Abstract

Although there have been many reports on the toxicity of tobacco smoke, fewer studies have reported the relationship between the smoke and carcinogenesis of head-and-neck cancers. It is assumed that direct stimulations due to tobacco smoke, such as chemical and mechanical stimulations, strongly influence the epithelium of the nasal cavity, paranasal sinuses, pharynx, and larynx. We investigated the influence of active and passive cigarette smoking on head-and-neck cancers. The subjects were 283 head-and-neck cancer patients examined at the otolaryngology department of Showa University Northern Yokohama Hospital in a 9-year and 2-month period from April 2001 to June 2010, in whom the presence or absence of active and passive cigarette smoking could be confirmed in detail. The active and passive smoking rates and the Brinkman index were retrospectively investigated according to the primary cancer site, gender, and histopathological classification. The active and passive smoking rates were high (about 90%) in patients with hypopharyngeal, laryngeal, and cervical esophageal cancers, and the Brinkman index was high in all. Squamous cell carcinoma (SCC) patients accounted for a high ratio of the head-and-neck cancer patients, and the active and passive smoking rates were significantly higher in SCC than in non-squamous cell carcinoma (non-SCC) patients (p < 0.0003). The active and passive smoking rates and the Brinkman index were high in patients with head-and-neck cancers in regions receiving strong direct stimulation from tobacco smoke, and the Brinkman index was also high in these patients, suggesting that carcinogenesis of head-and-neck cancers is strongly influenced by direct tobacco smoke stimulation.

Highlights

  • It is widely known that active and passive cigarette smoking is toxic for the human body [1,2,3]

  • 2) Active, passive, and total smoking rates and the Brinkman index according to the primary cancer site in each gender

  • The nasal cavity, paranasal sinuses, and a part of the larynx are covered with pseuodstratifiedcilliated epithelium, and the epipharynx is partially covered with columnar epithelium, but the mucoepithelium of the tongue/oral cavity, pharynx, laryngeal vocal cord, epiglottis, and cervical esophagus is comprised of stratified squamous epithelial cells

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Summary

Introduction

It is widely known that active and passive cigarette smoking is toxic for the human body [1,2,3]. Tobacco smoke contains about 200 toxic substances, and 69 of these have been identified as carcinogens [4]. There is no doubt that the carcinogens contained in tobacco smoke are closely involved in the carcinogenesis mechanism, as demonstrated by many epidemiological studies [5,6]. Tobacco smoke includes many carcinogenic substances, but among them benzopyrene and nitrosoamine are strong carcinogens. The association between active and passive cigarette smoking and carcinogenesis has been clarified in cancers of the lung, oral cavity, pharynx, larynx, nasal cavity, paranasal sinuses, esophagus, stomach, large intestine, liver, kidney, pancreas, urinary bladder, and uterine cervix [7,8,9,10]. The relative risk of active and passive smoking-induced carcinogenesis varies among cancer types. The sites we are concerned with are only those that come into direct contact with tobacco smoke, namely nasal cavity/paranasal sinus cancer, tongue/oral cavity cancer, epipharyngeal cancer, mesopharyngeal cancer, hypopharyngeal cancer, laryn-

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