2015 (English)In: Handbook on the toxicology of metals: Volume II: Specific metals / [ed] Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg, Academic Press, 2015, 4, 667-716 p.Chapter in book (Refereed)
Cadmium (Cd) occurs naturally with zinc and lead in sulfide ores. Elevated concentrations in air, water, and soil may occur close to industrial emission sources, particularly those of nonferrous mining and metal refining industries. Cadmium metal has been used as an anticorrosive when electroplated onto steel. Cd compounds are used in batteries and as pigments. Cd is increasingly used in solar panels. Dispersive use of Cd is restricted by law in the European Union. Absorption of Cd compounds through the skin is negligible. Between 10% and 50% of inhaled Cd will be absorbed. Humans absorb 5-10% of ingested Cd. A low intake of calcium, zinc, or iron increases the degree of absorption. Cadmium is transported in plasma when bound to metallothionein (MT), a low molecular weight protein, and/or to certain high molecular weight proteins. The accumulation of Cd occurs in many tissues, with particularly long half-lives (10-30 years) in muscle, bone, kidney, and liver. MT-bound Cd in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released. When not all Cd is bound, toxic effects occur. The average amount of Cd ingested in European and North American countries is 10-20 μg/day. The corresponding average urinary excretion is 0.5-1.0 μg/day and the blood concentration is 0.5-1.0 μg/L in nonsmokers; it is twice as high in smokers. The intake of Cd through food used to be higher in Japan than in Europe, but it has decreased and is currently similar to levels reported in European countries with high intakes. Acute inhalation of Cd in air, for example from soldering or welding fumes, may lead to severe chemical pneumonitis. Long-term exposure to low air levels may lead to chronic obstructive lung disease and possibly to lung cancer. Long-term excessive exposure from the air or food leads to renal tubular dysfunction. The first sign of damage is low molecular weight proteinuria. Long-term exposure from food, often combined with other means of delivery, may also lead to disturbance of calcium metabolism, osteoporosis, and osteomalacia, mainly among postmenopausal women. A disease exhibiting these features—called itai-itai disease—occurred in the 1950s in a Cd-polluted area of Japan: 124 cases were diagnosed up to 1970, and 196 cases in total were diagnosed up to 2011. In laboratory animals, Cd has been shown to induce cancer of the lungs, prostate, and other organs. Epidemiological studies have found increased rates of cancer of the lungs and in some studies also in other organs. Cadmium is classified as a human carcinogen (Group 1) by the International Agency for Research on Cancer (IARC). Exposure to Cd in the air at concentrations of 5-10 μg/m3 during a working life of 45 years may give rise to renal tubular dysfunction in a small proportion of exposed workers. At approximately 100 μg/m3, signs of chronic obstructive lung disease may develop. Epidemiological data shows that adverse kidney effects occur in sensitive occupational groups, as well as in general population groups, after lifelong exposures giving rise to urinary Cd (UCd) of 4 μg/g creatinine. At such exposures, bone effects including osteoporosis and increased risk of fractures may also occur in sensitive groups, mainly among postmenopausal women. Adverse bone and kidney effects may occur in a small but sensitive population group as a result of lifelong cadmium exposure with UCd of approximately 1 μg/g creatinine and higher, but the evidence is still inconclusive. Such exposure occurs in general population groups in many countries. There is no specific treatment for Cd poisoning. When there are signs of osteomalacia, large doses of vitamin D should be given. Because of the long half-life of Cd and the irreversibility of bone effects and some kidney effects primary prevention is essential.
Place, publisher, year, edition, pages
Academic Press, 2015, 4. 667-716 p.
cadmium toxicokinetics, biological monitoring of Cd, biological half-life of cd, Itai-Itai disease, kidney effects of Cd, osteomalacia, osteoporosis, bone mineral density and Cd, fractures and Cd, reproductive effects, endocrine disruption, carcinogenesis of Cd, dose-response relationships, risk assessment of Cd
Environmental Health and Occupational Health
IdentifiersURN: urn:nbn:se:umu:diva-112390DOI: 10.1016/B978-0-444-59453-2.00032-9ISBN: 9780123982933OAI: oai:DiVA.org:umu-112390DiVA: diva2:877366