TY - JOUR
T1 - Genetic susceptibility to benzene and shortened gestation
T2 - Evidence of gene-environment interaction
AU - Wang, Xiaobin
AU - Chen, Dafang
AU - Niu, Tianhua
AU - Wang, Zhaoxi
AU - Wang, Lihua
AU - Ryan, Louise
AU - Smith, Thomas
AU - Christiani, David C.
AU - Zuckerman, Barry
AU - Xu, Xiping
N1 - Funding Information:
This study is supported in part by grants R825818 from the Environmental Protection Agency, 1R01 HD32505-01 from the National Institute of Child Health and Human Development, 1R01 ES08337-01 from the National Institute of Environmental Health Science, and 1R01 OH03027 from the National Institute of Occupational Safety and Health; by the Barbara and Joel Alpert Children of the City Endowment Fund from the Department of Pediatrics, Boston University School of Medicine, and Boston Medical Center; and by grant 20-FY98-0701 from the March of Dimes Birth Defects Foundation. Dr. Dafang Chen is supported in part
PY - 2000/10/15
Y1 - 2000/10/15
N2 - This study investigated whether the association between low level benzene exposure and shortened gestation is modified by two susceptibility genes, CYP1A1 and GSTT1. This report includes 542 (302 nonexposed, 240 benzene-exposed) nonsmoking and nondrinking mothers of singleton live births at Beijing Yanshan Petrochemical Corporation between June 1995 and June 1997. Epidemiologic and clinical data and blood samples were obtained from mothers. Multiple linear regression models were used to estimate the associations of benzene exposure and genetic susceptibility with gestational age, adjusting for maternal age, education, parity, stress, passive smoking, prepregnancy weight and height, and infant's sex. Without consideration of genotype, benzene exposure was associated with a decrease in mean gestational age of 0.29 (standard error (SE), 0.12) week. When stratified by the maternal CYP1A1 genotype, the estimated decrease was 0.54 (SE, 0.12) week for the AA group, which was significantly greater (p = 0.003) than that for the Aa/aa group, which showed no decrease in gestational age. When both CYP1A1 and GSTT1 were considered, the greatest decrease was found among exposed mothers with the CYP1A1 AA-GSTT1 absent group (0.79 (SE, 0.25) week) and the CYP1A1 AA-GSTT1 present group (0.50 (SE, 0.22) week). Among the nonexposed, genetic susceptibility alone did not confer a significant adverse effect. This study provides evidence of gene-environment interaction and supports further assessment of the role of genetic susceptibility in the evaluation of reproductive toxins.
AB - This study investigated whether the association between low level benzene exposure and shortened gestation is modified by two susceptibility genes, CYP1A1 and GSTT1. This report includes 542 (302 nonexposed, 240 benzene-exposed) nonsmoking and nondrinking mothers of singleton live births at Beijing Yanshan Petrochemical Corporation between June 1995 and June 1997. Epidemiologic and clinical data and blood samples were obtained from mothers. Multiple linear regression models were used to estimate the associations of benzene exposure and genetic susceptibility with gestational age, adjusting for maternal age, education, parity, stress, passive smoking, prepregnancy weight and height, and infant's sex. Without consideration of genotype, benzene exposure was associated with a decrease in mean gestational age of 0.29 (standard error (SE), 0.12) week. When stratified by the maternal CYP1A1 genotype, the estimated decrease was 0.54 (SE, 0.12) week for the AA group, which was significantly greater (p = 0.003) than that for the Aa/aa group, which showed no decrease in gestational age. When both CYP1A1 and GSTT1 were considered, the greatest decrease was found among exposed mothers with the CYP1A1 AA-GSTT1 absent group (0.79 (SE, 0.25) week) and the CYP1A1 AA-GSTT1 present group (0.50 (SE, 0.22) week). Among the nonexposed, genetic susceptibility alone did not confer a significant adverse effect. This study provides evidence of gene-environment interaction and supports further assessment of the role of genetic susceptibility in the evaluation of reproductive toxins.
KW - Benzene
KW - Cytochrome P-450 CYP1A1
KW - Environmental exposure
KW - Genes
KW - Genetic predisposition to disease
KW - Gestational age
KW - Glutathione transferase
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U2 - 10.1093/aje/152.8.693
DO - 10.1093/aje/152.8.693
M3 - Article
C2 - 11052546
AN - SCOPUS:0034667674
SN - 0002-9262
VL - 152
SP - 693
EP - 700
JO - American journal of epidemiology
JF - American journal of epidemiology
IS - 8
ER -