Silicosis (also known as Grinder’s disease and Potter’s rot) is a form of pneumoconiosis 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.
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 1 micron 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 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.
The symptoms of silicosis include:
- Tachypnea or shortness of breath after physical exertion
- Dry or severe cough, often persistent and accompanied by hoarseness of the throat
- Fatigue or tiredness
- Changes in breathing pattern (rapid breathing or shallow breathing)
- Loss of appetite
- Chest pain
- Gradual dark shallow rifts in nails eventually leading to cracks
In advanced cases, the following may also occur:
- Cor pulmonale
- Respiratory insufficiency
Patients with silicosis are particularly susceptible to tuberculosis (TB) infection – known as silicotuberculosis. The reason for the increased risk – 10-30 fold increased incidence – is not well understood. It is thought that silica damages pulmonary macrophages, inhibiting their ability to kill mycobacteria.
Types of Silicosis
Classification of silicosis is made according to the disease’s severity, onset, and rapidity of progression. These include:
A form of the disease that develop after 20 years or longer of exposure to low levels of silica dust. Chronic silicosis itself is further subdivided into simple and complicated silicoses. This is the most common type of silicosis.
Early cases of the disease do not present any symptoms
Silicosis that develops after 1 to 3 years of exposure to very high concentration of silica dust.
Silicosis that develops after an average of 10 years of exposure to high concentration of silica dust.
Patient history should reveal exposure to silica dust due to occupation. Physical check up will reveal decreased chest expansion and abnormal breath sounds. Pulmonary function test will reveal reduced lung capacity.
Chest x-ray will confirm the presence of nodules in the lungs, especially in the upper lobes. Typically, it will also reveal eggshell calcification of the hilar lymph nodes. In rare cases, pulmonary nodules may also be calcified. In advanced cases of silicosis, coalescence of nodules may show up as large masses.
A computed tomography or CT scan can also provide a mode detailed analyses of the nodules, and can reveal cavitation due to concomitant mycobacterial infection.