Silicosis of the Lung – Acute, Accelerated and Chronic Types

What is silicosis?

Silicosis is a type of lung disease that is caused by inhaling silica particles. These particles may be present as free or crystalline silicon dioxide. It is a slow progressive condition that occurs decades after exposure to silica and is seen in a number of occupations, including mining, sand blasting, foundry work, construction and stone cutting. Silicosis is the most prevalent chronic occupational disease seen today and more common than other types of pneumoconiosis like coal worker’s pneumoconiosis and asbestosis.

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Silica can exist in different forms that can be broadly categorized into crystalline and amorphous silica. It is the crystalline form that appears to play a more significant role in lung disease due to its higher fibrinogenic properties. This means that it is more likely to promote fibrous scarring of the lung tissue. Some of the crystalline forms include quartz (most prevalent), crystobalite and tridymite. Crystalline silica may be combined with amorphous silica to form microcrystalline silica. Silicates are free silica combined with other compounds like talc, mica or asbestos.

Types of Silicosis

There are three types of silicosis :

  • Chronic silicosis
  • Accelerated silicosis
  • Acute silicosis

Most cases of silicosis is the classical chronic type. This means that the patient remains asymptomatic and symptoms first become apparent about 10 to 20 years after exposure. The accelerated form of silicosis is much more aggressive and patients may present with symptoms anywhere between 5 to 10 years. In some cases of accelerated silicosis, symptoms may appear after just 1 year of continued exposure to silica. An acute form of silicosis (silicoproteinosis) is seen within weeks or months of silica exposure. It occurs with constant exposure to large amounts of very fine silica dust.

How does silicosis occur?

Silica dust passes through the airways and into lungs. Here it interacts with the epithelial cells of the lung parenchyma and alveolar macrophages. Cell damage arises when silica particles make contact with the epithelial lining and leads toa build up of free radicals. Silica particles are also consumed by the macrophages (scavenger cells) where it causes these cells to release various chemical mediators like IL-1, TNF, fibronectin, lipid mediators, oxygen-derived free radicals, and fibrogenic cytokines.

Silicosis is a fibronodular pneumoconiosis meaning that the inflammation leads to confined areas of fibrotic scarring  of the lung tissue   This occurs over years and persists even if exposure to silica ceases. It first leads to tiny lumps that are spread throughout the lungs, primarily the upper zones. Gradually these lumps coalesce to form larger nodules and continues until there is widespread fibrosis of the lung. This affects gas exchange between the air that enters the lung sacs and blood stream and affects the flexibility of the lung.

Silicosos is not isolated to the lung tissue and there is usually involvement of the hilar lymph nodes and pleura (lining of the lungs). There is an increased chance of tuberculosis (silicotuberculosis), lung cancer and chronic obstructive pulmonary disease (COPD) in silicosis patients which can contribute to the pathogenesis and clinical presentation.

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