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I I I I I I I I I I I I I I I I I I I Arsenic would kill 50 percent of specimens in 4 days (96-h LC50). Average arsenic concentrations in the livers of adult frogs and toads were 0.164 mg/kg ww at an uncontaminated area (Hall and Mulhern 1984). This value was considerably lower than the leveLs of arsenic in many other freshwater animals (Wagemann et al. 1978). Birds There are great differences in tolerance to arsenic among bird species. As shown in table 4, female mallard (Anas platyrhynchos) ducklings showed a reduced growth rate when they were fed 30 mg As (V)/kg dw over 10 weeks (Camardese et al. 1990). In adult mallards, arsenic toxicity from sodium arsenate in the diet was significant at 400 mg/kg dw (Stanley et al. 1994). Other sensitive species, such as the brown-headed cowbird (Molothrus ater), showed SO-percent mortality in 11 days when fed copper acetoarsenite at 99.8 mg/kg dw (table 4). Opresko et aI. (1994) estimated thE~ no- observed-adverse-effect levels (NOAEL) for dietary concentrations of arsenic in several species of aquatic and terrestrial birds. The belted kingfisher (Ceryle alcyon) and great blue heron (Ardea herodias) are the mosl: relevant species for aquatic habitats. For those two species, the dietary NOAELs were 19 to 22 mg/kg ww when based on sodium arsenite in the diet and 3.4 to 3.9 mg/kg ww when based on copper acetoarsenite (Paris green). Stanley et al. (1994) found that adult mallards fed arsenic as sodium arsenate showed reduced weight gain, reduced liver weight, delayed egg laying, reduced egg weight, and eggshell thinning. Adult mallards exposed to dietary concentrations of 300 mg As/kg (dw) as sodium arsenate rapidly accumulated the compound but also rapidly eliminated it; the compound had a half-life of 1 to 3 days after removal from the diet and reached equili- brium levels in 10 to 30 days (Pendleton et al. 1995). The greatest accumulation of arsenic was in the liver, and lower levels were found in the blood and brain. Arsenic also reduced the growth and the body and liver weights in mallard ducklings (Stanley et al. 1994). Some studies indicate that arsenic is extremely toxic to avian eggs when injected (Birge and Roberts 1976, Gilani and Alibhai 1990). However, elevated levels of arsenic rarely occur naturally in eggs, even in those collected at agricultural drainwater evaporation ponds where arsenic was present at high concentra- tions. Among 81 eggs collected during 1987-89 in the San Joaquin Valley of California, only one contained arsenic above the detection limit of 0.4 mg/kg dw (Ohlendorf et al. 1993). Libby et aI. (1953) found that domestic poultry fed a diet containing high levels of arsenic (arsanilic acid at 180 mg/kg dw) nevertheless produced eggs that contained an average of only 1.3 mg As/kg and showed normal embryo viability. Many studies have shown that arsenic actually stimulates growth and egg pro- ductivity in poultry. Stute and Vogt (1968) fed 3-nitr0-4-hydroxyphenylarsonic acid to hens at 50 mg/kg dw and observed a 4-per- cent increase in egg production. Mammals Although arsenic is officially classified as a human carcinogen (EPA 1995), there is little evidence that it is carcinogenic to other mammals (Eisler 1988). It does, however, cause teratogenic effects in many species. Mammals are exposed to arsenic mainly by the ingestion of contaminated vegetation and water. Adverse effects were noted in rats at dietary levels of 20 mg/kg dw (table 4). Acute or subacute arsenic poisoning is much more common than chronic poisoning in mammals (National Academy of Sciences 1977). The probability of chronic arsenic exposure is rare because detoxification and excretion are rapid (Woolson 1975). As various studies have noted (see review by Talmage and Walton 1991), mammals normally are not good 0fJ