Updated: Dec 05, 2019
Author: Bathmapriya Balakrishnan, MBBS, BMedSc(Melb); Chief Editor: Zab Mosenifar, MD, FACP, FCCP 



Silicosis is a primary pneumoconiosis involving fibronodular lung disease caused by inhalation of silica dust.​ Quartz, the most common form of crystalline silica, is abundantly present in granite, slate, and sandstone.[1]  Although silicosis has been recognized for many centuries, its prevalence increased markedly with the introduction of mechanized mining.

The clinical picture of silicosis is variable, with three classified types.[1, 2] Acute (weeks to years of exposure) and chronic/classic forms (10-30 years after exposure), as well as accelerated silicosis (≤10 years of high-level exposure), have been recognized based on the duration of exposure to silica and on the latency of the symptoms.[1, 2] Simple silicosis is characterized by the radiographic presence of multiple nodules measuring 1-10 mm in diameter that are distributed predominantly in the superior and posterior segments of the upper lobes.[3] Complicated silicosis, also called progressive massive fibrosis (PMF), is characterized by the radiographic presence of large opacities with areas of homogeneous consolidation that mainly affect the superior and middle segments of the lungs.[4]

Complications of silicosis can cause related morbidity. As the disease progresses, airflow limitation occurs, manifested by dyspnea and cough, and results in chronic bronchitis. Eventually, cor pulmonale and respiratory failure develop. No specific therapy for silicosis cures or alters the course of the disease, thus prevention is essential.[1, 3]


Respirable silica particles (< 10 μm in diameter) are deposited within the distal airways and alveoli following inhalation. These particles are then phagocytized by macrophages. Several proinflammatory and profibrotic pathways are then activated, as follows[5] :

  1. Interleukin (IL)-1 is stimulated directly by macrophages and indirectly by toll-like receptors. This enhances the production of IL-1, tumor necrosis factor (TNF), caspase-1, and fibroblast growth factor (FGF).
  2. Modulation of the NALP3 protein inflammasomes induces regulatory T cells to express cytotoxic T-lymphocyte antigen 4, IL-10, and transforming growth factor-beta (TGF-β). This process occurs independently of lymphocyte interaction.

Subsequent exposure and ingestion of silica by alveolar macrophages leads to cell necrosis, autophagy, and the release of nondegraded intracellular silica. Thus, more macrophages are attracted, causing further release of cytotoxic oxidants and proteases, inflammatory cytokines, and arachidonic metabolites. This vicious cycle self-perpetuates, causing progressive alveolar inflammation and fibrosis.[5]

Excess collagen and fibronectin are constantly produced due to activation and recruitment of type II pneumocytes and fibroblast.[6]  Fibrotic changes are seen alongside silicotic nodules, causing distortion of the lung parenchyma and reduction in gas-exchange surfaces.

Complications and mortality related to silica exposure is dose-dependent.[5]  The current exposure limit has been set at 0.05 mg/m3, but even at these levels, the risk of developing simple silicosis over a life-time of work in the environment is 20%-40%.[7]  More recently, silicosis outbreaks have been associated with certain occupations; these include artificial stone benchtop fabricators, sandblasters and denim jean sandblasters, jewellery polishers, slatepencil stonemasons, metal grinders, agate mill workers, dental suppliers, electric cable manufacturers, and stone crushers.[8]  The incidence of silicosis (50%-60%) and mortality (10%-100%) for these occupations far outnumber the mortality (6 per 1000 workers) for chronic silicosis within the silica mining industry. Excess silica exposures have also been noted in the hydraulic fracturing industry and construction.[9]

Acute and high-intensity silica exposure can cause type II pneumocyte hyperthrophy and hyperplasia, such that excessive amounts of proteinaceous surfactant is produced within the alveoli. This leads to the histopathologic finding of silicoproteinosis.[5]  The effect of high-intensity brief exposure is much less understood; however, there are theories of the "plume effect" whereby silica exposure to more than 2 mg/m3 has an effect triple that of a cumulative equivalent of lower level, longer term exposure.[5]

Progressive massive fibrosis (PMF) occurs in 18%-37% of workers over an average of 5 years of exposure.[10]  Smoking and continued silica exposures play a significant role in the radiologic progression of silicosis, from simple to chronic, as well as PMF.[11]

Silicon and oxygen atoms are organized in a fixed pattern in crystalline silica, as opposed to the random orientation of atoms in amorphous silica. Examples of crystalline silica include include quartz, tridymite, and cristobalite. Opal, tripolite, silica-rich fiberglass, fume silica, mineral wool, and silica glass are examples of amorphous silica. Naturally occurring substances have varying concentration of silica. Sand, for example, is composed of 67% silica,[9] whereas granite has 25% to 40% silica. Crystalline silica is thought to be the most toxic form. Experimental data suggest the fibrogenic potential of silica is in the order of tridymite > cristobalite > quartz.[12]

The structure of crystalline silica produces opposite electric charges on opposite sides of the physical structure when pressure is applied onto the crystal. This property is called peizoelectric, which causes the formation of reactive oxygen species when exposed to airways and alveoli.[9]  Silica-induced oxidative stress stimulates specific transcription factors through interaction with toll-like receptors on alveolar macrophages, mediated through nuclear factor kappa-B (NF-κB) and activator protein (AP)-1, which further increases cytokine expression, inducing inflammation and fibrosis.[5]

Examples of occupations related to silica exposure include the following:

  • Mining or tunneling

  • Quarrying[13]

  • Drilling, chipping, or grinding

  • Crushing stone

  • Sandblasting[14]

  • Grinding or polishing in pottery or stone work[15]

  • Foundry work

  • Cement manufacturing

  • Glass manufacturing

  • Masonry

  • Blast furnace work

  • Coal mining[16]

  • Construction[17]

  • Cutting or manufacturing heat-resistant bricks

  • Dental laboratory work[18]


Accurate assessment of the frequency of silicosis and other pneumoconioses in the United States and in other countries is challenging for many reasons. The number of people who are at risk of silicosis and who are affected by the disease is unknown because of poor record-keeping practices, time delays from exposure to diagnosis, and poor understanding of the relationship between exposure and disease. Over 2 million workers have experienced an occupational exposure to silica,[2, 3]  with male workers predominantly affected, reflecting the occupations at risk.

Several epidemics of silicosis have been reported from a number of nations, including the United States. The worst epidemic of silicosis occurred in 1930-1931, during the construction of the Gauley Bridge tunnel in West Virginia; more than 400 of the estimated 2000 men who drilled rocks died of silicosis, and almost all the survivors developed silicosis.[9]  More recently, in 1996, silicosis was reported in 60 of 1072 workers in an automotive factory.[19] 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.[19]   

US data show a lessening of the rate of decline in deaths from silicosis after 1995, with an increased proportion of deaths in the age group younger than 45 years. These data indicate that intense overexposures to respirable crystalline silica continue to occur despite the existence of legally enforceable limits. A study of South African gold miners after they had left the mining industry documented a 25% cumulative risk of silicosis after 28 years of mining at a 0.33 mg/m3 silica exposure level.[20]  A death certificate study of South Dakota gold miners predicted that a 45-year cumulative exposure from ages 20 to 65 years at 0.09 mg/m3 would result in a 47% lifetime risk of silicosis.[20]  A study of Hong Kong granite quarriers indicated that cumulative silica exposure between 1 and 5 mg/m3 per year led to radiologic silicosis in 32% of men aged 50 years and older.[20]  In a study of Colorado miners who had left the hard rock mining industry, estimated exposures using silica measurements (in contrast to dust measurements) were associated with even higher risks of radiologic silicosis.[20]  In China, 23 million workers are exposed to silica, whereas in the United States, the National Institute for Occupational Safety and Health (NIOSH) has estimated that at least 1.7 million workers are exposed to silica, with between 1500 and 2360 of whom will develop silicosis each year.[12]


Previous studies of silicosis have shown that prognosis is dependent on various factors, including age at diagnosis, smoking history, clinical progression of disease, genetic polymorphisms, comorbid diseases, and conglomerate nodular disease on radiography.[5]  [21]

Genetic polymorphisms of tumor necrosis factor (TNF)-α2 and rs2076304 in the desmoplakin gene have also been associated with an increased risk of mortality.[22]

Patients who had profound silica exposure over a relatively shorter time course may develop accelerated silicosis. This entity is typically related to an exposure history of 5 to 15 years,[23]  usually 10 years or less.[2]  Disease progression may continue despite cessation of silica exposure. Autoimmune diseases are associated with accelerated silicosis.[9]

Patients with chronic silicosis may be asymptomatic despite potentially decades of exposure to silica dust.[24]  A subset of these patients, however, may develop progressive massive fibrosis (PMF).[5]  Retractions of PMF may cause emphysematous changes in the basilar lung regions. These patients are prone to develop hypoxic respiratory failure, mycobacterial infections, and pneumothoraces. Cause of death is invariably respiratory failure.[5]


Mycobacterium tuberculosis (TB) and non-TB mycobacterial infections

There is an 8- to 20-fold increased risk of mycobacterial infections in patients with silicosis.[5]  Dysregulated cell death pathways may cause macrophages exposed to silica to have an increased expression of tumor necrosis factor-alpha (TNFα), interleukin (IL)-1b, and caspase-9 expression. Following infection with mycobacteria, these macrophages favor necrosis over apoptosis, thus leading to the release of viable mycobacteria from necrotic cells and the progression of latent to active disease.[25]

Autoimmune disease

Epidemiologic evidence supports the increased risk between occupational exposure to crystalline silica dust and the development of autoimmune disorders such as systemic lupus erythematosus (SLE), systemic sclerosis, and rheumatoid arthritis (RA).[5]  The prevalence of SLE in males with high levels of silica exposure is 10 times higher than that of the general population.[26]  Rheumatoid arthritis (RA) is more common in men with silicosis than in the general population, most likely related to the effect of silica on the immune system. Caplan syndrome, originally described in coal workers, is characterized by pulmonary nodules with cavitation in silica workers with seropositive RA.[27]  It is thought that the presence of increased levels of autoantibodies, immune complexes, and hypergammaglobulinemia in silica-exposed workers may lead to this predisposition.[25]  Silica dust causes exposed macrophages to release antigenic polysaccharides that activate the reticuloendothelial system.[5]  Autoimmune disorders may accompany accelerated silicosis. Thus, it is important to screen affected inviduals, as treatment and prognosis may be altered.[5]

Chronic obstructive pulmonary disease (COPD)

Previous studies have noted that exposure to silica dust can lead to the development of chronic bronchitis, emphysema, and/or small airway diseases even without evidence of radiologically confirmed silicosis.[28]  Proposed mechanisms include the following:

  • Silica particles cause the release of mediators that potentiate the production of oxidants, cytokines, chemokines, and elastase, leading to airway inflammation and emphysema.
  • Silica particles cause epithelial cell injury that facilitates its penetration through the walls of small airways, leading to localized fibrosis.


Controversy regarding the carcinogenicity of silica[29, 30] is due varying methods of available studies, and the potential for bias due to confounders such as cigarette smoking, as well as exposure to chemicals such as radon, arsenic, or polycyclicaromatic hydrocarbons. According to the American College of Occupational and Environmental Medicine (ACOEM), the risk for lung cancer in silicotic persons tend to be greatest in workers with silicosis who smoke, but the cancer risk to nonsmoking silica-exposed workers without silicosis is less clear due to disparate results in available research.[31] Silica has been classified as a Group 1 human carcinogen since 1997 by the International Agency for Reasearch on Cancer (IARC).[32, 33]

Pulmonary alveolar proteinosis

Pulmonary alveolar proteinosis may occur following high level exposure of silica.[5]  Microscopic examination of bronchoalveolar lavage reveals positive periodic acid-Schiff stain (PAS), histologically known as silicoproteinosis.[9]

Chronic kidney disease (CKD)

Renal diseases such as nephrotic syndrome, glomerular nephritis, and end-stage renal disease (ESRD) may occur in silica-exposed individuals in the absence of overt pulmonary disease.[9]  There is an increased incidence of ESRD among workers in the manufacturing of industrial sand, granite, and ceramic.[34]

Patient Education

Since 1988, the National Institute for Occupational Safety and Health (NIOSH) has developed and continues to provide workplace surveillance and intervention programs.[8]  The Occupational Safety and Health Administration (OSHA) regulates workplace limits of exposure, termed permissible exposure limits (PEL), recommended by NIOSH. As of 2018, the new respirable silica standard PEL has been halved, to 50 mg/m3 from 100 mg/m3. Medical monitoring of silica-exposed workers is mandatory.

As there is a lack of effective therapy for silicosis, the mainstay of treatment remains preventative measures; for example, identification of high-risk occupations, enforced regulation of exposure standards, and health screening programs.

For patient education resources, please visit the CHEST Foundation[35]  and the American Lung Association.[2]




In obtaining a detailed occupational history for suspected silicosis and other pneumoconioses, note chronologically the periods of exposure, the type of work exposure, any respiratory protective devices used, and whether other people working in the same environment have any similar symptoms or disease.

Silicosis is typically divided into three distinct forms characterized by the duration of occupational exposure.[1, 2, 8]  

Acute silicosis

Acute silicosis, also known as silicopronteinosis, is typically associated with high-intensity exposure. Patients present within weeks up to 5 years from the initial insult. Specific occupations have been associated with acute silicosis, including silica flour processing, tombstone sandblasting, and surface drilling. The dose of exposure required to develop acute silicosis is poorly studied but thought to be in the order of 1-10 mg/m3/year.[36]

Presenting complaints include dyspnea, fatigue, weight loss, fever, and pleuritic pain. Clinical progression is often dramatic, with rapid progression to respiratory failure due to a decline in gas exchange and pulmonary function.

Accelarated silicosis

Accelerated silicosis develops within 10 years of moderate to high-level exposure. Disease progression may occur despite removal of the silica exposure. Accelerated silicosis is associated with autoimmune disorders.[9]

Chronic silicosis

Chronic silicosis occurs after 10 years or more following low- to moderate-level exposure. Patients either present with simple (nodular) silicosis or progressive massive fibrosis (PMF). Patients with simple silicosis can be asymptomatic, whereas those with PMF may have symptoms and signs of chronic respiratory failure. There is typically a long latency period for simple silicosis, in which most symptoms manifest after leaving the employment where exposure occurred.[12]

Simple silicosis is characterized radiologically by the presence of nodules (size < 1 cm), usually predominant in the upper lobes. Some case series report up to 70% of patients having symptoms of dyspnea, chronic cough, and sputum production.[37]

Silicotic nodules may coalesce to form conglomerate fibrotic masses (>1 cm), leading to the development of PMF. Central cavitation may occur, leading to complications like mycobacterial infections.

Mediastinal and hilar lymphadenopathy may be seen in up to 75% of patients with silicosis. Fibrosis and lung scarring lead to distortion of lung architecture and peribronchial vessels, resulting in pneumothoraces, pulmonary hypertension, and cor pulmonale. Pleural thickening may also be seen.[38]

Silicotic patients also develop airway diseases like asthma and chronic obstructive airway disease (COPD). Symptoms such as wheezing, exertional dyspnea and cough predominate.

Physical Examination

The symptoms and signs of chronic silicosis may be minimal. The main symptom is breathlessness, but in chronic silicosis, in the absence of other respiratory disease, even this symptom may be absent. In a small French observational study, the finger clubbing was noted in three patients and two patients had rales and crepitations on auscultation.[39] Four patients also had general debility with weight loss. Note that clubbing is typically not a feature associated with silicosis and should raise concern for lung cancer.[39]



Diagnostic Considerations

Diseases that cause diffuse parenchymal lung disease, including chronic hypersensitivity pneumonitis, idiopathic pulmonary fibrosis (IPF), and sarcoidosis, are among some of the differential diagnosis for silicosis.[40]  Furthermore, in a Korean study, patients diagnosed with IPF with occupational dust exposure had an earlier onset of disease and a worse prognosis.[41]  Obtain a good occupational exposure history, especially as there is a long latency period between symptom development and silica exposure.

Differential Diagnoses



Approach Considerations

The diagnosis of silicosis is based on a history of exposure, chest radiographic appearance consistent with silicosis, and an absence of other diagnoses that simulate the radiographic abnormalities of silicosis. Clinical manifestations, symptoms, and physical examination findings provide evidence to support the diagnosis.

Laboratory Studies

Although various serologic abnormalities have been noted in patients with silicosis, they are not diagnostic of the disease, and tests to detect these abnormalities are not indicated routinely. Humoral immune system abnormalities observed in silicosis include an increased incidence and titer of rheumatoid factor, antinuclear antibodies, and immune complexes. No consistent abnormality is noted in the cell-mediated immune system.

Some of the markers being considered for utilization in the evaluation of silicosis are discussed below.

Serum coppper (Cu)

The primary pathologic changes in silicosis are fibrosis in the lungs. Studies conducted on Cu levels in blood serum indicate that Cu plays a very important role in the progress of lung fibrosis, and it has a direct relationship with serum Cu levels. Ren and Jiang confirmed that an increase in ceruloplasmin levels in the silicosis group is one of the factors for elevated Cu.[42]  Each ceruloplasmin molecule contains eight Cu atoms, and the Cu level in blood serum is maintained by ceruloplasmin. The Cu increase may therefore be explained by an increase in the ceruloplasmin level in blood serum. Thus, fibrosis of lungs due to silicosis is accompanied by increases in ceruloplasmin as well as Cu levels in blood serum. Tiwari et a conducted an important study involving 134 workers in quartz stone crushing units to assess serum Cu activity and concluded the following[43] :

  • There was no significant difference among different categories of workers when mean serum Cu levels were compared according to duration of exposure.
  • When workers were categorized according to the presence or absence of respiratory diseases, those having respiratory diseases and exposed for at least 1 year had significantly higher levels of serum Cu compared to those with a similar duration of exposure but who were disease free.
  • Smokers had significantly higher serum Cu values relative to nonsmokers.
  • When pulmonary function tests were categorized according to respiratory morbidity, serum Cu levels were higher among those with respiratory disorders compared to those free from disease.

Clara cell protein (CC16)

CC16 is a 16-kDa protein secreted by nonciliated cells of the tracheobronchial tree. It has been proposed as a peripheral marker of respiratory epithelial injury. Broeckaert and Bernard[44]  and Bernard et al[45]  found that Clara cells are one of the most multifunctional and heterogeneous cell types in the mammalian lung, with their main function being protection of the respiratory tract. The highest concentrations of CC16 are in sputum and bronchoalveolar lavage fluid, reflecting intense secretion of the protein in the airways.[45]  The protein also occurs, but in smaller concentrations, in other fluids such as urine, amniotic fluid, and semen. 

In a study that measured the concentration of CC16 in the serum of 86 miners exposed to silica-rich dust in a quarry (average exposure: 15.2 months) and 86 control subjects matched for age, body mass index, and smoking status, no appreciable difference could be detected between exposed and control workers with regard to respiratory symptoms, chest radiograph findings, or lung function tests.[45] However, the concentration of CC16 in serum decreased in silica-exposed workers (geometric mean 12.3 μg/L) compared to control subjects (16.3 μg/L). The decrease was found both in lifelong nonsmokers (14.7 vs 21.9) and current smokers (11.3 vs 14.5). Tobacco smoking caused a decrease in serum CC16 that was further lowered after silica exposure.[45] These serum concentrations of CC16 probably reflect the very early toxic effects of silica particles on the respiratory epithelium. This reinforces the view that serum CC16 is a sensitive marker, which might improve our ability to detect exposure to chemicals potentially harmful to the respiratory tract.

Heme oxygenase-1 (HO-1)

HO-1, a rate-limiting enzyme in heme catabolism, has antioxidative, anti-apoptotic and anti-inflammatory activities. Studies indicate that crystalline silica induces the production of reactive oxygen species (ROS), which play a key role in the development of silicosis.

HO-1 is present in the lungs of humans and mice with silicosis, especially at sites of silica particle deposition. In mice, silica exposure is associated with acute leukocyte infiltration, leading to the development of silicotic lung lesions. Inflammation has been shown to be suppressed by treatment with hemin, an inducer of HO-1, and enhanced by zinc protoporphyrin, an inhibitor of HO-1. Pulmonary HO-1 expression is increased in silicosis.

HO-1 suppresses ROS activity and subsequent pathologic changes, thereby attenuating disease progression. A study by Sato et al showed that HO-1 is persistently expressed in lung lesions of patients with silicosis.[46]  This appears to reflect ROS induction by silica, leading to elevation in serum HO-1 levels. The increased HO-1 can protect the host by suppressing silica-induced ROS activity. Thus, regulation of HO-1 may represent a novel strategy for treatment of silicosis.

A major limitation of all these studies is that they were conducted in a lateral dimension over a small time period and within a group population, which gives only statistical and probabilistic results with respect to an individual subject. Therefore, a more conclusive finding may be obtained when the observations from these biomarkers are monitored in a cohort or for a specific subject over a long period and the data are interpreted with a time scale. Although such studies may take longer (in years) to provide any meaningful changes in the characteristics' values, they will be more conclusive and have a more definite prognostic value with respect to the health status of the subjects under monitoring.

Imaging Studies

Over the last seven decades the International Labour Organization (ILO) has published a series of guidelines on how to classify chest radiographs of persons with pneumoconioses. The goals have been to standardize classification methods and facilitate international comparisons of data on pneumoconioses, epidemiologic investigations, and research reports. The 2011 ILO guidelines accommodate the use of digital images, and a set of standards for digital images is available.[47] Apart from improving consistency in the reading of parenchymal disease, which is notoriously subject to reader variability, these guidelines enable the clinician to set an individual case in the context of the available epidemiologic information.

Small opacities in the parenchyma are classified by shape and size: p, q, or r for rounded opacities (diameter, < 1.5 mm, 1.5 to 3 mm, or >3 mm, respectively) and s, t, or u for irregular opacities (width, < 1.5 mm, 1.5 to 3 mm, or >3 mm, respectively). Profusion category (or concentration) is read on a 12-point scale (0/−, 0/0, 0/1, up to 3/2, 3/3, and 3/+) in comparison with the standard radiographs. Large opacities are classified as category A (for ≥1 such opacities with a diameter > 1 cm but not exceeding a combined diameter of 5 cm), category B (≥1 opacities > 5 cm in diameter and whose combined area does not exceed one upper zone), and category C (>B). Provision is made to grade pleural thickening for width ( a ≤5 mm, b >5 mm but < 10 mm, and c ≥ 10 mm) and extent (1 = up to one quarter, 2 = one quarter to one half, and 3 = over one half of the lateral chest wall). The extent of pleural calcification is also graded, and there are provisions for comment on other features.

Quality control in terms of radiographic technique and reading procedures using the ILO classification and reader training is incorporated. This involves training seminars for physicians who may qualify as “A” readers (ie, attended the seminars) or “B” readers, who passed a comprehensive examination on the basis of 120 radiographs read into the ILO classification.

Uncomplicated silicosis is characterized by the presence of small rounded opacities on the chest radiograph as graded in the ILO classification. In general, there is a good correlation among dust exposure, the amount of dust in the lungs, the lung pathology, and the chest radiograph. However, occasionally, even in advanced silicosis determined by histology, no chest radiographic changes may be apparent.

Silicotic nodules are usually symmetrically distributed and tend to appear first in the upper zones, later, although not invariably, involving other zones. Enlargement of the hilar nodes may precede the development of the parenchymal lesions. Eggshell calcification, when present, is strongly suggestive, although not pathognomonic, of silicosis.

Progressive massive fibrosis is characterized by the coalescence of small rounded opacities to form larger lesions; they are graded on the ILO scale according to size and extent (categories A to C). Computed tomography (CT) assessment is superior to the chest radiograph in not only assessing the presence and extent of silicotic nodulation but also in revealing early conglomeration. With time, the mass lesions tend to contract, usually to the upper lobes, leaving hypertranslucent zones at their margins and often at the lung bases. In this process, small rounded opacities, previously evident, may disappear, resulting in a picture that must be distinguished from tuberculosis.

Acute silicosis is characterized radiologically by diffuse changes that usually display an air space and interstitial pattern rather than the usual nodularity.

Other Tests

The lung function profile is determined by the extent of the silicosis, as well as the associated or concomitant airway and vascular changes. In chronic silicosis, spirometric tests (forced expiratory volume in 1 second [FEV1 ], FEV1 / forced vital capacity [FVC]) usually reflect airflow limitation. Reduction in the diffusing capacity of carbon monoxide (DLCO) is generally apparent in more advanced chronic silicosis and reflects associated emphysema. In the accelerated and acute forms of silicosis, functional changes are more marked and progression is more rapid. In acute silicosis, lung function shows a restrictive defect and impairment of gas exchange, which leads to respiratory failure.

Either interferon-gamma release assays (IGRA) or the Mantoux tuberculin skin test (TST) should be used to test for latent tuberculosis infection (LTBI). In individuals who have a positive skin test result, sputum samples should be examined for acid-fast bacilli (AFB) by microscopy and cultured for AFB to identify active disease.



Silicosis is diagnosed based on a history of exposure and the characteristic radiographic changes. Problems arise when the history of exposure is remote, forgotten, or missed, or it has taken place outside a recognized occupation.  

Although bronchoscopy is not required for the diagnosis of silicosis, it is useful to exclude other conditions. Bronchoalveolar lavage (BAL) fluid may demonstrate lymphocytosis (20%, compared to 6% in healthy controls) or neutrophilia (10%, compared to 0% in healthy controls) in acute silicosis; however, these findings are nonspecific and are noted in other radiologically similar diseases, such as sarcoidosis and pulmonary fibrosis.[5]

BAL from patients with acute silicoproteinosis has classically been reported to be a milky effluent with positive periodic-acid Schiff stain; however, cases from more recent outbreaks rarely describe this finding.[5]

Histologic Findings

Examination of lung tissue is seldom warranted in cases of silicosis. Lung biopsy is typically pursued to distinguish progressive massive fibrosis or other atypical features from lung cancer and tuberculosis. 

The characteristic histopathologic finding is the silicotic nodule mostly located near the respiratory bronchiole. The nodule is composed of refractile particles of silica surrounded by whorled collagen in concentric layers, with macrophages, lymphocytes, and fibroblasts in the periphery. Emphysematous blebs surround the silicotic nodule, especially in the subpleural area. Birefringent crystals of silica in the center of a silicotic nodule may be identified by polarized light microscopy. For definitive identification, scanning electron microscopy combined with x-ray spectroscopy may be needed.

Acute silicosis is seldom seen. The histology is similar to pulmonary alveolar proteinosis, in which the alveoli are filled with proteinaceous material that stains with periodic acid-Schiff stain.



Approach Considerations

Consulting a pulmonologist is appropriate for the evaluation of lung nodules, assessment of pulmonary function, and evaluation of disability, as well as treatment of mycobacterial disease and complications of advanced silicosis.

Treatment for silicosis-associated conditions (eg, mycobacterial infection, chronic obstructive pulmonary disease, lung cancer, autoimmune disorders, and chronic kidney disease) are principally similar to that of patients without silicosis. Please review resources pertinent to each condition.

Medical Care

Treatment strategies targeting the inflammatory pathway of silicosis have been investigated, however, consistently effective therapies yet to be developed,[5, 9]  and no cure currently exists.[1, 3]

Whole-lung lavage has previously been used for silicoproteinosis. Although the presence of dust particles, macrophages, and cytokines on bronchoalveolar lavage analyses decrease with whole-lung lavage, long-term outcomes, including mortality and pulmonary function parameters, have not demonstrated sustained improvement.[48]

Immunosuppressive therapies have yielded varying results. A study using corticosteroids reported a 300-mL improvement in forced vital capacity (FVC); however, there was no sustained improvement or reduction in mortality.[49]  Improvement in symptoms of dyspnea and cough also occurred, although the benefits were related to longer duration of silica exposure.[49]  Animal model studies using Infliximab have shown a reduction in inflammation and fibrosis histopathologically; however, these findings have yet to be translated into human studies.[50]

Inhaled aluminum citrate powder, which theoretically coats silica particles to reduce its solubility, have been studied. Controlled studies demonstrated symptomatic improvement; however, there was no change in lung function or mortality.[51]  Harmful side effects associated with aluminum powder use potentially outweight the benefits of treatment. 

Polyvinylpyridine-N-oxide (PVPNO) has been shown to decrease the potential for silica toxicity in animal models. It coats the surface of silica particles and decreases their potential for generating reactive oxygen species, thus limiting DNA damage.[52]  However, use of PVPNO is limited by liver and renal toxicity demonstrated in animal studies.

Nintedanib, an antifibrotic therapy used in idiopathic pulmonary fibrosis (IPF), have been studied in animal models, but it has yet to be studied in human trials.[53]  The Nintedanib in Progressive Pneumoconiosis Study (NiPPS), a prospective clinical pilot study evaluating occupational progressive pneumoconiosis (silicosis, coal pneumoconiosis, and asbestosis) with nintedanib 150 mg twice daily for 3 years, has not yet begun recruiting but has an expected start date of February 2020.

Cell-based therapy, including bone marrow-derived mononuclear cells[54] and mesenchymal cell transplantation,[55]  are currently undergoing trials in humans.

Surgical Care

Lung transplantation remains the only treatment option for end-stage silicosis. However, based on available data, patients with silicosis who underwent lung transplantation (4.9%) showed a nonstatistically significant survival advantage (hazard ratio: 0.6) compared to those undergoing lthe procedure for idiopathic pulmonary fibrosis (IPF).[56]


Primary prevention of silicosis through exposure control is important, because no effective medical treatment exists for this disease, which continues to progress even after a person is removed from further exposure. To achieve this, a sustained effort must be made to increase awareness of silicosis. Deaths from silicosis in younger subjects in the United States have been reported after exposure in the construction and manufacturing sectors, with none from mining.[57] Deaths of young people sandblasting denim are a reminder that there is often a lack of awareness of the hazards of silica outside the traditional occupations associated with silicosis.

Recommendations by the National Institute for Occupational Safety and Health (NIOSH) to reduce exposures to respirable crystalline silica in the workplace and to prevent silicosis and deaths in construction workers are outlined below.[58]

Recognize when silica dust may be generated and plan ahead to eliminate or control the dust at the source. Awareness and planning are keys to prevention of silicosis.

  • Use the dust collection systems available for many types of dust-generating equipment. When purchasing equipment, look for dust controls. Use local exhaust ventilation to prevent dust from being released into the air. Always use the dust control system, and keep it well maintained. Do not use equipment if the dust control system is not working properly.
  • During rock drilling, use water through the drill stem to reduce the amount of dust in the air, or use a drill with a dust collection system. Use drills that have a positive-pressure cab with air conditioning and filtered air supply to isolate the driller from the dust.
  • When sawing concrete or masonry, use saws that provide water to the blade.
  • Use good work practices to minimize exposures and to prevent nearby workers from being exposed. Eg, Remove dust from equipment with a water hose rather than with compressed air. Use vacuums with high-efficiency particulate air (HEPA) filters, or use wet sweeping instead of dry sweeping.
  • Use containment methods such as blast-cleaning machines and cabinets to prevent dust from being released into the air.

Do not use silica sand or other substances containing more than 1% crystalline silica as abrasive blasting materials. Substitute with less hazardous materials.

Practice good personal hygiene to avoid unnecessary exposure to other worksite contaminants, such as lead.

Take the following steps to assure that dusty clothes do not contaminate cars, homes, or worksites outside the dusty area:

  • Change into disposable or washable work clothes at the worksite.
  • Shower and change into clean clothes before leaving the worksite. 
  • Do not eat, drink, or use tobacco products in dusty areas.
  • Wash hands and face before eating, drinking, or smoking outside dusty areas.
  • Park cars where they will not be contaminated with silica and other substances such as lead.

Conduct air monitoring to measure worker exposures and ensure that controls are providing adequate protection for workers.

Use adequate respiratory protection when source controls cannot keep silica exposures below the NIOSH recommended exposure limitis (REL).

Do not use respirators as the primary means of preventing or minimizing exposures to airborne contaminants. Instead, use effective source controls such as substitution, automation, enclosed systems, local exhaust ventilation, wet methods, and good work practices. Such measures should be the primary means of protecting workers.

Respirators and respiratory protection program

The Occupational Safety & Health Administration (OSHA) and NIOSH offer general guidance on respiratory protection as well as provide information on standards for respiratory protection.[59]  Specific respiratory protection recommendations are summarized below.

When respirators are used, the employer must establish a comprehensive respiratory protection program, as outlined in the NIOSH Guide to Industrial Respiratory Protection [NIOSH 1987a][60]  and as required in the OSHA respiratory protection standard [29 CFR 1910.134 and 1926.103].[59]  Important elements of this standard are: 

  • Periodic environmental monitoring
  • Regular training of personnel
  • Selection of proper NIOSH-approved respirators
  • Evaluation of the worker’s ability to perform the work while wearing a respirator
  • Respirator fit testing
  • Maintenance, inspection, cleaning, and storage of respiratory protection equipment

The respiratory protection program should be evaluated regularly by the employer.

  • Provide periodic medical examinations for all workers who may be exposed to respirable crystalline silica.
  • Post warning signs to mark the boundaries of work areas contaminated with respirable crystalline silica.
  • Provide workers with training that includes information about health effects, work practices, and protective equipment for respirable crystalline silica.
  • Report all cases of silicosis to State health departments and OSHA.

Long-Term Monitoring

Medical monitoring

The National Institute for Occupational Safety and Health (NIOSH) indicates medical examinations should be available to all workers who may be exposed to respirable crystalline silica.[58] However, examinations should always supplement effective dust monitoring and controls—never substitute for them. Such examinations should occur before job placement or upon entering a trade, and at least every 3 years thereafter. Examinations should include at least the following items[58] :

  • A medical and occupational history to collect data on crystalline silica exposure and signs and symptoms of respiratory disease
  • A chest radiograph classified according to the 2011 International Labour Organization (ILO) International Classification of Radiographs of Pneumoconioses [47]
  • Spirometry
  • An annual evaluation for tuberculosis


Workers should receive safety training and education that includes the following[58] :

  • Information about the potential health effects of exposure to respirable crystalline silica.
  • Material safety data sheets for silica, masonry products, alternative abrasives, and other hazardous materials.
  • Instruction about the purpose and set-up of regulated areas marking the boundaries of work areas containing crystalline silica.
  • Information about safe handling, labeling, and storage of toxic materials.
  • Discussion about the importance of substitution, engineering controls, work practices, and personal hygiene in reducing crystalline silica exposure.
  • Instruction about the use and care of appropriate protective equipment (including protective clothing and respiratory protection).