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1978; Belton et al. 1985; Pershagen and Bjorklund 1985). Skin tumors, mainly of low malignancy, have been reported after consumption+2f arsenic-rich drinking waters; a total dose of several grams, probably as As , is usually required for the development of skin tumors (Pershagen and Vahter 1979). High incidences of skin cancer and hyperpigmentation were noted among several population groups, especially Taiwanese and Chileans, consuming water containing more than 0.6 mg As/1; the frequency of cancer was highest among people over age 60 who demonstrated symptoms of chronic arsenic poisoning (NRCC 1978). Arsenic reportedly inhibits cancer formation in species having a high incidence of spontaneous cancers (NRCC 1978). In fact, arsenic may be the only chemical for which there is sufficient evidence for carcinogenicity in humans but not in other animals (Woolson 1975; Belton et al. 1985; Lee et al. 1985). In general, animal carcinogenicity tests with inorganic and organic arsenicals have been negative (Hood 1985), even when the chemicals were administered at or near the highest tolerated dosages for long periods (NAS 1977). Most studies of arsenic carcinogenesis in animals were presumably of insufficient duration to simulate conditions in long-lived species such as humans (NRCC 1978). However, mice develope151eukemia and lymphoma after 20 subcutaneous injections of 0.5 mg As /kg body weight: 46% of the experimental group developed these signs vs. none in controls (NRCC 1978). Recently, pulmonary tumorogenicity has been demonstrated in hamsters administered calcium arsenate intratracheally (Pershagen and Bjorklund 1985). Cacodylic acid and other organoarsenicals are not carcinogenic, but may be mutagenic at very high doses (Hood 1985). Several inorganic arsenic compounds are weak inducers of chromosomal aberrations, sister chromatid exchange, and in vitro transformation of mammalian cells; however, there is no conclusive evidence that arsenic causes point mutations in any cellular system (Pershagen and Vahter 1979; Belton et al. 1985; Lee et al. 1985; Deknudt et al. 1986). Studies with bacteria suggest that arsenite is a comutagen, or may inhibit DNA repair (Belton et al. 1985). Arsenic is a known teratogen in several classes of vertebrates, and has been implicated as a cause of birth defects in humans. Specific developmental malSormation?5have been produced experimentally in mammals using inorganic As or As , either through a single dose or a continuous dose during embryogenesis (Hanlon and Ferm 1986b). Teratogenic effects are initiated no later than 4 hours postadministration of As; fetal abnormalities are primarily neural tube defects (Hanlon and Ferm 1985c), but may also include protruding eyes, incomplete development of the skull, abnormally ??all jaws.5 and other skeletal anomalies (NRCC 1978). Inorganic As and As but not organoarsenicals, cross placental barriers in many species of mammals, and result in fetal deaths and malformations (NRCC 1978; EPA 1980). Recent studies with hamsters, for example, showed that sodium arsenite can induce chromatid breaks and chromatid exchanges in Chinese hamster ovary cells in a 38