菸煙及油煙暴露與DNA修補酵素基因多形性對臺灣北部女性肺腺癌之交互作用

Interactive Effects of Exposures to Tobacco Smoke and Cooking Fume and Genetic Polymorphisms of DNA Repair Enzymes on Female Lung Adenocarcinoma in Northern Taiwan

吳慧真(Hui-Chen Wu) ； 廖國盟(Kuo-Meng Liao) ； 黃百婉(Pai-Wan Hung) ； 翁祖輝(Tsu-Huei Weng) ； 楊泮池(Pang-Chr Yang) ； 陳建仁(Chien-Jen Chen)

《台灣公共衛生雜誌》 20卷5期 (2001/10) Pp. 357-364

https://doi.org/10.6288/TJPH2001-20-05-04

摘要

目的：本研究在探討台灣北部地區女性肺腺癌與環境暴露和DNA修補酵素基因多形性的相關性，同時探討DNA修補酵素基因多形性與環境因子的交互作用對女性肺腺癌的影響。方法：本病例對照研究自臺大醫院選取107名女性肺腺癌病例和263名健康檢查對照個案為研究對象，以結構式問卷進行環境危險因子之訪問，DNA修補酵素基因多形性是以聚合酵素鍊鎖反應為基礎的方法進行限制酵素片段長度多行性分析。結果：控制年齡與受教育年數後，曾暴露於菸煙者罹患肺腺癌的危險對比值為未曾暴露者的1.73倍、曾暴露於未裝設排油煙機之廚房油煙者的危險對比值為未曾暴露者的2.42倍、曾使用木炭或煤炭為烹飪燃料者的危險對比值為使用電或瓦斯者的2.70倍、曾使用動物油烹飪者的危險對比值為使用值物油者的2.88倍。DNA修補酵素XRCC1-399 Gln/Gln基因型的危險對比值為Arg/Arg或Arg/Gln基因型的2.31倍(95%信賴區間：1.12-4.76)，XRCC3-241Thr/Met基因型的危險對比值為Thr/Thr基因型的2.08倍(95%信賴區間：0.99-7.81)，XDP-751Lys/Gln或Gln/Gln基因型的危險對比值為Lys/Lys基因型的2.08倍(95%信賴區間：1.51-4.82)，hMLH1 GA或AA基因型的危險對比值為GG基因型的3.69倍(95%信賴區間：1.42-9.62)。結論：菸煙及油煙廚房暴露是女性肺腺癌的重要環境危險因子；DNA修補酵素XRCC1、XRCC3、XPD和hMLH1之基因多形性和肺腺癌的發生有密切相關，菸煙及廚房油煙暴露和DNA修補酵素多形性基因，對女肺腺癌之發生有加成協同作用。

關鍵字

肺腺癌 ； DNA修補基因

並列摘要

Objective：This case-control study was carried out to investigate the association of female lung adenocarcinoma with environmental risk factors and genetic polymorphisms of DNA repair enzymes, and to assess the effect of gene-environment interaction on the disease. Methods： A total of 107 female patients affected with lung adenocarcinoma and 263 healthy controls were recruited serially from National Taiwan University Hospital. History of exposures to environmental risk factors was obtained through personal interview using on a structured Questionnaire, Genetic polymorphisms of DNA repair enzymes were determined by polymerase chain reaction with restriction fragment length polymorphism. Results: After adjustment for age and schooling Years. The odds ratio of developing .adenocarcinoma was 1.73 for exposures to tobacco smoking, 2.42 for exposures to cooking fume in unventilated kitchen, 2.70 for using coal and charcoal as cooking fuel, and 2.88 for using lard as cooking oil. The multivariate-adjusted odds ratio of developing lung adenocarcinoma was 2.31 (95% CI: 1.12-4.76) for XRCCl Gln/Gln genotype compared with Arg/Arg or Arg/Gln genotypes, 2.08(95%CI：0.99-7.81) for XRCC3 Thr/Met genotypes compared with Thr/Thr genotype,2.70(95%CI:1.42-9.62)for XPD Lys/Gln or Gln/Gln genotypes compared with Lys/Lys genotype, and 3.69 (95%CI: 1.42-9.62) for hMLHl GA or AA genotypes compared with GG genotype. Conclusions: Exposures to tobaccosmoking, and cooking fumes were important environmental risk factors for female lung adenocarcinoma. The genetic polymorphisms o DNA repair enzymes including XRCC1,XRCC3,SPD and Hmlh1 were associated with an increased risk of the disease.

並列關鍵字

female lung adenocarcinoma ； tobacco smoking ； cooking fume ； DNA repair enzyme