Journal of the National Cancer Institute Advance Access originally published online on June 12, 2007
JNCI Journal of the National Cancer Institute 2007 99(12):920-928; doi:10.1093/jnci/djm004
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© The Author 2007. Published by Oxford University Press.
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Fifty-Year Study of Lung and Bladder Cancer Mortality in Chile Related to Arsenic in Drinking Water
Affiliations of authors: Departamento de Salud Pública, Escuela de Medicina (GM, CF), and Departamento de Estadística, Facultad de Matemáticas (GM), Pontificia Universidad Católica de Chile, Santiago, Chile; Arsenic Health Effects Research Program, School of Public Health, University of California, Berkeley, CA (YY, CS, JL, AHS); School of Public Health, University of California, Berkeley, CA (MNB, SS)
Correspondence to: Allan H. Smith, MD, PhD, Arsenic Health Effects Research Program, School of Public Health, University of California, Berkeley, 140 Warren Hall, MC 7360, Berkeley, CA 94720-7360 (e-mail: ahsmith{at}berkeley.edu).
Background: Region II of Chile (the second most northerly administrative region) experienced dramatic increases in average arsenic water concentrations beginning in 1958, followed by marked declines in the 1970s when water treatment plants were installed. This history provides a unique opportunity to study time trends in the development of arsenic-related cancers, including lung and bladder cancers.
Methods: We investigated lung and bladder cancer mortality from 1950 to 2000 for region II compared with region V, where drinking water was not contaminated with arsenic. Mortality data were obtained from 218174 death certificates for the two regions for 1950–1970 and from mortality data tapes that identified 307 541 deaths in the two regions for 1971–2000. Poisson regression models were used to identify time trends in rate ratios (RRs) of mortality from lung and bladder cancers comparing region II with region V.
Results: Lung and bladder cancer mortality rate ratios for region II compared with region V started to increase about 10 years after high arsenic exposures commenced and continued to rise until peaking in 1986–1997. The peak lung cancer mortality RRs were 3.61 (95% confidence interval [CI] = 3.13 to 4.16) for men and 3.26 (95% CI = 2.50 to 4.23) for women. The peak bladder cancer RRs were 6.10 (95% CI = 3.97 to 9.39) for men and 13.8 (95% CI = 7.74 to 24.5) for women. Combined lung and bladder cancer mortality rates in region II were highest in the period 1992–1994, with mortality rates of 153 and 50 per 100000 men and women, respectively, in region II compared with 54 and 19 per 100000 in region V.
Conclusions: Such large increases in total population cancer mortality rates have, to our knowledge, not been documented for any other environmental exposure. The long latency pattern is noteworthy, with mortality from lung and bladder cancers continuing to be high until the late 1990s, even though major decreases in arsenic exposure occurred more than 25 years earlier.
| CONTEXT AND CAVEATS Prior knowledge Arsenic in drinking water is known to cause bladder, lung, and nonmelanoma skin cancer. However, little is known about the latency period. Study design Ecologic study comparing lung and bladder mortality for a period of 50 years in two regions of Chile—region II, which experienced a sudden rise and subsequent fall in arsenic levels in the drinking water during that time, and the sociodemographically similar region V, in which arsenic levels remained low. Contribution Lung and bladder cancer mortality in region II started to increase about 10 years after water arsenic levels increased and peaked 10–20 years after the levels dropped back down. At the peak, lung cancer mortality was about three times higher in region II than in region V in both men and women; bladder cancer was six times higher in men and 14 times higher in women. Implications A clear latency pattern for mortality from lung and bladder cancer after arsenic exposure is evident. Limitations This was an ecologic study that did not account for migration and did not have individual data on arsenic exposure or on other risk factors for lung and bladder cancer.
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Manuscript received July 10, 2006; revised April 9, 2007; accepted May 4, 2007.
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J Natl Cancer Inst 2007 99: 906-907.
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J Natl Cancer Inst 2007 99: 905.
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