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1 Department of Oral Pathology, Medical College of Virginia, Richmond, Virginia
For many years the tobacco habit and the development of oral cancer have been linked. Several studies have been conducted to determine the effect of whole cigarette smoke on epithelial tissues of mice and hamsters. When daily applications of smoke were made to the ears and lips of mice for up to 80 days, ears demonstrated some dyskeratotic change. This effect was enhanced by concurrent vitamin B complex deficiency. In no instance were lips altered by smoking. Prolongation of experimenetal periods to 20-24 months of daily smoking extended these findings, but still no neoplastic changes were observed. Intraoral smoke application to palatal and pouch mucosae of hamsters for similar periods also resulted in no evidence of neoplastic disease. Studies of cigarette smoke and concomitant exposure to ultraviolet irradiation likewise produced little evidence to implicate smoke as a direct carcinogen. However, when smoke was applied daily to oral mucosa that had first been treated with a suboptimal dose of a known carcinogen, squamous-cell carcinoma resulted in 56 per cent of animals. Hamsters treated with the initiating dose of the carcinogen only had a 24 per cent incidence of tumors. It appears that, in the oral epithelium, smoke is a cancer-promoting agent by chronic irritation.
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