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3
History and Analysis of Mustard Agentand Lewisite Research Programsin the United States

This chapter begins with an introduction that briefly describes sulfur mustard and Lewisite and their effects, accompanied by an overview of their development. This is followed by a description of the organization of chemical warfare research during World War I (WWI) and the postwar period of 1919 to 1940, including the development of Lewisite and nitrogen mustard. The major focus of this chapter, however, is to describe the research programs and protocols relating to mustard agents and Lewisite, initiated just prior to World War II (WWII) and continued throughout the war.

This committee also investigated as many protocols and supporting military documents as it could obtain for use in estimating the possible exposure levels experienced by the men who participated in the mustard and Lewisite tests. These estimates were intended to put into context the concentrations of vesicant used in animal and other types of experiments, which the committee was also charged to survey. As these protocols were investigated, it became apparent to the committee that the full body of knowledge available to the wartime scientists, especially information relevant to the long-term health outcomes of exposure to these agents, was not applied in the conduct of the human experimentation. Thus, this chapter begins to address compelling questions that emerged through the course of this study regarding the appropriate use of the existing scientific and medical literature in WWII testing programs, the lack of medical follow-up of human research subjects, and the probable exposure levels experienced by these subjects.

Finally, the chapter overviews the research programs since the end of WWII, including the continuing investigations concerning the mechanisms of toxicity of these agents. Description of the chemical stockpile



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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite 3 History and Analysis of Mustard Agentand Lewisite Research Programsin the United States This chapter begins with an introduction that briefly describes sulfur mustard and Lewisite and their effects, accompanied by an overview of their development. This is followed by a description of the organization of chemical warfare research during World War I (WWI) and the postwar period of 1919 to 1940, including the development of Lewisite and nitrogen mustard. The major focus of this chapter, however, is to describe the research programs and protocols relating to mustard agents and Lewisite, initiated just prior to World War II (WWII) and continued throughout the war. This committee also investigated as many protocols and supporting military documents as it could obtain for use in estimating the possible exposure levels experienced by the men who participated in the mustard and Lewisite tests. These estimates were intended to put into context the concentrations of vesicant used in animal and other types of experiments, which the committee was also charged to survey. As these protocols were investigated, it became apparent to the committee that the full body of knowledge available to the wartime scientists, especially information relevant to the long-term health outcomes of exposure to these agents, was not applied in the conduct of the human experimentation. Thus, this chapter begins to address compelling questions that emerged through the course of this study regarding the appropriate use of the existing scientific and medical literature in WWII testing programs, the lack of medical follow-up of human research subjects, and the probable exposure levels experienced by these subjects. Finally, the chapter overviews the research programs since the end of WWII, including the continuing investigations concerning the mechanisms of toxicity of these agents. Description of the chemical stockpile

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite disposal program is also included. The chapter concludes with an outline of some of the conclusions drawn by the committee from analysis of the historical records and calculations of exposure levels. INTRODUCTION Sulfur Mustard Sulfur mustard (C4H8Cl2S) is one of a class of chemical warfare agents known as vesicants because of their ability to form vesicles, or blisters, on exposed skin (see Figure 3-1). During WWI, exposed troops described the odor of this agent as a stench like mustard or garlic, hence its common name. Table 3-1 summarizes some characteristics of mustard agents and Lewisite. First noted for its toxic properties by dye chemists in the late 1880s, sulfur mustard has been referred to by a number of synonyms: S-mustard, to distinguish it from nitrogen mustard; ''Lost" or "S-Lost," from the names of two chemists who suggested it be used as a war gas (Lommel and Steinkopf); "yellow cross," for the identifying mark on WWI shells containing sulfur mustard; or Yperite, after the site of its first use in 1917. Although commonly and inaccurately referred to as mustard gas, the agent is a liquid at room temperature. Sulfur mustard produces skin blisters and damage to the eyes and respiratory tract, and it can be lethal at sufficiently high doses. It is a cellular poison and mutagen and a recognized human carcinogen. Battlefield use of sulfur mustard decreases the opponent's ability to fight by producing chemical burns on tissues that come into contact with either vapors or liquid droplets and aerosols. Exposed skin surfaces, eyes, and the linings of both the respiratory and the gastrointestinal tracts are all at risk, and the risks increase dramatically under hot, humid conditions. From a military standpoint, one of sulfur mustard's most useful properties is its persistence. Droplets of this agent released in an explosion can deposit on numerous surfaces, evaporating slowly and posing a risk from inhalation as well as contact with the skin. Indeed, this very set of conditions was observed in WWI after mustard shelling (Haber, 1986). One reason for this persistence is the characteristic freezing temperature of sulfur mustard (13°C to 15°C). Droplets or bulk quantities would thus be expected to remain where initially deposited during cool or winter weather, under forest canopies, or under overgrown vegetation. Under certain conditions, bulk quantities of mustard agent spilled or splashed onto the soil would not degrade for months. The exact date of the first sulfur mustard synthesis is somewhat unclear, but the first report may have been by Despretz in 1822. An 1860 report by Neimann describes a delayed-effect vesicant oil as a reaction product of ethylene on a mixture of sulfur chlorides. At that time, this

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite FIGURE 3-1 Vesicle formation on an Iranian patient, 16 hours after battlefield exposure to sulfur mustard. Reprinted from Willems, 1989, with permission from Annales Medicinae militaris Belgicae.

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite TABLE 3-1 Chemical and Physical Data   Sulfur Mustard Lewisite Nitrogen Mustard Chemical Abstracts Registry Number 505-60-2 541-25-3 51-75-2 Chemical formula C4H8Cl2S C2H2AsCl3 C5H11Cl2N Chemical structure CH2-CH2Cl H          AsCl2 CH2-CH2Cl   S   H3C-N   CH2-CH2Cl Cl H CH2-CH2Cl Synonyms 1,1'-Thiobis(2-chloroethane); 2,2'-dichloroethyl sulfide; bis(2-chloroethyl) sulfide; ,'-dichloroethyl sulfide; mustard gas; Schwefel-Lost; S-Lost; Yperite; yellow cross; Senfgas; Kampstoff "Lost"; dichlorodiethyl sulfide Chlorovinyldichloroarsine; 2-chlorovinyldichloroarsine; chlorovinylarsine dichloride; dichloro(2-chlorovinyl)arsine Mechlorethamine; chlormethine; 2-chloro-N-(2-chloroethyl)-Nmethylethanamine; Stickstofflost; di(chloroethyl)methylamine Abbreviations H (Levinstein mustard), HD (distilled mustard), HT (impure mixture) L HN2; related compounds include HN1, ethylbis(chloroethyl)amine; and HN3, tris(-chloroethyl)amine Melting point 13C-14C 0.1C -60C Boiling point 215C-217C at 760 mm Hg 190C at 760 mm Hg (decomposes) 87C at 18 Hg Molecular weight 159.08 207.32 156.1 Solubility Very sparingly soluble in water; soluble in oily solvents; high lipid solubility Insoluble in water, soluble in ordinary organic solvents Very slightly soluble in water Appearance and odor Colorless when pure, normally yellow to brown oily liquid, slight garlic-type odor Liquid, faint odor of geranium Liquid, faint fishy odor   SOURCES: Budavari, 1989; Hazardous Substances Databank, 1991; IARC, 1975; Somani, 1992; U.S. Army CRDEC, 1988, 1990.

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite product was identified as a compound [(C2H4)2S2Cl2] different from sulfur mustard; however, the observed severe skin blistering, latent period of several hours, and subsequent slow healing are all typical of skin exposure to sulfur mustard. At about the same time, Guthrie (1859, 1860) published investigations describing yet another variant compound (thought to be C4H4S2Cl2), also produced from sulfur chloride in reaction with ethylene. The odor was "pungent," resembling that of "oil of mustard." Guthrie noted destruction of the epidermis when the thin skin between the fingers and around the eyes was exposed to the ''vapour" of this compound. When the liquid was allowed to remain on the skin, blister formation was observed. Finally, in 1886, a process to produce significant quantities of pure sulfur mustard was described by Meyer using sodium sulfide, ethylene chlorohydrin, and hydrochloric gas (Jackson, 1936; Meyer, 1886; Prentiss, 1937; West, 1919). This process was the one eventually used by the German war factories to fill the shells fired at Ypres (Haber, 1986). Lewisite Lewisite (C2H2AsCl3) is a vesicant that contains organic arsenic. During WWI, a U.S. chemical warfare research laboratory investigating arsenic compounds as potential war gases developed the potent vesicant, subsequently named "Lewisite" after the research group director. Purified Lewisite is a colorless, oily liquid at room temperature with a faint "geranium-like" odor. More volatile than sulfur mustard, this agent can be used as a vapor over large distances and has been mixed with sulfur mustard to achieve greater effectiveness in combat. With a freezing point between -18°C and 0°C, Lewisite is effective over a wider temperature range than sulfur mustard. Lewisite is also a cellular poison, but works via a different mechanism than sulfur mustard. It is readily absorbed through the skin and respiratory tract, but moist tissues are particularly vulnerable and eyes exhibit the greatest sensitivity (Trammell, 1992; Watson and Griffin, 1992). In contrast to sulfur mustard, Lewisite exposure is characterized by immediate onset of pain. The agent is lethal at sufficient doses, produces chromosomal aberrations in some mammalian cellular assays, and is a systemic poison when absorbed into the bloodstream. Finally, some evidence suggests that Lewisite might be a carcinogen (Centers for Disease Control, 1988). The development of Lewisite as a war gas was made by W. Lee Lewis in 1918, while working at the Chemical Laboratory of the Catholic University of America in Washington, D.C. (Lewis and Perkins, 1923). The thrust of the work in this laboratory during WWI was the evaluation of substituted arsines (arsenic-containing chemicals) as potential chem-

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite ical warfare agents. Lewis had noticed a paragraph in a 1904 student dissertation by J.A. Nieuwland that documented the formation of an "extremely poisonous" substance after a reaction of arsenic chloride with dry acetylene in the presence of aluminum chloride (cited in Lewis and Perkins, 1923). The toxicity that had caused Nieuwland to stop further work on the reaction spurred Lewis to investigate the substance more fully. In addition, Lewis and his group worked out safer and more efficient production methods and elaborated plans for large-scale production (Lewis and Perkins, 1923; Lewis and Steigler, 1925). A production plant was eventually constructed in Willoughby, Ohio, and approximately 150 tons of Lewisite were in transit to Europe when the Armistice was signed in November 1918. The vessel was sunk at sea (Spiers, 1986; Tarbell and Tarbell, 1981; Trammell, 1992), and all experimental work with Lewisite in the U.S. Chemical Warfare Service abruptly ceased until WWII (Gates et al., 1946). RESEARCH PROGRAMS OF WORLD WAR I AND THE POSTWAR PERIOD As outlined above, prior to the actual use of sulfur mustard as a war gas in 1917, the substance was little more than an interesting compound produced, along with hundreds of other compounds, by the emerging science of industrial chemistry in the last half of the nineteenth century. Thus, tragically, the combat casualties of WWI became the first large group of experimental subjects in studies of the medical effects of sulfur mustard. Organized research into chemical warfare agents began in earnest in Britain and France after the German chlorine gas attack in 1915. In the United States, it was 1917 before a formally organized chemical warfare research program was established. The history of the program has been documented by various authors and summarized by Cochrane (1946) in a classified report released to the public in 1991. The program began with an offer from the Bureau of Mines to the National Research Council (NRC) to mobilize the bureau's unique and specialized laboratories toward the investigation of poison gases.1 With the U.S. declaration of war against Germany in 1917, the NRC Committee on Noxious Gases was formed to administer the research programs concerning poison gases, including sulfur mustard and later Lewisite. In the United States and Europe, much of the research was focused on methods of mass production of sulfur mustard, development of other vesicants and war gases, and development of better gas masks and other 1   The National Research Council was in 1917 and is today part of the National Academy of Sciences. The NRC was directly involved in defense research programs during both World War I and World War II. A description of this involvement is included in Appendix C.

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite equipment to protect troops from chemical attack. The overall research program was divided into sections, each of which was responsible for specific types of research, ranging from gas production processes to treatment of gas casualties. As the program  matured, the various organizational structures were modified. The details of these modifications are not presented here because they are largely irrelevant to consideration of the health effects of mustard agents and Lewisite. One modification, however, may have set the stage for how research into these substances' medical effects has been conducted and directed ever since. In 1918, a presidential order moved the research program from essentially civilian control under NRC to military control under the War Department. This move gave birth to the Chemical Warfare Service (CWS), which, to the present day, is responsible for the majority of research concerning chemical and biological warfare agents. As time went on this administrative change altered the direction of almost all investigations into the toxicology of vesicants and other chemical agents. Mainstream biomedical science is "hypothesis driven": when interesting results are obtained by an investigator, either that investigator or other groups begin further research to better understand what has been discovered, even if the interesting results are not directly relevant to the original questions being asked. In addition, the results of most biomedical research are published in "open literature," critically reviewed by outside experts and available to all. In contrast, most military research is "applications driven": priorities are determined on the basis of military needs (e.g., treatment of acute injuries, development of protective clothing), and results not directly relevant to the original questions are seldom pursued. Such research is commonly classified and is published only for other military groups. The tight controls and restrictions on military research can result in a "stunted" body of literature that presents major limitations to later assessments in areas that were never pursued—in this case, the long-term health effects caused by exposure to chemical agents in general, and mustard agents and Lewisite in particular. Researchers in the medical aspects of chemical warfare began their work in 1917 with few of the guideposts that are normally available from previous studies. The only literature available on the medical effects of sulfur mustard and Lewisite was that produced by the English and French, who had only a small head start with their research programs. Nevertheless, perusal of the significant papers published after the war from these groups reveals that multiple lines of investigation were quickly initiated and pursued. Some of the work done by the medical research groups examined the mechanisms of absorption of mustard agents into human skin, the effects of various ointments and antidotes

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite on the severity of blisters and skin damage, and the pathological changes in the respiratory tract following inhalation of sulfur mustard vapor. Cochrane's history lists 22 papers and books published by 1920, which stood as the distillation of all significant investigations completed in the United States during WWI (Cochrane, 1946). With the end of the war, the research program came to an end and CWS decreased drastically in size. The many research and production locations were also completely consolidated at the Edgewood Arsenal in Maryland. After a short period of relative uncertainty about its continued existence, CWS became part of the U.S. Army by an amendment to the National Defense Act on July 1, 1920. Two later books included comments on the long-term  effects of warfare gases. In 1925, Vedder published Medical Aspects of Chemical Warfare, in which he discounted any significant long-term sequelae of gassing and introduced the concept that "neurasthenic" conditions (an archaic term describing lassitude, decreased energy, and impaired functioning that, in Vedder's work, seemed to be used as a synonym for "psychosomatic") were the underlying factors in most veterans' claims of disability. Colonel Harry L. Gilchrist, in contrast, published an extensive comparative study on WWI casualties in 1928 that included detailed clinical descriptions of men who had been gassed in combat and a carefully researched chapter on the probable residual health effects of various gases (Gilchrist, 1928a,b). Gilchrist's work was a major contribution to knowledge about vesicant toxicity. Based on clinical examination of human gas victims and some animal experiments, as well as later follow-up studies of WWI veterans, Gilchrist found that the long-term effects of sulfur mustard were mainly respiratory, including emphysema, chronic asthma, and chronic bronchitis. Chronic conjunctivitis and corneal opacities were also described later by Gilchrist and Philip B. Matz (1933a,b; also see Appendix B for excerpt from Gilchrist and Matz, 1933b). The period from 1920 until 1936 also saw the establishment of a Medical Research Division within the CWS. This group continued toxicological studies of chemical warfare agents, including sulfur and nitrogen mustards and Lewisite; investigated the lethal and sublethal concentrations of the agents; and renewed investigations into protective ointments. In addition, the group formalized what was known regarding treatment of gas casualties and attempted to examine the residual effects of exposure to various chemical warfare agents. Its work involved both animal and human experimentation. The experiments with human subjects, however, used only a few subjects mostly drawn from personnel, including the scientists themselves, working at Edgewood Arsenal. For mustard agents and Lewisite, no major breakthroughs were made by the research efforts between 1920 and 1936. According to Cochrane,

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite the lack of progress was traceable to a variety of factors. One of these factors was funding, often in short supply in a peacetime environment. Also, to appease public concern about poison gas production, significant efforts were spent trying to find peacetime uses for these agents. Another factor was the constant struggles and competition between different branches of the military, different departments within the CWS, and different scientific disciplines. Cochrane reports that the medical researchers, in direct competition with apparently more productive chemists, were especially vulnerable to funding shifts. Thus, by the dawn of WWII, what was known about mustard agents and Lewisite (or many other agents, for that matter) was not organized into a cohesive body of literature. The clinical picture of the acute effects of exposure and some of the mechanisms of toxicity were well known (Gilchrist, 1928a,b; Vedder, 1925). There were clear guidelines for treatment of casualties, but the treatments were solely palliative. No effective ointments had been developed and nothing was available to prevent skin and lung damage. Even less was known about the long-term effects. So unorganized was the scientific base concerning vesicants that, when the 1941 version of the training manual for treatment of gas casualties (TM 8-285) was prepared for use in treating expected casualties in WWII, it did not include the carefully documented long-term effects of exposure reported by Gilchrist in 1928 and by Gilchrist and Matz in 1933. This omission, not explained in Cochrane's history or elsewhere, was surprising to this committee. It is improbable that CWS did not know of Gilchrist's work, because it had been published in "open, nonclassified" literature, including one journal. In retrospect, we know that such an omission may well have unfavorably influenced the treatment and long-term follow-up of gassed soldiers in WWII, had such casualties occurred. In terms of the WWII testing programs with human subjects, this omission—coupled with an apparent disregard for the long-term effects of gas exposure—may have contributed to the absence of follow-up of these human subjects, despite the fact that the end points of many of the experiments were skin injury and burns (also see Chapter 4). TESTING PROGRAMS AND CHEMICAL WARFARE PRODUCTION IN WORLD WAR II As the war in Europe eroded U.S. neutrality, preparations began to revitalize and expand the activities of the Chemical Warfare Service. In order to obtain a greater base of scientific expertise, the War Department again came to the National Research Council for help (see Appendix C). In 1941, the research effort was reorganized and subsumed under a newly established Office of Scientific Research and Development

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite FIGURE 3-2 Organization of World War II civilian scientific research and testing programs. Chamber and field tests were conducted by the Chemical Warfare Service and the Navy Department, Office of Research and Inventions. Civilian researchers from the NDRC and CMR worked in close communication with the military. SOURCE: OSRD, 1946; Stewart, 1948. (OSRD), eventually comprised of two working branches, the Committee on Medical Research (CMR) and the National Defense Research Committee (NDRC), and an Advisory Council. NRC's Committee on the Treatment of Gas Casualties (CTGC), experts in the fields of medicine and biological sciences, began working closely with the CMR to aid the effort by administering and supervising government grants to researchers and universities for a wide range of research regarding chemical warfare agents (see Figure 3-2 for OSRD organizational chart). One of the first assignments given to the CTGC was to review the scientific literature on the physiological effects of sulfur mustard and Lewisite, and on the methods tested for protection against injury and treatment of gas burns. The focus of the literature review was on acute

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite toxicity data, but included longer-term effects. The first reviews were distributed among the various NDRC and CMR groups in August 1943 (Smith, 1943). There is no evidence that these reviews resulted in any changes or modifications of the protocols for the treatment or follow-up of human subjects in the experimental programs. On the subject of long-term effects of exposure, only Vedder's work, and not Gilchrist's, is mentioned in this review. The focus of the following section is on the experiments conducted in the United States using human subjects; consideration of the animal experiments is included in later chapters, which survey the scientific literature. Similar experiments were also conducted in Great Britain, Canada, Australia, and the Soviet Union, as well as in Germany and Japan. The details of these experiments and these countries' chemical weapons programs are not included here. However, numerous references that provide information regarding these programs were examined by the committee, are included in the bibliography, and are specifically cited in this report where appropriate. One of the richest sources for information on the gas chamber experiments was reports released from the Naval Research Laboratory (NRL). Other primary source information regarding gas chamber experiments in locations other than the NRL was obtained by the committee from Edgewood Arsenal in Aberdeen, Maryland. CWS carried out three basic types of experiments with human subjects. According to Cochrane, these testing programs involved the use of approximately 60,000 human subjects. Patch, or drop, tests were the most common and were used to assess the efficacy of a multitude of protective or decontamination ointments, treatments for mustard agent and Lewisite burns, effects of multiple exposures on sensitivity, and the effects of physical exercise on the severity of chemical burns. In addition, drop application of liquid mustard agents was commonly used in basic training to raise single blisters to impress upon the trainees the toxicity of these agents and the need for immediate responses to any orders to don gas masks. Chamber tests of various types were conducted to test the effectiveness of protective clothing, all of which had been impregnated with chemicals to retard vapor penetration. Finally, field tests involved the contamination of large or small areas of land with sulfur mustard or Lewisite. Human subjects were used in field tests to test protective clothing, to monitor the effects of the agents on animals in the test sites, and to take measurements of agent concentrations in soil and water samples. Table 3-2 summarizes the known major locations of these tests and the types of experiments done in each location. Many veterans who were subjects in the chamber tests have obtained detailed records of their exposures from the Naval Research Laboratory. These reports often employ an outdated scientific notation. Table 3-3

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite Incineration remains a matter of continuing controversy among environmental groups, citizens who live near some of the proposed incineration sites, and the involved government agencies. The Programmatic Environmental Impact Statement, released by the Department of the Army in 1988, concludes that timely disposal of the stockpile of chemical weapons entails less of a hazard than continued storage. Technical support and oversight for the Chemical Stockpile Disposal Program (and the companion Chemical Stockpile Emergency Preparedness Program that assists nearby communities in developing emergency preparedness programs) is provided by numerous Army commands and a host of civilian institutions. These include the National Center for Environmental Health of the Centers for Disease Control (U.S. Department of Health and Human Services), Federal Emergency Management Agency, U.S. Environmental Protection Agency, U.S. Department of Agriculture, as well as state and local planning agencies in the 10 affected states, and two national laboratories (Oak Ridge National Laboratory, Oak Ridge, Tennessee; Argonne National Laboratory, Argonne, Illinois). Analyses of vesicant toxicity and long-term health risks from these groups have been considered, along with other information, in generating the present report. CONCLUSIONS AND FURTHER ANALYSIS The committee reached two principal conclusions based on its analysis of the chemical warfare testing programs from WWI through 1975. These conclusions relate directly to the estimated level of exposure to mustard agents and Lewisite experienced by the WWII chamber and field test subjects and to the exposures of workers in the Chemical Warfare Service during WWII. In addition, the committee's conclusions are pertinent to the health care concerns of those who have been injured by use of these agents in recent wars and conflicts, or who may be exposed in the future from belligerent use of these agents or through accidental exposure during their disposal. The lack of follow-up health assessments of the human subjects in WWII gas chamber tests and field tests severely diminished the amount and quality of information that could be applied in the assessment of long-term health consequences of exposure to mustard agents and Lewisite. Although the reasons underlying the lack of follow-up health assessments are not explicit from the numerous documents and materials considered by this committee, a number of factors may have played a role:  There was no unified body of information, based on WWI research and the research done in the period from 1918 to 1939, when

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite research was intensified in the early pre-WWII period. This lack of information seems to have contributed directly to a lack of appreciation for the serious long-term health risks associated with exposure to mustard agents and Lewisite, specifically chronic bronchitis, emphysema, chronic laryngitis, corneal opacities, chronic conjunctivitis, and keratitis.  Scientific inquiry was controlled by the military establishment, whose primary concern was with acute rather than long-term injury. This control also probably contributed to the paucity of animal or other types of studies, following WWII, aimed toward elucidation of long-term consequences of damage to specific physiological systems. For example, no long-term follow-up was done on workers involved in chemical warfare materials production, despite the high level of injuries that occurred.  The atmosphere of immediacy caused by the outbreak of war, and the resulting prioritization of expected combat injuries, at least strengthened the focus on acute damage from chemical warfare agents, and at worst dampened any sensitivities that were present regarding the future health of human subjects or chemical warfare production workers.  Once the war was over, there may also have been ambiguities about which federal department or agency should have had responsibility for follow-up of veterans. Although the former Veterans Administration (VA) had that role traditionally, the VA could not have been expected to know about the testing programs and their possible effects on the health of human subjects without communication from  the military.  Finally, and related to the issue of responsibility for follow-up, the continued secrecy maintained by the military regarding the WWII testing programs also created a barrier to follow-up assessments of exposed individuals. Even during the present study, which follows a five-year period of intensifying public scrutiny of these WWII programs, obtaining certain types of information was not easy and often involved piecing together bits of data from numerous sources. In fact, this committee was commonly required by many DoD and Department of the Army offices to file all requests under the Freedom of Information Act. These requirements were often imposed even on the present Department of Veterans Affairs (VA), when it attempted to aid this committee by making certain requests for information regarding the possible existence of records of individuals who participated in the testing programs (see Appendix E). The most valuable primary source data were received from the Naval Research Laboratory and NRC's Office of Archives and Information Services. This committee is especially grateful to the NRL for its commitment to open its files. The NRL

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite stands alone among sections of the Department of Defense in the maintenance of files and reports, and the sharing of those files with this committee and with the affected veterans. The levels of exposure to mustard agents or Lewisite experienced by the test human subjects may have been much higher than inferred in the summaries of the experiments and field tests. As in all chemical exposures, such exposure levels directly relate to the types and severities of exposure-induced injuries and diseases. One can infer the cumulative exposures to the skin of chamber subjects strictly on the basis that skin damage was the end point of these experiments (see Table 3-4). Therefore, if all other types of exposures were held to zero, these subjects received between 100 and 300 Ct. As has been documented, some of the subjects were hospitalized for as long as "a month or so" (Taylor et al., 1943). Thus, exposures to the skin may have been as high as 1,000-2,000 Ct. Under the hot, humid conditions in the chambers, however, lower exposure levels would have resulted in similar injuries (Papirmeister et al., 1991). The dose to the skin from such exposures would have been as high as those observed under battlefield and occupational conditions. Further, some sulfur mustard would also have been absorbed from the skin into the systemic circulation. In the chamber experiments, unmasked subjects were required to remain in their protective clothing from 4 to 24 hours following chamber trials, allowing ample opportunity for additional contact and inhalation exposures from contaminated surfaces and clothing. Another factor that probably resulted in some inhalation exposure of subjects in the chamber tests was vomiting during the period subjects were in the chamber. This was reported by at least one of the subjects who spoke at the public hearing; this person reported conjunctivitis and laryngitis following such a vomiting incident on his seventh day of testing (Elmer Hood, public hearing statement; see also Appendix G). Vomiting presumably would result in removal of the mask while in the chamber, with a resulting inhalation exposure of unknown duration at the chamber concentration being tested. The most important route of additional exposure in the chamber and field tests was probably gas mask leakage. From the information available to the committee, it appears that the vast majority of the human subjects in the chamber and field tests wore full-face gas masks during their exposures. In fact, the documented exposures at the Naval Research Laboratory were delivered at concentrations and for durations that would have caused lethal respiratory effects if the subjects had not been equipped with respiratory protection. Thus, exposure of the respiratory tract and eye to the agent would have depended on the

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite BOX 3-1 ODOR THRESHOLD FOR SULFUR MUSTARD AND LEWISITE: COMPARISON WITH TISSUE DAMAGE THRESHOLDS Even when enough agent had broken through their gas mask canisters to produce symptoms, chamber test subjects may not have noticed it, at least by odor. The odor threshold for sulfur mustard is reported to be about 0.6 mg/m3, and the median concentration of Lewisite detectable by odor is reported to be 14 to 23 mg/m3 (OSRD, 1946). However, both agents have effects on the eye and respiratory tract at lower concentrations (Papirmeister et al., 1991; Urbanetti, 1987). For example, sulfur mustard exposure at a concentration of 0.5 mg/m3 for 30 minutes (15 Ct) would result in both respiratory and eye symptoms (see Table 3-4). For Lewisite, such irritating effects are reported to be noticeable at concentrations estimated to be as low as 6 to 8 mg/m3 (Papirmeister et al., 1991; Urbanetti, 1987). Thus, for sulfur mustard exposures at 0.5 mg/m3, an exposure of only about 25 minutes (12.5 Ct) could be expected to cause eye and respiratory tract symptoms without the subject being aware of the exposure, at least by odor. protection factor (PF) afforded by the gas masks. The PF of a full-face respirator (e.g., a gas mask) is calculated as the ratio of the ambient concentration of the contaminant to the concentration inside the mask, which in turn depends on both leakage around the respirator and contaminant penetration of the gas mask canister. A PF of 100 equals a penetration of 1 percent of the contaminant into the mask (Adley and Uhle, 1969). A PF of 50 to 100, based primarily on leakage around facemasks, has been reported for relatively modern (post-WWII) full-face respirators (Hyatt, 1976). Estimates from industrial hygiene research, however, indicate that the level of protection achieved in actual use of a respirator is usually below the stated PF for that respirator (National Institute of Occupational Safety and Health, 1974). Thus, modern respirators are likely to function closer to the lower PF estimate of 50. In practical terms, even if the respirator actually achieved a PF of 100, subjects exposed to a concentration of 100 mg/m3 of sulfur mustard would be breathing a concentration as high as 1 mg/m3 inside the mask, corresponding to a cumulative exposure of 60 Ct over a single 60-minute trial. At even lower concentrations—under the odor threshold (0.6 mg/m3)—the subjects may well have been unaware of any leakage through their masks (see Box 3-1). Information on the breakthrough capacity of the gas mask cartridges used in the WWII chamber tests was not available to the committee, but it is known that prolonged use of cartridges can result in breakthrough of the agent by exceeding the capacity of the absorbent filter material (Stampfer, 1982). In the NRL chamber test reports examined by the present committee, when gas mask types were listed, the masks used were Mark III or Mark

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite IV Navy diaphragm gas masks. These masks were probably equipped with M9A1 (prior to July 1943) or M9A2 canisters that contained Whetlerite, a copper-, chromium-, and silver-impregnated activated charcoal as the sorbent (Brophy et al., 1959). The PF afforded by these masks for sulfur mustard or Lewisite was not available to the committee. However, an individual involved in this testing reported that the WWII British and U.S. masks were very effective in removing sulfur mustard (Howard Skipper, personal communication; see Appendix A). Yet some chamber tests were conducted at high concentrations. For example, a test conducted at chamber concentration of 100 mg/m3 for 60 minutes would have resulted in a cumulative, unprotected, exposure of 30,000 Ct over five trials. Even an assumed PF of 1,000 for the gas mask (10 times greater than that estimated for modern full-face respirators) would have resulted in concentrations as high as 0.1 mg/m3 in each trial, corresponding to a cumulative exposure of 6 Ct just from the inspired air in each trial. This would have been below the odor threshold for sulfur mustard and, over five trials, would have resulted in a cumulative inhalation exposure of 30 Ct, enough to cause signs and symptoms in the eyes and respiratory tract (see Table 3-4). If a more realistic estimate is used, such as a mask with a PF of 100, the per trial exposure would have been 60 Ct. Over five trials then, a subject could have had an inhalation exposure of 300 Ct, more than sufficient to cause an incapacitating injury (see Table 3-4). It is important to remember that any such inhalation exposure would have been in addition to any skin exposure through breakdown of the protective clothing. It is important to note also that the gas masks and clothing used in the NRL tests were worn repeatedly by the subjects. In at least one series of studies, it was reported that the rubber of the gas mask facepieces and connecting tubes absorbed enough sulfur mustard after 12 to 15 exposures to cause conjunctivitis, laryngitis, and erythema of the face (Taylor et al., 1943). Therefore it is clear that some exposure to the respiratory tract occurred from absorption of sulfur mustard on masks. Finally, as mentioned previously, the special diaphragm element in the types of gas masks used in the NRL chamber tests was eventually shown to provide an additional route of mask leakage, independent of the filter capacity (Brophy et al., 1959). The presence of erythema of the face, conjunctivitis, laryngitis, or bronchitis within 24 to 72 hours following an exposure to sulfur mustard or Lewisite would be clear evidence that a significant inhalation and eye exposure had occurred, even if the subject was wearing a mask during the exposure. Conversely, it would appear that a lack of such symptoms following even a low-level exposure of 5 to 6 days to sulfur mustard would indicate a cumulative exposure (Ct) of less than about 12 Ct (see Table 3-4). However, in terms of the Centers for Disease Control's

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite estimates of permissible exposure levels (CDC, 1988), the exposures actually reaching the breathing zone of chamber subjects (from the above example, 0.1 mg/m3 sulfur mustard breakthrough with a gas mask rated at 1,000 PF) may have been more than 1,000 times the general population agent control limits (0.0001 mg/m3 for sulfur mustard), and 33 times the control limits for occupational exposure (0.003 mg/m3 for sulfur mustard). In reality, some of the subjects in the chamber tests and field trials almost certainly breathed concentrations 10 or more times the 0.1 mg/m3 level for at least a part of their exposures. The focus here on chamber and field test subjects is not meant to discount the probable exposure levels experienced by those who were involved in the production or handling of mustard agents and Lewisite. Indeed, as outlined above, the poor safety record of the Chemical Warfare Service during the peak years of production, the high rate of agent-induced injuries, and the anecdotal reports of perceptible odors of sulfur mustard in the manufacturing areas argue that workers and gas handlers were often exposed to levels of mustard agents and Lewisite sufficient to cause short- and long-term health effects. Thus, these individuals should also be considered at risk for any of the adverse health effects this report identifies. In conclusion, the dose of sulfur mustard to the skin, eye, and respiratory tracts of the human subjects was substantial, especially in the case of the subjects involved in the chamber tests. Doses to the skin were probably equivalent to those received under combat conditions. Consideration of the probable gas mask leakage, additional exposures from contact or vapors from the clothing, accidents, and the documented signs and symptoms in the chamber test records indicate that the doses received by the human subjects were equivalent to those received in occupational exposures and, perhaps, even battlefield exposures. REFERENCES Adler FH. 1944. Report of consultant in ophthalmology on 6 cases of H vapor burns occurring at Bushnell Field Installation on April 20, 1944. Memo to Colonel C.P. Rhoads, dated May 1, 1944. Available at the National Archives, Suitland Reference Branch, Suitland, MD. Record Group 175, Group 4B, Folder 319.1. Adley FE, Uhle RJ. 1969. Protection factors and self-contained compressed-air breathing apparatus. American International Hygiene Association Journal 30:355-359. Alexander SF. 1947. Medical report of the Bari Harbor mustard casualties. Military Surgeon 101:1-17. Andrus EC, Bronk DW, Carden GA Jr, Keefer CS, Lockwood JS, Wearn JT, Winternitz MC, eds. 1948. Advances in Military Medicine. Science in World War II: Office of Scientific Research and Development. Boston: Little, Brown and Company. Balali-Mood M, Navaeian A. 1986. Clinical and paraclinical findings in 233 patients with sulfur mustard poisoning. In: Heyndricks B, ed. Terrorism: Analysis and Detection of

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Veterans at Risk: The Health Effects of Mustard Gas and Lewisite Gilchrist HL. 1928b. Chemical warfare and its medical significance. Military Surgeon 63:477-492. Gilchrist HL, Matz PB. 1933a. The residual effects of warfare gases. Medical Bulletin (US Veterans Administration) 9:339-390. Gilchrist HL, Matz PB. 1933b. The Residual Effects of Warfare Gases. Washington, DC: U.S. Government Printing Office. Gillis RG. 1985. Australian Field Tests with Mustard Gas 1942-1945. Department of Defence, Australia. Gilman A. 1946. Symposium on advances in pharmacology resulting from war research: therapeutic applications of chemical warfare agents. Federation Proceedings 5:285-292. Gilman A. 1963. The initial clinical trial of nitrogen mustard. American Journal of Surgery 165:574-578. Gilman A, Cattell M. 1948. Systemic agents: action and treatment. In: Andrus EC, Bronk DW, Carden GA Jr, Keefer CS, Lockwood JS, Wearn JT, Winternitz MC, eds. Advances in Military Medicine. Science in World War II: Office of Scientific Research and Development. Boston: Little, Brown. 546-564. Gilman A, Philips FS. 1946. The biological actions and therapeutic applications of the b-chloroethyl amines and sulfides. Science 103:409-415. Guthrie F. 1859. On some derivatives of the olefines. Quarterly Journal of the Chemical Society 12:109-126. Guthrie F. 1860. On some derivatives of the olefines. Quarterly Journal of the Chemical Society 13:129-135. Haber L. 1986. The Poisonous Cloud. Oxford:Clarendon Press. 250-257. Harris R, Paxman J. 1982. A Higher Form of Killing: The Secret Story of Chemical and Biological Warfare. New York: Hill and Wang. Heinen JH, Carhart HW, Taylor WH, Stolp BN, Conner JC, Clausen NM. 1945. Chamber Tests with Human Subjects. IX. Basic Tests with H Vapor. NRL P-2579. Washington, DC: Naval Research Laboratory. Heyndrickx A, Heyndrickx B. 1984. Treatment of Iranian soldiers attacked by chemical and microbiological war gases. Archives Belges (Supplement):157-159. Hyatt. 1976. Respirator Protection Factors. Los Alamos:Los Alamos Scientific Laboratory of the University of California. Infield GB. 1976. Disaster at Bari. London: New English Library. International Agency for Research on Cancer (IARC). 1975. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man. Vol. 9, Some Aziridines, N,S- & O-Mustards and Selenium. Lyon: IARC. Jackson KE. 1936. The history of mustard gas. Journal of the Tennessee Academy of Science 11:98-106. Lewis WL, Perkins GA. 1923. The ß-chlorovinylchloroarsines. Industrial and Engineering Chemistry 15:290. Lewis WL, Stiegler HW. 1925. The b-chlorovinyl chloroarsines and their derivatives. Journal of the American Chemical Society 47:2546-2556. Mandl H, Freilinger G. 1984. First report on victims of chemical warfare in the Gulf war treated in Vienna. Archives Belges (Supplement):330-340. McNamara BP, Owens EJ, Christensen MK, Vocci FJ, Ford DF, Rozimarek H. 1975. Toxicological Basis for Controlling Levels of Mustard in the Environment. Edgewood Arsenal Special Publication EB-SP-74030. Aberdeen Proving Ground, Maryland: U.S. Army Armament Command. Edgewood Arsenal Biomedical Laboratory. Medema J. 1986. Mustard gas: the science of H. Nuclear, Biological, and Chemical Defense and Technology International 1:66-71. Meyer V. 1886. Compounds of thiodiglycol. Chemischte Berichte 19:3259-3266. [In German]

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