Pharmacology and toxicology of heavy metals: Tellurium

Abstract

Tellurium (Te) dioxide is absorbed from the gastrointestinal tract of dogs. Te and tellurous acid are absorbed by the rat intestine. Increased Te excretion in urine of workers inhaling Te fumes suggests absorption via the respiratory tract. Labelled Na tellurite given i.v. to rabbits has produced the highest concentrations in kidney, heart, spleen, lungs and liver, in descending order, at 24 hr. Sheep and pigs have shown similar distribution. Labelled tellurous acid i.p. in rats has produced the highest concentrations in kidney, blood, liver and leg muscle through 200 days of observation, with the highest ultimate concentration in the femur. Na tellurite i.v. in chickens has been concentrated in kidney, gall bladder, liver and tibia at 96 hr. Excretion occurs in expired air, urine and bile mammals. Metabolism to dimethyl telluride accounts for the garlic-like odour of expired air and sweat. Kidney slices of rats, rabbits and humans reduce tellurite to Te. Te tetrachloride fed to ducklings has produced myocardial necroses and haemoperitoneum. Te dioxide and tartrate fed to dogs have inhibited gastric acid secretion. In rats and ducklings Te has caused patchy hepatic necrosis. Toxic doses of Na tellurate or tellurite have caused hair loss in rats, and dams fed Te metal during pregnancy have produced hydrocephalic offspring. Rats fed Te dioxide have developed hind limb paralysis and degeneration of proximal kidney tubules. Ducklings fed Te tetrachloride have shown cerebral necrosis. Humans inhaling Te fumes have reported headaches. In the treatment of Te intoxication dimercaprol is probably contraindicated since it tends to increase toxic effects, as with Se, and ascorbic acid is of doubtful value although it increases the production of dimethyl telluride. Medical uses of Te are confined to the inclusion of tellurite in microbiological culture media for differentiation and selection. (Cooper - Hindhead)