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| ==Case Studies== | | ==Case Studies== |
| [[Silicosis case study one|Case #1]] | | [[Silicosis case study one|Case #1]] |
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| ==Silica==
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| 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.
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| 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.
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| ==Pathology==
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| 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.
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| When fine particles of silica dust are deposited in the lungs, [[macrophage]]s 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 [[fibroblast]]s to proliferate and produce collagen around the silica particle, thus resulting in [[fibrosis]] and the formation of the nodular lesions.
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| 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.
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| 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.
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| ==Symptoms==
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| Because silicosis is progressive, signs of it may not appear until years after exposure.<ref name="WHO"/> Symptoms include:
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| * [[Tachypnea]] or shortness of breath after physical exertion
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| * Dry or severe cough, often persistent and accompanied by hoarseness of the throat
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| * Fatigue or tiredness
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| * Changes in breathing pattern (rapid breathing or shallow breathing)
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| * Loss of appetite
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| * Chest pain
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| * Fever
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| * Gradual dark shallow rifts in nails eventually leading to cracks
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| In advanced cases, the following may also occur:
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| * [[Cyanosis]]
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| * [[Cor pulmonale]]
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| * Respiratory insufficiency
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| 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.
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| ==Types of Silicosis==
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| Classification of silicosis is made according to the disease's severity, onset, and rapidity of progression. These include:
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| * ''Chronic silicosis''
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| 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.
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| * ''Asymptomatic silicosis''
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| Early cases of the disease do not present any symptoms
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| * ''Accelerated silicosis''
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| Silicosis that develops 5-10 years after high exposure to silica dust. Symptoms include severe shortness of breath, weakness, and weight loss.
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| * ''Acute silicosis''
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| 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.
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| ==Diagnosis==
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| 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.
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| 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 [[lymph node|hilar lymph node]]s. In rare cases, pulmonary nodules may also be calcified. In advanced cases of silicosis, coalescence of nodules may show up as large masses.
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| 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.
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| ==Treatment==
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| Silicosis is an irreversible condition with no cure. Treatment options currently focus on alleviating the symptoms and preventing complications. These include:
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| * Stopping further exposure to silica and other lung irritants, including [[tobacco smoking]].
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| * [[cough medicine|Cough suppressants]].
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| * [[Antibiotic]]s and antitubercular agents to prevent [[tuberculosis]]. These include [[isoniazid]], [[rifampin]], and [[pyrazinamide]].
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| * Chest [[physiotherapy]] to help the bronchial drainage of [[mucus]].
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| * [[Oxygen]] administration to avoid [[Hypoxia (medical)|hypoxemia]].
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| * [[Bronchodilator]]s to facilitate breathing.
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| * [[Lung transplantation]] to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.
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| Experimental treatments include:
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| * Whole-lung lavage (see [[Bronchoalveolar lavage]])
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| * Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.
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| * [[Corticosteroid]] therapy.
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| * The herbal extract tetrandine may slow progression of silicosis.<ref>{{cite paper
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| | author =Chao, D.H. ; Ma, J.Y.C. ; Malanga, C.J. ; Banks, D.E. ; Hubbs, A.F. ; Rojanasakul, Y. ; Castranova, V. ; Ma, J.K.H
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| | title =Multiple emulsion-mediated enhancement of the therapeutic effect of tetrandine against silicosis
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| | publisher =West Virginia University School of Pharmacy
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| | date =July 1996
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| | url =http://www.osti.gov/energycitations/product.biblio.jsp?osti_id=463739
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| | quote = Previously it was shown that the action of tetrandrine is attributed to its ability to inhibit the release of reactive oxygen metabolites and inflammatory cytokines by alveolar macrophages, and that targeted delivery of tetrandrine to alveolar macrophages using a multiple emulsion system minimizes drug toxicity, maintains the drug's pharmacological activity, and enhances tetrandrine distribution in the lungs while reducing systemic drug distribution. This study provides ''in vivo'' evidence of emulsion-mediated enhancement of drug action in the lungs against silica-induced lung injury using a rat model. }}</ref>
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| ==Prevention==
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| 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.
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| ==See also== | | ==See also== |