Abstract

Although alcohol is an established risk factor of head and neck cancer (HNC), insufficiencies exist in the literature in several aspects. We analyzed detailed alcohol consumption data (amount and type of alcoholic beverage) of 811 HNC patients and 940 controls to evaluate the association between alcohol and HNC by HNC sites and by genotypes of ADH1B and ALDH2. Alcohol was associated with an increased HNC risk in a dose-response relationship, with the highest risk observed for hypopharyngeal cancer, followed by oropharyngeal and laryngeal cancers. Liquor showed a stronger positive association with HNC than beer and wine. The highest HNC risk occurred in individuals with the slow ADH1B and slow/non-functional ALDH2 genotype combination. In our study population, 21.8% of HNCs, 55.7% of oropharyngeal cancers, and 89.1% of hypopharyngeal cancers could be attributed to alcohol. Alcohol accounted for 47.3% of HNCs among individuals with the slow ADH1B and slow/non-functional ALDH2 genotype combination. The HNC risk associated with alcohol became comparable to that of never/occasional drinkers after ten or more years of cessation from regular alcohol drinking. In conclusion, alcohol use is associated with an increased HNC risk, particularly for individuals with slow ethanol metabolism. HNC incidence may be reduced by alcohol cessation.

Highlights

  • Alcohol is an established risk factor of head and neck cancer (HNC), insufficiencies exist in the literature in several aspects

  • Alcohol showed a positive dose-response relationship with HNC risk, with the highest risk observed for hypopharyngeal cancer, followed by oropharyngeal cancer, and laryngeal cancer

  • The HNC risk associated with alcohol was the highest for individuals with the slow ADH1B and slow/non-functional ALDH2 genotype combination followed by individuals with the fast ADH1B and slow/non-functional ALDH2 genotype combination

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Summary

Introduction

Alcohol is an established risk factor of head and neck cancer (HNC), insufficiencies exist in the literature in several aspects. The highest HNC risk occurred in individuals with the slow ADH1B and slow/non-functional ALDH2 genotype combination. Betel quid, and human papillomavirus ( for oropharyngeal cancer), alcohol is an established risk factor of HNC2, 3; detailed assessment is needed to characterize the association between alcohol and HNC by dose-response, by different anatomic sites, by alcoholic beverage type, and by ethanol metabolizing gene polymorphisms, and to quantify the impact of alcohol cessation. A meta-analysis reported that compared to oral cancer and laryngeal cancer, pharyngeal cancer showed a stronger association with alcohol[4] Studies included in this meta-analysis analyzed oropharyngeal and hypopharyngeal cancers together as pharyngeal cancer. The association between ethanol metabolizing genes and HNC has been investigated, only a few studies have examined the combined effect of ADH1B and ALDH227, 28

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