Objective-To integrate recent understandings of the mechanisms of genotoxicity and carcinogenicity of the diVerent cobalt compounds. Method-A narrative review of the studies published since the last IARC assessment in 1991 (genotoxicity, experimental carcinogenesis, and epidemiology). Results-Two diVerent mechanisms of genotoxicity, DNA breakage induced by cobalt metal and especially hard metal particles, and inhibition of DNA repair by cobalt (II) ions contribute to the carcinogenic potential of cobalt compounds. There is evidence that soluble cobalt (II) cations exert a genotoxic and carcinogenic activity in vitro and in vivo in experimental systems but evidence in humans is lacking. Experimental data indicate some evidence of a genotoxic potential for cobalt metal in vitro in human lymphocytes but there is no evidence available of a carcinogenic potential. There is evidence that hard metal particles exert a genotoxic and carcinogenic activity in vitro and in human studies, respectively. There is insuYcient information for cobalt oxides and other compounds. Conclusion-Although many areas of uncertainty remain, an assessment of the carcinogenicity of cobalt and its compounds requires a clear distinction between the diVerent compounds of the element and needs to take into account the diVerent mechanisms involved. (Occup Environ Med 2001;58:619-625) Keywords: cobalt; DNA breakage; inhibition of DNA repair Cobalt and several of its compounds are used in various industrial applications (table 1). Workers are mainly exposed to cobalt by inhalation and varying toxic manifestations aVecting the respiratory system have been reported in these industries. Diseases of the upper respiratory tract, the bronchial tree, and the lung parenchyma have been reported and reviewed.

The GEMAS (geochemical mapping of agricultural soil) project collected 2108 Ap horizon soil samples from regularly ploughed fields in 33 European countries, covering 5.6 million km2. The <2 mm fraction of these samples was analysed for 53 elements by ICP-MS and ICP-AES, following a HNO3/HCl/H2O (modified aqua regia) digestion. Results are used here to establish the geochemical background variation and threshold values, derived statistically from the data set, in order to identify unusually high element concentrations for these elements in the Ap samples. Potentially toxic elements (PTEs),

Cadmium (Cd) and its compounds were classified as "carcinogenic to humans (Group 1)" by IARC in 1993. The observation of an increased number of lung cancers in a U.S. cohort of cadmium-exposed workers and the finding of tumors in animals exposed to various cadmium compounds apparently played an important role in this assessment. Since this evaluation, several cohorts of cadmium exposed workers have been updated and some additional data regarding environmental exposure to cadmium and cancer risk have been published. The main purpose of this systematic review was to examine whether inclusion of the studies that were not available for the 1993 evaluation might change the overall assessment of the carcinogenic potential of cadmium compounds. A second objective was to examine whether the recent studies are qualitatively better than the older ones and whether they should receive more weight in this assessment. A third issue was to investigate whether a competing effect between nonmalignant respiratory disease (NMRD) and lung cancer may have affected the results for lung cancer in occupationally exposed cohorts. Overall, considering the results of the most recent studies does not suggest that the effect of cadmium on lung cancer increases with improvement of the study design but points to a lower relative risk in the groups exposed to cadmium in the absence of arsenic and nickel. No evidence was found to support the hypothesis that NMRD represents a competing cause of death reducing the mortality from lung cancer. The association between cadmium exposure and prostate cancer was not confirmed in the latest available updates. Studies in environmentally exposed populations do not indicate an increased relative risk of cancer.

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