Journal
HANDBOOK ON THE TOXICOLOGY OF METALS, VOL I & II, 4TH EDITION
Volume -, Issue -, Pages 1217-1228Publisher
ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD
DOI: 10.1016/B978-0-444-59453-2.00054-8
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Food (e.g. meat, dairy products, and cereals) is the main source of tellurium exposure in the general population. In the working environment, inhalational exposure predominates. Small amounts of organic tellurium compounds can also be absorbed through the skin. No quantitative data have been published regarding the inhalational absorption of tellurium or tellurium compounds in humans. In experiments on healthy volunteers, a gastrointestinal absorption of 10-25% has been observed. In animal experiments, a similar absorption has been estimated. The highest tissue concentrations have been ob-served in the kidneys. Increased levels have also been noted in the blood, heart, lungs, liver, spleen, muscle, and bone. The main accumulation is in bone, which harbors >90% of the total body burden. Tellurium can pass both the placenta and the blood-brain barrier. Parenterally administered tellurium is predominantly excreted in the urine, whereas orally ingested tellurium salts are transferred through biliary secretion and mainly excreted in the feces. Small amounts, probably approximately 0.1%, of absorbed tellurium are exhaled, presumably as dimethyl telluride. In rat experiments, biological half-times ranging from 9 days in blood to 23 days in the kidney have been reported. The whole-body retention model for humans estimates a biological half-time of approximately 3 weeks. Elimination from bone is slow, with an estimated half-time of approximately 600 days. Acute systemic effects of tellurium toxicity in rats include listlessness, decreased locomotor activity, somnolence, anorexia, weight loss, gastrointestinal disturbances, changes in fur, and occasionally epilation and hind leg paralysis. Long-term studies of chronic effects are sparse. Dominant and critical effects have been reported from the nervous system, including peripheral neuropathy characterized by segmental demyelination and minor axonal degeneration. In the brain, black changes caused by dark tellurium particles localized to lipofuscin granules in neuronal cytoplasm have been observed. Other effects have been reported from the liver (fatty degeneration and necrosis), kidney (proximal tubular lesions, oliguria, or anuria), and heart (cell necrosis, edema, and congestion). Reproductive effects including, for example, hydrocephalus, edema, exophthalmia, and ocular hemorrhage have been described. Acute exposure to tellurium in occupational settings may cause acute respiratory irritation followed by the development of garlicky odor of the breath and sweat, drowsiness, headache, malaise, lassitude, weakness, and dizziness. Gastrointestinal symptoms such as anorexia, nausea, vomiting, metallic taste, dry mouth, and constipation may appear. Dermatitis and blue-black discoloration of the skin may follow exposure to tellurium hexafluoride. Severe intoxication may lead to depression of the respiratory system and circulatory collapse. No specific antidote for tellurium poisoning has been found. After inhalational exposure, treatment with fresh air, oxygen supply, assisted ventilation, beta(2)-adrenergic agonists, and oral or parenteral corticosteroids can be tried. Reviews of tellurium toxicology have been published by Browning (1969), Izrael'son (1973), Fishbein (1977), Alexander et al., (1988) and Kobayashi (2004).
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