• Clinical science

Silicosis (Miners phthisis…)

Summary

Silicosis is a common occupational lung disease that is caused by the inhalation of crystalline silica dust. Silica is the most abundant mineral on earth. Workers that are involved for example in constructions, mining, or glass production are among the individuals with the highest risk of developing the condition. Acute silicosis causes severe symptoms (e.g., exertional dyspnea, cough with sputum) and has a very poor prognosis. Chronic silicosis has a very variable prognosis and affected individuals may remain asymptomatic for several decades. However, radiographic signs are usually seen early on. Typical radiographic findings are calcifications of perihilar lymph nodes, diffuse ground glass opacities, large numbers of rounded, solitary nodules or bigger, confluent opacities. Avoiding further exposure to silica is crucial, especially since the only treatment available is symptomatic (e.g., bronchodilators). Silicosis is associated with an increased risk of tuberculosis and lung cancer.

Epidemiology

  • There are currently approx. 2.3 million workers exposed to silica dust
  • Overall incidence and mortality have significantly decreased over the last decades
  • Silicosis is a national notifiable disease.

References:[1][2][3]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

  • Inhalation of crystalline silica, most commonly as dust
  • High-risk occupations for the development of silicosis include sandblasting, mining; (e.g., coal mining), construction; (e.g., tunnel construction), hydraulic fracturing, ceramics production, quarrying, glass manufacturing; , and working in foundries.

To remember the high-risk occupations for the development of silicosis, think “I found (foundries) sand (sandblasting) on my (mining) window sill (silicosis)!”

References:[2][4]

Pathophysiology

  • Inhalation of silica dust → deposition in the airways; → interaction of crystalline silica surfaces with aqueous media produces oxygen radicals inflammatory reaction and injury to pulmonary cells (e.g., alveolar macrophages) → pulmonary fibrosis and scarring

References:[5][4]

Clinical features

Acute silicosis

Acute silicosis refers to a short-term exposure to a large amount of crystalline silica dust.

Chronic silicosis

Chronic silicosis refers to long-term exposure to crystalline silica dust. Patients may remain completely asymptomatic or develop symptoms only after several decades of exposure.

  • Chronic cough; (often with sputum; ) and exertional dyspnea
  • Fatigue and weight loss
  • Signs of respiratory failure and cor pulmonale
  • Caplan syndrome: pneumoconiosis in combination with rheumatoid arthritis; characterized by rapid development of basilar nodules and mild obstruction of ventilation [6]

Dyspnea upon exertion and cough with sputum are the key clinical features of silicosis!

Symptoms of chronic silicosis are variable and often occur only after several decades after constant/repeated exposure!References: [7][4]

Diagnostics

Silicosis is diagnosed based on the occupational history, respiratory symptoms, and the following diagnostic investigations.

In the early stages of the disease, there may not be any symptoms or findings on auscultation (wheezing or buzzing), while radiographic abnormalities can already be seen!

Silicosis features pathologic changes of both restrictive and obstructive lung disease.

Silica is found below the earth's surface, but the upper lobes of the lungs are primarily affected.

References: [7][4]

Treatment

  • There is no definitive treatment for either acute or chronic silicosis.
  • Avoid further exposure to crystalline silica
  • Lung transplantation (in patients with advanced respiratory failure)
  • Symptomatic treatment
    • Smoking cessation
    • Bronchodilators
    • Supplemental oxygen
    • Vaccination against pathogens causing respiratory infections (e.g., pneumococci)

References:[3][7][4]

Complications

References:[5][9]

We list the most important complications. The selection is not exhaustive.

  • 1. OSHA. OSHA's Final Rule to Protect Workers from Exposure to Respirable Crystalline Silica. https://www.osha.gov/silica/. Accessed July 29, 2017.
  • 2. Rose C, King TE Jr, Hollingsworth H. Silicosis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/silicosis. Last updated December 19, 2016. Accessed July 29, 2017.
  • 3. Centers for Disease Control and Prevention. Silicosis. https://wwwn.cdc.gov/nndss/conditions/silicosis/. Accessed July 29, 2017.
  • 4. Leung CC, Yu ITS, Chen W. Silicosis. The Lancet. 2012; 379(9830): pp. 2008–2018. doi: 10.1016/s0140-6736(12)60235-9.
  • 5. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Philadelphia, PA: Elsevier Saunders; 2015.
  • 6. Alaya Z, Braham M, Aissa S, Kalboussi H, Bouajina E. A case of Caplan syndrome in a recently diagnosed patient with silicosis: A case report. Radiology Case Reports. 2018; 13(3): pp. 663–666. doi: 10.1016/j.radcr.2018.03.004.
  • 7. Greenberg MI, Waksman J, Curtis J. Silicosis: A Review. Disease-a-Month. 2007; 53(8): pp. 394–416. doi: 10.1016/j.disamonth.2007.09.020.
  • 8. Joshi GN, Goetjen AM, Knecht DA. Silica particles cause NADPH oxidase-independent ROS generation and transient phagolysosomal leakage. Mol Biol Cell. 2015; 26(18): pp. 3150–64. doi: 10.1091/mbc.E15-03-0126.
  • 9. Sharma N, Kundu D, Dhaked S, Das A. Silicosis and silicotuberculosis in India. Bull World Health Organ. 2016; 94(10): pp. 777–778. doi: 10.2471/BLT.15.163550.
last updated 09/23/2020
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