Association of prenatal passive smoking and metabolic gene polymorphisms with child growth from birth to 3 years of age in the Hokkaido Birth Cohort Study on Environment and Children's Health

Abstract Although the effects of prenatal passive smoking on birth weight have been reported, the effects of metabolic gene polymorphisms on passive smoking have not been studied. Therefore, we investigated the effects of maternal passive smoking and metabolic gene polymorphisms on child growth up to 3 years of age using cotinine as a biomarker. We included 1356 Japanese participants in a prospective cohort between 2003 and 2007 (cotinine levels at the third trimester ≤ 0.21 ng/mL and 0.22 to 11.48 ng/mL for non-passive and passive smokers, respectively), and measured child outcomes such as weight, length, head circumference, and Kaup index. Additionally, we analyzed cytochrome P450 1A1 ( CYP1A1 ), epoxide hydrolase 1 ( EPHX1 ), and two N -acetyltransferase 2 ( NAT2 ) genotypes using real-time polymerase chain reaction methods. Associations were investigated using multiple regression models. Kaup index gain from birth up to 3 years of age was significantly smaller in children born to passive smokers than in those born to non-passive smokers (− 0.34 kg/m 2 ; 95% confidence interval: − 0.67, − 0.01). Maternal CYP1A1 genotype was not associated with prenatal passive smoking and Kaup index gain, but was significantly associated with prenatal passive smoking and head circumference gain from birth up to 3 years of age (− 0.75 cm; 95% confidence interval: − 1.39, − 0.12). Thus, this study suggests that prenatal passive smoking may have potent effects on postnatal growth from birth up to 3 years of age. Moreover, children with maternal CYP1A1 genotype may be more susceptible to the effects of prenatal passive smoking.