Tobacco Documents Online

! I I I I I I ! I I I I I I ! I I I AUTHOR: MATULIONIS, DANIEL H. AND ROBERT A. YOKEL DATE: 1988 TITLE: MURINE LUNG RESPONSE TO KAOLIN CONVEYED BY CIGARETTE SMOKE CITATION: VIRCHOWS ARCHIV A PATHOL ANAT 413:227-237 (1988) STUDY DESIGN:_C57BL/6 male mice were exposed to cigarette smoke or were sham-treated using a Tobacco and Health Research Institute mainstream-sidestream smoke exposure system. Mice were exposed to smoke twice/day for 3, 6 or 8.5 months. Mice were either 2 months (young) or 8-10 months old (old mice) when exposure was initiated. Young and old animals were exposed to smoke from 2A1 cigarettes to which no kaolin (hydrated aluminum silicate - AI=H40~Si ~ was added and to smoke from 2A1 cigarettes to which 0.1,1.0 or 10 mg of kaolin per gram tobacco was added._The lungs of mice (young and old) from each treatment group were assessed 3,6 or 8.5 months after onset of smoke exposure. FINDINGS/RESULTS: Amount of aluminum in right lungs of young mice were larger in mice which inhaled smoke from cigarettes laced with higher levels of kaolin. A more pronounced increase in lung parenchymal tissue and decrease of alveolar space was observed in old mice subjected to smoke from cigarettes containing higher doses of kaolin than in similarly treated young animals. The lung macrophage population did not increase as markedly in response to smoke inhalation in old mice nor did it increase in as clear a dose-response fashion to kaolin as it did in young animals. The Degree of ultrastructure alteration of phagocytes in the old mice suggested impaired cell function. Plate-like material resembling kaolin crystals was most conspicuous in lung macrophages of mice which inhaled largest amounts of kaolin. Manifestations of abnormal aggregates of lymphocytes and macrophages correlated with kaolin does inhaled in old mice but not in young animals. CONCLUSIONS: The above observations indicate that 1) kaolin gains access to lungs via cigarette smoke inhalation, 2) macrophages are important in maintaining pulmonary homeostasis and 3) the inorganic compound kaolin appears to impede macrophage function, resulting in potentiation of lung abnormalities.