The role of genetic polymorphisms in environmental health

被引:83
作者
Kelada, SN
Eaton, DL [1 ]
Wang, SS
Rothman, NR
Khoury, MJ
机构
[1] Univ Washington, Sch Publ Hlth & Community Med, Dept Environm Hlth, Seattle, WA 98195 USA
[2] Univ Washington, Ctr Ecogenet & Environm Hlth, Seattle, WA 98195 USA
[3] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA
[4] Ctr Dis Control & Prevent, Off Genom & Dis Prevent, Natl Ctr Environm Hlth, Atlanta, GA USA
关键词
disease susceptibility; environmental health; genetics; polymorphism;
D O I
10.1289/ehp.6065
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Interest is increasing in the role of variations in the human genome (polymorphisms) in modifying the effect of exposures to environmental health hazards (often referred to as gene-environment interaction), which render some individuals or groups in the population more or less likely to develop disease after exposure. This review is intended for an audience of environmental health practitioners and students and is designed to raise awareness about this rapidly growing field of research by presenting established and novel examples of gene-environment interaction that illustrate the major theme of effect modification. Current data gaps are identified and discussed to illustrate limitations of past research and the need for the application of more robust methods in future research projects. Two primary benefits of incorporating genetics into the existing environmental health research framework are illustrated: a) the ability to detect different levels of risk within the population, and b) greater understanding of etiologic mechanisms. Both offer opportunities for developing new methods of disease prevention. Finally, we describe a basic framework for researchers interested in pursuing health effects research that incorporates genetic polymorphisms.
引用
收藏
页码:1055 / 1064
页数:10
相关论文
共 168 条
[21]  
CAPORASO N, 1999, J NATL CANC I MONOGR, V26, P25
[22]   Characterization of single-nucleotide polymorphisms in coding regions of human genes [J].
Cargill, M ;
Altshuler, D ;
Ireland, J ;
Sklar, P ;
Ardlie, K ;
Patil, N ;
Lane, CR ;
Lim, EP ;
Kalyanaraman, N ;
Nemesh, J ;
Ziaugra, L ;
Friedland, L ;
Rolfe, A ;
Warrington, J ;
Lipshutz, R ;
Daley, GQ ;
Lander, ES .
NATURE GENETICS, 1999, 22 (03) :231-238
[23]   Drug-metabolizing enzyme induction by 2,2′-dipyridyl, 1,7-phenanthroline, 7,8-benzoquinoline and oltipraz in mouse [J].
Carr, BA ;
Franklin, MR .
XENOBIOTICA, 1998, 28 (10) :949-956
[24]  
CARTWRIGHT RA, 1982, LANCET, V2, P842
[25]  
Cascorbi I, 2001, CANCER RES, V61, P5051
[26]  
*CDC, 2001, NVECH PUBL
[27]  
*CDC OFF GEN DIS P, 2002, INF CONS PUBL HLTH P
[28]   Chinese alcoholic patients with esophageal cancer are genetically different from alcoholics with acute pancreatitis and liver cirrhosis [J].
Chao, YC ;
Wang, LS ;
Hsieh, TY ;
Chu, CW ;
Chang, FY ;
Chu, HC .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 2000, 95 (10) :2958-2964
[29]   Detection of three genetic polymorphisms in the 5′-flanking region and intron 1 of human CYP1A2 in the Japanese population [J].
Chida, M ;
Yokoi, T ;
Fukui, T ;
Kinoshita, M ;
Yokota, J ;
Kamataki, T .
JAPANESE JOURNAL OF CANCER RESEARCH, 1999, 90 (09) :899-902
[30]   Arsenic methylation capacity, body retention, and null genotypes of glutathione S-transferase M1 and T1 among current arsenic-exposed residents in Taiwan [J].
Chiou, HY ;
Hsueh, YM ;
Hsieh, LL ;
Hsu, LI ;
Hsu, YH ;
Hsieh, FI ;
Wei, ML ;
Chen, HC ;
Yang, HT ;
Leu, LC ;
Chu, TH ;
ChenWu, C ;
Yang, MH ;
Chen, CJ .
MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH, 1997, 386 (03) :197-207