Maternal smoking induced cotinine levels and genotoxicity in second trimester amniotic fluid.

Cotinine concentrations in amniotic fluid samples from 22 smoking and 37 non-smoking pregnant women and induction of sister-chromatid exchanges (SCE) in Chinese hamster ovary (CHO) cells by samples from 15 smokers and 15 non-smokers were studied as indicators of exposure to potential genotoxic activity during pregnancy. Analysis of cotinine revealed one individual in the non-smoking group with a high cotinine level apparently due to non-reported smoking. The mean cotinine concentration of smokers was 85 ng/ml whereas non-smokers had a concentration of 0.3 ng/ml. According to interview data 16 persons announced some passive exposure to tobacco smoke at home or at work; however this group did not differ from unexposed non-smokers in their amniotic fluid cotinine concentration. SCE inducing activity was tested with and without metabolic activation. The mean SCE frequency in CHO cells induced in the presence of exogenous metabolic activation by concentrated amniotic fluid of heavy smokers (> or = 10 cigarettes/day) was significantly higher (9.7 +/- 0.6 SCE/cell) than among non-smokers (8.9 +/- 0.6 SCE/cell) with metabolic activation. The results show that amniotic fluid cotinine measurements and induction of SCEs in CHO cells can be used to indicate fetal exposure by maternal smoking and support earlier studies suggesting a potential genotoxic hazard to the fetus of heavy smokers.