Cobalt in the environment and its toxicological implications.

Cobalt is an essential trace element which is widely distributed in nature. Most of cobalt consumed is used in the manufacture of alloys, and although not released extensively in the environment, it may represent a hazard to human health. In addition, excess dietary cobalt produces toxic effects in animals. Polycythemia and hyperglycemia with transitory damage to pancreatic alpha-cells have been widely reported after cobalt administration. Cobalt salts induce respiratory deficiency in yeast. CoCl2 increased sister chromatid exchange (SCE) in P388D1 cells and in lymphocytes from two donors. So far it has not been possible to induce cancer in experimental animals using cobalt by any other route than by injection. Ingestion of cobalt may lead to reproductive changes in the male rat such as loss of testicular volume and darkening of testicle color. On the other hand, oral administration of cobalt did not produce teratogenicity or significant fetotoxicity in the rat at daily doses as high as 100 mg CoCl2/kg. However, cobalt affected the period of late gestation as well as the postnatal development of the pups. Occupational toxicology of cobalt, hygienic and epidemiologic aspects, and treatment of cobalt poisoning are also topics of special interest. Cobalt is a metal with marked allergenic potential. Asthma, interstitial lung disease and combined asthma and alveolitis have been described as occupational health hazards. EDTA, DTPA, and N-acetyl-L-cysteine have been suggested as possible antidotes in cobalt intoxication.