 355

submarines, 355–362

temperature, 351–352

undersea operations, 348–349

underwater hazards, 354–355

visibility, 351

water quality, 352–354

Underwater breathing apparatuses, 293–296

United Nations Special Commission, 80

Universal gas equation, 316

Upshur, Abel, 45, 46

Uranium, depleted, 76–78

US Air Force occupational and environmental health program

critical elements of, 17

emerging developments in Air Force Occupational Medicine, 19

employee role and responsibilities, 16

execution of, 17–18

exposure assessment model, 17–18

headquarters level role and responsibilities, 12–13

installation level role and responsibilities, 13–16

major command roles and responsibilities, 13

management review, 19

overview, 12

planning process, 16–17

role and responsibilities, 12–16

supervisor role and responsibilities, 16

US Army Armament Research, Development and Engineering Center, 4

US Army Aviation and Missile Life Cycle Management Command, 5

US Army Center for Health Promotion and Preventive Medicine, 74

US Army Chemical Materials Activity, 8

US Army Communications-Electronics Command, 5

US Army Communications-Electronics Research, Development and Engineering Center, 4

US Army Contracting Command, 7

US Army Edgewood Chemical Biological Center, 4

US Army Environmental Hygiene Agency, 74

US Army ergonomics program, 244–245

US Army Joint Munitions Command, 5–7

US Army Materiel Command

Army Materiel Systems Analysis Activity, 8

The Logistics Support Activity, 8

mission of, 3

motto, 2

quality of work environment, 8–9

Research, Development and Engineering Command, 3–4

Tank-Automotive and Armaments Command Life Cycle Management Command, 4–5

US Army Aviation and Missile Life Cycle Management Command, 5

US Army Chemical Materials Activity, 8

US Army Communications-Electronics Command, 5

US Army Contracting Command, 7

US Army Joint Munitions Command, 5–7

US Army Military Surface Deployment and Distribution Command, 7–8

US Army Security Assistance Command, 8

US Army Sustainment Command, 7

US Army Military Surface Deployment and Distribution Command, 7–8

US Army Natick Soldier Research, Development and Engineering Center, 4, 5

US Army Occupational Health Programs

administrative medical examinations, 63–64

Army Occupational and Environmental Health Program, 115–124

in Bosnia, Herzegovina, and Kosovo, 83–86

credentialing and privileging, 60–61

disability retirement examinations, 64

emergency treatment, 66

employee health clinics, 60

employees, 62

epidemiological investigations, 65

evaluation, 59

evaluation of, 59

fitness-for-duty examinations, 64

health hazard education, 64

health promotion, 65–66

health providers, 61

immunizations, 65

industrial hygienists, 61

informatics, 100–103

laws, regulations, and guidance, 56–59

marketing, 58–59

medical centers, 59–60

medical directives, 58

medical records management, 62–63

medical surveillance, 63

monitoring absences due to illness, 64–65

nurses, 61

occupational health clinics, 59–60

Operation Enduring Freedom, 86–100

Operation Iraqi Freedom, 86–100

organization of, 59–62

during Persian Gulf War, 72–83

program document, 57–58

safety personnel, 61–62

staffing, 60–62

standard operating procedures, 58

status report, 57–58

supervisors, 62

worksite evaluations, 64

US Army Research Laboratory, 3

US Army Security Assistance Command, 8

US Army Sustainment Command, 7

US Army Tank Automotive Research, Development and Engineering Center, 4

US Department of Defense

Federal Employees Compensation Act program, 141–143, 146

Hearing Center of Excellence, 210

industrial hygiene exposure assessment model, 237–239

Laser Injury Hotline, 452

military workers’ compensation cost and rates, 143–144

needs for exposure assessment and biomarkers, 596–599

occupational health regulations and guidance, 57–58

personnel medical evaluations, 128–137

policy for handling exposures to depleted uranium, 434–435

program structure and management, 115–117

Protecting Our Workers and Ensuring Reemployment, 143, 146–148

radiation safety program, 429–434

reviews of military compensation programs, 144–146

Serum Repository, 553, 599

US Department of Labor

compensation program management efforts, 146–148

US Department of Transportation

commercial driver medical examination, 159

US Marine Corps

Navy and Marine Corps Public Health Center, 24, 26, 30, 34, 49–50

US Marine Corps War Memorial, 26

US Marine Corps safety and occupational health program

components of, 34–37

organization of, 30

Public Health Center technical manuals, 34

resources, 34–37

staffing, 30

US Navy

the colonial Navy, 42–43

comprehensive occupational health programs during World War II, 48–49

decompression sickness treatment tables, 335–337

development of steam-powered ships, 45–46

evolution of occupational medicine practice, 42–50

Navy and Marine Corps Public Health Center, 24, 26, 30, 34, 49–50

the new Navy, 43–46

occupational health programs during World War I, 48–49

organization of, 24–26

in the 20th Century, 46–50

US Navy Medical Department

the colonial Navy, 42–43

organization of, 27

US Navy Medicine

care for civilian employees, 47–48

establishment of flight and dive medicine, 46–47

organization of, 24–26

preventive medicine, 26–28

role of, 30

US Navy safety and occupational health program

audiology, 33

certification exams, 34–35

components of, 34–37

consultative support and oversight, 33–34

current strategic-level responsibilities, 29

hearing conservation program, 35–36

history of, 26–28

industrial hygiene, 31–32

laws, regulations, and guidance, 30

Medical Matrix Validation Committee, 34–35

medical surveillance, 34–35

occupational and environmental medicine, 32–33, 50

organization of, 30–34

process improvement, 37

program self-assessment, 37

Public Health Center technical manuals, 34

resources, 34–37

safety officers, 30–31

staffing, 30–34

worksite visits, 36

US Transportation Command, 285

USAEHA. See US Army Environmental Hygiene Agency

USS Constitution, 26, 43–44

USS Falcon, 47

USS Harry S. Truman, 35

USS Independence, 45

USS Ohio, 36

USS Princeton, 45–46

V

VA Airborne Hazards and Open Burn Pit Registry, 99

Vapor removing respirators, 222

Vehicle inspection systems radiation, 415–416

Very small aperture terminal communication systems, 456

Veterans Health Care Act of 1992, 73

VHF radio communications systems, 455

Vibration risks, 246, 252

Vietnam War, 72

Violence, workplace, 185

Vision, underwater effects, 317–318

Vision tests, 134

W

Walter Reed National Military Medical Center, 25

Waste anesthetic gases, 176

Water sampling, 85–86

Watervliet Arsenal, 5

Weaponry injuries, 275

Welding hazards, 389

White phosphorus, 383

Whole-blood tests, 90

Workers. See Federal workers’ compensation; Personnel

Workers’ compensation program. See also Federal workers’ compensation

systems analysis, 144–145

Workplace

risk categorization, 15

violence in, 185

Worksite evaluations, 64

Worksite task analyses, 250–252

Worksite visits, 36

World Trade Center terrorism attacks, 86–88

World War I

need for occupational health programs, 48

World War II

comprehensive Navy occupational health programs, 48–49

WRNMMC. See Walter Reed National Military Medical Center

X

X-rays

diagnostic uses, 405–406

digital radiography, 408

industrial uses, 407–408

medical uses, 402–407

therapeutic uses, 406–407

Y

Yellow sodium dichromate exposure, 89

Z

Zinc protoporphyrin test, 393