期刊
CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
卷 26, 期 5, 页码 756-761出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1055-9965.EPI-16-0281
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资金
- Ministry of Science and Technology of Taiwan [NSC: 94-2314-B-182-052, 95-2314-B-182-011, 96-2314-B-182-005, 104-2314-B-182-068]
- Chang Gung Medical Research Fund [CMRPD: 360013, 370031-3, 3E0021-3, 390041-3]
Background: Exposure to inorganic arsenic (InAs) has been documented as a risk factor for lung cancer. This study examined the association between InAs exposure, its metabolism, and lung cancer occurrence. Methods: We followed 1,300 residents from an arseniasis area in Taiwan, determined urinary InAs metabolites, and identified 39 lung cancer cases. Cox proportional hazards model was performed. Results: The results demonstrated that participants with either the primary methylation index [monomethylarsonic acid (MMA)/InAs] or the secondary methylation index [dimethy-larsenic acid (DMA)/MMA] lower than their respective median values were at a higher risk of lung cancer (HRs from 3.41 to 4.66) than those with high methylation capacity. The incidence density of lung cancer increased from 79.9/100,000 (year(-1)) to 467.4/100,000 (year(-1)) for residents with low methylation capacity and from 0 to 158.5/100,000 (year(-1)) for residents with high methylation capacity when the arsenic exposure dose increased from 2 to 10 ppb to >= 200 ppb, respectively. The analyses revealed a dose-response relationship between lung cancer occurrence and increasing arsenic concentrations in drinking water as well as cumulative arsenic exposure (monotonic trend test; P < 0.05 and P < 0.05, respectively) among the residents with low methylation capacity. The relationship between arsenic exposure and lung cancer among high methy-lators was not statistically significant. Conclusions: Hypomethylation responses to InAs exposure may dose dependently increase lung cancer occurrence. Impact: The high-risk characteristics observed among those exposed should be considered in future preventive medicine and research on arsenic carcinogenesis. (C) 2016 AACR.
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