Abstract

To evaluate the role of genetically controlled responsiveness to polycyclic aromatic hydrocarbons (PAH) in the effect of cigarette smoke on birth weight, pregnant mice were exposed to cigarette smoke from day 1 to day 17 of pregnancy and the offspring studied on day 18. An unequivocal phenotyping of foetuses with respect to responsiveness was achieved by measuring the activity of aryl hydrocarbon hydroxylase (AHH) in the foetal liver and corresponding placenta after pretreatment of the dam with β-naphthoflavone. The foetuses of dams exposed to standard non-filter cigarettes were consistently smaller than those of the controls, whereas smoke from commercial filter cigarettes was only marginally effective. No statistically significant association with the responsiveness to PAH could be found with respect to this effect on weight. These results suggest that genetically determined responsiveness to PAH, although of importance for PAH foetotoxicity in mice, is not important in the effect of cigarette smoke on birth weight in the strains studied.

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