eMedicine Specialties > Pulmonology > Occupational Lung Diseases

Silicosis

Basil Varkey, MD, FCCP, Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Medical College of Wisconsin; Consulting Pulmonologist, Froedtert Memorial Lutheran Hospital
Anita B Varkey, MD, Assistant Professor, Department of Medicine, Loyola University Medical Center; Associate Program Director, Internal Medicine Residency; Medical Director, General Internal Medicine Clinic, Loyola Outpatient Center

Updated: Apr 16, 2008

Introduction

Background

Pneumoconiosis is the general term for lung disease caused by inhalation of mineral dust. Silicosis is a fibronodular lung disease caused by inhalation of dust containing crystalline silica (alpha-quartz or silicon dioxide), which is distributed widely, or its polymorphs (tridymite or cristobalite), which are distributed less widely. Quartz, the most common form of crystalline silica, is abundantly present in granite, slate, and sandstone.

Silicosis has been a human scourge since antiquity. In 1705, Ramazzini cited Diembrock's description of the lungs of stonecutters "in whom he found heaps of sand that in running the knife through the pulmonary vesicles he thought he was cutting through some sandy body." In 1870, Visconti introduced the term silicosis, derived from Latin silex, or flint.

Although silicosis has been recognized for many centuries, its prevalence increased markedly with the introduction of mechanized mining. The prevalence has declined markedly in developed countries in recent decades because of effective industrial hygiene measures.

The eMedicine articles Silicosis and Coal Worker Pneumoconiosis and Pulmonary Fibrosis, Interstitial (Nonidiopathic) may be of interest, as may the Medscape CME course High-Resolution Chest Tomography in Idiopathic Pulmonary Fibrosis and Nonspecific Interstitial Pneumonia: Utility and Challenges.

Pathophysiology

Small (£ 1 µm) particles are more dangerous because they are more likely to be deposited distally in the respiratory bronchioles, alveolar ducts, and alveoli. The surface of these particles generates silicon-based radicals that lead to the production of hydroxyl, hydrogen peroxide, and other oxygen radicals that damage cell membranes by lipid peroxidation and inactivate essential cell proteins.

Alveolar macrophages ingest the particles, become activated, and release cytokines, including tumor necrosis factor, interleukin-1, and leukotriene B-4, as well as chemotactic factors that recruit other inflammatory cells. The ensuing inflammation damages resident cells and the extracellular matrix. Transforming growth factor–alpha induces proliferation of type 2 pneumocytes, and other cytokines (eg, platelet-derived growth factor, insulin - like growth factor) stimulate fibroblasts to proliferate and produce collagen; fibrosis results. Silica particles outlive the alveolar macrophages that ingested them, thereby continuing the cycle of injury.

Frequency

United States

Accurate assessment of the frequency of silicosis and other pneumoconioses in the United States and in other countries is impossible for many reasons. The number of people who are at risk 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. An estimated 200,000 miners and 1.7 million others have experienced an occupational exposure to silica.

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 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. 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.

Mortality/Morbidity

Over the past 4 decades, the number of people dying with silicosis in the United States has declined dramatically because of improved workplace protection. In 1968, 12 people per million population died with silicosis; in 1991, the number approximated 2 people per million population. Death certificates from 1968-1998 also reflect the declining number of silicosis cases. However, information gleaned from death certificates alone likely underestimates the prevalence of this disease in the population.

• As the disease progresses, airflow limitation occurs, manifested by dyspnea and cough. Eventually, cor pulmonale and respiratory failure develop. An increased incidence of mycobacterial diseases is reported in patients with silicosis. Probable reasons for the increased incidence of tuberculosis include impairment of macrophage function by silica and the crowded working and living conditions of the workers. When these diseases coexist, they often are referred to as silicotuberculosis. Silicotuberculosis is associated with rapid progression of silicosis and increased morbidity and mortality.
• Rheumatoid arthritis 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 rheumatoid arthritis.¹
• Cavitation caused by lung parenchymal necrosis in complicated silicosis may predispose individuals to Aspergillus colonization and to formation of an aspergilloma (mycetoma).

Race

No racial predilection is reported. The mortality rate among people of African descent exceeds that of whites.

Sex

Silicosis predominantly affects male workers, reflecting the occupations at risk.

Age

No precise information regarding age is available.

Clinical

History

In obtaining a detailed occupational history, the physician should 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.

The clinical picture of silicosis is variable; acute and chronic forms have been recognized. Acute silicosis follows a relatively brief exposure to silica dust. The more common chronic forms manifest after several years of exposure and may be asymptomatic (recognized by chest radiographic findings) or symptomatic, with indolent symptoms or progressive symptoms.

• Acute silicosis follows massive exposure to dust in unregulated environments. A subset of acute silicosis is silicoproteinosis, the chest radiographic appearance of which mimics pulmonary alveolar proteinosis with alveolar filling opacities. Acute silicosis causes symptoms weeks to a few years after exposure. Besides severe dyspnea, other symptoms include cough, fever, and weight loss. Pleuritic pain may be present.
• Chronic silicosis can be either simple silicosis or complicated silicosis (also called progressive massive fibrosis), a distinction based on the chest radiographic appearance (see Imaging Studies). Symptoms often manifest only 1-3 decades after initial exposure. Those who develop symptoms within 10 years after initial exposure have an accelerated form of silicosis and are more likely to develop progressive massive fibrosis (PMF).
  • Simple silicosis may be asymptomatic or may present with exertional dyspnea and cough with sputum production. Differentiating these symptoms from chronic bronchitis and emphysema in a smoker may be difficult.
  • In complicated silicosis, dyspnea and productive cough often are accompanied by constitutional symptoms of malaise and weight loss.

Physical

Physical findings vary with the type and extent of the disease.

• Physical findings are often unremarkable in simple silicosis.
• Tachypnea, expiratory prolongation, rhonchi, wheezing, and rales may be present in complicated silicosis.
• Digital clubbing is uncommon.
• Cyanosis may be noted in advanced cases of complicated silicosis.
• In advanced cases with cor pulmonale, characteristic signs may be present, including prominent jugular pulse, a left parasternal heave, loud pulmonary valve closure sound (P2), tender hepatomegaly, and pedal edema.

Causes

Silicosis is a fibronodular lung disease caused by inhalation of dust containing crystalline silica (alpha-quartz or silicon dioxide), which is distributed widely, or its polymorphs (tridymite or cristobalite), which are distributed less widely. The polymorphs of silica naturally present in lava can also be produced if amorphous silica is subjected to very high temperatures, and this has high toxicity to the lungs.

Because of the wide presence of crystalline silica in nature in an undisturbed form, as in rocks and the earth's crust, people in occupations that disturb the natural state or those involved in collecting or refining the material are at risk of developing silicosis. These occupations include the following:

• Mining or tunneling
• Quarrying
• Drilling
• Crushing stone
• Chipping
• Grinding
• Sandblasting
• Grinding or polishing in pottery and foundry work
• Cement manufacturing
• Glass manufacturing
• Masonry
• Blast furnaces
• Coal mining
• Construction
• Cutting or manufacturing heat-resistant bricks
• Dental laboratory technicians (a few cases have been reported)²

Differential Diagnoses

Other Problems to Be Considered

Pulmonary tuberculosis
Rheumatoid lung nodules
Metastatic lung cancer

Workup

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 (see Other Tests).
• Humoral immune system abnormalities observed in silicosis include increased incidence and titer of rheumatoid factor, antinuclear antibodies, and immune complexes. No consistent abnormality is noted in the cell-mediated immune system.

Imaging Studies

• Chest radiograph
  • Radiographic studies of the chest are essential to the diagnosis of silicosis. While some chest radiographic findings of silicosis may be nonspecific, others are sufficiently characteristic of the disease.
  • Bilateral alveolar filling and a ground-glass appearance mimicking alveolar proteinosis are observed in silicoproteinosis.
  • Simple silicosis manifests as multiple small (<10 mm) nodules that are scattered diffusely throughout the lungs but may be more prominent in the upper lung fields. These radiographic findings have been found to correlate well with pathologic findings. Chest radiographic findings in persons with simple silicosis have a high degree of sensitivity and specificity. Calcification of the hilar lymph nodes, particularly in the rim of the nodes (ie, eggshell calcification) is very characteristic of silicosis. However, eggshell calcifications are observed only in a minority of cases of silicosis. Other causes of eggshell calcification include sarcoidosis, histoplasmosis, and irradiation. Rarely, the pulmonary nodules also may show calcification.
  • Complicated silicosis (also known as PMF) manifests as bilateral upper lobe masses, which are formed by the coalescence of nodules. Cavitation may be seen. As these masses retract toward the hilum because of fibrosis, the lower lung fields may appear overinflated. Hilar calcifications may be present.
• CT scan
  • A high-resolution CT scan of the chest may be more sensitive than chest radiography in discerning the nodules of simple silicosis.
  • In progressive massive fibrosis, a CT scan provides more detail of emphysematous changes, pleural thickening, and the confluent masslike lesions (eg, the presence of cavitation) than a chest radiograph. Although cavitation in silicosis can occur without a mycobacterial infection, such a possibility should be considered when cavitation is observed.
  • Although pleural effusions are quite rare, pleural thickening is not an unusual finding.

Other Tests

• Pulmonary function tests
  • Pulmonary function test results may be normal in simple silicosis. However, silicosis is associated with an excessive decline in lung function.
  • In more advanced disease, airflow obstruction or a mixed pattern of obstruction and restriction is observed.
  • In smokers with airflow obstruction, separating the effect of silicosis from the confounding factor of tobacco smoke is difficult.
  • Progressive massive fibrosis causes severe restriction, decreased compliance, and hypoxemia.
• A tuberculin skin test using purified protein derivative (PPD) is indicated in all persons with silicosis. If the test result is positive (ie, 10 mm or more of induration at the site), treatment for latent or active infection is indicated. 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.

Procedures

• Bronchoscopy rarely is needed. The rare indication is in a cavitary or mass lesion when mycobacterial disease or lung cancer is suspected and examination of sputum samples is nondiagnostic.

Histologic Findings

Examination of lung tissue very seldom is necessary because the diagnosis of silicosis is based on history of exposure, symptoms, physical examination findings, and chest radiographic appearance.

The initial histopathologic changes of silicosis are pigmented macrophages and reticulin fibers in peribronchial, paraseptal, and perivascular areas.

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.

In PMF, the masslike areas may show cavitation caused by a necrotic process.

Acute silicosis silicotic nodules are seldom seen and the histology is similar to pulmonary alveolar proteinosis with alveolar filling with proteinaceous material that stains with periodic acid-Schiff stain.

Treatment

Medical Care

• Prevent further exposure to silica dust.
• Strongly advise patients to quit smoking and provide help in smoking cessation efforts.
• Immunize patients against influenza and pneumococcal pneumonia.
• No specific therapy for silicosis cures or alters the course of the disease.
• Corticosteroids may be of benefit in acute silicosis.³ In chronic silicosis, they are unlikely to be of benefit, although pulmonary function improvement was noted in one study.⁴
• Selectively in patients with very advanced disease without other comorbid conditions, lung transplantation may be an option. 
• Experimental (unproven) approaches to treatment include whole-lung lavage, aluminum inhalation, and parenteral administration of polyvinyl pyridine N-oxide.
• Latent tuberculosis infection (ie, positive tuberculin skin test result without active disease) should be treated with isoniazid (see Medication). A 10-mm induration is considered a positive test result in this population.
• Active tuberculosis (ie, Mycobacterium tuberculosis identified in smear or culture) should be treated with appropriate multiple drugs (see Medication) according to the most recently established guidelines.
• Complications (eg, airflow obstruction, cor pulmonale, respiratory failure), should they occur, should be treated appropriately.

Surgical Care

Selectively in patients with very advanced silicosis and without other significant comorbid conditions, lung transplantation should be considered.

Consultations

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

Diet

No dietary restrictions are necessary.

Activity

No restrictions on activity are necessary.

Medication

Latent tuberculosis: Isoniazid for 9 months, daily or intermittently (twice weekly directly observed treatment [DOT]), is the DOC.

Active tuberculosis: Several multidrug regimens are available using more drugs daily and reducing the number of drugs and converting to an intermittent DOT schedule. Treatment duration is 6-9 months and at least 3 months beyond negative culture results. Drugs used in treatment include isoniazid, rifampin, pyrazinamide, streptomycin, and ethambutol.

Antitubercular agents

Active against susceptible strains of M tuberculosis.

Isoniazid (Nydrazid)

Best combination of effectiveness, low cost, and minor adverse effects. First-line drug unless known resistance or another contraindication is present.

Dosing

Adult

5 mg/kg PO qd; not to exceed 300 mg qd
Alternatively, 15 mg/kg PO 2 times/wk; not to exceed 900 mg/dose

Pediatric

10-20 mg/kg PO qd; not to exceed 300 mg qd
Alternatively, 20-40 mg/kg 2 times/wk; not to exceed 900 mg/dose

Interactions

Higher incidence of isoniazid-related hepatitis can occur with alcohol ingestion on daily basis; aluminum salts may decrease isoniazid serum levels (administer 1-2 h before patient takes aluminum salts); may increase anticoagulant effects with coadministration; may inhibit metabolic clearance of benzodiazepines; carbamazepine toxicity or isoniazid hepatotoxicity may result from concurrent use (monitor carbamazepine concentrations and liver function); coadministration with cycloserine may increase CNS adverse effects (eg, dizziness); acute behavioral and coordination changes may occur with coadministration of disulfiram; coadministration with rifampin after halothane anesthesia may result in hepatotoxicity and hepatic encephalopathy; may inhibit hepatic microsomal enzymes and increase toxicity of hydantoin

Contraindications

Documented hypersensitivity; previous isoniazid-associated hepatic injury or other severe adverse reactions

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor patients with active chronic liver disease or severe renal dysfunction; periodic ophthalmologic examinations during therapy are recommended even when visual symptoms do not occur; associated with peripheral neuropathy

Rifampin (Rifadin)

For use in combination with at least 1 other antituberculous drug. Inhibits DNA-dependent bacterial, but not mammalian, RNA polymerase. Cross-resistance may occur. Treat for 6-9 mo and at least until 3 mo beyond negative culture results.

Dosing

Adult

10 mg/kg PO/IV qd; not to exceed 600 mg qd
Alternatively, 10 mg/kg PO/IV 2 times/wk; not to exceed 600 mg qd

Pediatric

10-20 mg/kg PO/IV; not to exceed 600 mg qd
Alternatively, 10-20 mg/kg PO/IV 2 times/wk; not to exceed 600 mg qd

Interactions

Induces microsomal enzymes, which may decrease effects of acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, oral contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with isoniazid may result in higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFTs occur)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Obtain CBCs and baseline clinical chemistries prior to and throughout therapy; in patients with liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur; orange discoloration of urine and secretions, nausea, vomiting, febrile reaction, and hepatitis have occurred

Pyrazinamide (PZA)

Pyrazine analog of nicotinamide that may be bacteriostatic or bactericidal against M tuberculosis, depending on concentration of drug attained at site of infection. Mechanism of action is unknown. This drug should be used only in combination with other antituberculous drugs.

Dosing

Adult

15-30 mg/kg PO qd; not to exceed 2 g/d; alternatively, 50-70 mg/kg PO 2 times/wk; not to exceed 4 g/d

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; severe hepatic damage; acute gout

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Clinical monitoring at week 2, 4, and 8 and blood tests as warranted; use only in combination with other effective antituberculous agents; inhibits renal excretion of urates; may result in hyperuricemia (usually asymptomatic); perform baseline serum uric acid determinations; discontinue if signs of hyperuricemia with acute gouty arthritis appear; perform baseline LFTs (closely monitor in patients with liver disease); discontinue if signs of hepatocellular damage appear; caution in patients with history of diabetes mellitus; associated with rash and GI distress; teratogenic potential is undetermined

Streptomycin

For treatment of susceptible mycobacterial infections. Use in combination with other antituberculous drugs (eg, isoniazid, ethambutol, rifampin).

Dosing

Adult

15 mg/kg/d IM qd; not to exceed 1 g qd; reduce dose in patient aged >60 y; not to exceed 750 mg qd
Alternatively, 25-30 mg/kg/d IM 2 times/wk; not to exceed 1.5 g/d

Pediatric

40 mg/kg/d IM; not to exceed 1 g/d
Alternatively, 25-30 mg/kg/d IM 2 times/wk; not to exceed 1.5 g/d

Interactions

Nephrotoxicity may be increased with aminoglycosides, cephalosporins, penicillins, amphotericin B, and loop diuretics

Contraindications

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Clinically monitor and check for acuity of hearing and renal function tests; narrow therapeutic index; not intended for long-term therapy; caution in patients with renal failure who are not on dialysis; caution in patients with myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; associated with ototoxicity; ototoxic to fetus

Ethambutol (Myambutol)

Diffuses into actively growing mycobacterial cells (eg, tubercle bacilli). Impairs cell metabolism by inhibiting synthesis of one or more metabolites, which in turn causes cell death. No cross-resistance demonstrated. This drug should be used only in combination with other antituberculous drugs.

Dosing

Adult

15-25 mg/kg PO qd; not to exceed 2.5 g/d
Alternatively, 50 mg/kg PO 2 times/wk

Pediatric

<13 years: Not recommended
>13 years: Administer as in adults

Interactions

Aluminum salts may delay and reduce absorption (administer several h before or after ethambutol dose)

Contraindications

Documented hypersensitivity; optic neuritis (unless clinically indicated)

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reduce dose in patients impaired renal function; associated with optic neuritis and rash; monitor color discrimination (ie, red-green) and visual acuity; treatment should not be deferred during pregnancy; preferred drugs in initial treatment are isoniazid, rifampin, and ethambutol

Follow-up

Deterrence/Prevention

• Monitoring of air quality and dust concentration in the workplace is essential to prevent silicosis and other pneumoconioses.
• Limiting exposure to harmful dusts can be achieved further by suppressing dust generation, filtering or capturing dust particles, diluting the concentration with fresh air, and using personal protective respiratory equipment as further possible means of preventing silicosis.
• The Occupational Safety and Health Administration (OSHA) has set a permissible exposure limit for respirable silica of 10 mg/m³. The National Institute for Occupational Safety and Health (NIOSH) standard is a more stringent exposure limit of 0.05 mg/m³.
• In addition to the primary prevention measures, secondary methods include monitoring workers with chest radiograph and spirometry to identify early disease and to stop further exposure to silica.

Complications

• Airflow obstruction
• Chronic bronchitis
• Cor pulmonale
• Respiratory failure
• Increased incidence of mycobacterial diseases
• Increased risk of lung cancer (see the Medscape Lung Cancer Resource Center)
• Association with connective-tissue disorders (eg, rheumatoid arthritis, systemic lupus erythematosus, mixed connective-tissue disease,⁵ systemic vasculitis⁶

Prognosis

• The clinical presentation at the time of diagnosis is somewhat predictive of the prognosis, but the rate of progression varies.
• Silicoproteinosis worsens quickly, and death may occur in months.
• Complicated silicosis shows gradual worsening of symptoms, deterioration of lung function, and increasing disability.
• On the other hand, patients with simple silicosis may be asymptomatic and may remain stable for many years both clinically and radiographically.

Patient Education

• Prevent further exposure to silica dust.
• Strongly advise patients to quit smoking and provide help in smoking cessation efforts.

Miscellaneous

Medicolegal Pitfalls

• Assessment of impairment and disability is difficult and is best left to experienced experts in this area. The degree of impairment demonstrated does not necessarily translate to the same degree of disability. Impairment may be defined as a physiological abnormality of function that persists after treatment. Disability may be defined as an inability to carry out a specific task or job, or the development of undue distress during the performance of the job or task. Therefore, to evaluate disability due to silicosis, one must document a reduction in pulmonary function that is sufficient to prevent the person from engaging in gainful employment or activities of daily living.
• Early diagnosis of other diseases emerging in patients with silicosis is important so that treatment can be started. Mycobacterial disease and lung cancer in patients with silicosis are examples of this scenario. Diagnosis is difficult because the symptoms of cough, malaise, and weight loss and the chest radiographic appearance of nodules and masses may not be discernibly different from that of complicated silicosis.
• Diagnosis of silicosis is based on exposure history of sufficient intensity and/or duration, chest radiograph and/or CT scan showing abnormalities consistent with silicosis, and absence of other diseases to account for the observed radiographic abnormalities.

References

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2. Centers for Disease Control and Prevention. Silicosis in dental laboratory technicians--five states, 1994-2000. MMWR Morb Mortal Wkly Rep. Mar 12 2004;53(9):195-7. [Medline].

3. Goodman GB, Kaplan PD, Stachura I, Castranova V, Pailes WH, Lapp NL. Acute silicosis responding to corticosteroid therapy. Chest. Feb 1992;101(2):366-70. [Medline].

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6. Mulloy KB. Silica exposure and systemic vasculitis. Environ Health Perspect. Dec 2003;111(16):1933-8. [Medline].

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Keywords

silicosis, pneumoconiosis, pneumoconioses, fibronodular lung disease, work-related illness, mining illness, mining, tunneling, quarrying, drilling, crushing stone, chipping, grinding, sandblasting, cement manufacturing, building construction, occupational hazard, cutting bricks, manufacturing bricks, silica dust, silica exposure

Contributor Information and Disclosures

Author

Basil Varkey, MD, FCCP, Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Medical College of Wisconsin; Consulting Pulmonologist, Froedtert Memorial Lutheran Hospital
Basil Varkey, MD, FCCP is a member of the following medical societies: American Association of Physicians of Indian Origin, American College of Chest Physicians, American Federation for Clinical Research, American Thoracic Society, and Royal College of Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Anita B Varkey, MD, Assistant Professor, Department of Medicine, Loyola University Medical Center; Associate Program Director, Internal Medicine Residency; Medical Director, General Internal Medicine Clinic, Loyola Outpatient Center
Anita B Varkey, MD is a member of the following medical societies: American College of Physicians and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Medical Editor

Gregory Tino, MD, Director of Pulmonary Outpatient Practices, Associate Professor, Department of Medicine, Division of Pulmonary, Allergy, and Critical Care, University of Pennsylvania Medical Center and Hospital
Gregory Tino, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H, Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine
Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine
Disclosure: Keck School of Medicine, USC None None

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

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