Polymorphisms in metabolic genes CYP1A1 and GSTM1 and quitting smoking during pregnancy

Background: Approximately 400,000 to 800,000 pregnant women smoke in the United States, exposing themselves and their developing fetus to tobacco. The role of metabolic enzyme genes in altering the effect from maternal smoking on child health has been documented. In this study we assessed the association of the MspI polymorphism in CYP1A1 (CYP1A1*2A) and the null GSTM1 with maternal smoking during pregnancy.

Methods: Survey data of cigarette smoking through in-person interview and genotyping data from buccal cell DNA were derived for 165 smoking mothers (85% African American) accompanying their children to Children's Hospital of Michigan, Detroit, Michigan.

Findings: The number of daily smokers declined from 157 (95.2%) 30 days prior to pregnancy to 126 (49.1%) by the last trimester. The polymorphic variations in CYP1A1 (eg, TC or CC) were positively associated with self reduction and spontaneous quitting and negatively associated with persistent smoking. After controlling for covariates using multiple logistic regression, OR = 2.25 (95% CI: 1.02-4.99) for self-reduction, OR = 1.75 (95% CI: 1.02-3.01) for quitting; and OR = 0.51 (95% CI: 0.29-0.88) for persistent smoking during pregnancy. There was no association between the null GSTM1 and maternal smoking.

Conclusions: The single base substitution in a non-coding region of the phase 1 metabolic gene CYP1A1 may facilitate self-reduction and quitting of tobacco smoking during pregnancy. This finding provides data on the genetic etiology of maternal smoking during pregnancy and it also warrants the necessity of assessing metabolic genes in modifying the effect of tobacco cessation programs.