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



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.




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.


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).


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


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


No precise information regarding age is available.