Ronald C Eldridge1, Michael Pawlita2, Lauren Wilson3, Philip E Castle4, Tim Waterboer2, Patti E Gravitt5, Mark Schiffman6, Nicolas Wentzensen6. 1. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD. Electronic address: ronald.eldridge@nih.gov. 2. German Cancer Research Center, Heidelberg, Germany. 3. National Institute of Environmental Health Sciences, Research Triangle Park, NC. 4. Albert Einstein College of Medicine, Bronx, NY. 5. The University of New Mexico, Albuquerque, NM. 6. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
Abstract
PURPOSE: Smoking is an established risk factor for a human papillomavirus (HPV) infection advancing to cervical precancer and cancer, but its role earlier in the natural history is less clear. Smoking is inversely associated with possessing HPV antibodies from a past infection suggesting that smoking may influence acquiring subsequent infections. METHODS: In a cohort of 1976 U.S. women, we evaluate whether reduced antibodies to HPV-16 is a mechanism for smoking's role on acquiring a subsequent HPV-16 infection, through the analytic technique of causal mediation analysis. We posit a causal model and estimate two counterfactually defined effects: a smoking impaired antibody-mediated indirect effect and a nonmediated direct effect representing all other potential mechanisms of smoking. RESULTS: Compared to never smokers, current smokers had increased odds of HPV-16 infection by the antibody-mediated indirect effect (odds ratio [OR] = 1.29; 95% confidence interval [CI]: 1.11, 1.73); the estimated direct effect was very imprecise (OR = 0.57; 95% CI, 0.26-1.13). We observed a stronger estimated indirect effect among women who smoked at least half a pack of cigarettes daily (OR = 1.61, 95% CI, 1.27-2.15) than among women who smoked less than that threshold (OR = 1.09; 95% CI, 0.94-1.44). CONCLUSIONS: This is the first study to directly test the mechanism underlying smoking as an HPV cofactor. The results support current smoking as a risk factor earlier in the natural history of HPV and are consistent with the hypothesis that smoking increases the risk of a subsequent infection by reducing immunity. Published by Elsevier Inc.
PURPOSE: Smoking is an established risk factor for a humanpapillomavirus (HPV) infection advancing to cervical precancer and cancer, but its role earlier in the natural history is less clear. Smoking is inversely associated with possessing HPV antibodies from a past infection suggesting that smoking may influence acquiring subsequent infections. METHODS: In a cohort of 1976 U.S. women, we evaluate whether reduced antibodies to HPV-16 is a mechanism for smoking's role on acquiring a subsequent HPV-16infection, through the analytic technique of causal mediation analysis. We posit a causal model and estimate two counterfactually defined effects: a smoking impaired antibody-mediated indirect effect and a nonmediated direct effect representing all other potential mechanisms of smoking. RESULTS: Compared to never smokers, current smokers had increased odds of HPV-16infection by the antibody-mediated indirect effect (odds ratio [OR] = 1.29; 95% confidence interval [CI]: 1.11, 1.73); the estimated direct effect was very imprecise (OR = 0.57; 95% CI, 0.26-1.13). We observed a stronger estimated indirect effect among women who smoked at least half a pack of cigarettes daily (OR = 1.61, 95% CI, 1.27-2.15) than among women who smoked less than that threshold (OR = 1.09; 95% CI, 0.94-1.44). CONCLUSIONS: This is the first study to directly test the mechanism underlying smoking as an HPV cofactor. The results support current smoking as a risk factor earlier in the natural history of HPV and are consistent with the hypothesis that smoking increases the risk of a subsequent infection by reducing immunity. Published by Elsevier Inc.
Entities:
Keywords:
Antibodies; HPV; Human papillomavirus; Indirect effect; Mechanism; Mediation; Smoking
Authors: R B Roden; A Armstrong; P Haderer; N D Christensen; N L Hubbert; D R Lowy; J T Schiller; R Kirnbauer Journal: J Virol Date: 1997-08 Impact factor: 5.103
Authors: A B Moscicki; N Hills; S Shiboski; K Powell; N Jay; E Hanson; S Miller; L Clayton; S Farhat; J Broering; T Darragh; J Palefsky Journal: JAMA Date: 2001-06-20 Impact factor: 56.272
Authors: Jill Koshiol; Lisa Lindsay; Jeanne M Pimenta; Charles Poole; David Jenkins; Jennifer S Smith Journal: Am J Epidemiol Date: 2008-05-15 Impact factor: 4.897
Authors: Matthew B Schabath; Luisa L Villa; Hui-Yi Lin; William J Fulp; Eduardo Lazcano-Ponce; Jorge Salmerón; Martha E Abrahamsen; Mary R Papenfuss; Manuel Quiterio; Anna R Giuliano Journal: Int J Cancer Date: 2013-11-13 Impact factor: 7.396
Authors: Jennifer C Spencer; Noel T Brewer; Tamera Coyne-Beasley; Justin G Trogdon; Morris Weinberger; Stephanie B Wheeler Journal: Cancer Epidemiol Biomarkers Prev Date: 2021-09-09 Impact factor: 4.254
Authors: Michelle B Shin; Gui Liu; Nelly Mugo; Patricia J Garcia; Darcy W Rao; Cara J Bayer; Linda O Eckert; Leeya F Pinder; Judith N Wasserheit; Ruanne V Barnabas Journal: Front Public Health Date: 2021-07-01
Authors: Mykhaylo Usyk; Christine P Zolnik; Philip E Castle; Carolina Porras; Rolando Herrero; Ana Gradissimo; Paula Gonzalez; Mahboobeh Safaeian; Mark Schiffman; Robert D Burk Journal: PLoS Pathog Date: 2020-03-26 Impact factor: 6.823