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

• Published in: American journal of epidemiology Vol. 166; no. 3; pp. 313 - 322
• Main Authors: Wu, Ting, Hu, Yonghua, Chen, Changzhong, Yang, Fan, Li, Zhiping, Fang, Zhian, Wang, Lihua, Chen, Dafang
• Format: Journal Article
• Language: English
• Published: Cary, NC Oxford University Press 01.08.2007; Oxford Publishing Limited (England)
• Subjects: Adult; Analysis. Health state; Biological and medical sciences; Birth Weight; China - epidemiology; cytochrome P-450 CYP1A1; Cytochrome P-450 CYP1A1 - genetics; Epidemiology; epoxide hydrolases; Epoxide Hydrolases - genetics; Female; General aspects; genetic; Genetic Predisposition to Disease; Genotype; Humans; infant; Medical sciences; Miscellaneous; Polymorphism; Polymorphism, Genetic; Prospective Studies; Public health. Hygiene; Public health. Hygiene-occupational medicine; Risk Factors; Tobacco smoke; tobacco smoke pollution; Tobacco Smoke Pollution - adverse effects; Women; Asia; China; birth weight; epoxide hydrolases; polymorphism, genetic; tobacco smoke pollution; infant; cytochrome P-450 CYP1A1; Human; Asiatic; genetic; tobacco smoke pollution; Enzyme; Cytochrome P450; Infant; Epoxide hydrolase; Prospective; Gene; Cohort study; Ether hydrolases; Passive smoking; Hydrolases; Genetics; Birth cohort; Birth weight; Woman; Public health; birth weight; cytochrome P-450 CYP1A1; epoxide hydrolases; infant; polymorphism; Polymorphism
• ISSN: 0002-9262; 1476-6256
• DOI: 10.1093/aje/kwm090

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.