Updated: Dec 31, 2015
Author: Basil Varkey, MD, FCCP; Chief Editor: Zab Mosenifar, MD, FACP, FCCP 



Pneumoconiosis is the general term for lung disease caused by inhalation and deposition of mineral dust, with asbestosis more specifically being pneumoconiosis caused by asbestos inhalation. (See Etiology.)

The word asbestos is derived from Greek and means inextinguishable. The term refers to a group of naturally occurring, heat-resistant fibrous silicates, the fibers of which are long and thin (length-to-diameter ratio >3) and either curved or straight. The curved fibers make up serpentine asbestos (chrysotile is the prime example), and the straight fibers make up amphibole asbestos. (See Etiology and Workup.)

Several different types of amphiboles (ie, amosite, anthophyllite, tremolite, actinolite, crocidolite) have been recognized. Chrysotile is by far the most common type of asbestos fiber produced in the world and accounts for virtually all asbestos used commercially in the United States.

The 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. (See Epidemiology and Prognosis.)

Patient education

Inform patients of the work-related causes of asbestosis (see Medical Care). For patient education information, see Bronchoscopy.


The incidence of asbestosis varies with the cumulative dose of inhaled fibers; the greater the cumulative dose, the higher the incidence of asbestosis. Experts estimate a 1% risk of developing asbestosis after a cumulative dose of 10 fiber-year/m3.

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]

As there is some continuing uncertainty about the mode(s) of action of asbestos in the genesis of diseases, an expert group proposed cooperative action by diverse scientific disciplines to address such issues as terminology, mineralogy, test materials, and experimental models.[2]

Antinuclear antibodies

Exposure to amphibole asbestos fibers is linked to the production of autoantibodies. Moreover, a study indicated that asbestos-related abnormalities occur more often in individuals who test positive for antinuclear antibodies (ANAs) than they do in persons who test negative for them. The study was conducted on the population of Libby, Montana, where mining, transportation, and processing of asbestos-contaminated vermiculite caused increased risk of asbestos-related pleural and lung diseases.[3]

Serum samples showed that the majority of persons sampled were positive for ANAs. It was also found that the risk of developing pleural or interstitial abnormalities was more than 3 times greater in the ANA-positive individuals than it was in persons who were ANA negative.[4, 5]

Sources of asbestos exposure

The risk of asbestos exposure 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 acoustic, thermal, and fireproofing purposes

Occupations associated with asbestosis include the following:

  • Insulation workers

  • Boilermakers

  • Pipefitters

  • Plumbers

  • Steamfitters

  • Welders

  • Janitors

The risk of uncontrolled removal of sprayed-on asbestos was highlighted, in a study of 2 workers, by the presence and persistence of asbestos fibers and bodies in the bronchoalveolar lavage (BAL) fluid of these workers even after several months.[6, 7]

Another study, published in 2012, provided a detailed assessment of the health hazards of exposure to asbestos-containing drywall accessory products.[8]


Occurrence in the United States

Asbestos consumption (per capita) peaked in 1951, declined gradually until 1971, and fell rapidly thereafter. No reliable information exists regarding the number of people presently at risk of asbestos exposure 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 on the level of asbestos fibers in the air) has drastically reduced the risk of asbestosis development. However, persons who have been previously exposed to asbestos continue to be at risk for asbestosis and other asbestos-related diseases.[9]

International occurrence

Bans on asbestos use are in place in several countries, including Australia, Japan, South Africa, and the nations of the European Union; use is restricted in the United States and Canada. However, trends in developing countries and countries that are emerging as economic powers indicate an increasing problem with asbestos-related diseases.[10] These shifts in the global epidemiology have prompted a call for a global ban on asbestos.[11, 12, 13]


The following complications can result from asbestos exposure:

  • Pulmonary hypertension

  • Cor pulmonale

  • Right-sided heart failure

  • Progressive respiratory insufficiency

  • Malignancy

Progressive respiratory insufficiency

See the list below:

  • The risk factors for developing this complication are as follows:

  • Cumulative amount of asbestos inhaled

  • Degree of dyspnea

  • Cigarette smoking

  • Combined pulmonary and pleural involvement

  • Honeycombing visible on radiographs

  • High number of neutrophils, eosinophils, and fibronectin in bronchoalveolar lavage (BAL) fluid


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 the upper respiratory tract, esophagus, biliary system, and kidney.

People who smoke are likely to develop chronic bronchitis and obstructive airway disease and are prone to respiratory tract infections. Moreover, 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 the development of lung carcinoma than are individuals who have neither exposure.[14]

Some studies show that asbestos exposure alone, without a smoking history, increases the risk of lung carcinoma 6-fold. Asbestos exposure also increases the risk of developing malignant mesothelioma and cancers of upper respiratory tract, esophagus, kidney, and biliary system.

In addition, a meta-analysis of several studies of women who were occupationally exposed to asbestos found sufficient evidence for a causal association between asbestos exposure and ovarian cancer.[15]

Concomitant diseases

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.

Airway obstruction

Ameille et al found no causal relationship between airway obstruction and asbestos exposure. Their study evaluated lung function in persons (n=3660) with previous occupational exposure to asbestos.[16] No significant correlation was shown between pulmonary function parameters and cumulative asbestos exposure.

Asbestosis-related mortality

Study of mortality trends in the United States has shown that, while deaths from other pneumoconioses are declining, deaths from asbestosis are increasing. Further, the death rate is not expected to decrease for several years. One model predicts 29,667 deaths from 2005 to 2027.[17]

Estimated annual 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.[18]



History and Physical Examination


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 report nonspecific chest discomfort, especially in advanced cases.

Physical examination

Rales are the most important finding during examination. Persistent and dry, they 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 rales in the end-inspiratory phase. In advanced disease, however, 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 them may not have this symptom.

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.



Diagnostic Considerations

Determining the cause of asbestosis depends on the clinicians’ 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.

Clinicians should be aware of the variety of diseases that may coexist with asbestosis and should keep in mind that the risk for bronchogenic carcinoma is increased with asbestos exposure and load, even without asbestosis.[19]

Conditions to consider in the differential diagnosis of asbestosis include collagen-vascular diseases and other interstitial pulmonary disorders.

Differential Diagnoses



Approach Considerations

The diagnosis of asbestosis is based on the following[20] :

  • 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 (ANAs), rheumatoid factor, and erythrocyte sedimentation rate lack diagnostic specificity and are not useful in diagnosis or in activity assessment.

A lung scan with gallium citrate (67 Ga) 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.

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 that exists 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 fibers or asbestos bodies (ie, ferruginous bodies; these 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.

Pleural plaques may coexist with asbestosis, but these plaques alone are usually not associated with impaired pulmonary function. Nonetheless, pleural plaques are a reliable indicator of asbestos exposure.


Chest radiographs (ie, posteroanterior and lateral views) are basic and required diagnostic imaging studies. However, the diagnosis of asbestosis requires multiple elements. A chest radiograph alone has only a modest positive predictive value for the condition, but when it is combined with abnormal signs (rales) and pulmonary function test results, the positive predictive value is markedly increased.[21]

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.

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.

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, which is affected by tuberculosis, or the lower third, which can be damaged by empyema, trauma, or past pleurodesis therapy. (An oblique-view radiograph may be helpful in recognizing pleura-based abnormalities.)

A calcified pleural plaque located in the diaphragmatic pleura is a reliable indicator of asbestos exposure but is not a required element for the 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. (See the image below.)

Asbestos pleural plaques. Asbestos pleural plaques.

Rarely, pleural adhesions may cause peripheral atelectasis with a rounded border (rounded atelectasis) that may simulate a lung tumor.[22]

The International Labor Office standardized classification of radiographic abnormalities is useful in grading the extent of disease in asbestosis and in other pneumoconioses.

CT Scanning

Computed tomography (CT) scanning is useful in the delineation of pleural or pleura-based abnormalities (eg, effusion, thickening, plaque, malignant mesothelioma, rounded atelectasis) and in the delineation of a parenchymal density that is suggestive of bronchogenic carcinoma.[23]

A high-resolution CT (HRCT) scan allows better definition of interstitial infiltrates and may be helpful in diagnosing asbestosis in the early stages.

Typical HRCT findings in asbestosis include subpleural linear opacities seen parallel to the pleura; basilar lung fibrosis and peribronchiolar, intralobular, and interlobular septal fibrosis; honeycombing; and pleural plaques.

In a minority of cases, HRCT abnormalities may be seen in individuals with normal chest radiographic findings.

Pulmonary Function Test

Diffusing capacity reduction precedes 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 on a pulmonary function test 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.


The 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.

Bronchoalveolar Lavage and Bronchoscopy

Bronchoalveolar lavage

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 and simulate asbestosis, and the procedure may aid in the diagnosis of a coexisting bronchogenic carcinoma. In workers who are exposed to asbestos, BAL can provide quantitative information through asbestos fiber counts. More than 1 asbestos body (ie, coated asbestos fiber) per milliliter of lavage effluent suggests significant exposure.[7]


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.

Histologic Findings

In most cases, physicians diagnose asbestosis without a histopathologic 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 the following 4 categories:

  • Grade 1 - Fibrosis in the wall of a respiratory bronchiole without extension to distant alveoli

  • Grades 2 and 3 - These define more extensive disease

  • Grade 4 - Alveolar and septal fibrosis with spaces larger than alveoli, ranging up to 1cm (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.

Lung biopsy

Open lung biopsy is not indicated in most cases. However, this procedure provides sufficient tissue for the pathologist to make a definitive diagnosis.



Approach Considerations

Remain aware of the complications of asbestosis in order to expedite detection and treatment. Inform patients about the work-related causation of the disease (potentially compensable) and report it to appropriate state or federal agencies. Additionally, advise smokers to quit smoking, and provide referral to a smoking cessation clinic.

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).

The treatment of asbestosis requires prompt antimicrobial therapy for respiratory infections, as well as immunization against influenza and pneumococcal pneumonia.

Assess the patient’s oxygenation status at rest and with exercise. If hypoxemia at rest or with exercise is detected, prescribe supplemental oxygen.

Provide palliative care for the relief of distressing symptoms in advanced disease; 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.

Prevention and deterrence

The 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 additional exposure increases the rate of progression. However, the disease may progress even after exposure has stopped.


Consult a pulmonologist to assess the need for long-term oxygen therapy and for the management of advanced cases and complications. Because of the likelihood of bronchogenic carcinoma, consult a thoracic surgeon if a solitary pulmonary nodule develops in a patient with asbestosis.