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Silicosis

  • Author: Basil Varkey, MD, FCCP; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Dec 16, 2015
 

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. Granite and slate have 30-40% free silica content, while sandstone is virtually all free silica.

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.[1]

The Medscape Drugs & Diseases articles Imaging in Silicosis and Coal Worker Pneumoconiosis and Interstitial (Nonidiopathic) Pulmonary Fibrosis may be of interest.

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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.

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Epidemiology

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, but it still accounts for potential life lost before age 65 years.[2] In 1968, 12 people per million population died with silicosis; in 1991, the number approximated 2 people per million population.[3] 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.

Disorders listed under in Complications cause related morbidity. 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.[4] 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.[5, 6]

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.[7] Polymorphisms of the interleukin 1 gene complex have been reported in coal miners with silicosis[8] ; the clinical significance of this has not been elucidated.

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.

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Contributor Information and Disclosures
Author

Basil Varkey, MD, FCCP Professor Emeritus, 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 College of Chest Physicians, American Association of Physicians of Indian Origin

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, Society of General Internal Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

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, American Thoracic Society

Disclosure: Nothing to disclose.

References
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  3. Rosenman KD, Reilly MJ, Kalinowski DJ, Watt FC. Silicosis in the 1990s. Chest. 1997 Mar. 111(3):779-86. [Medline].

  4. Sonnenberg P, Murray J, Glynn JR, Thomas RG, Godfrey-Faussett P, Shearer S. Risk factors for pulmonary disease due to culture-positive M. tuberculosis or nontuberculous mycobacteria in South African gold miners. Eur Respir J. 2000 Feb. 15(2):291-6. [Medline].

  5. de Oliveira Abrao C, de Araujo Filho JA. Mycobacterium sherrisii lung infection in a Brazilian patient with silicosis and a history of pulmonary tuberculosis. Case Rep Infect Dis. 2015. 2015:498608. [Medline].

  6. Chen S, Yuan J, Yao S, et al. Lipopolysaccharides may aggravate apoptosis through accumulation of autophagosomes in alveolar macrophages of human silicosis. Autophagy. 2015 Nov 9. [Medline].

  7. Caplan A, Payne RB, Withley JL. A broadened concept of Caplan's syndrome related to rheumatoid factors. Thorax. 1962. 17:205-209.

  8. Yucesoy B, Vallyathan V, Landsittel DP, et al. Polymorphisms of the IL-1 gene complex in coal miners with silicosis. Am J Ind Med. 2001 Mar. 39(3):286-91. [Medline].

  9. Verma DK, Vacek PM, des Tombe K, et al. Silica exposure assessment in a mortality study of vermont granite workers. J Occup Environ Hyg. 2011 Feb. 8(2):71-9. [Medline].

  10. Palabiyik SS, Girgin G, Tutkun E, Yilmaz OH, Baydar T. Immunomodulation and oxidative stress in denim sandblasting workers: changes caused by silica exposure. Arh Hig Rada Toksikol. 2013 Sep 1. 64(3):431-7. [Medline].

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

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

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  16. Sharma SK, Pande JN, Verma K. Effect of prednisolone treatment in chronic silicosis. Am Rev Respir Dis. 1991 Apr. 143(4 Pt 1):814-21. [Medline].

  17. American Thoracic Society, Centers for Disease Control and Prevention, Infectious Diseases Society of America. Treatment of tuberculosis. MMWR Recomm Rep. 2003 Jun 20. 52:1-77. [Medline].

  18. Rosenman KD, Moore-Fuller M, Reilly MJ. Connective tissue disease and silicosis. Am J Ind Med. 1999 Apr. 35(4):375-81. [Medline].

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

  20. Hogan SL, Cooper GS, Savitz DA, et al. Association of silica exposure with anti-neutrophil cytoplasmic autoantibody small-vessel vasculitis: a population-based, case-control study. Clin J Am Soc Nephrol. 2007 Mar. 2(2):290-9. [Medline].

 
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