期刊
ENVIRONMENTAL HEALTH PERSPECTIVES
卷 114, 期 8, 页码 1293-1296出版社
US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
DOI: 10.1289/ehp.8832
关键词
arsenic; bronchiectasis; childhood exposure; chronic obstructive pulmonary disease; drinking water; in utero exposure
资金
- NIEHS NIH HHS [R01 ES010033, P42 ES004705, R01 ES10033-03, P42-ES04705] Funding Source: Medline
Arsenic in drinking water is an established cause of lung cancer, and preliminary evidence suggests that ingested arsenic may also cause nonmalignant lung disease. Antofagasta is the second largest city in Chile and had a distinct period of very high arsenic exposure that began in 1958 and lasted until 1971, when an arsenic removal plant was installed. This unique exposure scenario provides a rare opportunity to investigate the long-term mortality impact of early-life arsenic exposure. In this study, we compared mortality rates in Antofagasta in the period 1989-2000 with those of the rest of Chile, focusing on subjects who were born during or just before the peak exposure period and who were 30-49 years of age at the time of death. For the birth cohort born just before the high-exposure period (1950-1957) and exposed in early childhood, the standardized mortality ratio (SMR) for lung cancer was 7.0 [95% confidence interval (CI), 5.4-8.9; p < 0.001] and the SMR for bronchiectasis was 12.4 (95% Cl, 3.3-31.7; p < 0.001). For those born during the high-exposure period (1958-1970) with probable exposure in utero and early childhood, the corresponding SMRs were 6.1 (95% Cl, 3.5-9.9; p < 0.001) for lung cancer and 46.2 (95% Cl, 21.1-87.7; P < 0.001) for bronchiectasis. These findings suggest that exposure to arsenic in drinking water during early childhood or in utero has pronounced pulmonary effects, greatly increasing subsequent mortality in young adults from both malignant and nonmalignant lung disease.
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