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Lung cancer rates among men and particularly among women, almost all of whom are non-smokers, in Xuan Wei County, China are among the highest in China and have been causally associated with exposure to indoor smoky coal emissions that contain very high levels of polycyclic aromatic hydrocarbons (PAHs). As such, this population provides a unique opportunity to study the pathogenesis of PAH-induced lung cancer that is not substantially influenced by the large number of other carcinogenic constituents of tobacco smoke. Aldo-keto reductases (AKRs) activate PAH dihydrodiols to yield their corresponding reactive and redox-activeo-quinones, which can then generate reactive oxygen species that cause oxidative DNA damage. We therefore examined the association between single nucleotide polymorphisms (SNPs) in four genes (AKR1C3-Gln5His,NQO1-Pro187Ser,MnSOD-Val16AlaandOGG1-Ser326Cys) that play a role in the generation, prevention or repair of oxidative damage and lung cancer risk in a population-based, case-control study of 119 cases and 113 controls in Xuan Wei, China. TheAKR1C3-Gln/Glngenotype was associated with a 1.84-fold [95% confidence interval (CI) = 0.98–3.45] increased risk and the combinedOGG1-Cys/CysandSer/Cysgenotypes were associated with a 1.93-fold (95% CI = 1.12–3.34) increased risk of lung cancer. Subgroup analysis revealed that the effects were particularly elevated among women who had relatively high cumulative exposure to smoky coal. SNPs inMnSODandNQO1were not associated with lung cancer risk. These results suggest that SNPs in the oxidative stress related-genesAKR1C3andOGG1may play a role in the pathogenesis of lung cancer in this population, particularly among heavily exposed women. However, due to the small sample size, additional studies are needed to evaluate these associations within Xuan Wei and other populations with substantial exposure to PAHs.

carcinogenesis

Oxidative damage-related genes               AKR1C3               and               OGG1               modulate risks for lung cancer due to exposure to PAH-rich coal combustion emissions