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1 Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut; 2 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda, Maryland; 3 Department of Epidemiology and Biostatistics, University of California at San Francisco, San Francisco, California; 4 Department of Health Research and Policy, Stanford University School of Medicine, Stanford, California; 5 Department of Preventive Medicine, Northwestern University Medical School, Chicago, Illinois; 6 Imperial College London, London, United Kingdom; 7 University of Torino, Turin, Italy; 8 Environmental Epidemiology and Biostatistics Unit, National Cancer Research Institute, Genoa, Italy; 9 Epidemiology and Genetics Unit, Department of Health Sciences, University of York, York, United Kingdom; 10 IARC, Lyon, France; 11 Servizio di Epidemiologia e Biostatistica, Centro di Riferimento Oncologico, Aviano, Italy; 12 Istituto di Ricerche Farmacologiche "Mario Negri" and Istituto di Statistica Medica e Biometria, University of Milan, Milan, Italy; 13 School of Public Health, University of Sydney, Sydney, New South Wales, Australia; 14 Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California; 15 Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center; 16 Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle, Washington; 17 Karmanos Cancer Institute and Department of Family Medicine, Wayne State University, Detroit, Michigan; 18 Department of Pathology, Carver College of Medicine, University of Iowa, Iowa City, Iowa; and 19 Department of Health Sciences Research, Mayo Clinic College of Medicine, Rochester, Minnesota
Requests for reprints: Lindsay M. Morton, Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, 6120 Executive Boulevard, EPS/7055, Rockville, MD 20852. Phone: 301-435-3972; Fax: 301-402-0916. E-mail: mortonli{at}mail.nih.gov
Background: The International Lymphoma Epidemiology Consortium (InterLymph) provides an opportunity to analyze the relationship between cigarette smoking and non-Hodgkin lymphoma with sufficient statistical power to consider non-Hodgkin lymphoma subtype. The results from previous studies of this relationship have been inconsistent, likely due to the small sample sizes that arose from stratification by disease subtype. To clarify the role of cigarette smoking in the etiology of non-Hodgkin lymphoma, we conducted a pooled analysis of original patient data from nine case-control studies of non-Hodgkin lymphoma conducted in the United States, Europe, and Australia.
Methods: Original data were obtained from each study and uniformly coded. Risk estimates from fixed-effects and two-stage random-effects models were compared to determine the impact of interstudy heterogeneity. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived from unconditional logistic regression models, controlling for study center, age, sex, and race.
Results: In our pooled study population of 6,594 cases and 8,892 controls, smoking was associated with slightly increased risk estimates (OR, 1.07; 95% CI, 1.00-1.15). Stratification by non-Hodgkin lymphoma subtype revealed that the most consistent association between cigarette smoking and non-Hodgkin lymphoma was observed among follicular lymphomas (n = 1452). Compared with nonsmokers, current smokers had a higher OR for follicular lymphoma (1.31; 95% CI, 1.12-1.52) than former smokers (1.06; 95% CI, 0.93-1.22). Current heavy smoking (
36 pack-years) was associated with a 45% increased OR for follicular lymphoma (1.45; 95% CI, 1.15-1.82) compared with nonsmokers.
Conclusions: Cigarette smoking may increase the risk of developing follicular lymphoma but does not seem to affect risk of the other non-Hodgkin lymphoma subtypes we examined. Future research is needed to determine the biological mechanism responsible for our subtype-specific results.
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