Cigarette smoking during pregnancy: comparison of biomarkers for inclusion in epidemiological studies

Abstract

Prenatal exposure to tobacco smoke represents an important confounding factor in epidemiological studies addressing developmental effects and requires careful controlling by the use of biomarkers. We compared the following biomarkers of exposure to tobacco smoke during pregnancy and related biological effects in 23 smokers and 17 non-smokers: placental concentrations of heavy metals (cadmium, chrome, lead and zinc), cotinine concentration in meconium, placental CYP1A1 activity (EROD) and bulky DNA adducts. Cadmium was detected in all samples and found in higher concentration in placentas of smokers compared with non-smokers (geometric mean ± GSD: 56.1 ± 1.8 vs 27.4 ± 1.6 μg kg -1 dry weight; p < 0.001). Cotinine was not detected in meconium samples from the non-smoker group, while samples from the smoker group contained a mean concentration of 114.1 ± 2.9 μg kg -1 . Correlation analysis of biomarkers among smokers revealed that daily cigarette consumption was strongly correlated to placental cadmium (Pearson's r = 0.83, p < 0.001) and to cotinine (r = 0.73, p < 0.001). EROD activity was also higher in smokers than in non-smokers (9.4 ± 3.4 vs 2.5 ± 1.8 pmol resorufin min -1 mg -1 protein; p < 0.001) and values were correlated to cotinine concentration in meconium (r = 0.80, p < 0.001) and placental cadmium level (r = 0.66, p < 0.001). The amount of bulky DNA adducts in placenta was highly variable and poorly associated with smoking status. Because of their high sensitivity and specificity to detect women who smoke during pregnancy, cotinine concentrations in meconium and placental EROD activity should be incorporated in epidemiological studies that investigate adverse developmental effects induced by in utero exposure to environmental contaminants.