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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 four 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. Sociodemographic and behavioral 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. What's new? Interactions between tobacco smoking and human papillomavirus (HPV) infection potentially result in supra‐additive effects on head and neck cancer (HNC) risk. The level of risk may be modified, however, by the timing of exposure to these factors over an individual's life course. Here, in a study population that included ever‐smokers and HNC patients, retrospective life course smoking trajectories among HPV‐positive HNC cases and controls were similar. Tobacco smoking even four decades prior to diagnosis was associated with elevated HNC risk, regardless of HPV status. HNC risk was increased particularly for HPV‐positive study participants who smoked before becoming sexually active. [ABSTRACT FROM AUTHOR]

The evidence for genetic polymorphisms in genes encoding cytochrome P450 (CYP) and glutathione S-transferase (GST) enzymes as risk factors for squamous cell carcinomas of the head and neck (SCCHN) in Caucasians is conflicting. Furthermore, the interactive effects with smoking have not been documented. We estimated the effects of five single nucleotide polymorphisms and two copy number variants associated with CYP and GST genes, as well as their interactive effects with smoking, on SCCHN risk among Caucasians from a case–control study conducted in Montreal, Canada. The study involved 389 incident SCCHN cases and 429 controls, frequency-matched by age and sex, recruited from four main hospitals between 2005 and 2013. Life-course-based interviews collected information on tobacco smoking history and other risk behaviors. DNA was isolated from oral exfoliated cells and genotyped for genetic variants. Unconditional logistic regression models estimated odds ratios (OR) and 95% confidence intervals (CI) for main, joint effect, stratum-specific and interaction estimates among non-, moderate and heavy smokers. Carriers of GSTP1 105Val (versus non-carriers) had a lower risk of SCCHN (OR = 0.71, 95% CI: 0.53, 0.95), which was observed for heavy smokers (OR = 0.59, 95% CI: 0.36, 0.95) and non-smokers alike (OR = 0.49, 95% CI: 0.24, 0.98). The decreased risk associations were also conserved among human papillomavirus negative individuals. There was no evidence for statistical interaction with smoking on additive or multiplicative scales for any of the variants analyzed. Of CYP and GST polymorphisms detected in Canadian Caucasians, only GSTP1 105Val was associated with a decreased risk for SCCHN. [ABSTRACT FROM AUTHOR]

Background: This study aimed to estimate the extent to which oral sex behavior is associated with an increased risk of oropharyngeal cancers (OPCs), and how much of the association is mediated by oral human papillomavirus (HPV) infection. Methods: We used data from a hospital‐based case‐control study conducted in Montreal, Canada. Information on oral sex behaviors was collected. Oral rinse and oral brush specimens were analyzed for HPV positivity and genotyping. Logistic regression estimated the odds ratios (OR) and 95% confidence intervals (CI) for the association between oral sex behaviors and OPC. Results: Onset of oral sex practice at age 16 years or younger had an increased risk of OPCs relative to those with onset after age 30 years (OR = 2.98; 95% CI 1.37‐6.47). This association decreased (OR = 1.09; 95% CI 0.25‐4.71) when restricted to those positive for HPV. Conclusions: Our results suggest that the association between oral sex and OPC seems mediated by oral HPV infection. [ABSTRACT FROM AUTHOR]