Silicosis overview

• Silicosis is caused by inhalation of one of the forms of crystalline silica, most commonly quartz. Silicosis is seen among sandblasters, underground miners, foundry and quarry workers, and in other dust-exposed trades.

• The term silicosis was first introduced by Visconti 1870, derived from the Latin word silex, or flint.
• Mining, tunneling, sand stone industry, stone quarrying and dressing, iron and steel foundries and flint crushing are the occupations most closely related to the hazards of silica exposure

• 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.

Silicosis is classified into five categories: Simple chronic, Complicated chronic, Interstitial Pulmonary Fibrosis, Acclerated silicosis, and Acute silicosis.

• Silicosis is caused by the inhalation of crystalline silica, including quartz, cristobalite, and trimidite.
• Of all three, quartz is most abundant and is frequently associated with the development of silicosis upon prolonged exposure and/or exposure at extremely high concentrations

Silicosis must be differentiated from other diseases that cause cough, dyspnea, pulmonary nodules and fibrosis seen on chest x-ray such as asbestosis, tuberculosis, aspergillosis and pulmonary malignancy.

• Protective measures such as respirators have brought a steady decline in death rates due to silicosis in Western countries. Unfortunately, this is not true of less developed countries where work conditions are poor and respiratory equipment is seldom used.

• All the occupations dealing with the siliceous rock are at risk for silicosis. Occupations include, excavations in mines, tunnels, quarries, underground galleries, dry cutting, grinding, sieving and manipulation of minerals and rock, manufacturing of silicon carbide, glass, porcelain, earthenware and other ceramic products, manufacturing and maintenance of abrasives and detergent powders, foundry work, milling work, sandblasting and grinding, pottery industry, handling quartz conglomerates and ornamental stone, dental prostheses.

• Silicosis develops very slowly in most cases. Often decades elapse in progression to clinical disease from the beginning. Usually starts as simple silicosis and progress further after not less than 10 years of exposure to silica. Accelerated silicosis is a variant of silicosis occurred due to intense exposure to silica for 5-10years. All forms of silicosis can progress in the absence of continued exposure.
• Tuberculosis, mycosis , pneumothorax are some of the complications of silicosis.

• Symptoms include dyspnea, cough, fatigue or tiredness, loss of appetite, chest pain andfever
• In advanced cases, cyanosis, cor pulmonale and respiratory insufficiency can occur

• Physical examination of the chest in silicosis is often unremarkable, although a variety of abnormal breath sounds, including crackles, rhonchi, or wheezes, occur as the disease progress.

• There are no specific laboratory tests for the diagnosis of silicosis, except a careful occupational history.
• A complete blood count with differential, granulocyte macrophage-colony stimulating factor (GM-CSF) antibodies, blood and sputum cultures and natriuretic peptide, are helpful in excluding other causes.
• Assessment of oxygenation is important, either with pulse oxygen saturation or arterial blood gas, to determine the severity of respiratory impairment and whether the patient will be able to tolerate diagnostic procedures.

• Other diagnostic studies, such as Pulmonary function tests, spirometry, bronchoscopy and lung biopsy, are not always necessary but may be required for the diagnosis of silicosis in the minority of patients, with no significant history of exposure and to differntiate silicosis from other diseases.

• Generally, management of silicosis aims to manage other respiratory comorbidities (e.g. COPD or tuberculosis) and to treat silicosis-associated complications
• Supportive therapy include smoking cessation, supplemental oxygen is administered to prevent complications of chronic hypoxemia and treatment with bronchodilators to facilitate breathing if airflow limitation is present on spirometry.

• Prevention of silicosis is by identification of work-place activities with high concentrations of crystalline silica dust and elimination or control of the exposure. Early intervention with the control or cessation of adverse exposures may result in reversal of symptoms and airflow limitation.

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