TY - JOUR
T1 - Maternal cigarette smoking, metabolic gene polymorphisms, and preterm delivery
T2 - New insights on G × E interactions and pathogenic pathways
AU - Tsai, Hui Ju
AU - Liu, Xin
AU - Mestan, Karen
AU - Yu, Yunxian
AU - Zhang, Shanchun
AU - Fang, Yaping
AU - Pearson, Colleen
AU - Ortiz, Katherin
AU - Zuckerman, Barry
AU - Bauchner, Howard
AU - Cerda, Sandra
AU - Stubblefield, Phillip G.
AU - Xu, Xiping
AU - Wang, Xiaobin
N1 - Funding Information:
Acknowledgments We are grateful to two reviewers for the very helpful comments. The study was supported in part by grants from the National Institute of Child Health and Human Development (R01 HD41702), National Institute of Environmental Health Sciences (R01ES11682, R21ES11666), March of Dimes Birth Defects Foundation (20-FY98¡0701, 20-FY02-56 and #21-FY07-605) and NICHD (K24 HD 042489).We thank the nursing staV of Labor and Delivery at Boston Medical Center for their continuous support and assistance to the study and Lingling Fu for data management, and Ann Ramsay for administrative support. We would like to particularly thank the outstanding expert consultants of the BMC Preterm Study team: Drs. Paul Wise, Jerome Klein, John M. Kasznica, and Milton Kotelchuck. Finally, we thank all of the participating mothers and their families.
PY - 2008/5
Y1 - 2008/5
N2 - Preterm delivery (PTD, <37 weeks of gestation) is a significant clinical and public health problem. Previously, we reported that maternal smoking and metabolic gene polymorphisms of CYP1A1 MspI and GSTT1 synergistically increase the risk of low birth weight. This study investigates the relationship between maternal smoking and metabolic gene polymorphisms of CYP1A1 MspI and GSTT1 with preterm delivery (PTD) as a whole and preterm subgroups. This case-control study included 1,749 multi-ethnic mothers (571 with PTD and 1,178 controls) enrolled at Boston Medical Center. After adjusting covariates, regression analyses were performed to identify individual and joint associations of maternal smoking, two functional variants of CYP1A1 and GSTT1 with PTD. We observed a moderate effect of maternal smoking on PTD (OR = 1.6; 95% CI: 1.1-2.2). We found that compared to non-smoking mothers with low-risk genotypes, there was a significant joint association of maternal smoking, CYP1A1 (Aa/aa) and GSTT1 (absent) genotypes with gestational age (β = -3.37; SE = 0.86; P = 9 × 10-5) and with PTD (OR = 5.8; 95% CI: 2.0-21.1), respectively. Such joint association was particularly strong in certain preterm subgroups, including spontaneous PTD (OR = 8.3; 95% CI: 2.7-30.6), PTD < 32 weeks (OR = 11.1; 95% CI: 2.9-47.7), and PTD accompanied by histologic chorioamnionitis (OR = 15.6; 95% CI: 4.1-76.7). Similar patterns were observed across ethnic groups. Taken together, maternal smoking significantly increased the risk of PTD among women with high-risk CYP1A1 and GSTT1 genotypes. Such joint associations were strongest among PTD accompanied by histologic chorioamnionitis.
AB - Preterm delivery (PTD, <37 weeks of gestation) is a significant clinical and public health problem. Previously, we reported that maternal smoking and metabolic gene polymorphisms of CYP1A1 MspI and GSTT1 synergistically increase the risk of low birth weight. This study investigates the relationship between maternal smoking and metabolic gene polymorphisms of CYP1A1 MspI and GSTT1 with preterm delivery (PTD) as a whole and preterm subgroups. This case-control study included 1,749 multi-ethnic mothers (571 with PTD and 1,178 controls) enrolled at Boston Medical Center. After adjusting covariates, regression analyses were performed to identify individual and joint associations of maternal smoking, two functional variants of CYP1A1 and GSTT1 with PTD. We observed a moderate effect of maternal smoking on PTD (OR = 1.6; 95% CI: 1.1-2.2). We found that compared to non-smoking mothers with low-risk genotypes, there was a significant joint association of maternal smoking, CYP1A1 (Aa/aa) and GSTT1 (absent) genotypes with gestational age (β = -3.37; SE = 0.86; P = 9 × 10-5) and with PTD (OR = 5.8; 95% CI: 2.0-21.1), respectively. Such joint association was particularly strong in certain preterm subgroups, including spontaneous PTD (OR = 8.3; 95% CI: 2.7-30.6), PTD < 32 weeks (OR = 11.1; 95% CI: 2.9-47.7), and PTD accompanied by histologic chorioamnionitis (OR = 15.6; 95% CI: 4.1-76.7). Similar patterns were observed across ethnic groups. Taken together, maternal smoking significantly increased the risk of PTD among women with high-risk CYP1A1 and GSTT1 genotypes. Such joint associations were strongest among PTD accompanied by histologic chorioamnionitis.
UR - http://www.scopus.com/inward/record.url?scp=42149164232&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=42149164232&partnerID=8YFLogxK
U2 - 10.1007/s00439-008-0485-9
DO - 10.1007/s00439-008-0485-9
M3 - Article
C2 - 18320229
AN - SCOPUS:42149164232
SN - 0340-6717
VL - 123
SP - 359
EP - 369
JO - Human genetics
JF - Human genetics
IS - 4
ER -