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enhancing duodenal As +5 absorption in rachitic chicks; and that As +5 and <br />phosphate did not appear to share a common transport pathway in the avian <br />duodenum (Fullmer and Wasserman 1986). <br />MAMMALS <br />Mammals are exposed to arsenic primarily by the ingestion of naturally <br />contaminated vegetation and water, or through human activity. In addition, <br />feed additives containing arsonic acid derivatives are often fed to domestic <br />livestock to promote growth and retard disease. Some commercial pet foods <br />contain up to 2.3 mg As/kg dry weight (NRCC 1978). Uptake may occur by <br />ingestion (the most likely route), inhalation, and absorption through skin and <br />mucous membranes. Soluble arsenicals are absorbed more rapidly and completely <br />than are the sparingly soluble arsenicals, regardless of the route of <br />administration (NRCC 1978). <br />Acute episodes of poisoning in warm-blooded organisms by inorganic and <br />organic arsenicals are usually characterized by high mortality and morbidity <br />over a period of 2 to 3 days (NAS 1977; Selby et al. 1977). General signs of <br />arsenic toxicosis include intense abdominal pain, staggering gait, extreme <br />weakness, trembling, salivation, vomiting, diarrhea, fast and feeble pulse, <br />prostration, collapse, and death. Gross necropsy shows a reddening of gastric <br />mucosa and intestinal mucosa, a soft yellow liver, and red edematous lungs. <br />Histopathological findings show edema of gastrointestinal mucosa and <br />submucosa; necrosis and sloughing of mucosal epithelium; renal tubular <br />degeneration; hepatic fatty changes and necrosis; and capillary degeneration <br />in gastrointestinal tract, vascular beds, skin, and other organs. In subacute <br />episodes, where animals live for several days, signs of arsenosis include <br />depression, anorexia, increased urination, dehydration, thirst, partial <br />paralysis of rear limbs, trembling, stupor, coldness of extremities, and <br />subnormal body temperatures (NAS 1977; Selby et al. 1977). In cases involving <br />cutaneous exposure to arsenicals, a dry, cracked, leathery, and peeling skin <br />may be a prominent feature (Selby et al. 1977). Nasal discharges and eye <br />irritation were documented in rodents exposed to organoarsenicals in <br />inhalation toxicity tests (Hood 1985). Subacute effects in humans and <br />laboratory animals include peripheral nervous disturbances, melanosis, anemia, <br />leukopenia, cardiac abnormalities, and liver changes. Most adverse signs <br />rapidly disappeared after exposure ceased (Pershagen and Vahter 1979). <br />Arsenic poisoning in most animals is usually manifested by acute or <br />subacute signs; chronic poisoning is infrequently seen (NAS 1977). The <br />probability of chronic arsenic poisoning from continuous ingestion of small <br />doses is rare, because detoxication and excretion are rapid (Woolson 1975). <br />Chronic toxicity of inorganic arsenicals is associated with weakness, <br />paralysis, conjunctivitis, dermatitis, decreased growth, and liver damage <br />(NRCC 1978). Arsenosis, produced as a result of chronic exposure to organic <br />arsenicals, was associated with demyelination of optic and sciatic nerves, <br />depressed growth, and decreased resistance to infection (NRCC 1978). <br />61