Relationship of the oxidative damage biomarker 8-epiprostaglandin F to risk of lung cancer development in the Shanghai Cohort Study

Jian Min Yuan, Steven G. Carmella, Renwei Wang, Yu Ting Tan, Jennifer Adams-Haduch, Yu Tang Gao, Stephen S. Hecht

Research output: Contribution to journalArticle

6 Scopus citations


It has been hypothesized that the pathogenesis of lung cancer induced by cigarette smoking involves oxidative damage by free radicals. Epidemiological data on biomarkers of oxidative damage and risk of lung cancer development are sparse. A nested case-control study of 610 lung cancer cases and 610 matched controls was conducted within a prospective cohort of 18 244 Chinese men in Shanghai, China. The concentrations of 8-epi-prostaglandin F (8-epiPGF), a biomarker of oxidative stress, were determined in baseline urine samples using a validated mass-spectrometry assay. Current smokers had significantly higher level of 8-epiPGF than former smokers or never smokers (P < 0.001). 8-epiPGF levels were significantly higher in lung cancer cases than their smoking-matched controls in former and current smokers, but not different in never smokers (P for interaction = 0.019). The relative risks of developing lung cancer for former and current smokers in the highest relative to the lowest quartile of 8-epiPGF were 5.25 (P trend = 0.035) and 1.99 (P trend =0.007), respectively. The effect of 8-epiPGF and biomarkers of cigarette smoke exposure on lung cancer risk was additive; the relative risk was 5.33 (95% confidence interval = 2.65-7.51) for current smokers with the highest thirds of 8-epiPGF and total cotinine compared with their lowest thirds. Smokers with a heightened state of oxidative stress in response to the insults of cigarette smoking may be more susceptible to smoking-induced lung carcinogenesis.

Original languageEnglish (US)
Pages (from-to)948-954
Number of pages7
Issue number7
StatePublished - Jul 3 2018


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