Silicosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Introduction

Silicosis (also known as Grinder's disease and Potter's rot) is a form of occupational lung disease 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.

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.

The full name for this disease when caused by the specific exposure to fine silica dust found in volcanoes is pneumonoultramicroscopicsilicovolcanoconiosis, and at 45 letters it is the longest word in any of the major English dictionaries. (The name has been described as a "trophy word" -- its only job is to serve as the longest word.)

Silica

Silica is the second most common mineral on earth. It is found in sand, many rocks such as granite, sandstone, flint and slate, and in some coal and metallic ores. 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 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.

Pathology

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.

Prevalence

Silicosis is the most common occupational lung disease worldwide, it occurs everywhere but is especially common in developing countries. From 1991 to 1995, China reported more than 24,000 deaths due to silicosis each year. In the United States, it is estimated that over one million(two million) workers are exposed to free crystalline silica dusts and 59,000 of these workers will develop silicosis sometime in the course of their lives.

According to CDC data, silicosis in the United States is relatively rare. The incidence of deaths due to silicosis declined by 84% between 1968 and 1999, and only 187 1999 deaths had silicosis as the underlying or contributing cause. Additionally, cases of silicosis in Michigan, New Jersey, and Ohio are highly correlated to industry and occupation.

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 Hawk's Nest incident (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.

There is some concern that a batch of cannabis contaminated with silica found in the UK may cause silicosis in some users.

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.

Silicosis is an occupational hazard to mining, sandblasting, quarry, ceramics 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.

Recently, silicosis in Turkish denim sandblasters was detected as a new cause of silicosis due to recurring, poor working conditions.

Silicosis is seen in horses associated with inspiration of dust from certain cristobalite-containing soils in California.

Symptoms

Because silicosis is progressive, signs of it may not appear until years after exposure. Symptoms 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
• Gradual dark shallow rifts in nails eventually leading to cracks

In advanced cases, the following may also occur:

• Cyanosis
• 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:

• Chronic silicosis

Occurs after 15-20 years of exposure to moderate 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. Patients with this type of silicosis may not have obvious symptoms, so a chest X-ray is necessary to determine if there is lung damage.

• Asymptomatic silicosis

Early cases of the disease do not present any symptoms

• Accelerated silicosis

Silicosis that develops 5-10 years after high exposure to silica dust. Symptoms include severe shortness of breath, weakness, and weight loss.

• Acute silicosis

Silicosis that develops a few months to 2 years after exposure to very high concentrations of silica dust. Symptoms of acute silicosis include severe disabling shortness of breath, weakness, and weight loss, often leading to death.

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 concomitant mycobacterial infection.

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 (see Bronchoalveolar lavage)
• Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.
• Corticosteroid therapy.
• The herbal extract tetrandine may slow progression of silicosis.

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. Water spray is often used where dust emanates. Dust can also be controlled through dry air filtering.

See also

• Pneumoconiosis
• Asbestosis
• COPD
• Philip D'Arcy Hart
• Hawk's Nest Incident
• John Haldane
• The Citadel

External links

• Imaging Findings in Silicosis by Daniel Powers, MD

Notes

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