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Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Environmental Medicine.
2007 (English)In: Handbook on the Toxicology of Metals, 3rd Edition / [ed] Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg and Lars T. Friberg, San Diego: Elsevier, 2007, 3, 445-486 p.Chapter in book (Other academic)
Abstract [en]

Cadmium (Cd) is chemically similar to zinc; it 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, electroplated onto steel, and Cd compounds are used as pigments, often in plastics. Cadmium and its compounds are also used in electric batteries, electronic components, and nuclear reactors. Because some of the applications of Cd can be performed by other less-toxic materials, the use of Cd has, therefore, been restricted by law in some countries. The absorption of Cd compounds through the skin is negligible. Between 10 and 50% of inhaled Cd will be absorbed, with the degree of absorption being greater for smaller particles and fumes than for larger dust particles. Humans absorb 5-10% of ingested Cd. A low intake of calcium, zinc, or iron increases the degree of absorption; for example, in iron-deficient individuals, the gastrointestinal absorption rate may be as high as 20%. Cadmium is transported in plasma when bound to metallothionein-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) having been reported for Cd in muscle, kidney, and liver tissue. Cadmium stimulates metallothionein production in the same manner as other bivalent metals, such as zinc, copper, and mercury. Metallothionein-bound Cd in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released after lysosomal degradation of the protein. The unbound Cd stimulates the production of new metallothionein, which binds the Cd in the renal tubular cells. When not all of this new Cd is bound, toxic effects occur, possibly because of the interference of Cd with zinc-dependent enzymes and/or membrane function. The average amount of Cd ingested in most European and North American countries is approximately 1020 mu g/day. The corresponding average urinary excretion is approximately 0.5-1.0 mu g/day. Most of the Cd in blood is located in the cells. The average blood concentration is approximately 0.5-1.0 mu g/L in nonsmokers; it is twice as high in smokers because of Cd absorption from cigarette smoke. Concentrations of 10-20 mu g/kg are usually found in the kidney cortex of nonsmokers in European countries. Although the intake of Cd through food has been higher in Japan than in Europe, and the reported tissue levels are correspondingly higher, the food intake of Cd has decreased in Japan during the last few decades. Ingestion of highly contaminated food or drink results in acute gastrointestinal effects with concomitant diarrhea and vomiting. 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 lung cancer. Long-term excessive exposure from the air or food leads to renal tubular dysfunction. The first sign of damage is a low-molecular-weight proteinuria. This condition is the critical effect of such exposure to Cd and is used in quantitative risk assessment. 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 Cd-polluted areas of Japan; 124 cases were diagnosed up to 1970, and decreasing numbers of clinical cases have been diagnosed later, with 66 cases during the period between 1970 and 2006. In animals exposed to Cd through injection, inhalation, or oral exposure, cancer may develop at the injection site, in the lungs and prostate, or in other organs. Although some epidemiological studies have found an increase in the rates of cancer of the lungs and prostate, other studies have not demonstrated such effects. Cadmium is classified as a human carcinogen (Group 1) by the International Agency for Research on Cancer. Exposure to Cd in the air at concentrations of 5-10 mu g/m(3) during a working life of 45 years may give rise to renal tubular dysfunction in a small proportion of exposed workers. At approximately 100 mu g/m(3), signs of chronic obstructive lung disease may develop even after exposure for a shorter duration. After a lifetime of exposure from food at an average intake of approximately 200 mu g/day, renal effects have been observed at age 50. There is considerable individual variation in the sensitivity of these renal effects. It has been suggested that such effects can be avoided if renal cortex levels are kept <50 mu g/kg and urine levels <2.5 mu g/g CR. Recent reports of low, but statistically significant, increases at even lower levels of urinary Cd are, however, noteworthy. Such increases are observed in the general population, particularly among people with diabetes. 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 in the kidneys, which are the critical organs and the irreversibility of the critical effect, primary prevention is essential. Prevention can be assisted through environmental and biological monitoring. The extensive literature on the toxicological and environmental aspects of Cd has been reviewed in detail by Friberg et al. (1974, 1985, 1986a), Tsuchiya (1978), Nriagu (1980, 1981), the WHO/IPCS (1992), the IARC (1993), Jarup et al. (1998c), the ATSDR (1999), Nordberg and Nordberg (2002), the EU (2003), Satarug and Moore (2004), and the WHO/FAO (2003, 2005).

Place, publisher, year, edition, pages
San Diego: Elsevier, 2007, 3. 445-486 p.
National Category
Pharmacology and Toxicology
URN: urn:nbn:se:umu:diva-76461DOI: 10.1016/B978-012369413-3/50078-1ISI: 000311285300025ISBN: 978-0-12-369413-3OAI: diva2:636767
Available from: 2013-07-12 Created: 2013-07-09 Last updated: 2013-07-12Bibliographically approved

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