Smoking and sister chromatid exchange.

ABSTRACT

Smokers were shown to have significantly higher SCE levels in peripheral lymphocytes than non-smokers. The increase of SCE was found to depend on the cigarette consumption, and to be significantly higher in subjects with a long than with a short history of smoking. Analysis of the frequency distribution of individual SCE levels and of SCE numbers in single cells gave no indication of subgroups of individuals of subpopulations of lymphocytes with an increased SCE response to smoking. Cells from smokers cultivated in plasma from non-smokers retained a high SCE level, and cells from non-smokers cultivated in plasma from smokers no increase of SCE, indicating that the increase of SCE caused by smoking is due to some type of (long-lived) cellular damage rather than to serum factors. The plasma levels of the primary nicotine metabolite cotinine were found to be increased in heavy smokers as compared to light smokers, and showed an excellent correlation with the cotinine levels in the amniotic fluid in pregnant female smokers. No correlation was found between the individual SCE and cotinine levels in smokers, which indicates that the degree of exposure to SCE-inducing genotoxic agents in the cigarette smoke is not related to plasma cotinine levels in any simple way. The induction of DNA strand breaks and SCE by two intermediary benzo(a)pyrene (BP) metabolites was studied in human lymphocytes in vitro. Both 9-OH-BP and BP-7,8-dihydrodiol were found to induce DNA breaks, but only the latter compound induced SCE. The SCE-inducing effect of BP-7,8-dihydrodiol was observed at a very low concentration (0.01 microM), which indicates a possible role for this BP derivative in the smoking-induced increase of SCE in vivo.