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Body Size, Physical Activity, and Risk of Hodgkin's Lymphoma in Women

¹ Northern California Cancer Center, Fremont, California; ² Stanford University Medical Center, Stanford, California; ³ Johns Hopkins University, Baltimore, Maryland; and ⁴ Hartford Hospital, Hartford, Connecticut

Requests for reprints: Theresa H.M. Keegan, Northern California Cancer Center, Suite 300, 2201 Walnut Avenue, Fremont, CA 94538-2334. Phone: 510-608-5040; Fax: 510-608-5095. E-mail: tkeegan{at}nccc.org

Few studies have examined the associations of body size and physical activity with the development of Hodgkin's lymphoma (HL) in women. In data from a population-based case-control study in women ages 19 to 79 years, we assessed the relation of self-report height, weight, body mass index (BMI), and strenuous physical activity to HL risk in 312 cases with diagnostic re-review and 325 random-digit dialed controls using logistic regression. Analyses were stratified by age group and tumor cell presence of EBV. After adjustment for social class measures, taller childhood and adult height were associated with higher HL risk. In women ages 19 to 44 years, HL risk was elevated for higher, but healthy, BMI values, whereas in women ages 45 to 79 years, associations with BMI were inverse. The odds of developing HL were lower with participation (versus nonparticipation) in strenuous physical activity in the past year [odds ratio (OR), 0.58; 95% confidence interval (95% CI), 0.39-0.87 in women 19-44 years; OR, 0.45; 95% CI, 0.19-1.06 in women 45-79 years] and throughout adult life, and with sports team membership (versus nonmembership) in high school and/or at ages 18 to 22 years. Results were similar in cases (n = 269) with and without tumor-cell EBV compared with controls, although the inverse association with physical activity was somewhat stronger for women with EBV-positive disease. These findings show that in women, body size and strenuous physical activity, both modifiable characteristics, are associated with HL risk in adult life possibly through immunologic, infectious, or genetic mechanisms. (Cancer Epidemiol Biomarkers Prev 2006;15(6):1095–101)

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