Evidence map›Paper›PMID 29107447›Full record

ArticleAnnals of epidemiology2017

Smoking and subsequent human papillomavirus infection: a mediation analysis.

Ronald C Eldridge, Michael Pawlita, Lauren Wilson, Philip E Castle, Tim Waterboer, Patti E Gravitt, Mark Schiffman, Nicolas Wentzensen

Open access · greenAbstract read
In one paragraph

Article in Annals of epidemiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 50 citations in OpenAlex.

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  19. Reducing Poverty-Related Disparities in Cervical Cancer: The Role of HPV Vaccination.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Ronald C EldridgeDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD. Electronic address: ronald.eldridge@nih.gov.
Michael PawlitaGerman Cancer Research Center, Heidelberg, Germany.
Lauren WilsonNational Institute of Environmental Health Sciences, Research Triangle Park, NC.
Philip E CastleAlbert Einstein College of Medicine, Bronx, NY.
Tim WaterboerGerman Cancer Research Center, Heidelberg, Germany.
Patti E GravittThe University of New Mexico, Albuquerque, NM.
Mark SchiffmanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
Nicolas WentzensenDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
National Cancer Institute · USGerman Cancer Research Center · DEAlbert Einstein College of Medicine · USTriangle · USUniversity of New Mexico · US

Funding

Human papillomavirus (HPV) infection and cervical and anal cancersZIACP010124 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI WENTZENSEN, NICOLAS · 2009 to 2025
$17.3M
CERVICAL CANCER AND HUMAN PAPILLOMAVIRUS (HPV) INFECTIONZ01CP010124 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI SCHIFFMAN, MARK · 1996 to 2008
$3.0M
Intramural NIH HHS Z01 CP010124Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

purposeSmoking 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.

methodsIn 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.

resultsCompared 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).

conclusionsThis 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.

Indexed as

AdultCase-Control StudiesFemaleHuman papillomavirus 16HumansMiddle AgedPapillomavirus InfectionsRisk FactorsSmokingUterine Cervical NeoplasmsAntibodiesHPVHuman papillomavirusIndirect effectMechanismMediationSmoking

Identifiers

PMID29107447
PMCPMC5705255
OpenAlexW2768773767

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.