Virginia Commonwealth University

VCU Massey Cancer Center

Causes and risk factors

Cigarettes and alcohol

Head and neck cancer is primarily a disease of cigarette and alcohol consumption. Moreover, a synergistic effect seems to exist between alcohol and tobacco with regard to carcinogenesis. Until recently, the incidence of laryngeal carcinoma has increased for both men and women, but overall the increase has been greater for women.

Malignant tumors of the salivary glands are not believed to be related to cigarette consumption and have declined in the general population. Cigarette use carries with it the risk of multiple primary tumors and about 10 percent of head and neck cancer patients manifest second tumors at the time of presentation.

Cigarette smoking is addictive, and approximately 40 percent of patients treated for head and neck cancer continue to smoke. In a study published by the VCU Department of Otolaryngology (head and neck surgery), the smoking cessation rate for head and neck cancer patients was 69 percent at 18 months after a cancer diagnosis. Treatment using combined modality therapy (radiation and surgery with or without chemotherapy) and total laryngectomy were positive predictors for smoking cessation (i.e., more likely to quit smoking). Past excessive alcohol consumption was a negative predictive factor. Unfortunately, as a consequence, patients with early stage lesions who are the most likely to benefit from prolonged smoking cessation are the least likely to quit. Frequent, short duration counseling beginning at the time of tumor diagnosis was found to be the best practical approach to achieve smoking cessation in head and neck cancer patients.

The number of cigarettes consumed by the average smoker has increased dramatically over the years. The average number of cigarettes consumed daily in 1935 was approximately 11.5 and increased to 33.3 in 1979. This increase may be attributed to the increasing use of filtered cigarettes. While smokers now inhale less smoke per cigarette, the number of cigarettes consumed has consequently increased. The proportion of low-tar cigarettes in the marketplace also has increased. Unfortunately, the definition of low tar is randomly set at 15 mg per cigarette and recent evidence has suggested that decreased tar has not led to a decrease in the incidence of smoking-related diseases.

Approximately 75 percent to 80 percent of all patients with oral carcinoma are noted to consume alcohol, particularly hard liquor. The disease is six times more common in drinkers than nondrinkers. Alcohol probably acts in various ways to induce oral carcinoma. First, ultrastructural analysis of the oral mucosa in nonsmoking alcoholic patients demonstrates epithelial dysplasia, including an increase in nuclear atypia, prominent nucleoli and fragmentation of the basal cell layer. This presence suggests that alcohol alone is carcinogenic. Alcohol and tobacco, as mentioned, are synergistic in the induction of carcinoma, which may be related to increased solubility of tobacco-related carcinogens. Finally, alcohol is known to cause nutritional deficiencies, which may result in diminished immune response to cancerous cells.

Other factors

  • Smokeless tobacco – has been directly linked to oral carcinomas. Despite little overall change in the rate of smokeless tobacco use, there has been a marked change in the age distribution of users. Consumption in the age group of 40 and above has diminished while regular use by children in third through 12th grade is estimated at 17 percent for boys and 2 percent for girls. Over six million Americans above the age of 12 are regular users.
  • Human papilloma virus (HPV 16 and 18) – widely distributed and has species and site specificity. It affects the skin, anogenital epithelium and upper aerodigestive tract epithelium and is associated with various histologic lesions at these sites. HPV 6, 11, 16 and 18 are often isolated from the genital and aerodigestive tract. HPV 6 and 11 are usually associated with benign lesions such as papillomata. HPV 16 and 18 have been identified in premalignant and malignant lesions. It has been proposed that the reservoir for HPV 6, 11, 16, 18, 31, 32 and 35 is the anogenital region and HPV 1, 2, 3, 4 and 5 reside in the skin. Further analysis of the role of HPV in head and neck cancer is ongoing.
  • Other – more than one-third of patients with carcinoma of the lip have an outdoor occupation. Prolonged exposure to sunlight seems to play a major role in the start of squamous cell carcinoma of the lip, especially the lower lip. Syphilis was thought previously to play an important role in oral carcinoma, but is thought less so today. Poor oral hygiene may be an etiologic factor in the development of oral cavity center. Ill-fitting dentures and jagged-fractured teeth causing chronic mucosal irritation also have been implicated in the genesis of oral carcinoma. Dietary deficiencies such as iron-deficient anemia and riboflavin deficiency have been noted. Even recurrent herpes stomatitis type-I has been observed in patients with oral carcinoma. Finally, environmental carcinogens such as sulfa, petroleum products and epoxy resins are suspect in head and neck carcinoma.