The damage produced by silica has some special characteristics that prompt us to call it a polyhedric disease.
The fact that it is a slowly progressing disease that is rare in terms of the overall population makes randomized trials difficult, and the reduced “market” limits the interest of the pharmaceutical industry. In contrast to other fibrotic lung diseases and common lung diseases such as asthma, very little use has been made of modern research techniques to understand this ancient disease or identify new therapeutic options.
However, our knowledge of the pathogenic mechanisms of damage caused by silica inhalation is steadily growing.
Firstly, silica-induced lung injury presumably results from the combined action of several interacting pathogenic mechanisms, including the direct cytotoxic effect of silica on macrophages, activation of macrophage surface receptors, lysosomal rupture, generation of reactive oxygen species (ROS), activation of inflammasome, cytokine and chemokine production, cell apoptosis/pyroptosis, and pulmonary fibrosis.
Then there is the accompanying immune dysfunction.
Silica inhalation causes the activation and apoptosis of macrophages, while the excess antigen generated is ingested by other activated macrophages.
These can migrate to lymph nodes, eventually leading to the activation of T and B lymphocytes.
The likelihood of developing connective tissue disease is enhanced in subjects with exposure to silica and silicosis.
Furthermore, there is strong evidence for a very high risk of tuberculosis in the presence of radiological silicosis