Risk assessment of nickel carcinogenicity and occupational lung cancer.

Abstract

Recent progress in risk assessment of nickel carcinogenicity and its correlation with occupational lung cancer in nickelexposed workers is reviewed. Epidemiological investigations provide reliable data indicating the close relation between nickel exposure and high lung cancer risk, especially in nickel refieries. The nickel species-specific effects and the doseresponse relationship between nickel exposure and lung cancer are among the main questions that are explored extensively. It is also suggested that some confounding factors such as cigarette smoking cannot be neglected. The determination of nickel concentration in lung tissue may be conducive to estimating the nickel exposure level, but it is uncertain whether the high nickel content in lung tissue indicates high lung cancer risk in nickel-exposed workers. Immunologic studies suggest that the suppressive effect ofnickel on NK cell activity and interferon production may also be involved in the mechanisms of nickel carcinogenesis. As a potential mutagen, nickel can cause chromosome damage both in vitro and in vivo; and on a molecular basis, nickel is found to induce DNA damage (DNA strandbreaks and crosslinks, infidelity of DNA replication, inhibition ofDNA repair, and the helical transition ofB-DNA toZ-DNA) by binding ofnickel ions to DNA and nuclear proteins. The discovery of oncogene promises both a challenge and an opportunity for nickel carcinogenesis research. It can be predicted that, with the rapid development ofmolecular biology and oncology, new approaches will be established for both understanding and controlling nickel-induced occupational lung cancer.

Occupational exposure to metal compounds and lung cancer. Results from a multi-center case–control study in Central/Eastern Europe and UK

“…In a similar lung cancer case-control study in Montreal [18,19], nickel was also found to be highly correlated with chromium, and the authors noted that the observed elevated risk for nickel (OR: 3.1, 95% CI: 1.9-5.0) may just as well be due to chromium, or both [18]. Also in cohort studies of nickel industries, the presence of other metals forms a major problem in evaluating nickelrelated risk [20]. Sorahan et al [21][22][23] carried out mortality studies in nickel-cadmium battery and nickel-chromium platers and found an association of lung cancer with cadmium and chromium exposure.…”

Trace elements in hazardous mineral fibres

“…A factor which is underestimated in fibre toxicity is the content of trace elements, which has been shown to be capable of inducing lung cancer (Bargagli et al, 2008;Baumgardt et al, 1986;Doll, 1958;Edel et al, 1990;Fukuda et al, 2004;Masironi, 1969;Shen and Zhang, 1994;Wei et al, 2014). As a matter of fact, there are both epidemiological and experimental indications that trace elements such as trace metals may provoke lung cancer (IARC, 1993;Nemery, 1990), and some researchers have claimed that asbestos fibres may play a passive role in producing diseases as carriers of trace elements (Dixon et al, 1970;Harington et al, 1967).…”

Molecular mechanisms in nickel carcinogenesis: modeling Ni(II) binding site in histone H4.

“…The main target areas are those in the respiratory system, depending on the size of nickel-containing dust particles. The coarsest particles are deposited in the nose, mouth, and larynx, whereas the finer grains can reach the bronchial tree (4,5).…”