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==Overview==
==Overview==
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.
*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 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.
==Historical Perspective==
*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
 
==Pathophysiology==
*When small [[silica]] dust particles are inhaled, they can embed themselves deeply into the tiny [[alveolar sac|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 [[fibrosis|fibrotic nodules]] with concentric "onion-skinned" arrangement of [[collagen]] fibers, [[hyalinization|central hyalinization]], and a cellular peripheral zone, with lightly [[birefringence|birefringent particles]] seen under [[polarized light]]. In acute silicosis, microscopic pathology shows a [[Periodic acid schiff|periodic acid-Schiff positive]] alveolar exudate (alveolar [[lipoproteinosis]]) and a cellular infiltrate of the alveolar walls.
 
==Classification==
Silicosis is classified into five categories: ''Simple chronic'', ''Complicated chronic'', ''Interstitial Pulmonary Fibrosis'', ''Acclerated silicosis'', and ''Acute silicosis''.
 
==Causes==
*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
 
==Differential Diagnosis==
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.
 
==Epidemiology and Demographics==
*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.
 
==Risk Factors==
*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]].
 
==Natural History, Complications and Prognosis==
*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.
 
==Diagnosis==
===History and Symptoms===
*Symptoms include [[dyspnea]], [[cough]], [[fatigue]] or [[tiredness]], [[loss of appetite]], [[chest pain]] and[[fever]]
*In advanced cases, [[cyanosis]], [[cor pulmonale]] and [[respiratory insufficiency]] can occur
 
===Physical Examination===
*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.
 
===Laboratory Findings===
*There are no specific laboratory tests for the diagnosis of silicosis, except a careful occupational history.
*A [[complete blood count]] with differential, [[GM-CSF|granulocyte macrophage-colony stimulating factor]] (GM-CSF) antibodies, [[Blood culture|blood]] and [[sputum cultures]] and [[BNP|natriuretic peptide]], are helpful in excluding other causes.
*Assessment of [[oxygenation]] is important, either with [[Pulse oximetry|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===
*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.
 
==Treatment==
===Medical Therapy===
*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]], [[oxygen|supplemental oxygen]] is administered to prevent complications of chronic [[hypoxemia]] and treatment with [[bronchodilators]] to facilitate breathing if airflow limitation is present on [[spirometry]].
 
===Primary Prevention===
*Prevention of silicosis is by identification of work-place activities with high concentrations of [[silica|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.


==References==
==References==

Latest revision as of 13:32, 24 June 2015

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aparna Vuppala, M.B.B.S. [2]

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.

Historical Perspective

Pathophysiology

Classification

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

Causes

  • 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

Differential Diagnosis

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.

Epidemiology and Demographics

  • 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.

Risk Factors

Natural History, Complications and Prognosis

  • 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.

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Diagnostic Studies

  • 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.

Treatment

Medical Therapy

Primary Prevention

  • 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.

References

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