Tobacco Documents Online

! I I I I I I I I I I I I I I I I I AUTHOR~ BOUFFANT, L. LE, J.C. Martin, H. Daniel, J.P Henin, and C. Normand ~AT~: 1980 ~J.T.J,~: ACTION OF INTENSIVE CIGARETTE SMOKE INHALATIONS ON RAT LUNG. ROLE OF PARTICULATE AND GASEOUS COFACTORS CITATION; JOURNAL NATIONAL CANCER INSTITUTE, 64, 273-284 (1980) ~: The actions of high doses of cigarette smoke alone or in combination with coal-dust or acrolein was investigated using non-inbred Sprague-Dawley rats. Gauloise brand black-tobacco cigarettes without filters were used for smoke inhalation studies. Rats were exposed to smoke inhalations either 2, 4 or 6/day, from 5 to 26 months. The amount of particulate smoke rats exposed to ranged from 0.46 g to 5.8 g depending upon the number of sessions. Dust inhalations studies used anthracite with 4% mineral matter and a particulate size less than 5 I~m. Exposure to dust at conc. 30 mg/m3 for 6 hours, 5 days per week. Rats exposed for either 8 exposures or 80 exposures, additionally some rats exposed 3 hr, twice a week for the duration of the experiment. Acrolein administered at rate of 1 hr/day at 8 ppm in air, for 10 or 18 months, FINDINGS/RESULTS= Smoke A/one:.Body weight of smoke exposed rats decreased compared to the controls, with the Intensity and total time of smoke inhalation having a marked influence. Macroscopic examination of lungs disclosed no visible tumors in smoke rats exposed after 30 months. A discrete brown pigmentation in the area of the pleura was observed which testified to the accumulation of tar. The sizes of the deposits were related to the intensity of inhalations (daily number of inhalations rather than to cumulative no. of sessions during the experiment. Results suggested that a comparatively fast physical or biochemical clearance was occurring. Histological examination of lungs also revealed no tumors, regardless of the rate and total number of smoke inhalations and of the duration of the experiment. When the number of sessions and the duration of the exp. were increased, the appearance of a hyperplasia of the alveolar lining involving type II cells and then at a later stage, areas of epidermoid metaplasia in the bronchial area were observed. However, emphysematous changes occurred that seemed to be more extensive in rats subjected to intensive inhalations. Coal Dust: When coal dust exposure was combined with smoke inhalations, the lesion inducing effects due to smoke were not appreciably altered. The pulmonary lesions produced by smoke plus dust, compared to those produced by smoke alone, the action of dust appeared to predominate. Macrophagic alveolitis was characteristic of intensive dust exposure. Hyperplasia and ciliated metaplasia were essentially localized in the area of dust deposits. Acrolein: The results obtained with acrolein plus smoke did not significantly differ from those obtained with smoke alone. CONCLUSIONS; The amount of tar found in lungs depended on the number of inhalation sessions per day, rather than total inhalations. Smoke inhalations caused emphysematous lesions, the extent of which depended on the total dose of smoke inhaled. No lung tumors were observed. Only a hyperplasia of the alveolar lining involving type II alveolar cells and, at a later stage, areas of metaplasia generally limited to the bronchial area were found. Association of coal dust with smoke did not alter the specific effects of smoke and resulted in effect peculiar to the action of dust. When smoke was combined with acrolein, the effects due to smoke were not appreciably altered. I