Our previous studies found the significant associations between cooking oil fume exposure and lung cancer risk in Chinese non-smoking females [5, 8]. The similar results were suggested in the present study. Individuals with exposure to cooking oil fume had a 1.61-fold increased risk of MS-275 cost developing lung adenocarcinoma (P = 0.009). It was reported that cooking oil fume condensates can induce DNA damage [9] and result in the increase of DNA cross-links in a certain concentration [10]. Some

study showed that exposure to cooking oil fume could inhibit cell growth, increase TGFbeta1 secretion, and induce oxidative stress in lung epithelial cells [11]. There are other studies suggesting the important roles of cooking oil fume exposure in lung cancer risk among nonsmoking women [12–14]. Based on our results, 751C variant allele of ERCC2 gene may contribute to risk of lung adenocarcinoma, whereas the ERCC2 312 and ERCC1 118 polymorphisms have no significant associations with lung adenocarcinoma among non-smoking females. The three SNPs selected in this study are all in exons of NER genes, which were considered to influence the

protein activity, then decrease selleckchem or increase the DNA repair capacity and finally associate with risk of cancer. The SNP at amino acid 751 of ERCC2 may be important in terms of ERCC2 protein activity [15], because it locate in the interactive domain, i.e. its helicase activator, p44, inside the TFIIH complex which is essential for transcription and NER [16]. The ERCC2 751 learn more polymorphism was associated with higher levels of chromatic aberrations [17] and DNA adducts levels in non-smokers

[18]. It was reported that ERCC2 751AC/CC was significantly defective in NER [19] and had a modulating effect on DRC [20]. These results suggested that ERCC2 751 polymorphism could result in a defect in NER and deficient DRC that may be responsible for increased susceptibility of cancer. Our results show that non-smoking females carrying GNA12 ERCC2 751C variant allele were at an increased risk for lung adenocarcinoma compared with those carrying AA genotype (adjusted OR = 1.64). It suggests that the polymorphism of ERCC2 codon 751 plays an important role in the development of lung adenocarcinoma in non-smoking females. Previous studies in whole population got the same results [21, 22]. However some reports found the non-correlation between the polymorphisms of ERCC2 gene and risk of lung cancer [23] or the opposite results [24]. The reason for these different conclusions is not clear now. Probably the size of the study population, the particularity of exposure to carcinogen in different populations and genetic differences of study subjects play important roles in it.