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Exposure to UV radiation and risk of Hodgkin lymphoma: A pooled analysis

  • Alain Monnereau
  • , Sally L. Glaser
  • , Clayton W. Schupp
  • , Karin Ekström Smedby
  • , Silvia De Sanjosé
  • , Eleanor Kane
  • , Mads Melbye
  • , Lenka Forétova
  • , Marc Maynadié
  • , Anthony Staines
  • , Nikolaus Becker
  • , Alexandra Nieters
  • , Paul Brennan
  • , Paolo Boffetta
  • , Pierluigi Cocco
  • , Ingrid Glimelius
  • , Jacqueline Clavel
  • , Henrik Hjalgrim
  • , Ellen T. Chang
  • Institut national de la santé et de la recherche médicale
  • Centre Georges-François Leclerc
  • Cancer Prevention Institute of California
  • Stanford University
  • Karolinska Institutet
  • Institute Catala Oncologia
  • CIBER Epidemiología y Salud Pública (CIBERESP)
  • University of York
  • Statens Serum Institut
  • Masaryk Memorial Cancer Institute
  • Université de Bourgogne
  • Dublin City University
  • German Cancer Research Center
  • University of Freiburg
  • International Agency for Research on Cancer
  • University of Cagliari
  • Exponent, Inc.

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

Ultraviolet radiation (UVR) exposure has been inversely associated with Hodgkin lymphoma (HL) risk, but only inconsistently, only in a few studies, and without attention to HL heterogeneity. We conducted a pooled analysis of HL risk focusing on type and timing of UVR exposure and on disease subtypes by age, histology, and tumor-cell Epstein-Barr virus (EBV) status. Four case-control studies contributed 1320HLcasesand 6381 controls. We estimated lifetime, adulthood, and childhood UVR exposure and history of sunburn and sunlamp use. We used 2-stage estimation with mixed-effects models and weighted pooled effect estimates by inverse marginal variances. We observed statistically significant inverse associations with HL risk for UVR exposures during childhood and adulthood, sunburn history, and sunlamp use, but we found no significant doseresponse relationships. Risks were significant only for EBV-positive HL (pooled odds ratio, 0.56; 95% confidence interval, 0.35 to 0.91 for the highest overall UVR exposure category), with a significant linear trend for overall exposure (P 5.03). Pooled relative risk estimates were not heterogeneous across studies. Increased UVR exposure may protect against HL, particularly EBV-positive HL. Plausible mechanisms involving UVR induction of regulatory T cells or the cellular DNA damage response suggest opportunities for new prevention targets.

Original languageEnglish
Pages (from-to)3492-3499
Number of pages8
JournalBlood
Volume122
Issue number20
DOIs
StatePublished - Nov 14 2013

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