| Affiliation: | (1) Channing Laboratory, Brigham and Women!["rsquo"]("/content/p68778v32488350p/xlarge8217.gif") s Hospital, Department of Medicine, Harvard Medical School, Boston, MA, USA;(2) Occupational Health Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA;(3) Department of Environmental and Occupational Health, Medical College, National Cheng-Kung University, Tainan, Taiwan;(4) Department of Biostatistics, Harvard School of Public Health, Boston, MA, USA |
| Abstract: | Objective: 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.Methods: 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.Results: 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.Conclusions: 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. |
