OBJECTIVES: To determine the role of maternal CYP1A1, GSTT1, and GSTM1 metabolic gene polymorphisms in modulating the association between pregnancy smoking exposure and fetal growth restriction. STUDY DESIGN: A case-control study was conducted to investigate if the association of pregnancy smoking and birth outcome was modulated by maternal gene polymorphisms. A total of 90 mothers with an IUGR baby (cases) and 180 mothers without IUGR (controls) were enrolled. RESULTS: Almost half of smokers who carried a CYP1A1 variant (51.3%), GSTT1 null (43.6%), or GSTM1 null genotypes (64.1%) delivered a baby with IUGR. Smokers with the variant CYP1A1 "aa" genotype had babies with lower mean birthweight than non-smokers with the same genotype (p=0.004). An interaction test showed increased prevalence of IUGR in smokers with the CYP1A1 (Aa/aa) variant (adjusted OR, 1.9; 95% CI, 1.4-5.5, p=0.01), or with the GSTT1 null (AOR, 1.5; 1.1-3.1, p=0.001), or GSTM1 null genotypes (AOR, 1.5; 1.2-3.7, p=0.001). CONCLUSIONS: Risk of fetal growth restriction in mothers who smoked during pregnancy was modulated by maternal metabolic gene polymorphisms. The genetic control of the conversion of toxic metabolites of tobacco smoke to less damaging substances is important for maternal and fetal health.
OBJECTIVES: To determine the role of maternal CYP1A1, GSTT1, and GSTM1 metabolic gene polymorphisms in modulating the association between pregnancy smoking exposure and fetal growth restriction. STUDY DESIGN: A case-control study was conducted to investigate if the association of pregnancy smoking and birth outcome was modulated by maternal gene polymorphisms. A total of 90 mothers with an IUGR baby (cases) and 180 mothers without IUGR (controls) were enrolled. RESULTS: Almost half of smokers who carried a CYP1A1 variant (51.3%), GSTT1 null (43.6%), or GSTM1 null genotypes (64.1%) delivered a baby with IUGR. Smokers with the variant CYP1A1 "aa" genotype had babies with lower mean birthweight than non-smokers with the same genotype (p=0.004). An interaction test showed increased prevalence of IUGR in smokers with the CYP1A1 (Aa/aa) variant (adjusted OR, 1.9; 95% CI, 1.4-5.5, p=0.01), or with the GSTT1 null (AOR, 1.5; 1.1-3.1, p=0.001), or GSTM1 null genotypes (AOR, 1.5; 1.2-3.7, p=0.001). CONCLUSIONS: Risk of fetal growth restriction in mothers who smoked during pregnancy was modulated by maternal metabolic gene polymorphisms. The genetic control of the conversion of toxic metabolites of tobacco smoke to less damaging substances is important for maternal and fetal health.
Authors: Digna R Velez Edwards; Roberto Romero; Juan Pedro Kusanovic; Sonia S Hassan; Shali Mazaki-Tovi; Edi Vaisbuch; Chong Jai Kim; Offer Erez; Tinnakorn Chaiworapongsa; Brad D Pearce; Jacquelaine Bartlett; Lara A Friel; Benjamin A Salisbury; Madan Kumar Anant; Gerald F Vovis; Min Seob Lee; Ricardo Gomez; Ernesto Behnke; Enrique Oyarzun; Gerard Tromp; Ramkumar Menon; Scott M Williams Journal: J Matern Fetal Neonatal Med Date: 2010-07-09
Authors: Laura R Stroud; George D Papandonatos; Nancy C Jao; Raymond Niaura; Stephen Buka; Neal L Benowitz Journal: Drug Alcohol Depend Date: 2022-02-17 Impact factor: 4.492