© 2003 by Oxford University Press
© 2003 Oxford University Press
ARTICLE |
Population Attributable Risks of Esophageal and Gastric Cancers
Affiliations of authors: L. S. Engel, W.–H. Chow, M. H. Gail, J. F. Fraumeni, Jr., Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; T. L. Vaughn, J. L. Stanford, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, and Department of Epidemiology, University of Washington, Seattle, WA; M. D. Gammon, School of Public Health, University of North Carolina, Chapel Hill; H. A. Risch, S. T. Mayne, R. Dubrow, Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT; J. B. Schoenberg (retired), Cancer Epidemiology Services, New Jersey Department of Health and Senior Services, Trenton, NJ; H. Rotterdam, Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, NY; A. B. West, Department of Pathology, New York University, New York, NY; M. Blaser, Department of Medicine, New York University School of Medicine, New York, NY; W. J. Blot, International Epidemiology Institute, Rockville, MD.
Correspondence to: Lawrence Engel, PhD, Memorial Sloan–Kettering Cancer Center, Epidemiology Service, 307 E. 63rd St., 3rd Floor, New York, NY 10021 (e-mail: engell{at}mskcc.org).
Background: Several risk factors have been identified for esophageal adenocarcinoma, gastric cardia adenocarcinoma, esophageal squamous cell carcinoma, and noncardia gastric adenocarcinoma, but no study has comprehensively examined their contributions to the cancer burden in the general population. Herein, we estimate the population attributable risks (PARs) for various risk factors observed in a multicenter population–based case–control study. Methods: We calculated PARs by using 293 patients with esophageal adenocarcinoma, 261 with gastric cardia adenocarcinoma, 221 with esophageal squamous cell carcinoma, 368 with noncardia gastric adenocarcinoma, and 695 control subjects. We included smoking for all four tumor types and Helicobacter pylori infection for noncardia gastric adenocarcinoma as established causal risk factors as well as several other factors for which causality is under evaluation. Results: Ever smoking, body mass index above the lowest quartile, history of gastroesophageal reflux, and low fruit and vegetable consumption accounted for 39.7% (95% confidence interval [CI] = 25.6% to 55.8%), 41.1% (95% CI = 23.8% to 60.9%), 29.7% (95% CI = 19.5% to 42.3%), and 15.3% (95% CI = 5.8% to 34.6%) of esophageal adenocarcinomas, respectively, with a combined PAR of 78.7% (95% CI = 66.5% to 87.3%). Ever smoking and body mass index above the lowest quartile were responsible for 45.2% (95% CI = 31.3% to 59.9%) and 19.2% (95% CI = 4.9% to 52.0%) of gastric cardia adenocarcinomas, respectively, with a combined PAR of 56.2% (95% CI = 38.1% to 72.8%). Ever smoking, alcohol consumption, and low fruit and vegetable consumption accounted for 56.9% (95% CI = 36.6% to 75.1%), 72.4% (95% CI = 53.3% to 85.8%), and 28.7% (95% CI = 11.1% to 56.5%) of esophageal squamous cell carcinomas, respectively, with a combined PAR of 89.4% (95% CI = 79.1% to 95.0%). Ever smoking, history of gastric ulcers, nitrite intake above the lowest quartile, and H. pylori infection were responsible for 18.3% (95% CI = 6.5% to 41.8%), 9.7% (95% CI = 5.4% to 16.8%), 40.7% (95% CI = 23.4% to 60.7%), and 10.4% (95% CI = 0.3% to 79.6%) of noncardia gastric adenocarcinomas, respectively, with a combined PAR of 59.0% (95% CI = 16.2% to 91.4%). Conclusion: In this population, a few known risk factors account for a majority of esophageal and gastric cancers. These results suggest that the incidence of these cancers may be decreased by reducing the prevalence of smoking, gastroesophageal reflux, and being overweight and by increasing the consumption of fruits and vegetables.
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