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Silicosis

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. more...

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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.

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 1μm 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.

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.

Prevalence

Although silicosis has been known for centuries, the industrialization of mining has lead to an increase in silicosis cases. 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.

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Endobronchial Silicosis
From CHEST, 10/1/00 by M. Lingat

M. Lingat, M.D., K.J. Malik, M.D., S. Raab, M.D., P.D. Kaplan, M.D.--Allegheny General Hospital, Pittsburgh, PA

Introduction: Silicosis is a fibrotic disease of the lung caused by pulmonary reaction to free crystalline silica. Radiographically it is manifested by small rounded opacities and occasionally by eggshell calcification of hilar nodes. It is predominantly a parenchymal disease. We report a case of endobronchial silicosis leading to broncholithiasis in the absence of other radiographic features typical of silica exposure.

Case Presentation: A 64-year-old retired coal miner was referred to the Pulmonary Clinic for evaluation of a 10 year history of recurrent pneumonias. He was a non smoker and had a benign past medical history. On physical exam, he was not dyspneic at rest. The breath sounds were normal with no adventitous sounds heard. Cardiac exam was normal. There was no clubbing, cyanosis, or peripheral edema. Chest roentogram demonstrated atelectasis. No rounded opacities were seen. CT scan revealed patchy infiltrates in both lower lung fields, associated with atelectasis. Spirometry was normal with an FVC of 4.78 (87%) and an [FEV.sub.l] of 3.81 (70%). The flow volume loop was normal. Flexible bronchoscopic examination revealed an exophytic endobronchial mass obstructing the right middle lobe bronchus. Biopsies of the lesion revealed fibrohistiocytic proliferation. On polatization, numerous small particles consistent with endobronchial silicotic nodules were found.

Discussion: The chronic fibrosing disease of the lungs caused by prolonged and extensive exposure to free silica has been recognized for centuries. Workers exposed to free silica may develop nodular lesions within the lungs that may coalesce into conglomerate or confluent lesions called massive fibrosis. This is defined as complicated silicosis, which may be associated with impaired lung function or even premature death. It is known that granulomatous infections such as Mycobacterium tuberculosis, Histoplasmosis and Coccidioidomycosis may cause broncholithiasis. Cahill, et al reported a case of broncholithiasis with silica exposure. Broncholiths can be deeply embedded into the wall of bronchus and erode into the lumen to cause symptoms such as cough, hemoptysis, lithotripsis, airway obstruction, pneumonia, and fistula formation. Radiographic manifestations include development of airway obstruction resulting in lobar or segmental atelectasis, mucosal impaction or air-trapping. Our patient had symptoms of cough and was treated for recurrent pneumonia twice in the year of diagnosis. Initially, his chest x-ray showed parenchymal densities without any nodules. A followup chest x-ray six months later showed atelectasis and consolidation of the right middle lobe. This was confirmed on CT scan. Bronchoscopy at the time showed an exophytic mass obstructing the right middle lobe. Upon biopsy, the histopathology was consistent with silicotic nodules reflecting his silica exposure. He developed endobronchial silicosis, which manifested as an exuberant growth of granulation tissue obstructing his airway causing atelectasis. Although Mycobacterial infection is often associated with patients, with silicosis, all his cultures were negative. Broncholithiasis may be ablated using YAG laser, and, at times, surgical resection may be necessary. Unfortunately, to-date, there is no specific treatment for silicosis. Current therapeutic measures include treatment of air flow obstruction or bronchodilators, treatment of respiratory tract infections with antibiotics, and the use of supplemental oxygen to prevent complications of chronic hypoxemia.

Conclusion: Endobronchial silicosis may present with radiographic features atypical of silicosis.

COPYRIGHT 2000 American College of Chest Physicians
COPYRIGHT 2001 Gale Group

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