Hm. Shen et Qf. Zhang, RISK ASSESSMENT OF NICKEL CARCINOGENICITY AND OCCUPATIONAL LUNG-CANCER, Environmental health perspectives, 102, 1994, pp. 275-282
Recent progress in risk assessment of nickel carcinogenicity and its c
orrelation with occupational lung cancer in nickel-exposed workers is
reviewed. Epidemiological investigations provide reliable data indicat
ing the close relation between nickel exposure and high lung cancer ri
sk, especially in nickel refineries. The nickel species-specific effec
ts and the dose-response 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 smo
king 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 in
dicates high lung cancer risk in nickel-exposed workers. Immunologic s
tudies suggest that the suppressive effect of nickel on NK cell activi
ty and interferon production may also be involved in the mechanisms of
nickel carcinogenesis. As a potential mutagen, nickel can cause chrom
osome damage both in vitro and in vivo; and on a molecular basis, nick
el is found to induce DNA damage (DNA strandbreaks and crosslinks, inf
idelity of DNA replication, inhibition of DNA repair, and the helical
transition of B-DNA to Z-DNA) by binding of nickel ions to DNA and nuc
lear proteins. The discovery of oncogene promises both a challenge and
an opportunity for nickel carcinogenesis research. It can be predicte
d that, with the rapid development of molecular biology and oncology,
new approaches will be established for both understanding and controll
ing nickel-induced occupational lung cancer.