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Ann Epidemiol. 2017 Nov;27(11):724-730.e1. doi: 10.1016/j.annepidem.2017.10.004. Epub 2017 Oct 17.

Smoking and subsequent human papillomavirus infection: a mediation analysis.

Author information

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.

KEYWORDS:

Antibodies; HPV; Human papillomavirus; Indirect effect; Mechanism; Mediation; Smoking

PMID:
29107447
PMCID:
PMC5705255
DOI:
10.1016/j.annepidem.2017.10.004
[Indexed for MEDLINE]
Free PMC Article

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