Polymorphisms in metabolic genes CYP1A1 and GSTM1 and changes in maternal smoking during pregnancy

Studies have documented the role of variations in genes that encode metabolic enzymes in altering the effects of maternal smoking on child health. We assessed the association of the MspI polymorphism in CYP1A1(*2A) and the null GSTM1 with maternal smoking behavior during pregnancy.

Smoking data for women during pregnancy were derived through in-person interviews and from genotyping data from buccal cell DNA for 165 smoking mothers (85% Black) accompanying their children to Children's Hospital of Michigan in Detroit. The number of daily smokers declined from 157 (95.2%) 30 days prior to pregnancy to 81 (49.1%) by the last trimester.

The polymorphic variants of CYP1A1*2A (TC or CC) were positively associated with self-reduction and spontaneous quitting and negatively associated with persistent smoking. After allowing for the effect from covariates, we found the adjusted odds ratio (OR) for the association of any C allele to be 2.12 (95% CI = 1.00-4.61) for self-reduction, 1.71 (95% CI = 1.00-2.91) for ever quit smoking, and 0.53 (95% CI = 0.31-0.91) for persistent smoking. The null GSTM1 polymorphism was not associated with any of the three smoking measures.

The single base substitution in the 3' noncoding region of the phase-1 metabolic gene CYP1A1 may facilitate self-reduction and quitting of tobacco smoking during pregnancy. This finding provides new data on the possible genetic etiology of maternal smoking during pregnancy and suggests the need to assess genetic factors (including metabolic genes) that modify the effectiveness of maternal tobacco cessation programs.