Association of alcohol consumption with oral high-risk human papillomavirus infection: a cross-sectional study within the multinational HPV infection in men (HIM) cohort.

Abstract

Human papillomavirus (HPV)-related oropharyngeal cancer arises from persistent high-risk HPV (HR-HPV) oral infection. Smoking is a risk factor for oral HPV, but alcohol's role is unclear. We investigated the association between alcohol consumption and oral HPV infection. This cross-sectional analysis used baseline data from the HIM Study. Oral HPV was detected with SPF10 PCR-DEIA-LiPA25 on oral gargle specimens. Associations between alcohol consumption and oral HPV were assessed using adjusted logistic regression models, exploring effect modification by smoking. Among 3121 males (median age 33 years, interquartile range [IQR] 25, 41), 39% were from Brazil (n = 1229), 32% from Mexico (n = 1014), and 28% from the United States (n = 878); 76% (n = 2365) reported alcohol use in the past month (median 8 drinks, IQR 0, 24). Oral HPV was detected in 20% (n = 469) participants reporting alcohol use, including 6.1% (n = 145) with HR-HPV and 14% (n = 324) low-risk HPV (LR-HPV). HR-HPV detection increased with alcohol intake, peaking at 7.6% (n = 75) among those consuming ≥16 drinks/month (p = 0.005). Consuming ≥16 drinks/month was independently associated with HR-HPV after adjustment (adjusted odd ratio [aOR] 1.60, 95% confidence interval [CI] 1.07, 2.40), whereas consuming 3-15 drinks was not (aOR 1.15, 95% CI: 0.76, 1.76). Exploratory stratified analyses showed aOR 2.57 (95% CI: 1.37, 4.96) in males who had never smoked and 1.12 (95% CI: 0.67, 1.88) in those who currently or formerly smoked, with no evidence of effect modification. Higher monthly alcohol consumption was modestly associated with oral HR-HPV in this cross-sectional analysis; longitudinal studies are needed to assess extension to oral HPV persistence, a recognized precursor of cancer. National Institute of Health, American Cancer Society.