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Cancer Epidemiology Biomarkers & Prevention 16, 385-391, March 1, 2007. Published Online First March 2, 2007;
doi: 10.1158/1055-9965.EPI-06-1057
© 2007 American Association for Cancer Research

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Benzene Exposure and Risk of Non-Hodgkin Lymphoma

Martyn T. Smith, Rachael M. Jones and Allan H. Smith

Center for Occupational and Environmental Health, School of Public Health, University of California, Berkeley, California

Requests for reprints: Martyn T. Smith, Division of Environmental Health Sciences, School of Public Health, 216 Earl Warren Hall, University of California, Berkeley, CA 94720-7360. Phone: 510-642-8770; Fax: 510-642-0427. E-mail: martynts{at}berkeley.edu

Exposure to benzene, an important industrial chemical and component of gasoline, is a widely recognized cause of leukemia, but its association with non-Hodgkin lymphoma (NHL) is less clear. To clarify this issue, we undertook a systematic review of all case-control and cohort studies that identified probable occupational exposures to benzene and NHL morbidity or mortality. We identified 43 case-control studies of NHL outcomes that recognized persons with probable occupational exposure to benzene. Forty of these 43 (93%) studies show some elevation of NHL risk, with 23 of 43 (53%) studies finding statistically significant associations between NHL risk and probable benzene exposure. We also identified 26 studies of petroleum refinery workers reporting morbidity or mortality for lymphomas and all neoplasms and found that in 23 (88%), the rate of lymphoma morbidity or mortality was higher than that for all neoplasms. A substantial healthy-worker effect was evident in many of the studies and a comprehensive reevaluation of these studies with appropriate adjustments should be undertaken. Numerous studies have also reported associations between benzene exposure and the induction of lymphomas in mice. Further, because benzene is similar to alkylating drugs and radiation in producing leukemia, it is plausible that it might also produce lymphoma as they do and by similar mechanisms. Potential mechanisms include immunotoxicity and the induction of double-strand breaks with subsequent chromosome damage resulting in translocations and deletions. We conclude that, overall, the evidence supports an association between occupational benzene exposure and NHL. (Cancer Epidemiol Biomarkers Prev 2007;16(3):385–91)




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2007 by the American Association for Cancer Research.