Environmental and occupational medicine. Rom WN, Renzetti AD Jr., Lee JS, Archer VE, eds. Boston, MA: Little, Brown and Company, 1983 Jan; :473-479
The toxicity of arsenic (7440382) and arsine (7784421) is reviewed. Major occupational exposure to arsenic occurs in smelting, as well as the chemical, pesticidal, and pharmaceutical industries. Inhalation of contaminated dust is the principal means of occupational exposure. Hair and urine concentrations of arsenic are used to monitor long and short term arsenic exposures, respectively. Acute arsenic poisoning usually follows the ingestion of contaminated food or drink. The clinical picture is described. Symptoms of chronic arsenic exposure are seen in the skin, nervous system, liver, cardiovascular system, hematopoietic system, and respiratory tract. Chronic arsenic exposure has been associated with cancer of the skin, liver, lungs, and lymphatic and hematopoietic tissues. Animal studies of arsenic carcinogenicity are examined. Reasons for inability to establish a model of arsenic carcinogenicity in any animal species continue to be sought. Mutagenic effects of arsenic are also examined. Arsenic has been shown to cause cell transformation in Syrian-hamster embryo cells, to induce aberrant DNA synthesis, and to produce chromosomal aberrations in tissue culture cells. Arsine is the most acutely toxic form of arsenic. Physical characteristics of arsine and the symptoms and mechanisms of arsine poisoning are discussed. The central mechanism of arsine poisoning is rapid intravascular hemolysis. Kidney failure apparently results from the precipitation of hemoglobin in the renal tubules. Two cases of arsine poisoning are reported in maintenance workers cleaning a drain clogged with the contents of a tank in which arsenical herbicides had been stored.