Interaction between tobacco and alcohol use and the risk of head and neck cancer: pooled analysis in the INHANCE consortium

By M. Hashibe, P. Brennan, Shu-Chun Chuang, S. Boccia, X. Castellsagué, Chu Chen, M. Curado, L. Maso, A. Daudt, E. Fabiánová and 33 more. Cancer Epidemiology, Biomarkers and Prevention, 2009

1,100 citations recorded by the source corpus.

Background The magnitude of risk conferred by the interaction between tobacco and alcohol use on the risk of head and neck cancers is not clear, since studies have used various methods to quantify the excess head and neck cancer burden. Methods We analyzed individual-level pooled data from 17 European and American case-control studies (11,221 cases and 16,168 controls) participating in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. We estimated the multiplicative interaction parameter (ψ) and population attributable risks (PAR). Results A greater than multiplicative joint effect between ever tobacco and alcohol use was observed for head and neck cancer risk (ψ=2.15, 95%CI=1.53–3.04). The PAR for tobacco or alcohol was 72% (95%CI=61%–79%) for head and neck cancer, of which 4% was due to alcohol alone, 33% was due tobacco alone and 35% was due to tobacco and alcohol combined. The total PAR differed by subsite (64% for oral cavity cancer, 72% for pharyngeal cancer, 89% for laryngeal cancer), by sex (74% for men, 57% for women) by age (33% for cases <45 years, 73% for cases >60 years) and by region (84% in Europe, 51% in North America, 83% in Latin America). Conclusions Our results confirm that the joint effect between tobacco and alcohol use is greater than multiplicative on head and neck cancer risk. However, a substantial proportion of head and neck cancers cannot be attributed to tobacco or alcohol use, particularly for oral cavity cancer, for head and neck cancer among women and among young onset cases.

Subfields: Otorhinolaryngology, Pathology and Forensic Medicine, Physiology

View Paper: https://www.semanticscholar.org/paper/5ec1d32b38ba3e083b219d02c6b53a54a41e1ebd

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In Pathology and Forensic Medicine

1. A. Jemal
2. humAn cArcinogens
3. Iarc Monographs
4. peRsonAl hAbIts
5. R. Siegel

In Physiology

1. A. Jemal

Citations in the corpus

• iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns (2012, background): “The results from case–control studies were similar to those observed for oral cancer (Olsen et al., 1985b; Choi & Kahyo, 1991; Schlecht et al., 1999b; Znaor et al., 2003; Hashibe et al., 2009).”
• Oral cavity and oropharyngeal squamous cell carcinoma—an update (2015, background): “Large-scale multicenter studies in Europe and Asia, as well as pooled analysis of European and American casecontrol studies, have attributed more than half of oral and oropharyngeal cancer cases to tobacco and/or alcohol.(59-61)”
• Global cancer statistics (2011, background): “Smoking, alcohol use, smokeless tobacco products, and HPV infections are the major risk factors for oral cavity cancer, with smoking and alcohol having synergistic effects.(126,127) The contribution of each of these risk factors to the burden varies across regions.”
• Global cancer statistics, 2012 (2015, background): “Smoking, alcohol use, smokeless tobacco use, and HPV infection are the major risk factors for oral cavity cancer, with smoking and alcohol having synergistic effects.(131,132) The contribution of each of these risk factors to the burden varies across regions.”
• Vitamin D and Clinical Outcomes in Head and Neck Cancer: A Systematic Review (2025, unknown): “…etiologies; tobacco and excessive alcohol use synergistically increase risk by up to five-fold, while environmental carcinogens and viral infections—human papillomavirus (HPV) in oropharyngeal cancers and Epstein–Barr virus (EBV) in nasopharyngeal cases—further complicate the landscape [18].”
• Unraveling the Role of Tumor-Infiltrating Immune Cells in Head and Neck Squamous Cell Carcinoma: Implications for Antitumor Immune Responses and Immunotherapy (2025, unknown): “…papillomavirus (HPV), particularly HPV-16 and, to a lesser extent, HPV-18, has emerged as a major etiological factor in oropharyngeal 2 of 29 HNSCC. HPV-positive tumors generally have a better prognosis and exhibit increased sensitivity to therapies such as chemotherapy and radiotherapy [3,4].”