Silica is the second most common mineral on earth. It is found in concrete, masonry, sandstone, rock, paint, and other abrasives. 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 1μm in diameter) containing crystalline alpha-quartz silica or silicon dioxide.

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.

Pathology

When the small silica dust particles are breathed into the lungs, they can embed themselves deeply into the tiny alveolar sacs and ducts 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 factor, 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.

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.

Characteristic lung tissue pathology in nodular silicosis consists of fibrotic nodules with concentric “onion-skinned” arrangement of collagen fibers, central hyalinization, and a cellular peripheral zone, with lightly birefringent particles seen under polarized light. In acute silicosis, microscopic pathology shows a periodic acid-Schiff positive alveolar exudate (alveolar lipoproteinosis) and a cellular infiltrate of the alveolar walls.

Prevalence

Although silicosis has been known for centuries, the industrialization of mining has lead to an increase in silicosis cases. In the United States, a 1930 epidemic of silicosis due to the construction of the Hawk’s Nest Tunnel near Gauley Bridge, West Virginia caused the death of more than 400 workers.

Also, the mining establishment of Delamar Ghost Town, Nevada was ruined a dry-mining process that produced a silicosis-causing dust. After hundreds of deaths from silicosis, the town was nicknamed The Widowmaker.

Indeed, silicosis is an occupational hazard to mining, sandblasting, quarry and foundry workers, as well as grinders, stonecutters and those continually exposed to silica dust.

Due to protective measures, such as using respirators, death rates of silicosis in Western countries have been steadily declining.