Relationship of lipid secretion and particle size to diffuse interstitial change in pneumoconiosis: A pathogenetic perspective

Simple pneumoconiosis due to compact particles, notably in coal workers, sometimes departs from its customary focal formations and a more diffuse distribution of dust‐impregnated fibrosis is superimposed. To account for this change, which may be reflected in the acquisition of radiologically irregular opacities in addition to rounded ones, attention is directed first toward type II alveolar epithelium. These cells come early into contact with inhaled particles and the lipid secretion provoked prevents their characteristic aggregation, so they remain in a more dispersed state and the consequent fibrotic reaction then tends to become diffuse. Second, submicron particles appear to act not from within the alveolus like the more usual larger ones, but after direct passage through type I epithelium into the interstitium, where lacking focal accumulation they are able to produce diffuse changes. Complexities, however, remain, among which are coalescence of focal lesions as their severity increases and interplay of agents producing interstitial fibrosis in the general population.