Researchers from Johns Hopkins Medicine have found an association between exposure to tobacco and the sexually transmitted human papillomavirus type 16. This virus is believed to be responsible for the development of both mouth and throat cancers.
The study, published in JAMA, followed up on the observation that there was an association between prevalence of the virus and the number of self-reported cigarettes smoked per day by an individual.
The researchers found that human papillomavirus type 16 (HPV16) infection was more prevalent among participants who had either used or recently been exposed to tobacco, regardless of their sexual behavior.
HPV16, a virus commonly transmitted through oral sex, is found in 80% of cancers located in the back of the throat. The number of mouth and throat cancer cases has risen by 225% in the US over the past 2 decades.
“The practice of oral sex is common, but this cancer is rare,” says study author Gypsyamber D’Souza. “So there must be cofactors in the process that explain why some people develop persistent HPV16 infections and HPV-positive oropharyngeal cancers when most other people don’t.”
For the study, the researchers examined 6,887 participants of the National Health and Nutrition Examination, a nationally representative sample of the US population. Of the 6,887 subjects, 2,012 (28.6%) were tobacco users and 63 (1.0%) were known to be infected with HPV16.
The participants were screened for biomarkers reflecting all forms of tobacco exposure – environmental, smoking and use of smokeless tobacco – and for oral HPV16 infection.
In addition to clinical testing – blood and urine testing and a 30-second oral rinse and gargle – the participants completed computer-assisted self-interviews in order to capture self-reported tobacco use and sexual behaviors.
Measures of tobacco exposure and oral sexual behavior were both found to be significantly associated with prevalence of oral HPV16 infection. The virus was more prevalent in participants who were current tobacco users (2.0%), compared with former users or those who had never used tobacco (0.6%).
Two tobacco-related chemicals, cotinine and NNAL (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol), were measured in the blood and urine of the participants. For every increase in the level of cotinine in the blood that was equivalent to smoking three cigarettes a day, the likelihood of HPV16 infection also increased by 31%.
Similarly, with each increase in the level of NNAL in the urine that was equivalent to smoking four cigarettes a day, the chances of HPV16 prevalence rose by 68%.
“These results may provide an additional reason for smoking cessation and suggest that even modest amounts of tobacco use are associated with higher oral HPV prevalence,” says Dr. Carole Fakhry, study author and assistant professor of otolaryngology-head and neck surgery at the Johns Hopkins University School of Medicine.
The researchers also emphasize that, despite finding a significant association between tobacco and the prevalence of oral HPV16, smoking and tobacco exposure do not in themselves cause HPV16 directly. People who are not exposed to tobacco are still able to develop HPV16 infections.
A limitation of the study is that it is unable to provide a causative explanation for the association between tobacco and oral HPV16. The researchers are also unable to completely exclude the possibility that people who use or are exposed to more tobacco might also have more oral sex, thus increasing the risk of HPV16 prevalence.
“It appears that tobacco exposure increases the likelihood of having oral HPV16 infection, and although we do not yet know why, we suspect that the virus may not be cleared from the body as easily in people who use tobacco,” says Dr. D’Souza.
The study authors believe that their findings highlight a need to assess the role of tobacco in the prevalence of oral HPV16 infection and its progression to malignancy.
Earlier this month, Medical News Today reported on a study suggesting that smoking during pregnancy could damage sons’ fertility.