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Mol. Hum. Reprod. Advance Access originally published online on February 15, 2006
Molecular Human Reproduction 2006 12(2):77-83; doi:10.1093/molehr/gal013
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Maternal smoking during pregnancy and genetic polymorphisms in the Ah receptor, CYP1A1 and GSTM1 affect infant birth size in Japanese subjects

S. Sasaki1,3, T. Kondo1, F. Sata1, Y. Saijo1, S. Katoh1, S. Nakajima1, M. Ishizuka2, S. Fujita2 and R. Kishi1

1Department of Public Health, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-ku, Sapporo 060-8638, Japan and 2Laboratory of Toxicology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Kita 18, Nishi 9, Kita-ku, Sapporo 060-0818, Japan

3 To whom correspondence should be addressed at: Department of Public Health, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-ku, Sapporo 060-8638, Japan. E-mail: sasakis{at}med.hokudai.ac.jp

Genetic susceptibility to tobacco smoke might have relation to adverse pregnancy outcomes. To estimate the effects of maternal smoking and genetic polymorphisms on infant birth weight and length, we conducted a prospective cohort study of 293 women who delivered singleton live births in Sapporo, Japan. Birth weight and length were significantly lower among infants born to continuously smoking women having the aryl hydrocarbon receptor (AhR) wild type genotype (Arg/Arg; 211 g ± 76 g; 1.2 cm ± 0.4 cm, p < 0.01 and p < 0.01, respectively), the CYP1A1 variant genotype (m1/m2 + m2/m2; 170 g ± 64 g, 0.8 cm ± 0.3 cm, p < 0.01 and p < 0.05, respectively), or the GSTM1 null genotype (171 g ± 58 g, 0.6 cm ± 0.3 cm, p < 0.01 and p < 0.05, respectively). When combinations of these genotypes were considered, birth weight and length were significantly lower for infants of continuously smoking women in the AhR wild type + CYP1A1 variant group (315 g ± 116 g; 1.7 cm ± 0.6 cm, p < 0.01 and p < 0.01, respectively) and in the CYP1A1 variant + GSTM1 null group (237 g ± 92 g; 1.3 cm ± 0.5 cm, p < 0.05 and p < 0.01, respectively). These genotypes did not confer adverse effects among women who had never smoked; therefore, maternal smoking in combination with maternal AhR, CYP1A1 and GSTM1 genetic polymorphisms may adversely affect infant birth size.

Key words: Ah receptor/CYP1A1/fetal development/GSTM1/maternal smoking


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