A rare lung pathology resulting from the inhalation of silica dust (quartz).
This condition is mainly seen in workers in slate mines and granite quarries, metal foundries, stone masonry and tunnelling.
The pathogenesis is thought to be a toxic effect on macrophages, which stimulate cytokine generation, precipitating fibrogenesis. Short heavy doses produce acute silicosis with pulmonary oedema and alveolar exudation. Prolonged exposure produces multiple fibrous nodules, which may expand causing extensive destruction of lung tissue and the development of progressive massive fibrosis.
In the early stages there may be no symptoms. The first symptom is usually breathlessness on exertion and a productive cough may follow. Progression leads to respiratory failure.
The nodules in silicosis are made up of collagen and contain silica particles which can be identified using polarised light.
The development of tuberculosis is a common complication of silicosis (silicotuberculosis). It is thought that this is due to impairment of local defences, as a result of the accumulation of silica in macrophages. Increased risk of lung cancer.
Chest X-ray in the early stages shows reticular/nodular shadowing. With progression there are radiological signs of massive fibrosis (destruction and lesions in the upper zones), and thin streaks of calcification around the hilar nodes (‘eggshell calcification’).
There is no specific treatment, primary prevention through education and exposure prevention remains the only effective stratergy.