Agency for Toxic Substances and Disease Registry
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Learning Objectives |
Upon completion of this section, you will be able to
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Introduction |
Depending on the route of exposure, cadmium has differing rates of absorption and varying health effects. Cadmium is a cumulative toxin. Its levels in the body increase over time because of its slow elimination. It accumulates chiefly in the liver and kidneys. However, it also accumulates in muscle and bone. The principal organs affected by cadmium’s toxicity, both acutely and chronically, are the:
The lungs can be damaged by acute inhalation exposures as well as suffering effects from more chronic occupational exposures. The kidneys can be damaged with both acute high-dose but more commonly, long-term chronic exposures. The bone disease that occurs with above average chronic exposures is thought to be secondary to cadmium’s effects on the kidney. |
Target Organs |
The chief organs acted upon by cadmium with its chronic toxic effects are
The lungs are a target organ in acute high-dose exposures to inhaled cadmium fumes. |
Mechanisms of Toxicity |
Cadmium is known to increase oxidative stress by being a catalyst in the formation of reactive oxygen species, increasing lipid peroxidation, and depleting glutathione and protein-bound sulfhydryl groups. Cadmium also can stimulate the production of inflammatory cytokines and downregulates the protective function of nitric oxide formation (Navas-Acien et al. 2004). |
Genotoxicity |
Cadmium expresses genotoxic activities in vitro in cells and in vivo in animals; and there is limited epidemiological evidence for in vivo human genotoxicity.
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Carcinogenicity |
There is sufficient evidence that cadmium metal and a number of cadmium compounds, such as cadmium chloride, oxide, sulfate, and sulfide, are carcinogenic in animals. Increased rates of testicular, prostate, and lung cancer in animals have been described (Sahmoun et al., 2005; ATSDR,1999). Current classification of cadmium’s carcinogenicity by health agencies.
Occupational cohort studies have suggested possible associations between chronic exposure to cadmium, particularly cadmium oxide, and cancers of the lung, prostate, and genitourinary system such as renal carcinoma. The strongest evidence for a linkage between occupational exposure to cadmium and cancer is that of lung cancer. This linkage is the reason cited by the IARC in 1993 for designating cadmium as a known human carcinogen and by the NTP for its characterization of cadmium as a known human carcinogen in 2000. The most positive evidence for the IARC’s decision came from a series of studies of the “globe cohort” that showed a positive association between occupational cadmium exposure and lung cancer. However, there have been updated studies of that cohort and other evidence (Sorhan and Esmen 2004) since then as reviewed by Verougstraete et al. in 2003. These studies conclude that, to date the epidemiological evidence shows “a small increase in the relative risk of lung cancer in workers exposed to cadmium and cadmium compounds” (Verougstraete et al. 2003). There is also a consensus that there is not enough evidence to definitely establish a link between cadmium exposure and renal and prostate cancer (Waalkes 2003; NTP 2004). There is no clinical or experimental evidence that background environmental exposures to cadmium causes cancer (Verougstraete et al. 2003). |
Key Points |
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Progress Check |