The pathogenesis of silica related diseases is discussed. The development of silicotic lesions depends on inhaling non combined forms of particulate silica of respirable size. The particles are ingested by alveolar macrophages and incorporated into a membrane bound vesicle called a phagosome. The phagosome is then merged with a lysosome. The membranes of these vesicles fuse together forming a single bound vesicle containing both phagocytized material and activated lysosomal enzymes known as a phagolysosomes.
Phagocytized silica disrupts lipoprotein membranes by an unknown mechanism.
It has been suggested that this phenomenon represents the starting point of the tissue reactions that result in silicosis. The effects of silica on human immunological competence are reviewed. Experimental silicosis in animal models is discussed. Such models have shown that silica is a selective macrophage toxin in all species. Interspecies variations occur with respect to the morphology of pulmonary lesions induced by silica.