Murine lung response to kaolin conveyed by cigarette smoke.

The effects of chronic (3 to 8.5 months) smoke inhalation from cigarettes laced with 0.1, 1.0 and 10.0 mg kaolin (hydrated aluminum silicate) per gram of tobacco on the morphological integrity of lungs and the pulmonary macrophage population were evaluated in young and old male C57BL/6 mice. Lacing procedures, monitored by determining aluminum content in acid-digested aliquots of tobacco via atomic absorption spectrometry (AAS), proved to be uniform. Amounts of aluminum in right lungs of young mice evaluated by AAS and of kaolin assessed by electron diffraction and polarizing light microscopy were larger in mice which inhaled smoke from cigarettes laced with more 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. Concomitant with the above, 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. Further, the degree of ultrastructural alteration of the 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 dose inhaled in old mice but not in young animals. The reported 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.