Silicosis

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Silicosis (also known as Grinder’s disease and Potter’s rot) is a form of occupational lung disease caused by inhalation of crystalline silica dust, and is marked by inflammation and scarring in forms of nodular lesions in the upper lobes of the lungs.

Silicosis (especially the acute form) is characterized by shortness of breath, fever, and cyanosis (bluish skin). It may often be misdiagnosed as pulmonary edema (fluid in the lungs), pneumonia, or tuberculosis.

This respiratory disease was first recognized in 1705 by Ramazzini who noticed sand-like substances in the lungs of stonecutters. The name silicosis (from the Latin silex or flint) was attributed to Visconti in 1870.

Silica is the second most common mineral on earth. It is found in sand, many rocks such as granite, sandstone, flint and slate, and in some coal and metallic ores. The cutting, breaking, crushing, drilling, grinding, or abrasive blasting of these materials may produce fine silica dust. It can also be in soil, mortar, plaster, and shingles. Silicosis is due to deposition of fine dust (less than 1 micrometre in diameter) containing crystalline silicon dioxide in the form of alpha-quartz, cristobalite, or tridymite.

The induction period between initial silica exposure and development of radiographically detectable nodular silicosis is usually 10 years. Shorter induction periods are associated with heavy exposures, and acute silicosis may develop within 6 months to 2 years following massive silica exposure.

When small silica dust particles are inhaled, they can embed themselves deeply into the tiny alveolar sacs and ducts in the lungs, where oxygen and carbon dioxide gases are exchanged. There, the lungs cannot clear out the dust by mucous or coughing.

When fine particles of silica dust are deposited in the lungs, macrophages that ingest the dust particles will set off an inflammation response by releasing tumor necrosis factors, interleukin-1, leukotriene B4 and other cytokines. In turn, these stimulate fibroblasts to proliferate and produce collagen around the silica particle, thus resulting in fibrosis and the formation of the nodular lesions. The inflammatory effects of crystalline silica are apparently mediated by the Nalp3 inflammasome.[1]

Furthermore, the surface of silicon dust can generate silicon-based radicals that lead to the production of hydroxyl and oxygen radicals, as well as hydrogen peroxide, which can inflict damage to the surrounding cells.

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