Pneumoconioses are interstitial lung diseases caused by inhalation of inorganic dusts. Asbestosis results from asbestos fibers (serpentine or amphibole) deposited in distal airways and alveoli. Asbestos fibers are incompletely phagocytosed by macrophages due to their length, causing frustrated phagocytosis with persistent release of reactive oxygen species, cytokines (TNF-alpha, TGF-beta), and fibrogenic mediators, leading to progressive interstitial fibrosis. Asbestos bodies (golden-brown, dumbbell-shaped structures with iron-protein coating around asbestos fiber) are pathognomonic on histology. Silicosis results from crystalline silica (quartz) inhalation in mining, sandblasting, and stone cutting. Silica particles are highly cytotoxic to macrophages — phagocytosed silica disrupts phagolysosome membranes, activating NLRP3 inflammasome and releasing IL-1beta, driving granuloma and nodule formation with progressive massive fibrosis. Both conditions increase the risk of TB (silicosis significantly), lung cancer (asbestos), and mesothelioma (asbestos — especially amphibole fibers).