Although not the major focus of most studies of mustard agents, gastrointestinal effects have been documented in some animal studies. The most common findings have been intestinal histopathological changes, including destruction of the mucosa and shedding of epithelial elements (Graef et al., 1948; Papirmeister et al., 1991). Gavage studies have also shown epithelial hyperplasia of the forestomach (Sasser et al., 1989b).
In humans, gastrointestinal effects of mustard agents are commonly seen in people with acute high exposures. Common symptoms include nausea and vomiting, both immediately after exposure and as a delayed effect (Papirmeister et al., 1991; Schonwald, 1992). Several mechanisms may account for these effects including (1) a direct and immediate cholinergic effect, (2) an inflammatory reaction of the upper gastrointestinal mucosa, (3) a delayed radiomimetic effect on the small intestine, and (4) physical stress secondary to skin and other effects from mustard agent exposure (Papirmeister et al., 1991). In some individuals there may be chronic gastrointestinal symptoms, but these appear to occur only secondarily to other chronic health problems due to acute high exposures to mustard agents.
Exposure of dogs to high doses of Lewisite produces some injury to the intestinal mucosa and focal necrosis of the liver with peribiliary hemorrhage (Cameron et al., 1946, 1947; Gates et al., 1946). Exposure of rats by lavage produced lesions of the forestomach including necrosis of the stratified epithelium (Sasser et al., 1989a). No information could be found on the effects of Lewisite on the human gastrointestinal systems.
In animals exposed to very high doses (i.e., LD50) of mustard agents, aplastic changes occur in the bone marrow. Lymphatic damage also occurs, including cellular depletion of the splenic sinuses and resultant disappearance of lymphocytes from the blood (Graef et al., 1948; Papirmeister et al., 1991). Similar hematological changes occur in humans after very high exposures to mustard agents. Marrow suppression including anemia, thrombocytopenia, and leukopenia has been seen (Papirmeister et al., 1991; Willems, 1989). Severe leukopenia appears to occur only after very high exposures, and secondary infections can be a significant contributor to the mortality in this group.
Laboratory studies have also demonstrated that exposure to Lewisite