Sulfur mustard depression

Acute exposures to sulfur mustard can result in skin and eye damage, gastrointestinal irritation, and depressed myelopoiesis (resulting in leukopenia and anemia) (Vogt et al., 1984). Damage to the respiratory tract, which is the principal cause of mortality in the first few days to weeks after exposure to sulfur mustard, involves acute edema, inflammation, and destruction of the airway epithelial lining (Institute of Medicine, 1993). Infection of the respiratory tract resulting in bronchopneumonia is a common complication of exposure to sulfur mustard. 

In addition to the acute toxic effects on the eyes, skin, and respiratory tract, both acute and longer-term neuropsychiatric effects (e.g. depression, anxiety, neurasthenia, insomnia, post-traumatic stress syndrome) have been documented for individuals exposed to sulfur mustard (Romano et al, 2008). Many of these effects have been documented for individuals exposed during noncombat (e.g. munitions plant workers) activities and are not always the result of high-level exposure that result in serious overt effects. Longer-term effects such as chronic bronchitis have been associated with occupational exposures that included episodes of acute toxicity, and delayed or recurrent keratitis may occur 8-40 years after a severe vapor exposure. Sulfur mustard-induced immunosuppression resulting in greater susceptibility to infections has also been reported. 

In general, a battlefield chemical casualty has also responded intensely to other stresses, such as sleep and food deprivation, dehydration, thermal extremes, and the summation of exposure to multiple blasts, concussions, and inhalation of smoke and combustion products. Reports of wartime sulfur mustard casualties show considerable variation in the occurrence of such findings as prostration, circulatory collapse, impaired cognition, severe headache, nausea and vomiting, lethargy, and depression (Vedder, 1925 Warthin et al., 1918 Willems, 1989). The extent of this variation suggests that factors other than sulfur mustard exposure may contribute to these problems. 

Lewisite, CHCl=CHAsCl2, 2-chlorovinyldichloroarsine, named after its discoverer W. L. Lewis, was produced by the USA and shipped to Europe in 1918, too late to be used in WWI. Between the wars it was also produced by Japan and the Soviet Union. It is relatively easily made from arsenic trichloride and acetylene, although the process is technically more difficult than the production of sulfur mustard. Lewisite is more volatile (bp 190 °C) than sulfur mustard and hence it is less persistent it also appears to be more sensitive to environmental moisture. In contrast to sulfur mustard, its initial effect (skin pain or irritation) is almost instant, and blisters appear within a few hours. There has been no confirmed instance of use, although Japan is suspected of having used lewisite in China in WWII. In addition to being stockpiled as a neat agent, lewisite was mixed with sulfur mustard to speed up the onset of action and to depress the freezing point of the latter. 

Lewisite was produced and stockpiled by various nations, including Japan, the United States, and the Soviet Union. Lewisite saw use, too, in mixtures with sulfur mustard, where lewisite acted as a freezing-point depressant. The Japanese might have used lewisite in combat... 

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