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American Journal of Epidemiology Advance Access originally published online on May 25, 2007
American Journal of Epidemiology 2007 166(3):313-322; doi:10.1093/aje/kwm090
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American Journal of Epidemiology © The Author 2007. Published by the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

ORIGINAL CONTRIBUTIONS

Passive Smoking, Metabolic Gene Polymorphisms, and Infant Birth Weight in a Prospective Cohort Study of Chinese Women

Ting Wu1, Yonghua Hu1, Changzhong Chen2, Fan Yang3, Zhiping Li3, Zhian Fang3, Lihua Wang1 and Dafang Chen1

1 Department of Epidemiology and Biostatistics, Peking University Health Science Center, Beijing, China
2 Brigham and Women's Hospital, Harvard Medical School, Boston, MA
3 Anhui Biomedical Institute, Anqing, Anhui Province, China

Correspondence to Dr. Yonghua Hu or Dr. Dafang Chen, Department of Epidemiology and Biostatistics, Peking University Health Science Center, 38 Xueyuan Road, Haidian District, Beijing 100083, People's Republic of China (e-mail: dafangchen{at}bjmu.edu.cn or yhhu{at}bjmu.edu.cn).

Received for publication September 18, 2006. Accepted for publication February 9, 2007.

The authors investigated whether polymorphisms in two maternal metabolic genes, cytochrome P-450 1A1 (CYP1A1) MspI and epoxide hydrolase 1 (EPHX1) Tyr113His, affect the association of maternal passive smoking with infant birth weight. The study was conducted in a cohort of 1,388 newly married mothers of liveborn singletons who worked in textile mills in Anqing, China, from 1996 to 2000. Multiple linear regression models were used to estimate the associations of passive smoking and genetic susceptibility with birth weight, with adjustment for important potential confounders. In the passive smoking group, there was a remarkable decrease in birth weight with the C/C6235 genotype (156.3 g, 95% confidence interval (CI): –283.6, –29.0) for CYP1A1 MspI and with Tyr/His113 (93.8 g, 95% CI: –188.6, –1.1) as compared with His/His113 (244.6 g, 95% CI: –491.0, –1.9) for EPHX1. When results were stratified by maternal genotype, passive smoking conferred a significantly negative effect in the EPHX1 Tyr/His113 group (103.5 g, 95% CI: –205.8, –9.2) and in the His/His113 group (687.3 g, 95% CI: –748.3, –178.3). The data further showed that there was a significant interaction between maternal passive smoking and maternal EPHX1 genotype for birth weight. The authors conclude that the CYP1A1 MspI and EPHX1 genotypes modified the association between maternal passive smoking and infant birth weight in this study, which is suggestive of possible gene-environment interaction.

birth weight; cytochrome P-450 CYP1A1; epoxide hydrolases; infant; polymorphism, genetic; tobacco smoke pollution


Abbreviations: CI, confidence interval; CYP1A1, cytochrome P-450 1A1; EPHX1, epoxide hydrolase 1; PCR, polymerase chain reaction


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