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  • Oskarsson, Agneta (författare)
  • Chapter 60. Vanadium
  • 2014
  • Ingår i: Handbook on the Toxicology of Metals. - 9780444594532 ; , s. 1347-1367
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
    • Absorption of vanadium from the gastrointestinal tract is poor, not exceeding 2% in humans. Soluble compounds of vanadium are absorbed to a considerable extent after inhalation and concentrated in the lung, but available information is not adequate for a reliable estimation of dose-response relationships. Absorbed vanadium is widely distributed in the body. In animals, the highest values are found in the bone, kidney, liver, and spleen. Bone maintains essentially unchanged levels for several weeks. Low concentrations have been detected in the brain, and in animal placenta and testes. Urine is the predominant route of excretion of absorbed vanadium. Animal and human data indicate that excretion occurs in at least two phases. A three-compartment model for elimination is described in humans, with half-times after intravenous injection of 1.2h, 26h, and 10-12 days. Vanadium is essential for certain bacteria and microorganisms. Some reports suggest that vanadium is essential for mammals, but no biochemical function has been defined in humans. The total dietary intake is estimated to be 6-30μg/day, and in some regions up to 50μg/day. The use of vanadium as a supplement for athletes and body builders has been reported. Point-of-contact non-neoplastic and neoplastic effects in experimental animals occur in the respiratory tract. Systemic effects have been observed in the liver, kidney, nervous system, cardiovascular system, and blood-forming organs. Metabolic effects include interference with the biosynthesis of cystine and cholesterol, depression and stimulation of phospholipid synthesis, and, at higher concentrations, inhibition of serotonin oxidation. Vanadate has been shown to inhibit sodium/potassium-transporting ATPase (Na+/K+ATPase), phosphatases, and several other enzyme systems. Vanadium compounds enhance the effects of insulin and have been shown to lower blood glucose in experiments in diabetic animals and humans. Both acute and chronic effects of occupational exposure to vanadium pentoxide (V2O5) and other vanadium compounds have been described. They are manifested mainly as delayed but reversible irritation of the respiratory tract involving excess mucus production and prolonged coughing, accompanied in cases of more severe exposure by bronchospasm, wheezing, and diarrhea. Eye irritation and conjunctivitis have been reported in workers. Tracheobronchitis may result from heavy, long-term exposure. Changes in lung function indicating obstructivity and increases in inflammatory biomarkers have been demonstrated in boiler cleaners after prolonged exposure. Vanadium is not mutagenic in the Ames test. However, pentavalent and tetravalent vanadium compounds have produced aneuploidy in somatic cells invitro and invivo. Clear evidence of carcinogenic activity has been shown in mice after inhalation of V2O5. The International Agency for Research on Cancer has classified V2O5as a possible carcinogen (Group 2B). Biological monitoring of vanadium in serum, blood, and urine is used to assess exposure to vanadium compounds in occupational and population studies. Reviews on environmental, toxicological and occupational health aspects of vanadium and vanadium compounds have been published (143,93,12,54,219,95,15,90,59,91,88,89and97).
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