US Army Medical Research Institute of Chemical Defense (USAMRICD) MEDICAL MANAGEMENT OF CHEMICAL CASUALTIES HANDBOOK Chemical Casualty Care Division (MCMR-UV-ZM) USAMRICD 3100 Ricketts Point Road Aberdeen Proving Ground, MD 21010-5400 THIRD EDITION July 2000 Disclaimer The purpose of this Handbook is to provide concise supplemental reading material for attendees of the Medical Management of Chemical Casualties Course. 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. ii Table of Contents Introduction...................................................................................................................1 Pulmonary Agents.......................................................................................................10 Cyanide........................................................................................................................19 Table. Cyanide (AC and AK). Effects From Vapor Exposure.............................25 Vesicants .....................................................................................................................30 Mustard.....................................................................................................................31 Table. Effects of Mustard Vapor.....................................................................................39 Lewisite....................................................................................................................46 Phosgene Oxime......................................................................................................52 Nerve Agents...............................................................................................................56 Table 1. Vapor Toxicity (mg-min/m3).....................................................................60 Table II. LD on Skin..............................................................................................61 50 Table III. Nerve Agent Effects. Vapor Exposure..................................................69 Table IV. Nerve Agent Effects. Liquid on Skin....................................................70 Incapacitating Agents.................................................................................................75 Riot-Control Agents....................................................................................................88 Decontamination.........................................................................................................95 Casualty Management in a Contaminated Area......................................................105 Chemical Defense Equipment..................................................................................112 Appendix A. Patient Decontamination...................................................................132 Appendix B. Casualty Receiving Area....................................................................145 Appendix C. Personnel Decontamination Station.................................................146 Appendix D. Toxicity Data.......................................................................................148 Appendix E. Physicochemical Data........................................................................150 Appendix F. Medical Equipment Set.......................................................................153 Appendix G. Table of Agents, Effects, First-Aid, Detection, and Skin Decontamination.......................................................................................................155 Appendix H. Glossary of Terms..............................................................................156 Index...........................................................................................................................158 ii i INTRODUCTION PURPOSE Chemical warfare is not a popular topic, and most military health care providers do not willingly become familiar with it. This was painfully obvious during Operation Desert Shield/Desert Storm when it soon became apparent that many health care providers knew little about the effects of chemical agents or the medical defense against them. This ignorance was particularly striking in view of the seven-decade long history of modern chemical warfare and the well-publicized use of mustard and nerve agent during the Iran-Iraq War in the 1980s. The prevailing attitude of military health care providers was that chemical agents would be used only on Hmong, Afghans, Kurds, or similarly unprepared and unprotected groups of people. Further, many health care providers believed if chemical weapons were used the outcome would be disastrous, defense would be impossible, and the casualty rate and loss of life would be high. Through education, however, medical professionals involved in Operation Desert Shield/Desert Storm learned that medical defenses were possible and effective, that chemical casualties could be saved and returned to duty, and that mortality could be minimized. Further, they realized that they might be the targets of chemical agents. More importantly, they rapidly learned that General Pershing's warning (written shortly after World War I) about chemical agents was still true: "...the effect is so deadly to the unprepared that we can never afford to neglect the question." The purpose of this handbook is to provide medical personnel in the field a concise, pocket-sized reference source for the medical management of chemical casualties. It is not intended to be a definitive text on the management of chemical casualties. HISTORY OF CHEMICAL WARFARE AND CURRENT THREAT The use of chemical weapons dates from at least 423 B.C. when allies of Sparta in the Peloponnesian War took an Athenian-held fort by directing smoke from lighted coals, sulfur, and pitch through a hollowed-out beam into the fort. Other conflicts during the succeeding centuries saw the use of smoke and flame, and the Greeks, during the seventh century A.D., invented Greek fire, a combination probably of rosin, sulfur, pitch, naphtha, lime, and saltpeter. This floated on water and was particularly effective in naval operations. During the fifteenth and sixteenth centuries, Venice employed 1 unspecified poisons in hollow explosive mortar shells and sent poison chests to its enemy to poison wells, crops, and animals. The birth of modern inorganic chemistry during the late eighteenth and early nineteenth centuries and the flowering of organic chemistry in Germany during the late nineteenth and early twentieth centuries generated both a renewed interest in chemicals as military weapons and also a spirited debate concerning the ethics of chemical warfare. The British admiralty rejected as, "against the rules of warfare," an 1812 request to use burning, sulfur-laden ships as a prelude to marine landings in France. Forty-two years later, the British War Office similarly condemned Sir Lyon Playfair's proposal to use cyanide-filled shells to break the siege of Sebastopol during the Crimean War, arguing that to use cyanide was "inhumane and as bad as poisoning the enemy's water supply." (Sir Lyon retorted, "There's no sense to this objection. It is considered a legitimate mode of warfare to fill shells with molten metal that scatters upon the enemy and produces the most frightful modes of death. Why a poisonous vapor that would kill men without suffering is to be considered illegitimate is incomprehensible to me. However, no doubt in time chemistry will be used to lessen the sufferings of combatants.") Other nineteenth-century proposals that were never put into practice included the idea of using chlorine-filled shells against the Confederacy during the American Civil War and the suggestion of Napoleon III during the Franco- Prussian War that French bayonets be dipped into cyanide. The Brussels Convention of 1874 attempted to prohibit the use of poisons in war. Delegates to the Hague Conventions in 1899 and 1907 considered the morality of chemical warfare but were unable to draft more than a weak and vaguely worded resolution against the use of chemicals on the battlefield. Against the background of this debate, World War I began. Early in the war, German units used the new, but as yet unreliable invention, the portable flamethrower; and France, where gendarmes had successfully employed riot-control agents for civilian crowd control, used small quantities of these agents in minor skirmishes against the Germans. Riot-control agents, although the first chemicals used on a modern battlefield, proved largely ineffective, and the search for more effective riot-control agents continued throughout the war. It should have been no surprise that the first large-scale use of chemical agents during the war was by heavily industrialized Germany, with its impressive scientific base of theoretical and applied chemistry and its capacity for mass production of chemicals. German units released an estimated 150 tons of chlorine gas from some 6000 cylinders near Ypres, Belgium, during the afternoon of 15 April 1915. Although this attack caused probably no more than 800 deaths, it was psychologically devastating to the 15,000 Allied troops, who promptly retreated. The Germans, however, were unprepared to take advantage of this victory, and chlorine and its successors were doomed to play a tactical, rather than a strategic role, during the war. 2 Shortly thereafter, the British were ready to respond in kind with chlorine, and the chemical armamentarium of both sides expanded with the addition of phosgene and chloropicrin. These three agents damaged primarily the upper and lower airways, and both sides developed a variety of masks to prevent inhalation injury. Masks also had the potential to protect against cyanide, which the French and the British (but not the Germans) also fielded to a limited extent during the war. However, on 12 July 1917, again near Ypres, Belgium, German artillery shells delivered a new kind of chemical agent, sulfur mustard, which in that attack alone caused 20,000 casualties and generated a series of new problems. Mustard, a relatively nonvolatile liquid, was persistent compared to the previously used agents, and thus not only the air that the soldier breathed, but also the objects that he touched, became potential weapons. It was effective at low doses. It affected not only the lungs, but also the eyes and the skin. Finally, the latent period of up to several hours with mustard meant there were no immediate clues to exposure as there had been with the earlier agents. Masks had to be augmented by hot, bulky, chemical protective clothing for soldiers and protection for their horses. The need for such a protective ensemble made fighting more difficult physically and psychologically. Diagnosis of mustard exposure was difficult, and mustard-exposed soldiers could easily overwhelm the medical system. Because the effects of mustard were delayed and progressive, most mustard casualties eventually presented for medical treatment. Although in most countries fewer than 5 percent of casualties from mustard who reached medical treatment stations died, mustard injuries were slow to heal and necessitated an average convalescent period of over six weeks. Between World War I and World War II, debate on chemical warfare continued in the United States (U.S.) and in international forums. The wording of the 1925 Geneva Protocol, which all of the major powers except for the U.S. and Japan ratified, implied the prohibition of the first use (but not the possession) of chemical and biological weapons. The treaty preserved the right to use such weapons in retaliation for a chemical attack. Russia, which had suffered half a million chemical casualties during World War I, worked with Germany in chemical agent offensive and defensive programs from the late 1920s to the mid-1930s. In contrast, the U.S. Chemical Corps struggled to stay alive in the face of widespread sentiment against chemical warfare. Evidence (not all of which is conclusive) suggests that the military use of chemical agents continued after the end of World War I. Following World War I, Great Britain allegedly used chemicals against the Russians and mustard against the Afghans north of the Khyber Pass, and Spain is said to have employed mustard shells and bombs against the Riff tribes of Morocco. During the next decade, the Soviet Union supposedly used lung irritants against tribesmen in Kurdistan; and Mussolini, who utilized tear gas during the war against Abyssinia in 1936 and 1937, also authorized massive aerial delivery of mustard (1) against Abyssinian tribesmen and (2) as an interdiction 3 movement on Italian flanks. Immediately prior to World War II and during the early part of that war, Japan is supposed to have used chemical weapons against China. In the late 1930s, a German industrial chemist, Dr. Gerhard Schrader, searching for more potent insecticides, synthesized tabun (GA), an extremely toxic organophosphate compound. Two years later, he synthesized sarin (GB), a similar but even more toxic compound. During World War II, Nazi Germany weaponized thousands of tons of these potent organophosphates that came to be called nerve agents. Why they were not used during the war is a matter of continuing discussion. Hitler, himself a mustard casualty during World War I, did not favor their use; neither did his senior staff who had fought on chemical battlefields during that war. Wrongly concluding from trends in Allied scientific publications on insecticides that the Allies had their own nerve agent program, German leaders may have been afraid of retaliation in kind to any Axis use of nerve agents. (President Roosevelt had in fact announced a no- first-use policy, but had promised instant retaliation for any Axis use of chemical agents.) Finally, during the later stages of the war, Germany lacked the air of superiority needed for effective delivery of chemical weapons. The well-organized German nerve agent program thus remained a complete secret until its discovery by the Allies during the closing days of the war. With the possible exception of Japan during attacks on China, no nation during World War II used chemical agents on the battlefield, although Germany employed cyanide and perhaps other chemical agents in its concentration camps. However, over 600 military casualties and an unknown number of civilian casualties resulted from the 1943 German bombing in Bari Harbor, Italy, of the John Harvey, an American ship loaded with two thousand 100-pound mustard bombs. The 14 percent fatality rate was due in large part to systemic poisoning following ingestion of and skin exposure to mustard-contaminated water by sailors attempting to keep afloat in the harbor following the attack. Civilian casualties, on the other hand, suffered more from the inhalation of mustard-laden smoke. The end of World War II did not stop the development, stockpiling, or use of chemical weapons. During the Yemen War of 1963 through 1967, Egypt in all probability used mustard bombs in support of South Yemen against royalist troops in North Yemen. The U.S., which used defoliants and riot-control agents in Vietnam and Laos, finally ratified the Geneva Protocol in 1975, but with the stated reservation that the treaty did not apply either to defoliants or riot-control agents. During the late 1970s and early 1980s, reports of the use of chemical weapons against the Cambodian refugees and against the Hmong tribesmen of central Laos surfaced, and the Soviet Union was accused of using chemical agents in Afghanistan. Widely publicized reports of Iraqi use of chemical agents against Iran during the 1980s led to a United Nations investigation that confirmed the use of the vesicant 4 mustard and the nerve agent GA. Later during the war, Iraq apparently also began to use the more volatile nerve agent GB, and Iran may have used chemical agents to a limited extent in an attempt to retaliate for Iraqi attacks. Press reports also implicated cyanide in the deaths of Kurds in the late 1980s. Because of the confirmed Iraqi possession and use of chemical agents, preparations for the liberation of Kuwait by the United Nations coalition included extensive planning for defense against possible chemical attacks by Iraq. Even though this threat never materialized, United Nations inspection teams discovered nerve agents and mustard at Al Muthanna (about 80 km northwest of Baghdad) after the February 1991 cease fire. Other chemical stockpiles may yet exist in Iraq, and inspection efforts continue. Other countries that have stockpiled chemical agents include countries of the former Soviet Union, Libya (the Rapta chemical plant, part of which may still be operational), and France. Over two dozen other nations may also have the capability to manufacture offensive chemical weapons. The development of chemical warfare programs in these countries is difficult to verify because the substances used in the production of chemical warfare agents are in many cases the same substances that are used to produce pesticides and other legitimate civilian products. The U.S.' stockpile consists almost entirely of nerve agents (GB and VX) and vesicants (primarily mustard [H, HD]). About 60 percent of this stockpile is in bulk storage containers, and 40 percent are stored in munitions, many of which are now obsolete. Since the Congressional passage of a bill mandating the destruction of all U.S. chemical agents, one incinerator plant has gone into operation at Johnston Atoll, and other facilities are in the planning stages. The chemical agents most likely to be used on a modern battlefield are the nerve agents and mustard; because of its alleged use by Iraq, cyanide may also pose a danger. Some intelligence analysts also consider the pulmonary intoxicants to be a credible threat. TERMS Chemical agents, like all other substances, may exist as solids, liquids, or gases, depending on temperature and pressure. Except for riot-control agents, 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, 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 when hot enough to boil water (212oF at sea level). 5 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 at a temperature lower than the boiling point of that substance at a given pressure. Liquid water, for example, becomes a gas 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 (steam) are composed not of water vapor, but rather suspensions of minute water droplets, that is, aerosols. 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 does, 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 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 generally more significant than the danger created by the 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 division 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. Biological effects occur following exposure to chemical agents dispersed as solids, liquids, gases, aerosols, or vapor. 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 6 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 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 ED (pronounced "ED50") and the ID denote the quantities (usually 50 50 measured as the weight in µg, mg, or g) of liquid agent that will predictably cause effects (E) or incapacitation (I) in 50 percent of a given group. Similarly, the LD is the 50 Lethal Dose or quantity (weight) of liquid agent that will kill 50 percent of a group. Note that the lower the LD , the less agent is required and thus the more potent is the agent. 50 Because of differences in absorption, the ED and LD values for a given agent are 50 50 site-specific; that is, the LD for mustard absorbed through dry, unabraded skin is much 50 higher than the LD for mustard absorbed through the eye. 50 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). That is, 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 one-minute exposure to 40 mg/m3. The ECt , ICt , and LCt then 50 50 50 correspond for vapor or gas exposures to the ED , ID , and LD , respectively, for 50 50 50 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 therefore not an exact measure of inhalation exposure. 7