A case-control study of CYP1A1, GSTT1 and GSTM1 gene polymorphisms, pregnancy smoking and fetal growth restriction.
OBJECTIVE
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.


METHODS
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.
Delpisheh
Ali
A
Child & Reproductive Health Group, Liverpool School of Tropical Medicine, UK.
Brabin
Loretta
L
Topping
Joanne
J
Reyad
Manal
M
Tang
Ai-Wei
AW
Brabin
Bernard J
BJ
D001724:Birth Weight; D016022:Case-Control Studies; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics*; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics*; D005982:Glutathione Transferase / Q000235:genetics*; D006801:Humans; D011110:Polymorphism, Genetic; D011247:Pregnancy; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*
D019363:Cytochrome P-450 CYP1A1; D005982:Glutathione Transferase; C413545:glutathione S-transferase T1