SMALL AIRWAYS DISEASE ASSOCIATED WITH MINERAL DUST EXPOSURE

Exposure to inorganic mineral dusts is associated with the development of pathologic changes in the small airways. The lesions consist of fibrotic thickening, often accompanied by pigment, of the walls of MBs and RBs, and sometimes of ADs as well. On casual inspection, the changes in the MBs are similar to those seen in cigarette smokers, but formal grading analysis indicates that they are more severe in those exposed to dusts compared with smoking-matched controls. The changes in the RBs and, where they occur, AD, are distinctive, and their presence usually indicates significant dust exposure. In man these lesions are seen with a broad spectrum of minerals, including asbestos, silica, iron oxide, aluminum oxide, several different sheet silicates, and coal. Similar changes have been found in experimental animals. Morphologically, these abnormalities have sometimes been called macules, but careful examination suggests there is a spectrum of changes characterized by the deposition of dust and pigment around small airways: True macules have no associated fibrosis, whereas the lesions described here have marked fibrosis. The pathogenesis of these lesions is unclear, but analysis of particle burdens within affected airways shows a strong correlation between number of particles and degree of fibrosis. Inhaled dusts of many kinds have been shown to evoke an inflammatory response that ultimately results in localized fibrosis of the airways. In this regard the development of fibrotic lesions in the distal small airways caused by mineral dusts is probably very similar to the development of fibrosis in small airways in cigarette smokers: Both processes appear to require long-term ongoing fairly low-grade inflammation. There is now a considerable body of literature that suggests that exposure to mineral dusts is associated with airflow obstruction. Some mineral dusts, most clealy coal, produce a form of centrilobular emphysema, and it has been proposed that emphysema is the cause of airflow obstruction in dust-exposed workers. However, experimental models reveal that lesions of the type described here in the small airways are capable of causing obstruction, and there are limited human data that leads to the same conclusion. The issue of the cause of airflow obstruction in those with dust exposure, and in particular of airways disease versus emphysema, requires further investigation.