• 12/2/2007
  • web-based article
  • Katie M Applebaum et al.
  • J Natl Cancer Inst, November 27, 2007

Background:
Human papillomavirus type 16 (HPV16) seropositivity and alcohol and tobacco use have been associated with risk of head and neck squamous cell carcinoma (HNSCC). However, it is less clear whether HPV16 influences HNSCC risk associated with alcohol and tobacco use.

Methods:
Incident cases of HNSCC diagnosed between December 1999 and December 2003 were identified from nine medical facilities in Greater Boston, MA. Control subjects were frequency matched to case subjects on age, sex, and town of residence. A total of 485 case subjects and 549 control subjects reported information on lifetime smoking and alcohol consumption and provided sera, which was used to determine presence of HPV16 antibodies. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) of HNSCC risk by alcohol consumption (drinks per week: <3, 3 to <8, 8 to <25, >/=25) and smoking (pack-years: none, >0 to <20, 20 to <45, >/=45), adjusting for age, sex, race, education, and HPV16 serology. Polytomous logistic regression was used to estimate odds ratios and 95% confidence intervals for the association of HPV16 serology, alcohol consumption, and tobacco use in site-specific analyses. All statistical tests were two-sided.

Results:
The strongest risk factors by tumor site were smoking for laryngeal cancer, alcohol for cancer of the oral cavity, and HPV16 for pharyngeal cancer. For pharyngeal cancer, risk increased with increasing alcohol consumption (OR(>/=25 versus <3 drinks per week) = 5.1, 95% CI = 2.4 to 11.0) and smoking (OR(>/=45 pack-years versus never smoker) = 6.9, 95% CI = 3.1 to 15.1) among HPV16-seronegative subjects but not among HPV16-seropositive subjects (P(interaction, HPV16 serology and alcohol) = .002; P(interaction, HPV16 serology and smoking) = .007). Among light drinkers or never smokers, HPV16 seropositivity was associated with a 30-fold increased risk of pharyngeal cancer.

Conclusions:
Alcohol or tobacco use does not further increase risk of HPV16-associated pharyngeal cancer. HNSCC risk associated with smoking, alcohol, and HPV16 differs by tumor site.

Authors:
Katie M Applebaum, C Sloane Furniss, Ariana Zeka, Marshall R Posner, Judith F Smith, Janine Bryan, Ellen A Eisen, Edward S Peters, Michael D McClean, and Karl T Kelsey

Authors’ affiliations:
Affiliations of authors: Departments of Environmental Health (KMA, EAE, KTK) and Genetics and Complex Diseases (CSF), Harvard School of Public Health, Boston, MA; Institute for the Environment, University of Brunel, West London, U.K. (AZ); Head and Neck Oncology Program, Dana-Farber Cancer Institute, Boston, MA (MRP); Department of Vaccine Biologics Research, Merck and Co, Inc, West Point, PA (JFS, JB); Epidemiology Program, Louisiana State University Health Sciences School of Public Health, New Orleans, LA (ESP); Department of Environmental Health, Boston University School of Public Health, Boston, MA (MDM); Departments of Community Health and Pathology and Laboratory Medicine, Center for Environmental Health and Technology, Brown University, Providence, RI