Journal Article

Less than additive interaction between cigarette smoke and chromium(VI) in inducing clastogenic damage in rodents

Roumen M. Balansky, Francesco D'Agostini, Alberto Izzotti and Silvio De Flora

in Carcinogenesis

Volume 21, issue 9, pages 1677-1682
Published in print September 2000 | ISSN: 0143-3334
Published online September 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.9.1677
Less than additive interaction between cigarette smoke and chromium(VI) in inducing clastogenic damage in rodents

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A combination of tobacco smoking with certain agents has been shown to exert synergistic carcinogenic effects. On the other hand, antagonism betweeen smoke and other pulmonary carcinogens has also been documented by both epidemiological and experimental data. In spite of a very large number of studies carried out for decades in workers exposed to hexavalent chromium, the influence of smoking habits on lung carcinogenesis induced by this metal has not been clarified. For this reason, we performed two studies evaluating clastogenic effects in rodents. In the first one, BDF1 mice were exposed whole-body to mainstream cigarette smoke for 5 days and, on the last day, they received an i.p. injection of potassium dichromate. In the second study, Sprague–Dawley rats were exposed whole-body to environmental cigarette smoke for 18 consecutive days and for the same period of time they received daily intra-tracheal instillations of sodium dichromate. Individually, the two hexavalent chromium salts and cigarette smoke, either mainstream or environmental, enhanced the frequency of micronuclei in bone marrow polychromatic erythrocytes of both mice and rats. Moreover, individual exposure to either environmental cigarette smoke or sodium dichromate enhanced the frequency of micronuclei and multiple nuclei in pulmonary alveolar macrophages of rats. In both studies, combined exposure to cigarette smoke and hexavalent chromium produced less than additive clastogenic effects. These results are consistent with our previous data, showing that hexavalent chromium and either benzo[a]pyrene or cigarette smoke condensate behave antagonistically in in vitro mutagenicity test systems and that the chromium reducing capacity of human pulmonary alveolar macrophages and peripheral lung parenchyma is enhanced in smokers. Taken together, in the absence of any epidemiological evidence, these findings rule out any occurrence of synergism between cigarette smoke and hexavalent chromium, at least in certain stages of the carcinogenesis process.

Keywords: CA, chromosomal aberrations; CS, cigarette smoke; ELF, epithelial lining fluid; ECS, environmental cigarette smoke; GSH, reduced glutathione; i.t., intra-tracheally; MCS, mainstream cigarette smoke; MN, micronucleated; NCE, normochromatic erythrocytes; PAM, pulmonary alveolar macrophages; PBS, phosphate-buffered saline; PCE, polychromatic erythrocytes; PN, polynucleated; SCE, sister chromatid exchanges; TPM, total particulate matter.

Journal Article.  5316 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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