Suppression of Inhaled Particle Cytotoxicity by Pulmonary Surfactant and Re-Toxification by Phospholipase-- Distinguishing Properties of Quartz and Kaolin

Inhaled particle contact with pulmonary surfactant in the hypophase lining pulmonary alveoli was modeled in vitro by exposing two respirable sized dusts, kaolin and silica quartz, to lecithin, a major component of pulmonary surfactant, emulsified in physiologic saline. Lecithin adsorbs to the dusts upon incubation at 37º C and suppresses their cytotoxicity as measured by pulmonary macrophage and erythrocyte assays, suggesting that pulmonary surfactant provides a defense system against prompt cell membrane lysis by inhaled dusts. Subsequent pulmonary macrophage phagocytosis and lysosomal enzyme digestion of the coated dusts was modeled in vitro by incubation with phospholipase A2 for one hour. With increasing lipase activity, silica hemolytic potential was restored to native silica levels. Kaolin was retoxified to levels far in excess of native kaolin hemolytic potential. Elution, thin layer chromatography and phosphate assay of treated dusts indicate most lecithin on silica is digested to lysolecithin and desorbed, silica retoxification being due to surface and adherent lysolecithin effects. Most lecithin on kaolin is not digested in this same time; that which is results in adherent lysolecithin which is responsible for the kaolin retoxification. Digestion with phospholipases A2 and C together produces only weakly retoxified kaolin. Results suggest that surface adsorption properties which control the adherence of prophylactic surfactant distinguish the pathogenic potentials of quartz, kaolin and mixed dust.