Pneumoconiosis is caused by the accumulation of dust in the lungs and the tissue reaction to its presence.
The appearance of pulmonary disability from pneumoconiosis is related to the amount of dust that has been inhaled. This amount will vary with the fibrogenicity of the dust. A dust which has a high fibrogenic potential is capable of incapacitating a larger amount of lung tissue following a shorter exposure than a dust having a low fibrogenic potential. In general, a very small percentage of workers exposed to a dust with a low fibrogenic potential (such a soft-coal miners) become incapacitated solely because they have developed simple pneumoconiosis. However, breathlessness and incapacitation may develop when simple pneumoconiosis becomes converted into the complicated variety and an excessive amount of functioning lung tissue is destroyed by progressive massive fibrosis. Of the pneumoconioses caused by fibrogenic dusts, silicosis and asbestosis are the most important. Silicosis is characterized by multifocal nodular fibrosis whereas asbestosis is typically a non-uniform diffuse pulmonary fibrosis that tends to be more pronounced in the basilar portions of the lungs. Silica and asbestos workers as well as coalminers and workers in non-dusty trades may develop breathlessness from chronic bronchitis or emphysema or both. The cause of this breathlessness is most often ascribable to the destruction of lung tissue or inflammation of the air passages (or both) by cigarette smoke. Cigarette smoke is also the main factor in the production of lung cancer in asbestos workers.