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
More on Silicosis |
 Overview: Silicosis |
| Differential Diagnoses & Workup: Silicosis |
| Treatment & Medication: Silicosis |
| Follow-up: Silicosis |
| References |
| Next Page » |
References
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Further Reading
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
