Silicosis
From Wikipedia, the free encyclopedia
| ICD-10 | J62 |
|---|---|
| ICD-9 | 502 |
Silicosis (also known as Grinder's disease) 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.
The full name for this disease is pneumonoultramicroscopicsilicovolcanoconiosis, and at 45 letters it is the longest word in the English language. (The name has been described as a "trophy word" -- its only job is to serve as the longest word <ref>"A Word A Day" comment on the longest "official" word</ref> .)
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.
This respiratory disease was first recognized in 1705 by Ramazzini who noticed sand-like substances in the lungs of stonecutters. The name silicosis (from the latin silex or flint) was attributed to Visconti in 1870.
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[edit] Silica
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 micrometre in diameter) containing crystalline alpha-quartz silica or silicon dioxide.
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.
[edit] Pathology
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.
[edit] Prevalence
Although silicosis has been known for centuries, the industrialization of mining has led to an increase in silicosis cases. Pneumatic drilling in mines and less commonly, mining using explosives, would raise rock dust. In the United States, a 1930 epidemic of silicosis due to the construction of the Hawk's Nest Tunnel near Gauley Bridge, West Virginia caused the death of more than 400 workers. The prevalence of silicosis led some men to grow what is called a miner's mustache, in an attempt to intercept as much dust as possible.
Also, the mining establishment of Delamar Ghost Town, Nevada was ruined by a dry-mining process that produced a silicosis-causing dust. After hundreds of deaths from silicosis, the town was nicknamed The Widowmaker. The problem in those days was somewhat resolved with an addition to the drill which sprayed a mist of water, turning dust raised by drilling into mud, but this inhibited mining work.
Indeed, silicosis is an occupational hazard to mining, sandblasting, quarry and foundry workers, as well as grinders, stonecutters and those continually exposed to silica dust.
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. For instance, life expectancy for silver miners in Potosí, Bolivia is around 40 years due to silicosis.
[edit] Symptoms
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
- Fever
In advanced cases, the following may also occur:
- Cyanosis
- Cor pulmonale
- Respiratory insufficiency
Patients with silicosis are particularly susceptible to tuberculosis (TB) infection.
[edit] Types of Silicosis
Classification of silicosis is made according to the disease's severity, onset, and rapidity of progression. These include:
- Chronic silicosis
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.
- Asymptomatic silicosis
Early cases of the disease do not present any symptoms
- Acute silicosis
Silicosis that develops after 1 to 3 years of exposure to very high concentration of silica dust.
- Accelerated silicosis
Silicosis that develops after an average of 10 years of exposure to high concentration of silica dust.
[edit] Diagnosis
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 concomittant mycobacterial infection.
[edit] Treatment
Silicosis is an irreversible condition, with no cure. Treatment options currently focus on alleviating the symptoms and preventing complications. These include:
- Stopping further exposure to silica and other lung irritants, including tobacco smoking.
- Cough suppressants.
- Antibiotics and antitubercular agents to prevent tuberculosis. These include isoniazid, rifampin, and pyrazinamide.
- Chest physiotherapy to help the bronchial drainage of mucus.
- Oxygen administration to avoid hypoxemia.
- Bronchodilators to facilitate breathing.
- Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.
Experimental treatments include:
- Whole-lung lavage.
- Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.
- Corticosteroid therapy.
- The herbal extract tetrandine may slow progression of silicosis.
[edit] Prevention
The best way to prevent silicosis is to identify work-place activities that produce crystalline silica dust and then to eliminate or control the dust.
[edit] See also
[edit] Notes
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[edit] External links
- Silicosis - eMedicine
- Silicosis - Health in Plain English (with pictures)bg:Силикоза
de:Silikose es:Silicosis fr:Silicose nl:Silicose pt:Silicose simple:Silicosis
