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as these exposure results would more accurately mimic human exposure. Certainly studying larger numbers of animals would provide a more sensitive measure of the possible magnitude of any reproductive risk associated with exposure to sulfur mustards. Short-term, high-dose exposures would also be helpful in attempting to examine any dose-rate effects. It should also be noted that the quality of the human data on the reproductive toxicity of sulfur mustards is quite poor. There has been insufficient follow-up of the occupational or battlefield cohorts to determine the nature of any reproductive toxicity or teratogenic effects attributable to these exposures.

Evidence suggests a causal relationship between sulfur mustard exposure and reproductive toxicity in laboratory animals, but the database is far too small and uncertain to allow a clear understanding of human reproductive risk from exposure to sulfur mustards. Sulfur mustards can cause genetic alterations in the sperm of male rats after inhalation or gastric exposure, but rodent and rabbit studies showed that sulfur mustards are not detectable teratogens in animals. The human data are difficult to interpret: it is unclear if it is significant that the Japanese child with one nonheritable variant protein had the same congenital malformation (cleft palate) that was reported in association with parental mustard exposure in Iran.



The literature addressing the reproductive toxicity of Lewisite is small; in fact, few data exist that advance the precise biologic fate of Lewisite in humans. Arsenic itself is known to be embryotoxic and teratogenic, and while Lewisite is an organic arsenical, in highly alkaline environments inorganic arsenic could be formed. These facts led the committee to examine the reproductive effects of inorganic and organic arsenicals, as well as Lewisite itself.

Inorganic Arsenicals. Ancel (1946) reported that sodium arsenate induced a significant reduction in size of offspring when chickens were given this compound orally. James and colleagues (1966) also reported a similar decreased size in offspring of ewes fed sodium arsenite during gestation. Ferm and Carpenter (1968) studied intravenous administration of sodium arsenate (20 mg/kg) in pregnant golden hamsters; the treatment resulted in exencephaly when injected on the eighth day of gestation. Genitourinary abnormalities, cleft lip, cleft palate, microanophthalmia, and ear deformities also were observed when exposure occurred at varying times during

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