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Silicosis 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. Acute silicosis 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, pain and other abrasives. The cutting, breaking, crushing, drilling, grinding or abrasive blasting of these materials may produce a fine silica dust. It can also be found in soil, mortar, plaster and shingles. Silicosis is due to deposition of fine dust (less than one 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. Acute silicosis may develop within 6 months to 2 years following massive silica exposure.
When 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 via mucous or coughing.
When fine particles of silica dust are deposited in the lungs, macrophages (body’s immune system of cellular defense) 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 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.
These include:
Tachypnea or Shortness of Breath
Dry or Severe Cough, often persistent or accompanied by hoarseness of the throat
Fatigue or tiredness
Changes in breathing pattern (rapid or shallow breathing)
Loss of Appetite
Chest Pain
Fever
Gradual dark shallow rifts in nails, eventually leading to cracks
Advanced cases may also include: Cyanosis; cor pulmonale (abnormal enlargement of the right side of the heart) and respiratory insufficiency.
Patients with silicosis are particularly susceptible to tuberculosis (TB) infection-known as silicotuberculosis. The reason for this is not fully understood, with an increased risk of 10-30 times more likely to develop. It is thought that silica damages pulmonary macrophages, thereby inhibiting their ability to destroy mycobacteria.
Classification of silicosis is made according to the disease’s severity, onset and rapidity of progression:
Chronic Silicosis-The most common which develops after 20 + years of prolonged exposure to low levels of silica dust. This can then be further divided into simple and complicated silicosis.
Asymptomatic Silicosis-Early cases that do not present symptoms.
Acute Silicosis-Develops after 1-3 years of exposure to very high concentration of silica dust.
Accelerated Silicosis-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 ups will reveal decreased chest expansion and abnormal breath sounds. Pulmonary function tests 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 in 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 (CT) scan can also provide more detailed analysis of the nodules and can reveal cavitation due to concomitant mycobacterial infection.