crease in other types of tumors now seems certain. Another long-term effect of nitrogen mustard treatment is pulmonary fibrosis, produced by damage to the pneumocytes.
Certainly, hematopoietic depression is seen with sulfur mustard exposure in man, although (except in massive exposures) the degree and frequency do not seem to be as intense or frequent as with the nitrogen mustards. This difference is likely due to the more direct exposure to the bone marrow of the nitrogen mustards when given by systemic exposure. This same rationale probably explains why acute leukemia has not been recognized as a consequence of sulfur mustard exposure. However, the increased incidence of solid tumors seen with nitrogen mustard would support the conclusion that exposure of the lungs and skin to sulfur mustard produces a carcinogenic effect on these tissues. Similarly, the delayed pulmonary toxicity seen in a small percentage of patients treated with nitrogen mustards would suggest that long-term damage to the lungs would be expected with intense exposure of the lungs to sulfur mustard.
The preparation of Lewisite (L-1) by the original procedure is complicated and dangerous. It involves the reaction of acetylene with arsenic trichloride, by using aluminum chloride as a catalyst. The reaction yields three principal products (5-19):
The optimum yield of Lewisite is about 20 percent, obtained along with L-2, L-3, tar, and an explosive material. Acetylene reacts with AsCl3 in hydrochloric acid solution, with mercuric chloride as a catalyst, to give Lewisite in 80 to 85 percent yield (based on AsCl 3). Cuprous chloride and ethanolamine hydrochloride used together, however, constitute the best catalyst for the reaction.
The hydrolysis of Lewisite by water involves the following equilibria (5-20):