Abstract
Twice daily exposure of 12–24 male inbred Syrian BIO 15.16 hamsters for 13 weeks to maximally tolerated doses of smoke from 12 types of investigational cigarettes under experimental conditions and with previously described instrumentation (Bernfeld et al., 1979) resulted in the following response: increased occurrence and aggregation of alveolar macrophages, increased occurrence of tracheal squamous metaplasia, and increased frequency and severity of laryngeal hyperplasia. The statistical significance of these changes was evaluated by means of loglinear models. The effect of varying the nicotine level in tobacco leaf between 0.2 and 1.5% caused no statistically significant changes in the subchronic response. Smoke from Bright tobacco with average tar yields of from 22.4 to 26.2 mg per cigarette caused significantly more alveolar macrophages and laryngeal hyperplasia but less tracheal squamous metaplasia than did smoke from Burley tobacco, with from 9.3 to 10.5 mg tar per cigarette. Deproteinization of tobacco did not change the response of the hamsters to the resulting smoke. Maleic hydrazide-field treatment of tobacco significantly reduced the alveolar macrophages, but spiking of tobacco with maleic hydrazide increased the response. Previous work had suggested that the tumorigenic response to cigarette smoke in chronic inhalation studies in hamsters may be predicted from subchronic inhalation studies in the same animal model (Bernfeld et al., 1983a). The present results then suggest that smoke from low-nicotine cigarettes is not less tumorigenic in the hamster than that from high-nicotine cigarettes, that smoke from high-tar Bright tobacco is more carcinogenic than that from low-tar Burley tobacco, that deproteinization of tobacco does not affect the tumorigenicity of the resulting smoke, and that maleic hydrazide-field treatment of tobacco does not increase the tumorigenicity of the resulting smoke, whereas spiking of tobacco with maleic hydrazide might do so.
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