Comparative histopathological and biochemical analysis of early stages of exposure to non-silicogenic aluminium silicate-and strongly silicogenic quartz-dust in rats

Abstract

One group of male CFY rats was given bentonite with high aluminium silicate content, the other group was given quartz dust, intratracheally. It has been stated that between 12-72 hours after the dust-exposure, the histological reactions developing upon the effect of non-silicogenic bentonite and silicogenic quartz are identical. Similarly in both groups lipid and phospholipid content of the lung shows a slight increase; the composition of phospholipids does not alter due to the effect of the two dusts. Between 12-72 hours after the exposure to both dusts the inflammatory response characterizing the histological reaction consists mainly of leukocytes; while between 48-72 hours macrophages appear in large numbers. The dust particles are swallowed both by leukocytes and macrophages. The confluating bronchopneumonia developed at the end of the 72nd hour is characterized by necrosis. Ninety days after exposure, bentonite causes storage-focal tissue reaction and quartz produces progressive pulmonary fibrosis; due to the effect of quartz, the lipid and phospholipid content of the lung significantly increases, the ratio of phospholipid fractions alters; bentonite does not increase the amount of pulmonary lipid and phospholipid. On the basis of the strong aldehyde bisulphite-toluidine blue (ABT) positivity of the macrophages containing bentonite, it may be assumed that the bentonite particle surface has an oriented polysaccharide and/or protein coat released from necrotized leukocytes, which protects the macrophage from the strong cytotoxic (necrotizing) effect of bentonite.