Long-term ambient hydrocarbon exposure and incidence of urinary bladder cancer

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作者
Han-Wei Zhang
Zhi-Ren Tsai
Victor C. Kok
Hsiao-Ching Peng
Yau-Hung Chen
Jeffrey J. P. Tsai
Chung Y. Hsu
机构
[1] China Medical University,Program for Aging
[2] National Health Research Institutes,Institute of Population Health Sciences
[3] National Yang Ming Chiao Tung University,Institute of Electrical Control Engineering, Department of Electrical and Computer Engineering
[4] Biomedica Corporation,Department of Computer Science and Information Engineering
[5] Asia University,Department of Medical Research, China Medical University Hospital
[6] China Medical University,Center for Precision Medicine Research
[7] Asia University,Department of Bioinformatics and Medical Engineering
[8] Asia University,Division of Medical Oncology
[9] Kuang Tien General Hospital Cancer Center,Department of Chemistry
[10] Tamkang University,Graduate Institute of Biomedical Science
[11] China Medical University,undefined
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Particulate matter and volatile organic compounds, including total hydrocarbons (THCs), are major ambient air pollutants. Primary nonmethane hydrocarbons (NMHCs) originate from vehicle emissions. The association between air pollution and urinary bladder cancer (UBC) is debatable. We investigated whether long-term exposure to ambient hydrocarbons increases UBC risk among people aged ≥ 20 years in Taiwan. Linkage dataset research with longitudinal design was conducted among 589,135 initially cancer-free individuals during 2000–2013; 12 airborne pollutants were identified. Several Cox models considering potential confounders were employed. The study outcomes were invasive or in situ UBC incidence over time. The targeted pollutant concentration was divided into three tertiles: T1/T2/T3. The mean age of individuals at risk was 42.5 (SD 15.7), and 50.5% of the individuals were men. The mean daily average over 10 years of airborne THC concentration was 2.25 ppm (SD 0.13), and NMHC was 0.29 ppm (SD 0.09). Both pollutants show long-term monotonic downward trend over time using the Mann–Kendall test. There was a dose-dependent increase in UBC at follow-up. UBC incidence per 100,000 enrollees according to T1/T2/T3 exposure to THC was 60.9, 221.2, and 651.8, respectively; it was 170.0/349.5/426.7 per 100,000 enrollees, corresponding to T1/T2/T3 exposure to NMHC, respectively. Without controlling for confounding air pollutants, the adjusted hazard ratio (adj.HR) was 1.83 (95% CI 1.75–1.91) per 0.13-ppm increase in THC; after controlling for PM2.5, adj.HR was even higher at 2.09 (95% CI 1.99–2.19). The adj.HR was 1.37 (95% CI 1.32–1.43) per 0.09-ppm increase in ambient NMHC concentration. After controlling for SO2 and CH4, the adj.HR was 1.10 (95% CI 1.06–1.15). Sensitivity analyses showed that UBC development risk was not sex-specific or influenced by diabetes status. Long-term exposure to THC and NMHC may be a risk factor for UBC development. Acknowledging pollutant sources can inform risk management strategies.
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