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Asbestosis
Article Last Updated: Nov 9, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Basil Varkey, MD, FCCP, Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Froedtert Memorial Lutheran Hospital, Medical College of Wisconsin
Basil Varkey is a member of the following medical societies: American Association of Physicians of Indian Origin, American College of Chest Physicians, American Federation for Clinical Research, American Thoracic Society, and Royal College of Physicians
Coauthor(s):
Anita B Varkey, MD, Consulting Staff, Division of General Medicine and Primary Care, John H Stroger Jr Hospital of Cook County; Assistant Professor, Department of Medicine, Rush Medical College
Editors: Sat Sharma, MD, FRCP(C), FCCP, FACP, DABSM, Program Director, Associate Professor, Department of Internal Medicine, Divisions of Pulmonary and Critical Care Medicine, University of Manitoba; Site Director of Respiratory Medicine, St Boniface General Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Om Prakash Sharma, MD, Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California; Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine; Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, Professor of Medicine, University of California at Los Angeles School of Medicine
Author and Editor Disclosure
Synonyms and related keywords:
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
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.
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
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.
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
- In 1992, nearly 6 of every 1 million deaths were attributed to asbestosis in the United States.
- People who smoke are likely to develop chronic bronchitis and obstructive airway disease and are prone to respiratory infections. People who smoke are at high risk for development of bronchogenic carcinoma because asbestos and tobacco smoke are synergistic in carcinogenicity. Individuals who both smoke and are exposed to asbestos are 59 times more susceptible to developing lung carcinoma than individuals who have neither exposure.
- 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.
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
Coal Worker's Pneumoconiosis
Dermatomyositis
Hypersensitivity Pneumonitis
Pulmonary Fibrosis, Idiopathic
Sarcoidosis
Silicosis
Other Problems to be Considered
Collagen-vascular diseases
Other interstitial pulmonary diseases
See Complications. Be aware of the predisposition for bronchogenic carcinoma and the variety of asbestos-related diseases that may coexist with asbestosis.
Lab Studies
- Briefly, the diagnosis of asbestosis is built upon 3 features: (1) reliable exposure history with an appropriate latency period; (2) evidence of fibrosis by radiographs (eg, chest radiographs, high-resolution computed tomography [HRCT]), consistent physical examination findings, and pulmonary function findings with or without histologic evidence (asbestos bodies in bronchoalveolar lavage [BAL] fluid2 or fibrosis in biopsy samples of lung tissue); and (3) absence of other causes for interstitial fibrosis.
- The diagnosis is based on the following:
- A reliable and significant (ie, dose x time) history of asbestos exposure and an appropriate latency period between exposure and detection of disease
- Characteristic changes of pulmonary fibrosis on imaging studies
- Absence of other fibrotic diseases that mimic asbestosis
- Dyspnea upon exertion
- Bilateral basilar inspiratory crackles
- Restrictive pattern on pulmonary function studies associated with impaired gas exchange
- Blood tests for antinuclear antibodies, rheumatoid factor, and erythrocyte sedimentation rate lack diagnostic specificity and are not useful in diagnosis or in activity assessment.
Imaging Studies
- Radiography
- Chest radiographs (ie, posteroanterior and lateral views) are basic and required diagnostic imaging studies.
- Typical findings include diffuse reticulonodular infiltrates, which are observed predominantly at the lung bases. The diffuse lung infiltrates cause the appearance of shaggy heart borders.
- Bilateral pleural thickening may be observed. Asbestos-related pleural thickening more often involves the middle third of the pleura as opposed to the upper third affected by tuberculosis and the lower third damaged by empyema, trauma, or past pleurodesis therapy.
- A calcified pleural plaque located in the diaphragmatic pleura is a reliable indicator of asbestos exposure but is not a required element for diagnosis of asbestosis. Besides the diaphragmatic pleura, other common sites for plaque formation in the parietal pleura are along the sixth through the ninth ribs. Noncalcified plaques may not be detected on chest radiographs.
- Rarely, pleural adhesions may cause peripheral atelectasis with a rounded border (rounded atelectasis) that may simulate a lung tumor.3
- In early disease, an increase in interstitial markings, mostly linear, is seen. Honeycombing, with cystic spaces surrounded by coarse interstitial infiltrates and small lung fields, characterizes advanced disease.
- The International Labor Office standardized classification of radiographic abnormalities is useful in grading the extent of disease in asbestosis and in other pneumoconioses.
- An oblique-view radiograph may be helpful in recognizing pleura-based abnormalities.
- Computed tomography scan
- CT scan is useful in delineation of pleural or pleura-based abnormalities (eg, effusion, thickening, plaque, malignant mesothelioma, rounded atelectasis) and in delineation of a parenchymal density that is suggestive of bronchogenic carcinoma.
- An HRCT scan allows better definition of interstitial infiltrates and may be helpful in diagnosing early stages of asbestosis.
- In a minority of cases, HRCT abnormalities may be seen in individuals with normal chest radiograph findings.
- Typical HRCT findings of asbestosis include subpleural linear opacities seen parallel to the pleura, basilar lung fibrosis and peribronchiolar, intralobular and interlobular septal fibrosis, honeycombing, and pleural plaques.
Other Tests
- Pulmonary function tests
- Diffusing capacity reduction may precede lung volume changes, but findings from a diffusing capacity measurement are not specific. Besides diffusing capacity reduction, the earliest physiologic abnormality is exertional hypoxemia.
- Total lung capacity is reduced in asbestosis as in other restrictive disorders.
- Using spirometry, vital capacity typically appears reduced, without a reduction in the ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1-to-FVC).
- Small airway flow rates (eg, midexpiratory forced expiratory flow, FEF25-75) are reduced but are nonspecific for a diagnosis of small airway obstructive disease.
- Oximetry
- Evaluation of oxygenation is important because uncorrected hypoxemia causes pulmonary hypertension and may lead to cor pulmonale.
- Physicians can use a noninvasive test of pulse oximetry as a screening test, especially if oximetry is performed during rest and during exercise (eg, 6-minute walk test).
- Obtain accurate information through measurement of arterial blood gases, which requires an arterial puncture. In selected cases, an exercise study may demonstrate desaturation during exercise.
- A lung scan with gallium citrate Ga 67 is a nonspecific test that may detect areas of inflammation in the lungs. However, the results do not always correlate with other measurements of inflammation. This test is no longer recommended.
Procedures
- Bronchoalveolar lavage
- BAL has only limited application in the diagnosis and management of asbestosis. BAL is helpful in diagnosing infections that may present with diffuse infiltrates, which simulate asbestosis, and BAL may aid in the diagnosis of a coexisting bronchogenic carcinoma.
- In workers who are exposed to asbestos, BAL can provide quantitative information by asbestos fiber counts. More than 1 asbestos body (ie, coated asbestos fiber) per milliliter of lavage effluent suggests significant exposure.
- Bronchoscopy
- Fiberoptic bronchoscopy is performed to facilitate BAL.
- In addition, bronchoscopy is indicated for airway examination when radiologic studies are suggestive of bronchogenic carcinoma.
- Transbronchoscopic lung biopsy is not recommended for diagnosis of asbestosis. This procedure yields inadequate tissue and may cause crush alterations to the tissue.
- Open-lung biopsy is not indicated in most cases. However, this procedure provides sufficient tissue for the pathologist to make a definitive diagnosis.
Histologic Findings
Most often, physicians diagnose asbestosis without histopathological examination of lung tissue. A pathologic diagnosis of asbestosis requires visualization of both fibrosis and asbestos bodies through light microscopy or a significant quantity of asbestos fibers observed through electron microscopy.
The American College of Pathologists' scheme for assessing the severity of asbestosis grades fibrosis in 4 categories. Grade 1 is fibrosis in the wall of a respiratory bronchiole without extension to distant alveoli. Grades 2 and 3 define more extensive disease, and Grade 4 is alveolar and septal fibrosis with spaces larger than alveoli ranging up to 1 cm (ie, honeycombing).
Asbestos bodies (ie, ferruginous bodies) are asbestos fibers that develop a ferritin-protein coat and have a characteristic long-beaded appearance. Asbestos bodies alone are not diagnostic for disease because occasionally examiners find asbestos bodies in people without known exposure.
Medical Care
- Control of asbestos in the workplace is the most effective method for preventing asbestosis. Cessation of further exposure to asbestos once the diagnosis of asbestosis is made is imperative because further exposure increases the rate of progression. However, the disease may progress even after cessation of exposure.
- Advise smokers to quit smoking, and provide referral to a smoking cessation clinic.
- Inform patients on the work-related causation of the disease (potentially compensable) and report it to appropriate state or federal agencies.
- Assessment of disease severity and functional impairment are important in tailoring a treatment and follow-up plan (ie, frequency of clinic visits, chest radiographs, pulmonary function testing).
- Treatment requires prompt attention to respiratory infections and immunizations against influenza and pneumococcal pneumonia.
- Perform prompt antimicrobial treatment of respiratory infections.
- Assess oxygenation status at rest and with exercise. If testing detects hypoxemia at rest or with exercise, prescribe supplemental oxygen.
- Remain aware of the complications of asbestosis to expedite detection and treatment.
- Provide palliative care for the relief of distressing symptoms in advanced disease.
Consultations
- Consult a pulmonologist to assess the need for long-term oxygen therapy and for the management of advanced cases and complications (see Mortality/Morbidity).
- If patients smoke, refer them to a smoking cessation clinic.
- Because of the likelihood of bronchogenic carcinoma, consult a thoracic surgeon if a solitary pulmonary nodule develops in a patient with asbestosis.
- Provide hospice referral (preferably at home) when disease reaches the terminal phase.
Drugs are not effective in the treatment of asbestosis. Corticosteroids and immunosuppressive drugs do not alter the course of the disease.
Deterrence/Prevention
- Control of asbestos in the workplace is the most effective method for preventing asbestosis.
Complications
- Pulmonary hypertension
- Cor pulmonale
- Right-sided heart failure
- Progressive respiratory insufficiency: The risk factors for developing this complication are cumulative amount of asbestos inhaled; degree of dyspnea; cigarette smoking; combined pulmonary and pleural involvement; honeycombing visible on radiographs; and a high number of neutrophils, eosinophils, and fibronectin in BAL fluid.
- Malignancy: A higher risk of lung carcinoma has been found in patients with asbestosis. Patients with asbestosis are also at risk for malignant mesothelioma and carcinomas of upper respiratory tract, esophagus, biliary system, and kidney.
Patient Education
- Inform patients of the work-related causes of asbestosis (see Medical Care).
- For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article Bronchoscopy.
Medical/Legal Pitfalls
- Diagnosis, causation, and impairment are the major issues with regard to medical/legal pitfalls.
- Physicians often make the diagnosis without histopathologic confirmation. Errors may occur because other more common interstitial diseases (eg, idiopathic pulmonary fibrosis) mimic the clinical, radiologic, and pulmonary functional features of asbestosis. Bear in mind the long latency period between patient exposure and the manifestation of symptoms and signs of asbestosis. When lung tissue is available for histopathologic examination, confirmation of diagnosis requires both fibrosis and accumulation of asbestos bodies or fibers.
- Determining the cause depends on assessment of the levels and duration of exposure and on knowledge of occupational epidemiologic studies.
- Assessment of impairment, which is a key ingredient in determining disability, is based mainly on pulmonary function studies.
- No evidence exists to confirm that small airway disease, which is detected by flow volume curves, progresses to asbestosis.
- Pleural plaques may coexist with asbestosis, but pleural plaques alone are usually not associated with impaired pulmonary function. Nonetheless, pleural plaques are a reliable indicator of asbestos exposure.
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Asbestosis excerpt Article Last Updated: Nov 9, 2007
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