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Gold is a rare, noble metal. It does not oxidize and occurs mainly in the elemental form; gold salts are not stable in aqueous solutions but tend to precipitate as elemental gold. In contrast, coordination complexes of gold are stable, and have the potential to pose a health hazard. Gold has been analyzed using flame atomic absorption (ore samples), flameless atomic absorption spectrometry (biological specimens of patients treated with gold), or inductively coupled plasma mass spectrometry (water samples, urine and blood from people not iatrogenically exposed). Levels of human exposure to gold from the air, food, and water are very low. Similarly, occupational exposure remains low. Measurable exposure can be caused by dental inlays, crowns, and bridges, but even this type of exposure apparently has little toxicological significance. Some thiol compounds of gold have been used extensively in medicine, notably in the treatment of rheumatic arthritis. They are rapidly metabolized, with those given orally apparently already metabolized before absorption. The coordination complex, Au(CN)2−, seems to be a common metabolite of all of these drugs, although its proportion of all metabolites is not known. Gold nanoparticles are extensively studied for use in different biomedical applications, including biomedical imaging methods, photothermal therapy, and targeted drug delivery. Particle size, surface properties, and route of exposure affect the absorption and distribution of gold nanoparticles. Gold nanoparticles have been shown to be taken up from the lungs and gastrointestinal tract. After intravenous administration, smaller particles show more widespread tissue distribution than larger gold nanoparticles, which tend to accumulate mainly in liver and spleen. Large doses, in the order of several grams, have been used in the treatment of rheumatic arthritis parenterally, and the incidence of side effects has been high. The most common effects are related to the skin and mucous membranes; the most serious, even fatal, effect is the suppression of bone marrow, aplastic anemia (anemia, thrombocytopenia, and agranulocytosis). Effects of gold therapy on the kidney are relatively frequent, and most usually occur in the form of membranous glomerulonephritis. This and other kidney effects are usually reversible upon cessation of the therapy. Gold-induced lung damage is rare, and usually reversible, but fatal cases have also been described. Mild gastrointestinal symptoms are very frequent; serious colitis is very rare, but may be fatal. In repeated dose studies in experimental animals, the kidney is the main target organ of gold toxicity; at high doses, tubular necrosis, and at lower doses, kidney cortex fibrosis has been observed. Such findings have not been reported in exposed humans. Repeated intramuscular (i.m.) administration of gold thiomalate has caused local injection site sarcomas in rats. Long-term i.m. administration of auranofin and triethylphosphine gold orally or aurothiomalate caused renal adenomas in rats. High doses of gold were embryotoxic and induced teratogenic effects in rats and rabbits. No information could be found on the mutagenic effects of gold compounds. Gold nanoparticles have generally shown low toxicity after oral or parenteral administration. Particle size, shape, and surface coating may modify the toxicity of gold nanoparticles. Subchronic inhalation exposure of rats to 4-5 nm gold nanoparticles resulted in only mild lung inflammation at doses ≥ 20 μg/m3. Gold nanoparticles have generally been negative in genotoxicity studies. Reproductive toxicity of gold nanoparticles has not been adequately studied but, according to available information, placental penetration of gold nanoparticles is limited. Interindividual variation in gold concentrations in the blood and urine are related to the internal exposure to gold from dental appliances, and this variation makes it impossible to use biological monitoring to meaningfully assess environmental or even occupational exposure to gold. While there are some studies indicating an association between therapeutic or adverse effects of gold and concentrations of gold in biological media, the majority of studies on the subject have not observed any such association. At present, therefore, biological monitoring cannot assist in predicting the outcome of gold therapy or the adverse effects of gold. In gold-mining operations, exposure to gold is negligible but, depending on the ore type and quality and mining technology, exposure to silica, mercury, arsenic, radon, diesel engine exhaust, lead, and cyanide are possible. In different parts of the world, very high incidences of even severe silicosis and subsequent pulmonary tuberculosis have been observed. Especially in small-scale gold mining, large amounts of mercury have been traditionally used, and are still being used, especially in the informal sector. Very significant exposure to inorganic mercury among miners and their families has been reported in many countries on all continents. In several instances, even outright mercury poisonings have occurred. In the vicinity of artisanal gold-mining areas, exposure to methylmercury has been demonstrated in different parts of the world. Release of arsenic to the environment from gold-mining activities has been well documented in many places, and even arsenic exposure, measured from arsenic concentrations in body tissues and fluids, has been documented in some populations. Spills and leakages of cyanide from gold mines have caused several environmental accidents, with very serious effects on aquatic wild life. Exposure to lead from the ore in an area of artisanal gold mining has caused a large and serious epidemic of lead poisoning, with many fatalities. |
