Changes in the composition of lung lipids and the "turnover" of dipalmitoyl lecithin in experimental alveolar lipo-proteinosis induced by inhaled quartz.

Specific pathogen-free rats, exposed to the inhalation of quartz for varying periods and surviving thereafter for several months, consistently developed alveolar lipo-proteinosis, but not typical silicosis as might have been expected. The overall lipid content of the lungs was much increased, notably the phospholipids and especially dipalmitoyl lecithin (DPL), whilst the lipid-free dry weight rose relatively little. In other rats, receiving brief but intenser exposures and surviving subsequently for a limited period so that the disease would be in an active phase, the rate of incorporation of labelled palmitic acid was measured and its rate of disappearance followed for 4 weeks. As compared with controls, the rate of synthesis of DPL was tripled and its rate of loss doubled. Accumulation of DPL in the lungs may thus be explained as an imbalance between formation and removal, though both are augmented. Our evidence conflicts with the view that the basic defect in alveolar lipo-proteinosis is a diminished capacity for elimination of alveolar secretion. The absolute plasma fatty acid content and the proportions of individual acids were unaffected in treated animals. It may therefore be concluded that the lipid accumulation derives from lung tissue rather than directly from the plasma, and type II epithelial cells appear to be a major source.