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.
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Abbreviations
- Environmental tobacco smoke:
-
(ETS)
- Arsenite:
-
As(III)
- arsenate:
-
As(V)
- monomethylarsonic acid:
-
MMA(V)
- monomethylarsonous acid:
-
MMA(III)
- dimethylarsinic acid:
-
DMA(V)
- cumulative arsenic exposure:
-
CAE
- primary arsenic methylation index:
-
PMI
- secondary arsenic methylation index:
-
SMI
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Chen, YC., Su, HJ.J., Guo, YL.L. et al. Interaction between environmental tobacco smoke and arsenic methylation ability on the risk of bladder cancer. Cancer Causes Control 16, 75–81 (2005). https://doi.org/10.1007/s10552-004-2235-1
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DOI: https://doi.org/10.1007/s10552-004-2235-1