Arsenic ingestion from well water linked to raised risk of lung cancer

Main Category: Lung Cancer
Article Date: 22 Dec 2004 - 0:00 PDT


Residents of Taiwan who consumed drinking water with high levels of arsenic have a higher risk of lung cancer, with cigarette smokers from this group having an even greater risk, according to a study in the December 22/29 issue of JAMA.

Arsenic is a naturally occurring element in soil, and can contaminate drinking water, according to background information in the article. Residents of the southwestern and northeastern coasts of Taiwan had been drinking well water contaminated with a high concentration of arsenic before the establishment of the public tap water system.

Chi-Ling Chen, Ph.D., of the College of Public Health, National Taiwan University, Taipei, Taiwan, and colleagues conducted a study to determine the dose-response relationship between ingested arsenic and lung cancer risk and the added effect of cigarette smoking on this risk.

The study included 2,503 residents in southwestern and 8,088 in northeastern arsenic-endemic areas in Taiwan, who were followed up for an average period of 8 years. Information on arsenic exposure, cigarette smoking, and other risk factors was collected at enrollment through standardized questionnaire interview.

During the study followup period, there were 139 newly diagnosed cases of lung cancer. Residents with the highest level of arsenic exposure had a 3.29 times increased risk for lung cancer, after adjusting for various factors including age, sex, and cigarette smoking status at recruitment. Among nonsmokers, those who were exposed to the highest arsenic level had about twice the risk for lung cancer when compared with those with the lowest level of exposure. Among participants with the lowest arsenic level, those who had the highest cumulative cigarette smoking exposure had a 4-fold risk of lung cancer compared with nonsmokers. When compared with nonsmokers with the lowest levels of arsenic exposure, those who consumed well water with the highest arsenic levels and smoked for more than 25 pack-years had a more than 11-fold risk of lung cancer.

"Approximately 32 percent to 55 percent of lung cancer cases were estimated to be attributable to the combined effect of cigarette smoking and ingested arsenic, depending on the levels of both exposures," the authors write. "The synergy indices ranged from 1.62 to 2.52, indicating a synergistic effect of ingested arsenic and cigarette smoking on lung cancer."

"The reductions in cigarette smoking would likely reduce the lung cancer risk accompanied by exposure to arsenic, and similarly, reductions in arsenic exposure would reduce the lung cancer risk among cigarette smokers. Appropriate public health interventions, such as cigarette smoking cessation programs and reduction in arsenic concentration of drinking water, are warranted. Furthermore, it is essential to take cigarette smoking into consideration in the risk assessment and the determination of the maximal contamination level of arsenic in drinking water," the authors conclude.

(JAMA. 2004; 292: 2984-2990. Available post-embargo at www.jama.com)

Editor's Note: This study was supported by grants from the National Science Council and from the Department of Health, Executive Yuan, Taiwan.

Editorial: Lung Cancer Etiology - Independent and Joint Effects of Genetics, Tobacco, and Arsenic

In an accompanying editorial, Habibul Ahsan, M.D., M.Med.Sc., of Columbia University, New York, N.Y., and Duncan C. Thomas, Ph.D., of the University of Southern California, Los Angeles, comment on the two lung cancer studies in this week's JAMA.

"Irrespective of the roles of familial aggregation and environmental exposures to arsenic or other carcinogens, lung cancer is primarily caused by tobacco smoking--an exposure that is largely preventable. If nicotine addiction genes or modifier genes play roles in subsets of patients with lung cancer, such cases can be prevented by preventing tobacco smoking. Although there are no addiction genes for arsenic or other environmental exposures, modifier genes could modulate the effects of these nontobacco carcinogens. Such genes, in combination with major genes, could lead to familial aggregation."

"Innovative epidemiological studies to detect and separate these effects, taking the lead from studies like those of Jonsson et al and Chen et al, need to be designed in the future. Even for individuals with such a familial risk, or for those who are already chronically exposed to arsenic or other lung carcinogens, avoiding tobacco smoking remains the most feasible option for reducing lung cancer risk," they write.

(JAMA. 2004; 292: 3026-3029. Available post-embargo at www.jama.com)

Contact: Chien-Jen Chen, Sc.D.
cjchen@ha.mc.ntu.edu.tw
JAMA and Archives Journals Website

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