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