Silicosis

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

• 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 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

• 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.

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

• 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

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.

• 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.

• 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.

• 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.

• Symptoms include dyspnea, cough, fatigue or tiredness, loss of appetite, chest pain andfever
• In advanced cases, cyanosis, cor pulmonale and respiratory insufficiency can occur

• 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.

• There are no specific laboratory tests for the diagnosis of silicosis, except a careful occupational history.
• A complete blood count with differential, granulocyte macrophage-colony stimulating factor (GM-CSF) antibodies, blood and sputum cultures and natriuretic peptide, are helpful in excluding other causes.
• Assessment of oxygenation is important, either with 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, 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.

• 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, supplemental oxygen is administered to prevent complications of chronic hypoxemia and treatment with bronchodilators to facilitate breathing if airflow limitation is present on spirometry.

• 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.

Template:WH Template:WS

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

• Silicosis was first described by Hippocrates when he reported a condition of breathlessness among miners. In 1870, the term Silicosis was first introduced by Visconti. The term was derived from the Latin word silex or flint.

• Hippocrates described a condition of “breathlessness” among miners.
• In 1690, Lohneiss noted that when “the dust and stones fall upon the lungs, the men have lung disease, breathe with difficulty.”
• Bernardo Ramazzini studied “miners’ phthisis,” among workers who inhaled substantial amounts of dusts.
• These dust-related afflictions have been known by various names, including “miners’ phthisis,” “dust consumption,” “mason’s disease,” “grinders’ asthma,” “potters’ rot,” and “stonecutters’ disease.” These problems are now collectively referred to as silicosis.^[1]
• In 1870, the term Silicosis was first introduced by Visconti. The term was derived from the Latin word silex or flint.

• In the 16th century, Agricola described the first outbreak among mine workers in the mines of the Carpathian mountains in Europe.
• Several epidemics of silicosis have been reported worldwide.
• In 1930-1931, the worst epidemic of silicosis occurred in USA during the construction of Gauley Bridge tunnel in West Virginia, where more than 400 of the estimated 2000 construction workers died of silicosis, and almost all survivors developed silicosis.^[2] In addition, the mining establishment of Delamar Ghost Town, Nevada was ruined by a dry-mining process that produced a silicosis-causing dust. Following hundreds of deaths from silicosis, the town was nicknamed The Widowmaker.^[3]

Template:WH Template:WS

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

There are 5 subtypes of silicosis that are differentiated according to the duration of exposure, development of symptoms, pulmonary function, and findings on chest imaging. Silicosis is classified as either simple chronic, complicated chronic, interstitial pulmonary fibrosis, accelerated silicosis, or acute silicosis.

There are 5 subtypes of silicosis that are differentiated according to the duration of exposure, development of symptoms, pulmonary function, and findings on chest imaging.^[1]

• Respiratory disease often develops > 10 years following exposure to low – moderate concentrations of silica dust.
• Patients usually remain asymptomatic, making the diagnosis of silicosis very difficult.
• Pulmonary function tests are typically normal but may also be reduced.
• On chest imaging, nodules are < 10 mm in diameter.

• Respiratory disease often develops > 10 years following exposure to silica dust.
• Patients may report dyspnea and cough.
• Pulmonary function may be either normal or reduced.
• On chest imaging, nodules > 1 cm with either obstructive or restrictive changes of variable severity

• Respiratory disease often develops > 10 years following exposure to silica dust.
• Patients may report dyspnea and cough.
• Pulmonary function may be either normal or reduced.
• On chest imaging, diffuse reticulonodular pattern similar to idiopathic pulmonary fibrosis is usually observed.

• Respiratory disease often develops 5 to 10 years following exposure to silica dust.
• Patients often report dyspnea, weakness, and weight loss.
• Pulmonary function is often reduced with rapid deterioration of FVC and FEV1.
• On chest imaging, rapidly progressive nodules and masses are observed.

• Respiratory disease often develops within 5 years of exposure to extremely high concentrations of silica dust.
• Patients often report severe, disabling dyspnea, weakness, weight loss, and progressive respiratory failure.
• Pulmonary function is usually reduced with restrictive changes and reduced diffusion capacity.
• On chest imaging, bilateral perihilar acinar-pattern consolidations with ground glass appearance is observed.

Template:WH Template:WS

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

The toxicity of crystalline silica results from the ability of crystalline silica surfaces to interact with aqueous media, to generate oxygen radicals, and to injure target pulmonary cells such as alveolar macrophages. Generation of inflammatory cytokines (eg, interleukin-1 and tumor necrosis factor beta) by target cells results in cytokine networking between inflammatory cells and resident pulmonary cells, which in turn leads to inflammation and fibrosis.

• The toxicity of crystalline silica appears to result from the ability of crystalline silica surfaces to interact with aqueous media, to generate oxygen radicals, and to injure target pulmonary cells such as alveolar macrophages.
• Generation of inflammatory cytokines (eg, interleukin-1 and tumor necrosis factor beta) by target cells results in cytokine networking between inflammatory cells and resident pulmonary cells, which in turn leads to inflammation and fibrosis.^[1]
• The alveolar macrophages are implicated as the major cell type in fibrogenesis^[2], but other immune cells, namely neutrophils^[3], T-lymphocytes, and mast cells are also involved.
• Following the interaction between effector immune cells (such as alveolar macrophage) and target tissue (such as bronchiolar/alveolar epithelial cells, fibroblasts), the progression of the disease is poorly understand.
  • Injury to the alveolar type I epithelial cell is regarded as an early event in fibrogenesis followed by hyperplasia and hypertrophy^[4] of type II epithelial cells.
  • Silica-induced cell hyperproliferation of mesenchymal cells is also a hallmark of the fibrotic lesion.
  • Proliferation may occur intially at sites of accumulation of inhaled minerals, but later at distal sites where particles or fibers are translocated over time.
  • Alternatively, mitogenic cytokines may mediate signaling events, leading to cell replication at sites physically remote from fibers.
  • The initiation of proliferation in epithelial cells and fibroblasts by silica may occur following the upregulation of the early response proto-oncogenes C-FOS, C-JUN, and C-MYC.^[5]
  • Increased expression of early response genes and protein products is also linked to the development of apoptosis^[6][7]

• Lower intensity exposures to silica evoke reversible inflammatory changes characterized by focal aggregations of mineral-laden alveolar macrophages.^[8]
• In contrast, higher exposures elicit intense and protracted inflammatory changes, cell proliferation in various compartments of the lung, and excessive deposition of collagen and other extracellular matrix components by mesenchymal cells.

Template:WikiDoc Sources

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

Silicosis is caused by the inhalation of crystalline silica, including quartz, cristobalite, and trimidite.

• 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.^[1]

• Silica (silicon dioxide) is the most abundant mineral on earth. Silica exists in crystalline and amorphous forms.
• Quartz is the most abundant form of crystalline silica. It is a major component of rocks including granite, slate, and sandstone.
  • Granite contains approximately 30% free silica
  • Slate contains approximately about 40%
  • Sandstone is almost pure silica^[2]
• In contrast, the amorphous forms, including vitreous silica and diatomite (formed from skeletons of prehistoric marine organisms), are relatively less toxic following inhalation than other forms of silica.
• Cristobalite and tridymite occur naturally in lava and are formed when either quartz or amorphous silica is subjected to very high temperatures.

Template:WH Template:WS

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

• Silicosis must be differentiated from other diseases that cause pulmonary fibrosis and pulmonary nodules on imaging, such as asbestosis, coal workers pneumoconiosis, mycobacterial, fungal, and parasitic infections, and pulmonary malignancy.

• The distinction between silicosis and other occupational disease (such as asbestosis or berylliosis) is made based on history of occupational exposure.
• Both coal workers pneumoconiosis and silicosis may result in the development of pulmonary nodules (diameter range from 1 to 10 cm) that are typically located in the upper pulmonary lobes .
• Beryllium-associated lung disease may present with multiple pulmonary nodules and mimic the radiologic appearance of sarcoidosis.
• Caplan’s disease is a combination of rheumatoid arthritis and coal-worker’s pneumoconiosis that manifests with multiple pulmonary nodules.^[1]

• Multiple pulmonary nodules that are ≥1 cm in diameter are likely to be metastatic disease from a malignant solid organ primary tumor.^[2].^[3]
• Multiple pulmonary nodules that are <5 mm in diameter, juxtaposed to either the visceral pleura or an interlobar fissure, and detected incidentally, are more likely to be benign lesions, such as granulomata, scars, or intraparenchymal lymph nodes.^[4]

• Both tuberculosis and atypical mycobacterial infections can result in the development of multiple nodules, which exceed 5 mm in diameter. Overall, multiple nodules caused by mycobacterial infections are relatively rare in comparison to the other characteristic imaging manifestations of tuberculosis and atypical mycobacterial infections.^[5]

• Multiple pulmonary nodules may be due to a fungal infection, namely histoplasmosis, coccidioidomycosis, blastomycosis, or cryptococcosis.
• Invasive aspergillosis is more common among immunocompromised hosts.
• Nodules due to fungal infection tend to be 0.5 to 3 cm in diameter and do not have a predilection for a specific region of the lungs. Fungal nodules usually demonstrate eithercavitation or calcification.^[6][7]

• Humans acquire the paragonimus westermani infection by ingesting either uncooked fresh water crabs or crayfish that harbor the metacercarial stage of the parasite.
• Paragonimus westermani is a fluke that is endemic in parts of China, Korea, Japan, the Philippines, and Taiwan.
• The typical radiographic appearance of Paragonimus is the development of multiple cavities with surrounding foci of hemorrhagic consolidation most commonly located in the lower and middle lung zones. CT may also demonstrate either linear adjacent to the nodules, suggestive of parasitic burrowing tracts.^[8]

Template:WH Template:WS

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

• In the USA, it is estimated that more than one million workers are occupationally exposed to free crystalline silica dusts (more than 100 000 of these workers are sandblasters), of whom some 59,000 will eventually develop silicosis. It is reported that each year in the USA about 300 people die from it, but the exact number is not known.
• Abrasive blasting with silica sand, often used to prepare surfaces for painting, has been associated with exposures 200 times greater than the level recommended by the US National Institute for Occupational Safety and Health. This agency recommended that silica sand be prohibited as an abrasive blasting agent.

• Workers in a broad range of industries are exposed to crystalline silica. Up to 200,000 miners and 1.7 million non-mining workers in the United States have experienced significant occupational exposure to inhaled silica.^[1]

• Several epidemics of silicosis have been reported worldwide, including the United States. The worst epidemic of silicosis occurred in 1930-1931, during the construction of Gauley Bridge tunnel in West Virginia (also known as hawks nest tunnel disaster ), more than 400 of the estimated 2000 men who drilled rocks died of silicosis, and almost all the survivors developed silicosis.
• It is estimated that there were between 3600 and 7300 cases per year of silicosis in the United States between 1987 and 1996 ^[2]. During that decade, nearly 3000 deaths were attributed to silicosis in the United States [13]. The overall mortality attributable to silicosis has decreased substantially in the United States over the past 30 years, largely because of improved workplace protection ^[3],^[4]. During 1999–2013, a total of 2,065 decedents had silicosis listed as the underlying or as a contributing cause of death. The annual number of silicosis deaths declined 40% from 185 in 1999 to 111 in 2013 (p-value for trend <0.001), but the decline appears to have leveled off during 2010–2013. The lowest number of silicosis deaths (88) occurred in 2011. Higher numbers of deaths occurred in 2012 (103) and 2013 (111), but remained within the 95% confidence interval predicted by the first-order autoregressive linear regression model used to evaluate trends for 1999–2013.More recently, in 1996, silicosis was reported in 60 of 1072 workers in an automotive factory. The risk of developing the disease increased as the number of years of exposure increased. Among workers who were employed for more than 30 years, 12% developed silicosis.

• African Americans have a two to seven times higher rate of developing silicosis compared with white workers with the same dust exposure ^[5]

• No precise information regarding age is available, usually seen at an older age as the disease progress over decades of exposure. Among all silicosis deaths, 47 (2.3%) decedents were aged 15–44 years; of these, 34 (72.3%) had silicosis coded as the underlying cause of death. The annual number of silicosis deaths in persons aged 15–44 years varied and was 4, 0, and 8 in 2011, 2012, and 2013, respectively.

• Silicosis predominantly affects predominantly male workers, reflecting the occupations at risk.^[3]

• Between 1991-1995, 500,000 cases recorded in China , and annually 6000 new cases and more than 24,000 deaths reported.
• In Vietnam 9,000 cases has been diagnosed so far. They constitute 90% of all cases of occupationally compensated diseases.
• In India, young males engaged in the quarrying and subsequent work in small, poorly ventilated sheds, a prevalence of 55% was found in that group
• In Brazil, in the state of Minas Gerais alone more than 4,500 workers have been diagnosed with silicosis.The state of Rio de Janeiro banned sandblasting after workers were found to have silicosis.
• In 1988-1994 Quebec, Canada, 40 newly diagnosed workers were compensated.
• The Colombian Government estimates that 1.8 million workers in the country are at risk of developing the disease.
• 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.
• 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.^[6]

Template:WH Template:WS

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

• Occupational exposure is the most significant risk factor of silicosis. Excavations in mines, tunnels, quarries, and underground galleries, quarrying, cutting and polishing siliceous rock, and manufacturing of silicon-based products are all associated with increased risk of developing silicosis.

The risk of developing silicosis is associated with the cumulative exposure of an individual to crystalline silica.

• Accumulated silica dose = Fraction of respirable dust × % of free silica in mg/m3 × Number of years of exposure^[1]
  
  

Occupational exposure is the most significant risk factor of silicosis.

• The most common occupations that involve exposure to silicosis are shown below:

• Excavations in mines, tunnels, quarries, underground galleries
• Quarrying, cutting and polishing siliceous rock
• 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: cast shakeout, sprue removal and blast cleaning
• Milling work: polishing, filing products containing free silica
• Sandblasting^[2] and grinding
• Pottery industry
• Handling quartz conglomerates and ornamental stone
• Dental prostheses

• A few cases of non-occupational silicosis have been reported in communities at proximity to industries like quarries and sand works.
• In addition to environmental, genetic factors such as polymorphisms for TNF-α gene is associated with more severe silicosis^[3]

Template:WH Template:WS

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

Individuals with history of past or present exposure to silica are screened with chest x-ray and PPD skin test to diagnose latent tuberculosis.

Template:WH Template:WS

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

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.

• More recent findings show that exposure to silica, even without silicosis, may also predispose individuals to Tuberculosis^[1]The increased risk of both pulmonary and extra-pulmonary TB is lifelong even after the exposure ceases^[2]. The risk increases with severity of silicosis. Acute and accelerated silicosis are at increased risk compared to simple chronic. The TB rates can be extremely high in silica-exposed groups with high rates of TB and HIV in the community. In many instances, it is the chest radiograph rather than clinical features that gives the first indication of TB in the presence of silicosis.
• Aggressive treatment of active tuberculosis is indicated as high treatment failure and relapse rates were noted due to direct impairment of macrophage function by crystalline silica and poor drug penetration into silicotic lung nodules.

• Screening for latent TB and early treatment with a 9-month course of Isoniazid is recommended in people with silicosis^[3]

• Silica-exposed workers (without silicosis) may be at increased risk for fungal infections, as they are for mycobacterial infections as silica dust impairs cellular defense. Aspergillosis was the most common mycosis among persons with pneumoconiosis^[4], in which silica-impaired macrophages are incapable of targeting inhaled conidia ^[5]
• Silica-exposed workers are protected from exposure to fungi by the following measures :

• Wetting soil and bird droppings to suppress fungal-contaminated dust
• Maintaining good personal hygiene; and,
• In areas with endemic inhaled fungi, use enclosed operator cabs with high-efficiency particulate air filtration or personal respiratory protection for particulates.

• Spontaneous pneumothorax is a rare pleural complication that can develop in patients with silicosis. Usually in these cases pneumothorax is unilateral and rarely bilateral^[6] Many studies state the association of pneumothorax with the presence of bullae ^[7] and it can also be due to direct toxic injury by silica, products of inflammatory response affect the elastic fibres of the alveolar wall leading to formation of bleb ^[8]

• Many Studies are going on to understand the pathogenesis of silicosis causing lung cancer.The risk is additive if there is associated smoking^[9]. One recent study reports the LTB4 dependent inflammation promotes lung tumour growth ^[10]

• silica-induced nephropathy has been associated with both glomerular and tubular dysfunction. The hypotheses for the pathophysiology of silica’s effect on the kidney include either a direct toxic effect on the kidney or as an adjuvant to enhance an immunologic mechanism^[11]

• Silica exposure effects are not just limited to the lungs, it also has a relationship with some rheumatic diseases, such as rheumatoid arthritis (RA) , scleroderma , systemic lupus erythematosus , Wegener’s granulomatosis and polyarteritis nodosa^[12]
• The association with scleroderma and silicosis is known as Erasmus syndrome and that with rheumatoid arthritis is known as Caplan’s syndrome^[13]

• Simple silicosis may remain stable for many years and hence the prognosis is good. The prognosis of accelerated silicosis and acute silicosis is poor, and associated mycobacterial and fungal infections make the prognosis worse.
• Accelerated silicosis and acute silicosis worsens quickly and progress to death. It is not known to what extent deaths among younger workers were caused by acute or accelerated forms of silicosis.
• Complicated silicosis shows gradual worsening of symptoms; lung function deteriorates and disability increases.

Template:WH Template:WS