Cadmium

Cadmium (Cd) occurs with zinc and lead in sulfide ores. Elevated concentrations in air, water, and soil may occur close to nonferrous mining and metal refining industries. Cadmium metal has been used as an anticorrosive when electroplated onto steel. Cd compounds are used in batteries, as pigments and in solar panels. Between 10% and 50% of inhaled Cd will be absorbed and 5%–10% of ingested Cd. The accumulation of Cd in humans occurs in many tissues, with particularly long half-lives (10–30 years) in muscle, bone, kidney, and liver. Cd bound to metallothionein in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released and toxic effects occur. The average amount of Cd ingested in Japan and most European and North American countries is <10–20 μg/day. The corresponding average urinary excretion of Cd is <0.5–1.0 μg/day and the blood concentration is 0.2–0.7 μg/L in nonsmokers; it is twice as high in smokers. 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 with low molecular weight proteinuria. It 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. Cd-induced cancer of the lungs, prostate, and other organs in animals and increased rates of cancer of the lungs and other organs in humans. The International Agency for Research on Cancer (IARC) classified Cd as a human carcinogen (Group 1). 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 2–4 μg/g creatinine. At such exposures, bone effects including osteoporosis and fractures may also occur in sensitive groups. 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. This level of exposure occurs within general population groups in many countries. Osteomalacia is treated with large doses of vitamin D, but there is no effective treatment for other Cd-related effects. Because of the long half-life of Cd and the irreversibility of bone effects and some kidney effects, primary prevention is essential. The toxicological and environmental aspects of Cd have been reviewed in detail by Friberg et al. (1974, 1985, 1986), Tsuchiya (1978), Nriagu (1980, 1981), the WHO/IPCS (1992), the IARC (1993, 2012), Järup et al. (1998c), the Agency for Toxic Substances and Disease Registry (ATSDR, 1999), Nordberg and Nordberg (2002), the European Union (EU, 2003, 2007; ECHA 2020), Satarug and Moore (2004), and the World Health Organization Food and Agriculture Organization (JECFA, 2004, 2012), the European Food Safety Authority (EFSA, 2009, 2012), Akesson et al. (2014), the Scientific Committee on Occupational Exposure Limits (SCOEL, 2017), and the International Union of Pure and Applied Chemistry (Nordberg et al., 2018).