Interaction between environmental tobacco smoke and arsenic methylation ability on the risk of bladder cancer

• DOI: 10.1007/s10552-004-2235-1
• Publication Date: 2005-04-27T11:42:03Z
• Authors: Yen-Ching Chen; Huey-Jen Jenny Su; Yu-Liang Leon Guo; E. Andres Houseman; David C. Christiani
• Keywords: Male; Air Pollutants; Carcinoma, Transitional Cell; Smoking; Taiwan; Middle Aged; Methylation; Cataract; Arsenic; 3. Good health; Fractures, Bone; 03 medical and health sciences; Sex Factors; 0302 clinical medicine; Urinary Bladder Neoplasms; Risk Factors; Case-Control Studies; Inactivation, Metabolic; Humans; Environmental Pollutants; Female; Tobacco Smoke Pollution; Aged

Arsenic exposure and environmental tobacco smoke (ETS) have been suspected to be associated with bladder cancer risk. We hypothesize that interaction between ETS and the ability to methylate arsenic, a detoxification pathway, modifies the risk of bladder cancer.From January 1996 to December 1999, we identified 41 newly diagnosed bladder cancer patients and 202 fracture and cataract patients at the National Cheng-Kung University (NCKU) Medical Center. The levels of urinary arsenic species [As(III), As(V), MMA(V), and DMA(V)] were determined in all subjects.We found significant interaction between ETS and secondary methylation index (SMI) on the risk of bladder cancer (p=0.02). Among non-smokers with a high primary methylation index (PMI), the risk of bladder cancer was lower in subjects exposed to ETS (OR, 0.37; 95% CI, 0.14-0.96) than in subjects without exposure to ETS. Among non-smokers without ETS, the risk of bladder cancer was 4.7 times higher in subjects with a low SMI (95% CI, 1.30-16.81) than in subjects with a high SMI.Ability to methylate arsenic plays an important role in reducing the risk of bladder cancer attributable to the continuation of arsenic exposure from drinking water and from ETS exposure.