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Continuing Education Activity

Silica is the most plentiful mineral on earth and is the primary constituent in most rocks. The respirable form of silica is small enough to reach the terminal bronchioles and alveoli of the respiratory system. Typical immune mechanisms cannot clear these particles from the lung, initiating a pathologic cycle of inflammation and parenchymal damage that ultimately leads to silicosis. Silicosis is the world's most prevalent occupational lung disease and is characterized by irreversible, progressive pulmonary fibrosis leading to restrictive lung disease. Silicosis is a preventable disease with significant morbidity and mortality that has no cure. Education on prevention, screening, timely diagnosis, avoidance of exacerbating factors, and treatment of complications is imperative. This activity reviews the etiology, epidemiology, pathogenesis, pathophysiology, clinical evaluation, and management of silicosis and highlights the role of the interprofessional team in caring for patients with this occupational pneumoconiosis.


  • Identify patients at risk of developing silicosis based on their exposure history.
  • Differentiate between the major forms of silicosis by clinical presentation and radiographic findings.
  • Counsel patients with silicosis about lifestyle changes to reduce their risk of associated complications.
  • Develop and employ interprofessional team strategies to improve outcomes for patients with silicosis.


Silica, or silicon dioxide (SiO2), comprises a silicon atom and 2 oxygen atoms.[1] Silica is the most plentiful mineral on Earth,  distributed throughout the Earth's crust as silicate minerals. Silica is the main constituent of more than 95% of rocks and stones.[2] 

Occupational exposure to silica dust is one of the oldest known forms of lung disease, first documented by Hippocrates in 400 BC describing breathing disorders in metal diggers. In the 1600s, van Diemerbrock noted the harmful effects of inhaling granite dust. Ramazzini provided a detailed description in the 1700s of the lung scarring observed in stone and coal workers. During the industrial revolution, advancing mechanization of production techniques increased workers' risk of contact with higher concentrations of silica dust. In 1832, it was noted that sandstone workers had significantly shorter life expectancies compared to limestone and brick workers, often dying by the age of 40. The Hawks Nest Tunnel disaster of the 1930s was one of the worst industrial disasters in American history. To create a large tunnel that would redirect a river to power a hydroelectric plant in West Virginia, workers drilled through rock in a confined space without ventilation or respiratory protection. Many developed disabling lung damage within a few months due to exposure to high silica concentrations.[2]

The burden of silica-associated disease remains high, and silicosis is currently the world's most prevalent chronic occupational disease.[2] Many industries place workers at risk of inhaling silica-containing dust, including abrasive blasting, denim jean manufacture, artificial stone production, brickwork, pottery, porcelain work, tunneling, mining, and structural construction and demolition.[3]

Silica exists in amorphous and crystalline forms that have unique physiochemical properties.[4] Amorphic silica is found in biological matter such as plants, sponges, algae, fungi, and bacteria and nonvegetative matter such as volcanic glass, colloidal sols, and powders.[2][5] Amorphic silica is not considered toxic.[5] Crystalline silica is a mineral commonly known as quartz, present in granite and sandstone.[1] In contrast to the random orientation of molecules in amorphous silica, crystalline silica exhibits a fixed, repeating, polymerized silicon-oxygen tetrahedral framework. Crystalline silica exists in various forms, including α-quartz, β-quartz, α-tridymite, β-tridymite, α-cristobalite, β-cristobalite, keatite, coesite, stishovite, and moganite. α-Quartz is the most common crystalline silica and the most biologically toxic form.[2]

Particles of crystalline silica are considered biologically active when small enough in diameter to reach the distal bronchioles and alveoli of the lungs. Such particles are denoted as "respirable crystalline silica" (RCS) and are less than 5 μm in diameter.[2][3] RCS is released into the atmosphere by crushing, grinding, or cutting silica-containing matter.[4] RCS can easily go unnoticed as it is odorless, colorless, and nonirritating. In 1997, the International Agency for Research on Cancer labeled RCS as a human carcinogen.[2]

Silica also exists as "silica nanoparticles" (SiNPs), particles of nanoform silicon dioxide that measure less than 100 nm in diameter. SiNPs have physiochemical characteristics distinct from the bulk form of silica.[6] SiNPs are colloidal metal oxides comprising a siloxane (Si-O-Si-O) core with abundant silanol (Si-OH) surface groups. SiNPs are either mesoporous or solid. The silica matrix of mesoporous SiNPs has many channels and pores, whereas solid SiNPs have no pores.[7] Mesoporous SiNPs have a controllable, uniform pore size, large volume-to-surface ratio, easily modifiable surface chemistry, and exceptional biocompatibility.[8] The silica framework of SiNPs yields many advantageous qualities, such as its stability in acidic conditions, temperature fluctuations, and organic solvents.[8] The pores of mesoporous SiNPs can be filled with various biomolecules.[7]

Silicosis, a type of pneumoconiosis, occurs secondary to the inhalation of RCS and causes progressive, irreversible, and fatal lung inflammation and fibrosis.[3] While the condition is preventable, no treatment exists. Silicosis increases susceptibility to Mycobacterial diseases, autoimmune diseases, and bronchogenic carcinoma.[1] This activity reviews the etiology, epidemiology, pathophysiology, clinical findings, evaluation, and management of patients with silicosis.


The many diverse forms of silica can be used in various ways. The Consumer Federation of America and the United States Food and Drug Administration have deemed amorphous silica and salicylates safe for human use when manufactured in larger, non-respirable particle sizes.[9] These non-respirable particles are often used in hair, skin, and nail products.[10] Since the early 1990s, denim and artificial stone production have been some of the largest silica-based industries. Denim is often sandblasted with minerals containing silica particles to obtain a look of worn- or washed-out denim. Artificial stone, commonly used for countertops and benchtops, comprises quartz, decorative glass, and metal pieces bound by a polymer resin. The crystalline silica component constitutes over 90% of the finished stone.[2] These contemporary manufacturing processes have contributed to the reemergence of silicosis.[2]

SiNPs are frequently used in the cosmetic, food, and agriculture industries.[6]  SiNPs are also used in the production of processed foods and food storage. The average daily consumption of silica from foodstuffs is approximately 9.4 mg/kg. Amorphous silica is an anti-caking, anti-foaming, or flow-aiding agent in powdered foods such as cake mixes or spices. Silica is also occasionally used as an aroma carrier or filtering agent. There are future opportunities for silica nano-additives to adjust specific properties of food, including taste, texture, and shelf life. SiNPs could also be used to fortify essential foods with vitamins and nutrients.[10]

SiNPs have become powerful medical tools with diagnostic and therapeutic applications in cancer.[7] SiNPs can provide improved clearance, solubility, and targeted release of drugs. The adjustable surface chemistry of silica particles enables diverse surface modifications, which alter drug biodistribution and pharmacokinetics.[10] For example, the reactive silanol groups on the surface of the silica can be conjugated with biomolecules, such as organic groups, antibodies, or DNA, to functionalize the nanoparticles and allow them to bind target surfaces or cells or to evade the reticuloendothelial system, thus providing longer circulation times.[7]

SiNPs have also become invaluable in imaging studies, allowing for less invasive diagnostic studies and speeding up treatment-based decision-making. Most imaging dyes are hydrophobic, making them incompatible with the aqueous environment of the body. However, the hydrophobic dye particles are trapped in the silica matrix, which protects them from direct contact with the environment and increases their stability.[10] 

Little is known about the adverse effects of SiNPs, and there is inadequate evidence to draw any firm conclusions about their toxicity except that toxicity is likely multifactorial and affected by surface modifications, pore size, particle size, route of exposure, and dosage.[10]


Between 1991 and 1995, more than 500,000 individuals in China alone were diagnosed with silica-related lung disease. The World Health Organization pledged in 1995 to eliminate silicosis by the year 2030, but silicosis currently remains a prominent health issue internationally.[2] 

Cumulative respiratory exposure to silica has been identified as the primary factor associated with the development of lung pathology and is impacted by the exposure duration and intensity. Occupational exposure to RCS is regulated by most countries by the time-weighted average (TWA). The TWA is the average concentration of an airborne substance encountered over an average work week of 40 hours. Generally, the accepted exposure limit of RCS is between 0.05 mg/m3 to 0.1 mg/m3. However, it was proven in 2002 that even at exposure levels equal to a TWA of 0.05 mg/m3 over a working career of 40 to 45 years, workers still had a significant risk of at least 1 in 100 developing radiographic silicotic lung disease.

Although short-term exposures are not generally regulated, even short periods of exposure to high concentrations of RCS markedly increase the risk of developing silicosis. It is generally recommended that the RCS level not surpass 3 times the 8-hour TWA for more than 30 minutes and should certainly never exceed 5 times the 8-hour TWA.[2]

The newer industries of sand-blasting denim and engineered stone have been associated with alarmingly high rates of silicosis.[9] In the United States, individuals who work with artificial stone countertops are frequently exposed to hazardous concentrations of silica dust released into the air with cutting, drilling, grinding, and polishing stone slabs.[11] One study revealed that grinding or cutting artificial stone without water dust suppression produced nearly 300 times the recommended 30-minute TWA exposure limit.[2] Studies have also indicated a significant increase in the prevalence of autoimmune disease in patients with silicosis from occupational exposure to the artificial stone industry.[2] Certain smaller industries or hobbies, such as ceramics or pottery, may also be associated with exposure to substantial RCS levels.[9]

Although SiNPs show much promise, little is known about their potential adverse effects on humans. In vitro and in vivo studies have demonstrated that SiNPs can induce inflammation, oxidative stress, and apoptosis.[6] However, these studies evaluated SiNPs with various physiochemical properties, likely contributing to the significant variations in their toxicity.[12] Further research must be done, as the increasing production and usage of SiNPs will increase human exposure.[6] 


Long-term occupational exposure to RCS is associated with the development of silicosis, a devastating interstitial lung disease characterized by diffuse pulmonary fibrosis.[1] 

RCS particles are small enough to bypass the pulmonary mucociliary defense system and into the terminal airways and alveoli, where they are coated with pulmonary surfactant.[4] The surfactant is believed to modify the surface chemistry of the particles in a protective manner, temporarily decreasing their toxicity. In response to immune stimulation by the silica particles, alveolar macrophages influence alveolar type II cells and bronchiolar epithelial cells to produce a copious amount of surfactant. However, the protective effect of the surfactant against silica-induced lung damage is only temporary, lasting approximately 3 days, after which the surfactant undergoes enzymatic proteinaceous digestion.[1] The sustained overproduction of surfactant and the accumulation of the denatured protein is an acute pathological feature of silica exposure. This leads to a build-up of proteinaceous debris in the alveoli, recognized as silicoproteinosis.[1][4]

In the terminal airways, the RCS particles are engulfed by alveolar macrophages to clear the lung of the inhaled debris. Particles become entrapped in lysosomes, where they are resistant to degradation.[1] Within the lysosome, silica produces reactive oxygen species, which damage the lysosomal membrane, leading to the spillage of the digestive enzymes into the cytoplasm of the macrophage and promoting cell death.[4] Any dysfunctional alveolar macrophages persisting in the alveoli cannot maintain surfactant homeostasis or effectively clear debris from the alveoli, leading to a collection of intra-alveolar material.[2]

Macrophages collect at damaged pulmonary tissue, stimulating the activity of fibroblasts, leading to pulmonary fibrosis, formation of silicotic nodules, and reduction of lung area available for gas exchange.[2][13] The silica particles released by macrophage destruction are either excreted via the mucociliary escalator, transported through lymphatic drainage, or engulfed by other alveolar macrophages, stimulating a vicious cycle of cellular destruction, inflammation, and pulmonary damage.[2][4] The lymphatic spread of pulmonary macrophages likely explains the origin of any extrapulmonary manifestations of silicosis, including lymphadenopathy.[3] These pathologic changes are much more indolent than the abrupt silicoproteinosis experienced in voluminous acute exposures.


The classic histopathological finding of silicosis is the silicotic nodule. Microscopically, silicotic nodules have 2 zones, central and peripheral. Concentrically arranged collagen fibers characterize central zones. The peripheral zone is poorly organized and contains fibroblasts, lymphocytes, and dust-laden macrophages. Visualization with polarized light microscopy reveals weakly birefringent polyhedral particles and brightly birefringent needle-like silicate crystals.[14][15][14]

History and Physical

Three major forms of silicosis have been described, each distinguished by the latency period between the initial exposure to RCS and the onset of symptoms. Histopathological disease occurs before the onset of radiological or clinical disease. The 3 major forms of silicosis are acute, accelerated, and chronic. Chronic silicosis, the most commonly encountered form of silicosis, is also known as classic silicosis and may be simple or complicated. Complicated chronic silicosis is also known as pulmonary massive fibrosis (PMF).[9]

All patients with silicosis will have a history of exposure to RCS. Professions with a particularly high risk of excessive RCS exposure include quartz millers, abrasive blasting, denim jean manufacture, brick masons, miners, potters, ceramicists, and those who help construct underground subways and dams.[1][3] However, many patients with silicosis are asymptomatic with a normal physical examination, making clinical suspicion based on occupational history imperative.[13] Symptoms and physical examination findings, if present, are often dictated by the form of silicosis present.

Acute silicosis or silicoproteinosis is a rare condition only observed in patients with high-intensity RCS exposure.[16] Acute silicosis usually presents within a few weeks to less than 5 years after RCS exposure. While anyone with high-intensity exposure to RCS may develop silicoproteinosis, it is most commonly identified in individuals who have performed abrasive sandblasting or work in tunnels. The pathology of acute silicosis is unique and is characterized by significant alveolitis and alveolar proteinosis.[2] Patients with acute silicosis are generally symptomatic, reporting pulmonary and systemic symptoms, including dyspnea, pleurisy, cough, fevers, fatigue, and weight loss. Physical examination frequently reveals hypoxia.[9]

Accelerated silicosis is characterized by a disease progression that is more rapid than chronic silicosis.[2] Specifically, the accelerated form of silicosis develops within 5 to 10 years of RCS exposure.[9] Accelerated silicosis exhibits features that overlap acute and chronic silicosis. While there may be evidence of silicoproteinosis, patients also demonstrate the silicotic nodules of chronic disease. However, the pulmonary nodules intensify more quickly.[4][9][4] 

Chronic silicosis is the most common presentation of this pneumoconiosis, usually presenting 10 to 30 years after prolonged exposure to low concentrations of RCS.[2] Radiographic findings differentiate between simple and complicated chronic silicosis.[9] Simple chronic silicosis is also called nodular silicosis, characterized by pulmonary nodules less than 10 mm in diameter.[2] Patients with simple chronic silicosis are frequently asymptomatic but may present with a dry cough or dyspnea on exertion. Simple silicosis may transition to complicated silicosis as the nodules progress.[9] Complicated chronic silicosis, or PMF, develops when the pulmonary nodules expand and fuse to form conglomerate masses with a diameter of greater than 10 mm.[4] Patients with PMF usually develop debilitating respiratory impairment due to the profound destruction of lung tissue, which results in decreased perfusion capacity, impairment in lung function, and elevated pulmonary resistance.[16] Pulmonary hypertension and cor pulmonale may result.[16]

The physical examination of patients with accelerated or chronic silicosis may reveal lymphadenopathy. Interestingly, in lower levels of silica exposure, the development of lymphadenopathy may precede the development of pulmonary findings.[16][17] Theoretically, lymph node fibrosis would hinder the elimination of silica dust from the lungs, potentially leading to a higher silica burden and increased likelihood of developing lung damage from parenchymal silicosis.[2]


There is no specific laboratory test to diagnose silicosis; the diagnosis rests on a history of RCS exposure and consistent radiological features.[1][2] 

Chest radiographs are often performed first in evaluating suspected occupational lung disease, as radiographs are inexpensive, widely available, and administer a low radiation dose. As most patients with silicosis are asymptomatic, the first signs of disease are often discovered on chest radiography as part of an occupational health screen or as an incidental finding.[2]  Chest radiography may reveal multiple nodules in the middle and upper lungs bilaterally, often with enlargement of the hilar and mediastinal lymph nodes.[13] However, chest radiography is often unable to detect early disease.[3] High-resolution computerized tomography (HRCT) is more sensitive during early disease stages and provides greater diagnostic confidence (see Image. Silicosis, Computed Tomography).

Features consistent with chronic simple silicosis include well-defined nodules less than 10 mm in diameter. These nodules are characteristically located in the upper lobes and may be accompanied by mediastinal and hilar lymphadenopathy with nodules in the peri-lymphatic distribution. Radiological features consistent with chronic complicated silicosis include conglomerate masses greater than 10 mm in diameter. These masses are usually located in the posterior apical lung and may migrate toward the hilum. These large nodules often have irregular margins, vary in shape, and can lead to lung volume loss with mediastinal or tracheal distortion.[16]

Knowledge of the specific radiographical features of acute silicosis is limited to a small number of case series and reports. Radiographic features that may be revealed with HRCT imaging include numerous bilateral centrilobular nodular and ground-glass opacities. If there is also focal consolidation with air bronchograms caused by a buildup of intra-alveolar material and alveolar and septal wall thickening, the images may show a “crazy-paving” pattern.[2][16]

Pulmonary function in patients with silicosis will vary depending on the stage of the disease. In early disease, lung function may be unaffected.[4] In later stages, pulmonary function tests may reveal reduced lung volume, forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and diffusion capacity.[1]

Many countries have silica surveillance programs for workers exposed to RCS that focus on early disease detection, which includes meeting with a medical practitioner for a detailed medical and work history, physical examination, appropriate imaging studies, and pulmonary function tests. If the worker begins to exhibit signs or symptoms of silicosis, they should be referred to a pulmonologist or an occupational health specialist.[9] 

Treatment / Management

There is currently no effective treatment for silicosis.[14] Most interventions are supportive and consist of supplemental oxygen in those with hypoxia, recommended vaccinations, prompt treatment of infection, and pulmonary rehabilitation.[1] The primary modality for the treatment of end-stage silicosis is a lung transplant.[3] Transplantation is expensive, carries significant risk, and is a limited resource for a median survival of only 6 to 7 years after transplant.[2]

Although silicosis is currently untreatable, it is undoubtedly preventable.[9] Primary prevention by controlling RCS exposure is critical.[9] In individuals exposed to silica, diagnosing silicosis early and counseling patients on avoiding further RCS exposure and smoking cessation is essential to disease management.[2] 

Our advancing understanding of the pathophysiology of silicosis has opened the door to more targeted treatments such as anti-fibrotic and anti-cytokine therapy; there have been no large randomized controlled trials to assess the efficacy and safety of such drugs.[4] 

Differential Diagnosis

The radiographical opacities of patients with silicosis often resemble other pulmonary diseases such as sarcoidosis, tuberculosis, or malignancy.[16] The diagnosis of silicosis requires that alternative diagnoses must be excluded. If the diagnosis remains uncertain, a lung biopsy may be considered. Microscopic evaluation of biopsied nodules from patients with silicosis would reveal acellular whorls of hyaline collagen. Birefringent crystals will be observed when tissue is viewed under polarized light, confirming the presence of silica.[15]


Silicosis is a devastating and incurable condition marked by irreversible lung scarring.[4] The fibrosis is progressive, leading to irreversible and often fatal restrictive lung function.[2] The prognosis is poor, with a gradually worsening decline in pulmonary function, often leading to the eventual development of respiratory failure and cor pulmonale. Infection with tubercular or nontubercular Mycobacteria is also common. Deterioration may be indolent or more accelerated, based on the intensity and duration of exposure.[1] Pulmonary inflammation and damage will progress even with complete cessation of silica exposure.[13]


Silica exposure and exposure to cigarette smoke have a significant additive, almost multiplicative, effect on the development of lung cancer.[2] Exposure to RCS is associated with an increased risk of all histologic forms of lung cancer.[9] Animal models suggest that the initial inflammation, followed by an immunosuppressive environment caused by silica exposure, promotes the growth of pulmonary neoplasms.[2] Additionally, the progression of silicosis may be confused for malignancy or mask the development of early lung cancers.[9] As the two disease processes are difficult to distinguish with CT, magnetic resonance (MR) imaging is helpful. On T2-weighted images, the large conglomerate masses of PMF are of low intensity, whereas cancerous cells display high-intensity signals. Notably, positron emission tomography (PET) does not help distinguish cancer from PMF, as both display an intense uptake of FDG.[16]

Another important complication of silicosis is the development of infection with Mycobacterium tuberculosis (TB). TB is one of the main contributors to morbidity and mortality in workers exposed to silica, particularly in regions with high rates of TB and human immunodeficiency virus (HIV).[12] The large conglomerate masses characteristic of complicated silicosis may develop central cavitation, increasing the risk of tuberculosis and other Mycobacteria infections.[9] International guidelines recommend chemoprophylaxis for latent TB and TB screening in workers exposed to silica.[2][18]

Additionally, although the exact mechanism is not well understood, evidence supports that exposure to silica is linked with the development of certain autoimmune diseases such as systemic lupus erythematosus, systemic sclerosis (scleroderma), glomerulonephritis, and rheumatoid arthritis.[1]

Deterrence and Patient Education

Patients should be counseled on preventing initial or further exposure to RCS to avoid the development or acceleration of silicosis. Patients should also be advised of the significantly increased risk of pulmonary malignancy experienced in individuals exposed to crystalline silica and nicotine smoke.[2]

Enhancing Healthcare Team Outcomes

Silicosis is a devastating and incurable disease that is often difficult to diagnose. Once diagnosed, proper patient education is invaluable and may lead to a significant extension and improved quality of life.[19] A coordinated effort of primary care practitioners, pulmonologists, nursing staff, occupational health specialists, and transplant surgeons will lead to the best patient outcomes.

Practitioners performing the primary evaluation of the patients at risk of silicosis should perform a thorough physical examination and obtain a comprehensive exposure history, with specific questions regarding occupational exposure. Healthcare personnel should know the benefit of treatment of coexisting conditions, such as latent tuberculosis and nicotine addiction.[2] It is also imperative for healthcare practitioners to report any new diagnosis of silicosis to local and state health departments.[9] 

Silica surveillance registries help public health programs tailor their outreach, education, and prevention strategies.[9] A new diagnosis of silicosis should prompt a detailed review of the occupational hygiene measures in place at the workplace.[15] Wet-cutting saws, dust extraction systems, and personal respiratory equipment are essential primary prevention methods.[19] Random measurement of environmental RCS levels is also important to ensure effective control measures.[2] Consultation with public health agencies may be required if there is concern that individuals working with silicosis continue to face high exposure to RCS.[1]

Nursing staff members are a valuable part of the healthcare team, as they often spend the most time in close contact with the patient and frequently form interpersonal relationships with them. Nurses may pick up crucial medical history details that were previously missed. They also help to provide timely and compassionate care. Reassurance and gentle encouragement to reinforce essential lifestyle changes can immensely impact patients’ lives. In particular, occupational health nurses are specifically beneficial, as they are trained to provide education on risk factors and prevention strategies at worksites.[19] 

Although there is now a wealth of knowledge on the cause of silicosis and its detrimental health effects, millions of workers worldwide continue to endure exposure to hazardous levels of RCS.[3] We could eliminate this preventable and devastating disease with the conjoined effort of medical professionals, public health systems, and industry employers.[20]

(Click Image to Enlarge)
Silicosis, Computed Tomography
Silicosis, Computed Tomography. This CT of a patient with silicosis reveals the characteristic nodules in the middle lobes of both lungs accompanied by peri-hilar lymphadenopathy.
Contributed by S Bhimji, MD


Lauren Baum


8/6/2023 7:49:01 AM



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