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).
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