Pulmonary Pathology Online
Pathology of Silicosis
Silicosis is caused by the inhalation of silicon dioxide, of which there are three molecular configurations.
The most important is quartz, and the others are cristobalite and tridymite.
The earth’s crust is composed largely of silicon and its oxides, and these often combine with other minerals to form silicates.
Visit: Silicone granulomas
Silicon dioxide, often referred to as "free silica", has the distinction of producing the best-known and the most widespread pneumoconiosis.
Silicosis is acquired in sandblasting. Mining also involves exposure to silica, as do numerous other occupations, including stone cutting, polishing and sharpening of metals, ceramic manufacturing, foundry work, and the cleaning of boilers.
Simple Nodular Silicosis:
Simple nodular silicosis is the most common form of silicosis and is almost inevitable in any worker chronically exposed to silica.
The lungs contain silicotic nodules (always less than 1 cm in diameter, and usually 2mm to 4mm in diameter) that, on histologic examination, have a characteristic whorled appearance, with concentrically arranged collagen that forms the largest part of the nodule.
At the periphery there are aggregates of mononuclear cells, mostly lymphocytes, and fibroblasts.
Polarized light reveals doubly refractile silicates within the nodule, but these are not related to the pathogenesis of silicosis (only free silica is responsible).
Hilar nodes become enlarged and calcified, often at the periphery of the node (“eggshell calcification”).
It has now become apparent that simple silicosis is not usually associated with significant disability, as assessed by pulmonary function.
Progressive Massive Fibrosis:
Progressive massive fibrosis (PMF) is defined radiologically as nodular masses of more than 1 cm diameter in a background of simple silicosis.
Most of these lesions are considerably large (about 5-10 cm in diameter) and are usually located in the upper zones of the lung.
Morphologically, the lesions often exhibit central necrosis, although in some instances they consist of aggregates of nodules of simple silicosis ("conglomerate silicosis" ).
It is well recognized that tuberculosis is much more common in patients with silicosis than in others and that it is a serious complication.
This complication was first described in South Africa. Most of the gold miners there are migrant workers who are employed on a short-term contract.
Lesions of tuberculosis in the miners closely resemble PMF, hence the notion that PMF is due to tuberculosis.
Most observers give less importance to the tuberculous theory of PMF now than was once the case.
Progressive massive fibrosis is related to the amount of silica in the lung.
Disability is caused by the destruction of lung tissue that has been incorporated into the nodules.
Now uncommon, acute silicosis results from heavy exposure to finely particulate silica during sand blasting or boiler scaling.
It is associated with diffuse fibrosis of the lung in which classic silicotic nodules are not found.
Dense eosinophilic material accumulates in the alveolar spaces to produce an appearance that resembles alveolar lipoproteinosis.
Indeed, experimental administration of finely particulate silica has been used as a model for that condition.
The disease progresses rapidly over a few years, in contrast to other forms of silicosis, the progression of which is measured in decades.
On radiologic examination, acute silicosis shows diffuse linear fibrosis and a reduction in lung volume.
Clinically, there is a severe restrictive defect.
Etiology and Pathogenesis:
It was originally thought that the varying degrees of fibrosis associated with different forms of silica reflected differing solubilities.
The popular view today is that following the ingestion of silica, macrophages produce a fibroblast-stimulating factor.
Because of the toxicity of silica, the macrophage dies, thereby releasing the ingested silica and the fibroblast-stimulating factor.
The silica is then reingested by macrophages and the process is amplified.
The cytotoxicity of silica results from the contact between the mineral particle and the target macrophages.
For many years, the death of these cells has been related to the fate of the particles after this contact.
In particular, the release of lysosomal enzymes into the cytosol follows rapidly on the phagocytosis of silica particles.
It has been suggested that the breakdown of cellular components as a result of the release of lysosomal components produces irreversible cell injury.
Although intracellular lysosomal rupture has been documented in silica-treated macrophages, the evidence that it causes cell death is only circumstantial.
Experimentally, it has been possible to dissociate intracellular lysosomal rupture from cell death after exposure to silica particles.
It is likely that the macrophages are killed because of direct damage to the plasma membrane.
Immunologic mechanisms may also be involved in the pathogenesis of silicosis.
Immunoglobulins are present in the silicotic nodules, and abnormal serum immunoglobulins (Example: Antinuclear antibodies) are also often present.
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