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Int J Cancer. 2019 Oct 4. doi: 10.1002/ijc.32708. [Epub ahead of print]

Latency of tobacco smoking for head and neck cancer among HPV-positive and HPV-negative individuals.

Author information

1
Faculty of Dentistry, McGill University, Montréal, Canada.
2
Epidemiology and Biostatistics Unit, INRS-Institut Armand-Frappier, Laval, Canada.
3
Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montréal, Canada.
4
Department of Microbiology and Infectious Diseases, Hôpital Notre-Dame du Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, Canada.
5
Department of Cancer Prevention and Control, Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA.
6
Department of Oncology, Faculty of Medicine, McGill University, Montréal, Canada.

Abstract

Human papillomavirus (HPV) infection and tobacco smoking are well known risk factors for head and neck cancers (HNC). Although an effect modification between oral HPV infection and tobacco smoking may exist, evidence is lacking on how they interact temporally. We investigated the latency and life course effects of tobacco smoking on risk of HNC among HPV-positive (HPV+ve ) and negative (HPV-ve ) individuals. We used data from 631 ever-smoker participants of a hospital-based case-control study conducted in 4 major hospitals in Montréal, Canada. Cases (n=320), incident, histologically confirmed, primary squamous cell carcinomas, were frequency-matched to controls (n=311) by age and sex. Socio-demographic and behavioural factors (e.g., tobacco and alcohol use and sexual history) were collected using a structured interview applying a life grid technique. Oral exfoliated cells were used for HPV DNA detection and genotyping. Latency effects were estimated flexibly using a Bayesian relevant exposure model and further extended with a life course approach. Retrospective smoking trajectories for HPV+ve cases and controls had similar shapes. Exposure to tobacco smoking even 40 years before diagnosis was associated with an increased HNC risk among both HPV+ve and HPV-ve participants. The effect of smoking before the start of sexual activity compared to afterwards was higher among HPV+ve individuals. This pattern of association was less profound among HPV-ve participants. Temporal interactions may exists between oral HPV infection and life course smoking trajectories in relation to HNC risk. This article is protected by copyright. All rights reserved.

KEYWORDS:

Latency effect, Head and Neck Cancer, Tobacco Smoking, Bayesian Inference

PMID:
31584196
DOI:
10.1002/ijc.32708

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