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Season, Sun, Sex, and Cervical Cancer

¹ Department of Epidemiology and Biostatistics, Norman J. Arnold of Public Health; ² Cell and Developmental Biology and Anatomy, School of Medicine, University of South Carolina; ³ WJB Dorn Veterans Affairs Medical Center, Columbia, South Carolina; ⁴ College of Biological Sciences University of Minnesota, St. Paul, Minnesota; ⁵ Department of Physiology, Leiden University and ⁶ Leiden Cytology and Pathology Laboratory, Leiden, the Netherlands

Requests for reprints: William J.M. Hrushesky, WJB Dorn Veterans Affairs Medical Center/Network 7, University of South Carolina School of Medicine, 6439 Garners Ferry Road (Mail Code 151), Columbia, SC 29209. Phone: 803-647-5654; Fax: 803-647-5656. E-mail: william.hrushesky{at}med.va.gov

Introduction: Sunlight's UV B component, a known cellular immunosupressant, carcinogen, and activator of viral infections, is generally seasonally available. Venereal human papillomavirus (HPV) transmission, at least in part, causes cervical cancer. We have previously inspected the monthly rates of venereal HPV infection and sunlight fluency in Southern Holland over 16 consecutive years. Both peak in August with at least 2-fold seasonality. The amount of available sunlight and the rate of Papanicolaou (Pap) smear screen–detected HPV are positively correlated. We now investigate whether premalignant and malignant cervical epithelial changes are also seasonal and related to seasonal sunlight fluency.

Methods: We have studied >900,000 consecutive, serially independent, interpretable screening Pap smears obtained by a single cervical cancer screening laboratory in Leiden, Holland, during a continuous 16-year span from 1983 through 1998. The average monthly rates of premalignant and malignant epithelial change were inspected and the annual patterns contrasted to the annual pattern of sunlight fluency at this global location and to monthly average HPV infection rate. Because HPV is venereally transmitted, Dutch seasonal sexual behavior was evaluated by assessment of the annual pattern of Dutch conception frequency as a competing cause for cervical cancer seasonality.

Results: (a) Twice as many premalignant and malignant epithelial changes were found among Pap smears obtained in the summer months, with an August peak concurrent with histopathologic evidence of HPV infection and sunlight fluency in Southern Holland. (b) Monthly sunlight fluency is correlated positively with both the monthly rates of Pap smear–detected cervical epithelial dysplasia and carcinomatous histopathology, as well as HPV. (c) Conception frequency, in this location, peaks in Spring not summer, and has a 4.8% annual amplitude.

Conclusions: (a) Cervical epithelial HPV infection and HPV-induced cervical epithelial dysplasia and carcinomatous change may each be novel sun exposure risks and thereby behaviorably avoidable. (b) Because screening Pap smears uncover many abnormalities that resolve spontaneously (false positives), these data may argue for screening and follow-up Pap smear examinations in seasons other than summer in the Northern Hemisphere, to diminish the false-positive smear rate. Global data are available to confirm and further test each of these conclusions.

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