U.S. Army Medical Research Institute 

of Chemical Defense (USAMRICD) 

MEDICAL MANAGEMENT 

OF CHEMICAL 

CASUALTIES 

HANDBOOK 

Chemical Casualty Care Division 

USAMRICD 

MCMR-CDM 

3100 Ricketts Point Rd 

Aberdeen Proving Ground, MD 21010-5400 

FOURTH EDITION 

February 2007 
Emergency Response Numbers

National Response Center: 1-800-424-8802 

 or (for chem/bio hazards and terrorist events): 

 1-202-267-2675 

USAMRICD Emergency Response Line: 

 1-410-436-3276 or 1-410-322-6822 

CDC’S Emergency Response Line: 1-770-488-7100 

HANDBOOK 

REPRINTING POLICY 

The US Army Medical 

Research Institute of Chemical Defense, Chemical 

Casualty Care Division, requests that users of this 

handbook, prior to distributing or reprinting parts of or 

this entire handbook, notify: 

Chemical Casualty Care Division 

US Army Medical Research Institute of 

Chemical Defense 

3100 Ricketts Point Road 

Aberdeen Proving Ground, MD 21010-5400 
USAMRICD 

Chemical Casualty Care Division’s 

MEDICAL MANAGEMENT OF CHEMICAL 

CASUALTIES HANDBOOK 

Fourth Edition 

February 2007 

EDITORS

COL (Ret) Gary Hurst, MC, USA 

LTC Shirley Tuorinsky, AN, USA 

COL James Madsen, MC, USA 

COL Jonathan Newmark, MC, USA 

LTC Benjamin Hill, MC, USA 

Lt Col Charles Boardman, USAF 

SFC Jeffrey Dawson, USA 

ACKNOWLEDGEMENTS

Ms. Patricia Hurst 

Ms. Leslie Key 

Mr. Laukton Rimpel 

Mr. Daniel Boehm 

Ms. Crystal Chadwick 
Disclaimer

 The purpose of this Handbook is to provide 

concise, supplemental reading material for 

attendees of the Medical Management of 

Chemical Casualties Course. It is to be used as 

a guide in the chemical arena and not to replace 

official doctrine. 

 Every effort has been made to make the 

information contained in this Handbook 

consistent with official policy and doctrine. 

 This Handbook, however, is not an official 

Department of the Army publication, nor is it 

official doctrine. It should not be construed as 

such unless it is supported by other documents.
TABLE OF CONTENTS 

INTRODUCTION ...............................................1 

LUNG-DAMAGING AGENTS..........................18 

CYANIDE.........................................................40 

VESICANTS.....................................................62 

NERVE AGENTS...........................................122 

INCAPACITATING AGENTS ........................157 

RIOT-CONTROL AGENTS ...........................194 

DECONTAMINATION ...................................212 

CASUALTY MANAGEMENT ........................227 

CHEMICAL DEFENSE EQUIPMENT ...........246 

APPENDICES................................................275 
Introduction 

Lung-Damaging Agents 

Cyanide 

Vesicants 

Nerve Agents 

Incapacitating Agents 

Riot-Control Agents 

Decontamination 

Casualty Management 

Chemical Defense Equipment 

Appendices
1 

INTRODUCTION 

PURPOSE 

 Poisoning, that is, exposure to toxic 

chemicals, a process also called intoxication, 

has been an important medical issue for 

centuries. A particularly frightening type of 

poisoning is the generation of military mass 

casualties on the battlefield by the use either of 

chemicals developed specifically for that 

purpose, or of chemicals produced for industry 

and co-opted for battlefield use. In addition, 

these agents can produce civilian casualties 

during warfare and can lead to both military and 

civilian casualties from terrorist use in settings 

remote from a defined battlefield. 

 Military healthcare providers have a special 

responsibility to recognize and manage chemical 

casualties whatever the setting. First, military 

healthcare providers will likely be the first 

medical personnel to receive exposed 

warfighters, sailors, or airmen. Secondly, 

because of the preeminence of the U.S. military 

medical establishment in research, response, 

and training concerning chemical warfare 

agents, military medical personnel must be able 

to respond to chemical exposures at U.S. 

stockpile sites of chemical warfare agents and to 

provide expert consultation to their civilian 
2 

counterparts in the event of a terrorist attack 

involving these agents. Knowledge of the 

medical aspects of the prevention, 

preparedness, response, and recovery phases 

of any military or civilian event involving 

chemical exposure is expected of every military 

medical care provider. 

 This handbook has been produced to help 

address the need for training military medical 

officers. Its primary use is as an adjunct, 

together with a companion biological agents 

handbook, to the Medical Management of 

Chemical and Biological Casualties (MCBC) 

Course. It is not designed to replace the handson training afforded by this course, but it has 

been designed to help MCBC students both 

during the course and after its completion. 

 Medicine is a changing art and science, and 

the treatment protocols and drug dosages 

described in this handbook are not to be 

construed as replacements for sound clinical 

judgment or to be inflexible rules incapable of 

change as new information becomes available. 

It is the responsibility of the users to avail 

themselves of the latest available resources. 

One such resource is the Internet site of the 

Chemical Casualty Care Division of the U.S. 

Army Medical Research Institute of Chemical 

Defense (USAMRICD): 

http://ccc.apgea.army.mil. Registration at this 
3 

site is strongly encouraged so that access to the 

user-restricted portions of the site in an 

emergency will not be delayed. The userrestricted area of this site includes the text of the 

latest published edition of this handbook as well 

as other important references for chemical 

casualty care. 
4 

CHEMICAL AGENTS 

GENERAL CONCEPTS AND 

TERMINOLOGY 

 To paraphrase Paracelsus, any substance 

delivered in excess can act as a poison; it is the 

dose that makes the poison. Nevertheless, the 

term poison traditionally refers to chemicals that 

are sufficiently potent to induce poisoning in 

relatively low doses. The terms toxic chemical, 

chemical agent, and chemical warfare agent are 

often defined in different ways, and their use in 

this handbook needs to be clarified at the outset 

along with the use of related terms. 

 The Chemical Warfare Convention defines a 

toxic chemical as “any chemical which through 

its chemical action on life processes can cause 

death, temporary incapacitation or permanent 

harm to humans or animals;" specifies that this 

definition includes “all such chemicals, 

regardless of their origin of their method of 

production;” and specifically includes toxins such 

as ricin and saxitoxin. 

 The U.S. Army defines chemical warfare 

(CW) agents (often called simply chemical 

agents) as toxic substances developed for 

military use to produce death, serious injury, or 

incapacitation through their toxicological effects 
5 

in exposed humans or animals and officially 

excludes from this definition three broad 

categories of chemicals: (1) riot-control agents, 

(2) herbicides, and (3) smoke and flame 

materials

 Toxic industrial materials, or TIMs, are 

industry-associated materials with harmful 

effects on humans; they can be subdivided into 

toxic industrial biologicals, or TIBs; toxic 

industrial chemicals, or TICs; and toxic industrial 

radiologicals, or TIRs. The North Atlantic Treaty 

Organization (NATO) has a more restricted 

definition for toxic industrial chemical as a 

chemical that (1) is more toxic than ammonia 

(that is, has an LCt50 of 100,000 mg-min/m3

 or 

less [see later in this section] and (2) is 

produced in quantities greater than 30 tons per 

year at a given production facility. However, 

TICs are also commonly defined as any 

industrially produced chemicals that could be 

used to produce mass casualties. 

Toxicant is a general synonym for poison

and can be used interchangeably with the latter 

term. Toxin is also commonly used as a 

synonym for poison but in discussions of 

chemical and biological agents is best defined in 

its more restricted sense as a toxic chemical 

synthesized by a living organism. Toxins have 

characteristics of both chemical and biological 

agents and are increasingly being separately 
6 

classified as mid-spectrum agents, which 

include not only toxins but also bioregulators 

(small molecules with regulatory functions in the 

body in physiological doses but with toxic effects 

in larger doses), synthetic viruses, and 

genocidal weapons. 

 Chemical, biological, and mid-spectrum 

agents are often referred to as weapons of mass 

destruction, or WMD, and the official military 

definition of WMD in fact includes these three 

kinds of agents. However, in the strict sense of 

the word, weapons of mass destruction are 

weapons capable of causing extensive damage 

to physical structures, such as buildings, and 

include high explosives and nuclear and 

thermonuclear bombs. Chemical agents, 

biological agents, toxins, and point sources of 

radiation may cause mass casualties while 

leaving structures intact; and a better term for 

these kinds of weapons is mass-casualty 

weapons, or MCW, a term that is gradually 

gaining currency and that this handbook 

recommends when referring to chemical agents. 

Unconventional weapons is a term used to refer 

to chemical agents, biological agents, toxins, 

nuclear and thermonuclear bombs, radiological 

dispersal devices (also called RDDS, or “dirty 

bombs”), and point sources of radiation used as 

weapons. It does not, however, include 

conventional high explosives. 
7 

 The list of chemical warfare agents officially 

designated as such by the U.S. military includes 

those chemicals that are intended to cause 

death or serious injury and also those intended 

to cause incapacitation, that is, temporary 

inability to perform one’s military duties. The 

former are called toxic agents and include (1) 

lung-damaging agents (also called pulmonary or 

choking agents), (2) “blood” agents (specifically, 

cyanide compounds), (3) vesicants (blistering 

agents), and (4) nerve agents; those designed to 

produce only temporary incapacitation are 

referred to as incapacitating agents. This 

handbook will address each of these groupings 

of “official” chemical warfare agents as well as 

riot-control agents, which are technically not 

chemical warfare agents according to the U.S. 

military definition, but they are widely used in 

law enforcement for mass incapacitation. 

 Chemical agents may have chemical names 

and may also have common names. Every 

chemical agent developed for military use in the 

U.S. also has a NATO code, a one- to threeletter designation assigned after World War II 

(WWII) by the NATO to provide a standard 

shorthand recognizable in any of the languages 

used by NATO countries. Thus, the chemical 

compound O-isopropyl 

methylphosphonofluoridate has the common 

name sarin and the NATO code GB. This 

handbook will make extensive use of NATO 
8 

codes as well as common names for chemical 

agents. 

PHYSICAL FORMS OF CHEMICAL AGENTS 

 Chemical agents, like all other substances, 

may exist as solids, liquids, or gases, depending 

on temperature and pressure. Except for riotcontrol agents and the incapacitating agent BZ, 

which are solids at usually encountered 

temperatures and pressures, chemical agents in 

munitions are liquids. Following detonation of 

the munitions container, the agent is primarily 

dispersed as liquid or as an aerosol, defined as 

a collection of very small solid particles or liquid 

droplets suspended in a gas (in this case, in the 

explosive gases and the atmosphere). Thus, 

"tear gas," a riot-control agent, is not really a gas 

at all, but rather an aerosolized solid. Likewise, 

mustard "gas" and nerve "gas" do not become

true gases even at the boiling point of water 

(212o

F/100oC at sea level). 

 Certain chemical agents, such as hydrogen 

cyanide, chlorine, and phosgene, may be gases 

when encountered during warm months of the 

year at sea level. The nerve agents and mustard 

are liquids under these conditions, but they are 

to a certain extent volatile; that is, they volatilize 

or evaporate, just as water or gasoline does, to 

form an often invisible vapor. A vapor is the 

gaseous form of a substance that is normally a 
9 

liquid at usual environmental temperatures. 

Another way of conceptualizing a vapor is to 

regard it as the gaseous form of a substance at 

a temperature lower than the boiling point of that 

substance at a given pressure. Liquid water, for 

example, becomes a gas (steam) when heated 

to its boiling point at a given pressure, but below 

that temperature, it slowly evaporates to form 

water vapor, which is invisible. Visible water 

clouds (including “clouds of steam”) are 

composed neither of water vapor nor water gas 

(steam) but rather are suspensions of minute 

water droplets, i.e., an aerosol.

 The tendency of a chemical agent to 

evaporate depends not only on its chemical 

composition and on the temperature and air 

pressure, but also on such variables as wind 

velocity and the nature of the underlying surface 

with which the agent is in contact. Just as water 

evaporates less quickly than gasoline but more 

quickly than motor oil at a given temperature,

pure mustard is less volatile than the nerve 

agent GB but is more volatile than the nerve 

agent VX. However, all of these agents 

evaporate more readily when the temperature 

rises, when a strong wind is blowing, or when 

they are resting on glass rather than on, for 

example, porous fabric. 

 Volatility is thus inversely related to 

persistence, because the more volatile a 
10 

substance is, the more quickly it evaporates and 

the less it tends to stay or persist as a liquid and 

contaminate terrain and materiel. The liquid 

hazard of a persistent agent is often more 

significant than the danger created by the 

relatively small amounts of vapor that it may 

generate. The converse is true of nonpersistent 

agents, which may pose a serious vapor hazard 

but which also evaporate quickly enough not to 

create a liquid hazard for an extended time. The 

arbitrary but generally accepted divisions 

between persistent and nonpersistent agents is 

24 hours, meaning that a persistent agent will by 

definition constitute a liquid hazard and 

contaminate surfaces for 24 hours or longer. 

Such agents (mustard and VX) are thus suitable 

for contaminating and denying terrain and 

materiel to the enemy. Nonpersistent agents, 

such as GB and cyanide, find tactical 

employment in the direct line of assault into 

enemy territory since they will have evaporated 

within a day and will no longer contaminate 

surfaces. These generalizations are obviously 

subject to the modifying factors of temperature, 

environmental factors such as wind, and surface 

characteristics. 

EXPOSURE, ABSORPTION, AND 

TOXICITY OF CHEMICAL AGENTS

 Toxicologically speaking, exposure means 

contact of a poison with an epithelial surface 
11 

(such as the skin, respiratory epithelium, eyes, 

or gastrointestinal mucosa) and is quantified as 

external dose. Penetration of an epithelial barrier 

is called absorption and results in an absorbed 

dose, or internal dose. Furthermore, an 

absorbed agent may exert local effects at or 

near the site of exposure and absorption or 

systemic effects following distribution in the 

circulation to sites remote from the exposure 

site. Biological effects occur following exposure 

to chemical agents dispersed as solids, liquids, 

gases, aerosols, or vapors. Eye or skin injury 

may follow direct exposure to the suspended 

solid particles of aerosolized riot-control agents, 

and inhalation of these agents brings the 

aerosolized solid in contact with the epithelium 

of the respiratory tree. Nevertheless, systemic 

effects from exposure to riot-control agents are 

rare. Contact of the eyes, or more likely the skin, 

with liquid nerve or vesicant agents may 

produce local effects or lead to absorption and 

systemic effects. 

 Liquid exposure is the most important 

hazard associated with persistent agents and 

necessitates the proper wearing of chemical 

protective clothing. At low temperatures, 

hydrogen cyanide (AC), cyanogen chloride (CK), 

and phosgene (CG) exist as liquids. However, 

because of their high volatility (low persistence), 

they seldom present a significant liquid hazard 

unless the area of exposure is large or 
12 

evaporation is impeded by trapping of liquid 

agent in saturated, porous clothing. Penetration 

of shrapnel or clothing contaminated with liquid 

chemical agent of any type may also lead to 

intramuscular or intravenous exposure and 

subsequent systemic effects. 

 Chemical agents in the form of aerosolized 

liquid droplets, vapor, or gas may directly 

contact the eyes, skin, or (through inhalation) 

the respiratory tree. Local damage is possible at 

any of these sites, but systemic absorption 

through dry, intact skin is usually less important 

than with the other routes. Vapor or gas 

exposure to the eyes, and especially the 

respiratory tree, is the most important hazard 

associated with nonpersistent agents and 

necessitates the proper wearing of a mask that 

provides both ocular and inhalation protection. 

 Specialized terms refer to the amount of 

chemical agent encountered during an 

exposure. The ED50 and the ID50 denote the 

quantities (usually measured as the weight in 

μg, mg, or g) of liquid agent that will predictably 

cause effects (E) or incapacitation (I) in 50% of a 

given group. Similarly, the LD50 is the lethal dose 

or quantity (weight) of liquid agent that will kill 

50% of a group. Note that the lower the LD50, 

the less agent is required and thus the more 

potent is the agent. Because of differences in 

absorption, the ED50 and LD50 values for a given 
13 

agent are site-specific; i.e., the LD50 for mustard 

absorbed through dry, unabraded skin is much 

higher than the LD50 for mustard absorbed 

through the eye. 

 Comparison of the amounts of chemical 

agent encountered as aerosol, vapor, or gas 

requires use of the concentration-time product or 

Ct, which refers to the agent concentration 

(usually in mg/m3

) multiplied by the time (usually 

in minutes) of exposure. For example, exposure 

to a concentration of 4 mg/m3

 of soman (GD) 

vapor for 10 minutes results in a Ct of 40 

mg·min/m3

. Exposure to 8 mg/m3 for 5 minutes 

results in the same Ct (40 mg·min/m3

). For 

almost any given agent (with the notable 

exception of cyanide, which will be discussed in 

a separate chapter), the Ct associated with a 

biological effect is relatively constant even 

though the concentration and time components 

may vary within certain limits (Haber's Law). 

Therefore, a 10-minute exposure to 4 mg/m3

 of 

soman causes the same effects as a 5-minute 

exposure to 8 mg/m3

 of the agent or to a oneminute exposure to 40 mg/m3

. The ECt50, ICt50., 

and LCt50, then correspond for vapor or gas 

exposures to the ED50, ID50, and LD50, 

respectively, for liquid exposure and are likewise 

site-specific. However, the concentration-time 

product does not take into account variables 

such as respiratory rate and depth and is 
14 

therefore not an exact measure of inhalation 

exposure. 

GENERAL PRINCIPLES OF CHEMICAL 

CASUALTY CARE

 Chemical casualties must be recognized

and appropriately managed. Management 

includes triage (i.e., sorting for medical 

treatment), medical treatment, decontamination

(if liquid contamination is present), and 

disposition, which may include evacuation and, 

hopefully, eventual return to duty. 

 Casualty Recognition. Recognition of a 

chemical casualty is heavily dependent upon 

recognition and differential diagnosis of 

toxidromes, i.e., constellations of symptoms and 

signs that characterize exposure to a specific 

agent or kind of agent. This handbook will 

present distinct toxidromes characteristic of 

exposure to central-compartment lung-damaging 

agents, peripheral-compartment lung-damaging 

agents, cyanide compounds, sulfur mustard, 

Lewisite, phosgene oxime, nerve agents, 

anticholinergic incapacitating agents, 

“traditional” riot-control agents, and vomiting 

agents (a subset of riot-control agents). It is 

important to recognize these toxidromes and 

also to recognize other conditions that could 

mimic them. 
15 

 Chemical agent casualties may be exposed 

to more than one agent and may also have other 

diagnoses, such as concomitant exposure to 

other kinds of mass-casualty agents, preexisting medical or surgical conditions, or 

trauma. It is just as important to view the 

casualty, and the situation, as a whole as it is to 

identify chemical exposure. The best way to 

accomplish this is to use a toxicological 

perspective, i.e., to consider the triad of agent, 

environment, and host. Specifically, the astute 

clinician will think of (1) the agent; (2) the form(s) 

or state(s) of the agent in the environment; (3) 

the passage of agent from the environment to 

the host, i.e., the route or routes of entry; (4) 

whether exposure and absorption of the host are 

producing only local effects (restricting to the 

site of exposure) or are also generating systemic 

effects (effects remote from the site of 

exposure); (5) the severity of effects and of 

exposure; (6) the time course of effects; (7) 

other possible diagnoses (instead of the 

originally considered diagnosis, i.e., differential 

diagnoses; and in addition to the originally 

considered agent, i.e., concomitant diagnoses); 

and (8) any possible interaction or synergism 

among co-existing diagnoses. Without a 

consideration of these factors, treating 

healthcare providers have a tendency to focus 

on the chemical exposure, sometimes to the 

neglect of other life-threatening conditions. 
16 

 Casualty Management. Once a chemical 

casualty has been recognized, appropriate 

management must begin. Triage is the process 

of sorting casualties for medical treatment when 

not all casualties can receive care 

simultaneously. It is in some ways both an 

assessment step and a management step and 

can act as a bridge between initial assessment 

and management. The triage categories used by 

the U.S. military are (1) immediate (those who 

are in danger of losing their lives unless action is 

taken within a few minutes), (2) delayed (those 

who require significant medical intervention but 

who can tolerate a somewhat longer delay in 

treatment), (3) minimal (casualties who have 

minor injuries, illnesses, or intoxications, often 

amenable to self or buddy care), and (4) 

expectant (those who are gravely ill and who 

cannot be treated with available resources 

without causing the death, by misallocation of 

resources, of other casualties). In this handbook, 

triage for specific kinds of chemical agents will 

be addressed within the chapter devoted to that 

agent type. 

 Initial management for severely affected 

chemical casualties (especially those who are 

triaged as immediate) can conveniently be 

summarized as an application of the ABCDDs, 

i.e., A) Airway, B) Breathing, C) Circulation, D1) 

immediate Decontamination, and D2) Drugs, i.e., 

specific antidotes. These interventions will be 
17 

described in specific agent chapters and also in 

the sections on decontamination and casualty 

management in a contaminated area. The latter 

section will also address the issues of patient 

disposition, including evacuation and return to 

duty. 

 Eight appendices (Appendices A through H) 

at the end of this handbook summarize and 

illustrate major concepts from the preceding 

sections of this publication, and following the 

index, review cards for each type of agent will 

help the reader review the material presented 

previously. 

 This handbook is meant to be as userfriendly as possible. New editions build upon 

new information and also are heavily dependent 

upon reader feedback. Please consider helping 

with the next edition by sending your comments 

and suggestions to the Chemical Casualty Care 

Division at ccc@apg.amedd.army.mil. 
18 

LUNG-DAMAGING AGENTS: 

Toxic Industrial Chemicals 

CG, Cl 

SUMMARY 

Signs and Symptoms: Central effects: Eye 

and airway irritation, dyspnea. Peripheral 

effects: Chest tightness, and delayed

pulmonary edema. 

Field Detection: The Chemical Agent 

Detector Kit and the M93A1 FOX 

RECONNAISSANCE System will detect small 

concentrations of CG; however, they will not 

detect Cl. 

Decontamination: Vapor - fresh air; Liquid - 

copious water irrigation. 

Management: Termination of exposure, 

ABCs of resuscitation, enforced rest and 

observation, oxygen with or without positive 

airway pressure for signs of respiratory 

distress, other supportive therapy as needed. 
19 

LUNG-DAMAGING AGENTS: 

TOXIC INDUSTRIAL 

CHEMICALS 

OVERVIEW 

Over 1,800 toxic industrial chemicals (TICs) 

are used in industry, stored at industrial sites, 

and transported on the world’s road and rail 

systems. Some of these chemicals were 

deployed as chemical warfare agents during 

World War I (WWI), killing and injuring 

thousands, and can have the same deadly 

consequences today if released during an 

accident or through terrorist sabotage. Death 

from exposure to TICs is more frequent when 

they are inhaled. Inhaling TICs in the form of a 

gas, vapor (gas coming from a liquid), or aerosol 

(liquid or solid particles suspended in a gas) can 

cause a sudden closure of the larynx 

(laryngospasm) causing the victim to become 

unconscious and collapse. TICs can also cause 

damage to the tissues of the upper airways, 

resulting in swelling, scarring, and airway 

narrowing, which can restrict breathing. TICs 

can damage lung tissues, allowing body plasma 

and other fluids to leak into the lung air sacs 

(alveoli), causing pulmonary edema and death 

from asphyxiation. 
20 

 Warfighters are frequently exposed to TICs 

and military medical personnel must know about 

these agents so that they can help reduce troop 

exposure and prevent serious injury from them. 

 Understanding the Respiratory System. 

The respiratory system can be divided into two 

parts. Understanding these parts can greatly 

simplify the treatment problem-solving process. 

 Central Airway. This includes the 

nasopharynx (nose), oropharynx (mouth), larynx 

(vocal cords), trachea and bronchi (airway from 

the throat into the lungs). Tissues in this area 

are very moist and thin and can be damaged by 

TICs. 

 Peripheral Airway. This includes the lung 

sacs (alveoli) distributed throughout the lung 

tissue. During normal respiration, inhaled 

gasses fill the alveoli and then move slowly 

through their walls. The gasses then move 

through the thin walls of the blood vessels, 

capillaries, surrounding the alveoli and into the 

blood. TICs can damage the walls of alveoli and 

the capillaries surrounding them, allowing blood 

plasma and cells to leak into the air space of the 

alveoli. 
21 

PHYSIOCHEMICAL CHARACTERISTICS 

 Lung-damaging TICs are typically heavier 

than air and hang close to the ground when 

released. They tend to evaporate and disperse 

very quickly, depending on temperature and 

wind conditions. If the TIC is in liquid form at 

room temperature, then it will tend to give off a 

vapor. Vapors can become trapped in clothing 

fibers and “off-gas” to affect those who are 

nearby and have no respiratory protection. 

Although skin decontamination after vapor 

exposure is not a high priority, clothing should 

be removed and the underlying skin 

decontaminated with soap and water.
Molecular 

Weight 

Boiling Point Freezing 

Point 

Phosgene (CG) 

99 7.6oC -128oC 

Hydrogen Chloride (HCl) 

36.46 -85oC -114oC 

Ammonia 17.03 -33.35 oC -77.7oC SPFIB Polymer 214 - 217oC 257- 263oC Oxides of Nitrogen (NOx) 

28.1 -195.8 oC -210oC 

White Phosphorus Smoke (P4) 

123.895 280oC 44.1oC 
22 

DETECTION 

 Chlorine and ammonia have their own 

distinctive odors. Phosgene smells like newly cut 

grass, newly mown hay, or green corn. It is 

important to remember that odor is not a reliable 

detection method, and this does not protect 

against toxic inhalation effects. There are no 

specific field detection devices for these 

compounds; however, the ACADA can detect 

battlefield agent vapors when deployed as an 

area surveillance tool. 

PROTECTION 

 The military mask, if fitted with a C2A1 filter 

canister, will protect against chlorine, phosgene, 

PFIB, NOx, and HC smoke in the open 

battlefield. Specific filters, or the use of a selfcontained breathing apparatus with its own air 

supply, are mandated for other TICs such as 

ammonia. Masks will not be effective in 

environments where the TIC displaces oxygen, 

such as occurs with carbon dioxide. 

TOXICITY 

 The LCt50 of phosgene is approximately 

3200 mg-min/m3

, which is half the LCt50 (6,000 

mg-min/m3

) of chlorine. Since only half as much 

phosgene is required to kill half of an exposed 
23 

group, phosgene is thus twice as potent as 

chlorine. Perfluoroisobutylene (PFIB) is 10 times 

more toxic than phosgene. Listed below are the 

OSHA standards for exposure limits in parts per 

million.
AGENT CG Cl Ammonia PFIB NOx 

Concen. Exposure Limits (ppm) 

0.1 5 50 0.01 25 
24 

Lung-Damaging Agents 

 TICs are numerous. Those that pose a 

frequent threat to the warfighter in the field are 

listed here. Though the list is not complete, 

casualties from other lung-damaging agents are 

managed the same way as these examples. In 

low doses highly reactive TICs have a greater 

effect on the central airway; other TICs act on 

both airways; and still others that are not as 

reactive in the central airway travel deeper in the 

respiratory tract and destroy the tissues of the 

alveoli in the peripheral airways. Any TIC 

inhaled in large doses will cause damage to both 

central and peripheral airways. 

CENTRALLY-ACTING TICs 

 Ammonia. This highly caustic and reactive 

gas is used for industrial refrigeration, for 

cleaning, for the processing of some illicit drugs, 

and for numerous legitimate industrial 

processes. It is a good example of a TIC that, in 

low doses, is primarily centrally acting. It rapidly 

forms a strong base (alkali) when it contacts the 

moist tissues of the central airway. The alkali 

burns and destroys the tissues it contacts. The 

victim may suddenly go into laryngospasm and 

collapse. The tissues of the airway will also 

become swollen. Scar tissue may form along the 

airway. Frequently, damaged tissue in the 

airway will die, slough off, and obstruct it. 
25 

Sulfur Mustard (HD) is an example of a 

chemical agent produced solely for warfare that 

acts on the central airway if inhaled. HD will 

cause tissue to slough off in large sheets, known 

as pseudomembranes, which block the airway. 

The various degrees of airway restriction cause 

casualties with central airway 

restriction/obstruction to be unable to breathe, or 

to sneeze and cough, to have hoarseness when 

they talk, and to make wheezing noises when 

they breathe. 

PERIPHERALLY-ACTING TICs 

Phosgene. Today phosgene is a major 

industrial chemical used in many manufacturing 

processes. More importantly, it is released from 

heating or burning many common chemicals or 

solvents. Carbon tetrachloride, 

perchloroethylene (a degreasing compound), 

methylene chloride (used in paint removal), and 

many other compounds break down to 

phosgene with flame or heat. Also, common 

substances such as foam plastics release 

phosgene when they burn. A warfighter 

presenting with shortness of breath in the 

absence of a chemical attack or other obvious 

cause should be questioned very carefully about 

whether he/she has been near any burning 

substances or chemical vapors that were near 
26 

flame or other hot materials (e.g., a heater with 

open coils). 

Perfluoroisobutylene (PFIB ) is given off 

when Teflon® burns at high temperatures, such 

as in a vehicle fire. Teflon® is used to line the 

interior of many military vehicles, particularly 

armored vehicles and aircraft. Closed-space 

fires in these vehicles release PFIB. Survivors of 

vehicle fires who are short of breath should be 

questioned carefully regarding their exposure to 

the smoke. 

Oxides of Nitrogen, or NOx, are 

components of photochemical smog that can be 

produced by the burning of gunpowder or the 

burning of industrial waste. These substances 

can build up to high concentrations where 

artillery is fired and there is inadequate 

ventilation. Warfighters who become short of 

breath after heavy firing should be suspected of 

exposure to this lung-damaging agent. 

HC Smoke is a mixture of equal amounts of 

hexachloroethane, zinc oxide, and 

approximately 7% grained aluminum or 

aluminum powder used in the military for 

obscuration. The zinc oxide can cause lung 

damage if inhaled in toxic amounts. Appropriate 

precautions, such as the wearing of protective 

masks, must be taken when HC smoke is used. 
27 

TICs THAT ACT BOTH CENTRALLY AND 

PERIPHERALLY

 Chlorine: This is a good example of a 

combination agent, one that acts on both airway 

compartments in low doses. It is widely used in 

industry for the manufacture of plastics, 

lubricants, and to purify water. It was the first 

chemical agent used effectively on the WWI 

battlefield against unprotected military troops. Its 

effectiveness as a weapon was greatly reduced 

once protective masks were widely available for 

wear on the battlefield. Chlorine turns to 

hydrochloric acid when it contacts the moisture 

of the airway; it then causes chemical burns to 

the tissue. It produces signs and symptoms 

seen with exposure to both central and 

peripherally- acting agents. Its action is a 

reminder that even though central damage may 

seem like the primary concern in some patients 

(e.g., they are coughing and wheezing), the 

medic must always treat the casualty as if they 

could develop peripheral symptoms and take 

seriously any patient complaints about feeling 

chest tightness or having breathing difficulty. 
28 

Site of Action 

Agent Central Peripheral 

CG Large dose Yes 

NOx Large dose Yes 

HC Smoke Large dose Yes 

Ammonia Yes Large dose 

Cl Yes Yes 

PFIB Large dose Yes 

TOXICODYNAMICS 

MECHANISM OF ACTION

 Central Airway. Centrally-acting TICs like 

ammonia and HD, will form strong acids or 

bases (alkali) with the water in the tissues of the 

central airway and then destroy these tissues. 

Damaged tissues will swell and can slough into 

the airway and restrict breathing. 

Peripheral Airway. Phosgene is the most 

studied peripheral agent. It causes pulmonary 

edema, which is life threatening. Less is known 

about the other compounds; however, it is 

believed that they are very similar. 
29 

 Phosgene causes effects in the lung by 

inhalation only. It does not cause lung effects 

when absorbed through the skin, injected, or 

orally ingested. 

 When inhaled, phosgene travels to the very 

end of the smallest airways, the bronchioles, 

and causes damage to these airways. 

Additionally, it causes damage to the thin 

membrane that separates the smallest blood 

vessels (the capillaries) and the air sacs (the 

alveoli). Phosgene reacts with the proteins and 

enzymes in these alveolar-capillary membranes 

to cause damage to the membranes. These 

membranes usually function to separate the 

blood in the capillaries from the air in the alveoli, 

but when the membranes are damaged, they 

cannot do this. Blood, or at least the liquid part 

of the blood, the plasma, can leak through the 

damaged membrane into the alveoli. When the 

plasma leaks into the alveoli, the air sacs 

become full of fluid, and air cannot enter them. 

Therefore, exchange of oxygen from the air into 

the blood is hindered, and the casualty suffers 

oxygen deprivation. The extent of the lack of 

oxygen depends on the extent of the phosgene 

exposure and the number of alveoli filled with 

plasma. This is similar to what happens with 

drowning, in that the alveoli fill up with fluid; 

however, in this instance, it is fluid from the 

blood, not from an external source. For this 
30 

reason, phosgene poisoning is sometimes 

referred to as “dry land drowning.” 

CLINICAL EFFECTS 

Centrally-acting agents: Immediately or 

shortly after exposure to these gasses or 

vapors, the individual can develop 

laryngospasm, though this is not true in all 

exposures. As the airways are irritated and 

damaged the individual will sneeze and have 

pain in the nose (nasopharynx inflammation); 

can develop painful swallowing (oropharynx 

inflammation); hoarseness, a feeling of choking 

and noise with exhalation (larynx inflammation); 

pain in the chest, coughing, and wheezing 

during breathing (trachea and bronchi 

inflammation). This can progress to peripheral 

effects if the exposure is great enough where 

the TIC has reached the peripheral airway. 

Scarring of the central airway can create 

permanent airway narrowing depending on the 

agent involved and the dose received. 

 Peripherally-acting agents: Very shortly 

after exposure to phosgene or other agents 

affecting the peripheral airway, the casualty may 

typically have an asymptomatic period of 30 

minutes to 72 hours, but most significant 

exposures have a latent period less than 24 

hours. The duration and concentration of the 

exposure will determine the time to symptom 
31 

onset. The casualty may notice irritation of the 

eyes, nose, and throat, but more commonly, 

there may be no effects during or immediately 

after exposure. The major effects from 

phosgene exposure and other peripherallyacting agents do not occur until hours later. 

HD signs are also delayed, but the damage is 

more in the central compartment.

 The casualty with peripheral damage who is 

developing pulmonary edema will notice 

shortness of breath between 2 and 24 hours 

after exposure. Initially, this may be mild, and 

the eventual severity of the shortness of breath 

(dyspnea) will depend on the amount of 

exposure. As the damage progresses, the 

dyspnea will become more severe, and soon a 

cough will develop. If the damage is severe, the 

casualty will start coughing up clear, foamy 

sputum, the plasma from his blood that has 

leaked into his alveoli. 

 A casualty with a very mild exposure to 

phosgene (or another of these compounds) will 

develop dyspnea 6 to 24 hours after exposure. 

He will notice it first after heavy exertion; 

however, later he will become short of breath 

after any activity. With proper care, he will do 

well and recover completely. 

 A casualty with a severe exposure to 

phosgene (or another of these compounds) will 
32 

notice shortness of breath within 4 to 6 hours

after exposure. Increased difficulty to breathe, 

even at rest, will occur, and even with intensive 

pulmonary care, the casualty may not survive. 

 The average casualty from a lung-damaging 

agent will be in between these two extreme 

cases. When the onset of dyspnea is greater 

than 6 hours after exposure, there may be 

progression to dyspnea at rest. However, with 

good pulmonary care beginning early after the 

onset of effects, the individual should recover 

completely. 

DIFFERENTIAL DIAGNOSIS 

 Many TICs can be distinguished by their 

odor; they generally irritate the mucous 

membranes and can lead to dyspnea, and 

pulmonary edema of delayed onset. 

Riot-control agents produce a burning 

sensation predominantly in the eyes and upper 

airways. This irritation is typically more intense 

than that caused by TICs and is unaccompanied 

by the distinctive odor. 

 Nerve agents induce the production of 

watery secretions as well as respiratory distress; 

however, their other characteristic effects 

distinguish nerve agent toxicity from TIC 

inhalation injury. 
33 

The respiratory toxicity associated with 

vesicants is usually delayed but predominantly 

affects the central, rather than the peripheral, 

airways. Vesicant inhalation severe enough to 

cause dyspnea typically causes signs of airway 

necrosis, often with pseudomembrane formation 

and partial or complete upper airway 

obstruction. Finally, pulmonary parenchymal 

damage following vesicant exposure usually 

manifests itself as hemorrhage rather than 

pulmonary edema. 

LABORATORY FINDINGS 

 No commonly available laboratory tests exist 

for the specific identification or quantification of 

exposure to lung-damaging agents. However, 

an increase in the hematocrit may reflect the 

hemoconcentration induced by transudation of 

fluid into the pulmonary parenchyma from the 

peripherally-acting agents. Arterial blood gases 

may show a low PaO2 or PaCO2, which is an 

early, nonspecific warning of increased 

interstitial fluid in the lung. 

 Peak expiratory flow rate may decrease 

early after a massive exposure to peripherallyacting agents. This nonspecific test helps to 

assess the degree of airway damage and the 

effect of bronchodilator therapy. Decreased lung 

compliance and carbon monoxide diffusing 
34 

capacity are particularly sensitive indicators of 

interstitial fluid volume in the lung but are 

complex tests for hospital use only. 

With peripherally-acting agents, early 

findings on chest x-ray are hyperinflation, 

followed later by pulmonary edema without 

cardiovascular changes of redistribution or 

cardiomegaly. Ventilation profusion ratio (V/Q) 

scanning is very sensitive but is nonspecific and 

for hospital use only. 

MEDICAL MANAGEMENT 

Terminate exposure as a vital first 

measure. This may be accomplished by 

physically removing the casualty from the 

contaminated environment or by isolating him 

from surrounding contamination by supplying a 

properly fitting mask. Decontamination of any 

liquid agent on skin, and removal of clothing if 

vapors are trapped there, fully terminates 

exposure from that source. 

Execute the ABCs of resuscitation as 

required. Establishing an airway is especially 

crucial in a patient exhibiting hoarseness or 

stridor; such individuals may face impending 

laryngeal spasm and require intubation. 

Establishing a clear airway also aids in 

interpretation of auscultatory findings. Steps to 

minimize the work of breathing must be taken. 
35 

Because of the always present danger of 

hypotension induced by pulmonary edema or 

positive airway pressure, accurate determination 

of the casualty's circulatory status is vital not just 

initially, but also at regularly repeated intervals 

and whenever indicated by the clinical situation. 

Enforce rest. Even minimal physical 

exertion may shorten the clinical latent period 

and increase the severity of respiratory 

symptoms and signs in a lung-damaging agent 

casualty. Physical activity in a symptomatic 

patient may precipitate acute clinical 

deterioration and even death. Strict limitation of 

activity (i.e., forced bed rest) and litter 

evacuation are mandatory for patients 

suspected of having inhaled any of the 

edematogenic agents. This is true whether or 

not the patient has respiratory symptoms and 

whether or not objective evidence of pulmonary 

edema is present. 

Prepare to manage airway secretions and 

prevent/treat bronchospasm. Unless 

superinfection is present, secretions present in 

the airways of lung- damaging agent casualties 

are usually copious and watery. They may serve 

as an index to the degree of pulmonary edema 

and do not require specific therapy apart from 

suctioning and drainage. Antibiotics should be 

reserved for those patients with an infectious 

process documented by sputum gram staining 
36 

and culture. Bronchospasm may occur in 

individuals with reactive airways, and these 

patients should receive theophylline or betaadrenergic bronchodilators. Steroid therapy is 

also indicated for bronchospasm as long as 

parenteral administration is chosen over topical 

therapy, which may result in inadequate 

distribution to damaged airways. 

Methylprednisolone, 700-1000 mg or its 

equivalent, may be given intravenously in 

divided doses during the first day and then 

tapered during the duration of the clinical illness. 

The increased susceptibility to bacterial infection 

during steroid therapy mandates careful 

surveillance of the patient. There is some 

support in the literature for steroid use in those 

exposed to HC smoke (zinc/zinc oxide) and 

oxides of nitrogen, as it is theorized that these 

can reduce autoimmune reactions that can 

foster scar development and subsequent 

bronchiolitis obliterans. The literature does not 

give strong support for the use of steroids in the 

treatment of other toxic inhalants. Thus, steroids 

are not recommended in individuals without 

evidence of overt or latent reactive airway 

disease. 

 
37 

Prevent/treat pulmonary edema. Positive 

airway pressure provides some control over the 

clinical complications of pulmonary edema. Early 

use of a positive pressure mask may be 

beneficial. Positive airway pressure may 

exacerbate hypotension by decreasing thoracic 

venous return, necessitating intravenous fluid 

administration and perhaps judicious use of the 

pneumatic anti-shock garment. 

Prevent/treat hypoxia. Oxygen therapy is 

definitely indicated and may require 

supplemental positive airway pressure 

administered via one of several available 

devices for generating intermittent or continuous 

positive pressure. Intubation, with or without 

ventilatory assistance, may be required, and 

positive pressure may need to be applied during 

at least the end-expiratory phase of the 

ventilator cycle. 

Prevent/treat hypotension. Sequestration 

of plasma-derived fluid in the lungs may cause 

hypotension that may be exacerbated by 

positive airway pressure. Urgent intravenous 

administration of either crystalloid or colloid 

(which in this situation appears equally effective) 

may need to be supplemented by the judicious 

application of the pneumatic anti-shock garment. 

The use of vasopressors is a temporary 

measure until fluids can be replaced. 
38 

TRIAGE 

 Patients seen within 12 hours of 

exposure. A patient with pulmonary edema 

only is classified immediate if intensive 

pulmonary care is immediately available. In 

general, a shorter latent period portends a more 

serious illness. A delayed patient is dyspneic 

without objective signs and should be observed 

closely and retriaged hourly. An asymptomatic 

patient with known exposure should be 

classified minimal and observed and retriaged 

every two hours. If this patient remains 

asymptomatic 24 hours after exposure, 

discharge the patient. If exposure is doubtful and 

the patient remains asymptomatic 12 hours 

following putative exposure, consider discharge. 

An expectant patient presents with pulmonary 

edema, cyanosis, and hypotension. A casualty 

who presents with these signs within six hours of 

exposure generally will not survive; a casualty 

with the onset of these signs six hours or longer 

after exposure may survive with immediate, 

intensive medical care. If ventilatory support is 

not available, but adequate evacuation assets 

are available, these patients should have priority 

for urgent evacuation to a facility where 

adequate ventilatory support is available. 

Patients seen more than 12 hours after 

exposure. A patient with pulmonary edema is 

classified immediate provided he will receive 
39 

intensive care within several hours. If cyanosis 

and hypotension are also present, triage the 

patient as expectant. A delayed patient is 

dyspneic and should be observed closely and 

retriaged every two hours. If the patient is 

recovering, discharge him 24 hours after 

exposure. An asymptomatic patient or patient 

with resolving dyspnea is classified minimal. If 

the patient is asymptomatic 24 hours after 

exposure, discharge him. A patient with 

persistent hypotension despite intensive medical 

care is expectant. 

RETURN TO DUTY 

 If the patient has only eye or upper airway 

irritation and is asymptomatic with normal 

physical examination 12 hours later, he may be 

returned to duty. If the patient's original 

complaint was dyspnea only, yet physical 

examination, chest x-ray, and arterial blood 

gases are all normal at 24 hours, he may be 

returned to duty. If the patient presented initially 

with symptoms and an abnormal physical 

examination, chest x-ray, or arterial blood gas, 

he requires close supervision but can be 

returned to duty at 48 hours if physical 

examination, chest x-ray, and arterial blood 

gases are all normal at that time. 
40 

CYANIDE 

AC, CK 

SUMMARY 

Signs and Symptoms: few. After exposure 

to high concentrations, seizures, respiratory 

and cardiac arrest. 

Field Detection: The M256A1 Samplerdetector, M18A2, and M90 Chemical agent 

detectors detect Hydrogen Cyanide (AC) as 

vapor or gas in the air, and the M272 

chemical water testing kit detects AC in water.

Decontamination: Skin decontamination is 

usually not necessary because the agents are 

highly volatile. Wet, contaminated clothing 

should be removed and the underlying skin 

decontaminated with water or other standard 

decontaminants to prevent off-gassing as a 

hazard. 

Management: Antidote: intravenous (IV) 

sodium nitrite and sodium thiosulfate. 

Supportive: oxygen, correct acidosis. 
41 

OVERVIEW 

Cyanide is a rapidly acting, lethal agent that 

is limited in its military usefulness by its high 

LCt50 and high volatility. Death occurs around 

eight minutes after inhalation of a high Ct. 

Sodium nitrite and sodium thiosulfate are 

effective antidotes. 

HISTORY/MILITARY RELEVANCE 

 The French used cyanide in WWI without 

notable military success, possibly because of 

the insufficient amounts delivered and the nature 

of the chemical. After WWI, the Nazis in 

Germany used cyanide in the extermination of 

death camp prisoners. Zyklon B was used in 

enclosed chambers. Nazi leaders themselves 

chose to commit suicide using cyanide The U.S. 

maintained a small number of cyanide munitions 

during WWII. Japan allegedly used cyanide 

against China before and during WWII, and Iraq 

may have used cyanide against the Kurds in the 

1980s. In 1978 cyanide contamination of Tylenol 

led to the production of tamper-proof bottle caps 

and caplets. The Jim Jones cult staged a final 

mass suicide in Guyana in 1982, where over 

900 followers drank a cyanide-laced beverage. 

In 1995, the Aum Shinrikyo used cyanide in train 

station restrooms with poor success. Today 

there are rebel cults like the Tamils of Sri Lanka 
42 

who wear cyanide capsules to take in the event 

they are captured. 

Terms. The term cyanide refers to the anion 

CN-

, or to its acidic form, hydrocyanic acid 

(HCN). Cyanogen (C2N2) is formed by the 

oxidation of cyanide ions; however, the term 

cyanogen has also come to refer to a substance 

that forms cyanide upon metabolism and 

produces the biological effects of free cyanide. 

Simple cyanide (HCN, NaCN) is a compound 

that dissociates to the cyanide anion (CN-

) and a 

cation (H, Na+

). A nitrile is an organic 

compound that contains cyanide. A cyanogen

usually refers to a nitrile that liberates the 

cyanide anion during metabolism and produces 

the biological effects of the cyanide anion. 

Cyanogens may be simple (cyanogen chloride) 

or complex (sodium nitroprusside). 

 Cyanides are also called "blood agents," an 

antiquated term still used by many in the 

military. At the time of the introduction of cyanide 

in WWI, the other chemical agents in use 

caused mainly local effect. In contrast, inhaled 

cyanide produces systemic effects and was 

thought to be carried in the blood, hence, the 

term "blood agent." The widespread distribution 

of absorbed nerve agents and vesicants via the 

blood invalidates this term as a specific 

designator for cyanide. Also, the use of "blood 

agent" carries the connotation that the main site 
43 

of action of cyanide is in the blood, whereas 

cyanide actually acts primarily outside the 

bloodstream. 

 Materials of interest as chemical agents are 

the cyanide hydrogen cyanide (hydrocyanic 

acid, AC) and the simple cyanogen, cyanogen 

chloride (CK). Cyanogen bromide was used 

briefly in WWI but is of no present interest. 

Sources other than military. The cyanide 

ion is ubiquitous in nearly all living organisms 

that tolerate and even require the ion in low 

concentrations. The fruits and seeds (especially 

pits) of many plants of the Roseacae family, 

such as cherries and peaches, as well as 

almonds and lima beans contain cyanogens 

capable of releasing free cyanide following 

enzymatic degradation. The edible portion (the 

roots) of the cassava plant (widely used as a 

food staple in many parts of the world) contains 

the cyanogenic glucoside linamarin. The 

combustion of any material containing carbon 

and nitrogen has the potential to form cyanide; 

some plastics (particularly acrylonitriles) 

predictably release clinically significant amounts 

when burned. Industrial concerns in the U.S. 

manufacture over 300,000 tons of hydrogen 

cyanide annually. Cyanides find widespread use 

in chemical syntheses, electroplating, mineral 

extraction, dyeing, printing, photography, 
44 

agriculture, and in the manufacture of paper, 

textiles, and plastics. 

PHYSIOCHEMICAL CHARACTERISTICS 

 The cyanides exist as liquids in munitions 

but rapidly vaporize upon detonation of the 

munitions. The major threat is from the vapor. 

The liquid toxicity is approximately that of 

mustard (see Toxicity, below). 

 The preferred way to deliver cyanide on the 

battlefield is by large munitions (bombs, large 

shells), because smaller weapons will not 

provide the concentrations needed for effects. In 

reality, the low efficiency of cyanide on the 

tactical battlefield over time has led to its disuse 

in combat operations. 

DETECTION AND PROTECTION 

 The immediately-dangerous-to-life-andhealth (IDLH) concentration of hydrogen cyanide 

(AC) is 50.0 parts per million (ppm); that for 

cyanogen chloride (CK) is 0.6 mg/m3

. The 

military detectors are capable of detecting AC 

and CK at the threshold limits given. 
45 

DETECTOR 

AC 

(Hydrocyanic 

Acid) 

CK 

(Cyanogen 

Chloride) 

M256A1 7.0 mg/m3 

M272 (in 

water) 20.0 mg/m3 

M18A2 8.0 mg/m3

M90 30 mg/m3

M93A1 Fox 46 mg/m3 

 Because the odor of cyanide may be faint or 

lost after accommodation, olfactory detection of 

the odor of bitter almonds is not a reliable 

indicator of cyanide exposure, even for those 

who possess the gene required to smell 

cyanide. The activated charcoal in the canister 

of the chemical protective mask adsorbs 

cyanide, and the mask affords full protection 

from this gas in an open field environment. 

MECHANISM OF TOXICITY 

 Cyanide salts in solid form or in solution are 

readily absorbed from the gastrointestinal (GI) 

tract when ingested. Moreover, the lower the pH 

in the stomach, the more hydrogen cyanide is 

released as gas from ingested salts. Liquid 

cyanide and cyanide in solution can be 

absorbed even through intact skin, but this route 
46 

of entry is usually not clinically significant. 

Parenteral absorption of liquid cyanide can also 

occur from wounds. Cyanide is readily absorbed 

through the eyes, but the most important route 

of entry in a battlefield or terrorist scenario would 

likely be by inhalation. Following absorption, 

cyanide is quickly and widely distributed to all 

organs and tissues of the body. Ingestion leads 

to particularly high levels in the liver when 

compared with inhalation exposure, but both 

routes lead to high concentrations in plasma and 

erythrocytes and in the heart, lungs, and brain. 

 An example of the ability of cyanide to react 

with metals in the body is its reaction with the 

cobalt in hydroxycobalamin (vitamin B12a) to form 

cyanocobalamin (vitamin B12). The reactions of 

cyanide with metals are reversible and exhibit 

concentration-dependent equilibria, but the 

reactions of cyanide with sulfur-containing 

compounds are catalyzed by the enzyme 

rhodanese and are essentially one-way and 

irreversible. The rate-limiting factor in the 

rhodanese-mediated reactions is usually the 

availability of sulfur donors in the body. These 

reactions can be accelerated therapeutically by 

providing a sulfane such as sodium thiosulfate. 

The reaction products, thiocyanates and sulfites, 

are significantly less toxic than cyanide itself and 

are eliminated in the urine. Cyanide also reacts 

with carbonyl and sulfhydryl groups (directly or 

via 3-MPST and other enzymes). However, the 
47 

two most important kinds of reactions from the 

perspective of understanding the classical 

mechanism of action of cyanide and its 

response to specific antidotal therapy are the 

reactions with metals and the enzyme-catalyzed 

reactions with sulfur-containing compounds. 

 Cyanide is eliminated unchanged from the 

body in breath, sweat, and urine--as sodium 

thiocyanate in the urine, and as 

iminothiocarboxylic acid (ITCA) from reaction 

with sulfhydryl groups. High concentrations of 

cyanide in the body will also lead to measurable 

increases in urinary elimination of 

cyanocobalamin (vitamin B12). 

TOXICITY 

 The LCt50s of AC and CK by inhalation have 

been estimated to be 2500-5000 mg-min/m3

 for 

AC and about 11,000 mg-min/m3

 for CK. LD50s

for hydrogen cyanide have been estimated to be 

1.1 mg/kg for IV administration and 100 mg/kg 

after skin exposure. The oral LD50s for sodium 

and potassium cyanide are about 100 and 200 

mg/kg, respectively. 

 Cyanide is unique among military chemical 

agents because it is detoxified at a rate that is of 

practical importance, about 17 μg/kg·min. As a 

result, the LCt50 is greater for a long exposure 
48 

(e.g., 60 minutes) than for a short exposure 

(e.g., 2 minutes). 

MECHANISM OF ACTION 

 Cyanide has a high affinity for certain sulfur 

and for certain metallic complexes, particularly 

those containing cobalt and the trivalent form of 

iron (Fe3+). The cyanide ion can rapidly combine 

with iron in cytochrome a3 (a component of the 

cytochrome aa3 or cytochrome oxidase complex 

in mitochondria) to inhibit this enzyme, thus 

preventing intracellular oxygen utilization. The 

cell then utilizes anaerobic metabolism, creating 

excess lactic acid and a metabolic acidosis. 

Cyanide also has a high affinity for the ferric iron 

in methemoglobin, and one therapeutic 

stratagem induces the formation of 

methemoglobin to which cyanide preferentially 

binds. 

 The small quantity of cyanide always 

present in human tissues is metabolized at the 

approximate rate of 17 μg/kg·min, primarily by 

the hepatic enzyme rhodanese, which catalyzes 

the irreversible reaction of cyanide and a sulfane 

to produce thiocyanate, a relatively nontoxic 

compound excreted in the urine. (An elevated 

concentration of thiocyanate in either blood or 

urine is evidence of cyanide exposure.) The 

limiting factor under normal conditions is the 

availability of a sulfane as a substrate for 
49 

rhodanese, and sulfur is administered 

therapeutically as sodium thiosulfate to 

accelerate this reaction. The lethal dose of 

cyanide is time dependent because of the ability 

of the body to detoxify small amounts of cyanide 

via the rhodanese-catalyzed reaction with 

sulfane. A given amount of cyanide absorbed 

slowly may cause no biological effects even 

though the same amount administered over a 

very short period of time may be lethal. In 

contrast, the LCt50 of each of the other chemical 

agents, which are not metabolized to the same 

extent as is cyanide, is relatively constant over 

time. A lethal amount causes death whether 

administered within minutes or over several 

hours. 

CLINICAL EFFECTS 

 The organs most susceptible to cyanide are 

the central nervous system (CNS) and the heart. 

Most clinical effects are of CNS origin and are 

nonspecific. 

 Approximately 15 seconds after inhalation of 

a high concentration of cyanide, there is a 

transient hyperpnea, followed within 15 to 30 

seconds by the onset of convulsions. 

Respiratory activity stops two to three minutes 

later, and cardiac activity ceases several 

minutes later still, or approximately six to eight 

minutes after exposure. 
50 

 The onset and progression of signs and 

symptoms after ingestion of cyanide or after 

inhalation of a lower concentration of vapor are 

slower. The first effects may not occur until 

several minutes after exposure, and the time 

course of these effects depends on the amount 

absorbed and the rate of absorption. The initial 

transient hyperpnea may be followed by feelings 

of anxiety or apprehension, agitation, vertigo, a 

feeling of weakness, nausea with or without 

vomiting, and muscular trembling. Later, 

consciousness is lost, respiration decreases in 

rate and depth, and convulsions, apnea, and 

cardiac dysrhythmias and standstill follow. 

Because this cascade of events is prolonged, 

diagnosis and successful treatment are possible. 

 The effects of cyanogen chloride include 

those described for hydrogen cyanide. 

Cyanogen chloride is also similar to the riotcontrol agents in causing irritation to the eyes, 

nose, and airways, as well as marked 

lacrimation, rhinorrhea, and bronchosecretions. 

Physical Findings. Physical findings are 

few and nonspecific. The two that are said to be 

characteristic are in fact not always observed. 

The first is severe respiratory distress in an 

acyanotic individual. The natural complexion of 

the casualty may mask any “cherry-red” skin. 

When seen, "cherry-red" skin suggests either 
51 

circulating carboxyhemoglobin from carbon 

monoxide poisoning or high venous oxygen 

content from failure of extraction of oxygen by 

tissues poisoned by cyanide or hydrogen sulfide. 

However, cyanide victims may have normal 

appearing skin and may even be cyanotic, 

although cyanosis is not classically associated 

with cyanide poisoning. 
52 

Table. Cyanide (AC and CK): 

Effects from Vapor Exposure 

Moderate, 

from low 

concentration 

Transient 

increase in 

rate and 

depth of 

breathing, 

dizziness, 

nausea, 

vomiting, 

headache.

These may 

progress to 

severe 

effects if 

exposure 

continues.

The time of 

onset of 

these 

effects 

depends on 

the 

concentrati

on but is 

often within 

minutes 

after onset 

of 

exposure.

Severe, 

from high 

concentration

Transient 

increase in 

rate and 

depth of 

breathing - 

15 seconds. 

Convulsions - 

30 seconds. 

Cessation of 

respiration- 2 

to 4 minutes. 

Cessation of 

heartbeat - 4 

to 8 minutes.

 In addition to the preceding effects, CK 

causes intense irritation of the eyes, nose, and 

airways. 
53 

 The second classic sign of cyanide 

poisoning is the odor of bitter almonds; however, 

approximately 50% of the population is 

genetically unable to detect the odor of cyanide. 

 The casualty may be diaphoretic with normal 

sized or large pupils. A declining blood pressure 

and tachycardia follow an initial hypertension 

and compensatory bradycardia. Terminal 

hypotension is accompanied by bradyrhythmias 

before asystole. 

TIME COURSE OF EFFECTS 

 Effects begin 15 seconds following 

inhalation of a lethal Ct; death ensues in about 6 

to 8 minutes. The onset of effects following 

inhalation of lower Cts may be as early as 

minutes after the onset of exposure. After 

exposure is terminated by evacuation to fresh air 

or by masking, there is little danger of delayed 

onset of effects. 

 The time course for ingested cyanide is 

longer with the victim initially complaining of 

stomach upset, due to the alkaline nature of 

potassium cyanide. This is followed after a 

period of approximately 7 minutes by 

hyperpnoea, a feeling of anxiety in the patient, 

and within 15 minutes, the patient feels 

weakness and experiences a loss of 
54 

consciousness. Convulsions follow. Within 25 

minutes apnea occurs, and soon the heart stops 

and death occurs. Typically, death occurs within 

30 minutes after cyanide ingestion, depending 

on the dose ingested and the physiological 

make-up of the victim. 

DIFFERENTIAL DIAGNOSIS 

 Inhalation exposure to either cyanide or a 

nerve agent may precipitate the sudden onset of 

loss of consciousness, followed by convulsions 

and apnea. The cyanide casualty has normal 

sized or dilated pupils, few secretions, and 

muscular twitching, but no fasciculations. In 

contrast, the nerve agent casualty has miosis 

(until shortly before death), copious oral and 

nasal secretions, and muscular fasciculations. In 

addition, the nerve agent casualty may be 

cyanotic, whereas the cyanide casualty usually 

is not. 

LABORATORY FINDINGS 

 There are several laboratory tests that can 

be requested, but antidotal treatment must be 

provided immediately if signs and symptoms are 

clearly indicative of cyanide poisoning since the 

rapid timeline will not allow the provider to wait 

for confirmatory lab results without 

compromising the patient. 

 
55 

 1. An elevated blood cyanide concentration.

Mild effects may be apparent at concentrations 

of 0.5 to 1.0 μg/ml, and concentrations of 2.5 

μg/ml and higher are associated with coma, 

convulsions, and death and are used primarily 

for forensic confirmation. 

 2. Acidosis. Metabolic acidosis with a high 

concentration of lactic acid (lactic acidosis) or a 

metabolic acidosis with an unusually high anion 

gap (if the means to measure lactic acid are not 

available) may be present. Because oxygen 

cannot be utilized, anaerobic metabolism with 

the production of lactic acid replaces aerobic 

metabolism. Lactic acidosis, however, may 

reflect other disease states and is not specific 

for cyanide poisoning. Test results are fairly 

rapid and valuable as an early confirmatory lab 

result. 

 3. Oxygen content of venous blood greater 

than normal. This also is a result of poisoning of 

the cellular respiratory chain and the resulting 

failure of cells to extract oxygen from arterial 

blood. This finding is also not specific for 

cyanide poisoning. It is helpful in confirming a 

diagnosis and for evaluating methemoglobin 

levels for later adjusting the levels of 

methemoglobin-forming antidotes. 
56 

MEDICAL MANAGEMENT 

 Management of cyanide poisoning begins 

with self protection, then removal of the casualty 

to fresh air. Dermal decontamination is 

unnecessary if exposure has been only to vapor. 

With liquid exposure, wet clothing should be 

removed, and the underlying skin should be 

washed either with soap and water or water 

alone if liquid on the skin is a possibility. A 

casualty that has ingested cyanide does not 

require decontamination. 

 Attention to the basics of intensive cardiorespiratory supportive care is critical and 

includes mechanical ventilation as needed, 

circulatory support with crystalloids and 

vasopressors, correction of metabolic acidosis 

with IV sodium bicarbonate, and seizure control 

with benzodiazepine administration. The fact 

that cyanide inhibits cellular utilization of oxygen 

would lead to the expectation that supplemental 

oxygen would not be of use in cyanide 

poisoning. However, in fact, administration of 

100% oxygen has been found empirically to 

exert a beneficial effect and should be a part of 

general supportive care for the cyanide casualty. 

 Gavage and administer activated charcoal if 

the cyanide was ingested. All vomitous should 

be collected so that vapors from it do not sicken 

the staff. 
57 

 Symptomatic patients, especially those with 

severe manifestations, may further benefit from 

specific antidotal therapy. This is provided in a 

two-step process. First, a methemoglobinforming agent such as amyl nitrite (available in 

civilian antidote kits, but not in military kits, as 

crushable ampoules for inhalation) or sodium 

nitrite (for IV use) is administered, since the 

ferric ion (Fe3+) in methemoglobin has an even 

higher affinity for cyanide than does cytochrome 

a3. The equilibrium of this reaction causes 

dissociation of bound cyanide from cytochrome 

a3 and frees the enzyme to help produce 

adenosine triphosphate ( ATP) again. 

Hypotension, produced by nitrite administration, 

should be monitored. Further, a prudent concern 

for overproduction of methemoglobin must be 

realized as this may compromise oxygencarrying capacity. Thus, nitrite is relatively 

contraindicated in, for example, smokeinhalation victims. The initial adult dose, 

equivalent to 1 of the 2 sodium nitrite vials in the 

standard Cyanide Antidote Kit, is 10 ml. 

Pediatric nitrite dosing (in the case of a military 

response to a civilian terrorist incident) is 

dependent on body weight and hemoglobin 

concentration. The recommended pediatric 

dose, assuming a hemoglobin concentration of 

12 g/dl, is 0.33 ml/kg of the standard 3% solution 

given slowly, IV, over 5 to 10 minutes. 
58 

 The second step for treatment is the infusion 

of a sulfur donor, typically sodium thiosulfate, 

which is utilized as a substrate by rhodanese for 

its conversion of cyanide to thiocyanate. Sodium 

thiosulfate itself is efficacious, relatively benign, 

and also synergistic with oxygen administration 

and thus may be used without nitrites empirically 

in situations such as smoke inhalation with high 

carboxyhemoglobin levels. In the cyanide 

antidote kit, the antidotes are already prepared 

in premeasured vials. The initial adult dose, 

equivalent to 1 of the 2 large bottles in the 

Cyanide Antidote Kit, is 50 ml; the initial 

thiosulfate dose for pediatric patients is 1.65 

ml/kg of the standard 25% solution, IV. Second 

treatments with each of the two antidotes may 

be given at up to half the original dose if needed. 

Directions are also found on the inside of the kit 

lid. 

 It is important to realize that, although the 

combination of sodium nitrite and sodium 

thiosulfate may save victims exposed to 10 to 20 

lethal doses of cyanide and are effective even 

after breathing has stopped, many patients will 

recover even without specific antidotal treatment 

if vigorous general supportive care is 

emphasized. Lack of availability of antidotes is 

therefore not a reason to consider even apneic 

cyanide casualties expectant. It is also important 

to realize that administration of antidotes, 

especially if not given slowly enough or if given 
59 

in extremely large doses, is also associated with 

morbidity, and even mortality. Antidotes should 

not be withheld in a patient with suspected 

cyanide poisoning, but infusion rates should be 

slow, and the drugs should be titrated to effect. 

Overdosage should be avoided. 

 Several alternative therapies and 

experimental antidotes are used in other NATO 

countries. Germany uses dimethylaminophenol 

(DMAP), a rapid methemoglobin former 

developed for intramuscular (IM) and IV use. 

However, muscle necrosis at the site of injection 

occurs, and only the IV route of administration is 

recommended. 

 Certain cobalt compounds directly chelate 

cyanide to reduce its toxicity. Because cobalt 

compounds do not depend upon the formation of 

methemoglobin, they may exert their antidotal 

activity more quickly than do methemoglobinformers. Great Britain and France use cobalt 

edetate (Kelocyanor), but clear superiority to the 

methemoglobin formers has not been 

demonstrated, and cobalt toxicity is occasionally 

seen, particularly if the patient has only a mild 

exposure. The other cobalt compound 

sometimes used in France is hydroxycobalamin 

(vitamin B12a), which complexes with cyanide on 

a molar basis. Clinical trials of this compound 

are underway in the U.S. All of these have been 
60 

found to be most effective when combined with 

the administration of thiosulfate. 

 Ongoing research is examining whether 

slow methemoglobin formers can be used as 

pretreatment to induce clinically asymptomatic 

methemoglobinemia in troops at high risk for 

cyanide exposure. 

TRIAGE 

 An immediate casualty is one who presents 

within minutes of inhalation exposure with 

convulsions or the recent onset of apnea, but 

with circulation intact. Immediate antidote 

administration will be lifesaving. 

 A minimal casualty is one who has inhaled 

less than a lethal amount and has mild effects. 

The antidotes may reduce his symptoms but are 

not lifesaving. 

 The delayed casualty is one recovering 

from mild effects or successful therapy. 

Generally, it will be hours before full recovery. 

Evacuation is not necessary but might be 

considered until full recovery takes place. 

 An expectant casualty is apneic with 

circulatory failure (more likely to triage as 

expectant here if there are limited resources and 

the casualty has a co-exposure to other 
61 

toxicants or serious trauma resulting in anoxic 

encephalopathy). 

 Generally, a casualty who has had 

inhalation exposure and survives long enough to 

reach medical care will need little treatment. A 

severely compromised logistical capability to 

provide adequate respiratory support might be a 

basis for re-triage to a different category. 

RETURN TO DUTY 

 Full recovery is usually relatively fast after 

cyanide intoxication. Those with mild to 

moderate effects from the agent can usually 

return to duty within hours, and those 

successfully treated after severe effects can 

return within a day as long as there is no 

neurological damage caused by significant 

hypoxia. 
62 

 VESICANTS 

HD, H, L, CX 

OVERVIEW 

 Sulfur mustard has posed a military threat 

since its introduction on the battlefield in WWI. 

Most of this chapter concerns this agent. Unless 

otherwise noted, the term "mustard" refers to 

sulfur mustard. 

 The nitrogen mustards (HN1, HN2, and 

HN3) were synthesized in the 1930s, but were 

not produced in large amounts for warfare. 

Mechlorethamine (HN2, Mustargen) became the 

prototypical cancer chemotherapeutic compound 

and remained the standard compound for this 

purpose for many years. 

 Lewisite (L) was synthesized during the late 

stages of WWI but probably has not been used 

on a battlefield. The Lewisite antidote, British 

Anti-Lewisite (BAL), finds medicinal use today 

as a heavy-metal chelator. 

 Although classified as a vesicant, phosgene 

oxime (CX) is a corrosive urticant that also has 

not seen battlefield use. 
63 

 Lewisite and phosgene oxime pose only 

minor potential military threats and will be 

discussed briefly at the end of this chapter. 
64 

MUSTARD 

HD, H 

SUMMARY 

Signs and Symptoms: Asymptomatic latent 

period (hours). Erythema and blisters on the 

skin; irritation, conjunctivitis, corneal opacity, 

and damage in the eyes; mild upper 

respiratory signs to marked airway damage; 

also gastrointestinal (GI) effects and bone 

marrow stem cell suppression. 

Field Detection: M256A1 Kit, M18A2 

chemical agents detector kits; individual 

Chemical Agents Alarm (ICAM), M90 

chemical agents detector, M8 and M9 

chemical agent detector papers, M21 Remote 

Sensing Chemical Agent Alarm (RSCAAL), 

M93A1 FOX NBC RECONNAISSANCE 

System, M272 chemical water testing kit, M22 

automatic chemical agent (ACADA) detection 

alarm 

Decontamination: 0.5% hypochlorite, M291 

kit, and water in large amounts. 

Management: Decontamination immediately 

after exposure is the only way to prevent 

damage. Supportive care of patients; there is 

no specific therapy. 
65 

OVERVIEW 

 Vesicant agents, specifically sulfur mustard 

(H, HD), have been major military threat agents 

since their introduction in WWI. They constitute 

both a vapor and a liquid threat to all exposed 

skin and mucous membranes. Mustard's effects 

are delayed, appearing hours after exposure. 

The organs most commonly affected are the 

skin (with erythema and vesicles), eyes (with 

mild conjunctivitis to severe eye damage), and 

airways (with mild irritation of the upper 

respiratory tract, to severe bronchiolar damage 

leading to necrosis and hemorrhage of the 

airway mucosa and musculature). Following 

exposure to large quantities of mustard, 

precursor cells of the bone marrow are 

damaged, leading to pancytopenia and 

increased susceptibility to infection. The GI tract 

may be damaged, and there are sometimes 

CNS signs. There is no specific antidote, and 

management is symptomatic therapy. Immediate 

decontamination is the only established way to 

reduce damage. 

HISTORY/MILITARY RELEVANCE 

 Sulfur mustard was first synthesized in the 

early 1800s and was first used on the battlefield 

during WWI by Germany in July 1917. Despite 

its introduction late in that conflict, mustard 

produced the most chemical casualties, 
66 

although fewer than 5% of the casualties who 

reached medical treatment facilities died. Italy 

allegedly used mustard in the 1930s against 

Abyssinia. Egypt apparently employed mustard 

in the 1960s against Yemen, and Iraq used 

mustard in the 1980s against Iran and the 

Kurds. Most recently, 2005, the Burmese 

military has allegedly used a substance against 

the Karenni people of Burma causing many of 

the clinical symptoms seen in mustard victims. 

Accidental exposure from old ordinance also 

occurs frequently with recent events in China in 

2003 and Delaware in 2004. Mustard is still 

considered a major threat agent. 

 The U.S. manufactured mustard during WWI 

and WWII. Most of its stockpile has been or is 

being destroyed. 

Nomenclature. Sulfur mustard 

manufactured by the Levinstein process 

contains up to 30% impurities (mostly sulfur) and 

is known as H. Mustard made by a distillation 

procedure is almost pure and is known as HD 

(distilled mustard). An early term for the German 

agent was HS (probably derived from the WWI 

slang term Hun Stoffe). 

PHYSIOCHEMICAL CHARACTERISTICS 

 Mustard is an oily liquid with a color ranging 

from light yellow to brown. Its odor is that of 
67 

garlic, onion, or mustard (hence its name), but 

because of accommodation of the sense of 

smell, odor should not be relied on for detection. 

Under temperate conditions, mustard 

evaporates slowly and is primarily a liquid 

hazard, but its vapor hazard increases with 

increasing temperature. At 100o

F/37.7oC or 

above, it is a definite vapor hazard. Mustard 

freezes at 57o

F/13.9 oC, and since a solid is 

difficult to disperse, mustard is often mixed with 

substances with a lower freezing point, e.g., 

Lewisite (the mixture is HL), so that the mixture 

will remain liquid at lower temperatures. The 

mixture HT also refers to mustard that has been 

thickened with small quantities of newer 

thickening agents to make it even more 

persistent. 

DETECTION AND PROTECTION 

 The immediately-dangerous-to-life-andhealth (IDLH) concentration of sulfur mustard 

(H) is 0.003 mg/m3. The M8A1 automatic 

chemical agent detector alarm is incapable of 

detecting mustard. However, liquid mustard 

turns M8 paper a ketchup red, and M9 paper will 

turn pink, red, reddish-brown, or purple when 

exposed to liquid nerve agents or vesicants, but 

does not specifically identify either the class of 

agent or the specific agent. The detectors in the 

following chart have the capacity to detect sulfur 

mustard (H) at the threshold limits given. 
68 

DETECTOR H 

M256A1 3.0 mg/min3 

M272 (in water) 2.0 mg/min3

M18A2 0.5 mg/min3

M21 150 mg/min3

M90 0.2 mg/min3

M93A1 Fox 0.01 - 1 mcg/l 

CAM 0.1 mg/min3

 Because the odor of sulfur mustard may be 

faint or lost after accommodation, olfactory 

detection of the odor of mustard, garlic, onions, 

or horseradish is not a reliable indicator of 

mustard exposure. The activated charcoal in the 

canister of the chemical protective mask 

adsorbs mustard, as does the charcoal in the 

chemical protective overgarment. The butyl 

rubber in the chemical protective gloves and 

boots is impermeable to mustard. Proper wear 

of the chemical protective mask and the 

chemical protective ensemble affords full 

protection against sulfur mustard. 

MECHANISM OF TOXICITY 

 Mustard vapor and liquid readily penetrate 

thin layers of most fabrics (but not the chemical 

protective ensemble) to reach underlying skin. 
69 

Although mustard dissolves relatively slowly in 

aqueous solutions such as sweat, the 

lipophilicity of mustard guarantees effective 

absorption through even intact skin. Penetration 

is rapid (1 to 4 mcg/cm2

-min) and is enhanced 

by moisture, heat, and thin skin. This explains 

the otherwise baffling observation that WWI 

mustard burns involved the scrotum in 42% of 

cases, but the presumably more readily exposed 

hands in only 4% of cases. Ocular and 

respiratory routes of entry are also important, as 

is parenteral absorption in casualties with 

conventional wounds. Ingestion (enteral 

absorption) was an important route of entry for 

mustard in the sailors who jumped into mustard 

floating on the sea from the exploding, mustard 

carrying ship, the SS John Harvey, docked at 

Bari Harbor, Italy during WWII. 

 Approximately 10% of the amount of 

mustard that begins to penetrate the skin will 

bind to the skin as "fixed" (reacted) mustard; the 

remaining 90% of the dose reaches the 

circulation and is systemically distributed as 

"free" (unreacted and hydrolyzed) mustard. 

Distribution is to almost all organs and tissues 

including the kidneys, liver, intestines, and 

lungs; although, because of dilutional effects 

and reactions of mustard in the bloodstream, 

clinical effects from systemic distribution are 

seen only at high doses. After IV administration, 

mustard disappears from the blood within 
70 

seconds to minutes. Because of the rapid 

fixation of mustard to tissue, the fluid inside the 

blisters that eventually develop at the sites of 

skin contact contains no free mustard and does 

not pose a contamination hazard to health care 

providers. Mustard participates in a variety of 

biotransformative (metabolic) reactions in the 

body. Some of these reactions are catalyzed by 

enzymes, but most absorbed mustard reacts 

directly by forming covalent bonds (via 

alkylation) with DNA, RNA, proteins, 

components of cell membranes, and other 

macromolecules in the body. Mustard is 

eliminated primarily in the urine as by-products 

of alkylation. 

TOXICITY 

 The LCt50 of sulfur mustard dispersed as a 

vapor is 1500 mg-min/m3

 in an unprotected 

group and 10,000 mg-min/m3

 in a group with 

respiratory protection. This demonstrates not 

only the importance of respiratory protection, but 

also the fact that sufficient concentrations of 

vapor and sufficient exposure times render 

mustard vapor lethal, even in masked 

individuals. The LD50 of liquid mustard on the 

skin is 100 mg/kg. Thus, administration of 7 g 

(about a teaspoon) of liquid mustard to each 

member of a group of individuals weighing 70 kg 

would be expected to cause the death of half of 

those exposed. Although 7 g of a liquid applied 
71 

evenly to the surface of the skin may cover 

approximately 20 to 25% of the total body 

surface area (BSA), the correlation between 

BSA involvement and deaths from mustard in 

the field is poor. One plausible reason for this 

discrepancy is that using BSA figures by 

themselves ignores the inhalational component 

of mustard exposure. Another conceivable 

explanation is that measurement solely of 

affected BSA neglects factors such as the 

thickness of coverage, subsequent spread, 

contact time, and continued exposure. A 10 mcg 

droplet of sulfur mustard can produce a small 

vesicle on exposed skin. 

TOXICODYNAMICS 

(MECHANISM OF ACTION) 

 Absorbed mustard must first dissolve in 

aqueous solution such as sweat or extracellular 

fluid. Although mustard molecules dissolve 

slowly in such solutions, once they dissolve they 

rapidly (within seconds to a minute or two) 

rearrange to form extremely reactive cyclic 

ethylene sulfonium ions that immediately bind to 

intracellular and extracellular enzymes, proteins, 

and other cellular components. Mustard has 

many biological actions, but the exact 

mechanism by which it produces tissue injury is 

not known. According to one prominent 

hypothesis, biological damage from mustard 

results from DNA alkylation and crosslinking in 
72 

rapidly dividing cells, such as basal 

keratinocytes, mucosal epithelium, and bone 

marrow precursor cells. This leads to cellular 

death and inflammatory reaction, and in the skin, 

protease digestion of anchoring filaments at the 

epidermal-dermal junction and the formation of 

blisters. 

 Mustard also possesses mild cholinergic 

activity, which may be responsible for effects 

such as early GI symptoms and miosis. 

 It should be re-emphasized that mustard 

reacts with tissue within minutes of entering the 

body and that blood, tissue, and blister fluid do 

not contain free mustard, nor do they represent 

a contamination risk for medical personnel. 

CLINICAL EFFECTS 

 Topical effects of mustard occur in the eye, 

airways, and skin. Systemically absorbed 

mustard may produce effects in the bone 

marrow, GI tract, and CNS. Direct injury to the 

GI tract may also occur following ingestion of the 

compound. 

 Combined data from U.S. forces in WWI and 

Iranians in the Iraq-Iran conflict suggest equal 

incidence of eye, airway, and skin involvement 

(between 80 and 90% for each). However, there 

were higher incidences of eye and lung damage 
73 

in Iranian casualties than in WWI casualties, 

probably because of the larger amount of 

evaporation of the agent in the hot climate. 

Skin. Erythema is the mildest and earliest 

form of skin injury after exposure to mustard. It 

resembles sunburn and is associated with 

pruritus or burning, stinging pain. Erythema 

begins to appear in 2 to 48 hours after vapor 

exposure with time of onset dependent on Ct, 

ambient temperature and humidity, and skin site 

exposed. The skin sites most sensitive are the 

warm, moist locations with thinner skin such as 

the perineum, external genitalia, axillae, 

antecubital fossae, and neck. 

Within the erythematous areas, small 

vesicles can develop which may later coalesce 

to form bullae. The typical bulla, or blister, is 

large, dome-shaped, thin-walled, translucent, 

yellowish, and surrounded by erythema. The 

blister fluid is clear, at first thin and strawcolored, but later yellowish and tending to 

coagulate. The fluid does not contain mustard 

and is not a vesicant. 

 At extremely high doses such as those from 

liquid exposure, lesions may develop a central 

zone of coagulation necrosis with blister 

formation at the periphery. These lesions take 

longer to heal and are more prone to secondary 
74 

infection than the uncomplicated lesions seen at 

lower exposure levels. 

Pulmonary. The primary airway lesion from 

mustard is necrosis of the mucosa with later 

damage to the musculature of the airways if the 

amount of agent is large. The damage begins in 

the upper airways and descends to the lower 

airways in a dose-dependent manner. Usually 

the terminal airways and alveoli are affected 

only as a terminal event. Pulmonary edema is 

not usually present unless the damage is very 

severe, and then it usually is hemorrhagic. 

 The earliest effects from mustard, perhaps 

the only effects from a low Ct, involve the nose, 

sinuses, and pharynx. There may be irritation or 

burning of the nares, epistaxis, sinus pain or 

irritation, and irritation or soreness of the 

pharynx. As the Ct increases, other effects 

occur, such as laryngitis with voice changes and 

a nonproductive cough, and damage to the 

trachea and upper bronchi leads to a cough 

productive of sputum. Lower airway involvement 

causes dyspnea and an increasingly severe 

cough with increased quantities of sputum. 

Terminally, there may be necrosis of the smaller 

airways with hemorrhagic edema into 

surrounding alveoli. This hemorrhagic 

pulmonary edema is rarely a feature. 
75 

 Necrosis of the airway mucosa with resulting 

inflammation can cause pseudomembrane 

formation. Pseudomembranes may occur from 

the most proximal parts of the airways to the 

most distal portions. These membranes may 

cause local airway obstruction at the sites of 

formation, and detachment may lead to 

obstruction of lower airways. 

 The cause of death in mustard poisoning is 

commonly respiratory failure. Mechanical 

obstruction by pseudomembranes and agentinduced laryngospasm are important causes of 

death in the first 24 hours after exposure. 

Deaths occurring from the third to the sixth day 

after exposure result from secondary bacterial 

pneumonia caused by bacterial invasion of 

denuded respiratory mucosa and necrotic 

debris. Agent-induced bone marrow suppression 

is a contributory factor in later, septic deaths 

from pneumonia. 

Eyes. The eyes are the organs most 

sensitive to mustard vapor injury. The latent 

period is shorter for eye injury than for skin injury 

and is also Ct dependent. 

 After low-dose vapor exposure, irritation 

evidenced by reddening of the eyes may be the 

only effect. As the dose increases, the spectrum 

of injury includes progressively more severe 
76 

conjunctivitis, photophobia, blepharospasm, 

pain, and corneal damage. 

 Blisters do not normally form in the eyes. 

Instead, swelling and loosening of corneal 

epithelial cells lead to corneal edema and 

clouding with leukocytes (which affects vision). 

Corneal vascularization with secondary edema 

may last for weeks. Scarring between the iris 

and lens may follow severe effects; this scarring 

may restrict pupillary movements and may 

predispose victims to glaucoma. 

 The most severe damage is caused by liquid 

mustard from airborne droplets or by selfcontamination. After extensive eye exposure, 

severe corneal damage with possible perforation 

of the cornea and loss of the eye can occur. Eye 

loss also results from panophthalmitis if 

appropriate therapy is not instituted. 

 During WWI, mild conjunctivitis accounted 

for 75% of eye injuries, with recovery in 1 to 2 

weeks. Moderate conjunctivitis with minimal 

corneal involvement, blepharospasm, edema of 

the lids and conjunctivae, and orange-peel 

roughening of the cornea accounted for 15% of 

the cases, with recovery in 4 to 6 weeks. Severe 

corneal involvement accounted for 10% of the 

cases. Those with permanent corneal damage 

accounted for less than 1% of cases. About 
77 

0.1% of these severe casualties would meet the 

criteria for legal blindness today. 

 Miosis noted after mustard exposure in both 

humans and experimental animals is probably 

from the cholinomimetic activity of mustard. 

Gastrointestinal (GI) tract. The mucosa of 

the GI tract is very susceptible to mustard 

damage, either from systemic absorption or 

ingestion of the agent. However, reports of 

severe GI effects from mustard poisoning are 

relatively infrequent. 

 Mustard exposure, even exposure to a small 

amount, will often cause nausea, with or without 

vomiting, lasting 24 hours or less. The nausea 

and vomiting appear not to be a direct effect of 

the agent on the GI tract, but rather they are 

from a stress reaction, a nonspecific reaction to 

the odor, or cholinergic stimulation by mustard. 

Further GI symptoms are usually minimal unless 

the exposure was severe (even then, GI signs 

are not common) or exposure resulted from 

ingestion of contaminated food or drink. 

Diarrhea has been reported; constipation is 

equally common. Diarrhea (rarely bloody) and 

vomiting beginning days after a high-dose 

exposure imply a poor prognosis. 

Central nervous system (CNS). The CNS 

effects of mustard remain poorly defined. Animal 
78 

work demonstrated that mustards (particularly 

the nitrogen mustards) are convulsants, and 

there are several human case reports describing 

victims who were exposed to very large amounts 

and had neurological effects within several 

hours after exposure just prior to death. Reports 

from WWI, and again from Iran, described 

people exposed to small amounts of mustard 

that appeared sluggish, apathetic, and lethargic. 

These reports suggest that minor psychological 

problems could linger for a year or longer. 

TIME COURSE OF EFFECTS 

 Mustard binds irreversibly to tissue within 

several minutes after contact. If decontamination 

is not done immediately after exposure, there is 

no way to prevent injury, although later 

decontamination might prevent a more severe 

lesion. 

 The clinical effects of mustard are delayed. 

Signs and symptoms may appear as early as 2 

hours after a high-dose exposure, whereas 

following a low-dose vapor exposure, the latent 

or asymptomatic period may extend to 48 hours. 

There are several reports of individuals exposed 

to very large amounts who died within hours; 

this type of occurrence is extremely rare. The 

typical onset time is between four and eight 

hours. The concentration (C) of the mustard 

vapor, time (t) of exposure, ambient weather, 
79 

and body site exposed are factors in the onset 

time. 

 It must be emphasized that mustard 

causes tissue damage within several 

minutes after contact without causing any 

concomitant clinical effects, e.g., burning or 

erythema. Because of the lack of immediate 

effects, the contaminated person is often 

unaware of the exposure and does not 

decontaminate. To prevent injury, 

decontamination must be done immediately 

after contact. Later decontamination may 

prevent further damage, absorption, or spread of 

the agent. 
80 

Table: Effects of Mustard Vapor

ORGAN SEVERITY EFFECTS 

ONSET 

OF 

FIRST 

EFFECT 

Eye Mild 

Tearing, itchy, 

burning, gritty 

feeling 

4-12 

hours 

Moderate 

Above, plus 

reddening, 

swelling of lids, 

moderate pain 

3-6 hours 

Severe 

Marked 

swelling of lids, 

possible 

cornea 

damage, 

severe pain 

1-2 hours 

Airways Mild 

Runny nose, 

sneezing, 

nosebleed, 

hoarseness, 

hacking cough 

12-24 

hours 

Severe 

Above, plus 

severe 

productive 

cough, 

shortness of 

breath 

2-4 hours 

Skin Mild to 

Severe 

Erythema 

(redness), 

blisters 

2-24 

hours 
81 

DIFFERENTIAL DIAGNOSIS 

 Of the three vesicant agents, mustard is the 

only one that does not cause immediate pain. 

The casualty is asymptomatic until the lesion 

becomes apparent hours later. 

 Lewisite and phosgene oxime, in contrast, 

cause immediate pain or irritation to the eye, 

skin, or respiratory tract. This causes sufficient 

stimulus to decontaminate immediately or to 

mask. 

 Isolated small blisters or a small group of 

blisters suggest possible exposure to mustard, 

to plants such as poison ivy or poison oak, 

drugs, or other substances. The physical 

characteristics of the lesion are not distinctive; 

therefore, the history of exposure is invaluable. 

 Although the blisters of mustard and 

Lewisite are slightly different (there is less 

erythema around the Lewisite blister), this 

information is of little value in individual cases. 

LABORATORY FINDINGS 

 Leukocytosis occurs during the first day, and 

the magnitude of increase in leukocytes during 

the subsequent days correlates roughly with the 

amount of tissue injury, primarily to skin or 

pulmonary tissue. If systemic absorption is large, 
82 

leukocytes in the peripheral blood will decrease 

beginning on day three to day five; this decrease 

indicates damage to precursor cells in the bloodforming organs. The fall may be precipitate, e.g., 

a decrease of 5000 to 10,000 cells/day. If the 

marrow damage is severe, erythrocytes and 

thrombocytes may later decrease, but the 

casualty usually recovers or dies before this is 

apparent. A leukocyte count of 500 or fewer is a 

sign of an unfavorable prognosis. 

 Signs of a chemical pneumonitis may 

appear within the first 2 to 3 days after inhalation 

exposure. Leukocytosis, fever, and sputum 

production suggest a bacterial process, but 

within this time period sputum cultures are 

usually negative for pathogens. Organisms 

commonly invade the damaged airway tissue at 

days 3 to 5. A change in the fever pattern, an 

increase in leukocytosis, and a change in the 

character of the sputum in this time period 

suggest a bacterial process. Sputum Gram Stain 

and culture should be done for identification of 

the specific organism. 

 Damaged skin should be cultured routinely, 

particularly if there is an increase in the exudate 

or in the inflammatory reaction. 

 Although GI bleeding is unusual, declining 

hematocrit values should prompt serial analyses 

of stool for occult blood. 
83 

 Thiodiglycol, a urinary metabolite of sulfur 

mustard, can be measured by the Army Medical 

Laboratory (AML) that will be deployed. There is 

no clinical laboratory test for mustard in blood or 

tissue, nor is one expected, since mustard is 

biotransformed and bound to tissues within 

minutes after absorption. However, ways to 

measure blood and tissue adducts produced in 

the body after reaction with sulfur mustard are 

being studied. 

MEDICAL MANAGEMENT

 The management of a patient exposed to 

mustard may be simple, as in the provision of 

symptomatic care for a sunburn-like erythema, 

or extremely complex, as in providing total 

management for a severely ill patient with burns, 

immunosuppression, and multi-system 

involvement. Suggested therapeutic measures 

for each organ system are provided below. 

Guidelines for general patient care are not 

intended to take the place of sound clinical 

judgment, especially in the management of 

complicated cases. 

Skin. Erythema should be treated with 

calamine or other soothing lotion or cream (e.g., 

0.25% camphor and menthol, calamine) to 

reduce burning and itching. Small blisters (under 

1-2 cm) should be left intact, but because larger 
84 

ones will eventually break (the blister fluid does 

not contain mustard), they should be carefully 

unroofed. Denuded areas should be irrigated 

three to four times daily with saline, another 

sterile solution, or soapy water and then liberally 

covered with a topical antibiotic such as silver 

sulfadiazine or mafenide acetate to a thickness 

of 1-2 mm. If an antibiotic cream is not available, 

sterile petrolatum will be useful. Modified Dakins 

solution (sodium hypochlorite) was used in WWI 

and in Iranian casualties for irrigation and as an 

antiseptic. 

 Multiple or large areas of vesication suggest 

the need for hospitalization and whirlpool bath 

irrigation. 

 Systemic analgesics should be used 

liberally, particularly before manipulation of the 

patient or irrigation of the burn areas. Systemic 

antipruritics such as trimeprazine should be tried 

if needed. Monitoring of fluids and electrolytes is 

important in any sick patient, but it must be 

recognized that fluid loss is not of the magnitude 

seen with thermal burns. Clinicians accustomed 

to treating patients with thermal burns must 

resist the temptation to over-hydrate a mustard 

casualty with a similar amount of burned body 

surface. 

Eyes. Conjunctival irritation from a low Ct 

will respond to any of a number of available 
85 

ophthalmic solutions after the eyes are 

thoroughly irrigated. Regular application of 

homatropine (or other anticholinergic drug) 

ophthalmic ointment will reduce or prevent future 

synechiae formation. A topical antibiotic applied 

several times a day will reduce the incidence 

and severity of infection. Vaseline or a similar 

substance should be applied to the edges of the 

lids regularly to prevent them from sticking 

together. This prevents adhesions and later 

scarring during healing and also permits 

drainage of any underlying infection or pus. 

Topical analgesics may be useful initially if 

blepharospasm is too severe to permit an 

adequate examination, but topical analgesics 

should otherwise be avoided, and systemic 

analgesics should be given for eye pain. Topical 

steroids are not of proven value, but their use 

during the first day or two might reduce 

inflammation. Further use should be relegated to 

an ophthalmologist. Sunglasses may reduce 

discomfort from photophobia. 

 The patient should be constantly reassured 

that complete healing and restoration of vision 

will be the outcome. 

Pulmonary. Upper airway symptoms (sore 

throat, nonproductive cough, and hoarseness) 

may respond to steam inhalation and cough 

suppressants. Although a productive cough and 

dyspnea accompanied by fever and leukocytosis 
86 

occurring 12 to 24 hours after exposure may 

suggest a bacterial process to the clinician, he 

must resist the urge to use antibiotics for this 

process, which in fact is a sterile bronchitis or 

pneumonitis. Infection often occurs on about the 

third day. Its presence is signaled by an 

increased fever, an increase in the pulmonary 

infiltrate by x-ray, and an increase in sputum 

production and a change in sputum character to 

purulent. Appropriate antibiotic therapy should 

await confirmation of the clinical impression by 

positive sputum studies (Gram stain and 

culture). 

 Intubation should be performed early, before 

laryngeal spasm or edema makes it difficult or 

impossible. Intubation permits better ventilation 

and facilitates suction of the necrotic and 

inflammatory debris. Oxygen may be needed, 

and early use of PEEP or CPAP may be of 

benefit. If there is a suggestion of 

pseudomembrane formation, bronchoscopy 

should be done to permit suctioning of the 

necrotic debris by direct vision. 

 Bronchodilators may be of benefit for 

bronchospasm. If they fail, steroids may be tried. 

There is little evidence that the routine use of 

steroids is beneficial. The need for continuous 

use of assisted or controlled ventilation suggests 

a poor prognosis. 
87 

 Death often occurs between the fifth and 

tenth day after exposure because of pulmonary 

insufficiency and infection complicated by a 

compromised immune response from agentinduced bone marrow damage. 

Gastrointestinal. Atropine (0.4-0.6 mg, IM 

or IV), another anticholinergic drug or antiemetic 

should control the early nausea and vomiting. 

Prolonged vomiting or voluminous diarrhea 

beginning days after exposure suggests direct 

involvement of the GI tract by severe systemic 

poisoning, a poor prognostic sign. 

Bone marrow. Sterilization of the gut by 

nonabsorbable antibiotics should be considered 

to reduce the possibility of sepsis from enteric 

organisms. Cellular replacement (bone marrow 

transplants or transfusions) may be successful, 

as intact mustard does not persist beyond the 

few minutes following absorption and would not 

damage the new cells. 

General. A patient severely ill from mustard 

poisoning requires the general supportive care 

provided for any severely ill patient, as well as 

the specific care given to a burn patient. Liberal 

use of systemic analgesics and antipruritics, as 

needed, maintenance of fluid and electrolyte 

balance, and other supportive measures are 

necessary. Parenteral food supplements 

including vitamins may also be helpful. 
88 

Other. Sulfur donors such as sodium 

thiosulfate decreased systemic effects and 

elevated the LD50 when given before exposure 

or within 20 minutes after exposure in 

experimental animals. Activated charcoal given 

orally to casualties was of no value. 

Hemodialysis was not only ineffective, but 

actually harmful in several casualties. The rapid 

biotransformation of the mustard molecule 

suggests that none of these measures would be 

beneficial hours or days after exposure. 

TRIAGE 

 Most mustard casualties will be triaged as 

delayed. Those with skin lesions covering 

several percent to 50% of the BSA will require 

further medical care but do not need immediate 

lifesaving assistance. (In contrast, patients with 

thermal burns covering 20 to 70% of their BSA 

are considered immediate because of their fluid 

requirements.) Those with mild to moderate 

pulmonary effects will also eventually require 

further care but are not in the immediate 

category for triage. Eye injuries from other 

causes require immediate care, but by the time 

the mustard eye lesion develops, there is no 

possibility of reducing the injury. These 

casualties are also in the delayed category. 
89 

 Patients with skin lesions covering a small 

percentage of BSA (under 5%) when the lesions 

are not in vital areas (a burn on the face might 

prevent mask donning) are triaged as minimal. 

Clinical judgment should dictate whether these 

patients should be evacuated for care or 

whether they can return to duty. The tactical 

situation will also be a factor in the decision. 

Patients with minor eye injuries to include 

irritation and reddening can be treated and 

returned to duty. Those with slight upper 

respiratory complaints of a hacking cough and 

an irritated throat that developed 12 hours or 

longer after exposure might be given 

symptomatic therapy and returned to duty. 

 The only mustard casualties that might be 

triaged as immediate are those with moderately 

severe to severe pulmonary signs and 

symptoms. Two factors should temper this 

decision. First, casualties who develop severe 

pulmonary effects within four to six hours of 

exposure will probably not survive despite 

maximal medical care, and it might be better to 

expend limited medical resources elsewhere. 

Second, if evacuation to a maximal medical care 

facility is required, the casualty may survive the 

lengthy trip, but during the delay, his lesion may 

progress to an irreversible stage. 

 A mustard casualty who has severe 

pulmonary effects that developed within four to 
90 

six hours of exposure should be triaged as 

expectant. A casualty who has over 50% BSA 

burns from mustard liquid might also be 

categorized as expectant, but this decision 

would depend on available medical resources at 

the far rear echelons of medical care. (The LD50

for liquid mustard is about 7 grams, or between 

1 and 11⁄2 teaspoons of liquid. This amount will 

cover about 25% BSA, so an individual with a 

50% BSA burn could possibly have 2 LD50s on 

his skin. This person might be saved, but at 

great expenditure of medical resources.) 

RETURN TO DUTY 

 Casualties with minor skin, eye, or 

pulmonary injuries might be returned to duty as 

soon as they are given symptomatic therapy at a 

medical facility. The range of return to duty times 

for those with more severe but treatable injuries 

is from one week to a year or longer. 

 Those with eye injuries should recover in 

one to three weeks, except for the low 

percentage of casualties with severe injuries or 

complications. Casualties with mild to moderate 

pulmonary injuries should return to duty in a 

week to a month. Healing of mild skin lesions 

will enable the casualty to return within several 

weeks, but patients with large skin lesions will 

require hospitalization for many months. 
91 

LONG-TERM EFFECTS 

 Repeated symptomatic exposures to 

mustard over a period of years (as in 

manufacturing workers) seem to be well 

established as a causal factor in an increased 

incidence of upper airway cancer. However, the 

association between a single exposure to 

mustard and airway cancer is not well 

established. A single, severe exposure to 

mustard may have contributed to other airway 

problems, such as chronic bronchitis, based on 

WWI data. A new complication seen in Iranian 

casualties from the Iran-Iraq War in the 1980s 

was late-onset tracheobronchial stenosis, which 

presumably would have been seen in WWI 

casualties had antibiotic therapy been available 

to allow those who died from secondary 

bacterial pneumonia to survive. 

 Several eye diseases, such as chronic 

conjunctivitis and delayed keratitis, may follow a 

single, severe exposure of the eye to mustard. 

Skin scarring and pigment changes may follow a 

severe skin lesion from mustard; cancer 

sometimes develops in scarred skin. 

 Mustard is classed as a mutagen and 

carcinogen, based on laboratory studies. 

However, there are no data to implicate mustard 

as a reproductive toxin in man, and there is no 
92 

evidence that mustard is a causative factor in 

nonairway, non-skin cancer in man. 

Supplemental Considerations for 

Treatment and Disposition Written for 

Iraqi Freedom War Effort 

 In addition to the treatment modalities listed 

in the references above, there has been ongoing 

animal research dealing with the management of 

mustard injuries and observation of accidents 

that have occurred with sulfur mustard in the 

U.S. and abroad. (We do not have major human 

experience dealing with mustard casualties 

other than WWI and the Iran/Iraq conflict in the 

1980s. It is unethical to perform human mustard 

injury research.) 

 A. Eye. 

 Research at the U.S. Army Medical 

Research Institute of Chemical Defense 

(USAMRICD) with rabbits exposed to sulfur 

mustard showed remarkable results using 

steroids and antibiotic eye combinations. Eyes 

that would have been all but destroyed 

appeared almost normal when these 

combinations were applied early and frequently. 

In the study, they were given both by injection 

and topically in the form of solutions and 

ointments. These results were so remarkable 

that it was recommended this past year that 
93 

commercially available ophthalmologic 

steroid/antibiotic solutions or ointments be 

added to the field medical sets. Recommended 

use would be as soon as possible in connection 

with even the mildest mustard eye injury. The 

frequency of use would be every one to two 

hours until the full extent of the developing 

mustard injury became known. The treatment 

would then be modified accordingly, with 

consultation and examination by an 

ophthalmologist at the earliest time possible. 

This initial treatment would be applied only in the 

absence of a penetrating injury to the eye or in 

the case of obvious, secondary bacterial 

infection. Eye pain could be severe enough to 

require narcotic analgesia. 

 Exposure to sulfur mustard can lead to a 

chronic eye inflammation with associated pain, 

erosions, and even frank ulceration. This 

keratitis has been seen to develop as early as 8 

months and as late as 20 years after initial 

exposure. It does not seem to be associated 

with severity of exposure, although one would 

suspect a higher incidence with more severe 

exposures. Mustard-induced chronic keratitis 

was either infrequent or undetected in the years 

following WWI. 

 
94 

B. Lung. 

 No specific antidotes for mustard injury to 

the lung exist; however, a tremendous amount 

of supportive care is available for all pulmonary 

injuries. 

 Mustard lung injuries in the trachea and 

bronchi have a high rate of secondary bacterial 

infection starting as early as three days and 

developing as late as two to three weeks after 

exposure. The late development is especially 

frequent with doses leading to significant bone 

marrow depression. Prophylactic administration 

of antibiotics is contraindicated and will lead to 

the selection of resistant bacterial infections. 

Vigilant watch for the earliest signs and 

symptoms of infection with Gram stain and 

cultures to help choose the most appropriate 

antibiotic are the watch words. 

 The sloughing of the necrotic bronchial 

mucosa, pseudomembranes, either as 

amorphous debris or as pseudomembranes, can 

be severe enough to cause mechanical 

blockage and suffocation. Treatment is rigorous 

percussion and postural drainage and provision 

of humidified air with supplemental moisturized 

air/oxygen. At times, fiberoptic bronchoscopy 

may be needed to remove the blockage. 

Warfighters in WWI died from these blockages. 
95 

 A complication not reported from WWI, but 

seen in casualties from the Iran/Iraq War in the 

1980s, was severe tracheobronchial stenosis, 

which may be irreversible. Bronchospasm with 

asthma-like symptoms can be a frequent 

complication of the mustard lung injury. The 

medicines used for the bronchospasm are the 

same as in asthma: beta- adrenergic dilators, 

steroids, and theophylline-type drugs. 

 Steroidal anti-inflammatory agents have 

never been shown scientifically to be beneficial 

in cases of mustard lung injury. However, if beta 

adrenergic bronchodilators are not providing 

complete relief, many physicians would be quick 

to add steroids to aid in breaking the 

bronchospasm. Again, caution is warranted 

because of the likelihood of secondary bacterial 

infection in cases of exposure to sulfur mustard. 

 With significant irritation to the larynx, acute 

closure caused by laryngospasm is possible and 

could result in death if a patent airway is not 

maintained. 

 Pulmonary edema is not a normal feature of 

the mustard lung injury, except in the case of 

very large exposures where hemorrhagic 

pulmonary edema may be seen. 
96 

 Mounting circumstantial evidence suggests 

the possibility of chronic bronchial disease 

developing after significant pulmonary exposure. 

 Mustard is a proven carcinogen, but no 

cases of cancer have been documented with 

acute exposures. However, some factory 

workers chronically exposed to low doses of 

sulfur mustard in WWI developed cancers of the 

respiratory tract (nasopharynx, larynx, and lung). 

 A small amount of laboratory data in rats 

and mice exists pointing to reproductive 

abnormalities. Anecdotal stories are now coming 

out of Iran and Iraq that will take years to 

substantiate if good epidemiological studies are 

performed. 

 The possibility of a causal link between 

mustard exposure and late onset or chronic 

health effects should always be investigated in 

patients with a documented or suspected history 

of exposure. 

 C. Skin. 

 In general, mustard skin burns are more 

superficial than thermal burns, but the services 

of an intensive care unit or surgical burn unit can 

easily be a necessity. Judicious IV fluid and 

electrolyte therapy are required with significant 

mustard skin burns, but fluid requirements are 
97 

less than with corresponding thermal burns. 

Fluids and electrolytes should be closely 

monitored, as fluids may be lost to edematous 

areas, with resultant dehydration. Medical 

personnel are cautioned not to over-hydrate the 

patient, as hypervolemia and pulmonary edema 

can be iatrogenically induced in mustard 

casualties. The exact fluid replacement 

requirements for cutaneous mustard injuries 

should be based on patient status and 

considered on a case-by-case basis. 

 Vesication may take several days to 

complete. Mustard blister fluid does NOT 

contain active sulfur mustard. Once a patient 

has been adequately decontaminated, medical 

personnel do not have to fear contamination. 

 Multiple techniques exist for caring for the 

mustard skin burns/blisters/wounds: (1) leaving 

the blisters intact; (2) removing/debriding the 

roof of large blisters; (3) leaving the blister roof 

intact with sterile needle aspiration of the fluid; 

and (4) removing the blister roof with temporary 

placement of artificial or pig skin. A universal 

measure is the use of a topical antibiotic cream 

or ointment whether the blister is intact or not. 

The topical antibiotic depends on individual 

experience and preference, starting with 

traditional surgical preparations and working 

down to whatever is available. A moist woundhealing environment should be maintained 
98 

during the re-epithelialization process for optimal 

outcome. Initially, the attachment of the 

neoepidermis to the underlying dermis may be 

weak, and protective dressings may be needed 

to avoid or minimize damage as a result of 

friction with clothing or bedding. 

Mustard skin wounds can easily develop a 

secondary bacterial cellulitis requiring the use of 

appropriate systemic antibiotics. We have been 

impressed by the tremendous inflammation 

caused by sulfur mustard in human skin. To the 

uneducated eye, this can easily be confused 

with bacterial cellulitis. Infection surveillance and 

specialty consultation may be necessary. 

 Mustard casualties with skin injury may 

require narcotics for analgesia. 

 It has long been recognized that mustard 

skin wounds are slow to heal, taking sometimes 

twice the time that would be expected with a 

conventional wound or a thermal burn. The 

hypothesis explaining these observations is that 

abnormal compounds of DNA (DNA adducts) 

are produced, delaying the healing time. Also, 

the skin histologically very often looks more like 

scar tissue than normal skin. Recent studies in 

the U.S. (USAMRICD) and England (Porton 

Down) have shown that appropriate 

debridement of the deeper mustard burns leads 

to more normal healing times and return to 
99 

regular skin architecture. Good results were 

obtained with both laser debridement and 

traditional mechanical techniques. Accurate 

depth assessment is important, because it 

dictates how aggressive treatment needs to be 

to minimize or prevent cosmetic and functional 

deficits (e.g., deep injuries will need to be 

excised and grafted). Microcutaneous blood flow 

is a good prognostic indicator and should be 

monitored using laser Doppler perfusion imaging 

or indocyanine green fluorescence imaging, if 

available. 

 Surgeons are encouraged to contact the 

USAMRICD or the U.S. Army Institute of 

Surgical Research (ISR). 

D. Bone Marrow. 

 Sulfur mustard, like nitrogen mustard and 

certain chemotherapeutic compounds, is an 

alkylating agent. Systemic absorption of sulfur 

mustard usually above what would be 25% of a 

lethal dosage can lead to significant bone 

marrow depression. This is why the systemic 

effects of sulfur mustard sometimes have been 

described as radiomimetic. The earliest indicator 

that a patient may have received a significant 

systemic exposure is nausea and vomiting 

persisting longer than the first hour or two after 

exposure. Nausea and vomiting 24 hours later is 

definitely a warning sign. The next most 
100 

sensitive indicator is a fall in the lymphocyte 

count; this lymphopenia may occur as early as 

the first 24 hours. The polymorphonuclear cell 

count may actually rise in the first 24 hours. 

Other cellular components of blood may show a 

significant decline as early as three days after 

exposure, and patients can be in profound 

marrow suppression by one to three weeks 

following exposure. The usual life- threatening 

complication is sepsis and septic pneumonia. 

Transfusions, isolation techniques, hormonal 

stimulation of the marrow and appropriate 

antibiotics may all be utilized. 

 Studies in the non-human primates 

conducted by the Navy using nitrogen mustard 

and by the Army with sulfur mustard showed an 

improved bone marrow recovery time using 

granulocyte colony stimulating factor (GCSF). 

GCSF is a commercially available product for 

use in more standard cases of marrow 

suppression. Physicians are encouraged to 

contact the USAMRICD should the need arise. 

E. Gastrointestinal. 

 Severe hemorrhagic diarrhea may be 

caused either by direct ingestion of sulfur 

mustard or by systemic absorption following 

exposure by other routes. High doses of sulfur 

mustard can induce a necrosis and sloughing of 

the gastrointestinal mucosa. The most important 
101 

aspect of treatment is IV fluids and electrolytes. 

Anticholinergics to control bowel spasm and 

possibly narcotic analgesia are indicated as long 

as an acute surgical abdomen is not a 

complication. Hemorrhage could be severe 

enough to require transfusion. 

 F. Central Nervous System. 

 In the first few hours of exposure to sulfur 

mustard, patients can experience mood swings 

ranging from depression to euphoria. The 

mechanism for these mood changes is not 

understood. Supportive care is indicated. 

 A few individuals in WWI who received 

massive exposures to sulfur mustard 

experienced seizures and died rapidly. This 

same phenomenon has been observed in 

animals. 

I. Guidelines for Return to Duty

 Due to the slow healing properties of sulfur 

mustard injuries, any casualties with significant 

injury to the eyes, respiratory tract, skin, GI tract, 

or CNS will not be returning to duty for weeks to 

months. 

 
102 

A. Eye. 

 Only the mildest eye irritations to sulfur 

mustard, those requiring perhaps only soothing 

eye drops, will be able to return to duty. The 

mildest form of conjunctivitis causes a functional 

blindness from pain, photophobia, and spasm of 

the eyelid muscles; this conjunctivitis takes an 

average of two weeks to resolve. As the severity 

of the injury increases, so does the time for 

healing. A moderate conjunctivitis may require a 

full two months before return to duty is possible. 

In a few rare instances, blindness may result 

from severe exposures. 

 B. Lung. 

 

 Only those individuals experiencing an 

irritation without significant tissue injury will be 

able to return to duty. Determining who has 

received only an irritation or the mildest of 

injuries will require observation from three to 

seven days. Anyone with documented mustard 

lung injury producing a bronchial pneumonia or 

pseudomembrane formation will not be able to 

return to duty for several months. Severe cases 

may never return to duty. 
103 

 C. Skin. 

 Only small percentage surface areas (less 

than 5%) in non-critical areas will be able to 

return to duty following treatment with topical 

antibiotic, dressings, and oral analgesics. Burns 

to the hands, feet, face, axillae, and groin are all 

potentially disabling. (A recent accident victim 

required hospitalization in a burn center for 

burns on the left arm and left leg amounting to 

6% body surface area. The disability caused by 

this injury for such a relatively small surface area 

was striking.) 

Return to duty will require weeks to months 

in all but the mildest of injuries. 

 Burns by liquid on the skin and in the eye 

cause the most severe injury. It is possible in 

some instances to receive a nearly total body 

burn with mustard vapor with effects no more 

severe than those from a second-degree 

sunburn. A vapor burn of this milder level of 

severity would take 48 hours or more to develop. 

However, a vapor burn developing in only a few 

hours could be as severe as a liquid burn. 

Severity of a mustard burn is dependent upon 

the total absorbed dose of vapor and liquid. 
104 

II. Guidelines for Medical Evacuation to 

Either Landstuhl, Germany or CONUS. 

 

 A casualty that requires hospital care for 

longer than two weeks, specialty care not 

available in theater, or intensive care or burn 

center-level treatment should be medically 

evacuated as soon as feasible. 

III. Physical Examination, Laboratory, and 

Procedures at Medical Center. 

 These recommendations pertain ONLY to 

patients requiring evacuation to the MEDCEN 

level of care. 

 There should be a full, appropriate internal 

medicine, dermatology, ophthalmology, or burn 

surgical examination on admission and 

documentation. Serial evaluations should focus 

on any abnormalities until these abnormalities 

have resolved with time and appropriate 

treatment. Patients with injury involving specific 

organ systems (for example the eyes, 

respiratory tract, GI tract, blood, or CNS) should 

at a minimum receive consultative care by the 

appropriate specialists. 

 Return to duty should be delayed until after 

full recovery. Temporary duties during 

convalescence should be appropriate to the 
105 

patient’s condition while awaiting full return to 

duty or medical retirement. 

 After full recovery, the patient should have 

follow-up evaluations every six months with 

appropriate studies for specific injuries. If 

problems are found at follow-up visits, 

appropriate care should be given with return 

visits as frequently as necessary. Once a 

patient has had two six-month follow-up visits 

without problems arising, he or she should start 

annual follow-up visits for five years. Any 

associated medical problems will extend the 

period of close follow-up until complete 

resolution or maximal medical improvement. 

Once a patient goes five years without related 

medical problems, he or she may be discharged 

to an as-indicated, follow-up status. 

 All patients should have access to military or 

veterans’ health care for life for effects of 

exposure to sulfur mustard. 

 Patients with a mustard eye injury should 

have ophthalmology evaluations every five years 

(and more frequently as necessary) for the rest 

of their lives. 

 Patients with mustard lung injury to the 

respiratory tract (including any of the 

nasopharynx, larynx, trachea, and lung) should 
106 

have a pulmonary evaluation as indicated, but at 

least every five years, for life. 

 Patients who have recovered from 

pancytopenia caused by sulfur mustard should 

have a hematology evaluation as indicated, but 

at least every five years, for life. 
107 

LEWISITE 

L 

SUMMARY 

Signs and Symptoms: Lewisite causes 

immediate pain or irritation of skin and mucous 

membranes. Erythema and blisters on the skin 

and eye and airway damage similar to those 

seen after mustard exposures develop later. 

Field Detection: M256A1 kit, M18A2 chemical 

agent detector kits; Individual Chemical Agent 

Alarm (ICAM), M90 chemical agents detector, 

M8 and M9 chemical agent detector paper, M21 

Remote Sensing Chemical Agents Alarm 

(RSCAAL), M93A1 FOX NBC 

RECONNAISSANCE System, M272 Chemical 

water testing kit, M22 Automatic Chemical Agent 

(ACADA) Detection Alarm. 

Decontamination: M291, soap and water, 

0.5% bleach solution. 

Management: Immediate decontamination; 

symptomatic management of lesions the same 

as for mustard lesions; a specific antidote (BAL) 

will decrease systemic effects. 
108 

OVERVIEW 

 Lewisite is a vesicant that damages the 

eyes, skin, and airways by direct contact. After 

absorption, it causes an increase in capillary 

permeability to produce hypovolemia, shock, 

and organ damage. Exposure to Lewisite 

causes immediate pain or irritation, although 

lesions require hours to become full-blown. 

Management of a Lewisite casualty is similar to 

management of a mustard casualty, although a 

specific antidote, British Anti-Lewisite (BAL, 

dimercaprol), will alleviate some effects. 

HISTORY/MILITARY RELEVANCE 

 Dr. Wilford Lee Lewis first synthesized 

Lewisite in 1918, but production was too late for 

its use in WWI. It has not been used in warfare, 

although some countries may stockpile it. 

Lewisite is sometimes mixed with mustard to 

achieve a lower freezing point of the mixture for 

ground dispersal and aerial spraying. 

PHYSIOCHEMICAL CHARACTERISTICS 

 

 Lewisite is an oily, colorless liquid with the 

odor of geraniums. It is more volatile than 

mustard. 
109 

DETECTION AND PROTECTION 

 The immediately-dangerous-to-life-andhealth (IDLH) concentration of Lewisite (L) is 

0.003 mg/m3

. The M8A1 automatic chemicalagent detector alarm is incapable of detecting 

Lewisite. However, liquid Lewisite turns M8 

paper a ketchup red, and M9 paper will turn 

pink, red, reddish-brown, or purple when 

exposed to liquid nerve agents or vesicants, but 

does not specifically identify either the class of 

agent or the specific agent. The detectors in the 

chart below can detect Lewisite (L) at the 

threshold limits given. 

DETECTOR L 

M256A1 14.0 mg/min3

M272 (in water) 2.0 mg/min3

M18A2 Kit 10.0 mg/min3

M21 (RSCAAL) 150.0 mg/min3

M90 0.2 mg/min3

M93A1 Fox 10 - 100 mcg/l 

ICAM 2.0 mg/min3
110 

 Because the odor of Lewisite may be faint or 

lost after accommodation, olfactory detection of 

the odor of geraniums is not a reliable indicator 

of Lewisite exposure. The activated charcoal in 

the canister of the chemical protective mask 

adsorbs Lewisite, as does the charcoal in the 

chemical protective overgarment. Lewisite 

attacks the butyl rubber in the chemical 

protective gloves and boots, which nevertheless 

are expected to protect against field 

concentrations of Lewisite until they can be 

exchanged for fresh gloves and boots. Proper 

wear of the chemical protective mask and 

chemical protective ensemble affords full 

protection against Lewisite. 

MECHANISM OF TOXICITY 

Lewisite is readily absorbed from the skin, 

eyes, and respiratory tract, as well as by 

ingestion and via wounds. It is systemically 

distributed to almost all organs and tissues of 

the body where it participates in a variety of 

chemical reactions. It is eventually eliminated 

primarily as reaction products in the urine. 

TOXICITY 

 Lewisite causes nasal irritation at a Ct of 

about 8 mg-min/m3

, and its odor is noted at a Ct 

of about 20 mg-min/m3

. Lewisite causes 

vesication and death from inhalation at the same 
111 

Ct as mustard. Liquid Lewisite causes vesication 

at about 14 mcg, and the LD50 of liquid Lewisite 

applied to the skin is about 2.8 grams. 

TOXICODYNAMICS 

(MECHANISM OF ACTION) 

 Although Lewisite contains trivalent arsenic 

and combines with thiol groups in many 

enzymes, its exact mechanism of biological 

activity is unknown. 

CLINICAL EFFECTS 

Organ Systems. Unlike mustard, Lewisite 

vapor or liquid causes immediate pain or 

irritation. A person with a droplet of Lewisite on 

his skin will note the burning and will 

immediately take steps to try and remove it. The 

vapor is so irritating that a person will seek to 

mask or leave the contaminated area if possible. 

Because this warning causes the person 

exposed to take immediate steps to 

decontaminate, the Lewisite lesion will probably 

not be as severe as the lesion from mustard, 

since exposure to mustard is often undetected 

and decontamination is not done. 

 There are almost no data on humans 

exposed to Lewisite. The following information is 

based on animal investigations. 
112 

Skin. Within about five minutes after 

contact, liquid Lewisite will produce a grayish 

area of dead epithelium. Erythema and blister 

formation follow more rapidly than in a similar 

lesion from mustard, although the full lesion 

does not develop for 12 to 18 hours. The lesion 

has more tissue necrosis and tissue sloughing 

than does a mustard lesion. 

Eye. Lewisite causes pain and 

blepharospasm on contact. Edema of the 

conjunctiva and lids follows, and the eyes may 

be swollen shut within an hour. Iritis and corneal 

damage may follow if the dose is high. Liquid 

Lewisite causes severe eye damage within 

minutes of contact. 

Respiratory. The extreme irritancy of 

Lewisite to the nasal area and upper airways 

causes the person to mask or exit the area. 

Scanty data indicate that Lewisite causes the 

same airway signs and symptoms as mustard. 

The airway mucosa is the primary target, and 

damage progresses down the airways in a dosedependent manner. Pseudomembrane formation 

is prominent. Pulmonary edema, which occurs 

rarely and usually only to a minimal degree after 

mustard exposure, may complicate exposure to 

Lewisite. 

Other. Available data suggest that Lewisite 

causes an increase in permeability of systemic 
113 

capillaries with resulting intravascular fluid loss, 

hypovolemia, shock, and organ congestion. This 

may lead to hepatic or renal necrosis with more 

prominent GI effects (including vomiting and 

diarrhea) than after mustard. 

Physical Findings. The findings are similar 

to those caused by mustard. As noted, the 

tissue damage at the site of the skin lesion may 

be more severe. 

TIME COURSE OF EFFECTS 

 Pain and irritation from either liquid or vapor 

Lewisite are immediate. Early tissue destruction 

is more obvious than after mustard, but the 

lesion is not full-blown for 12 hours or longer. 

DIFFERENTIAL DIAGNOSIS 

 Although differences have been reported 

between the skin lesions from mustard and 

Lewisite (less surrounding erythema and more 

tissue destruction characterize Lewisite blisters), 

these are of little diagnostic assistance in a 

single patient. The history of immediate pain on 

contact is absent after mustard exposure and 

present after Lewisite or phosgene oxime 

exposures. 
114 

 Other substances cause erythema and 

blisters, and often the history of exposure is the 

most helpful tool in diagnosis. 

LABORATORY FINDINGS 

 There is no specific diagnostic test for 

Lewisite. Leukocytosis, fever, and other signs of 

tissue destruction will occur. 

MEDICAL MANAGEMENT 

 Early decontamination is the only way of 

preventing or lessening Lewisite damage. Since 

this must be accomplished within minutes after 

exposure, this is self-aid rather than medical 

management. 

 The guidelines for the management of a 

mustard casualty will be useful. Lewisite does 

not cause damage to hematopoietic organs as 

mustard does; however, fluid loss from the 

capillaries necessitates careful attention to fluid 

balance. 

 BAL was developed as an antidote for 

Lewisite and is used in medicine as a chelating 

agent for heavy metals. There is evidence that 

BAL in oil, given intramuscularly, will reduce the 

systemic effects of Lewisite. However, BAL itself 

causes some toxicity, and the user should read 
115 

the package insert carefully. BAL skin and 

ophthalmic ointment decreases the severity of 

skin and eye lesions when applied immediately 

after early decontamination; however, neither is 

currently manufactured. 

TRIAGE 

 Casualties should be triaged using the 

guidelines for triage of mustard patients. 

RETURN TO DUTY 

 Casualties with minor skin lesions who 

receive symptomatic therapy can be returned to 

duty quickly. Because Lewisite generally causes 

more tissue damage than mustard, casualties 

with eye and larger skin lesions should be 

triaged as delayed and evacuated. Whether to 

triage those with pulmonary injury as immediate, 

delayed, or expectant depends on the severity of 

the injury and how quickly after exposure it 

occurred. 
116 

PHOSGENE OXIME 

CX 

SUMMARY 

Signs and Symptoms: Immediate burning and 

irritation followed by wheal-like skin lesions and 

eye and airway damage.

Field Detection: M256A1 and M18A2 chemical 

agent detector kits; M90 chemical agent 

detector, M93A1 FOX NBC 

RECONNAISSANCE SYSTEM. 

Decontamination: M291, soap and water, 

0.5% bleach solution.

Management: Immediate decontamination, 

symptomatic management of lesions. 

 
117 

OVERVIEW 

 Phosgene oxime (CX) is an urticant or nettle 

agent that causes a corrosive type of skin and 

tissue lesion. It is not a true vesicant since it 

does not cause blisters. The vapor is extremely 

irritating, and both the vapor and liquid cause 

almost immediate tissue damage upon contact. 

There is very scanty information available on 

CX. 

MILITARY SIGNIFICANCE 

 There is no current assessment of the 

potential of CX as a military threat agent. 

PHYSIOCHEMICAL CHARACTERISTICS 

 Phosgene oxime is a solid at temperatures 

below 95o

F/35oC, but the vapor pressure of the 

solid is high enough to produce symptoms. 

Traces of many metals cause it to decompose; 

however, it corrodes most metals. 

DETECTION AND PROTECTION 

 The IDLH concentration of CX has not been 

defined. The M272 water testing kit, MINICAMS, 

ICAD, M21 remote sensing alarm, CAM, 

ACAMS, DAAMS, and M8A1 automatic 

chemical agent detector alarm are incapable of 

detecting CX. Likewise, M8 and M9 paper 
118 

should not be depended upon to detect this 

agent. The M256A1 detector ticket reacts to the 

presence of CX, but the detection threshold is 

not known with certainty. The detectors in the 

following chart are capable of detecting CX at 

the threshold limits given. 

DETECTOR CX 

M18A2 0.5 mg/min3

M90 0.15 mg/min3

M93A1 Fox 10 - 100 mcg/l 

 Because the odor of phosgene may be faint 

or lost after accommodation, olfactory detection 

of a pepperish or pungent odor is not a reliable 

indicator of the presence of CX. The activated 

charcoal in the canister of the chemical 

protective mask adsorbs CX, as does the 

charcoal in the chemical protective overgarment. 

Phosgene oxime may attack the butyl rubber in 

the chemical protective gloves and boots, which 

nevertheless are expected to protect against 

field concentrations of CX until they can be 

exchanged for fresh gloves and boots. Proper 

wear of the chemical protective mask and 

chemical protective ensemble affords full 

protection against CX. 
119 

MECHANISM OF TOXICITY 

 The toxicokinetics of CX are not known in 

detail. Penetration of exposed surfaces is rapid, 

and systemic distribution to most organs and 

tissues, including the GI tract, is probably 

important. 

TOXICITY 

 The estimated LCt50 by inhalation is 1500-

2000 mg·min/m3

. The LD50 for skin exposure has 

been estimated as 25 mg/kg. 

TOXICODYNAMICS 

(MECHANISM OF ACTION) 

 The mechanism by which CX causes 

biological effects is unknown. 

CLINICAL EFFECTS 

Skin. Phosgene oxime liquid or vapor 

causes pain on contact, which is followed in turn 

by blanching with an erythematous ring in 30 

seconds, a wheal in 30 minutes, and necrosis 

later. The extreme pain may persist for days. 

Eye. Phosgene oxime is extremely painful 

to the eyes. The damage is probably similar to 

that caused by Lewisite. 
120 

Pulmonary. Phosgene oxime is very 

irritating to the upper airways. This agent causes 

pulmonary edema after inhalation and after skin 

application. 

Other. Some animal data suggest that CX 

may cause hemorrhagic inflammatory changes 

in the GI tract. 

TIME COURSE OF EFFECTS 

 Phosgene oxime causes immediate pain 

and irritation to all exposed skin and mucous 

membranes. The time course of damage to 

other tissue probably parallels that of damage to 

the skin. 

DIFFERENTIAL DIAGNOSIS 

 Other causes of urticaria and skin necrosis 

must be considered. Common urticants do not 

cause the extreme pain that CX does. 

LABORATORY FINDINGS 

 There are no distinctive laboratory findings. 
121 

MEDICAL MANAGEMENT 

 Management is supportive. The skin lesion 

should be managed in the same way that a 

necrotic ulcerated lesion from another cause 

would be managed. 

TRIAGE 

 Because of the continuing pain, most 

casualties should be placed in the delayed

category and evacuated. 

RETURN TO DUTY 

 The decision to return a CX casualty to duty 

should be based on healing of the lesion(s) and 

the casualty's freedom from discomfort. 
122 

NERVE AGENTS 

GA, GB, GD, GF, VX 

SUMMARY 

Signs and Symptoms: 

 Vapor: 

Small exposure -- miosis, rhinorrhea, mild 

difficulty breathing. 

 Large exposure -- sudden loss of 

consciousness, convulsions, apnea, flaccid 

paralysis, copious secretions, miosis. 

 Liquid on skin: 

 Small to moderate exposure -- localized 

sweating, nausea, vomiting, feeling of weakness. 

Large exposure -- sudden loss of 

consciousness, convulsions, apnea, flaccid 

paralysis, copious secretions. 

Field Detection: M256A1 chemical agent detector kit, 

M8 chemical agent detector paper, M9 chemical agent 

detector paper; Improved Chemical Agent Alarm (ICAM), 

M93A1 FOX NBC RECONNAISSANCE System, M18A2 

chemical agent detector kit, M21 Remote Sensing 

Chemical Agent Alarm (RSCAAL), M90 chemical agent 

detector, M22 Automatic Chemical Agents Detection 

Alarm (ACADA). 

Decontamination: M291 SDK, soap and water, 0.5% 

Hypochlorate solution. 

Immediate management: Administration of MARK I Kits 

(atropine and pralidoxime chloride); diazepam in addition 

if casualty is severe; ventilation and suction of airways for 

respiratory distress.
123 

OVERVIEW 

 Nerve agents are the most toxic of the 

known chemical agents. They are hazards in 

their liquid and vapor states and can cause 

death within minutes after exposure. Nerve 

agents inhibit acetylcholinesterase in tissue, and 

their effects are caused by the resulting excess 

acetylcholine. 

HISTORY/MILITARY RELEVANCE 

 Nerve agents were developed in pre-WWII 

Germany. Germany had stockpiles of nerve 

agent munitions during WWII but did not use 

them for reasons that are still unclear. In the 

closing days of the war, the U.S. and its allies 

discovered these stockpiles, developed the 

agents, and manufactured nerve agent 

munitions. The U.S. chemical agent stockpile, 

which is in the process of being destroyed, 

contains the nerve agents sarin (GB) and VX. 

 Nerve agents are considered major military 

threat agents. The only known battlefield use of 

nerve agents was in the Iraq-Iran conflict. 

Intelligence analysts indicate that many 

countries have the technology to manufacture 

nerve agent munitions. 
124 

PHYSICAL CHARACTERISTICS 

 Nerve agents are liquids under temperate 

conditions. When dispersed, the more volatile 

ones constitute both a vapor and a liquid hazard. 

Others are less volatile and represent primarily a 

liquid hazard. The "G-agents" are more volatile

than VX. Sarin (GB) is the most volatile, but it 

evaporates less readily than water. GF is the 

least volatile of the G-agents. 

 Nerve agents can be dispersed from 

missiles, rockets, bombs, howitzer shells, spray 

tanks, land mines, and other large munitions. 

DETECTION AND PROTECTION 

 The IDLH concentrations of nerve agents 

are 0.0001 mg/m3 for tabun (GA), 0.0001 mg/m3

for sarin (GB), 0.0003 mg/m3 for soman (GD), 

0.0001 mg/m3 for GF, and 0.0001 mg/m3

 for VX. 

Liquid G agents turn M8 paper a "gold" yellow, 

and VX turns M8 paper a "verdana" or "olive" 

green. M9 paper will turn pink, red, reddish 

brown, or purple when exposed to liquid nerve 

agents or vesicants but does not specifically 

identify either the class of agent or the specific 

agent. 

Because the odor of nerve agents may be 

faint or lost after accommodation, olfactory 

detection of the odor of fruit or fish is not a 
125 

reliable indicator of mustard exposure. The 

activated charcoal in the canister of the chemical 

protective mask adsorbs nerve agents present 

as vapor or gas, as does the charcoal in the 

chemical protective overgarment; and the butyl 

rubber in the chemical protective gloves and 

boots is impermeable to nerve agents. Proper 

wear of the protective mask and the chemical 

protective ensemble affords full protection 

against nerve agents. 
Table: The following detectors have the capacity to detect nerv

threshold limits given. 

Detector 

GA 

(Tabun) 

GB 

(Sarin) 

GD 

(Soman) GF 

M256A1 Unknown 0.05 mg/m3 Unknown UnknowM272 (in water) 0.02 mg/m3 0.02 mg/m3 0.02 mg/m3 M18A2 0.02 mg/m3 M21 RSCAAL 3.0 mg/m3 3.0 mg/m3 3.0 mg/m3M90 0.04 mg/m3 0.04 mg/m3 0.04 mg/m3 0.04 mg/M93A1 Fox 62 mg/m3 0.1-1 mcg/l CAM 0.03 mg/m3 0.03 mg/m3 0.03 mg/m3 0.03 mg/M22 ACADA 0.001 PPM 0.002 PPM 0.002 PPM 
126 

MECHANISM OF TOXICITY 

 Nerve agents are organophosphorus 

cholinesterase inhibitors. They inhibit the 

butyrylcholinesterase in the plasma, 

acetylcholinesterase on the red cell, and 

acetylcholinesterase at cholinergic receptor sites 

in tissue. The three enzymes are not the same; 

even the two acetylcholinesterases have slightly 

different properties, although both have a high 

affinity for acetylcholine. The blood enzymes 

provide an estimate of the tissue enzyme 

activity. After acute exposure to a nerve agent, 

the erythrocyte enzyme activity most closely 

reflects the activity of the tissue enzyme, but 

during recovery the plasma enzyme activity 

more closely parallels tissue enzyme activity. 

 After a nerve agent inhibits the tissue 

enzyme, the enzyme cannot hydrolyze 

acetylcholine, the neurotransmitter, at 

cholinergic receptor sites. Acetylcholine 

accumulates and continues to stimulate the 

affected organ. The clinical effects from nerve 

agent exposure are caused by excess 

acetylcholine. 

 The attachment of the agent to the enzyme 

is permanent (unless removed by therapy). 

Erythrocyte enzyme activity returns at the rate of 

erythrocyte turnover, about 1% per day. Tissue 

and plasma enzyme activities return with 
127 

synthesis of new enzymes. The rate of return of 

the tissue and plasma enzymes is not the same, 

nor is the rate the same for all tissue enzymes. 

However, the agent can be removed from the 

enzyme and the enzyme "reactivated" by 

several types of compounds, the most useful of 

which are the oximes. If the agent-enzyme 

complex has not "aged," oximes are useful 

therapeutically. Aging is a biochemical process 

by which the agent-enzyme complex becomes 

refractory to oxime reactivation of the enzyme. 

For most nerve agents, the aging time is longer 

than the time within which acute casualties will 

be seen. However, the aging time of the GDenzyme complex is about two minutes, and the 

usefulness of oximes in GD poisoning is greatly 

decreased after this period. 

 Organs with cholinergic receptor sites 

include the smooth muscles, skeletal muscles, 

CNS, and most exocrine glands. In addition, 

cranial efferents and ganglionic afferents are 

cholinergic nerves. 

 Muscarine will stimulate some of the 

cholinergic sites, and these are known as 

muscarinic sites. Organs with these sites include 

the smooth muscles and glands. Nicotine will 

stimulate other cholinergic sites, known as 

nicotinic sites, which are those in skeletal 

muscle and ganglia. The CNS contains both 

types of receptors, but the pharmacology in the 
128 

CNS is more complex and less well understood. 

Atropine and similar compounds block the 

effects of excess acetylcholine more effectively 

at muscarinic sites than at nicotinic sites. 

 Some commonly used pesticides (for 

example, the organophosphate [OP] Malathion 

and the carbamate Sevin) and some common 

therapeutic drugs (the carbamates 

pyridostigmine [Mestinon] and physostigmine 

[Antilirium]) also inhibit acetylcholinesterase and 

can be considered "nerve agents." However, 

while the OP pesticides cause the same 

biological effects as nerve agents, there are 

some important differences in the duration of 

biological activity and response to therapy. 

CLINICAL EFFECTS 

 The initial effects of exposure to a nerve 

agent depend on the dose and route of 

exposure. The initial effects from a sublethal 

amount of agent by vapor exposure are different 

than the initial effects from a similar amount of 

liquid agent on the skin. 

Toxicities. The estimated amounts to 

cause certain effects in man are shown in 

Tables I and II. In Table I, L indicates lethal, I 

indicates incapacitating (severe), and M 

indicates miosis. The large amounts of GA and 

GB required to produce effects after skin 
129 

application reflect the volatility of these agents. 

They evaporate rather than penetrate the skin. 

However, if these agents are occluded and 

prevented from evaporating, they penetrate the 

skin very well. 

Table I. 

Vapor Toxicity (mg-min/m3)

Agent LCt50 ICt50 MCt50

GA 400 300 2-3 

GB 100 75 3 

GD 70 Unknown <1 

GF Unknown Unknown <1 

VX 50 35 0.04 

Table II. 

LD50 on Skin

Agent Amount 

GA 1000 mg 

GB 1700 mg 

GD 50 mg 

GF 30 mg 

VX 10 mg 
130 

 Sarin (GB), the agent studied most 

thoroughly in man, will cause miosis, rhinorrhea, 

and a feeling of tightness in the throat or chest 

at a Ct of 3 to 5 mg·min/m3

. 

Effect. Exposure to a small amount of nerve 

agent vapor causes effects in the eyes, nose, 

and airways. These effects are from local 

contact of the vapor with the organ and do not 

indicate systemic absorption of the agent. In this 

circumstance, the erythrocyte-ChE may be 

normal or depressed. A small amount of liquid 

agent on the skin causes systemic effects 

initially in the (GI) tract. Lethal amounts of vapor 

or liquid cause a rapid cascade of events 

culminating within a minute or two with loss of 

consciousness and convulsive activity, followed 

by apnea and muscular flaccidity within several 

more minutes. 

Eye. Miosis is a characteristic sign of 

exposure to nerve agent vapor. It occurs as a 

result of direct contact of vapor with the eye. 

Liquid agent on the skin will not cause miosis if 

the amount of liquid is small. A moderate 

amount of liquid may or may not cause miosis. A 

lethal or near-lethal amount of agent usually 

causes miosis. A droplet of liquid in or near the 

eye will also cause miosis. Miosis will begin 

within seconds or minutes after the onset of 

exposure to agent vapor, but it may not be 

complete for many minutes if the vapor 
131 

concentration is low. Miosis is bilateral in an 

unprotected individual, but occasionally may be 

unilateral in a masked person with a leak in his 

mask eyepiece. 

 Miosis is often accompanied by complaints 

of pain, dim vision, blurred vision, conjunctival 

injection, nausea, and occasionally, vomiting. 

The pain may be sharp or dull, in or around the 

eyeball, but more often is a dull ache in the 

frontal part of the head. Dim vision is due in part 

to the small pupil, and cholinergic mechanisms 

in the visual pathways also contribute. The 

complaint of blurred vision is less easily 

explained, as objective testing usually indicates 

an improvement in visual acuity because of the 

"pin-hole" effect. Conjunctival injection may be 

mild or severe, and occasionally subconjunctival 

hemorrhage is present. Nausea (and sometimes 

vomiting) is part of a generalized complaint of 

not feeling well. Topical homatropine or atropine 

in the eye can relieve miosis, pain, dim vision, 

and nausea. 

Nose. Rhinorrhea may be the first indication 

of nerve agent vapor exposure. Its severity is 

dose dependent. 

Airway. Nerve agent vapor causes 

bronchoconstriction and increased secretions of 

the glands in the airways in a dose-related 

manner. The exposed person may feel a slight 
132 

tightness in his chest after a small amount of 

agent and may be in severe distress after a 

large amount of agent. Cessation of respiration 

occurs within minutes after the onset of effects 

from exposure to a large amount of nerve agent. 

This apnea is probably mediated through the 

CNS, although peripheral factors (skeletal 

muscle weakness, e.g., the intercostal muscles, 

and bronchoconstriction) may contribute. 

GI tract. After they are absorbed, nerve 

agents cause an increase in the motility of the 

GI tract and an increase in secretions by the 

glands in the wall of the GI tract. Nausea and 

vomiting are early signs of liquid exposure on 

the skin. Diarrhea may occur with large amounts 

of agent. 

Glands. Nerve agent vapor causes 

increases in secretions from the glands it 

contacts, such as the lacrimal, nasal, salivary, 

and bronchial glands. Localized sweating 

around the site of liquid agent on the skin is 

common, and generalized sweating after a large 

liquid or vapor exposure is common. Increased 

secretions of the glands of the GI tract occur 

after systemic absorption of the agent by either 

route. 

Skeletal muscle. The first effect of nerve 

agents on skeletal muscle is stimulation 

producing muscular fasciculations and twitching. 
133 

After a large amount of agent, fatigue and 

weakness of muscles are rapidly followed by 

muscular flaccidity. 

 Fasciculations are sometimes seen early at 

the site of a droplet of liquid agent on the skin, 

and generalized fasciculations are common after 

a large exposure. These may remain long after 

most of the other acute signs decrease. 

Central nervous system (CNS). The acute 

CNS signs of exposure to a large amount of 

nerve agent are loss of consciousness, seizure 

activity, and apnea. These begin within a minute 

after exposure to a large amount of agent vapor 

and may be preceded by an asymptomatic 

period of 1 to 30 minutes after contact of liquid 

with the skin. 

 After exposure to smaller amounts of nerve 

agents, CNS effects vary and are nonspecific. 

They may include forgetfulness, an inability to 

concentrate fully, insomnia, bad dreams, 

irritability, impaired judgment, and depression. 

They do not include frank confusion and 

misperceptions (i.e., hallucinations). These may 

occur in the absence of physical signs or other 

symptoms of exposure. After a severe exposure, 

these symptoms occur upon recovery from the 

acute severe effects. In either case, they may 

persist for as long as four to six weeks. 
134 

Cardiovascular. The heart rate may be 

decreased because of stimulation by the vagus 

nerve, but it is often increased because of other 

factors such as fright, hypoxia, and the influence 

of adrenergic stimulation secondary to 

ganglionic stimulation. Thus, the heart rate may 

be high, low, or in the normal range. 

Bradyarrhythmias such as first-, second-, or 

third-degree heart block may occur. The blood 

pressure may be elevated from adrenergic 

factors, but is generally normal until the terminal 

decline. 

PHYSICAL FINDINGS 

 Physical findings depend on the amount and 

route of exposure. After exposure to small to 

moderate amounts of vapor, there are usually 

miosis and conjunctival injection, rhinorrhea, and 

pulmonary signs, although the latter may be 

absent even in the face of mild to moderate 

pulmonary complaints. In addition to these 

signs, an exposure to a high Ct may precipitate 

copious secretions from the nose and mouth, 

generalized muscular fasciculations, twitching or 

seizure activity, loss of consciousness, and 

apnea. Cyanosis, hypotension, and bradycardia 

may be present just before death. 

 Exposure to a small droplet of liquid on the 

skin may produce few physical findings. 

Sweating, blanching, and occasionally, 
135 

fasciculations, at the site may be present soon 

after exposure, but may no longer be present at 

the onset of GI effects. After a large exposure, 

the signs are the same as after vapor exposure. 

 Miosis is a useful sign of exposure to vapor 

but does not occur after a liquid exposure unless 

the amount of exposure is large or the exposure 

is in or close to the eye. 

TIME COURSE OF EFFECTS 

 Effects from nerve agent vapor begin within 

seconds to several minutes after exposure. Loss 

of consciousness and onset of seizure activity 

have occurred within a minute of exposure to a 

high Ct. After exposure to a very low Ct, miosis 

and other effects may not begin for several 

minutes, and miosis may not be complete for 15 

to 30 minutes after removal from the vapor. 

There is no latent period or delay in onset from 

vapor exposure. Effects may continue to 

progress for a period of time, but maximal 

effects usually occur within minutes after 

exposure stops. 

 A large amount of liquid on the skin causes 

effects within minutes. Commonly there is an 

asymptomatic period of 1 to 30 minutes, and 

then the sudden onset of an overwhelming 

cascade of events, including loss of 

consciousness, seizure activity, apnea, and 
136 

muscular flaccidity. After small amounts of liquid 

agent on the skin, the onset of effects has been 

delayed for as long as 18 hours after contact. 

These effects are initially gastrointestinal and 

are usually not life-threatening. Generally, the 

longer the interval, the less severe are the 

effects. 

DIFFERENTIAL DIAGNOSIS 

 The effects caused by a mild vapor 

exposure, namely, rhinorrhea and tightness in 

the chest, may easily be confused with an upper 

respiratory malady or an allergy. Miosis, if 

present, will help to distinguish these, but the 

eyes must be examined in very dim light to 

detect this. Similarly, GI symptoms from another 

illness may be confused with those from nerve 

agent effects, and in this instance there will be 

no useful physical signs. History of possible 

exposure will be helpful, and laboratory 

evidence (decreased RBC-ChE activity), if 

available, will be useful to distinguish the two. 

 The diagnosis is easier in the severely 

intoxicated patient. The combination of miosis, 

copious secretions, and generalized muscular 

fasciculations in a gasping, cyanotic, and 

convulsing patient is characteristic. 
137 

LABORATORY FINDINGS 

 Nerve agents inhibit the cholinesterase 

activity of the blood components, and estimation 

of this activity is useful in detecting exposure to 

these agents. The erythrocyte enzyme activity is 

more sensitive to acute nerve agent exposure 

than is the plasma enzyme activity. 

 The amount of inhibition of this enzyme 

activity does not correlate well with the severity 

of local effects from mild to moderate vapor 

exposure. The enzyme activity may be from 0 to 

100% of the individual's normal activity in the 

face of miosis, rhinorrhea, and/or airway 

symptoms. Normal or nearly normal erythrocyte 

acetylcholinesterase activity may be present 

with moderate effects in these organs. At the 

other extreme, the enzyme may be inhibited by 

60 to 70% when miosis or rhinorrhea is the only 

sign of exposure. Severe systemic effects 

generally indicate inhibition of the erythrocyte 

acetylcholinesterase by 70 to 80% or greater. 

 Other laboratory findings will relate to 

complications. For example, acidosis may occur 

after prolonged hypoxia. 
138 

MEDICAL MANAGEMENT 

 Management of a casualty with nerve agent 

intoxication consists of decontamination, 

ventilation, administration of the antidotes, and 

supportive therapy. The condition of the patient 

dictates the need for each of these and the order 

in which they are done. 

 Decontamination is described elsewhere in 

this manual. Skin decontamination is not 

necessary after exposure to vapor alone, but 

clothing should be removed because it may 

contain "trapped" vapor. 

 The need for ventilation will be obvious, 

and the means of ventilation will depend on 

available equipment. Airway resistance is high 

(50 to 70 cm of water) because of 

bronchoconstriction and secretions, and initial 

ventilation is difficult. The resistance decreases 

after atropine administration, after which 

ventilation will be easier. The copious secretions 

that may be thickened by atropine also impede 

ventilatory efforts and require frequent 

suctioning. In reported cases of severe nerve 

agent exposure, ventilation has been required 

from 0.5 to 3 hours. 

 Three drugs are used to treat nerve agent 

exposure, and another is used as pretreatment 

for potential nerve agent exposure. The three 
139 

therapeutic drugs are atropine, pralidoxime 

chloride, and diazepam. The use of the 

pretreatment drug pyridostigmine bromide is 

discussed later in this chapter. 

Atropine is a cholinergic blocking or 

anticholinergic compound. It is extremely 

effective in blocking the effects of excess 

acetylcholine at peripheral muscarinic sites. 

When small amounts (2 mg) are given to normal 

individuals without nerve agent intoxication, 

atropine causes mydriasis, a decrease in 

secretions (including a decrease in sweating), 

mild sedation, a decrease in GI motility, and 

tachycardia. The amount in three MARK I Kits 

may cause adverse effects on military 

performance in a normal person. In people not 

exposed to nerve agents, amounts of 10 mg or 

higher may cause delirium. Potentially, the most 

hazardous effect of inadvertent use of atropine 

(2 mg, IM) in a young person not exposed to a 

cholinesterase-inhibiting compound in a warm or 

hot atmosphere is inhibition of sweating, which 

may lead to heat injury. In the military, atropine 

is packaged in autoinjectors, each containing 2 

mg. 

Pralidoxime chloride (Protopam chloride, 

2-PAMCl) is an oxime. Oximes attach to the 

nerve agent that is inhibiting the cholinesterase 

and break the agent-enzyme bond to restore the 

normal activity of the enzyme. Clinically, this is 
140 

noticeable in those organs with nicotinic 

receptors. Abnormal activity in skeletal muscle 

decreases and normal strength returns. The 

effects of an oxime are not apparent in organs 

with muscarinic receptors; oximes do not cause 

a decrease in secretions, for example. They also 

are less useful after aging occurs, but with the 

exception of GD (soman) intoxicated individuals, 

casualties will be treated before significant aging 

occurs. Pralidoxime chloride (600 mg) is in an 

autoinjector for self-use along with the atropine 

injector. These atropine and pralidoxime chloride 

autoinjectors are packaged together in a MARK I 

Kit. Each warfighter is issued three MARK I Kits. 

Diazepam is an anticonvulsant drug used to 

decrease convulsive activity and reduce the 

brain damage caused by prolonged seizure 

activity. Without the use of pyridostigmine 

pretreatment, experimental animals died quickly 

after superlethal doses of nerve agents despite 

conventional therapy. With pyridostigmine 

pretreatment (followed by conventional therapy), 

animals survived superlethal doses of soman 

but had prolonged periods of seizure activity 

before recovery. They later had performance 

decrements and anatomic lesions in their brains. 

The administration of diazepam with other 

standard therapy to soman-poisoned animals 

pretreated with pyridostigmine reduced the 

seizure activity and its sequelae. Current military 

doctrine is to administer diazepam with other 
141 

therapy (three MARK I Kits) at the onset of 

severe effects from a nerve agent, whether or 

not seizure activity is among those effects. Each 

warfighter carries one autoinjector containing 10 

mg of diazepam for his buddy to administer to 

him (if he could self-administer it, he would not 

need it). Diazepam should be administered 

with the three MARK I Kits when the 

casualty's condition warrants the use of 

three kits at the same time. Medical personnel 

can administer more diazepam to a casualty if 

necessary. The medical corpsman carries extra 

diazepam injectors and is authorized to 

administer two additional injectors at ten-minute 

intervals to a convulsing casualty. 

 The doctrine for self-aid for nerve agent 

intoxication states that if an individual has 

effects from the agent, he/she should selfadminister one MARK I Kit. If there is no 

improvement in 10 minutes, he/she should seek 

out a buddy to assist in the evaluation of his/her 

condition before further MARK I Kits are given. If 

a buddy finds an individual severely intoxicated 

(e.g., gasping respirations, twitching, etc.) so 

that the individual cannot self-administer a 

MARK I Kit, the buddy should administer three 

MARK I Kits and diazepam immediately. The 

discussion below is advice for medical 

assistance. 
142 

 The appropriate number of MARK I Kits to 

administer initially to a casualty from nerve 

agent vapor depends on the severity of the 

effects. Systemic atropine will not reverse miosis 

(unless administered in very large amounts), 

and miosis alone is not an indication for a MARK 

I Kit. If the eye or head pain and nausea 

associated with the miosis are severe, topical 

application of atropine (or homatropine) in the 

eye will bring relief. Topical atropine should not 

be used without good reason (severe pain), 

because it causes blurred vision for a day or 

longer. A casualty with miosis and rhinorrhea 

should be given one MARK I Kit only if the 

rhinorrhea is severe and troublesome (he cannot 

keep his mask on because of fluid). A casualty 

with mild to moderate dyspnea should be given 

one or two MARK I Kits, depending on the 

severity of his distress and the time between 

exposure and therapy. Some of the respiratory 

distress from a mild exposure will spontaneously 

decrease within 15 to 30 minutes after 

termination of exposure, so if the casualty is not 

severely uncomfortable, only one MARK I Kit 

should be used initially. Atropine is quite 

effective, and care should be taken not to give 

too much in a casualty who does not need it. 
143 

 A severe casualty from nerve agent vapor 

has miosis, copious secretions from the nose 

and mouth, severe difficulty breathing or apnea, 

possibly some degree of cyanosis, muscular 

fasciculations, and twitching or convulsive 

activity, and is unconscious. He should be given 

three MARK I Kits and diazepam immediately. 

Ventilation will be needed and should be done 

via an endotracheal airway if possible. 

Suctioning of the excessive airway secretions 

will be necessary to enhance air exchange and 

will make ventilatory efforts easier. Atropine, 2 

mg, should be repeated at three- to five-minute 

intervals and should be titrated to a reduction of 

secretions and to reduction of ventilatory 

resistance. When the IV preparation is available, 

the preferred route of atropine administration is 

via the IV route, but this route should be avoided 

until hypoxia is corrected, because intravenously 

administered atropine in hypoxic animals has 

produced ventricular fibrillation. In a hypotensive 

patient or a patient with poor veins, atropine 

might be given intratracheally, either via the 

endotracheal tube or directly into the trachea, for 

more rapid absorption via the peribronchial 

vessels. 

 The medical care provider might err in giving 

too much atropine to a mild to moderate 

casualty. More importantly, the care provider 

might err by giving too little atropine to a severe 

casualty. In a severe casualty, atropine should 
144 

be pushed at frequent intervals until secretions 

are dry (or nearly dry) and until ventilation can 

be accomplished with ease. In reported cases 

this has required 10 to 20 mg of atropine within 

the first several hours. A conscious, less 

severely exposed casualty should receive 

atropine until he is breathing comfortably, and 

he will be able to communicate this. Dry 

secretions need not be an endpoint in mild to 

moderate casualties. 

 The casualty with skin exposure to liquid is 

more difficult to evaluate and manage than is a 

vapor exposure casualty. Agent on the surface 

of the skin can be decontaminated, but agent 

absorbed into the skin cannot be removed. The 

initial effects from absorbed liquid agent can 

start two to three hours after thorough 

decontamination of agent droplets on the skin. A 

casualty from liquid exposure on the skin may 

continue to worsen because of continued 

absorption of the agent from the skin depot. 

 The first effects of a liquid droplet on the 

skin are sweating with or without blanching, and 

occasionally, muscular fasciculations at the site. 

Gastrointestinal effects (nausea, vomiting, and 

sometimes diarrhea) are the first systemic 

effects, and these may start from 0.5 to 18 hours 

after contact with the agent. If these effects 

occur within the first several hours after 

exposure, they may portend more severe 
145 

effects, and initial therapy should be two MARK I 

Kits. If effects begin later, initial therapy should 

be one MARK I Kit. 

 A large amount of liquid agent on the skin 

will cause effects 1 to 30 minutes after contact, 

whether or not decontamination was done. 

Nevertheless, early decontamination may lessen 

the magnitude of the effects. After a 1- to 30-

minute latent or asymptomatic period, the 

casualty will suddenly lose consciousness and 

begin seizure activity. The condition of the 

casualty and management are the same as 

described for a severe casualty from vapor 

exposure. 

 Further care of the severe casualty consists 

of atropine administration to minimize secretions 

and ventilation until spontaneous respiration 

resumes. Oxime administration should be 

repeated at hourly intervals for two or three 

additional doses. The preferred method of 

administration of the oxime is by IV drip of 1 

gram over 20 to 30 minutes (more rapid 

administration will cause hypertension), but 3 

additional oxime autoinjectors (total dose of 1.8 

grams) may be given if the IV route cannot be 

used. The need for ventilation may continue for 

0.5 to 3 hours. Unless prolonged hypoxia or 

other complications have occurred, the casualty 

will eventually begin having spontaneous 

muscular activity and make sporadic attempts to 
146 

breathe. Muscles will become stronger and 

breathing more regular, and the casualty will 

have intermittent episodes of conscious 

behavior. Within an hour or two, he will be 

breathing, moving, and conscious, although he 

will be weak and intermittently obtunded. 
147 

Table III. 

Nerve Agent Effects: Vapor Exposure

Mild

• Eyes: miosis, dim vision, headache 

• Nose: rhinorrhea 

• Mouth: salivation 

• Lungs: dyspnea ("tightness in the 

chest") 

• Time of onset: seconds to minutes 

 after exposure 

• Self-aid: one MARK I Kit 

• Buddy-aid: stand by 

Severe

• All of the above, plus 

• Severe breathing difficulty or cessation 

of respiration 

• Generalized muscular twitching, 

weakness, or paralysis 

• Convulsions 

• Loss of consciousness 

• Loss of bladder, bowel control 

• Time of onset: seconds to minutes 

after exposure 

• Self-aid: None - warfighter will be 

unable to help self 

• Buddy-aid: 3 MARK I Kits and 

diazepam immediately
148 

Table IV. 

Nerve Agent Effects: Liquid on Skin

Mild/moderate

• Muscle twitching at site of exposure 

• Sweating at site of exposure 

• Nausea, vomiting 

• Feeling of weakness 

• Time of onset: 10 minutes to 18 hours 

after exposure 

• Self-aid: 1 to 2 MARK I Kits, 

depending on severity of symptoms 

• Buddy-aid: stand-by 

Severe

 All of the above, plus 

• Severe breathing difficulty or cessation 

of breathing 

• Generalized muscular twitching, 

weakness, or paralysis 

• Convulsions 

• Loss of consciousness 

• Loss of bladder and bowel control 

• Time of onset: minutes to an hour after 

exposure 

• Self-aid: none - warfighter will be 

unable to help himself 

• Buddy-aid: 3 MARK I Kits and 

diazepam immediately 
149 

PRETREATMENT 

 In late 1990, the U.S. military fielded 

pyridostigmine bromide as a pretreatment for 

nerve agent exposure. Each individual received 

a blister pack containing twenty-one 30-mg 

tablets. The dose regimen is one 30-mg tablet 

every 8 hours. When to start and stop dosing is 

a division or corps' command decision and is 

made with the advice of the intelligence, 

chemical, and medical staffs. To use or to stop 

the pretreatment is not a local decision, nor is it 

an individual decision. Thus, pyridostigmine is, 

in a sense, not a medical treatment, but a 

defensive weapons system. 

 Pyridostigmine bromide (Mestinon) is the 

drug of choice for myasthenia gravis and has 

been approved for the treatment of this disease 

since 1951. In 2003, the additional on-label use 

of pyridostigmine bromide for pretreatment 

against soman was approved by the Food and 

Drug Administration. Consequently, 

commanders have the authority to order its use 

in this situation without warfighter consent, 

exactly as they may order an approved vaccine. 

 When given before soman exposure and 

when that exposure is followed by the standard 

MARK I therapy, the use of pretreatment will 

increase the LD50 several fold over the LD50

obtained without the use of the pretreatment. 
150 

Functionally, this means that a warfighter can 

survive what would have been otherwise a lethal 

dose; pyridostigmine converts what would have 

been a dead warfighter to a very sick patient 

who can be saved only if the antidotes are 

properly and promptly administered. When 

soman is the nerve agent, the use of 

pyridostigmine increases survival. When the 

agent is GB or VX, survival after standard MARK 

I therapy is essentially the same whether or not 

pyridostigmine pretreatment is used, i.e., 

pyridostigmine use provides no benefit in GB or 

VX poisoning. Current data are not adequate to 

evaluate the effectiveness of pyridostigmine 

pretreatment for GA or GF exposure. 

 Pyridostigmine is not an antidote, and it 

should not be taken after soman exposure. Its 

use will not decrease the effects of soman. It is 

ineffective unless standard MARK I therapy is 

also used in the appropriate manner. 

 One consequence of the greater survival 

from the use of pyridostigmine is prolonged 

seizure activity and subsequent possible brain 

damage in the survivors. The early 

administration of diazepam will decrease these 

effects. 

 About 50 years ago, it was noted that 

carbamates bind to the active site of 

cholinesterase in a similar manner to the binding 
151 

of organophosphonate cholinesterase inhibitors 

to cholinesterase. Additionally, while the 

carbamate was attached to the active site, an 

organophosphorus compound could not attach 

to the enzyme. The carbamate-enzyme binding, 

or carbamylation, lasts only for hours, rather 

than for the lifetime of the enzyme as the 

organophosphorus compound attachment does, 

and is therefore spontaneously reversible. While 

the enzyme is carbamylated, the active site is 

protected from attack by other compounds such 

as organophosphorus cholinesterase inhibitors, 

including nerve agents. After several hours, the 

carbamate leaves the enzyme (i.e., 

decarbamylation occurs), and the enzyme 

becomes completely functional again. Thus, the 

carbamate provides temporary protection for the 

enzyme against nerve agent attack. Luckily, 

people have far more AChE than they need, so 

the use of pyridostigmine to carbamylate a small 

proportion of AChE converts that proportion into 

a reserve that will be available to save the 

patient if soman attack inactivates all of the rest. 

 Over the past several decades, many 

carbamates have been investigated for their 

effectiveness in animals and their safety in man. 

Pyridostigmine was chosen and underwent 

extensive testing in humans. It already had a 

long safety record, having been in use for over 

40 years; there are over 16,000 myasthenic 

patients in the U.S. who use it on a daily basis. 
152 

Investigations indicated that it did not interfere 

with the performance of military tasks and 

caused no adverse physiological disturbances. 

The incidence of side effects from the drug 

during these studies was reported as fewer than 

5%. 

 Tens of thousands of U.S. troops took 

pyridostigmine during the 1990-91 Gulf War. 

The incidence of side effects (primarily 

gastrointestinal and urinary) was over 50%, but 

only a few percent of the troops sought medical 

help because of the severity of these effects. 

The drug was discontinued by the warfighters’ 

medical officers in less than 1% of cases. 

TRIAGE 

 A severe nerve agent casualty who is 

unconscious, convulsing or post-ictal, breathing 

with difficulty or apneic, and possibly flaccid will 

survive with appropriate, immediate therapy, 

including ventilation, if he still has an intact 

circulation. He should be triaged as immediate

if that therapy can be provided. If a blood 

pressure cannot be obtained, he may be 

considered expectant. 

 The casualty with severe symptoms who is 

spontaneously breathing, has not lost 

consciousness, and has not seized has an 

excellent chance of survival with a minimal 
153 

amount of therapeutic effort. He should be 

categorized as immediate and given three 

MARK I Kits and diazepam. He may worsen if 

his exposure was to liquid, and atropine 

administration should be repeated at frequent 

intervals. If he loses consciousness, seizes, and 

becomes apneic, he will be retriaged, and his 

further care will depend on available resources. 

 Casualties who are walking and talking and 

are no longer being exposed to agent will 

usually be triaged as minimal. If a casualty can 

walk and talk, he is breathing and his circulation 

is intact. He would not appear to need 

immediate, life-saving care. This does not 

preclude self-administration or medicadministration of further antidotes for symptoms, 

and these should be given as necessary. 

 A casualty recovering from a severe 

exposure that has received large amounts of 

antidotes and has been ventilated will be triaged 

as delayed, because he is in need of further 

medical observation or care. A casualty who 

suffered liquid exposure and has been both 

treated and decontaminated may also be triaged 

as delayed. 
154 

RETURN TO DUTY 

 Return to duty depends on the status of the 

casualty, his military assignment, and the 

tactical situation. 

 Studies indicate that animals with decreased 

erythrocyte AChE activity from a nerve agent 

exposure have a decreased LD50 for another 

nerve agent exposure (they are more 

susceptible to the agent) until that 

cholinesterase activity returns to at least 75% of 

its baseline, or pre-exposure activity. Nerve 

agent-exposed workers in a depot or research 

facility are prevented from returning to work with 

agents until this recovery occurs. In a battlefield 

situation, this conservative management should 

be balanced against the need for the person and 

his risk of being exposed to a large amount of 

agent. 

 In a military field situation, the capability to 

analyze blood for erythrocyte cholinesterase 

activity is usually not available, and the "normal" 

or baseline activity of each individual is not 

known. The erythrocyte cholinesterase activity in 

a casualty with severe systemic effects will be 

inhibited by 70% or greater (30% or less of his 

pre-exposure activity), and 45 days or longer will 

be required for cholinesterase activity to return 

to 75% of pre-exposure activity. The enzyme 

activity of a casualty with mild or moderate 
155 

effects from agent vapor might be nearly normal 

or might be markedly inhibited. A prediction of 

erythrocyte cholinesterase recovery time is 

unreliable. 

 Most individuals triaged as minimal could 

return to duty within several hours if the tactical 

situation required all available manpower. The 

lingering ocular and CNS effects may be limiting 

factors in these cases. These individuals might 

be able to fire a rifle, but their performance on a 

tracking screen might be severely decremented 

because of both visual problems and difficulty in 

concentrating. These prolonged effects must be 

thoroughly evaluated before the casualties are 

returned to duty. 

 A casualty who had severe effects might be 

walking and talking after 6 to 24 hours but will 

still be unfit for most duties. Ideally, he should be 

kept under medical observation for a week or 

longer and not returned to duty until recovery of 

cholinesterase activity. However, the tactical 

situation may lead to modification of these 

guidelines. 

LONG-TERM EFFECTS 

 Minor electroencephalographic changes 

were noted more than a year after nerve agent 

exposure when averaged EEGs in a group of 

people who had been exposed to a nerve agent 
156 

were compared to a control group. Changes 

could not be identified in individuals. 

 Neuropsychiatric changes have been noted 

in individuals for weeks to months after 

exposure to insecticides. Both in the Tokyo 

subway attack and in the Iran-Iraq war, reports 

of long-term neuropsychiatric changes after 

exposure to nerve agent have surfaced. Little is 

known about the pathophysiology of these 

syndromes, as they are clearly not dose-related 

and overlap with post-traumatic stress disorder. 

 Polyneuropathy, reported after OP 

insecticide poisoning, has not been reported in 

humans exposed to nerve agents and has been 

produced in animals only at doses of nerve 

agents so high that survival would be unlikely. 

The intermediate syndrome has not been 

reported in humans after nerve agent exposure, 

nor has it been produced in animals by nerve 

agent administration. Muscular necrosis has 

been produced in animals after high dose nerve 

agent exposure but reverses within weeks; it has 

not been reported in humans. 
157 

INCAPACITATING AGENTS 

BZ, Fentanyl Derivatives 

SUMMARY 

Signs and Symptoms: BZ and other glycolates:

mydriasis; dry mouth; dry skin; increased DTRs; 

decreased level of consciousness; confusion; 

disorientation; disturbances in perception and 

interpretation (illusions and/or hallucinations); 

denial of illness; short attention span; impaired 

memory. Fentanyl derivatives (carfentanil):

dizziness, sleepiness, ataxia, miosis (if there is no 

hypoxia, with hypoxia there is pupil dilation), rapid 

unconsciousness, vomiting, decreased 

respirations, central apnea, coma. 

Field Detection: No field detector is available for 

either BZ or fentanyl derivatives. 

Decontamination: BZ: Gentle, but thorough 

flushing of skin and hair with water or soap and 

water is all that is required. Remove clothing. 

Fentanyl derivatives (carfentanil): No 

decontamination required. 

Management: BZ: Antidote: physostigmine. 

Supportive: monitoring of vital signs, especially 

core temperature. Fentanyl derivatives 

(carfentanil): Antidote: opioid antagonist 

naloxone/naltrexone. Supportive: monitoring of vital 

signs. Proper positioning of patient to maintain 

airway is critical until effects of central respiratory 

depression diminish. 
158 

OVERVIEW 

 BZ and other glycolates. BZ is a glycolate 

anticholinergic compound dispersed as an 

aerosolized solid (primarily for inhalation) or as 

agent dissolved in one or more solvents for 

ingestion or percutaneous absorption (physical 

properties). Acting as a competitive inhibitor of 

acetylcholine at postsynaptic and postjunctional 

muscarinic receptor sites BZ causes peripheral

nervous system (PNS) effects that in general are 

the opposite of those seen in nerve agent 

poisoning. CNS effects include stupor, 

confusion, and confabulation with concrete and 

panoramic illusions and hallucinations, and with 

regression to automatic "phantom" behaviors 

such as plucking and disrobing. The U.S. 

weaponized BZ, but demilitarization began in 

1988 and is complete. Refugees fleeing 

Yugoslavia in 1993 were probably exposed to a 

glycolate like substance based on anecdotal 

reports of their behaviors. The combination of 

anticholinergic PNS and CNS effects aids in the 

diagnosis of patients exposed to these agents. 

Physostigmine, which increases the 

concentration of acetylcholine in synapses and 

in neuromuscular and neuroglandular junctions, 

is a specific antidote. 

 Fentanyl derivatives (carfentanil).

Fentanyl, an opioid, has more than a dozen 

derivatives. While the exact fentanyl derivative 
159 

used by the Russians in 2002 is not known at 

this time, it is believed that it is related to the 

most potent of the known analogs, carfentanil. It 

is 10,000 times more potent than the opioid 

morphine. Carfentanil, produced under the trade 

name Wildnil®, is a large animal tranquilizer 

approved for veterinary use. Some believe that it 

may have been mixed with the anesthetic gas 

halothane to increase its potency. The U.S. does 

not use fentanyl analogs as incapacitants, 

although these were considered through the 

1970s. The identification of signs and symptoms 

aids in the diagnosis of the patients who 

succumb to a gas. Maintenance of the patient’s 

airway is critical for his survival as well as the 

rapid administration of the antidote, an opioid 

antagonist, naloxone or naltrexone. 

HISTORY/MILITARY RELEVANCE 

 

BZ and other glycolates. The use of 

chemicals to induce altered states of mind dates 

to antiquity and includes the use of plants such 

as thorn apple (Datura stramonium) that contain 

combinations of anticholinergic alkaloids. The 

use of nonlethal chemicals to render an enemy 

force incapable of fighting dates back to at least 

600 B.C. when Solon's warfighters threw 

hellebore roots into streams supplying water to 

enemy troops, who then developed diarrhea. In 

184 B.C., Hannibal's army used belladonna 

plants to induce disorientation, and the Bishop of 
160 

Muenster in A.D. 1672 attempted to use 

belladonna-containing grenades in an assault on 

the city of Groningen. In 1881, members of a 

railway surveying expedition crossing Tuareg 

territory in North Africa ate dried dates that 

tribesmen had apparently deliberately 

contaminated with Hyoscyamus falezlez. In 

1908, 200 French warfighters in Hanoi became 

delirious and experienced hallucinations after 

being poisoned with a related plant. More 

recently, accusations of Soviet use of 

incapacitating agents internally and in 

Afghanistan were never substantiated. 

 

 Following WWII, the U.S. military 

investigated a wide range of possible nonlethal, 

psychobehavioral, chemical incapacitating 

agents to include psychedelic indoles such as 

lysergic acid diethylamide (LSD-25) and 

marijuana derivatives, certain tranquilizers, as 

well as several glycolate anticholinergics. One of 

the anticholinergic compounds, 3-quinuclidinyl 

benzilate, was assigned the NATO code BZ and 

was weaponized beginning in the 1960s for 

possible battlefield use. Although BZ figured 

prominently in the plot of the 1990 movie 

Jacob's Ladder as the compound responsible for 

hallucinations and violent deaths in a fictitious 

American battalion in Vietnam, this agent never 

saw operational use. Destruction of American 

stockpiles began in 1988 and is now complete. 
161 

 In February 1998, the British Ministry of 

Defence released an intelligence report that 

accused Iraq of having stockpiled large amounts 

of a glycolate anticholinergic incapacitating 

agent known as Agent 15. As stated above, this 

compound is speculated either to be identical to 

BZ or a closely related derivative. Also in 1998, 

there were allegations that elements of the 

Yugoslav People's Army used incapacitating 

agents that caused hallucinations and irrational 

behavior against fleeing Bosnian refugees. 

Physical evidence of BZ use in Bosnia remains 

elusive, however.

 

Terms. The term "incapacitation," when 

used in a general sense, is roughly equivalent to 

the term "disability" as used in occupational 

medicine and denotes the inability to perform a 

task because of a quantifiable physical or mental 

impairment. In this sense, any of the chemical 

warfare agents may incapacitate a victim; 

however, again by the military definition of this 

type of agent, incapacitation refers to 

impairments that are temporary and nonlethal. 

Thus, riot-control agents are incapacitating 

because they cause temporary loss of vision 

due to blepharospasm, but they are not 

considered military incapacitants because the 

loss of vision does not last long. 

 Although incapacitation may result from 

physiological changes such as mucous 
162 

membrane irritation, diarrhea, or hyperthermia, 

the term "incapacitating agent" as militarily 

defined refers to a compound that produces 

temporary and nonlethal impairment of military 

performance by virtue of its psychobehavioral or 

CNS effects. 

 Sources other than military. BZ and 

related anticholinergic compounds can be 

synthesized in clandestine laboratories, but its 

illicit use is low possibly because of some 

unpleasant effects. The anticholinergics 

atropine, oxybutynin, and scopolamine find use 

in clinical medicine and are available as 

pharmaceuticals, as are antihistamines that 

have prominent anticholinergic side effects. 

Finally, anticholinergic hallucinogenic 

compounds are present in plants of the family 

Solanaceae, which include thorn apple (Jimson 

weed, Datura stramonium), black henbane 

(Hyoscyamus niger), belladonna (deadly 

nightshade, Atropa belladonna), woody 

nightshade (Solanum dulcamara), and 

Jerusalem cherry (Solanum pseudocapsicum). 

These plants contain varying proportions of the 

anticholinergic glycolates atropine, 

hyoscyamine, and hyoscine. Finally, BZ itself, 

now called QNB in the scientific community, is 

widely used in pharmacology as a muscarinic 

receptor marker. 
163 

 Fentanyl derivatives (carfentanil). 

Fentanyl was first synthesized by Belgian 

scientists in the 1950s. Since that time more 

than a dozen analogs of fentanyl have been 

developed, each more potent than the original 

fentanyl. Long used as an anesthetic and 

analgesic for surgery and chronic pain 

management, fentanyl analogs were considered 

for use as an incapacitating agents by several 

nations, including the U.S., up through the 

1970s. To date the U.S. has never weaponized 

fentanyl analogs or used any as an incapacitant. 

The Russian government admitted that on 

October 23, 2002, its Special Forces used a 

knockout gas containing a “fentanyl derivative” 

to incapacitate 50 Chechen terrorists, who 

threatened to blow up a Moscow theater and 

their 800 hostages before storming the building 

at the end of a 3-day stand-off. At the end of the 

siege all of the terrorists were dead, shot by the 

Russian Special Forces after many succumbed 

to the gas, and 129 of the 800 hostages (16%) 

died as a result of medical complications from 

the gas. The hostage death toll would assuredly 

have been greater if the Russian forces had 

stormed the theater without the incapacitating 

gas and the explosives had been successfully 

detonated by the terrorists. 

 It is reported by survivors that the gas was 

released into the theater through a hose or pipe 

near the floor at the front of the theater. The 
164 

release took place in the early morning when 

most inside the theater were sleeping after a 

tense night of negotiation. The ventilation 

system in the theater was not operating, as it 

had been disabled by the terrorists. Food and 

water were limited, so hostages were 

dehydrated. Hostages ranged in age from 13 

years old to the elderly, and all were seated at 

different locations in the theater relative to the 

source of the gas. These factors resulted in 

vastly different dosing of the individuals in the 

theater. While a majority of those sleeping inside 

the theater succumbed quickly to the gas, not all 

did so completely or immediately. In fact, one 

hostage stumbled out of the theater and some of 

the male terrorists fled to the rear of the theater. 

Because of this, some survivors have reported 

that Special Forces allowed the gas to flow into 

the theater for up to an hour before beginning 

their entry. This further increased the dose 

received by the hostages who succumbed early 

to the gas. While medical providers had some 

supplies of the antidote naloxone, there 

reportedly was not enough and it did not work 

for all patients. Many medical providers at 

hospitals were unaware of the antidote needed 

and tried a variety of remedies before 

discovering that naloxone worked for some of 

the survivors. Many hostages, upon going 

unconscious, slumped in their seats with their 

necks positioned in ways that restricted already 

suppressed breathing efforts for the long period 
165 

between release and rescue. Others became 

unconscious and then vomited, choking on their 

own vomit. Some patients, unconscious but still 

breathing when Special Forces entered the 

building, were positioned on the pavement 

outside the theater in supine or on city buses 

with necks hyper-extended for transport. These 

actions caused airways to become 

compromised, resulting in asphyxiation. In one 

instance a bus driver was unable to find a 

hospital and became lost, further prolonging 

medical care. 

PHYSIOCHEMICAL CHARACTERISTICS 

 BZ is the NATO code for 3-quinuclidinyl 

benzilate (QNB). BZ is odorless. It is stable in 

most solvents, with a half-life of three to four 

weeks in moist air; even heat-producing 

munitions can disperse it. It is extremely 

persistent in soil and water and on most 

surfaces. It is also soluble in propylene glycol, 

DMSO, and other solvents. Agent 15 

presumably shares many of the physiochemical 

properties of BZ. 

Fentanyl derivatives (carfentanil). At 

standard room temperature, fentanyl and 

carfentanyl exist in liquid form that, while 

difficult, could potentially be aerosolized. Some 

surviving hostages near the release area 

reported seeing a bluish gray cloud that left a 
166 

sweet taste in their mouths, which could indicate 

the addition of halothane, a halogenated 

anesthetic, to the gas. Halothane was also in the 

blood of two German hostages who were taken 

to German hospitals. Halothane is a liquid at 

standard temperature and pressure that 

volatilizes rapidly. Other hostages reported that 

they did not recall seeing any gas with a 

distinctive taste, odor, or color before passing 

out. The vapors of the agent used in Moscow 

quickly dissipated in the open air once the 

theater was ventilated by opening doors and 

breaking windows. 

DETECTION AND PROTECTION 

 BZ. Because BZ is odorless and 

nonirritating, and because clinical effects are not 

seen until after a latent period of 30 minutes to 

24 hours, exposure could occur without the 

knowledge of casualties. No currently available 

field military or civilian detector is designed to 

disclose the presence of BZ or other 

anticholinergic compounds in the environment. 

Confirmation of the exact chemical involved in 

an incapacitating agent exposure would have to 

await laboratory analysis of environmental 

specimens containing the agent. The HEPA filter 

in the canister of the chemical protective mask 

prevents exposure of the face and respiratory 

tract to aerosolized BZ. The chemical protective 

ensemble protects the skin against contact with 
167 

BZ or other incapacitating agents dispersed as 

fine solid particles or in solution. Protection 

against ingestion would depend upon a high 

index of suspicion for BZ-contaminated food or 

drink. 

Fentanyl derivatives (carfentanil). There 

are no chemical detectors for fentanyl 

derivatives and they have no odor, so they 

cannot be detected by smell. While the charcoal 

filter canister of a chemical protective mask 

should protect against concentrations in a 

ventilated environment, as they were worn by 

Special Forces personnel when first entering the 

theater, the filter effectiveness in an enclosed, 

unventilated space is unknown. 

TOXICOKINETICS 

 BZ may be dispersed as an aerosolized 

collection of small particles. Alternately, it may 

be dissolved in a solvent such as DMSO to 

enhance percutaneous absorption. 

Bioavailability via ingestion and by inhalation of 

one-micron particles approximates 80%, and 40 

to 50%, respectively, of a parenterally delivered 

dose of BZ. Percutaneous absorption of BZ 

dissolved in propylene glycol yields, after a 

latent period of up to 24 hours, serum levels 

approximately 5 to 10% of those achieved with 

intravenous or intramuscular administration. 

Although inhalation of aerosolized BZ is 
168 

probably the greatest risk on the battlefield, 

terrorists may choose to disseminate BZ in 

forms that provide significant opportunities for 

ingestion and absorption through the skin. 

 Following absorption, BZ is systemically 

distributed to most organs and tissues of the 

body. Its ability to reach synapses and 

neuromuscular and neuroglandular junctions 

throughout the body is responsible for its PNS 

effects, whereas its ability to cross the bloodbrain barrier is responsible for its CNS effects. 

Atropine and hyoscyamine both cross the 

placenta and can be found in small quantities in 

breast milk; whether this is also true for BZ is 

unclear. 

 Metabolism of BZ would be expected to 

occur primarily in the liver, with elimination of 

unchanged agent and metabolites chiefly in the 

urine. 

Fentanyl derivatives (carfentanil).

Fentanyl and its derivatives are opioids, 

synthetic non-opium derived narcotics that 

perform like opium. They bind to opioid 

receptors in the CNS and the GI tract. The 

fentanyl derivative was released in the form of a 

gas in an enclosed space. It may have been 

combined with an inhalation anesthetic such as 

halothane. Once inhaled it is quickly delivered to 

the blood stream for distribution throughout the 
169 

body. While the gas incapacitated most of those 

in the theater within the first few minutes, there 

were some who were awake at the time of 

release, and away from the source of the 

release, and were able to flee the theater. In the 

CNS carfentanil binds selectively to mu opioid 

receptors, which are predominantly found in the 

gray regions of the brain and the spinal cord. 

This causes a depression in the function of the 

CNS. Activation of mu receptors by opioids 

causes loss of pain sensation, miosis, 

decreased intestinal paristalsis (constipation), 

nausea and vomiting, respiratory depression, 

and diminished mental alertness resulting in a 

feeling of drowsiness, euphoria, sleepiness, and 

unconsciousness. With increased dosing this 

can result in brain-mediated apnea. These 

products are eventually eliminated in the urine. 

TOXICITY 

 BZ and other glycolates. The characteristic 

that makes BZ an incapacitating rather than a 

toxic chemical warfare agent is its high safety 

ratio. The amount required to produce effects is 

a thousand or more fold less than a fatal dose of 

the compound. In terms of Ct products 

(admittedly a sometimes problematic way of 

measuring dosage received after aerosol 

exposure), the ICt50 (the Ct product needed to 

produce incapacitation in 50% of an exposed 

group) for BZ is 112 mg-min/m3

, whereas the 
170 

LCt50 is estimated to be 200,000 mg-min/m3

. 

 Fentanyl derivatives (carfentanil). The 

effective dose (ED50), the amount needed to 

cause incapacitation, for carfentanil, a very 

potent fentanyl derivative and a likely candidate 

for the agent used in Moscow, is 0.0034 mg/kg 

while the lethal dose (LD50) is 3.4 mg/kg. This 

gives carfentanil the relatively wide safety index 

of 10,000, making it a good choice as an 

incapacitant. Two German hostages taken to 

Germany for treatment tested positive for 

halothane, but it is believed that one of these 

patients received halothane during life-saving 

procedures. Therefore, fentanyl could have been 

mixed with the halogenated anesthetic 

halothane to make it more potent. 

TOXICODYNAMICS 

(MECHANISM OF ACTION) 

 BZ and other glycolates. The agent BZ 

and other anticholinergic glycolates act as 

competitive inhibitors of the neurotransmitter 

acetylcholine neurons (1) at postjunctional 

muscarinic receptors in cardiac and smooth 

muscle and in exocrine (ducted) glands and (2) 

at postsynaptic receptors in neurons. As the 

concentration of BZ at these sites increases, the 

proportion of receptors available for binding to 

acetylcholine decreases and the end organ 

"sees" less acetylcholine. (One way of 
171 

visualizing this process is to imagine BZ coating 

the surface of the end organ and preventing 

acetylcholine from reaching its receptors.) 

Because BZ has little to no agonist activity with 

respect to acetylcholine, high concentrations of 

BZ essentially substitute a "dud" for 

acetylcholine at these sites and lead to clinical 

effects reflective of understimulation of end 

organs. 

 Fentanyl derivatives (carfentanil). These 

analogs act to bind to mu opioid receptors found 

throughout the brain (hippocampus, cerebral 

cortex, periaqueductal grey and thalamus) and 

spinal cord (dorsal horn). When the binding 

occurs the receptors produce effects such as 

analgesia, miosis, euphoria, constipation, and 

respiratory depression. 

CLINICAL EFFECTS 

BZ and other glycolates: 

Peripheral Effects

• Mydriasis, blurred vision 

• Dry mouth, skin 

• Initially rapid heart rate; later, normal or 

slow heart rate 

• Possible atropine flush 

 

 The PNS effects of BZ are, in general, 

readily understood as those of understimulation 
172 

of end organs and are qualitatively similar to 

those of atropine. Decreased stimulation of 

eccrine and apocrine sweat glands in the skin 

results in dry skin (an affected patient can be 

"dry as a bone") and a reduction in the ability to 

dissipate heat by evaporative cooling. The skin 

becomes warm ("hot as a hare") partly from 

decreased sweating and partly from 

compensatory cutaneous vasodilatation (the 

patient becomes "red as a beet," with a socalled atropine flush) as the body attempts to 

shunt a higher proportion of core-temperature 

blood as close as possible to the surface of the 

skin. With decreased heat loss, the core 

temperature itself rises. 

 Understimulation of other exocrine glands 

leads to xerostomia (dry mouth, another way in 

which the patient is "dry as a bone"), thirst, and 

decreased secretions from lacrimal, nasal, 

bronchial, and gastrointestinal glands. 

 Decreased cholinergic stimulation of 

pupillary sphincter muscles allows alphaadrenergically innervated pupillary dilating 

muscles to act essentially unopposed, resulting 

in mydriasis. (In fact, the cosmetic effect of 

mydriasis in women who applied extracts of 

deadly nightshade topically to their eyes 

explains the name "belladonna" ["beautiful lady"] 

given to this plant.) Similar effects on cholinergic 

ciliary muscles produce paralysis of 
173 

accommodation. Classically, the patient is 

described as being "blind as a bat." Other 

smooth muscle effects from BZ intoxication 

include decreased bladder tone and decreased 

urinary force with possibly severe bladder 

distention (yet another way in which the patient 

may be said to be "dry as a bone"). 

 BZ typically raises the heart rate initially, but 

hours later, depending on the dose of BZ, the 

heart rate falls to normal or may become slow. 

Either the peripheral vagal blockade has 

ceased, or the stimulation of the vagal nucleus 

has occurred. 

 Neither atropine nor BZ can act directly at 

the postjunctional nicotinic receptors found in 

skeletal muscle, but BZ-exposed patients 

nonetheless exhibit muscle weakness. This 

weakness, along with incoordination, heightened 

stretch reflexes, and ataxia, is probably due to 

the effects of BZ at CNS sites. 

 The PNS effects of BZ are essentially side 

effects that are useful in diagnosis, but incidental 

to the CNS effects for which the incapacitating 

agents were developed. These CNS effects 

include a dose-dependent decrease in the level 

of consciousness, beginning with drowsiness 

and progressing through sedation to stupor and 

coma. The patient is often disoriented to time 

and place. Disturbances in judgment and insight 
174 

appear. The patient may abandon socially 

imposed restraints and resort to vulgar and 

inappropriate behavior. Perceptual clues may no 

longer be readily interpretable, and the patient is 

easily distracted and may have memory loss, 

most notably short-term memory. In the face of 

these deficits, the patient still tries to make 

sense of his environment and will not hesitate to 

make up answers on the spot to questions that 

confuse him. Speech becomes slurred and often 

senseless, and loss of inflection produces a flat, 

monotonous voice. References become 

concrete and semiautomatic with colloquialisms, 

clichés, profanity, and perseveration. 

Handwriting also deteriorates. Semiautomatic 

behavior may also include disrobing (perhaps 

partly because of increased body temperature), 

mumbling, and phantom behaviors such as 

constant picking, plucking, or grasping motions 

("woolgathering" or carphology). 

Central Effects

• Disturbances in level of consciousness 

• Misperceptions and difficulty in 

interpretation (delusions, hallucinations) 

• Poor judgment and insight (denial of 

illness) 

• Short attention span, distractibility, 

impaired memory (particularly recent) 

• Slurred speech, perseveration 

• Disorientation 
175 

• Ataxia 

• Variability (quiet/restless) 

 Central nervous system mediated 

perceptual disturbances in BZ poisoning include 

both illusions (misidentification of real objects) 

and hallucinations (the perception of objects or 

attributes that have no objective reality). 

(Although the phrase "mad as a hatter" refers to 

poisoning from mercury formerly used by hatters 

on felt, it can just as well serve as a reminder of 

CNS effects from anticholinergics.) 

Anticholinergic hallucinations differ from the 

often vague, ineffable, and often transcendentappearing hallucinations induced by 

hallucinogenic indoles such as LSD. 

Hallucinations from BZ tend to be realistic, 

distinct, easily identifiable (often commonly 

encountered objects or persons), and 

panoramic. They also have the tendency to 

decrease in size during the course of the 

intoxication. 

 Another prominent CNS finding in BZ 

poisoning is behavioral lability, with patients 

swinging back and forth between quiet confusion 

and self-absorption in hallucinations to frank 

combativeness. Moreover, as other symptoms 

begin to resolve, intermittent paranoia may be 

seen. Automatic behaviors common during 

resolution include the crawling or climbing 
176 

motions called "progresso obstinato" in old 

descriptions of dementia. 

 BZ produces effects not just in individuals, 

but also in groups. Sharing of illusions and 

hallucinations (folie à deux, folie en famille, and 

"mass hysteria") is exemplified by two BZintoxicated individuals who would take turns 

smoking an imaginary cigarette clearly visible to 

both of them but to no one else. 

 Fentanyl derivatives (carfentanil). Effects 

of the gas agent used in the Moscow theater 

incident were reportedly almost immediate for 

those near the area of the release. For others 

there was a period of a feeling of drowsiness 

which quickly transitioned to unconsciousness. 

Some not near the release were less affected 

and showed drowsiness and ataxia, but were 

able to escape the area. Some of those who 

were unconscious vomited while sleeping, which 

caused their airway to be blocked. They also 

slumped in the theater seats, which placed their 

airways in restricted positions and blocked them. 

Those exposed to lethal doses of the agent who 

continued to breathe it in after becoming 

unconscious could also have experienced 

centrally-mediated respiratory depression and 

finally, apnea. 

 The general effects of opioids are that they 

are analgesic and sedative; they commonly 
177 

cause euphoria, dysphoria, and drowsiness. 

They will depress the central respiratory centers, 

constrict the pupils, and depress the cough 

reflex. Effective doses of fentanyl will stimulate 

the chemoreceptor trigger zone that causes 

nausea and vomiting. Opioids increase smooth 

muscle tone and therefore slow gastrointestinal 

propulsion. The effect on urinary smooth muscle 

is variable, so urinary urgency may increase or 

decrease. 

 Halothane is a halogenated hydrocarbon 

that causes general anesthesia, with a much 

reduced analgesic effect compared to fentanyl. It 

causes cerebral vasodilatation, increasing 

cerebral blood flow, but decreases cerebral 

consumption of oxygen. There is a decrease in 

skeletal muscle tone throughout the body, 

decreased salivation and gastric motility and like 

fentanyl, respiratory depression, which may 

produce a decreased tidal volume but increased 

respiratory rate. It causes the bronchial smooth 

muscles to dilate. Myocardial contractility and 

cardiac output also decrease due to vagal 

stimulation. This causes a drop in mean arterial 

pressure. It can trigger myocardial dysrhythmias, 

especially when hypoxia is present. 
178 

TIME COURSE OF EFFECTS 

BZ and other glycolates. 

 Clinical effects from ingestion or inhalation 

of BZ appear after an asymptomatic or latent 

period that may be as little as 30 minutes or as 

long as 20 hours; the usual range is 0.5 to 4 

hours, with a mean of 2 hours. However, effects 

may not appear up to 36 hours after skin 

exposure to BZ. 

 Once effects appear, their duration is 

typically 72 to 96 hours and dose-dependent. 

Following an ICt50 of BZ, severe effects may last 

36 hours, but mild effects may persist for an 

additional day. 

 The clinical course from BZ poisoning can 

be divided into the following four stages: 

 1. Onset or induction (zero to four hours 

after exposure), characterized by 

parasympathetic blockade and mild CNS effects. 

 2. Second phase (4 to 20 hours after 

exposure), characterized by stupor with ataxia 

and hyperthermia. 

 3. Third phase (20 to 96 hours after 

exposure), in which full-blown delirium is seen 

but often fluctuates from moment to moment. 

 4. Fourth phase, or resolution, 

characterized by paranoia, deep sleep, 
179 

reawakening, crawling or climbing automatisms, 

and eventual reorientation. 

Fentanyl derivatives (carfentanyl). Immediate 

unconsciousness given an effective dose. 

DIFFERENTIAL DIAGNOSIS 

 The differential diagnosis for irrational and 

confused patients is a long one and includes 

anxiety reactions as well as intoxication with a 

variety of agents, to include hallucinogenic 

indoles (such as LSD), cannabinoids (such as 

the delta-9-tetrahydrocannabinol in marijuana), 

lead, barbiturates, and bromides. All of these 

conditions can lead to restlessness, 

lightheadedness (with associated vertigo and 

ataxia), confusion, and erratic behavior with or 

without vomiting. Clues that specifically point to 

BZ or a related compound are the combination 

of anticholinergic PNS effects ("dry as a bone," 

"hot as a hare," "red as a beet," and "blind as a 

bat") with the CNS effects ("mad as a hatter") of 

slurred and monotonous speech, automatic 

behavior (perseveration, disrobing, and phantom 

behaviors ["woolgathering"]), and vivid, realistic, 

describable hallucinations (decreasing in size 

over time) in a patient slipping into and out of 

delirium. 
180 

SIGNS AND SYMPTOMS POSSIBLE 

ETIOLOGY

Restlessness, dizziness, or 

giddiness; failure to obey 

orders, confusion, erratic 

behavior; stumbling or 

staggering; vomiting. 

Anticholinergics 

(e.g., BZ) indoles 

(e.g., LSD), 

cannabinols (e.g. 

marijuana), anxiety 

reaction, other 

intoxications (e.g., 

alcohol, bromides, 

barbiturates, lead).

Dryness of mouth, 

tachycardia at rest, 

elevated temperature, 

flushing of face; blurred 

vision, pupillary dilation; 

slurred or nonsensical 

speech; hallucinatory 

behavior; disrobing; 

mumbling and picking 

behavior; stupor and coma. 

Anticholinergics 

Inappropriate smiling or 

laughter, irrational fear, 

distractibility, difficulty 

expressing self, perceptual 

distortions; labile increase 

in pupil size, heart rate, 

blood pressure. Stomach 

cramps and vomiting may 

occur.

Indoles 

(Schizophrenic 

psychosis may 

mimic in some 

respects.) 
181 

Euphoric, relaxed, 

unconcerned daydreaming 

attitude, easy laughter; 

hypotension and dizziness 

on sudden standing.

Cannabinols 

Tremor, clinging or 

pleading, crying; clear 

answers, decrease in 

disturbance with 

reassurance; history of 

nervousness or immaturity, 

phobias.

Anxiety reaction 

Sleepiness, ataxia, rapid 

unconscious, miosis, 

reduced quality of 

respirations decrease with 

resulting respiratory 

depression. 

 Fentanyl 

(carfentanyl) 

 Atropine intoxication from MARK I 

autoinjector use in a patient not exposed to 

nerve agents may create similar PNS effects to 

those seen in BZ intoxication. However, marked 

confusion from atropine is not normally seen 

until a total of six or seven autoinjectors have 

been given (in a hot, dehydrated, or battlestressed individual, less atropine would probably 

suffice). Circumstantial evidence may be helpful 

in this situation. Heat stroke may also generate 

hot, dry, and confused or stuporous casualties 

and needs to be considered in the differential 
182 

diagnosis. Patients with anxiety reactions are 

usually oriented to time, place, and person but 

may be trembling, crying, or otherwise panicked. 

The classic picture of unconcern, or "la belle 

indifférence," may characterize a patient with a 

conversion reaction, but these patients are also 

likely to be oriented and lack the anticholinergic 

PNS signs of BZ poisoning.

MEDICAL MANAGEMENT 

 Guidelines for general patient care are not 

intended to take the place of sound clinical 

judgment, especially in the management of 

complicated cases. 

 BZ and other glycolates. The admonition 

to protect oneself first may be difficult when 

dealing with any intoxication involving a latent 

period, since initially asymptomatic exposure to 

health care providers may already have 

occurred during the same time frame in which 

patients were exposed. Protection of medical 

staff from already absorbed and systemically 

distributed BZ in a patient is not needed. 

 

 General supportive management of the 

patient includes decontamination of skin and 

clothing (ineffective for already absorbed agent 

but useful in preventing further absorption of any 

agent still in contact with the patient), 

confiscation of weapons and related items from 
183 

the patient, and observation. Physical restraint 

may be required in moderately to severely 

affected patients. The greatest risks to the 

patient's life are (1) injuries from his or her own 

erratic behavior (or from the behavior of similarly 

intoxicated patients) and (2) hyperthermia, 

especially in patients who are in hot or humid 

environments or are dehydrated from 

overexertion or insufficient water intake. A 

severely exposed patient might be comatose 

with serious cardiac arrhythmias and electrolyte 

disturbances. Management of heat stress 

assumes a high priority in these patients. 

Because of the prolonged time course in BZ 

poisoning, consideration should always be given 

to evacuation to a higher care level. 

 As a competitive inhibitor of acetylcholine, 

BZ effectively decreases the amount of 

acetylcholine "seen" by postsynaptic and 

postjunctional receptors throughout the body. 

Specific antidotal therapy in BZ poisoning is 

therefore geared toward raising the 

concentration of acetylcholine in these synapses 

and junctions. Any compound that causes a rise 

in acetylcholine concentration can potentially 

overcome BZ-induced inhibition and restore 

normal functioning; even the nerve agent VX 

has been shown to be effective when given 

under carefully controlled conditions. The 

specific antidote of choice in BZ poisoning is the 

carbamate anticholinesterase physostigmine 
184 

(eserine; Antilirium®), which temporarily raises 

acetylcholine concentrations by binding 

reversibly to anticholinesterase on the 

postsynaptic or postjunctional membrane. 

Physostigmine is similar in many ways to 

pyridostigmine and is equally effective when 

used as a pre-exposure antidotal enhancer 

("pretreatment") in individuals at high risk for 

subsequently encountering soman. However, 

physostigmine is not used for this purpose 

because the doses required cause vomiting 

through CNS mechanisms. In the case of BZ 

poisoning, a nonpolar compound such as 

physostigmine is used specifically because 

penetration into the brain is required in those 

individuals who already have CNS effects from 

BZ. 

 In BZ-intoxicated patients, physostigmine is 

minimally effective during the first four hours 

after exposure but is very effective after four 

hours. Oral dosing generally requires one and a 

half times the amount of antidote as does IM or 

IV administration. However, effects from a single 

intramuscular injection of physostigmine last 

only about 60 minutes, necessitating frequent 

re-dosing. It must be emphasized that 

physostigmine does not shorten the clinical 

course of BZ poisoning and that relapses will 

occur if treatment is discontinued prematurely. 

The temptation to substitute a slow intravenous 

infusion for intramuscular injections should be 
185 

tempered by the awareness that IV infusion may 

lead to nerve-agent-like bradycardia, and too 

rapid infusion might cause arrhythmias, 

excessive secretions (to the point of 

compromising air exchange), and convulsions. 

Moreover, the sodium bisulfite in commercially 

available preparations of physostigmine may 

cause life-threatening allergic responses. 

 Suggested dosages for physostigmine in the 

treatment of BZ poisoning follow: 

Test dose. If the diagnosis is in doubt, a 

dose of 1 mg might be given. If a slight 

improvement occurs, routine dosing should be 

given. 

Routine dosing. Adult doses of about 45 

mcg/kg have been recommended. This might be 

modified by the response. A mental status 

examination should be done every hour, and the 

dose and time interval of dosing should be 

modified according to whether the mental status 

is improved or not. As the patient improves, the 

dosage requirement will decrease. Oral dosing 

is the preferred route after the initial IV dose. 

This will decrease the risk of overdose that could 

be created by further IV administration.
186 

Routes of administration. 

 

 IM: 45 mcg/kg in adults (20 mg/kg in 

children) 

 

 IV: 30 mcg/kg slowly (1 mg/min) 

 

 PO: 60 mcg/kg if patient is cooperative 

(because of bitter taste, consider diluting in 

juice) 

 For each route, titrate about every 60 

minutes to mental status. 

 Fentanyl derivatives (carfentanil). It is 

critical to assess the patient’s respiration and 

insure that his airway is not obstructed. A quick 

check of the patient’s head and body should 

also be conducted to insure that he did not 

bump his head or other parts of his body on the 

floor or on objects if he collapsed quickly. Check 

for airway obstruction from vomitous and clear 

the airway and position the patient on his side. 

Administer the antidote, naloxone, and check for 

improved respiration. Even after the 

administration of the antidote, the patient’s 

breathing must be checked periodically, as 

naloxone effects are known to be short-lived 

with a potent opioid such as carfentanil. Preexisting medical conditions may also interfere 

with breathing, which could be exacerbated as 

fentanyl derivatives tend to depress respiration. 
187 

 The individual who has aspirated vomit may 

be at risk for aspiration pneumonia, so a followup chest radiograph may be indicated. A CT 

head scan should be ordered if a fall injury to the 

head is suspected. Patients with preexisting 

cardiac disease may be at risk for cardiac 

ischemia, so an ECG should be ordered for 

these patients. Urine drug screenings must 

specifically detect for fentanyl and carfentanyl as 

they will not be identified by morphine screens. 

Other precautionary lab tests to assess 

rhabdomyolysis, electrolytes, renal and liver 

function and clotting are appropriate to assess 

clearance and general status. If the agent is 

unknown, then it is wise to collect additional 

blood and urine samples for testing to help rule 

out other analgesics, sedatives, or toxins. 

 The antidotes for opioids, naloxone 

hydrochloride (Narcan), or naltrexone have long 

been used to treat heroine addicts. These are 

opioid receptor antagonists that bind to the 

opioid receptors more strongly than a fentanyl 

derivative, but do not activate the receptor. As 

these replace the opioid on the opioid receptor 

the signs and symptoms are quickly reversed, 

especially life-threatening respiratory 

depression. It is important to remember that 

these have a relatively short half life, so 

symptoms may return in an apparently stabilized 

patient. This means that the patient, though 
188 

recovering, must be monitored closely and 

airway support maintained until full 

consciousness is achieved. If the agent is 

composed of multiple substances, then 

naloxone, an opioid inhibitor, may demonstrate 

only limited effectiveness. The administration of 

naloxone can be diagnostic as well as 

therapeutic. The dosage guidelines noted here 

are for those with opioid dependency. Some 

individuals may be hypersensitive to naloxone; 

otherwise there are no life-threatening side 

effects with normal dosing. When uncertain of 

the agent, naloxone should be titrated slowly 

and the patient observed closely for change. 

 The adult dose is 0.4 to 2 mg IV, repeated 

every 2 to 3 minutes as needed for stabilization 

of breathing. IV administration will bring the 

quickest improvement. If injected either IM or 

subcutaneously, increments of 0.1 to 0.2 mg are 

recommended at 2- to 3-minute intervals until 

adequate patient ventilation is achieved. Larger 

than suggested dosage may result in increased 

blood pressure, sweating, and vomiting. 

Dosages may need to be repeated every 20 to 

60 minutes after initial stabilization if signs 

return. Supplemental IM doses may have longer 

effect. If no response is noted after 10 mg of 

naloxone have been administered, the toxic 

agent should be questioned. 
189 

 The pediatric dose is 0.1 mg/kg of body 

weight if given IV. If this dose does not allow for 

adequate patient ventilation, a follow-on dose of 

0.1 mg/kg of body weight can be administered. If 

IV is not available, it can also be administered 

IM or subcutaneously. Titrate to respiratory 

stabilization. 

HISTORY AND TOXICITY OF THE BZ 

ANTIDOTE PHYSOSTIGMINE 

 

 The antagonism between physostigmine 

(the elixir or calabar bean) and atropine (tincture 

of belladonna) was first reported in 1864 by a 

physician who successfully treated prisoners 

who had become delirious after drinking tincture 

of belladonna. Physicians did not notice this 

report until the 1950s when atropine coma (in 

which 50 mg or so of atropine were given to 

certain psychiatric patients) was successfully 

treated with physostigmine after the "therapeutic 

benefit" had been attained. Again, this went 

unnoticed until a controlled study reported in 

1967 indicated that anticholinergic intoxication 

could be successfully, albeit transiently, 

reversed by physostigmine. 

 A recent textbook of emergency medicine 

stated that physostigmine should be used only 

as "a last resort." It would seem that when a 

patient needs "last resort" care is the absolute 
190 

wrong time to administer a potent cholinesterase 

inhibitor. 

 The administration of physostigmine by the 

IV route in a delirious but conscious and 

otherwise healthy patient is not without peril. It is 

sometimes difficult to keep a delirious patient 

quiet long enough to administer the drug (at 1 

mg/min is the marketed solution of 1 mg/ml). 

Even if administered correctly (very slowly), the 

heart rate may decline from 110 bpm to 45 bpm 

over a period of 1 to 2 minutes. The difference in 

the onset of the effects after IM and IV 

administration of physostigmine is a matter of 

only several minutes. Since its use is rarely 

lifesaving, this slight difference in time of 

response is inconsequential. 

 Physostigmine is a safe and effective 

antidote if used properly. In a conscious and 

delirious patient it will produce very effective but 

transient reversal of both the peripheral and 

central effects of cholinergic blocking 

compounds. Its use by the IV route is not without 

hazards. It absolutely should NOT be used in a 

patient with cardiorespiratory compromise, 

hypoxia, or acid-base imbalance with a history of 

seizure disorders or arrhythmias. 
191 

TRIAGE 

BZ and other glycolates. 

An immediate casualty (possible, but 

unlikely) would be one with cardiorespiratory 

compromise or severe hyperthermia. Immediate 

attention to ventilation, hemodynamic status, 

and temperature control could be lifesaving. 

Because of its dangers in a hypoxic or 

hemodynamically challenged patient, 

physostigmine should be considered a secondline management option to be used only if 

adequate attention can simultaneously be given 

to temperature and other vital signs. 

 The delayed casualty would present with 

pronounced or worsening anticholinergic signs. 

Physostigmine should definitely be considered in 

this kind of patient. 

 A minimal casualty from a strictly medical 

standpoint might have mild PNS or CNS 

anticholinergic effects. Given the time course of 

BZ intoxication, however, these patients should 

not be considered able to manage themselves 

or capable of routine return to duty and should 

be relieved of their weapons, observed, and if 

the holding capacity at the current echelon is 

exceeded, evacuated. 
192 

 An expectant casualty (also possible, but 

unlikely) would have severe cardiorespiratory 

compromise in a situation in which treatment or 

evacuation resources are too limited to allow the 

necessary attention to be directed to him or her. 

Fentanyl derivatives (carfentanyl). 

 An immediate casualty would be one with 

cardiorespiratory compromise due to central 

apnea or airway obstruction. Immediate 

attention to maintenance of the airway, 

supplemental oxygen and ventilatory support, 

and administration of antidotes will be lifesaving. 

These patients should be considered a priority 

for rapid evacuation to a facility with respiratory 

care assets if their condition does not improve 

with the administration of antidotes and 

supplemental oxygen at the incident scene. 

 The delayed casualty would present with 

independent breathing that could be 

compromised if the patient vomits or central 

dyspnea increases. Respiration needs to be 

monitored closely. This patient must be placed 

in a side-lying position to help maintain a clear 

airway. Supplemental oxygen and administration 

of antidotes should be considered for this 

patient. 

 A minimal casualty might be an individual 

who has walked out of the contaminated area 
193 

unassisted and is able to converse, but may be 

somewhat drowsy. In these patients breathing is 

not restricted. They should be placed in an area 

where they can be observed for 24 hours before 

being released. 

 An expectant casualty (also possible, but 

unlikely) would have severe cardiorespiratory 

compromise in a situation in which antidotal 

treatment, respiratory assistance, and 

evacuation resources are too limited to allow the 

necessary attention to be directed to him or her. 

RETURN TO DUTY 

 BZ and other glycolates. Given the time 

course of the intoxication, early return to duty is 

probably not a realistic possibility for the majority 

of casualties who may require observation and 

management for several days at the least. 

 Fentanyl derivatives (carfentanil). Those 

with mild to moderate symptoms should be able 

to return to duty within 24 hours. Those who 

require ventilatory support will require longer 

periods of hospitalization until cardiopulmonary 

function is normalized, barring any complications 

such as pulmonary infection or brain damage 

from hypoxia following periods of sustained 

apnea. 
194 

RIOT-CONTROL AGENTS 

CS, CN, CR, DM, and OC 

SUMMARY 

Signs and Symptoms: Burning and pain on 

exposed mucous membranes and skin, eye 

pain and tearing, burning in the nostrils, 

respiratory discomfort, and tingling of the 

exposed skin. DM: Will cause prolonged 

periods of vomiting and a feeling of malaise. 

Field Detection: No field detector is available 

for any of the RC Agents. 

Field Decontamination: Eyes: Thoroughly 

flush with water, saline, or similar substance. 

CS, CN, CR, DM: Skin: Flush with copious 

amounts of water, soap and water, or a mildly 

alkaline solution (sodium bicarbonate or 

sodium carbonate). Generally, 

decontamination is not needed if the wind is 

brisk. OC: The pain from OC will increase with 

water, especially warm water. It is best 

decontaminated with baby shampoo, milk, 

alcohol, or vegetable oil. Without 

decontamination pain will subside over time. 

Immediate management: Usually none is 

necessary; effects are self-limiting and 

diminish or cease within 45 minutes. DM is 

the exception, where effects may last several 

hours. 
195 

OVERVIEW 

 Riot-control agents, also called irritants, 

lacrimators, and "tear gas," produce transient 

discomfort and eye closure to render the 

recipient temporarily incapable of fighting or 

resisting. Law enforcement agencies use them 

for riot control, and military forces use them for 

training and in combat (see below). They have a 

high LCt50 and a low effective Ct50, and therefore 

have a high safety ratio. Their major activity is to 

cause pain, burning, or discomfort on exposed 

mucous membranes and skin; these effects 

occur within seconds of exposure but seldom 

persist more than a few minutes after exposure 

has ended. 

HISTORY/MILITARY RELEVANCE 

 Paris police used riot-control agents to 

dispel rioters before WWI, and these 

compounds were the first chemical agents 

deployed during that war. French warfighters 

used them with limited success in small 

skirmishes. About 30 riot-control agents were 

developed and used, but their use decreased 

following the advent of more potent compounds. 

After WWI, military and law enforcement 

agencies used CN for various purposes until CS, 
196 

a more potent and less toxic compound, 

synthesized by Corson and Stoughton (hence 

the nomenclature) in 1928, replaced it in about 

1959. Today CN is in commercially available 

devices for self-protection (Mace®

), but CS and 

oleoresin capsicum (OC) are fast becoming the 

favorites among law enforcement agencies. The 

military forces of most countries use CS in 

training as a confidence builder for the protective 

mask (the "gas chamber exercise"), and the 

U.S. used it extensively in Vietnam primarily for 

tunnel denial. Worldwide, police forces of many 

countries, e.g., Ireland, France, Russia, and the 

U.S., use it for crowd control or during riots. 

 Introduced in 1974 in the U.S., oleoresin 

capsaicin (OC) is quickly replacing other riot 

control agents used in law enforcement across 

the U.S. because of its safety and the fact that it 

can be dispensed as a liquid, foam, aerosol, or 

as a powder in paint ball delivery systems. It is 

best used for individual protection. Derived from 

the resin of cayenne peppers, it has been used 

in various ways. In small amounts it is used for 

pain relief; in larger amounts it is used as an 

irritant and as a tool of torture. Examples include 

its use historically by the Japanese police and 

the ninja, in the form of a powder, metsubishi, 

blown on an attacker, and as an irritant during 

the Indo-China wars of 2,000 B.C. The U.S. 

excludes these agents from international treaty 

provisions. They may be used in military 
197 

situations by Presidential Order. OC can be 

used by military law enforcement.

 The agents in use today are OC, CS, and 

CN. CA is a very old and outmoded riot-control 

agent because of its low safety margin and 

caustic nature, so it will not be discussed here; 

CR is a British agent similar to CS, and DM 

(Adamsite) is an irritant as well as a vomiting 

agent. While OC, CS, and CN are used in the 

U.S., CA and DM are not, but may be used by 

other nations for riot control. 

PHYSIOCHEMICAL CHARACTERISTICS 

 Unlike most agents, which are liquids under 

temperate conditions, the riot-control agents CS, 

CN, CR, and DM are crystallized solids with low 

vapor pressures and are dispersed as fine 

particles or in solution. Dispersion devices 

include small, handheld spray cans, large spray 

tanks, grenades, and larger weapons. OC is an 

oily resin, which can be dried to form an offwhite powder and aerosolized, or combined with 

a medium such as alcohol or oil to make a liquid 

or foam spray.

MECHANISM OF TOXICITY 

 The mechanism of biological activity is less 

well characterized for riot-control agents than for 

most other agents. Fortunately, a detailed 
198 

knowledge of the mechanism of action is not 

necessary for appropriate medical management. 

 CS and CN are SN2 alkylating agents 

(mustard, in contrast, is an SN1 alkylator) and 

react readily at nucleophilic sites. Prime targets 

include sulfhydryl-containing enzymes such as 

lactic dehydrogenase. In particular, CS reacts 

rapidly with the disulfhydryl form of lipoic acid, a 

coenzyme in the pyruvate decarboxylase 

system. It has been suggested that tissue injury

may be related to inactivation of certain of these 

enzyme systems. 

 Pain can occur without tissue injury and may 

be bradykinin mediated. CS causes bradykinin 

release in vivo and in vitro, and elimination of 

bradykininogen in vivo abolishes the systemic 

response to CS. 

 The initial response to aerosolized CS is an 

increase in blood pressure and irregular 

respiration, suggestive of the Sherrington 

pseudoaffective response. Bypassing the pain 

receptors of the nose and upper airway by 

endotracheal administration of CS leads to the 

same decrease in blood pressure and in 

respiration seen after IV injection. This suggests 

that the initial pressor effect and irregular 

respiration are responses to a noxious stimulus 

rather than pharmacological effects of CS. 
199 

 OC produces a burning and painful 

sensation in the individual it contacts as it binds 

to ion-channel receptors in the nervous system 

resulting in rapid cell depolarization and a 

massive release of substance P, a neuropeptide 

that is a neurotransmitter of pain. This release of 

high levels of substance P signals the brain that 

the body is experiencing extreme pain and 

burning. This continues until the substance P is 

used up. The body then releases endorphins to 

inhibit the pain sensation, which can create a 

period of euphoria, a “runners high” as an after 

effect for the individual exposed. Those who 

regularly eat hot peppers are less susceptible to 

the painful effects of pepper spray. The use of 

capsaicin in pain relieving ointments causes a 

slower release and depletion of substance P, 

creating an analgesic effect without causing the 

extreme pain sensation experienced with OC 

exposure. 

CLINICAL EFFECTS 

 The main effects of riot-control agents are 

pain, burning, and irritation of exposed mucous 

membranes and skin. These effects do not differ 

appreciably from one agent to another except in 

the case of DM, which will be discussed in a 

separate section. 

Eyes. The eye is the organ most sensitive to 

riot-control agents. Contact with any of the riot-
200 

control agents produces a sensation of 

conjunctival and corneal burning and leads to 

tearing, blepharospasm, and conjunctival 

injection. The severe blepharospasm causes the 

lids to close tightly and produces transient 

"blindness," an effect that could inhibit the 

recipient's ability to fight or resist. However, if 

the recipient opens his eyes, his vision is near 

normal even if a significant concentration of the 

agent persists. 

 Because these compounds are solids, with 

the exception of OC, it is possible for a particle 

or clump to become embedded in the cornea or 

conjunctiva to cause tissue damage. With the 

caveat noted below, there is no evidence that 

this complication has ever occurred; however, a 

recipient seeking medical care for eye pain after 

exposure should have his eyes thoroughly 

decontaminated and undergo thorough 

ophthalmic examination. It could be necessary 

to pick out the particles of agent from tissue. The 

carriers' solvents in some OC sprays can cause 

corneal erosion, so eyes should be 

decontaminated with copious amounts of water 

or baby shampoo and water. Follow-up with an 

ophthalmologist is indicated if complications 

appear. 

 Reviewers examined the evidence for 

permanent eye damage from riot-control agents. 

In each instance, the damage was from a 
201 

weapon fired from close range (about 50% were 

self-inflicted). The reviewers concluded that the 

blast force driving the agent deep into tissue 

(with or without the wadding of the weapon) was 

the major cause of permanent injuries. This 

should not happen under normal use. 

Nose and mouth. Contact with the delicate 

mucous membranes of the nose produces a 

burning sensation, rhinorrhea, and sneezing; a 

similar burning sensation accompanied by 

increased salivation occurs after contact with the 

mouth. 

Airways. Inhalation causes burning and 

irritation of the airways with bronchorrhea, 

coughing, and a perception of a "tight chest" or 

an inability to breathe. In research studies, 

pulmonary function studies done immediately 

after exposure have shown minimal alterations. 

In one reported instance, nine Marines who 

were without respiratory protection were 

exposed to high CS concentrations during 

training and developed transient pulmonary 

syndrome. All had coughs and shortness of 

breath, five had hemoptysis, and four who 

needed to be hospitalized had hypoxia. It was 

discovered that those hospitalized underwent 

strenuous physical exercise within 36 to 84 

hours after exposure to high amounts of CS. 

One week after exposure all nine had normal 
202 

lung function measured by spirometry before 

and after exercise.

 An inhaled irritating compound might be 

expected to exacerbate a chronic pulmonary 

disease such as asthma, emphysema, or 

bronchitis, but this appears not to happen after 

CS or CN, even though these agents have been 

used widely in mixed populations. The medical 

care provider should nevertheless anticipate 

airway problems in individuals with lung disease, 

particularly if they are exposed to higher than 

the average field use concentrations. The onset 

of extreme pain for those exposed to OC has 

resulted in a few cases of laryngospasm as a 

reaction to the pain caused by the OC. These 

cases have responded well with standard airway 

management. 

 There is no evidence that CS causes 

permanent lung damage after one or several 

exposures to field concentrations. Following 

inhalation of lethal amounts, animals died from 

severe airway damage 12 to 24 hours postexposure, but survivors from large exposures 

had minimal or no pulmonary abnormalities. 

After multiple (50 or more) daily exposures to 

smaller amounts, animals developed laryngitis 

and tracheitis. 

Skin. Contact with the skin causes a tingling 

or burning sensation and may cause erythema, 
203 

particularly if the skin is raw or freshly abraded 

(e.g., shortly after shaving). The erythema 

begins several minutes after exposure and 

generally subsides 45 to 60 minutes after 

termination of exposure.

 Under conditions of high temperature, high 

humidity, and high concentration of agents such 

as CS, there may be more severe dermatitis 

starting with erythema hours after exposure and 

followed by vesication. Generally these are 

second-degree burns not unlike, but more 

severe than sunburn. Firemen who entered 

buildings contaminated with CS after summer 

riots several decades ago developed these 

lesions. After stirring up the contaminating 

particles, they later developed erythema and 

blisters on their exposed skin. Hypersensitivity 

may develop for those who have reacted to CS 

in the past. In one instance, an individual 

developed generalized vesication and high fever 

after an uneventful exposure to CS more than 

20 years after his only and equally uneventful 

previous exposure. OC will cause skin redness 

and irritation and with prolonged exposure to 

high concentrations can cause skin rash, but not 

the blistering seen with CS or CN. 

GI tract. Gastrointestinal effects usually do 

not occur with most riot-control agents (DM is an 

exception), although there may be retching or 

vomiting if the agent concentration is high, 
204 

exposure is prolonged, or the individual is 

sensitive. 

 Cardiovascular. A transient increase in 

heart rate and blood pressure has occurred in 

people immediately prior to an exposure to all of 

these riot-control agents or immediately after 

onset of exposure. The heart rate and blood 

pressure returned essentially to pre-test ranges 

while exposure continued and may have been 

caused by the anxiety or the initial pain rather 

than a pharmacological effect of these agents. 

This "alarm reaction" may cause adverse effects 

in one with pre-existing cardiovascular disease. 

 Oral ingestion. Taking large amounts of 

capsicum orally can increase the production of 

stomach acid, but this would not be caused by 

ingestion of minute amounts of OC from a spray 

or foam. Children occasionally eat CS, and 

several adults have swallowed CS pellets. Aside 

from bouts of diarrhea and abdominal cramps 

(which might have been from the cathartics and 

antacids used as therapy), their courses have 

been uneventful. In animals, the LD50 for CS is 

about 200 mg/kg (which is about 14 grams/70-

kg person), an amount unlikely to be ingested, 

even deliberately. A few animals fed lethal 

amounts (or greater) of CS had gastric irritation 

or erosions, and several had signs of intestinal 

perforation. Recommended therapy after 
205 

ingestion consists of cathartics, antacids, and 

surgical observation. 

Lethality. CN, occasionally in combination 

with DM, has caused deaths in people who 

refused to exit a confined space. In each case 

the agent was used in excess. Death generally 

occurred hours after initial exposure, and postmortem findings were those of severe airway 

damage similar to that seen in animals. Deaths 

directly attributed to OC exposure are not easily 

found in the literature, though theoretically 

severe laryngospasm could cause respiratory 

obstruction, hypoxia, and unconsciousness. 

Those in police custody who died after exposure 

to OC died from pre-existing cardiopulmonary 

conditions, drug intoxication, or positioning while 

restrained that restricted breathing, but no 

deaths were directly attributed to the actions of 

OC. 

 Metabolism. Animals given lethal amounts 

of CS by IV or intraperitoneal (IP) administration 

developed increased blood thiocyanate 

concentrations hours later, indicating that the 

malononitrile portion of CS had been 

metabolized to cyanide. Cyanide was not a 

factor in causing death (lung damage was). A 

significant increase in blood concentration of 

thiocyanate has not been noted after aerosol 

administration of CS. Several popular databases 

mention this cyanogenic potential of CS and 
206 

suggest that treatment of a CS casualty might 

require therapy for cyanide poisoning (this 

recommendation is apparently based on the IV 

or IP administration data). After receiving lethal 

amounts of CS by inhalation, animals died 12 to 

24 hours later from severe airway damage; 

cyanide was not implicated in their deaths. 

 OC will cause depletion of substance P over 

time; once substance P is depleted, pain stops. 

The body rebuilds substance P stores over 

several hours to days. OC is absorbed in the 

body. Those who are exposed to capsaicin for 

long periods of time, such as in food or topical 

salves for pain management, have depleted 

stores of substance P and may not demonstrate 

as extreme a pain reaction to the administration 

of OC. 

ADAMSITE (DM) 

 DM typically appears as a canary yellow 

crystalline solid and has the same unique color 

when dispensed as a cloud. The effects of usual 

field concentrations of DM are similar to those of 

the other riot-control agents, except that DM has 

little irritancy to the skin. However, at higher 

concentrations, DM causes nausea, vomiting, 

and a feeling of generalized malaise. For this 

reason, it is called a vomiting agent.
207 

TIME COURSE OF EFFECTS 

 Except for those produced by DM, the 

biological effects from these agents begin 

seconds after exposure and continue for 15 

minutes or so after one exits the contamination 

to fresh, clean air. The effects from DM begin 

two to four minutes after the onset of exposure 

and may last an hour or two. (This is 

advantageous militarily, as an individual 

unaware of the agent will continue to inhale it for 

several minutes and absorb a larger dose. He 

may then vomit, requiring mask removal, which 

leads to continued inhalation of agent.) 

DIFFERENTIAL DIAGNOSIS 

 Usually the circumstances of exposure 

make the diagnosis obvious. The history and the 

few physical signs (conjunctival injection with 

normal pupils, tearing, etc.) are usually 

adequate. On a battlefield, the sudden onset of 

burning pain and irritation might lead one to 

consider Lewisite or phosgene oxime exposure, 

but the signs and symptoms of riot-control 

agents gradually recede, whereas those from 

the vesicants worsen.
208 

LABORATORY FINDINGS 

 There are no specific laboratory tests that 

will confirm the diagnosis. Complications, e.g., 

infection of a skin lesion, will produce the 

laboratory findings characteristic of the 

complication. 

MEDICAL MANAGEMENT 

 The effects of exposure to these agents 

under the usual field conditions generally are 

self-limiting and require no specific therapy. 

Most will disappear in 15 to 30 minutes, 

although erythema may persist for an hour or 

longer. 

 The following section discusses potential 

complications occurring only under exceptional 

circumstances, such as exposure to a very large 

amount of agent (as in an enclosed space), 

exposure in adverse weather, or experimental 

studies in humans or animals. They are not to 

be expected with normal use of these agents. 

 Less than 1% of exposed people will have 

effects severe or prolonged enough to cause 

them to seek medical care. Those who do 

probably will have eye, airway, or skin 

complaints. Because there is no antidote for 

these agents, treatment consists of symptomatic 

management. 
209 

Eyes. The eye should be carefully flushed 

with water or saline and impacted particles 

should be sought. General care consists of a 

topical solution (many are available) to relieve 

the irritation and topical antibiotics. An 

ophthalmologist should be consulted for further 

evaluation and care. With exposure to OC, milk, 

vegetable oil, or baby shampoo and copious 

amounts of water can be effective for eye 

washing.

Pulmonary. These agents may exacerbate 

chronic disease or unmask latent disease, 

although there is little evidence of this. 

Bronchospasm with wheezing and mild distress 

continuing hours after exposure may occur in a 

latent asthmatic. More severe effects and 

respiratory distress may occur in one with 

chronic bronchitis or emphysema. Management 

includes oxygen administration (with assisted 

ventilation, if necessary), bronchodilators if 

bronchospasm is present, and specific 

antibiotics dictated by the results of sputum 

studies (Gram stains of smears followed by 

culture). A specialist skilled in the treatment of 

inhalation injury should be consulted early. 

Animal studies and very limited human data 

indicate that maximal effects occur 12 hours 

after exposure. 

Skin. The early erythema requires 

reassurance, but no specific therapy unless 
210 

severe and prolonged more than an hour or two. 

The later onset erythema precipitated by a larger 

exposure in a hot and humid atmosphere is 

usually more severe and less likely to resolve 

quickly. It may require the use of soothing 

compounds such as calamine, camphor, and 

mentholated creams. Small vesicles should be 

left intact, but larger ones will ultimately break 

and should be drained. Irrigation of denuded 

areas several times a day should be followed by 

the application of a topical antibiotic. Large, 

oozing areas have responded to compresses 

containing substances such as colloidal 

oatmeal, Burrow's solution, and other 

dermatologic preparations. 

DECONTAMINATION 

 The crystallized solids, CS, CN, CR, and 

DM, can be released from hair, skin, and 

clothing by flapping the arms or the use of fans. 

While many of these are not directly soluble in 

water, washing with soap and water will 

effectively remove these agents from the skin. 

Washing with soap and water is particularly 

important for those exposed to these agents for 

long periods of time, such as an individual 

operating a mask confidence chamber. Water 

will increase the pain of OC, so if it is used it 

should be with copious volumes to help remove 

the OC from the skin surface. A mild soap, such 

as baby shampoo, will help loosen resin, as will 
211 

vegetable oil or alcohol. Casein in milk will help 

to reduce the further release of substance P. 

Milk, with its lipophilic casein, will also effectively 

combine with the capsaicin resin to help wash it 

away. 

TRIAGE 

 A person exposed to the usual field 

concentrations of riot-control agents will 

probably not be seen at a triage area. Those 

presenting with complications should be triaged 

according to the nature of their injuries. 

RETURN TO DUTY 

 Because the effects of field concentrations 

clear within minutes, the casualty should be 

returned to duty as soon as possible. Casualties 

with complications may require evacuation and 

further medical treatment before returning to 

duty. 
212 

DECONTAMINATION 

OVERVIEW 

 Decontamination is the reduction or removal 

of hazardous agents. Decontamination of 

chemical agents may be accomplished by 

removal of these agents by physical means or 

by chemical neutralization or detoxification. 

 There are three levels of patient 

decontamination: (1) immediate 

decontamination primarily protects the patient by 

reducing or eliminating the amount of chemical 

agent on the skin; (2) patient operational 

decontamination reduces the spread of 

contamination from the contaminated patient to 

“dirty” designated transport vehicles; and (3) 

patient thorough decontamination primarily 

protects the medical facility and its staff from 

cross contamination by agent on the patient’s 

skin and clothing. 

 Prompt removal of an agent from the skin by 

any nontoxic means is the key to patient 

decontamination. Immediate decontamination by 

the warfighter can mean the difference between 

minor and significant medical effects from agent 

exposure. 
213 

 The M291 Skin Decontamination Kit (SDK) 

or soap and water are currently the best 

decontaminants for skin. Reactive Skin 

Decontamination Lotion (RSDL), a liquid skin 

decontaminant, is expected to replace the M291 

(SDK), a dry resin-based decontaminant, in the 

future. 

INTRODUCTION 

 Decontamination is the process of removing 

or reducing a hazardous agent, whether 

chemical, biological, or radiological, from a 

person or object. Chemical contamination can 

present as a vapor, aerosol, liquid, or dry solid. 

The key reference for patient decontamination in 

the military is FM 4-02.7, Health Service Support 

in an NBC Environment. 

 Decontamination is not as critical for those 

contaminated only by vapor exposure, because 

vapor will continue to volatilize in the open air; 

rapidly brushing the hair if vapor is trapped in it 

and removing a patient’s clothing where vapors 

can be trapped will usually remove the vapor 

hazard. Exposures to aerosols, liquid, and dry 

solids on the other hand will require more 

thorough decontamination if a patient is to enter 

a facility where staff are not in protective 

clothing. 
214 

 In the military there are three levels of 

patient decontamination. (1) Immediate 

decontamination is performed by the exposed 

individual or a buddy if that individual is unable 

to decontaminate themselves. It reduces the 

dose of agent the patient receives by removing 

agent from the skin. It also reduces agent on 

equipment worn by the patient. (2) Patient 

operational decontamination is decontamination 

that is performed at the unit level to reduce the 

spread of contamination from a patient during 

evacuation in a “dirty vehicle.” Here the patient 

remains in full protective ensemble, and gross 

contamination is removed from the ensemble 

prior to transport. (3) Finally, patient thorough 

decontamination occurs prior to a contaminated 

patient being allowed into a medical treatment 

facility (MTF). A patient decontamination station 

(PDS) is usually established to perform this task. 

Here the patient’s equipment and clothing are 

removed and a more thorough decontamination 

of contaminated skin is performed. 

 Other techniques of decontamination include 

detailed troop decontamination (DTD), which is 

performed by units for those who are not 

casualties but need to exit the contaminated 

battlefield, and technical decontamination, which 

is the decontamination of PDS operators before 

they cross to the uncontaminated side of the 

PDS. 
215 

 The most important decontamination to 

minimize injury to the patient is immediate 

decontamination since it reduces the patient’s 

exposure to a toxic agent. It is most effective if 

performed within one or two minutes after 

exposure, particularly with HD, but the dose will 

still be reduced to some degree if 

decontamination is performed later than this. 

The key is to remove the agent from the skin 

with whatever means are available that are not 

toxic or abrasive to the skin. 

 Decontamination studies have been 

conducted using common household products. 

The goal of these studies was identification of 

decontaminants for civilians, as well as field 

expedients for the warfighters. Timely use of 

water, soap and water, or flour, followed by wet 

tissue wipes, produced results equal, nearly 

equal, or, in some instances, better than those 

produced by the use of Fuller's Earth, Dutch 

Powder, and other compounds. (Fuller's Earth 

and Dutch Powder are decontamination agents 

currently fielded by some European countries.) 

This is easily understood because (1) no topical 

decontaminant has ever shown efficacy with 

penetrated agent, (2) agents in large enough 

quantity, especially vesicants, may begin 

penetrating the skin before complete reactive 

decontamination (detoxification) takes place, 

and (3) early physical removal is most important.
216 

 Copious amounts of water or soap and 

water are effective for washing away most 

agents. A low pressure, high volume of water 

should be used combined with wiping of the 

skin. Fat-based soaps should be used and not 

detergents. The fat-based soaps, such as castile 

soap or other mild liquid soaps, help to emulsify 

thickened agents such as VX and HD. 

 Physical removal is imperative because 

none of the chemical means of destroying these 

agents does so instantaneously. While 

decontamination preparations such as fresh 

hypochlorite react rapidly with some agents 

(e.g., the half time for destruction of VX by 

hypochlorite at a pH of 10 is 1.5 minutes), the 

half times of destruction of other agents, such as 

mustard, are much longer. If a large amount of 

agent is present initially, a longer time is needed 

to completely neutralize the agent to a harmless 

substance.

 The preferred methods of skin 

decontamination in the military are: 

 1. The use of the M291 Skin 

Decontamination Kit (SDK), which contains pads 

impregnated with Ambergard-555 Resin. As the 

pad is scrubbed over the contaminated skin, the 

chemicals are rapidly transferred into and 

trapped in the interior of the resin particles. The 

presence of acidic and basic groups in the resin 
217 

promotes the destruction of trapped chemical 

agents by acid and base hydrolysis. Because 

the resin is black, it maps out the areas that 

have been decontaminated. It is used on intact 

skin, but not in open wounds. Since the M291 

Kit is small and dry and easily carried by the 

warfighter, it is well suited for field use. It will be 

the early intervention with the use of this kit that 

will reduce chemical injury and save lives in 

most cases. Decontamination of the casualty 

using an M291 Kit does not obviate the need for 

decontamination at a field facility. 

 2. Soap and water is a low-cost 

decontaminant that removes agents by washing 

them off the skin. It is effective for removing 

chemical, biological and radiological 

contaminants. It does not destroy biological 

agents or neutralize radioactive particles. Both 

fresh water and sea water have the capacity to 

remove chemical agents not only through 

mechanical force, but also via slow hydrolysis; 

however, the generally low solubility and slow 

rate of diffusion of chemical warfare agents in 

water significantly limit the agent hydrolysis rate. 

The predominant effect of water and water/soap 

solutions is the physical removal or dilution of 

agents; however, slow hydrolysis does occur 

particularly with alkaline soaps. Fat-based liquid 

soap (e.g. baby shampoo, castile liquid soap, or 

soft soap) attract and help emulsify chemical 

agent so that the action of the water can wash it 
218 

away. Detergents that can dry the skin should 

not be used. Clean water can be used to irrigate 

wounds; only copious amounts of water, normal 

saline, or eye solutions are recommended for 

the eye. 

 3. A 0.5% hypochlorite solution with an 

alkaline pH is an alternate skin decontaminant 

that can be used when the others are not 

available and water is limited. It is a solution of 

nine parts water to one part bleach which at this 

dilution is not harmful to the skin. It is wiped on 

the skin and can be rinsed off several minutes 

later with fresh water. This chemical 

decontamination reaction involves very slow 

oxidative chlorination and hydrolysis. The term 

oxidative chlorination covers the "active 

chlorine" chemicals like hypochlorite. 

Hypochlorite solutions act universally against the 

organophosphorus and mustard agents. Both 

VX and HD contain sulfur atoms that are readily 

subject to oxidation and hydrolysis. The 

decontamination effectiveness of these solutions 

increases as the hypochlorite pH levels go 

above 8; but this is harmful to the skin, so at the 

dilution level of 0.5% the oxidation and 

hydrolysis effects are present but very limited. 

Hypochlorite should not be used in abdominal 

wounds, open chest wounds, on nervous tissue, 

or in the eye. Irrigation of the abdomen may lead 

to adhesions and is therefore also 

contraindicated. The use of hypochlorite in the 
219 

thoracic cavity may be less of a problem, but the 

hazard is still unknown. 

 4. Finally, while not yet in the inventory, 

Reactive Skin Decontamination Lotion (RSDL) is 

a new decontaminant that is expected to replace 

the M291 in the future. It is a packaged sponge 

that contains a liquid solution that effectively 

wipes away chemical agents and simultaneously 

provides oxime protection against nerve agents. 

CERTIFICATION OF DECONTAMINATION

 Certification of decontamination for chemical 

agents is accomplished by any of the following: 

processing through the decontamination station, 

M8 paper, or the ICAM (Improved Chemical 

Agent Monitor). If proper procedure is followed, 

the possibility of admitting a contaminated 

casualty to an MTF is extremely small. Fear is 

the worst enemy, not the contaminated 

warfighter. 

WOUND DECONTAMINATION 

 The initial management of a casualty 

contaminated by chemical agents will require 

removal of IPE and skin decontamination before 

treatment within an MTF. 

 When thorough decontamination is 

performed, contaminated bandages are 
220 

removed and wounds are flushed with sterile 

water. Any contaminated debris (such as 

clothing in the wound that may hold agent) is 

irrigated and removed from the wound by 

decontaminated gloved hand, instruments, or 

other no touch technique. The bandages are 

then replaced only if bleeding recurs or the 

wound needs to be protected from further 

contamination. Contaminated tourniquets are 

replaced with clean tourniquets and the sites of 

the original tourniquets decontaminated. Splints 

are thoroughly decontaminated by rinsing with a 

0.5% hypochlorite solution or copious amounts 

of soap and water, but removed only by a 

physician or a medical aidman directly 

supervised by a physician. 

 

 General consideration. Of the agents 

discussed, only two types, the vesicants and 

nerve agents, might present a hazard from 

wound contamination. Cyanide is quite volatile, 

so it is extremely unlikely that liquid cyanide will 

remain in a wound, and it requires a very large 

amount of liquid cyanide to produce vapor 

adequate to cause effects. 

 Mustard converts to a cyclic compound 

within minutes of absorption into a biological 

milieu, and the cyclic compound rapidly 

(minutes) reacts with blood and tissue 

components. These reactions will take place 

with the components of the wound -- the blood, 
221 

the necrotic tissue, and the remaining viable 

tissue. If the amount of bleeding and tissue 

damage is small, mustard will rapidly enter the 

surrounding viable tissue where it will quickly 

biotransform and attach to tissue components 

(and its biological behavior will be much like an 

intramuscular absorption of the agent).

 Although nerve agents cause their toxic 

effects by their very rapid attachment to the 

enzyme acetylcholinesterase, they also quickly 

react with other enzymes and tissue 

components. As they do with mustard, the blood 

and necrotic tissue of the wound will "buffer" 

nerve agents. Nerve agent that reaches viable 

tissue will be rapidly absorbed, and since the 

toxicity of nerve agents is quite high (a lethal 

amount is a small drop), it is unlikely that 

casualties who have had much nerve agent in a 

wound will survive to reach medical care. 

 Potential risk to the surgeon from possibly 

contaminated wounds arises from agent on 

foreign bodies in the wound and from thickened 

agents. 

Thickened agent. Thickened agents are 

chemical agents that have been mixed with 

another substance (commonly an acrylate) to 

increase their persistency. They are not 

dissolved as quickly in biological fluids, nor are 

they absorbed by tissue as rapidly as other 
222 

agents. VX, although not a thickened agent, is 

absorbed less quickly than other nerve agents 

and may persist in the wound longer than other 

nerve agents. 

 Thickened agents in wounds require more 

precautions. Casualties with thickened nerve 

agents in wounds are unlikely to survive to reach 

surgery. Thickened HD has delayed systemic 

toxicity and can persist in wounds even when 

the large fragments of cloth have been removed. 

Though the vapor hazard to surgical personnel 

is extremely low, contact hazard from thickened 

agents does remain and should always be 

assumed. 

 No country is currently known to stockpile 

thickened agents. In a chemical attack, the 

intelligence and chemical staffs should be able 

to identify thickened agents and to alert medical 

personnel of their use. 

Off-gassing. The risk from vapor offgassing from chemically contaminated shrapnel 

and cloth in wounds is very low and not 

significant. Further, there is no vapor release 

from contaminated wounds without foreign 

bodies. Off-gassing from a wound during 

surgical exploration will be negligible (or zero). 

No eye injury will result from off-gassing from 

any of the agents. A chemical-protective mask is 

not required for surgical personnel. 
223 

 Foreign material. The contamination of 

wounds with mustard or nerve agents is 

basically confined to the foreign material (e.g., 

battle dress uniform (BDU) and protective 

garment in the wound). The removal of this cloth 

from the wound effectively eliminates the 

hazard. There is little chemical risk associated 

with individual fibers left in the wound. No further 

decontamination of the wound for chemical 

agent is necessary. 

Wound exploration/debridement.

Surgeons and assistants are advised to wear a 

pair of well-fitting (thin), butyl rubber gloves or 

double latex surgical gloves and to change them 

often until they are certain there are no foreign 

bodies or thickened agents in the wound. This is 

especially important where puncture is likely 

because of the presence of bone spicules or 

metal fragments. 

 The wound should be explored with surgical 

instruments rather than with fingers. Pieces of 

cloth and associated debris must not be 

examined closely, but quickly disposed of in a 

container of 5% hypochlorite. The wound can 

then be checked with the ICAM, which may 

direct the surgeon to further retained material. It 

takes about 30 seconds to get a stable reading 

from the ICAM. A rapid pass over the wound will 

not detect remaining contamination. The wound 

is debrided and excised as normal, maintaining 
224 

a no-touch technique. Removed fragments of 

tissue are dropped into hypochlorite. Bulky 

tissue such as an amputated limb should be 

placed in a plastic or rubber bag (chemicalproof), which is then sealed. 

 Hypochlorite solution (0.5%) may be instilled 

into noncavity wounds following the removal of 

contaminated cloth. This solution should be 

removed by suction to an appropriate disposal 

container. Within a short time, i.e., five minutes, 

this contaminated solution will be neutralized 

and nonhazardous. Subsequent irrigation with 

saline or other surgical solutions should be 

performed. 

 Penetrating abdominal wounds caused by 

large fragments or containing large pieces of 

chemically contaminated cloth will be 

uncommon. Surgical practices should be 

effective for the majority of wounds in identifying 

and removing the focus of remaining agent 

within the peritoneum. Saline, hydrogen 

peroxide, or other irrigating solutions do not 

necessarily decontaminate agents, but may 

dislodge material for recovery by aspiration with 

a large bore sucker. The irrigation solution 

should not be swabbed out manually with 

surgical sponges. The risk to patients and 

medical attendants is minuscule. However, safe 

practice suggests that any irrigation solution 

should be considered potentially contaminated. 
225 

Following aspiration by suction, the suction 

apparatus and the solution should be disposed 

of in a solution of 5% hypochlorite. 

 Superficial wounds should be subjected to 

thorough wiping with soap and water or a 0.5% 

hypochlorite solution and subsequent irrigation 

with normal saline. 

 Instruments that have come into contact with 

possible contamination should be placed in 5% 

hypochlorite for ten minutes prior to normal 

cleansing and sterilization. Reusable linen 

should be checked with the ICAM or M-8 paper 

for contamination; if found to be contaminated, it 

should be disposed of in a 5 to 10% hypochlorite 

solution. 

CONCLUSIONS 

 Decontamination at the MTF is directed 

toward (1) eliminating any agent transferred to 

the patient during removal of protective clothing, 

(2) decontaminating or containing contaminated 

clothing and personal equipment, and (3) 

maintaining an uncontaminated treatment 

facility. 

 Current doctrine specifies the use of the 

M291 (SDK), soap and water, or a 0.5% 

hypochlorite solution. These decontaminants 
226 

have been tested and found to be effective when 

used appropriately. 
227 

CASUALTY MANAGEMENT IN 

 A CONTAMINATED AREA 

OVERVIEW 

 In a contaminated environment, casualties 

enter an MTF through the patient 

decontamination station (PDS). This occurs at 

all levels of medical care where contaminated 

casualties might be received. The purpose of the 

PDS is to remove all contamination, or as much 

as possible, from the casualty before he/she 

enters the clean MTF; this ensures that 

unprotected medical staff inside the facility are 

not made ill or become cross-contaminated by 

the agent that is on the arriving patient. The key 

military reference for the decontamination of 

patients is FM 4-02.7, Health Service Support in 

an NBC Environment, which offers detailed 

instructions on the establishment and operation 

of a PDS. The key reference for the 

establishment of stateside MTF patient 

decontamination is the Occupational Safety and 

Health (OSHA) Best Practices for Hospitalbased First Receivers of Victims from Mass 

Casualty Incidents Involving the Release of 

Hazardous Substances, January 2005. This 

section outlines the key points found in those 

documents. More detailed PDS procedures are 

also found in Appendix A.
228 

ZONES OF CONTAMINATION 

Hot Zone. This is the area that is directly 

contaminated by CBRN agents. In combat, this 

is the contaminated battlefield or TIM release 

site (e.g., factory storage tank or terrorist bomb). 

Casualties usually undergo immediate 

decontamination in the hot zone or on the 

periphery of it. 

Warm Zone. This is an area where low 

levels of dry, liquid, and vapor contamination 

can be expected once contaminated individuals 

enter this area. The contamination hazard is 

essentially the agent that remains on the 

patients that are brought into this area. In this 

zone immediate, patient operational, and patient 

thorough decontamination take place. The PDS 

is initially set up in an area free of 

contamination. This area becomes part of the 

warm zone once contaminated casualties begin 

to arrive. 

 Cold Zone. The cold zone is an area free 

from liquid, dry, and vapor contamination. All 

personnel and patients entering this zone have 

been decontaminated. Protective ensemble and 

mask are usually not required for personnel in 

the cold zone unless the area becomes 

contaminated. Standard precautions must be 
229 

practiced if the patient is infectious from a 

biological agent. 

 The principal components of the PDS are: 

• Entry control point (ECP)/arrival point 

• Triage area 

• Emergency treatment area 

• Decontamination area(s) 

• "Hot line" 

 After crossing the hot line, the casualty 

enters the clean triage and treatment area. From 

there, the now contamination-free casualty is 

brought into that MTF or prepared for “clean” 

disposition to another MTF. 

 The size of the MTF will dictate the 

personnel support needed to staff the PDS to 

ensure that it is functional. At a Battalion Aid 

Station (BAS), for example, staffing is limited 

and the same senior medical NCO serving as 

the triage officer may also provide emergency 

care. The decontamination areas will be staffed 

by a limited number of augmented personnel, 

and very limited medical care can be provided in 

the clean treatment area. At larger MTFs there 

will be a medical professional to triage and 

others to provide emergency care. There will be 

more decontamination lanes and more 

augmentees to man these lanes. If augmented 

personnel are not plentiful, the decontamination 
230 

team will be supplemented by non-medical 

personnel from the hospital staff. Manning a 

PDS can take 19 to 45 people, depending on its 

size and the time that the PDS needs to be in 

continuous operation. 

 The following is intended as an introduction 

to each of these stations. More detailed 

information can be found in the Appendix or in 

the references noted previously. 

KEY COMPONENTS OF A PDS

All PDS operations must have the following 

key components to operate effectively. 

WARM SIDE 

Protection. All staff on this side of the PDS 

wear MOPP Level IV, roughly equivalent to 

OSHA Level C. 

Entry Control Point (ECP) and Arrival 

Area. Patients pass through the ECP where 

access is controlled to the PDS. Vehicles with 

casualties then proceed to the arrival point 

where they are unloaded. This is manned by 

augmentees. Key activities here are (1) routing 

of vehicles, (2) unloading of vehicles, and (3) 

quick pat down searches to remove ordinance 

from patients. All staff are in MOPP Level IV 

when contaminated patients arrive. 
231 

Warm Side Triage Area. This is located 

near the arrival area; patients are moved to this 

area from the arrival point. Here casualties are 

simultaneously triaged as to their need for 

medical care, their priority for patient thorough 

decontamination, and their priority for 

evacuation to the next level of care. Within the 

triage area casualties are moved to either the 

immediate [warm side Emergency Medical 

Treatment (EMT)], delayed, minimal, or 

expectant treatment areas. A patient is retriaged 

as their condition changes. The placement of 

treatment areas in relation to the 

decontamination lanes is suggested to improve 

patient flow through the PDS. 

• The immediate patients are moved to the 

warm side, EMT. This area is located 

between patient triage (closer to triage to 

minimize the time it takes to move from 

triage to dirty EMT) and the entrance to the 

litter decontamination lanes. This way a 

patient can be moved to litter 

decontamination without interfering with the 

traffic flow from other patient groups. 

• The delayed patient area should be 

positioned nearer to the entrance to both the 

litter and ambulatory decon lines. This way 

delayed patients can be processed through 
232 

ory lanes when the 

lanes become available. 

•

e 

interfere with the flow to the litter 

nes. 

• r to 

if the EMT area no longer has patients in it. 

through the EMT and decontamination process. 

either the litter or ambulat

Minimal patients should be positioned near 

to the ambulatory patient area so that if 

medical care on the clean side of the hot line 

is needed they can process through the 

ambulatory lane when it becomes availabl

and not 

la

Expectant patients should be located nea

the EMT area, but farther away from the 

decontamination lanes so that they can be 

retriaged and stabilized for decontamination 

Casualties are retriaged as they progress 

Warm Side Emergency Treatment (EMT) 

Area. Patients triaged as immediate for m

treatment are sent to this area until their 

condition is stabilized for patient thorough

decontamination at this PDS or for dirty 

evacuation to another medical facility. An initial 

quantity of medical supplies are located in this

area to provide antidotes to chemical agents, 

bandages for wounds, equipment to establ

access, intubation equipment to establish 

edical 

ish IV 
233 

to 

d 

ld 

ined and experienced aidmen 

(EMT, c sman, etc.), nurses, or physician 

ss

emergency airways, and decontamination kits 

provide immediate or operational 

decontamination to patients. It is important to 

only put enough supplies here for the anticipate

number of patients so that unused supplies are

not in danger of contamination. The warm side 

EMT area should be large enough to expand

and handle an influx of patients. Staffing shou

consist of tra

orp

a istants. 

Warm Side Disposition (Dirty 

Evacuation). Located in the vicinity 

side EMT. Here patients remain in prote

ensemble and undergo operational 

decontamination and staging for “dirty” 

evacuation (ground, water, 

of the warm 

ctive 

or rotor wing aircraft) 

to another MTF where adequate resources are 

available to care for them. 

Contaminated Waste Dump. Located at 

least 75 meters down wind from the hot line. 

Bags of contaminated clothing and bandages 

are taken to this area where they are buried and 

marked with the appropriate hazard markers. 

The position is communicated to headquarters 

so that the waste can be disposed of properly. 

 Temporary Morgue. A shaded area 

located on the warm side where the 
234 

policy until they are retrieved by the services unit 

contaminated remains of those who die while 

being processed through the PDS are stored. 

These remains stay on the warm side of the hot 

line and are handled in accordance with theater 

that turns them over to mortuary affairs. 

Litter Patient Decontamination Lane(s). 

This area is located between the warm side 

EMT and the hot line where litter patients have 

their clothing removed, contaminated bandage

and splints replaced, and personal effects and 

field medical card (FMC) placed in plastic, zip

lock bags, and where they are decontamin

Patients must be medically stable enoug

undergo decontamination before they are 

brought to this area. Those performing 

decontamination also wear a toxicological agent 

protective (TAP) apron over their protective 

ensemble to keep their protective ensemble d

and to allow them to decontaminate their aprons 

before conducting patient transfers. With the 

exception of the Air Force and some Navy units

who have trained medical teams throughout the

decontamination pro

s 

-

ated. 

h to 

ry 

cess, this area is manned 

by augmentees who are closely supervised by 

an aidman. 

Ambulatory Patient Decontamination

Lane. This area is usually located parallel to the

litter patient decontamination lane. Ambulatory 
235 

al 

ts 

sing 

roop 

le, to 

sup bulatory patients as they process 

patients who need to see the physicians at the 

MTF are processed through this area where 

they have their clothing removed, contaminated 

bandages and splints replaced, and person

effects and FMC placed in plastic, zip-lock bags, 

and they are decontaminated. Ambulatory 

individuals who do not have medical complain

needing to be seen at this MTF are treated in 

the treatment area and returned to their unit 

without undergoing decontamination or cros

the hot line, or they are processed through t

decontamination lanes and not through the 

medical ambulatory decontamination lane. 

Those performing decontamination also wear a 

TAP apron to keep their protective ensemble 

dry. This area is usually manned by at least one

aidman, and other augmentees if availab

ervise am

through the line and assist one another. 

Contamination Check Area. T

located between the decontamination l

the hot line. Here, completeness of 

decontamination is checked using the 

appropriate monitoring devices (e.g., chemical:

ICAM or M8 paper). Zip-lock bags c

patient’s personal items can also be unzipped

and the monitors used to check for 

contamination of the items inside them. The 

decontamination check of patients may not be

necessary where

his area is 

anes and 

ontaining the 

 fully plumbed decontamination 
236 

tents provide adequate soap and water for a 

thorough wash. 

Litter Decontamination Station. 

warm side litters are washed and readied for u

again. Buckets and sponges with 5% 

hypochlorite solution are available as well as 

water to rinse the litters. With a shower/rolle

system,

 Here, 

se 

r 

 litters only need to be sent back through 

the decon station for a wash with soap and 

sonal 

water.

Weapons and Contaminated Per

Effects Storage Area. Here, patient

and personal effects are secured and 

inventoried. Items from this area are 

decontaminated and moved through the 

contamination check area before being sent 

across the hot line. If personnel are limited, this 

area may need to be well o

 weapons 

rganized and under 

the observation of personnel serving as security 

augmentees. 

Warm Side Rest Area. A shaded rest area 

where PDS team members can rest and drink 

water while remaining in their protective 

ensemble. 

Hot Line and Shuffle Pit. The hot line 

separates the PDS warm zone (dirty side) fro

the cold zone (clean side) where the MT

m 

F is 
237 

e 

y 

uch as 

ity. 

ed 

ated 

s 

e warm 

mbers 

augmen es for litter patients and one 

augmentee for ambulatory patients. 

located. No liquid or solid contamination 

crosses the hot line. The line must be 

indicated in some way (e.g., by a barrier, tap

line, or air lock) so that all personnel know the

cannot cross the line until they are properly 

decontaminated. In the battlefield it is best to 

indicate this area with a specific barrier, s

concertina wire, to protect the medical facil

Shuffle pits or boot rinses are located at 

openings along the hot line to ensure that 

footwear worn by individuals moving across the 

hot line is decontaminated. At the hot line, 

information on the patient’s FMC is transferred 

to a clean card, and litter patients are transferr

to a clean litter to ensure that no contamin

cards or litters cross the hot line. A blanket is 

also placed on the patient once they are 

transferred to a clean litter. Team members on 

the clean side receive the patient. Staffing on 

the dirty side consists of the team in TAP apron

that decontaminated the patient and th

side aidman, if available. Receiving me

consist of one medic and at least two 

te
238 

Vapor Control Line (VCL). This line is 

typically upwind of the hot line by approximately 

10 meters. Patients and PDS team members 

remain masked until they cross this line. This 

line can be established using chemical vapor 

detectors such as the ACADA. 

CLEAN SIDE 

 Protection. Personnel assigned to this area 

do not need to wear protective equipment as the 

patients in this area are free from contamination. 

When processing infectious biological 

casualties, staff should practice universal 

precautions and wear appropriate respiratory 

protection. 

Triage/EMT Area (Cold Zone). This 

contamination-free area is located beyond the 

hot line and vapor control line where patients are 

retriaged and treated. It can be a holding and 

staging area for admission to an MTF, for clean 

evacuation to another MTF, or for ambulance 

transport from a co-located (troop and patient) 

PDS to a nearby MTF. 

Disposition (Cold Zone - Clean 

Evacuation). This area is adjacent to the cold 

zone triage/EMT. From this area, contaminationfree patients that have been stabilized are 

staged for transport to another treatment facility. 
239 

Supply Point. This point is located outside 

the VCL. PDS supplies are kept here and are 

handed across the hot line to the warm side 

when needed. 

PDS CRITICAL CONCERNS 

 

Warm Side Triage and Treatment 

 It is important that the triage officer be 

practiced enough to effectively triage patients so 

that the PDS is not overwhelmed with patients 

who can be treated on the warm side and 

returned to their unit; should be dirty evacuated 

to a larger MTF (if that is possible); or stabilized 

in the warm area until they are ready for 

decontamination. The triage officer might be a 

senior medic in a BAS. In larger medical units 

the triage officer might be a physician or 

physician's assistant. His ability to evaluate the 

casualty will be limited because both he and the 

casualty will be in MOPP Level IV. 

Warm Side EMT Care 

 Those casualties needing immediate care 

will be sent to the warm side EMT. Casualties 

classified as minimal might also be sent to this 

area, if the appropriate care can be provided in a 

contaminated environment. The purpose of this 

is to return them to duty quickly and to lessen 

the workload on the decontamination teams. 
240 

However, the types of injuries that can be 

treated without breaking the integrity of the 

protective garment are small; once the integrity 

of the protective garment is violated, the minimal 

casualty will need to be treated and sent through 

troop decontamination to don replacement IPE 

before being returned to the battle area. For 

those patients being processed through patient 

decontamination who might be returned to their 

unit, arrangements will need to be made with 

supported units to have replacement IPE 

available for these casualties. Decontaminated 

litter patients will be placed in a patient 

protective wrap (PPW) if they need to be 

transported on dirty evacuation assets or 

through contaminated areas. Administration of 

MARK I Kits is an example of treatment that can 

be given without breaking the seal of the 

protective garment. 

 Those casualties classified as delayed will 

be sent through the PDS for decontamination if 

they require care in the clean treatment area. 

Otherwise, they will be dirty evacuated to the 

next level of care that can better handle them. 

 The expectant casualty will be temporarily 

set aside, adjacent to the warm side EMT, for 

later re-evaluation as there are no more patients 

in the EMT station. 
241 

 The amount of vapor arising from patient 

IPE should not be enough to preclude an apneic 

patient from being ventilated. Ideally, in a 

battlefield environment a resuscitation device 

individual chemical (RDIC) with its filtered ambubag should be used. Ventilation of a newly 

apneic patient will be limited more by the lack of 

personnel to squeeze the ambu-bag than by the 

risk of forcing more chemical vapor into the 

casualty's lungs. Intravenous injections can be 

given and IV fluids can be started after 

decontamination of the skin at the IV insertion 

site and the care provider's gloves. Minor 

suturing can be done in this area using the same 

precautions. The time needed by the single 

medical care provider to perform these 

procedures is probably the limiting 

consideration, not the risk of further 

contamination. 

Preventing Musculoskeletal and Heat Injury 

 A safety officer must be appointed for 

operations on the warm side of the PDS. This 

can be the NCOIC, OIC, or some other 

individual. It must be someone who can observe 

the PDS workers, travel freely around the PDS, 

and manage work/rest cycles. 

 Worker musculoskeletal injury can easily 

occur from patient lifting and litter carrying or 

injuries caused by falls while wearing protective 
242 

ensemble. To reduce these, clear routes within 

the PDS to reduce tripping hazards; establish 

decontamination lanes far apart to reduce 

clutter; enforce frequent garbage bag removal to 

reduce trip hazards; train and enforce safe-lifting 

techniques; ensure there are adequate rest 

breaks; and use work-saving equipment, e.g., 

NATO litter carriers, if available. 

 Patient triage, treatment, and 

decontamination involve moderate and heavy 

work. Wearing IPE generates heat that is not 

easily dissipated by the process of sweating 

since the wearer’s skin does not contact the air 

to cool. This can create heat injury and increase 

accident frequency as overheated workers 

overlook safety procedures. 

Heat Stroke. Cause: The body’s 

temperature regulatory system fails and 

sweating becomes inadequate. Signs and 

Symptoms: Body temperature is usually 105°F 

(40.5°C) or higher. The victim is mentally 

confused, delirious, perhaps in convulsions, or 

unconscious. Medical Attention: First-aid must 

be administered immediately since death can 

occur without quick treatment. Move the victim 

to a cool shaded area. Process the victim 

quickly across the hot line. Remove the victim’s 

IPE, soak the underclothing with water, and fan 

the body to increase cooling. Evacuate to 
243 

nearest MTF for medically monitored fluid 

replacement. 

Heat Exhaustion. Cause: Loss of large 

amounts of fluid by sweating, sometimes with 

excessive loss of salt. Signs and Symptoms:

Sweating, extreme weakness or fatigue and may 

show giddiness, nausea, or headache; can 

resemble the early heat stroke symptoms. The 

skin is clammy and moist, the complexion is pale 

and flushed, and the body temperature is normal 

or slightly elevated. The victim may lose 

consciousness. Medical Attention: Notify 

medical personnel immediately. Move the victim 

to a cool place and rest. Process the victim 

across the hot line as operation tempo permits. 

Have him drink plenty of liquid. His status 

should be monitored by an aidman. 

Heat Cramps. Cause: Painful spasms of 

the muscles in those who sweat profusely, drink 

large quantities of water, but don’t adequately 

replace salt loss. Medical Attention: Cramps 

may occur during or after work hours and may 

be relieved by taking salted liquids by mouth. 

Move the individual to the warm side rest area 

and seek medical attention. Return to work; can 

be put in a less physically demanding position if 

contention improves; or process across the hot 

line when operations tempo allows. 
244 

Fainting. Cause: Typically seen in a worker 

who is not accustomed to hot environments. The 

heat will cause blood vessels in the skin and the 

lower part of the body to enlarge to try to cool 

the body. The blood may pool there rather than 

return to the heart to be pumped to the brain 

causing the person to faint. Medical Attention: 

The worker should be guided to lie down in the 

warm side rest area. Elevate the legs. Seek 

medical advice. He should recover quickly. 

Return the individual to duty when recovered, or 

process across the hot line when operations 

tempo allows. 

Work/Rest Cycles. These are carried out 

on the warm side of the hot line. Enforcing 

adequate worker rest ensures adequate worker 

hydration, gives the body an opportunity to get 

rid of excessive heat, slows down the production 

of internal body heat that is created during 

physical work, and provides greater blood flow 

to the skin. Wearing protective overgarments 

adds 10°F (5.6°C) to the wet bulb globe 

temperature (WBGT) index, and wearing body 

armor increases this by another 5°F (2.8°C).
MODERATE WORK 

HEAT CATEGORY 

WBGT INDEX 

o F 

WORK/ REST MIN 

WATER INTAKE QT/HR 

WORKREST MIN 

1 

(WHITE) 

78-81.9 NL 3/4 40

2 

(GREEN) 

82-84.9 50/10 3/4 30

3 

(YELLOW) 

85-87.9 40/20 3/4 30

4 

(RED) 

88-89.9 30/30 3/4 20

5 

(BLACK) 

> 90 20/40 1 10
245 

CAUTION: 

Drinking Fluids. A worker may produce as 

much as two to three gallons of sweat in the 

course of a day’s work. A worker, therefore, 

should not depend on thirst to signal when and 

how much to drink. Five to 7 ounces of liquid 

should be consumed every 15 to 20 minutes to 

replenish the necessary fluids in the body. Water 

intake should not exceed 1 quart per hour or 12 

quarts per day, since excessive water 

consumption can dilute the salt content of the 

blood to the point where it interferes with brain, 

heart, and muscle function. This “water 

poisoning” can result in heat attack and 

seizures. 
246 

CHEMICAL DEFENSE 

EQUIPMENT 

 This overview is divided into four sections: 

• Individual Protection 

• Individual Decontamination 

• Detection and Alarms 

• Patient Protective Equipment 

INDIVIDUAL PROTECTION 

 This section includes standard "A" chemical 

defense equipment (CDE) issued to each 

warfighter depending on their MOS and 

consisting of the following: 

• M40 Series Field Protective Mask 

• M42A2 Combat Vehicle Protective Mask 

• M45 Air Crew/Land Warrior Chem-Bio 

Mask System 

• MCU-2A/P Protective Mask 

• Battle Dress Overgarment 

• Joint Service Lightweight Integrated Suit 

Technology 

• Suit Contamination Avoidance and Liquid 

Protective 

• Chemical Protective Gloves and 

Overboots 
247 

• Skin Exposure Reduction Paste Against 

Chemical Warfare Agents (SERPCWA) 

Chemical-Biological Mask: Field M40/M42A2/ 

M45 

TM 3-4240-346-10 

TM 3-4240-348-10 

 This section focuses on three variations of 

protective masks, the M40A1, the M42A2, and 

the M45. These masks share many of the same 

design characteristics, capabilities, and 

features. Each mask has been designed for 

very specific mission requirements, such as 

aircraft or combat vehicle operation. This 

section is not designed to highlight specific 

mask operational capabilities; it is intended to 

provide technical information pertaining to 

overall mask operations. 

 Protective masks provide users with 

respiratory, eye, and face protection against CB 

agents and radioactive fallout particles. If a 

mask is properly fitted and worn correctly it 

provides a gas-tight face seal, which prevents 

contaminated air from reaching the wearer’s 

respiratory, ocular, and dermal systems. 

 

 Masks described in this section have not 

been designed for use TIC environments and 

are known to be ineffective against chemicals 

such as ammonia and carbon monoxide. The 
248 

masks are also not suitable for confined spaces 

where oxygen is insufficient to support life. 

 Each mask is constructed of silicone rubber 

with an in-turned sealing surface so it can form 

a comfortable seal on the wearer’s face, an 

external second skin for additional protection. 

Binocular eye lens system is used for improved 

vision, clear and tinted outserts provide eye 

protection against laser and low speed 

fragmentation, and optical inserts may be 

inserted if the user requires corrective lenses. 

An elastic head harness secures the mask to 

the user’s face. Other common features include 

front and side voicemitters to allow for face-toface and phone communications. Each of the 

masks is furnished with drinking tubes to allow 

for hydration. A key design feature of each of 

the discussed protective masks is the use of a 

standard C2/C2A1 NATO threaded filter 

canister. The C2 filter canister contains 

Chromium VI; damaged or unusable canisters 

are considered hazardous waste and are known 

to be carcinogenic if inhaled or swallowed. The 

C2A1 canister is chromium free but must be 

disposed of in accordance with state and local 

environmental laws. Both canisters are qualified 

to withstand and protect against a maximum of 

15 nerve, choking, and blister agent attacks. 

The canister is externally mounted and may be 

mounted on the left or right side of the user’s 

face depending on the preference of the user. 
249 

Additionally a quick-doff hood is used to provide 

protection to the user’s head and neck. 

MCU-2A/P Protective Mask 

Air Force Technical Order 14P4-15-1 

 The MCU-2A/P Series Mask is designed to 

protect the face, eyes and respiratory tract of the 

user from tactical concentrations of chemical 

and biological agents, toxins and radioactive 

fallout particles. The mask has a unimolded, 

silicone rubber face piece and a single flexible 

lens bonded onto the face piece. The large lens 

gives the user a wide field of vision. It has a 

single filter and two voicemitters, one on the 

front of the mask for speaking directly into a 

telephone or radio handset and one at the side 

to allow personnel nearby to hear. A nosecup 

with two inlet valves fits over the nose and 

mouth. It directs incoming air across the inside 

of the lens to reduce fogging. The mask has a 

drinking tube that connects to a canteen with an 

M1 cap. The mask is not authorized for use 

during TIC spills, and the mask is not effective 

against chemicals such as ammonia, chlorine, or 

even carbon monoxide fumes. The mask is not 

effective in confined spaces where oxygen 

levels are insufficient to sustain life. 
250 

Battle Dress Overgarment (BDO) 

TM 10-8415-209-10 

 The Battle Dress Overgarment will hereafter 

be referred to as the BDO. The BDO chemical 

protective overgarment is a two-piece 

overgarment consisting of a coat and separate 

trousers. The BDO is available in a factorysealed, vacuum-packaged, vapor-barrier (VB) 

bag. The VB bag assists in protecting the BDO 

from environmental impacts associated with 

storage. Each VB bag contains a jacket and 

trousers. The suit is composed of an outer layer 

constructed of 50/50 nylon cotton tightly woven 

material that has been treated with waterresistant sealant. The liner or inner layer is 

constructed of charcoal-impregnated 

polyurethane foam, nylon tricot laminate. BDOs 

are available in various camouflage patterns 

with sizes ranging from extra extra small (XXXS) 

to double extra large (XXL). Once the BDO has 

been removed from the vacuum-sealed 

packaging, the suit offers 22 days of wear. With 

slight increase in risk commanders may increase 

wear time to 30 days. Wear time for the BDO 

begins when the seal is broken on the VB bag. 

To properly maintain the BDO when not in use, it 

should be sealed in the original VB bag or other 

similar material bag. The bag can be sealed with 

duct tape, 100 mile per hour tape, or other 

suitable tape. Donning the BDO regardless of 

the amount of time within a 24-hour period 
251 

constitutes a day of use. The BDO is currently 

qualified to offer 24 hours of protection against 

CB agents in solid, liquid, or vapor form; the suit 

also protects against alpha and beta radioactive 

particles. 

Joint Service Lightweight Integrated Suit 

Technology (JSLIST) 

TM 10-8415-220-10 

 The Joint Service Lightweight Integrated 

Suit Technology (JSLIST) Chemical Protective 

Overgarment (CPO) has been designed to 

replace its predecessor, the battle dress 

overgarment (BDO). The JSLIST CPO is a twopiece overgarment consisting of a coat with an 

integrated hood and separate trousers. The 

CPO has been designed to be lighter weight, 

more flexible and have the ability to be 

laundered up to six times. In addition the system 

has also been designed to reduce the stresses 

of protective gear. The JSLIST CPO is available 

in four- color woodland and three-color desert 

camouflage patterns. The JSLIST suit is 

composed of an outer layer of 50/50 

nylon/cotton poplin, rip-stop material with 

camouflage pattern facing outward. The liner or 

inner layer is polyester knit coated with activated 

carbon spherical absorbers covered by a 

nonwoven laminate that is bonded to a tricot knit 

back. Unlike the BDO, JSLIST suits are not 

packaged as sets; JSLIST suits consist of a coat 
252 

and trousers. Each component is separately 

packed in a factory-sealed vacuum bag 

containing the ensemble item and a resealable 

bag. JSLIST suits are available in seven sizes 

ranging from short extra small (SXS) to large 

long (LL). The JSLIST overgarment is currently 

qualified to offer 24 hours of protection against 

CB agents in solid, liquid, or vapor form; the suit 

will also protect against alpha and beta 

radioactive particles. 

 

 Once the CPO has been removed from the 

vacuum- sealed packaging, the suit offers 45 

days of wear and 120 days of service life. To be 

properly maintained and stored when not in use, 

the JSLIST CPO should be placed in the 

resealable bag that is furnished with each 

component of the ensemble. 

 Both the BDO/JSLIST ensemble will be 

worn in all environments when under threat of 

an imminent nuclear, biological, or chemical 

attack or after chemical operations have been 

initiated. 

 Once the suit has been contaminated, the 

Warfighter must replace the suit by using the 

MOPP gear exchange procedure described in 

STP 21-1-SMCT, Warfighter's Manual of 

Common Tasks, October 2003, Task 

#031-503-1023, Exchange MOPP Gear. The 

BDO/JSLIST adds weight to the Warfighter’s 
253 

workload. In addition, the BDO/JSLIST prevents 

heat exchange with the environment and may 

add, depending on the Warfighter's level of 

exertion, 10o

F to 15oF to his ambient 

temperature and heat burden. When wearing the 

BDO/JSLIST at MOPP 1 or MOPP 2, and 

complete encapsulation is not required, certain 

modifications to the uniform are authorized: 

• The trouser leg closures may be unzipped. 

• The waist tabs may be loosened. 

• The jacket may be unzipped. 

• The sleeve Velcro closures may be 

opened. 

 This overall loosening of the BDO/JSLIST 

will allow heat to escape as walking and other 

movements induce a bellows action of the suit 

against underlying clothing and skin. 

Suit, Contamination Avoidance and Liquid 

Protective (SCALP) 

TM 10-8415-209-10 

 The SCALP is an impermeable, lightweight, 

inexpensive, disposable ensemble that provides 

supplemental liquid protection. The SCALP is a 

four- piece ensemble that consists of a jacket, 

trousers, and two footwear covers. It is designed 

to be worn over the BDO or JSLIST with 

protective overboots. The footwear covers are 

constructed with 12 mil embossed polyethylene 
254 

soles. The SCALP ensemble provides protection 

from gross liquid contamination for up to one 

hour. Operationally the SCALP is used to protect 

personnel who are conducting decontamination 

procedures from becoming soaked during decon 

operations. 

Chemical Protective Gloves and Overboots

• Green/Black Vinyl Overboots (GVO) 

(BVO) 

• The Multipurpose Overboot (MULO) 

• Gloves, 0.025-inch thickness 

• Gloves, 0.014-inch thickness 

• Gloves, 0.007-inch thickness 

Green or Black Vinyl Overboots (GVO) (BVO)

 The overboots have been designed to be 

worn over combat boots to protect the user’s 

feet. The boots are available in sizes 3-14. The 

GVO/BVO are constructed of vinyl, making them 

impervious to all known chemical and biological 

agents and alpha and beta radiological particles. 

They also protect against environmental effects 

such as rain, mud, and snow. Both boots are 

similar except for the color and the enlarged, 

elastic pull-tab fasteners on the BVO. The 

GVO/BVO are qualified to offer 60 days of 

protection. If the GVO/BVO become 

contaminated, they provide 24 hours of 

protection. Following contamination, use a 5% 
255 

HTH and water solution or a 5% household 

bleach and water solution to decontaminate the 

GVO/BVO. Ensure boots are serviceable and no 

signs of deterioration are present after the 

decontamination process. If boots are deemed 

to be unserviceable, replace them. 

Multipurpose Overboot (MULO)

 The multipurpose rain/snow/CB overboot 

(MULO) replaces the older black vinyl 

overboot/green vinyl overboot (BVO/GVO). The 

MULO is made by injection molding an 

elastomer blend, compounded to provide the 

characteristic chemical and environmental 

protection required. It incorporates two quickrelease side buckles and is designed to be worn 

over the standard issue combat boot, jungle 

boot, and intermediate cold/wet boot. The 

MULO provides 60 days of durability and 24 

hours of protection against liquid chemical 

agents. The MULO is capable of being 

decontaminated to an operationally safe level 

using standard field decontaminants. 

Environmental protection is provided against 

water, snow and mud, in addition to petroleum, 

oil, and lubricant (POL). Additionally, the MULO 

is flame resistant. 
256 

Chemical Protective Glove Set

 Chemical protective glove sets are qualified 

to offer protection against chemical and 

biological agents, as well as alpha and beta 

radiological particles. The chemical protective 

glove set consists of an outer glove for 

protection and an inner glove for absorption of 

perspiration. The outer gloves are made from 

black butyl rubber and are impermeable to 

chemical agents. The inner gloves are made of 

thin, white cotton. 

 Glove sets are available in three 

thicknesses, 7 mil to 25 mil, and in sizes ranging 

from extra small (XS) to extra large (XL). 

 The 25-mil glove offers the most durable 

protection and may be utilized to perform close 

combat tasks or other types of heavy labor. 

The 14-mil glove is less durable and is used in 

an environment in which much less physical 

demand is placed on the glove. Such users 

could include vehicle mechanics, aviators, or 

weapons crews. 

If either glove becomes contaminated, 

decontaminate or replace within 24 hours after 

exposure. Contaminated gloves may be 

decontaminated with a 5% chlorine solution or a 

5% HTH and water solution. 
257 

 The 7-mil gloves offer the most tactility and 

are used by individuals who require extreme 

sensitivity to accomplish tasks without 

subjecting the glove to harsh treatment. If the 7-

mil glove becomes contaminated, replace or 

decontaminate it after six hours of exposure. 

Contaminated gloves may be decontaminated 

with a 5% chlorine solution or a 5% HTH and 

water solution. 

Skin Exposure Reduction Paste Against 

Chemical Warfare Agents (SERPACWA) 

NSN 6505-01-483-7162 

 SERPACWA is used by service members in 

conjunction with MOPP) gear to enhance 

protection against chemical warfare agents. 

Approved by the FDA for military use only, it is a 

cream containing chemically inert perfluorinated 

polymers. It is applied to susceptible areas of 

the skin before donning MOPP gear. Not 

intended for use by itself, SERPACWA will 

provide additional protection at those locations 

where the MOPP is susceptible to leakage or 

separation, including the waist, groin, armpits, 

wrists, ankles, and neck. In conjunction with 

personal decontaminating materials, the use of 

SERPACWA will prevent or reduce the toxicity 

resulting from exposure to chemical warfare 

agents. When used as directed, SERPACWA 

will provide between five and eight hours of 

protection. 
258 

For further information on these items, see 

Multiservice Tactics, Techniques, and 

Procedure for Nuclear, Biological, and 

Chemical (NBC) Protection FM 3-11.4 June 

2003, Chapters VI, Appendix A.

INDIVIDUAL DECONTAMINATION 

 The preceding section provided an overview 

of the primary items of chemical defense 

equipment which, when used correctly, will 

prevent contact with agent in typical battlefield 

concentrations. The problem of 

decontamination arises when some warfighters, 

because of bad training, bad discipline, or bad 

luck, become exposed to liquid agent despite 

the availability of protective masks and clothing. 

 This section addresses two 

decontamination kits currently in the inventory--

the M291 Decontaminating Kit Skin and the 

M295 Decontamination Kit Individual 

Equipment. The kits are fairly simple in design 

and function, and instructions for their use are 

straightforward and easily committed to 

memory. Because of the potency of liquid nerve 

agents and the rapidly occurring tissue damage 

caused by vesicants, every warfighter must be 

able to conduct an effective decontamination of 

all exposed skin without referring to the 

instructions printed on the kits. 
259 

Decontaminating Kit, Skin: M291

NSN 4230-01-276-1905 

TM 3-4230-229-10 

 The M291 Skin Decontamination Kit 

consists of a wallet-like carrying pouch 

containing six individually sealed 

decontamination applicator pads. Each pad is 

filled with FDA-approved Ambergard XE-555 

decontaminating resin. Each kit allows 

personnel to decontaminate their skin of liquid 

nerve and vesicant agents through physical 

removal, absorption, and neutralization of 

chemical agents. The M291 kit is nontoxic and 

has been designed for external use. Since it 

may be slightly irritating to eyes or skin, 

decontamination powder should be kept out of 

eyes, cuts, and wounds. Inhalation of the 

powder should be avoided as it can irritate the 

lungs. 

 Each of the individual decontamination pads 

is capable of providing decontamination 

coverage to the face and hands or an equivalent 

area of skin from exposure to chemical agents. 

Effective decontamination will result in blacking 

of decontaminated skin areas. 
260 

Decontamination Kit, Individual Equipment: 

M295 (DKIE)

NSN 4230-01-357-8456 

TM 3-4230-235-10 

 The M295 DKIE consists of a pouch 

containing four individually sealed wipe down 

mitts. Each wipe-down mitt is comprised of a 

sorbent decontaminating powder containing 

alumina and silica. Each kit allows personnel to 

decontaminate their individual equipment 

through sorption of contamination by both the 

pad and the decontaminating powder. 

Decontamination is effective against liquid nerve 

and vesicant chemical agents. Kits are worn 

over protective ensembles and are capable of 

decontaminating approximately 1,200 square 

feet. (M291 kits may be used to decontaminate 

such items as the CB mask and hood, gloves, 

footwear, weapons, helmet, and load-bearing 

vest.) 

 M295 kits are issued in boxes of 20 kits. The 

kits should be stored at the squad level in a box 

capable of being decontaminated. 

DETECTION AND ALARMS 

 This section will describe the equipment 

issued for detection and identification of 

chemical agent liquid and vapor in the 

environment. For both the individual warfighter 
261 

and the unit, these items of equipment (listed 

below) are the primary means of identifying the 

presence and type of chemicals on the 

battlefield and determining when a safe 

condition exists. 

• Paper, CM Agent Detector: M9 

• Paper, CM Agent Detector: M8 

• Chemical Agent Detector Kit: M256A1 

• Chemical Agent Monitor 

• Automatic Chemical Agent Alarm: M8A1 

• Water Test Kit, Chemical Agents: M272 

Paper, CM Agent Detector: M9

NSN 6665-01-049-8982 

TM 3-6665-311-10 

 M9 detector paper is placed on personnel 

and equipment to detect and identify the 

presence of liquid nerve or blister agents in 

exposures as small as 100 microns in diameters. 

The paper contains an indicator chemical dye 

that will turn pink, red, reddish brown, or red 

purple when exposed to liquid agents. The paper 

is capable of detecting but cannot identify 

specific agents. M9 paper is manufactured in 30-

feet x 2-inch adhesive-backed rolls of dull, offwhite/cream-colored paper. The rolls are 

packaged with a reusable plastic storage bag in 

a vacuum-sealed, vapor-barrier package. The 

detector paper dye may be a potential 

carcinogen, so chemical protective gloves should 
262 

be worn when handling M9 detector paper. 

Placement of M9 is dictated by the dominant 

hand of the user. If the user is right-handed, M9 

detector paper should be placed around the right 

upper arm, left wrist, and right ankle. If the user 

is left-handed, M9 detector paper should be 

placed around the left upper arm, right wrist, and 

left ankle. If a color change is indicated, proper 

masking, decontamination, and MOPP 

procedures must be followed. 

NOTE: *M9 Chemical Agent Detector Paper will 

not detect cyanide. 

 Many substances are known to cause false 

positive responses on M9 paper. The following 

are common false positive indicators: antifreeze, 

liquid insecticide, or petroleum products. 

Attention to possible interfering substances on 

the battlefield can help in the later interpretation 

of a color change on the M9 paper in the 

absence of confirmation tests for agents. This 

does not relieve the service member of the 

obligation to mask and take other appropriate 

measures. 

Paper, CM Agent Detector: M8

NSN 6665-00-050-8529 

 M8 Chemical Agent Detector Paper is used 

to detect the presence of liquid V type nerve, G 

type nerve, and H type blister agents. M8 paper 
263 

is issued in booklets containing 25 tan-colored 

sheets of chemically treated, dye-impregnated 

paper. Each page is perforated and staplebound for easy removal. The reverse side of the 

front cover contains a color comparison bar 

chart for color comparison agent recognition. 

 If M8 paper is exposed to chemical agents, 

the dye impregnated paper will convert from tan 

to an agent-specific color, depending on the 

agent. The following agents will cause the dye to 

change to one of three colors. 

• G: Nonpersistent Nerve: Yellow 

• H: Blister: Red 

• V: Persistent Nerve: Olive Green or Black 

NOTE: *M8 Chemical Agent Detector Paper will 

not detect cyanide. 

 If indicated by M9 chemical agent detector 

paper or encountering a liquid suspected of 

being a chemical agent, service members must 

follow proper masking, decontamination, and 

MOPP procedures. 

 To prepare M8 paper to conduct agent 

identification, tear one half sheet from the 

booklet and affix the sheet to a stick or other 

object. Use the stick as a handle, blot the paper 

onto the unknown liquid, and wait for 30 

seconds. Once 30 seconds has elapsed, 
264 

compare the tested M8 paper to the color 

comparison bar chart located on the inside cover 

of the booklet. 

 The following are common false positive 

indicators: antifreeze, liquid insecticide, or 

petroleum products. Attention to possible 

interfering substances on the battlefield can help 

in the later interpretation of a color change on the 

M8 paper 

Improved Chemical Agent Detector Kit: 

M256A1

NSN 6665-01-133-4964 

TM 3-6665-307-10 

 The M256A1 Chemical Agent Detection Kit is 

designed to detect and identify chemical agents 

in liquid or vapor and consists of the following: 

• A booklet of M8 paper (previously 

described) to detect agents in liquid form; 

and 

• 12 foil-wrapped detector tickets containing 

eel enzymes as reagents to detect very 

low concentrations of chemical vapors. 

 Instructions for the use of the detector 

tickets appear on the outside of each of the foil 

packets and in a separate instruction booklet in 

the kit. The chart below shows the agents 

detected by the M256A1 Kit.
265 

Agent Detected Symbol Class 

Hydrogen 

Cyanide AC "Blood" (cyanide) 

Cyanogen 

Chloride CK "Blood" (cyanide) 

Mustard H Blister 

Nitrogen 

Mustard HN Blister 

Distilled Mustard HD Blister 

Phosgene 

Oxime CX Blister 

Lewisite L Blister 

Nerve Agents V and G 

Series 

Nerve 

By following the directions on the foil 

packets or in the instruction booklet, service 

members can conduct a complete test with the 

liquid-sensitive M8 paper and the vaporsensitive detector ticket in approximately 20 

minutes. During the test, the sampler must be 

kept out of direct sunlight, which speeds 

evaporation of the reagents. Waving the 

detector sampler in the air also accelerates 
266 

evaporation, so the sampler should be held 

stationary during all parts of the test. 

Simulator, Detector Tickets, Chemical 

Agents: Training, M256A1

NSN 6665-01-112-1644 

TM 3-6665-320-10 

 The M256 trainer simulator was developed 

to provide realistic training while avoiding 

unnecessary exposure to potentially 

carcinogenic reagents in the M256A1 detector 

kit. The M256 trainer contains 36 preengineered detector tickets and an instruction 

booklet. The pre-engineered detector tickets 

show color changes comparable to those seen 

when the M256A1 detector kit is used in clean or 

contaminated environments. 

Improved Chemical Agent Monitor (ICAM)

NSN 6665-01-199-4153 

TM 3-6665-331-12&P 

 The ICAM, which is used to detect nerve and 

blister agents as vapors only, uses a 10-mCi 

nickel-63 (Ni63) beta-particle radiation source to 

ionize airborne agent molecules that have been 

drawn into the unit by a pump. The resulting ion 

clusters vary in mass and charge and thus also 

travel at different rates in an applied electrical 

field. Comparison of the mobilities of the different 

ionic species to electronically stored standards 
267 

allows an on-board microcomputer to determine 

the type of agent and its relative concentration. A 

liquid crystal display (LCD) presents these data 

as a series of concentration-dependent bars in a 

G mode for G agents and VX and in an H mode 

for blister agents. 

 

 The ICAM detects agent vapor in that 

volume of air drawn by the pump into the 

sampling chamber of the instrument. It follows 

that the inlet port must not come into contact with 

a suspected area of evaporating agent on a 

surface but must nevertheless approach within a 

few inches of the site of suspected 

contamination. Because of the variation in agent 

concentration from one spot to another, 

depending upon wind velocity and other 

environmental factors, numerical displays of 

agent concentration in typical units would be 

impractical and unreliable. Accordingly, the 

display warns of a low vapor hazard (1 to 3 bars 

visible), a high vapor hazard (4 to 6 bars visible), 

or a very high vapor hazard (7 to 8 bars visible). 

M22 Automatic Chemical Agent Alarm 

ACADA)

NSN 6665-01-438-6963 

TM 3-6665-321-12&P 

 The M22 is an automatic agent alarm 

system capable of detecting and identifying 

standard blister and nerve agents. The 
268 

system is man-portable, operates 

independently after system start-up, and 

provides an audible and visual alarm. The 

M22 system also provides communications 

interface for automatic battlefield warning. 

The system consists of the M88 detector, as 

many as five M42 alarm units, a confidence 

sample, protective caps, square inlet, rain 

caps, a carrying case, and various power 

supplies. 

 The M22 ACADA samples the air for the 

presence of nerve agent vapors (GA, GB, 

GD, VX) and blister agent vapors (HD, L), 

and provides simultaneous detection and 

warning of these agents. It operates in cold 

and hot climates (-30o

F to +125oF). Tactical 

operations of the M22 system are basically 

the same as the M8A1 Automatic Chemical 

Agent Alarm, except for some improvements 

over the M8A1. The M88 detectors normally 

are placed facing into the wind no more than 

150 meters outside of the unit perimeter, 

with no more than 300 meters between 

detectors. They are connected to the alarm 

units with WD-1/TT telephone wire; 

whenever possible, the distance between 

the detector units and the alarm units should 

not exceed 400 meters. Improvements over 

the M8A1 system are as follows: 
269 

• Simultaneous detection and warning 

of nerve and blister agents 

• Significantly more sensitive than the 

M8A1 

• Much less response to interference 

 The following items can interfere with 

the normal operation of the M22 ACADA 

and will sound a false alarm: 

• CS Tear Gas 

• JP8 Fuel 

• Brake Fluid 

• Aqueous Fire Fighting Foam (AFFF) 

• M18 Marking Grenade (Red and 

Violet) 

Water Testing Kit, Chemical Agents: M272

NSN 6665-01-134-0885

TM 3-6665-319-10 

 The M272 Water Test Kit was designed and 

fielded to answer the need for a test to detect 

water contamination by nerve agent, blister 

agent, cyanide ("blood" agent), or Lewisite. The 

kit will operate between 32o

F and 125oF. An 

enclosed instruction card enables the warfighter 

to conduct all the tests required to identify the 

threat agents. The kit will detect the chemical 

agents at the concentrations indicated on the 

following chart. 
270 

Chemical 

Agent Symbol(s) 

Concentration 

(mg/l)-* 

Cyanide AC 20.0 as CNMustard HD 2.0 -- 

Lewisite L 2.0 as As+++ 

Nerve G/V 0.02 -- 

 *Concentration reliably detected by kit tests. 

Water-containing agents in lesser 

concentrations are permissible for short-term 

use (up to 7 days) in both cold and warm 

regions as long as the daily consumption per 

person does not exceed 5 quarts. Each kit 

contains enough reagents for tests on 25 

separate water samples. The operator can 

easily conduct the full range of tests in 20 

minutes when the temperature is between 50-

105°F; at lower temperatures, the water samples 

and the nerve agent ticket should both be 

warmed for 10 minutes before beginning testing. 

Water that is too hot may cause foaming in the 

detector tubes for Lewisite, mustard, and 

cyanide; therefore, water at temperatures 

between 105-125°F should be cooled for at least 

5 minutes to reduce its temperature to 105° or 

cooler. 
271 

PATIENT PROTECTIVE EQUIPMENT 

 In this section, the following three items that 

have been fielded will be discussed: 

• Patient Protective Wrap 

• Decontaminable Litter 

• Resuscitation Device Individual Chemical 

(RDIC) 

Patient Protective Wrap

Wrap, Patient, Chemical Protective 

NSN 6530-01-383-6260 

Blower, Lightweight 

NSN 4240-01-442-8415 

Hose Assembly 

NSN 4240-01-442-2314 

 Many protective garments have been 

developed for military personnel; however, 

protection for patients who are unable to wear 

standard chemical protective garments was 

lacking. The Chemical Warfare Patient 

Protective Wrap was developed to satisfy this 

requirement. The addition of the blower unit 

serves as a modification for the improvement of 

the performance of the Patient Wrap by 

increasing airflow to the patient. The Wrap 

resembles a lightweight sleeping bag. It is 107 

cm wide x 249 cm long and weighs 2.7 kg. It is 
272 

constructed of a permeable sheet of carbonimpregnated fabric and an impermeable bottom 

sheet. The top sheet has an impermeable 

transparent window to permit observation of the 

patient during transit. A port to provide a 

protective entryway for the insertion of IV tubing 

is located at each side of the window. 

 The blower unit is a small, lightweight unit 

that provides a continuous flow of clean, filtered 

air for breathing. The benefit of the addition of 

this item is a considerable reduction in the 

danger of heat stress on the casualty, and an 

increase in the operational effectiveness of the 

wrap while in hot climates. 

 The system consists of: 

• Wrap, Patient, Chemical Protective 

• Blower, Lightweight 

• Hose Assembly 

NOTE: Patients should not be left in the wrap 

for longer than six hours. 
273 

Decontaminable Litter

NSN 6530-01-290-9964 

 Contaminated casualties arriving at a 

medical treatment location will in most cases 

require decontamination prior to definitive 

treatment. This decontamination process will 

require the use of the limited supplies of 

equipment organic to the treatment unit. Ideally, 

equipment in limited supply should be capable of 

complete decontamination using field-available 

methods. However, in tests conducted by the 

U.S. Army Research, Development, and 

Engineering Command, canvas litters exposed 

to liquid blister agents and then decontaminated 

still desorbed vapors for 72 hours after all 

surface contaminants were removed. 

 The decontaminable litter was developed to 

replace the canvas litters. The new litter is made 

from a monofilament polypropylene that has 

high tensile strength and low elasticity. The 

fabric does not absorb liquid chemical agents 

and is not degraded by decontaminating 

solutions. The fabric is flame retardant, highly rip 

resistant, and treated to withstand exposure to 

weather and sunlight. The fabric has a 

honeycomb weave that results in a rough, nonslip surface, and liquids easily pass through the 

40% of surface area that is open. The carrying 

handles retract into the metal pole frame for a 

closed total length of 83.5 inches (212.1 cm) to 
274 

allow for loading the litter onto the UH-60 

helicopter. The handles have TWO open 

positions, 90.0 inches (228.1 cm) and 91.6 

inches (232.7 cm). The first position is a NATO 

standard, and litter bearers provided the second 

position to allow increased gripping comfort. The 

aluminum poles have been designed to provide 

direct gripping surfaces for litter stanchions. All 

metal parts have been painted with Chemical 

Agent Resistant Coating (CARC) paint. 

Resuscitation Device, Individual Chemical

NSN 6515-01-338-6602 

 The RDIC is a ventilatory system consisting 

of a compressible butyl rubber bag, a NATO 

standard C2 canister filter, a nonrebreathing 

valve, a cricothyroid cannula adapter, and a 

flexible hose connected to an oropharyngeal 

mask. The mask is removable from the distal 

end of the flexible hose for connection of the 

hose to the cannula adapter. The butyl rubber 

bag resists the penetration of liquid chemical 

agent that may be on the chemical protective 

gloves of the operator and is easily 

decontaminated. The elasticity of the outer cover 

limits airway pressure to a maximal value of 70 

cm H2O (70 mbar). The device will deliver up to 

600 ml of filtered air per cycle at a rate of 30 

cycles per minute. 
275 

APPENDIX A

PATIENT DECONTAMINATION 

OVERVIEW 

 Patient decontamination is personnel, time, 

and equipment intensive. Nevertheless, with a 

little ingenuity and attention to just a few basic 

principles, an effective patient decontamination 

procedure can be accomplished with minimal 

cost. The first part of this appendix briefly 

discusses considerations in establishing a 

patient decontamination station (PDS), followed 

by step-by-step procedures. 

 The PDS is part of the MTF, and the same 

considerations for establishing the treatment 

facility apply to the decontamination area. The 

decontamination area is located about 50 

meters downwind from the treatment area (i.e., 

wind blowing from the clean treatment area to 

the dirty decontamination area). 

KEY PRINCIPLES 

• Wind direction 

• Security of the decontamination station 

• Area control of the decontamination 

station 

• Litter patient decontamination 
276 

• Ambulatory patient decontamination 

 The important considerations of personnel 

and equipment requirements are discussed in 

other publications. 

Wind Direction 

 Wind direction is important because a vapor 

hazard may be present downwind from a liquid 

contaminated area (i.e., patient arrival/triage 

area). Patient decontamination is always 

performed upwind, or at least not downwind, 

from the patient arrival area. 

 The decontamination station will initially be 

set up to take advantage of the prevailing wind; 

however, setup should be adaptable to allow for 

quick rearrangement when the wind comes from 

another direction. 

 If the wind changes direction by more than 

30o

, the decontamination station will need to be 

adjusted accordingly. A wait of 10 to 15 minutes 

to determine if the change is permanent should 

precede the move. When the station is moved, it 

must be moved at least 75 meters upwind from 

any contaminated area. 
277 

Security of Decontamination Site 

 When choosing a decontamination site, the 

same security considerations must be given as 

for any other site chosen for medical operations. 

The decontamination site is at the same 

potential risk from attack as is the actual MTF. 

Area Control of Decontamination Site 

 An entry control point (ECP) can be 

established to control movement of clean and 

contaminated vehicles to the MTF or the 

Decontamination Station. The ECP should be 

located at a distance far enough from the MTF 

to keep vapor hazard from contaminated 

vehicles to the minimum. 

 Traffic control at the decontamination site 

involves routing a clearly marked, one-way 

course from the ECP to the decontamination 

station. 

 Control of personnel movement is necessary 

to ensure that contaminated walking personnel 

do not accidentally contaminate clean areas. 

The hot line must be secured. Concertina wire 

works well to keep personnel in the desired 

areas, and a clearly marked, one-way route 

helps to ensure that correct entry and exit points 

are used. 
278 

Litter Patient Decontamination

Personnel. Two people are required per 

litter patient. These two augmentees will link up 

with one litter patient in the triage area and work 

with that same litter patient until hand-off at the 

“hot line.” These two people conduct both 

clothing removal and any required skin 

decontamination. To assist these two 

augmentees, two other augmentees will be 

needed, one to assist the first two augmentees 

in picking up the patient from the clothing 

removal litter, and the second to remove the 

contaminated clothing and litter and replace it 

with a clean litter. These four augmentees will 

conduct all patient decontamination and 

movement of the patient while in MOPP Level IV 

and the Toxicological Agent Protective (TAP) 

apron.

 Personnel working in the patient 

decontamination area will be at MOPP level IV 

plus the Toxicological Agent Protective (TAP) 

apron. At least two people from this area will 

move to the triage area and carry the patient 

from this area to the first decontamination 

station. 

Hypochlorite Solutions. Hypochlorite 

solution is used as an alternative decontaminant 

in patient decontamination; however, the 
279 

hypochlorite solution must be prepared. Two 

concentrations of the hypochlorite solution are 

required. A 5% solution is used to 

decontaminate gloves, aprons, litters, cutting 

devices, the patient’s mask hood, and other nonskin contact areas. A 0.5% solution is used to 

decontaminate the patient’s mask, skin, splints, 

and tourniquets and to irrigate their soft tissue 

wounds. 

 The chlorine solutions are placed in buckets 

for use in their particular area. The buckets 

should be distinctly marked because it is very 

difficult to tell the difference between the 5% and 

0.5% chlorine solutions. These solutions may be 

made using the 6-ounce Calcium Hypochlorite 

(HTH) containers that come with the Chemical 

Agent Decon Set. The 0.5% solution can be 

made by adding one 6-ounce container of 

calcium hypochlorite to 5 gallons of water. The 

5% CL solution is made by adding eight 6-ounce 

containers of calcium hypochlorite to 5 gallons of 

water. These solutions evaporate quickly at high 

temperatures, so if they are made in advance, 

they should be stored in closed containers. 

Procedure

1. Decontaminate the hood and mask. 

Wipe/sponge down the voicemitter, eyelets 

and outserts with the M291 SDK, or 5% 

bleach solution. While wiping around the 
280 

filter, cover the inlet of the C2A1 filter 

canister with a hand or gauze momentarily 

to keep liquid out of the inside of the canister 

where it could wet the charcoal, reduce filter 

efficiency, and clog the filter. To decon the 

hood (quick doff hood or integrated 

hood/hooded overgarment), wipe down the 

hood using M291 SDK or 5% bleach 

solution (starting at the top of the head and 

wiping down towards the litter and 

shoulders). 

2. Remove hood. 

a. Remove the quick doff hood of the M40 

mask 

(1) Dip the cutting device in a bucket of 5% 

bleach solution or decon/scrub-cutting 

tool with the M295 or M291. 

(2) Cut the hood shoulder straps. 

(3) Cut the quick-doff hood from the front 

bottom center to the chin through the 

elastic band under the chin. 

(4) Cut from the center of the forehead and 

over the top of the head toward the litter 

so that the hood will lay flat on the litter. 

b. Remove the hood of the JSLIST. 

(1) Dip the cutting device in a bucket of 5% 

bleach solution or decon/scrub-cutting 

tool with the M295 or M291. 
281 

(2) Cut the hood starting at the front center 

and continue cutting across the top of 

the head toward the litter. 

(3) Fold the left and right sides of the hood 

away from the head onto the litter. 

3. Decontaminate head. After the hood is 

laying flat on the litter under the patient’s 

head, decontaminate any exposed areas of 

the patient’s head, hair, back of the ears, 

and neck that were not protected by the 

hood. The mask remains on the patient. This 

exposed skin is decontaminated using either 

the M291, soap and water, or 0.5% bleach 

solution. Do not use 5% bleach solution on 

skin. 

4. Remove the Field Medical Card (FMC). 

a. The medic at the litter patient 

decontamination station should view the 

FMC prior to removal. 

b. Cut the patient’s FMC tie wire, allowing the 

FMC to fall into a plastic, “zip-lock” bag. Seal 

the plastic bag and decontaminate the 

outside of the bag with the M291, M295, or 

rinse the outside of the bag with 0.5% 

bleach solution. Place the plastic bag with 

the FMC under the back of the protective 

mask head harness straps. The FMC will 

remain with the patient until he reaches the 
282 

hot line, where it will be transcribed onto a 

clean FMC. 

5. Remove gross contamination from the 

patient’s protective overgarment. Wipe all 

evident contamination spots with M291 SDK 

or 5% bleach solution. 

6. Remove patient’s personal effects from 

overgarment. Remove all items from the 

protective overgarment pockets and place 

them in a plastic “zip-lock” bag. Label the 

bag with the patient’s identification and seal 

the bag. If the articles are not contaminated, 

place them in a separate bag from 

suspected contaminated items. Wipe down 

the outside of the bag with the M291 or dip it 

in a bucket of 5% hypochlorite solution. The 

bags are sent on the litter with the patient 

and checked for contamination at the 

contamination check area.

NOTE: The patient's identification tags stay 

around their neck throughout the 

decontamination process. They are 

decontaminated with soap and water, M291, or 

0.5% bleach. 
283 

7. Cut the patient’s overgarment. 

a. The overgarment jacket and trousers may 

be cut simultaneously. Two persons may be 

cutting clothing at the same time. 

b. Cutting is performed using sharp bandage 

scissors or long-handled seatbelt cutters (J 

knife). 

c. Cut around bandages, tourniquets, and 

splints, leaving them in place. Only medical 

personnel remove bandages, tourniquets, 

and splints. 

NOTE: Dip cutting device in a bucket of 5% 

bleach solution after each complete line of cut to 

avoid contaminating inner parts of the clothing or 

exposed skin. If bleach solution is not available, 

then cutting tools must be scrubbed using the 

M295 or M291. 

8. Remove overgarment jacket. 

a. Unfasten or cut the Velcro closures at the 

wrists. 

b. Start cutting at the collar and make two cuts, 

one up each sleeve from the wrist to the 

shoulder and then to the collar. Keep the 

cuts close to the insides of the arms so that 

most of the sleeve material is folded 

outward. An alternative is to start at the 

collar and cut down the sleeve to the wrist. 
284 

c. Cut the jacket drawstring at the bottom of 

the jacket and unfasten Velcro closures, 

moving from the waist to the neck, and then 

unzip the jacket. If the jacket will not unzip, 

make a cut parallel to the zipper. 

d. Carefully fold the sleeves of the 

overgarment away from the patient’s arms, 

exposing only the black liner. Avoid 

aerosolizing any dust particles on the 

garment or allowing the outside of the 

garment to touch the patient. 

e. Instruct the patient to keep his hands to the 

sides, away from the pieces of overgarment 

lying on his chest. If the casualty is unable to 

lift his arms, then one augmentee will hold 

the casualty’s gloved hand and perform this 

action. Another augmentee then carefully 

folds the chest sections over the outside of 

the litter. The patient’s arms are then 

lowered to the sides, keeping the arms away 

from the area where the overgarment has 

been removed. 

9. Remove overgarment trousers. 

a. Cut the trouser suspenders. 

b. Cut the leg closure cord and hook and pile 

fasteners at the ankle cuff. 

c. Cut from the ankle along the inseam of the 

left trouser leg until the crotch area is 

reached, and then cut across the zipper. 
285 

d. Cut along the inseam of the right trouser leg 

until the crotch area is reached, then go 

sideways into the first cut at the zipper. 

e. Allow the trouser halves to drape over the 

sides of the litter. Carefully roll and tuck the 

remaining cloth (that at the crotch and on 

the inside of the legs) in on itself ensuring 

that only the black liner of the cloth is 

showing. 

10. Remove outer gloves. Do not remove the 

inner gloves. 

a. Decontaminate your own gloves with the 

M295, M291, or 5% bleach solution. 

b. Decontaminate the casualty's gloves with 

the M295, M291, or 5% bleach solution. 

c. Instruct the casualty to hold his arms away 

from the litter and upper body or, if he 

cannot comply with instructions, hold his 

gloves by the fingers. 

 

NOTE: Always remove the gloves over the 

sides of the litter.

d. Grasp the cuff of the glove, turning the glove 

inside out, and remove it. 

e. Carefully lower the patient’s arm(s) across 

his chest as each glove is removed. Avoid 

touching the patient’s cloth glove liner or 

arm with your rubber glove. 
286 

CAUTION: Do not allow the arms to contact 

the exterior (camouflage) side of the 

overgarment. 

f. Dispose of the contaminated gloves by 

placing them in a trash bag. 

g. Decontaminate your own gloves with the 

M295, M291, or 5% bleach solution. 

11. Remove black vinyl overboots (BVO) or 

Multi-purpose overboot (MULO). 

a. Unfasten the three elastic closures. 

b. Gently pull the overboot by the heel until it is 

removed. 

c. If the overboot will not come off, cut the boot 

from top to bottom along the centerline of 

the boot or along the inside of the boot. Fold 

the overboot down and gently pull the heel 

until it is removed. 

12. Remove personal effects from BDU. Place 

personal effects in a plastic, zip-lock bag. 

This can be the same bag used for items 

taken from the overgarment pockets if they 

were not contaminated; otherwise, place 

these items in a separate bag. Seal the bag 

and decontaminate the outside of the bag. 

Keep the bag with the patient or take to a 

contaminated item holding area where they 

can be decontaminated. 
287 

13. Remove combat boots without touching 

body surfaces. 

a. Cut the boot laces along the tongue. 

b. Pull the boots downward and toward you 

until removed. 

c. Place the boots in the plastic bag containing 

the chemical overboots and gloves. 

14. Remove inner clothing. 

a. Cut or unbuckle belt. 

b. Cut the BDU pants following the same 

procedures as for the overgarment trousers. 

c. Cut the BDU jacket following the same 

procedures as for the overgarment jacket. 

15. Remove undergarments. 

a. Remove the patient’s T-shirt. Dip the cutting 

device in the 5% hypochlorite solution 

between each cut. Cut both sleeves from the 

inside, starting at the elbow, up to the 

armpit. Continue cutting across the shoulder 

to the collar. Cut around bandages or 

splints, leaving them in place. Next, peel the 

T-shirt away from the body to avoid 

spreading contamination. 

b. If the patient is wearing a brassiere, cut it 

between the cups. Cut both shoulder straps 

where they attach to the cups and lay them 

back off of the shoulders. 
288 

c. Remove the patient’s undershorts/panties by 

cutting from the lower side of the hip to the 

waist on both sides. 

d. Remove the socks and cotton glove liners. 

e. Do not remove the patient’s identification 

tags. 

16. Litter transfer and decontamination. 

Transfer the patient to a decontamination 

litter. After the patient’s clothing has been 

cut away, he is transferred to a 

decontaminable litter. The decontamination 

team members decontaminate their gloves 

and apron with the 0.5% hypochlorite 

solution or M291. One member places his 

hands under the patient’s legs and thigh, a 

second member places his arms under the 

patient’s back and buttocks, and the third 

member places his arms under the patient’s 

shoulders and supports the head and neck. 

They carefully lift the patient using their 

knees, not their backs, to minimize back 

strain. While the patient is elevated, another 

decontamination team member removes the 

litter from the litter stands and another 

member replaces it with a clean 

decontaminable litter. The patient is carefully 

lowered onto the clean litter. Two 

decontamination members carry the litter to 

the skin decontamination station. The 

contaminated clothing and overgarment are 

placed in bags and moved to the 
289 

decontaminated waste dump. The dirty litter 

is rinsed with the 5% bleach solution or 

M295 for reuse. 

17. Skin and Wound Decontamination. 

a. The casualty is now decontaminated with 

soap and water, the M291, or 0.5% bleach 

solution. 

b. If the patient was in IPE, the best method is 

to decontaminate only those skin areas 

where there was a break in the IPE (e.g., 

around wounds, areas where the underlying 

uniform is wet with agent, or where there is 

a tear in the overgarment). 

c. If the patient is not wearing IPE or had 

significant uniform tears or damaged 

underlying uniform, an alternate method is to 

decontaminate the entire skin surface by 

wiping the skin with a sponge and soapy 

water, or 0.5% bleach solution with a water 

rinse. Wash the casualty from the midline 

outward, constantly washing from clean to 

dirty and not placing a dirty sponge back on 

a clean area without first rinsing the sponge. 

The complete topside of the casualty is 

washed in this manner, paying particular 

attention to hairy areas of the body (groin 

and axillary regions) and sweaty areas (beltline, just above the boots, the crease of the 

buttocks, and wrists). After log-rolling the 

patient onto his side, wash the backside of 
290 

the casualty. Then wash the casualty's back 

from the shoulders to over halfway down the 

backside, taking care not to miss any areas. 

The upper side of the litter is deconned prior 

to rolling the patient to their back again. 

Wash the opposite side of the casualty in 

exactly the same manner, and 

decontaminate the litter with soap and 

water. 

d. After the patient is decontaminated, his 

dressings and tourniquet are changed. 

Superficial (not body cavities, eyes, or 

nervous tissue) wounds are flushed with the 

0.5% CL solution and new dressings are 

applied as needed. Cover massive wounds 

with plastic or plastic bags. New tourniquets 

are placed 0.5 to 1 inch proximal to the 

original tourniquet, and then the old 

tourniquets are removed. Splints are not 

removed but saturated to the skin with 0.5% 

CL solution. If the splint cannot be saturated 

(air splint or canvas splint), it must be 

removed sufficiently so that everything 

below the splint can be saturated with the 

0.5% CL solution. The patient, his wounds, 

and the decontaminable litter have now 

been completely decontaminated. 

18. Final monitoring and movement to treatment 

area. The patient is monitored for 

contamination using the (ICAM) or M8 

paper. Once the casualty is confirmed clean 
291 

of chemical agent, he is transferred via a 

shuffle pit over the hot line. The shuffle pit is 

composed of two parts Super Tropical 

Bleach (STB) and three parts earth or sand. 

The shuffle pit should be deep enough to 

cover the bottom of the protective overboots. 

The buddy system wash of the TAP apron 

and gloves in 0.5% hypochlorite solution 

precedes the transfer of the patient to a 

new, clean canvas litter if the 

decontaminable stretchers are in limited 

supply. A three-person patient lift is again 

used as the litter is switched. If the litter as 

well as the patient was checked, both 

patient and the same litter can be placed 

over the hot line. 

AMBULATORY PATIENT DECON 

 Casualties that are decontaminated in an 

ambulatory area are those who require 

treatment that can be provided in the clean 

treatment area/MTF. These casualties will have 

their clothing removed during the 

decontamination process before crossing the 

hotline to the clean side. 

 Casualties who require only minimal care 

will undergo spot decon of their overgarment. 

They will be treated in the contaminated EMT 

area and return to duty. 
292 

Personnel

 Personnel from the decontamination station 

might assist the casualty, or the casualties might 

assist each other during this process under 

close supervision. 

Procedure

 Decontamination of ambulatory casualties 

closely follows the methods described in FM 4-

02.7 Health Service Support in an NBC 

Environment and FM 3-5, NBC 

Decontamination. 

 The step-by-step procedure outlined below 

is the prescribed doctrine for decontaminating 

an ambulatory patient, but it is by no means the 

only method. Knowing this method, however, 

ensures that correct and essential steps are not 

omitted, and when they are, other measures are 

taken to preclude a hazardous outcome. 

 The M291 Skin Decontamination Kit or a 

soap solution and water are used for chemical 

contamination on the skin. (The least desired 

alternative for skin decontamination is bleach 

[hypochlorite solution]). A 0.5% hypochlorite 

solution with water rinse is useful if water is 

limited and the M291 kits are not available. Only 

a 0.5% hypochlorite solution is used for skin 

decontamination; higher concentrations will 
293 

irritate and burn the skin, allowing agents to 

enter the skin more rapidly. 

 The M295 Decontamination Kit Individual 

Equipment is used to remove obvious 

contamination from the patient and help to 

control the spread of contamination on IPE 

(MOPP ensemble) and other equipment. If it is 

not available, then either soap solution or a fieldexpedient adsorbent material, such as clean dry 

earth or flour, can be substituted. 
294 

 The first five steps are the same as in litter 

patient decontamination and are not described 

in detail. 

1. Decontaminate mask and hood. 

2. Remove hood. 

3. Decontaminate head. 

4. Remove the FMC. 

5. Remove gross contamination from the 

outergarment. 

6. Remove casualty's overgarment. 

a. Cut overgarment around tourniquets, 

bandages, and splints. One augmentee 

medic or an augmentee will supervise the 

patients to cut one another’s overgarments 

off if there are not adequate numbers of 

augmentees to assist. 

NOTE: Dip cutting device in a bucket of 5% 

bleach solution after each complete line of cut to 

avoid contaminating inner parts of the clothing or 

exposed skin. If bleach solution is not available, 

cutting tools must be scrubbed using the M295 

or M291.
295 

b. Remove overgarment jacket by cutting. 

 (1) The casualty is standing and can hold 

on to a support such as a chair or litter 

stand. 

 (2) First, cut around all bandages and 

tourniquets. 

 (3) Cut the Velcro wrist closures. 

 (4) Cut the BDO jacket drawstring or the 

JSLIST drawcord at the jacket bottom. 

On the BDO, unzip the three snaps that 

connect the back of the BDO jacket and 

pants. 

 (5) Cut the BDO/JSLIST jacket starting at 

the waist and cut toward the collar in a 

line parallel to the zipper. 

 (6) Instruct the casualty to clench his fists; 

stand with arms held down and 

extended backward at about a 30-

degree angle if the jacket was unzipped 

or cut in the front. If the jacket was cut 

along the rear have the patient extend 

the arms forward at about a 30-degree 

angle. 

 (7) Grasp the jacket collar at the sides of 

the neck and peel the jacket off the 

shoulders in a down and away motion, 

smoothly pulling the jacket inside out 

over the casualty's fists. 

 (8) Place the jacket in a plastic trash bag. 
296 

NOTE: The jacket may need to be cut along the 

sleeve if bandages are in the way and sleeves 

cannot be rolled over the bandaged area. 

c. Remove the overgarment trousers by 

cutting. 

 (1) The casualty should have an object to 

help steady him in standing, such as a 

chair or litter stand. 

NOTE: Do not cut the trouser suspenders until 

the end of the process; you do not want the 

trousers to fall and interfere with the cutter. 

 (2) Keep the pants zipped. Unfasten Velcro 

ankle fasteners and begin cutting at the 

ankle. Cut along the inseam and move 

up toward the waist of the trousers. After 

cutting both trouser legs from ankle to 

waist, cut each suspender and allow the 

trousers to fall to the ground. Take the 

trousers and lay them on the ground, 

black side up, next to the patient. Later 

the patient will step onto this as he 

removes his overboots. 

NOTE: After each long cut, dip the cutting 

device in a bucket of 5% bleach solution or 

decon the scrub-cutting tool with the M295 or 

M291. 
297 

7. Remove the overboots. 

a. Unfasten all boot closures. 

b. Step on the heel of the boot and have the 

patient step out of the overboot and onto the 

black side of the cut trousers that are lying 

on the ground. Repeat this process for both 

boots. The overboots can be 

decontaminated and issued to other 

individuals. 

c. If the overboot will not come off, cut the boot 

from top to bottom along the centerline of 

the boot until the boot is loose enough to 

remove. 

8. Remove outer gloves. Do not remove the 

inner glove liners. 

a. Decontaminate your own gloves with the 

M295, M291, or 5% bleach solution. 

b. Decontaminate the casualty's gloves with 

the M295, M291, or 5% bleach solution. 

c. Instruct the casualty to hold his arms up, if 

possible, and away from his upper body. If 

the patient cannot do this, hold his gloves at 

the fingers. 

d. Grasp the cuff of the glove. 

e. Pull the cuff over the fingers, turning the 

glove inside out. 

f. Dispose of the contaminated gloves by 

placing them in a trash bag. 

g. Decontaminate your own gloves again with 

the M295, M291, or 5% bleach solution. 
298 

9. Remove inner gloves. The patient should 

remove the liners to reduce the possibility of 

spreading contamination. The augmentee 

instructs the casualty to remove the white 

glove inner liner using the following 

guidance: 

a. Grasp heel of glove liner without touching 

exposed skin. 

b. Peel liner downward and off. 

c. Drop it into the plastic trash bag. 

d. Remove the remaining liner in the same 

manner. 

e. Drop it into the plastic trash bag. 

f. The patient then moves to the monitoring 

station. 

NOTE: Waste material from two ambulatory 

patients, including the cut trousers, are placed 

into one 35-gallon trash bag along with the 5% 

bleach and soapy water that was used on the 

two patients. Tie the bag shut and transport it to 

the dirty dump. 
299 

10. Monitor xx.

a. Monitor with ICAM or M8 detection paper. 

b. Check all areas of the casualty's clothing 

and combat boots. Pay particular attention 

to: 

 (1) Combat boots 

 (2) Protective mask 

 (3) Hair and neck area 

 (4) Discolored areas 

 (5) Damp spots 

 (6) Wrist closure area 

 (7) Areas under tears in BDO 

 (8) Around dressings and splints 

c. If clean, send the casualty to the hot line. 

d. If contaminated areas are found, 

decontaminate the areas using the M291 or 

soap and water. If the BDOs are 

contaminated they must be removed (see 

following). After decontamination or BDO 

removal, recheck the area with the ICAM or 

the M8 detection paper. 

11. Remove the BDU. 

a. Remove personal effects from BDU

 (1) Have the casualty remove all items from 

his BDU and deposit them into a ziplock bag. 

 (2) Check for contamination. If not 

contaminated, they remain with the 
300 

patient. If contaminated, they are moved 

to a contaminated item holding area. 

b. Remove inner clothing (if contaminated). 

 (1) Cut or unbuckle belt. 

 (2) Cut the BDU pants following the same 

procedures as for the overgarment 

trousers. 

 (3) Cut the BDU jacket following the same 

procedures as for the overgarment 

jacket. 

c. Remove undergarments (if contaminated). 

 (1) Remove the patient’s T-shirt. 

 (a) Dip cutting devices in 5% bleach 

solution or scrub them with the 

M295 or the M291 between each 

cut. 

 (b) Cut around bandages or splints, 

leaving them in place. 

 (c) Cut up the front (back) of the 

patient’s T-shirt from the waist up to 

the collar. 

 (d) Cut both sleeves from the elbow to 

the shoulder and then to the collar. 

 (e) Next, peel the T-shirt away from the 

body to avoid spreading 

contamination. 

 (2) Remove the patient’s brassiere. 
301 

 (a) Cut it between the cups. 

 (b) Cut both shoulder straps where they 

attach to the cups and remove the 

brassiere. 

 

 (3) Remove the patient’s 

undershorts/panties. 

 (a) Cut from the lower side of the hip to 

the waist on both sides. 

 (b) Place the undergarments into the 

plastic garbage bag containing the 

other contaminated items. 

12. Check Patient for Contamination. 

a. After the patient’s BDU and underwear have 

been removed, check the skin, hair, and 

boots for contamination by using M8 

detector paper or the ICAM. 

b. Carefully survey all areas of the patient’s 

skin, paying particular attention to areas 

around the neck, wrist, ears, dressings, and 

splints. 

13. Final Decontamination. At the 

contamination check area, use the M291, 

soap and water, or a 0.5% hypochlorite 

solution followed by a water rinse on any 

areas of the patient that still indicate 

contamination. 
302 

14. Remove any contaminated bandages and 

tourniquets (the medic does this procedure). 

a. Place new tourniquets 1/2 to 1 inch above 

the old tourniquets. 

b. Remove old tourniquets. 

c. Decontaminate the exposed skin area. 

d. Cut away bandages. 

e. Decontaminate the exposed skin area. 

f. Replace bandages only to control bleeding. 

g. Decontaminate exposed skin. 

15. Conduct final check for completeness of 

decontamination with the ICAM or M8 

detection paper. 

16. Move to the hot line. The augmentee 

instructs the patient to move 10 to 30 meters 

to the shuffle pit/hot line. 

The Hot-Line and Clean Side Actions for the 

Ambulatory Patient 

NOTE: Straddling the hot line is the casualty 

pass-over point, which is in a shuffle pit. The 

shuffle pit is composed of two parts super 

tropical bleach (STB) and three parts earth (by 

volume). The ambulatory patient shuffle pit 

should be wide enough for the ambulatory 

patient and two assistants. 
303 

1. At the shuffle pit, an augmentee from the 

clean side meets the patient and opens a 

blanket or other covering for the patient that 

is appropriate for the environmental 

conditions. 

2. The patient shuffles through the shuffle pit 

wearing combat boots. 

3. Once across the vapor control line, the 

ambulatory patient can remove his mask. 

4. In the clean treatment area, the patient is 

now retriaged, treated, and evacuated. 

a. In a hot climate, the patient will probably be 

significantly dehydrated; the rehydration 

process must begin immediately. 

b. Overhead cover should be provided for 

casualties in the holding area. It is here that 

the mask may be removed for treatment 

unless circumstances dictate that the 

casualty remains closer to the Hot line. 
304 

Comments 

 The clean area is the resupply point for the 

patient decontamination station. Water is 

needed for rehydration of persons working in the 

decontamination area. The resupply section 

should have an adequate stock of canteens with 

the M1 cap. 

 An area should be established 50 meters 

perpendicular to the litter casualty 

decontamination line and approximately 5 

meters from the hot line for workers to use as a 

rest and rehydration point. Prior to using this 

point, workers must decontaminate the TAP 

aprons they are wearing using a 5% bleach 

solution and doff the apron near the 

decontamination line. Mask quick doff hoods, if 

worn, should also be decontaminated. After 

completion of this decontamination process, the 

warfighters are checked for contamination; then 

moved to the rest/rehydration point. If it is not 

safe to remove the mask, warfighters can 

rehydrate using their mask drink tubes. 
305 

APPENDIX B 

PATIENT DECONTAMINATION 

STATION 

 The diagram shows a set-up for casualty 

management in a contaminated environment. 

The chapter on casualty management describes 

the various areas. 

 The actual set-up of this station may vary 

depending on the assets and circumstances.

307 

APPENDIX C 

TOXICITY DATA 

 The following tables provide estimated 

human toxicity data on the agents discussed in 

this handbook. 

 Agent Effect Ct50 (mg-min/m3) Liquid on 

skin 

GA Miosis ~2-3 

Death 200-400 

GB. Miosis ~3 

Death 100-200 

GD. Miosis ~2-3 

Death 50-70 

VX Death 10-50 

HD Eye 12-200 

HD Pulmonary 100-200 

Erythema 200-1000 10 μg 

Death 

1500 inhalation 

10,000 skin 100 mg/kg 

L Erythema >1500 10-15 μg 

Death ~1500 inhalation 40-50 mg/kg
308 

 Agent Effect Ct50 (mg-min/m3) Liquid on 

skin 

CX Eye 200? 

Erythema 2500? 

Death 3200? 

CG Pulmonary 

effects >1600 

Death 3200 

AC Death 2500-5000 

CK Death 11,000 

CN Irritation 10-20 

Death 14,000 

CS Irritation 5-10 

Death >50,000 
309 

APPENDIX D 

PHYSIOCHEMICAL DATA 

The following tables provide physiochemical data on 

the agents discussed in this handbook.
GA 

Tabun 

GB 

Sarin 

GF G

So

Molecular Weight 162 140 180 1

Vapor Density 

(compared to air) 

5.63 4.86 6.2 6

Liquid Density 

(g/cc) 

1.07@25oC 1.102@20oC 1.17@20oC 1.02@

Freezing/Melting 

Point (oC) 

-50 -56 -30 -

GA 

Tabun 

GB 

Sarin 

GF G

So

Boiling Point (oC) 

(@ 750mm HG ) 

247 147 239 

(@20oC) 

1

Vapor Pressure 

(mm HG @25oC) 

0.07 2.9 0.04(@20o

C) 

0

Volatility (mg/m3 at 

25oC) 

610 17,000 581 3,
HD 

(Distilled Mustard)

L 

(Lewisite)

Molecular Weight 159 207 

Vapor Density 

(compared to air) 

5.4 7.1 

Liquid Density(g/cc) 1.27@20oC 1.89@20oC 

Freezing/Melting 

Point (oC) 

14.5 -18 

Boiling Point (oC) 

(@750mm HG) 

(227.8) 190 

Vapor Pressure (mm 

HG@ oC) 

0.07@20oC 0.2239@20oC 

Volatility (mg/m3) 600@20oC 4480@20oC 
AC 

(Hydrogen 

Cyanide)

CK 

(Cyanogen Choride)

Molecular Weight 27 61.5 

Vapor Density 

(compared to air)

0.94 2.1 

Liquid Density(g/cc) 0.69 1.18 

Freezing/Melting 

Point (oC)

-13.3 -6.9 

Boiling Point (oC) 

@750mm HG) 

25.7 12.8 

Vapor Pressure 

(mg/m3) 

630@20oC 1230@25oC 

Volatility (mg/m3) 1,080,000@25oC 2,600,000@12.8oC 
CN

(Mace)

CS 

Molecular Weight 154.59 189 

Vapor Density (compared to 

air) 

5.3 -- 

Liquid Density(g/cc) 1.32 (solid) @20oC 1.04@2

Freezing/Melting Point (oC) 58 -94 

Boiling Point (oC) (@750mm 

HG) 

248 315 

Vapor Pressure (mm HG) 0.0041@20oC 0.00034@

Volatility (mg/m3) 115@20oC 0.71@2
310 

APPENDIX E 

EQUIPMENT LIST 

MEDICAL EQUIPMENT SET 

CHEMICAL AGENT PATIENT TREATMENT 

(30 patients) 

6545-01-5187565, MES CHEM AG TRMT-2003 

4240014422314 HOSE ASSEMBLY, 

AIR B EA 12 

4240014428415 BLOWER, 

LIGHTWEIGHT EA 12 

4720014061637 HOSE METALLIC EA 12 

6130015009675 BATTERY CHARGER 

4POSI EA 1 

6140015009672 RECHARGEABLE 

BATTERY EA 24 

6505009269083 ATROPINE INJ 0.7ML EA 500

6505011253248 PRALIDOXIM CHL 

INJ2ML EA 50 

6505013321281 ATROPINE SULF 

INHAL6S PG 1 

6505014542525 ATROPINE SULFATE 

OPHT TU 12 

6505014578901 ANTIDOTE 

TREATMENT EA 5 

6505015053476 DIAZEPAM INJ 2ML 10S PG 10 
311 

6515006878052 AIRWAY PHARY 

100MM10S PG 1 

6515007540412 SYRINGE 

HYPODERMI100S PG 1 

6515007542834 NEEDLE HYPO 18GA 

100S PG 2 

6515009582232 AIRWAY PHARYN 

80MM10S PG 1 

6515013386602 RESUSCITATOR HAND 

OPR EA 4 

6515014123099 SYRINGE 

HYPODERMIC20S PG 1 

6515014355350 SUCTION APPAR 

OROPHAR EA 2 

6515015195876 ADMINISTRATION 

SET60S PG 1 

6530013836260 WRAP AND LITTER PAT EA 12 

6530015196886 BAG STERILIZATION 

10S PG 1 

6545009143490 CHEST NO4 30X18X12 

EM EA 3 

6640015007717 CARTRIDGE 

RESPIRATOR EA 48 

6640015007721 INDICATOR AIRFLOW EA 1 

7520009357135 PEN BALL-POINT 

BLACK DZ 1 

8415011382503 GLOVES CHEM PROT 

LGE PR PR 4 
312 

MEDICAL EQUIPMENT SET 

CHEMICAL AGENT DECONTAMINATION 

(60 patients) 

6564-01-15187568, CHEM AGT PA-2003 

6515009357138 SCISSORS 

BANDAGE7.25" EA 15

6515011688108 SYRINGE HYPO 

10ML100S PG 1 

6515014123099 SYRINGE 

HYPODERMIC20S PG 1 

6530006600034 SUPPORT LITTER 

FOLDNG PR 8 

6530013807309 LITTER FOLDING 91.60" EA 4 

6545009143490 CHEST NO4 30X18X12 

EM EA 3 

6545009143510 CHEST MED INS SUP 

NO6 EA 1 

6665000508529 PAPER CHEM AGENT 

25S BK 6 

6665012265589 PAPER CHEMICAL 

AGEN RO 1 

6840002550471 DISINFECTANT CALC 

6OZ BT 49

6850012761905 DECONTAMINATING KIT BX 2 

7240002461097 PAIL UTILITY PLAS3GAL EA 10

7520009357135 PEN BALL-POINT BLACK DZ 1 

7540014608995 FORM PRINTED BK 1 
313 

7920008841115 SPONGE CELLULOSE 

RECT EA 60

8105001913902 BAG PLASTIC RO 2 

8135006181783 PLASTIC SHEET RO 

POLY RO 1 

8415002817813 APRON TAP SMALL EA 2 

8415002817814 APRON TAP MEDIUM EA 4 

8415002817815 APRON TAP LARGE EA 2 

8415010333517 GLOVE SET CHEM 

PROTEC SE 2 

8415010333518 GLOVE SET CHEM 

PROTEC SE 4 

8415010333519 GLOVE SET CHEM 

PROTEC SE 4 

8415011382494 GLOVE INSERTS CHEM 

SM PR 25

8415011382495 GLOVE INSERTS 

MEDIUM PR 25

MCU-2A/P Protective Mask 

Item Size NSN 

MCU-2A/P Protective 

Mask S 4240-01-327-4148 

MCU-2A/P Protective 

Mask M 4240-01-327-4149 
314 

MCU-2A/P Protective 

Mask L 4240-01-327-4150 

M40-A1 Protective Mask 

Item Size NSN 

M40-A1, 

Protective Mask S 4240-01-258-0061 

M40-A1, 

Protective Mask M 4240-01-258-0062 

M40-A1, 

Protective Mask L 4240-01-258-0063 

M42-A2 Protective Mask 

Item Size NSN 

M42-A2, 

Protective Mask S 4240-01-413-4100 

M42-A2, 

Protective Mask M 4240-01-413-4101 

M42-A2, 

Protective Mask L 4240-01-413-4102 
315 

M45 Protective Mask 

Item Size NSN

M45 Protective 

Mask 

XS 4240-01-414-4034 

M45 Protective 

Mask 

S 4240-01-414-4035 

M45 Protective 

Mask 

M 4240-01-414-4051 

M45 Protective 

Mask 

L 4240-01-414-4052 

DESERT JSLIST COAT 

Item Size NSN 

JSLIST COAT 

DESERT XLL 8415-01-505-1616 

JSLIST COAT 

DESERT XLR 8415-01-509-8314 

JSLIST COAT 

DESERT 2XLL 8415-01-505-1622 

JSLIST COAT 

DESERT 3XLL 8415-01-506-7710 
316 

JSLIST COAT 

DESERT LL 8415-01-444-6131 

JSLIST COAT 

DESERT LR 8415-01-444-6138 

JSLIST COAT 

DESERT ML 8415-01-444-6131 

JSLIST COAT 

DESERT MR 8415-01-444-5926 

JSLIST COAT 

DESERT MS 8415-01-444-5913 

JSLIST COAT 

DESERT SS 8415-01-444-5905 

JSLIST COAT 

DESERT SXS 8415-01-444-5902 

DESERT JSLIST TROUSERS 

Item Size NSN 

JSLIST 

TROUSERS 

DESERT 

XLL 8415-01-505-1567 

JSLIST 

TROUSERS 

DESERT 

XLR 8415-01-509-8269 
317 

JSLIST 

TROUSERS 

DESERT 

2XLL 8415-01-505-1591 

JSLIST 

TROUSERS 

DESERT 

3XLL 8415-01-506-7713 

JSLIST 

TROUSERS 

DESERT 

LL 8415-01-444-5900 

JSLIST 

TROUSERS 

DESERT 

LR 8415-01-444-5898 

JSLIST 

TROUSERS 

DESERT 

ML 8415-01-444-5892 

JSLIST 

TROUSERS 

DESERT 

MR 8415-01-444-5893 

JSLIST 

TROUSERS 

DESERT 

MS 8415-01-444-5506 

JSLIST 

TROUSERS 

DESERT 

SS 8415-01-444-5504 
318 

JSLIST 

TROUSERS 

DESERT 

SXS 8415-01-444-5417 

WOODLAND JSLIST COAT 

Item Size NSN 

JSLIST COAT 

WOODLAND XLL 8415-01-444-1241 

JSLIST COAT 

WOODLAND XLR 8415-01-509-8296 

JSLIST COAT 

WOODLAND 2XLL 8415-01-505-1591 

JSLIST COAT 

WOODLAND 3XLL 8415-01-506-7546 

JSLIST COAT 

WOODLAND LL 8415-01-444-1270 

JSLIST COAT 

WOODLAND LR 8415-01-444-1265 

JSLIST COAT 

WOODLAND ML 8415-01-444-1249 

JSLIST COAT 

WOODLAND MR 8415-01-444-1238 
319 

JSLIST COAT 

WOODLAND MS 8415-01-444-1200 

JSLIST COAT 

WOODLAND SS 8415-01-444-1169 

JSLIST COAT 

WOODLAND SXS 8415-01-444-1163 

WOODLAND JSLIST TROUSERS 

Item Size NSN 

JSLIST 

TROUSERS 

WOODLAND 

XLL 8415-01-505-1274 

JSLIST 

TROUSERS 

WOODLAND 

XLR 8415-01-509-8265 

JSLIST 

TROUSERS 

WOODLAND 

2XLL 8415-01-505-1591 

JSLIST 

TROUSERS 

WOODLAND 

3XLL 8415-01-506-7698 

JSLIST 

TROUSERS 

WOODLAND 

LL 8415-01-444-2338 
320 

JSLIST 

TROUSERS 

WOODLAND 

LR 8415-01-444-2325 

JSLIST 

TROUSERS 

WOODLAND 

ML 8415-01-444-2308 

JSLIST 

TROUSERS 

WOODLAND 

MR 8415-01-444-2310 

JSLIST 

TROUSERS 

WOODLAND 

MS 8415-01-444-1613 

JSLIST 

TROUSERS 

WOODLAND 

SS 8415-01-444-1439 

JSLIST 

TROUSERS 

WOODLAND 

SXS 8415-01-444-1435 

BDO (Four Color Woodland Camouflage 

Pattern)

Item Size NSN 

BDO XXL 8415-01-137-1707 

BDO XL 8415-01-137-1706 

BDO LR 8415-01-137-1705 
321 

BDO MD 8415-01-137-1704 

BDO SM 8415-01-137-1703 

BDO XS 8415-01-137-1702 

BDO XXS 8415-01-137-1701 

BDO XXXS 8415-01-137-1700 

DBDO (Three Color Desert Camouflage 

Pattern)

Item Size NSN 

DBDO XXL 8415-01-327-5353 

DBDO XL 8415-01-327-5352 

DBDO LR 8415-01-327-5351 

DBDO MD 8415-01-327-5350 

DBDO SM 8415-01-327-5349 

DBDO XS 8415-01-327-5348 

DBDO XXS 8415-01-327-5347 

DBDO XXXS 8415-01-327-5346 
322 

Suit Contamination Avoidance and Liquid 

Protective (SCALP) 

Item Size NSN 

Footwear 

Covers, Liquid 

Contamination 

SM 8430-01-364-3458 

Footwear 

Covers, Liquid 

Contamination

M/L 8430-01-364-3459

Footwear 

Covers, Liquid 

Contamination

XL/XXL 8430-01-364-3460

Clothing Outfit, 

Liquid 

Contamination, 

Trousers, 

Poncho 

Attached Hood 

(Green) 

SM 8415-01-364-3320 

Clothing Outfit, 

Liquid 

Contamination, 

Trousers, 

Poncho 

Attached Hood 

(Green)

M/L 8415-01-364-3321
323 

Clothing Outfit, 

Liquid 

Contamination, 

Trousers, 

Poncho 

Attached Hood 

(Green)

XL/XXL 8415-01-364-3322

Clothing Outfit, 

Liquid 

Contamination, 

Trousers, 

Poncho 

Attached Hood 

(Tan)

SM 8415-01-333-0987 

Clothing Outfit, 

Liquid 

Contamination, 

Trousers, 

Poncho 

Attached Hood 

(Tan)

M/L 8415-01-333-0988 

Clothing Outfit, 

Liquid 

Contamination, 

Trousers, 

Poncho 

Attached Hood 

(Tan)

XL/XXL 8415-01-333-0989 
324 

Chemical Protective Glove Sets 

Item Size NSN

25-Mil Gloves 

with liners 

Butyl 

XS 8415-01-144-1862 

25-Mil Gloves 

with liners 

Butyl 

SM 8415-01-033-3517 

25-Mil Gloves 

with liners 

Butyl 

MD 8415-01-033-3518 

25-Mil Gloves 

with liners 

Butyl 

LG 8415-01-033-3519 

25-Mil Gloves 

with liners 

Butyl 

XL 8415-01-033-3520 

14-Mil Gloves 

with liners 

Butyl 

SM 8415-01-138-2497 

14-Mil Gloves 

with liners 

Butyl 

MD 8415-01-138-2498 
325 

14-Mil Gloves 

with liners 

Butyl 

LG 8415-01-138-2499 

14-Mil Gloves 

with liners 

Butyl 

XL 8415-01-138-2500 

7-Mil Gloves 

with liners 

Butyl 

SM 8415-01-138-2501 

7-Mil Gloves 

with liners 

Butyl 

MD 8415-01-138-2502 

7-Mil Gloves 

with liners 

Butyl 

LG 8415-01-138-2503 

Chemical Protective Overboots (MULO) 

Item Size NSN 

Overboot 

(Black) 

Multipurpose 

3 8430-01-464-9453 

Overboot 

(Black) 

Multipurpose 

4 8430-01-464-9458 
326 

Overboot 

(Black) 

Multipurpose 

5 8430-01-464-9459 

Overboot 

(Black) 

Multipurpose 

6 8430-01-464-9461 

Overboot 

(Black) 

Multipurpose 

7 8430-01-464-9462 

Overboot 

(Black) 

Multipurpose 

8 8430-01-464-9464 

Overboot 

(Black) 

Multipurpose 

9 8430-01-464-9474 

Overboot 

(Black) 

Multipurpose 

10 8430-01-464-9475 

Overboot 

(Black) 

Multipurpose 

11 8430-01-464-9477 

Overboot 

(Black) 

Multipurpose 

12 8430-01-464-9480 
327 

Overboot 

(Black) 

Multipurpose 

13 8430-01-464-9479 

Overboot 

(Black) 

Multipurpose 

14 8430-01-464-9484 

Chemical Protective Overboots (BVO) 

Item Size NSN

Overboot 

(BVO) 

3 8430-01-317-3374 

Overboot 

(BVO) 

4 8430-01-317-3375 

Overboot 

(BVO) 

5 8430-01-317-3376 

Overboot 

(BVO) 

6 8430-01-317-3377 

Overboot 

(BVO) 

7 8430-01-317-3378 

Overboot 

(BVO) 

8 8430-01-317-3379 
328 

Overboot 

(BVO) 

9 8430-01-317-3380 

Overboot 

(BVO) 

10 8430-01-317-3381 

Overboot 

(BVO) 

11 8430-01-317-3382 

Overboot 

(BVO) 

12 8430-01-317-3383 

Overboot 

(BVO) 

13 8430-01-317-3384 

Overboot 

(BVO) 

14 8430-01-317-3385 

Chemical Protective Overboots (GVO) 

Item Size NSN

Overboot 

(GVO) 

3 8430-01-084-6305 

Overboot 

(GVO) 

4 8430-01-084-6306 

Overboot 

(GVO) 

5 8430-01-049-0878 
329 

Overboot 

(GVO) 

6 8430-01-049-0879 

Overboot 

(GVO) 

7 8430-01-049-0880 

Overboot 

(GVO) 

8 8430-01-049-0881 

Overboot 

(GVO) 

9 8430-01-049-0882 

Overboot 

(GVO) 

10 8430-01-049-0883 

Overboot 

(GVO) 

11 8430-01-049-0884 

Overboot 

(GVO) 

12 8430-01-049-0885 

Overboot 

(GVO) 

13 8430-01-049-0886 

Overboot 

(GVO) 

14 8430-01-049-0887 
330 

APPENDIX F 

 The following table is intended to serve as a 

reminder of the agents, their effects, first-aid 

measures, detection, and skin decontamination. 

 It is in no way complete, nor is it intended to 

be complete. Consult the appropriate chapter for 

further details. 
Type of 

Agent 

Effects Onset First-aid Skin 

Dec

Pulmonary TIC: CG (PFIB, HC) 

Dyspnea, coughing Hours None Non

usuaneed

Cyanide: AC, CK 

Loss of consciousness, convulsions, apnea 

Seconds None (nitrite and 

thiosulfate) 

Nonusuaneed

Vesicants: H, HD, L 

Erythema, blisters; irritation of eyes; cough, dyspnea Vapor: miosis, rhinorrhea, dyspnea 

Hours (immediate pain after L) 

None 

Vapor: seconds 

M29and 0.5% blea
Type of 

Agent 

Effects Onset First-aid Skin 

Dec

Nerve: GA, GB, GD, GF, VX 

Vapor: miosis, rhinorrhea, dyspnea Liquid: sweating, vomiting Both: convulsions, apnea 

Vapor: seconds Liquid: minutes to hours 

MARK I (1 to 3); diazepam 

M29and 0.5% blea

Incapacitating: BZ, Agent 15 

Mydriasis, increased body temperature; dry mouth and skin; confusion; visual hallucinations 

Minutes to hours 

Remove from harming themselves or others 

Remouteclothwatesoap wate

Riot-control: CS, CN 

Burning, stinging of eyes, nose, airways, skin 

Seconds None Wat
331 

APPENDIX G 

 Acronyms are helpful for remembering the 

toxicologically important aspects of a poisoned 

casualty. Choose the one that you find easiest to 

remember and commit it to memory. The logical 

progression of each acronym from agent 

through environment and to host should aid 

memorization. 

ASBESTOS: 

A: Agent(s): Type(s) and estimated doses 

S: State(s): Solid, liquid, vapor, gas, aerosol 

B: Body sites: Where exposed (routes of entry) 

[exposure and absorption] 

E: Effects: Local vs. systemic 

S: Severity: Of a) effects and b) exposure 

T: Time course: Past, present, and future 

[prognosis]) 

O: Other diagnoses: (a) Instead of (DDx) and 

(b) in addition to (additional diagnoses) 

S: Synergism: Interaction among multiple coexisting diagnoses 
332 

TOXICANT: 

T: Toxicant(s)/Toxidrome: Agent; does it fit 

with a specific toxidrome? 

O: Outside the body: Form: Solid, liquid, vapor, 

gas, aerosol? 

X: Xing into the body: Where did the agent 

cross into the body? [exposure and 

absorption] 

 I: Inside the body: Where did the agent go 

inside the body? [distribution] 

C: Chronology: Time course of exposure (past, 

present, and future) 

A: Additional diagnoses: Possible co-existing 

diagnoses 

N: Net effect of diagnoses: Interaction among 

all diagnoses; patient as a whole 

T: Triage: Priority for treatment, 

decontamination, and transport 

POISON: 

P: Poison(s): Type(s) and estimated doses 

O: Outside the body: Form: Solid, liquid, vapor, 

gas, aerosol? 

 I: Into/Inside the body: Where did it get into 

the body and where did it go inside the 

body? 

S: Sequence of events: Time course [past, 

present, and future] 
333 

O: Other diagnoses: a) Instead of (DDx) and b) 

in addition to (additional diagnoses) 

N: Net effects of diagnoses: Interaction among 

all diagnoses; patient as a whole 

The ABCDDs of Chemical Casualty Care 

A: Airway attention should be focused on 

establishing an airway (by positioning or by 

procedures) if needed, and maintaining the 

airway. No matter what else is done to try to 

save a casualty, death will be guaranteed if the 

airway is lost. 

B: Breathing may require intubation and 

ventilation of casualties. Keep in mind that once 

a casualty has been intubated, someone will be 

required to stay with the casualty to provide and 

monitor ventilations until the victim leaves the 

area, is capable of breathing spontaneously 

again, or expires or until the resources devoted 

to the casualty are critically required elsewhere 

to save other lives. 

C: Circulation may require chest compressions 

to maintain circulation in the absence of effective 

cardiac contractions will probably not be feasible 

for more than a few patients in a mass-casualty 

event, and most casualties without a pulse will 

have to be triaged as expectant. 
334 

D: Decontamination: Immediate, along with 

thorough patient decontamination and technical 

decontamination constitutes one of the main 

types of personnel decontamination 

D: Drugs, refers to specific antidotal treatment 

for selected agents and also to ancillary 

supportive medications. 

Remembering and applying the ABCDDs is as 

crucial to organizing initial treatment as 

ASBESTOS, POISON, or TOXICANT is to a 

systematic evaluation of a chemical casualty. 
335 

APPENDIX H 

GLOSSARY OF TERMS 

ACAA. Automatic Chemical Agent Alarm. 

ACADA. Automatic Chemical Agent Detector 

Alarm; this area monitoring detector sounds a 

warning when it senses the vapors of blister and 

nerve agents. 

Acid. A substance with a pH less than 7. 

Aerosol. A gaseous suspension of fine solid or 

liquid particles. 

Alkali. A substance with a pH greater than 7. 

Alveoli. Microscopic air sacs in the lungs where 

oxygen and carbon dioxide diffusion (movement) 

takes place through alveolar walls. 

AMEDD. Army Medical Department. 

Asphyxiation. Unconsciousness or death 

caused by lack of oxygen. 

BAL. British Anti-Lewisite. 

BDO. Battle Dress Overgarment. 

BDU. Battle Dress Uniform. 

Bronchi. The finer, smaller, divisions of the wind 

pipe into the lungs. 

CAM. Chemical Agent Monitor. 

CANA. Convulsive Antidote, Nerve Agent. 

Capillaries. Small blood vessels. 

CARC. Chemical Agent Resistant Coating. 

C/B. Chemical/Biological. 

CDC. Chemical Decontamination Center. 
336 

CBPS. Chemical and Biological Protective 

Shelter. 

Central airway. The main airway that transports 

air from the nose and mouth to the lungs. 

CPS. Chemical Protective Shelter. 

C2A1 filter canister. The standard filter used on 

the military mask. Protects against historic 

chemical warfare agents. 

DAAMS. Depot Area Air Monitoring System. 

DBDO. Desert Battle Dress Overgarment. 

DTD. Detailed Troop Decontamination. 

ECP. Entry Control Point. 

EMT. Emergency Medical Treatment. 

FMC. Field Medical Card. 

GREGG. Graves Registration. 

HC smoke. Military tactical smoke. 

HTH. High Test Hypochlorite. 

KPH. Kilometer Per Hour. 

ICAD. Individual Chemical Agent Monitor. 

Intubation. The process of enhancing respiration 

by providing an artificial airway. 

IDLH. Immediately-dangerous-to-life-andhealth. 

JSLIST. Joint Service Lightweight Integrated 

Suit Technology. 

Laryngospasm. Spasmodic closure of the 

larynx (voice box at the top of the trachea/wind 

pipe). 

Larynx. Voicebox and vocal cords. 

LBE. Load Bearing Equipment. 

LCL. Liquid Control Line. 

MCW. Mass-casualty Weapon.
337 

MES. Medical Equipment Set. 

MOPP. Mission Oriented Protective Posture. 

MTF. Medical Treatment Facility. 

MTO&E. Modified Table of Organization and 

Equipment. 

NAAK. Nerve Agent Antidote Kit. 

Nasopharynx. The area of the nose and upper 

airway. 

NATO. North Atlantic Treaty Organization. 

NBC. Nuclear/Biological/Chemical. 

NCO. Noncommissioned Officer. 

NCOIC. Noncommissioned Officer-in-Charge. 

NOx. Toxic smoke that can cause pulmonary 

edema. Produced by exploding munitions, 

industrial smoke, and in grain silos as a product 

of grain fermentation. 

OIC. Officer-in-Charge. 

Oropharynx. The mouth and upper airway. 

PFIB. Toxic smoke produced by Teflon® 

burning at more than 700o

F. 

Pulmonary edema. Fluid in the lungs, 

associated with an outpouring of fluids from the 

capillaries into the pulmonary spaces (air sacs 

or alveoli) producing severe shortness of breath. 

In later stages, produces expectoration of frothy, 

pink, fluid and blue lips (cyanosis). 

SDK. Skin Decontamination Kit. 

TAP. Toxicological Agent Protective, e.g., TAP 

apron. 

TC. Training Circular. 

TIC. Toxic Industrial Chemical; a chemical with a 

toxicity equal to or greater than ammonia and is 
338 

produced more than 30 times a year by an 

industrial facility. 

TIM. Toxic Industrial Materiel. 

Trachea. Wind pipe. 

Vapor. Fumes given off by a liquid. 

VCL. Vapor Control Line. 

WMD. Weapon of Mass Destruction. 
339 

INDEX

2-PAMCl · 139 

A

AC · 11, 40, 43, 44, 45, 

47, 52, 265, 270, 308, 

312 

acetylcholine · 123, 

126, 139, 158, 170, 

171, 183, 184 

acetylcholinesterase · 

123, 126, 128, 137, 

221 

aerosol · 8, 9, 13, 19, 

169, 196, 205, 213, 

332, 333 

Agent 15 · 161, 165 

airway(s) · 16, 18, 19, 

20, 24, 25, 27, 28, 29, 

30, 32, 33, 34, 35, 36, 

37, 39, 50, 52, 64, 65, 

72, 74, 75, 80, 82, 85, 

91, 95, 107, 108, 112, 

116, 120, 122, 130, 

131, 137, 143, 157, 

159, 165, 176, 186, 

188, 192, 198, 201, 

202, 205, 206, 208, 

233, 274, 310, 334, 

337, 351, 352, 353 

alveoli · 19, 20, 29, 31, 

74, 338 

anticholinergic · 14, 85, 

87, 101, 139, 158, 

159, 160, 161, 162, 

166, 170, 175, 179, 

180, 182, 189, 191 

antidotes · 16, 41, 55, 

58, 59, 60, 94, 138, 

150, 153, 187, 192, 

232 

apnea · 50, 54, 60, 122, 

130, 132, 133, 134, 

135, 143, 157, 169, 

176, 192, 193, 353 

atropine · 85, 87, 122, 

128, 131, 138, 139, 

140, 142, 143, 144, 

145, 153, 162, 168, 

171, 172, 173, 181, 

189, 310, 353 

autoinjector · 139, 140, 

141, 145, 181 

B

BAS · 229, 239 

BDU · 223, 286, 287, 

299, 300, 301, 336 

blister agent · 7 
340 

blister agent · 248, 261, 

262, 266, 267, 268, 

269, 273 

blister(s) · 64, 70, 72, 

73, 76, 80, 81, 83, 84, 

97, 107, 112, 113, 

114, 117, 149, 203, 

263, 265, 269, 351 

blood agent · 42 

breathing · 16, 19, 22, 

27, 28, 30, 34, 52, 58, 

122, 143, 144, 146, 

147, 152, 153, 164, 

165, 186, 188, 192, 

193, 205, 272, 334, 

353 

BZ · 8, 157, 158, 159, 

160, 161, 162, 165, 

166, 167, 168, 169, 

170, 171, 173, 175, 

176, 178, 179, 180, 

181, 182, 183, 184, 

185, 189, 191, 193 

C

CAM · 117, 126 

cholinesterase · 126, 

137, 139, 150, 151, 

154, 155, 190 

CK · 11, 40, 43, 44, 45, 

47, 52, 265, 308, 312 

CNS · 49, 65, 72, 77, 

101, 104, 127, 128, 

132, 133, 155, 158, 

162, 168, 169, 173, 

175, 178, 179, 184, 

191 

convulsions · 49, 50, 

54, 55, 60, 122, 185, 

242, 353 

Ct · 13, 41, 53, 73, 74, 

75, 84, 110, 111, 130, 

134, 135, 169 

CX · 62, 116, 117, 118, 

119, 120, 121, 265, 

308, 311 

cyanide · 7, 10, 13, 14, 

41, 42, 43, 44, 45, 46, 

47, 48, 49, 50, 51, 52, 

53, 54, 55, 56, 57, 58, 

59, 60, 61, 205, 206, 

220, 262, 263, 269, 

270 

cyanogen chloride · 

11, 42, 43, 44, 45, 50, 

265 

D

decon · 231, 236, 254, 

279, 280, 291, 296 

decontamination · 14, 

16, 17, 18, 21, 34, 56, 

64, 65, 78, 79, 107, 

111, 114, 115, 116, 

122, 138, 144, 145, 

157, 182, 194, 210, 
341 

212, 213, 214, 215, 

216, 217, 218, 219, 

223, 225, 227, 228, 

229, 231, 232, 233, 

234, 235, 236, 239, 

240, 241, 242, 246, 

254, 255, 258, 259, 

260, 262, 263, 273, 

275, 276, 277, 278, 

281, 282, 288, 289, 

291, 292, 293, 294, 

299, 301, 302, 304, 

305, 312, 331, 333, 

335, 351, 352, 353 

diazepam · 122, 139, 

140, 141, 143, 147, 

150, 153, 310, 353 

distilled mustard · 66, 

265 

E

erythema · 64, 65, 73, 

79, 80, 81, 83, 107, 

112, 113, 114, 202, 

203, 208, 209, 210, 

307, 308, 351 

F

fasciculations · 54, 

132, 133, 134, 135, 

136, 143, 144 

G

GA · 122, 124, 126, 128, 

129, 150, 268, 307 

GB · 7, 9, 10, 122, 123, 

124, 126, 128, 129, 

130, 150, 268, 307 

GD · 13, 122, 124, 126, 

127, 129, 140, 268, 

307 

GF · 122, 124, 126, 129, 

150 

GI tract · 45, 65, 72, 77, 

87, 101, 104, 119, 

120, 132, 168 

gloves · 68, 110, 118, 

125, 223, 241, 246, 

254, 256, 257, 260, 

261, 274, 279, 285, 

286, 287, 288, 291, 

297, 298, 311, 324 

glycolate · 157, 158, 

159, 160, 161, 162, 

169, 170, 171, 178, 

182, 191, 193 

H

H · 42, 62, 64, 65, 66, 

67, 68, 262, 263, 265, 

267 

HD · 25, 28, 31, 62, 64, 

65, 66, 215, 216, 218, 
342 

222, 265, 268, 270, 

307, 311 

heart · 46, 49, 54, 134, 

171, 173, 180, 190, 

204, 244, 245 

HL · 67 

hood · 249, 251, 260, 

279, 280, 281, 294, 

322, 323 

hydrogen cyanide · 8, 

11, 43, 44, 45, 47, 50, 

265 

hyoscyamine · 162, 

168 

I

ICAM · 266 

ICt50 · 13, 129, 169, 178 

incapacitating agent · 

7, 8, 14, 157, 160, 

161, 162, 163, 166, 

167, 173 

L

L · 62, 107, 109, 265, 

268, 270, 311 

LCt50 · 5, 13, 22, 41, 47, 

49, 70, 119, 129, 170, 

195 

Lewisite · 14, 62, 63, 

67, 81, 107, 108, 109, 

110, 111, 112, 113, 

114, 115, 119, 207, 

265, 269, 270, 311, 

351 

litter · 35, 231, 232, 234, 

236, 237, 240, 241, 

242, 271, 273, 274, 

278, 280, 281, 282, 

284, 285, 288, 289, 

290, 291, 294, 295, 

296, 304, 311, 312 

M

M18A2 · 45, 68, 109, 

118, 126 

M256A1 · 45, 68, 107, 

109, 118, 126, 261, 

264, 266, 350, 351 

M272 · 45, 68, 109, 

117, 126, 261, 269 

M291 · 64, 107, 213, 

216, 217, 219, 225, 

258, 259, 260, 279, 

280, 281, 282, 283, 

285, 286, 288, 289, 

292, 294, 296, 297, 

299, 300, 301, 351 

M40 · 246, 247, 280, 

314 

M40A1 · 247 

M42A2 · 246, 247 

M8 · 44, 67, 109, 117, 

124, 235, 261, 262, 
343 

263, 264, 265, 290, 

299, 301, 302 

M8A1 · 44, 67, 109, 

117, 261, 268, 269 

M9 · 44, 67, 109, 117, 

124, 261, 262, 263 

MARK I · 122, 139, 140, 

141, 142, 143, 145, 

147, 149, 150, 153, 

181, 240, 353 

MOPP · 230, 239, 252, 

253, 257, 262, 263, 

278, 293 

mouth · 20, 134, 143, 

157, 166, 171, 172, 

180, 201, 243, 249, 

312, 337 

muscle · 59, 102, 127, 

132, 133, 140, 146, 

170, 172, 173, 177, 

243, 245 

mustard · 8, 9, 10, 13, 

14, 25, 44, 62, 64, 65, 

66, 67, 68, 69, 70, 71, 

72, 73, 74, 75, 76, 77, 

78, 79, 80, 81, 83, 84, 

87, 88, 89, 90, 91, 92, 

93, 94, 95, 96, 97, 98, 

99, 100, 101, 102, 

103, 105, 106, 107, 

108, 111, 112, 113, 

114, 115, 125, 198, 

216, 218, 220, 221, 

223, 265, 270, 351 

N

nausea · 50, 52, 77, 87, 

99, 122, 131, 132, 

142, 144, 169, 177, 

206, 243, 353 

nerve agent · 7, 9, 14, 

32, 42, 54, 67, 109, 

122, 123, 124, 125, 

126, 127, 128, 130, 

131, 132, 133, 135, 

136, 137, 138, 139, 

140, 141, 142, 143, 

147, 148, 149, 150, 

151, 152, 154, 155, 

156, 158, 181, 183, 

219, 220, 221, 222, 

223, 258, 265, 267, 

268, 269, 270, 336 

nitrogen mustard · 62, 

78, 99, 100, 265 

nose · 20, 30, 31, 50, 

52, 74, 80, 130, 131, 

134, 143, 147, 198, 

201, 249, 337 

NOx · 22, 24, 26, 338 

O

overboots · 246, 253, 

254, 255, 286, 287, 

291, 297, 325, 327, 

329 
344 

oxides of nitrogen · 22, 

26, 36 

P

paralysis · 122, 147, 

172, 353 

percutaneous · 158, 

167 

perfluoroisobutylene · 

23 

peripheral nervous 

system · 158 

PFIB · 18, 22, 23, 24, 26 

phosgene oxime · 14, 

62, 63, 81, 113, 207 

photophobia · 76, 85, 

102 

physostigmine · 128, 

157, 158, 183, 184, 

185, 189, 190, 191 

PNS · 158, 168, 171, 

173, 179, 181, 182, 

191 

pralidoxime chloride · 

122, 139, 140, 353 

pretreatment · 60, 138, 

139, 140, 149, 150, 

184 

prognosis · 77, 82, 86, 

332 

protective wrap · 240, 

271 

pyridostigmine · 128, 

139, 140, 149, 150, 

151, 152, 184 

R

respiration · 20, 50, 52, 

132, 141, 145, 147, 

157, 181, 186, 192, 

198 

respiratory · 11, 12, 13, 

18, 20, 21, 24, 32, 33, 

35, 49, 50, 55, 56, 61, 

64, 65, 69, 70, 75, 81, 

89, 96, 101, 104, 105, 

110, 112, 122, 136, 

142, 157, 166, 169, 

171, 176, 177, 181, 

187, 189, 192, 193, 

194, 201, 205, 209, 

238, 247, 249, 353 

resuscitation · 18, 34 

RSDL · 213, 219 

S

sarin · 7, 123, 124, 130 

scopolamine · 162 

secretions · 32, 35, 54, 

122, 131, 132, 134, 

136, 138, 139, 140, 

143, 144, 145, 172, 

185, 353 
345 

SERPACWA · 257 

soman · 13, 124, 140, 

149, 150, 151, 184 

suction · 86, 122, 224, 

225, 311, 353 

symptoms · 14, 18, 27, 

35, 39, 50, 54, 60, 64, 

66, 72, 77, 78, 85, 89, 

94, 95, 107, 112, 116, 

117, 122, 133, 136, 

137, 152, 153, 157, 

159, 175, 180, 187, 

193, 194, 207, 242, 

243, 351, 352, 353 

T

tabun · 124, 126 

Teflon® · 26, 338 

triage · 14, 16, 38, 39, 

60, 61, 88, 115, 121, 

152, 191, 211, 229, 

231, 238, 239, 242, 

276, 278, 333 

U

unconscious · 19, 143, 

152, 164, 165, 176, 

181, 242 

V

ventilation · 26, 34, 56, 

86, 122, 138, 143, 

144, 145, 152, 164, 

188, 189, 191, 209, 

241, 334, 353 

vomiting · 14, 50, 52, 

77, 87, 99, 113, 122, 

131, 132, 144, 157, 

169, 177, 179, 180, 

184, 188, 194, 197, 

203, 206, 353 

VX · 9, 10, 122, 123, 

124, 126, 129, 150, 

183, 216, 218, 222, 

267, 268, 307 

W

weakness · 50, 53, 122, 

132, 133, 147, 173, 

243, 353 
Introduction 

Lung-Damaging Agents 

Cyanide 

Vesicants 

Nerve Agents 

Incapacitating Agents 

Riot-Control Agents 

Decontamination 

Casualty Management 

Chemical Defense Equipment 

Appendices
LUNG-DAMAGING AGENTS: 

Toxic Industrial Chemicals 

Cl, CG 

SUMMARY 

Signs and Symptoms: Central effects: Eye 

and airway irritation, dyspnea. Peripheral 

effects: Chest tightness, and delayed

pulmonary edema. 

Field Detection: The Chemical Agent 

Detector Kit and the M93A1 FOX 

RECONNAISSANCE System will detect small 

concentrations of CG; however, they will not 

detect Cl. 

Decontamination: vapor - fresh air; liquid - 

copious water irrigation. 

Management: termination of exposure, ABCs 

of resuscitation, enforced rest and observation, 

oxygen with or without positive airway pressure 

for signs of respiratory distress, other 

supportive therapy as needed. 
CYANIDE 

AC, CK 

SUMMARY 

Signs and Symptoms: few. After exposure 

to high concentrations, seizures, respiratory 

and cardiac arrest. 

Field Detection: The M256A1 Samplerdetector, M18A2, and M90 Chemical agent 

detectors detect Hydrogen Cyanide (AC) as 

vapor or gas in the air, and the M272 

chemical water testing kit detects AC in water.

Decontamination: Skin decontamination is 

usually not necessary because the agents are 

highly volatile. Wet, contaminated clothing 

should be removed and the underlying skin 

decontaminated with water or other standard 

decontaminants to prevent off-gassing as a 

hazard. 

Management: Antidote: intravenous (IV) 

sodium nitrite and sodium thiosulfate. 

Supportive: oxygen, correct acidosis. 
MUSTARD 

HD, H 

SUMMARY 

Signs and Symptoms: asymptomatic latent 

period (hours). Erythema and blisters on the 

skin, chemical burns; irritation, conjunctivitis, 

corneal opacity, and damage in the eyes; mild 

upper respiratory signs to marked airway

damage; also gastrointestinal (GI) effects and 

bone marrow stem cell suppression. 

Field Detection: M256A1 kit, M18A2 

chemical agent detector kits; Individual 

Chemical Agent Alarm (ICAM), M90 chemical 

agents detector, M8 and M9 chemical agent 

detector paper, M21 Remote Sensing 

Chemical Agents Alarm (RSCAAL), M93A1 

FOX NBC RECONNAISSANCE System, 

M272 Chemical water testing kit, M22 

Automatic Chemical Agent (ACADA) 

Detection Alarm. 

Decontamination: M291, soap and water, 

0.5% bleach solution. 

Management: Decontamination immediately 

after exposure is the only way to prevent 

damage. Supportive care of patients - there is 

no specific therapy. 
LEWISITE 

L 

SUMMARY 

Signs and Symptoms: Lewisite causes 

immediate pain or irritation of skin and mucous 

membranes. Erythema and blisters on the skin 

and eye and airway damage similar to those 

seen after mustard exposures develop later. 

Field Detection: M256A1 kit, M18A2 chemical 

agent detector kits; Individual Chemical Agent 

Alarm (ICAM), M90 chemical agents detector, 

M8 and M9 chemical agent detector paper, M21 

Remote Sensing Chemical Agents Alarm 

(RSCAAL), M93A1 FOX NBC 

RECONNAISSANCE System, M272 Chemical 

water testing kit, M22 Automatic Chemical Agent 

(ACADA) Detection Alarm. 

Decontamination: M291, soap and water, 

0.5% bleach solution. 

Management: Immediate decontamination; 

symptomatic management of lesions the same 

as for mustard lesions; a specific antidote (BAL) 

will decrease systemic effects. 
PHOSGENE OXIME 

CX 

SUMMARY 

Signs and Symptoms: Immediate burning 

and irritation followed by wheal-like skin 

lesions and eye and airway damage. 

Field Detection: M256A1 and M18A2 

chemical agent detector kits; M90 chemical 

agent detector, M93A1 FOX NBC 

RECONNAISSANCE SYSTEM. 

Decontamination: M291, soap and water, 

0.5% bleach solution.

Management: Immediate decontamination, 

symptomatic management of lesions. 
NERVE AGENTS 

SUMMARY 

Signs and Symptoms: 

Vapor: 

Small exposure -- miosis, rhinorrhea, mild difficulty 

breathing. 

Large exposure -- sudden loss of consciousness, 

convulsions, apnea, flaccid paralysis, copious 

secretions, miosis. 

Liquid on skin: 

Small to moderate exposure -- localized sweating, 

nausea, vomiting, feeling of weakness. 

Large exposure -- sudden loss of consciousness, 

convulsions, apnea, flaccid paralysis, copious 

secretions. 

Field Detection: M256A1 chemical agent detector kit, 

M8 chemical agent detector paper, M9 chemical agent 

detector paper; Improved Chemical Agent Alarm (ICAM), 

M93A1 FOX NBC RECONNAISSANCE System, M18A2 

chemical agent detector kit, M21 Remote Sensing 

Chemical Agent Alarm (RSCAAL), M90 chemical agent 

detector, M22 Automatic Chemical Agents Detection 

Alarm (ACADA). 

Decontamination: M291 SDK, soap and water, 0.5% 

Hypochlorate solution. 

Immediate management: Administration of MARK I Kits 

(atropine and pralidoxime chloride); diazepam in addition 

if casualty is severe; ventilation and suction of airways for 

respiratory distress.
INCAPACITATING AGENTS 

BZ, Fentanyl Derivatives

SUMMARY 

Signs and Symptoms: BZ: mydriasis; dry 

mouth; hot, red, dry skin; increased DTRs; 

decreased level of concentration; disturbance 

in perception and interpretation (illusions 

and/or hallucinations); denial of illness; short 

attention span; impaired memory. Fentanyl 

(carfentanil): miosis, drowsiness, 

unconsciousness, vomiting, central apnea. 

Detection: No field detector is available for 

BZ or fentanyl derivatives. 

Decontamination: BZ: Remove clothing. 

Gentle, but thorough washing of skin and hair 

with water or soap and water is required. 

Bleach is not necessary. Fentanyl 

(carfentanil): no decontamination needed. 

Management: BZ Antidote: physostigmine. 

Supportive: monitoring of vital signs, 

especially core temperature. Fentanyl 

(carfentanil): Antidote: Naloxone/naltrexone. 

Supportive: monitoring of vital signs, airway 

maintenance is critical until the effects of the 

agent wear off. 
RIOT-CONTROL AGENTS 

CS, CN, CR, and OC 

SUMMARY 

Signs and Symptoms: CS, CN, CR, and OC: feeling of 

intense burning and pain on exposed mucous 

membranes and skin, eye pain and tearing, burning in the 

nostrils, respiratory discomfort, and tingling of the 

exposed skin. With severe exposure: laryngospasm 

which can compromise breathing if not attended to. CS, 

CN, CR, with severe exposure: respiratory discomfort and 

skin blistering. DM: delayed skin irritation by several 

minutes, vomiting and malaise that can last for hours. 

Field Detection: No field detector is available. 

Decontamination: Eyes: thoroughly flush with water, 

saline, or similar substance. Skin: flush with copious 

amounts of water, alkaline soap and water, or a mildly 

alkaline solution (sodium bicarbonate or sodium 

carbonate). Generally, decontamination is not needed if 

the wind is brisk. Hypochlorite exacerbates the skin lesion 

and should not be used. OC: use of water for 

decontamination will increase pain. If water must be used 

it must be in copious amounts. OC is best 

decontaminated using baby shampoo, milk, or vegetable 

oil. Pain will diminish over time, once the individual’s 

substance P is depleted. 

Immediate management: Usually none is necessary; 

effects are self-limiting.