Bismuth human exposure

Bismuth has similar human exposure pathways as lead. Its overall exposure opportunity to the human population is much less than lead since bismuth has seen many fewer uses in industry. The opportunity for exposure from ingestion is low, except in its use in medicines. The general population is not subject to bismuth exposure by direct contact. Bismuth is a byproduct of lead smelting and thus there is human exposure from airborne lead smelting emissions. 

The specific cytotoxicity of Bi-anti-Tac has been blocked by excess of unlabelled anti-Tac but not by human IgG. Anti-Tac alone is unable to inhibit the proliferation or protein synthesis of most leukemic T-cell lines . Toxins conjugated to anti-Tac bound to the surface of the leukemic cells are poorly and slowly internalized into endosomes, and toxin conjugate of anti-Tac does not pass easily from endosome vehicles to the cytosol in order to kill the cells.a-Particles emitted from bismuth-212bound to the surface of the leukemic cells are much more effective cytotoxic reagents. Hits of one or two a-particles are sufficient for cell inactivation. The one-hour half-life of Bi makes it appropriate for rapid targetting of leukemic cells without prolonged exposure of the normal tissue. 

Oral human LDlq is equal to 221 mgkg Adverse acute reactions to bismuth include acute renal failure following ingestion of excessive concentrations. Bismuth can cause nausea, vomiting, and abdominal pain within hours of exposure. Muscle cramps and weakness, blurred vision, and hyperreflexia may be exhibited. Liver transaminase activities may be elevated. 

There does not appear to be an antidote of choice for bismuth toxicity in humans. Gastric lavage can be used within 1 h of exposure. Replace fluids and electrolytes. Monitor renal and liver function for several days and treat failure conventionally. The newer chelating agents, meso-2,3-dimercaptosuccinic acid and D,L-2,3-dimercapto-propane-l-sufonic acid, are being investigated experimentally as antidotes for bismuth toxicity, and the latter has been shown to be effective. In mice, D-penicillamine has proven effective. 

Metals A wide range of metals induce nephrotoxicity in humans and/or in animal models (Table 5). Some of these metals (e.g., iron, cobalt, copper) are essential elements required for normal body function, while others can be useful in treating diseases. For example, gold salts are useful in treating rheumatoid arthritis lithium salts are indicated for the treatment of manic-depressive illness and aluminum and bismuth salts are available to treat indigestion and stomach aches. However, exposure to these and other metals can occur from environmental sources and in excessive concentrations, can lead to nephropathy. 

Paschal DC, Ting BG, Morrow JC et al (1998) Trace metals in urine of United States residents reference range concentrations. Environ Res 76(l) 53-59 Poon R, Chu I (2000) Effects of trivalent antimony on human erythrocyte glutathione-S-transferases. J Biochem Mol Toxicol 14(3) 169-176 Poon R, Chu I, Lecavalier P et al (1998) Effects of antimony on rats following 90-day exposure via drinking water. Food Chem Toxicol 36(l) 21-35 Rahman L, Corns WT, Bryce DW et al (2000) Determination of mercury, selenium, bismuth, arsenic and antimony in human hair by microwave digestion atomic fluorescence spectrometry. Talanta 52(5) 833-843... 

Lead and other heavy metals such as silver, copper, cadmium, lead and bismuth have been known to have toxic effects on humans and our environment since ancient time [3]. These metals have become mainstays in the electronic world in which we live. As a result, human and environmental exposure to these metals has increased significantly over the past several decades, leading to significant health concern and environmental degradation. Lead and other metals enter the environment and the human body through several routes, which environmental and health regulations seek to reduce or eliminate. 

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