Maternal cigarette smoking, metabolic gene polymorphisms, and preterm delivery: New insights on G × E interactions and pathogenic pathways

Hui Ju Tsai; Xin Liu; Karen Mestan; Yunxian Yu; Shanchun Zhang; Yaping Fang; Colleen Pearson; Katherin Ortiz; Barry Zuckerman; Howard Bauchner; Sandra Cerda; Phillip G. Stubblefield; Xiping Xu; Xiaobin Wang

doi:10.1007/s00439-008-0485-9

Maternal cigarette smoking, metabolic gene polymorphisms, and preterm delivery: New insights on G × E interactions and pathogenic pathways

Hui Ju Tsai^*, Xin Liu, Karen Mestan, Yunxian Yu, Shanchun Zhang, Yaping Fang, Colleen Pearson, Katherin Ortiz, Barry Zuckerman, Howard Bauchner, Sandra Cerda, Phillip G. Stubblefield, Xiping Xu, Xiaobin Wang

^*Corresponding author for this work

Pediatrics

Research output: Contribution to journal › Article › peer-review

69 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	359-369
Number of pages	11
Journal	Human Genetics
Volume	123
Issue number	4
DOIs	https://doi.org/10.1007/s00439-008-0485-9
State	Published - May 2008

Funding

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.

ASJC Scopus subject areas

Genetics(clinical)
Genetics

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10.1007/s00439-008-0485-9

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Tsai, H. J., Liu, X., Mestan, K., Yu, Y., Zhang, S., Fang, Y., Pearson, C., Ortiz, K., Zuckerman, B., Bauchner, H., Cerda, S., Stubblefield, P. G., Xu, X., & Wang, X. (2008). Maternal cigarette smoking, metabolic gene polymorphisms, and preterm delivery: New insights on G × E interactions and pathogenic pathways. Human Genetics, 123(4), 359-369. https://doi.org/10.1007/s00439-008-0485-9

@article{38cf46b0fbdd4ac5890815142ba0785e,

title = "Maternal cigarette smoking, metabolic gene polymorphisms, and preterm delivery: New insights on G × E interactions and pathogenic pathways",

abstract = "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.",

author = "Tsai, {Hui Ju} and Xin Liu and Karen Mestan and Yunxian Yu and Shanchun Zhang and Yaping Fang and Colleen Pearson and Katherin Ortiz and Barry Zuckerman and Howard Bauchner and Sandra Cerda and Stubblefield, {Phillip G.} and Xiping Xu and Xiaobin Wang",

note = "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.",

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doi = "10.1007/s00439-008-0485-9",

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Tsai, HJ, Liu, X, Mestan, K, Yu, Y, Zhang, S, Fang, Y, Pearson, C, Ortiz, K, Zuckerman, B, Bauchner, H, Cerda, S, Stubblefield, PG, Xu, X & Wang, X 2008, 'Maternal cigarette smoking, metabolic gene polymorphisms, and preterm delivery: New insights on G × E interactions and pathogenic pathways', Human Genetics, vol. 123, no. 4, pp. 359-369. https://doi.org/10.1007/s00439-008-0485-9

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.

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Maternal cigarette smoking, metabolic gene polymorphisms, and preterm delivery: New insights on G × E interactions and pathogenic pathways

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UN SDGs

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