Silicosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Silica (silicon dioxide) is the most abundant mineral on earth. Silica exists in crystalline and amorphous forms. Crystalline silica (quartz, cristobalite, and tridymite) is associated with a spectrum of pulmonary diseases. Amorphous forms, including vitreous silica and diatomite (formed from skeletons of prehistoric marine organisms), are relatively less toxic after inhalation [18].
Quartz is the most abundant form of crystalline silica and is a major component of rocks including granite, slate, and sandstone. Granite contains about 30 percent free silica, slate about 40 percent, and sandstone is almost pure silica [19]. Cristobalite and tridymite occur naturally in lava and are formed when quartz or amorphous silica is subjected to very high temperatures.
The toxicity of crystalline silica appears to result from the ability of crystalline silica surfaces to interact with aqueous media, to generate oxygen radicals, and to injure target pulmonary cells such as alveolar macrophages. Resultant generation of inflammatory cytokines (eg, interleukin-1 and tumor necrosis factor beta) by target cells lead to cytokine networking between inflammatory cells and resident pulmonary cells, resulting in inflammation and fibrosis [20].
"Free" crystalline silica is unbound to other minerals. "Combined" forms of silica, called silicates, are compounds in which silica is bound to other minerals. Examples of silicates used in industry include asbestos (hydrated magnesium silicate), talc (Mg3Si4O10(OH)2), and kaolinite (Al2Si2O5(OH)4), a major component of kaolin (china clay) [21]. The pulmonary effects of asbestos inhalation are substantial, and are discussed separately
Silica probably exerts it effects on the macrophages that ingest it and alter their function rather than disrupting it. The
stimulated macrophage appears to secrete mediator substances such as Interleukin-1. The macrophages has been implicated to be the major cause of fibrosis that accompanies silicosis.
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.
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.