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A meta-analysis of oropharyngeal cancer studies conducted on the Indian subcontinent calculated a statistically significant fourfold increase in risk for betel quid with tobacco and a statistically significant twofold increase in risk for betel quid alone.[12] Studies of head and neck cancer (without specification of subsite) suggest that increases in risk are positively correlated with chewing frequency and duration.[4] Human Papillomavirus (HPV) Infection HPV type 16 (HPV-16) infection is a sufficient, but not necessary, cause of head and neck cancers, with a greater causal relationship with oropharyngeal cancer.[13,14] A meta-analysis of five case-control studies of HPV-16 positivity in either serum or tissue calculated an odds ratio of 15.1 (95% confidence interval [CI], 6.833.7) for cancer of the tonsils, 4.3 (95% CI, 2.18.9) for other oropharyngeal sites, and 2.0 for both oral cavity (95% CI, 1.23.4) and larynx (95% CI, 1.04.2).[14] In a case-control study, the observed strong association of HPV-16 serologic status and oropharyngeal cancer did not vary at different levels of tobacco or alcohol use.[15] HPV-16 E6 seroconversion was shown to occur over a range of 6 to 28 years before oropharyngeal cancer diagnosis, at a median age of 52 years.[16] Thus, the HPV-16 infection that increases the risk of oropharyngeal cancer may occur in individuals aged 20 to 40 years

The most popular mass-market vape products, like the JUUL and Vuse Alto pod-style vapes, remain under FDA review

In addition, cigarette smoking can weaken local immune defences in the throat, which makes it easier for various types of throat infections to develop or linger longer than usual

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