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[Cancer Research 59, 5932-5937, December 1, 1999]
© 1999 American Association for Cancer Research

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[Cancer Research 59, 5932-5937, December 1, 1999]
© 1999 American Association for Cancer Research


Epidemiology and Prevention

Occupational Exposures and Risk of Gastric Cancer in a Population-basedCase-Control Study1

Anna Mia Ekström2, Mikael Eriksson, Lars-Erik Hansson, Anders Lindgren, Lisa Beth Signorello, Olof Nyrén3 and Lennart Hardell

Department of Medical Epidemiology, Karolinska Institutet, S-171 77 Stockholm, Sweden [A. M. E., L. B. S., O. N.]; Department of Oncology, University Hospital, S-221 85 Lund, Sweden [M. E.]; Department of Surgery, Mora Hospital, S-792-85 Mora, Sweden [L. E. H.]; Department of Pathology, Falu Hospital, S-791 82 Falun, Sweden [A. L.]; and Department of Oncology, Örebro Medical Center, S-701 85 Örebro, Sweden [L. H.]

Gastric cancer trends seem to follow improvements in the environment of blue-collar workers, but the etiological role of occupational exposures in gastric carcinogenesis is scantily investigated. The risk of gastric adenocarcinoma in 10 common occupational industries, and particularly the long-term effects of asbestos, organic solvents, impregnating agents, insecticides, and herbicides, were evaluated in a population-based case-control study, including data on most established risk factors. The study base included all individuals of ages 40–79, born in Sweden and living in either of two areas (total population, 1.3 million) with differing gastric cancer incidences, from February 1989 through January 1995. We interviewed 567 cases classified to site (cardia/noncardia) and histological type, and 1165 population-based controls, frequency-matched for age and sex. Metal workers had a 46% excess gastric cancer risk [adjusted odds ratio (OR), 1.46; 95% confidence interval (CI), 1.10–1.94], increasing to 1.65 (95% CI, 1.17–2.32) for >10 years in the industry. The elevated risk after exposure to herbicides (OR, 1.56; 95% CI, 1.13–2.15) was attributable to phenoxyacetic acids (adjusted OR, 1.70; 95% CI, 1.16–2.48), similarly across tumor subtypes, and not modified by smoking, body mass index, or Helicobacter pylori. The absence of interaction was demonstrated by the pure multiplicative effect found among those exposed to both H. pylori and phenoxyacetic acids (OR, 3.42; 95% CI, 1.41–8.26). Organic solvents, insecticides, impregnating agents, and asbestos were not associated with gastric cancer risk. Employment in the metal industry and exposure to phenoxyacetic acids were both positively and independently associated with gastric cancer risk. The fractions of all gastric cancers attributable to these job-related exposures were small but not negligible (7 and 5%, respectively) in the Swedish population.




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Copyright © 1999 by the American Association for Cancer Research.