Introduction
Background
Pulmonary fibrosis caused by asbestos inhalation is called asbestosis. The word asbestos is derived from Greek and means inextinguishable, and asbestos is a group of naturally occurring, heat-resistant fibrous silicates. Pneumoconiosis is the general term for lung disease caused by inhalation and deposition of mineral dust.
Asbestos fibers are long and thin (length-to-diameter ratio >3) and may be either curved or straight. The curved fibers are called serpentine (chrysotile is the prime example), and the straight fibers are amphiboles. Researchers recognize 5 different amphiboles: (1) amosite, (2) anthophyllite, (3) tremolite, (4) actinolite, and (5) crocidolite. Chrysotile is by far the most common type of asbestos fiber produced in the world.
Production and use of asbestos increased greatly between 1877 and 1967. In the 1930s and 1940s, scientists recognized a causal link between asbestos exposure and asbestosis. In the 1950s and 1960s, researchers established asbestos as a predisposing factor for bronchogenic carcinoma and malignant mesothelioma.
Also see Asbestos-Related Disease and Asbestosis for a radiological focus.
Pathophysiology
The cumulative dose of fibers inhaled over a period of time and the type, durability, and dimensions of the fiber influence carcinogenicity and fibrogenicity. The incidence of asbestosis varies with the cumulative dose of inhaled fibers; the greater the cumulative dose, the higher the incidence of asbestosis. All types of asbestos fibers are fibrogenic to the lungs. Amphiboles, particularly crocidolite fibers, are markedly more carcinogenic to the pleura. Fibers with diameters smaller than 3 micrometers are fibrogenic because they penetrate cell membranes. Long fibers (ie, >5 micrometers) are incompletely phagocytosed and stay in the lungs, setting up cycles of cellular events and the release of cytokines.The initial inflammation occurs in the alveolar bifurcations and is characterized by the influx of alveolar macrophages. Asbestos-activated macrophages produce a variety of growth factors, including fibronectin, platelet-derived growth factor, insulinlike growth factor, and fibroblast growth factor, which interact to induce fibroblast proliferation. Oxygen free radicals (eg, superoxide anion, hydrogen peroxide, hydroxy radicals) that are released by the macrophages damage proteins and lipid membranes and sustain the inflammatory process. A plasminogen activator, which is also released by macrophages, further damages the interstitium of the lung by degrading matrix glycoproteins.
Individuals probably differ in their susceptibility to asbestosis based on respiratory clearance and other unidentified host factors. People who smoke have an increased rate of asbestosis progression likely due to impaired mucociliary clearance of asbestos fibers.1
Frequency
United States
Asbestos consumption (per capita) peaked in 1951, declined gradually until 1971, and declined rapidly thereafter.
No reliable information exists regarding the number of people presently at risk in the United States and in other countries. Since the early 1940s, as many as 10 million workers in the United States may have been exposed to asbestos. In 1972, reports estimated that 250,000 persons were at risk. By the 1980s, the number of active asbestos miners and millers had fallen to a few hundred. Strict regulation (eg, prohibition of asbestos sprays in buildings, controls in the level of asbestos fibers in the air) has drastically reduced the risk of developing asbestosis. However, those who have been previously exposed continue to be at risk for asbestosis and other asbestos-related diseases.
International
Trends in usage of asbestos and observational studies suggest that asbestosis and other asbestos-related diseases are likely to be continuing problems in developing countries.
Mortality/Morbidity
- Study of mortality trends in the United States show that while deaths from other pneumoconioses are declining, deaths from asbestosis are increasing. Further, they are not expected to decrease in the next 15 years. One model predicts 29,667 deaths from 2005 to 2027.2
- Estimated annua years of potential life lost before age 65 years attributable to asbestosis totaled 7267 in the years 2001-2005 and represented a significant increase from 1968-1972.3
- People who smoke are likely to develop chronic bronchitis and obstructive airway disease and are prone to respiratory tract infections. People who smoke are at high risk for the development of bronchogenic carcinoma because asbestos and tobacco smoke are synergistic in carcinogenicity. Individuals who both smoke and are exposed to asbestos are several times more susceptible to developing lung carcinoma than individuals who have neither exposure.4
- Some studies show that asbestos exposure alone, without a smoking history, increases the risk of lung carcinoma 6-fold.
- Asbestos exposure increases the risk of developing malignant mesothelioma and cancers of upper respiratory tract, esophagus, kidney, and biliary system.
- Asbestosis may coexist with other asbestos-related diseases, including calcified and noncalcified pleural plaques, pleural thickening, benign exudative pleural effusion, rounded atelectasis, and malignant mesothelioma of the pleura.
Clinical
History
- Because the development of asbestosis is dose dependent, symptoms appear only after a latent period of 20 years or longer. This latent period may be shorter after intense exposure.
- Dyspnea upon exertion is the most common symptom and worsens as the disease progresses.
- Patients may have a dry (ie, nonproductive) cough. A productive cough suggests concomitant bronchitis or a respiratory infection.
- Patients may complain of nonspecific chest discomfort, especially in advanced cases.
Physical
- Rales (ie, end-inspiratory crackles) are the most important finding during examination. The rales are persistent and dry and are described as fine cellophane rales or coarse Velcro rales. The rales are best auscultated at the bases of the lungs posteriorly and in the lower lateral areas. Initially, physicians hear the rales in the end-inspiratory phase. However, in advanced disease, rales may be heard during the entire inspiratory phase. Occasionally, the presence of rales precedes radiographic finding abnormalities and pulmonary function test abnormalities. Rales are not to be expected in all patients; one third of patients may not have them.
- Finger clubbing is observed in 32-42% of cases. This finding is not necessarily related to the severity of disease.
- Reduced chest expansion in advanced disease correlates with restrictive ventilatory impairment and reduced vital capacity.
- In advanced disease, patients may show the following signs associated with cor pulmonale: cyanosis, jugular venous distention, hepatojugular reflux, and pedal edema.
Causes
- See Pathophysiology for a discussion of various factors that cause asbestosis. Among them, the level of asbestos fiber exposure is of prime importance. Experts estimate a 1% risk of developing asbestosis after a cumulative dose of 10 fiber-year/m3.
- In modern times, the risk to persons in the United States occurs mainly through the processing, manufacturing, and end-use of asbestos.
- Manufacturers commonly use asbestos in the following products:
- Products containing asbestos cement - Pipes, shingles, clapboards, sheets
- Vinyl-asbestos floor tiles
- Asbestos paper in filtering and insulating products
- Material in brake linings and clutch facings
- Textile products - Yarn, felt, tape, cord, rope
- Spray products used for acoustical, thermal, and fireproofing purposes
- Examples of occupations associated with asbestosis include the following:
- Insulation workers
- Boilermakers
- Pipefitters
- Plumbers
- Steamfitters
- Welders
- Janitors
More on Asbestosis |
 Overview: Asbestosis |
| Differential Diagnoses & Workup: Asbestosis |
| Treatment & Medication: Asbestosis |
| Follow-up: Asbestosis |
| Multimedia: Asbestosis |
| References |
| Next Page » |
References
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Further Reading
Keywords
asbestosis, pneumoconiosis, pulmonary fibrosis, lung disease, bronchogenic carcinoma, malignant mesothelioma, coal worker's pneumoconiosis, dermatomyositis, hypersensitivity pneumonitis, idiopathic pulmonary fibrosis, sarcoidosis, silicosis, collagen vascular diseases, interstitial pulmonary diseases, asbestos inhalation, chrysotile fibers, amphibole fibers, calcified pleural plaques, noncalcified pleural plaques, pleural thickening, benign exudative pleural effusion, rounded atelectasis, malignant mesothelioma of the pleura
