Genetic susceptibility to benzene and shortened gestation: Evidence of gene-environment interaction

Citation
Xb. Wang et al., Genetic susceptibility to benzene and shortened gestation: Evidence of gene-environment interaction, AM J EPIDEM, 152(8), 2000, pp. 693-700
Citations number
38
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Envirnomentale Medicine & Public Health","Medical Research General Topics
Journal title
AMERICAN JOURNAL OF EPIDEMIOLOGY
ISSN journal
0002-9262 → ACNP
Volume
152
Issue
8
Year of publication
2000
Pages
693 - 700
Database
ISI
SICI code
0002-9262(20001015)152:8<693:GSTBAS>2.0.ZU;2-#
Abstract
This study investigated whether the association between low level benzene e xposure and shortened gestation is modified by two susceptibility genes, CY P1A1 and GSTT1. This report includes 542 (302 nonexposed, 240 benzene-expos ed) nonsmoking and nondrinking mothers of singleton live births at Beijing Yanshan Petrochemical Corporation between June 1995 and June 1997. Epidemio logic and clinical data and blood samples were obtained from mothers. Multi ple linear regression models were used to estimate the associations of benz ene exposure and genetic susceptibility with gestational age, adjusting for maternal age, education, parity, stress, passive smoking, prepregnancy wei ght and height, and infant's sex. Without consideration of genotype, benzen e 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 gen otype, the estimated decrease was 0.54 (SE, 0.12) week for the AA group, wh ich was significantly greater (p = 0.003) than that for the Aa/aa group, wh ich 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 suscep tibility alone did not confer a significant adverse effect. This study prov ides evidence of gene-environment interaction and supports further assessme nt of the role of genetic susceptibility in the evaluation of reproductive toxins.