title: Green tea consumption, genetic susceptibility, PAH-rich smoky coal, and the risk of lung cancer.
abstract: Experimental evidence suggests that green tea (Camellia sinesis) may reduce the risk of lung cancer through several hypothesized mechanisms including scavenging oxidative radicals, inhibition of tumor initiation, and modulation of detoxification enzymes. However, epidemiologic results have not been consistent as to the relationship between green tea consumption and lung caner prevention. We employed a population-based case-control study of 122 cases and 122 controls to investigate the effect that green tea consumption may have on the risk of lung cancer and whether polymorphisms in 8-oxoguanine-DNA glycosylase (OGG1), glutathione-S-transferase M1 (GSTM1), and aldo-keto reductase 1C3 (AKR1C3) modify such an association. Daily green tea consumption was associated with a non-significant reduction in lung cancer risk. However, the effect of smoky coal exposure was higher for non-drinkers (odds ratio (OR)=4.93; 95% confidence interval (95% CI)=1.27-19.13) than for drinkers (OR=1.88; 95% CI=1.01-3.48). Further, among individuals with the OGG1 Cys(326) allele, daily consumption was associated with a 72% reduction (95% CI=0.09-0.94). Among GSTM1 null homozygotes, those who consumed green tea daily had a non-significant reduction in risk compared with non-consumers. Green tea consumption had no effect among OGG1 Ser(326) homozygotes or GSTM1 carriers. In addition, AKR1C3 genotype did not modulate the effect of green tea consumption. The chemopreventive effects of green tea in this population may be restricted to individuals who are particularly susceptible to oxidative stress and oxidative DNA damage.
authors.affiliation: Division of Cancer Epidemiology and Genetics, Occupational and Environmental Epidemiology Branch, National Cancer Institute, NIH, DHHS, 6120 Executive Blvd., EPS 8121, MSC 7240, Bethesda, MD 20892-7240, USA. bonnerm@mail.nih.gov
authors.forename: Matthew R
authors.initials: MR
authors.lastname: Bonner
authors.forename: Nathaniel
authors.initials: N
authors.lastname: Rothman
authors.forename: Judy L
authors.initials: JL
authors.lastname: Mumford
authors.forename: Xingzhou
authors.initials: X
authors.lastname: He
authors.forename: Min
authors.initials: M
authors.lastname: Shen
authors.forename: Robert
authors.initials: R
authors.lastname: Welch
authors.forename: Meredith
authors.initials: M
authors.lastname: Yeager
authors.forename: Stephen
authors.initials: S
authors.lastname: Chanock
authors.forename: Neil
authors.initials: N
authors.lastname: Caporaso
authors.forename: Qing
authors.initials: Q
authors.lastname: Lan
mesh_terms: D000429:Alcohol Oxidoreductases / Q000235:genetics; D000449:Aldehyde Reductase; D000074408:Aldo-Keto Reductases; D016022:Case-Control Studies; D003031:Coal / Q000032:analysis*; D045647:DNA Glycosylases / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D008175:Lung Neoplasms / Q000209:etiology / Q000235:genetics / Q000517:prevention & control*; D008297:Male; D011083:Polycyclic Compounds / Q000032:analysis*; D013662:Tea
chemical_list: D000429:Alcohol Oxidoreductases; D000449:Aldehyde Reductase; D000074408:Aldo-Keto Reductases; D003031:Coal; D045647:DNA Glycosylases; D005982:Glutathione Transferase; D011083:Polycyclic Compounds; D013662:Tea; C479058:oxoguanine glycosylase 1, human