Asbestosis

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Background

Asbestosis is a process of diffuse interstitial fibrosis of the lung resulting from exposure to asbestos dust.[1, 2, 3]  Asbestos is the name given to a group of naturally occurring minerals that are resistant to heat and corrosion; these include mineral fibers such as chrysotile, amosite, and crocidolite, among others. Chrysotile is by far the most common type of asbestos fiber produced in the world, and it accounts for virtually all commercial use of asbestos in the United States.

Exposure to asbestos occurs through inhalation of fibers in air in the working environment, ambient air in the vicinity of factories handling asbestos, or indoor air in housing and buildings containing asbestos materials. Heavy exposures to asbestos can occur in the construction or shipping industries, particularly during the removal of asbestos materials for renovation, repairs, or demolition. Workers are also likely to be exposed during the manufacture and use of asbestos products (eg, textiles, floor tiles, friction products, insulation [pipes], other building materials), as well as during automotive brake and clutch repair work. Asbestos stopped being manufactured in US materials in the 1970s.

Although the most common exposure to commercial asbestos is occupational, workers' families are also at risk from indirect “take-home” exposures transported by contaminated items such as clothing. Contamination of the living environment from asbestos-containing products is another source of exposure.[4]

The development of asbestosis is dose-dependent, with symptoms typically appearing only after a latent period of 20 years or longer. After intense exposure, however, the latency period may be shorter.

Pathophysiology and Etiology

The incidence of asbestosis varies with the cumulative dose of inhaled fibers; the greater the cumulative dose, the higher the incidence of asbestosis. The risk of developing asbestosis after a cumulative dose of 10 fiber-year/m3 has been estimated at approximately 1%.[5]

All types of asbestos fibers are fibrogenic to the lungs. Amphiboles, particularly crocidolite fibers, are markedly more carcinogenic to the pleura.[5]  The dimensions of the fibers are also important.[6, 7] Fibers with diameters smaller than 3 μm are fibrogenic because they penetrate cell membranes. Long fibers (ie, >5 μm) are incompletely phagocytosed and stay in the lungs, leading to cytokine release and cell destruction.

The initial inflammation of asbestosis occurs in the alveolar bifurcations, characterized by the influx of alveolar macrophages. Asbestos-activated macrophages produce a variety of growth factors, including fibronectin, platelet-derived growth factor (PDGF), insulinlike growth factor (IGF), and fibroblast growth factor (FGF), which interact to induce fibroblast proliferation.

Reactive oxygen species (ROS; eg, superoxide anion, hydrogen peroxide, and hydroxy radicals) released by the macrophages damage proteins and lipid membranes, potentiating 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 vary in their susceptibility to asbestosis on the basis of differences in 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.[8]  In addition, although the data regarding the association between MUC5B promoter polymorphism and idiopathic pulmonary fibrosis (IPF) appear to be clear, the data regarding whether the MUC5B promoter variant is a potential genetic risk factor for asbestosis have been mixed.[9, 10, 11]

Uncertainty remains about the mode(s) of action of asbestos in the genesis of diseases; in an effort to reduce this uncertainty, an expert group has proposed cooperative action by diverse scientific disciplines to address such issues as terminology, mineralogy, test materials, and experimental models.[12]

Antinuclear antibodies

Exposure to amphibole asbestos fibers is linked to autoantibody production. Studies have indicated that asbestos-related abnormalities occur more often in individuals who test positive for antinuclear antibodies (ANAs) than in those who test negative.[13] These studies were conducted in Libby, Montana, where mining, transportation, and processing of asbestos-contaminated vermiculite caused an increased risk of asbestos-related pleural and lung diseases. Serum samples showed that most of the people sampled were ANA-positive.[14, 15] In addition, the risk of developing pleural or interstitial abnormalities was more than three times higher in ANA-positive individuals than in ANA-negative individuals.[14]

Despite the association with ANA seropositivity, there is no clear link between asbestos exposure and the development of autoimmune disorders such as systemic lupus erythematosus. This lack of association with autoimmune disease is in stark contrast to silicate dust exposure, for which there is a clear association with the development of autoimmune disorders.[16, 17, 18]

Sources of asbestos exposure

As noted earlier, exposure to asbestos occurs through inhalation of fibers in air in the working environment, ambient air in the vicinity of factories handling asbestos, or indoor air in housing and buildings containing asbestos materials. Asbestos has commonly been used in the following products:

Occupations associated with asbestosis include the following:

The risk of uncontrolled removal of sprayed-on asbestos was highlighted in a study of two workers, in whom the presence and persistence of asbestos fibers and bodies in their bronchoalveolar lavage (BAL) fluid was noted even after several months.[20, 21]  A separate study provided a detailed assessment of the health hazards of exposure to asbestos-containing drywall accessory products.[22]

Epidemiology

In 2014, the World Health Organization (WHO) estimated that 125 million people worldwide are exposed to asbestos in the workplace, that more than 100,000 people die each year from asbestos-related lung cancer, mesothelioma, and asbestosis, and that nearly 400 deaths are attributable to nonoccupational exposure to asbestos.[5]  

According to mortality data from the US National Center for Health Statistics (NCHS), 6290 deaths were attributed to asbestosis in the period 1999-2010, of which the majority (95%) were in White males (median age, 79 y).[23]  A 2024 study using data from the Global Burden of Disease (GBD) study reported that during the period 1990-2019, the overall number of deaths due to occupational exposure to asbestos increased by 20.2% in the United States, but the age-standardized mortality rate (ASMR) and the age-standardized disability-adjusted life years (DALYs) rate (ASDR) declined.[24]

A 2024 study reported that in 2019, occupational asbestos exposure was responsible for 239,330 deaths and 4,189,000 disability-adjusted life years (DALYs) globally.[25]  Over the period 1990-2019, deaths attributed to occupational asbestos exposure increased by 65.65% globally, and DALYs increased by 43.66%.

According to World Trade Center Health Registry estimates, about 410,000 people were exposed to asbestos when as much as 400 tons of it was released following the collapse of the the Twin Towers on September 11, 2001.[26]  Those at highest risk for developing 9/11-related illnesses were workers who participated in the rescue, recovery, and cleanup efforts at the sites of the towers, along with those living and working in lower Manhattan during the cleanup.

 A substantial amount of asbestos remains in buildings and eventually will be removed, either during remediation or renovations or demolition. It has been estimated that approximately 1.3 million workers in construction and general industry may be exposed to asbestos during maintenance activities or remediation of buildings containing asbestos.[23]  In the United States, vermiculite mined in Libby, Montana, was found to be contaminated with asbestos; this vermiculite was used in 70% of vermiculite insulation in the United States between 1919 and 1990. In a study of 128 Libby miners, 119 had asbestos-related findings on high-resolution computed tomography (HRCT).[27]  

Asbestos has not been mined in the United States since 2002, but in 2016, approximately 340 metric tons of asbestos was imported for use in the chloralkali industry to manufacture semipermeable diaphragms in electrolytic cells; in addition, an unknown quantity of asbestos was imported within manufactured products, possibly including brake linings and pads, building materials, gaskets, millboards, and yarn and thread, among others.[28]  In 2024, however, no asbestos was imported.[29]

Globally, bans on asbestos use are in place in several countries, including Australia, Japan, South Africa, and the nations of the European Union; asbestos use is restricted in the United States and Canada. However, persons who have been previously exposed to asbestos continue to be at risk for asbestosis and other asbestos-related diseases as a consequence of the long latency periods following exposure.[30, 31]  In addition, trends in developing countries and countries that are emerging as economic powers indicate an increasing problem with asbestos-related diseases.[32]

Prognosis

The following complications can result from asbestos exposure:

Progressive respiratory insufficiency

The risk factors for developing progressive respiratory insufficiency are as follows:

Malignancy

A higher risk of lung carcinoma has been found in patients with asbestosis. Specifically, asbestos exposure raises the risk for bronchogenic carcinoma. Patients with asbestosis are also at risk for developing malignant mesothelioma and carcinomas of the upper respiratory tract, esophagus, biliary system, and kidney. Exposure to commercial materials made or contaminated with asbestos has been the main preventable cause of malignant mesothelioma. 

In a prospective cohort study (N = 544) examining the incidence of malignancy in patients with asbestosis from chrysotile exposure, Wang et al found the rate of occurrence to be 16.36% (n = 89).[33]  The standardized incidence ratios for the various malignancies were 16.61 for lung cancer, 175 for mesothelioma, 5.23 for breast cancer, and 8.77 for endometrial carcinoma.

A mortality study that included 3984 Italian shipyard workers employed in Genoa between 1960 and 1981 and followed them to 2014 reported a death rate of 83.6%, with excess mortality for all cancers, pleural mesothelioma, and cancers of the larynx and lung, as well as for respiratory diseases, including asbestosis.[34] Of the 399 deaths from lung cancer, 90 (22.6%) were attributed to asbestos exposure.

People who smoke are likely to develop chronic bronchitis and obstructive airway disease, and they 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 have synergistic carcinogenicity.[35] Individuals who both smoke and are exposed to asbestos are several times more susceptible to the development of lung carcinoma than individuals without either exposure.[36]

Some studies have found that asbestos exposure alone, without a smoking history, increases the risk of lung carcinoma sixfold.

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.[37] This association should be interpreted with caution, in that some cohort studies included in earlier meta-analyses reported disease misclassification for peritoneal mesothelioma.[38]

Concomitant diseases

Asbestosis may coexist with other asbestos-related diseases, including calcified and noncalcified pleural plaques, pleural thickening,[39] benign exudative pleural effusion, rounded atelectasis, and malignant mesothelioma of the pleura. A study of 102 asbestosis cases diagnosed since January 2001 found that pleural plaques were present in 94% (n = 96) and malignancies in 76% (n = 78; 38 lung cancers, 29 pleural mesotheliomas, 8 peritoneal mesotheliomas).[40]

Airway obstruction

A large study (N = 3660) that evaluated lung function in persons with previous occupational exposure to asbestos found no causal relation between airway obstruction and asbestos exposure.[41] No significant correlation was shown between pulmonary function parameters and cumulative asbestos exposure.

Patient Education

Patients should be informed regarding the work-related causes of asbestosis (see Medical Care). In addition, it is useful for patient education efforts to address the following questions.

What is asbestos?

Asbestos is a group of minerals shaped as long fibers. Sources of asbestos, up to the 1970s, included insulation, car brakes, ships, and construction materials. 

Who gets exposed to asbestos?

People get exposed to asbestos through their work. Occupations at high risk include construction workers, roofers, welders, and insulation workers, among others. Because asbestos can linger on articles of clothing, family members of people who work in these occupations may also be exposed if sufficient care is not taken.

What health problems can result from exposure to asbestos?

Asbestos can causes many health problems. The mnemonic CAP can serve as a useful reminder of the health problems associated with asbestos exposure, as follows:

Symptoms of asbestos exposure do not occur immediately after contact with the mineral. Some people may not have symptoms for 15-30 years. Most patients who develop asbestosis or another related disease due to asbestos exposure will have shortness of breath. Other symptoms include coughing up blood and chest pain. If any of these symptoms occur, medical attention should be sought.

History

A detailed occupational and potential exposure history is essential. The following information should be obtained[2] :

The development of asbestosis is dose-dependent, with symptoms typically appearing only after a latent period of 20 years or longer; however, the latency period may be shorter after intense exposure.

Dyspnea on exertion is the most common symptom of asbestosis and worsens as the disease progresses. Patients may have a dry (ie, nonproductive) cough. A productive cough, however, suggests concomitant bronchitis or a respiratory infection. Patients may report nonspecific chest discomfort, especially in advanced cases.

Physical Examination

Bibasilar rales are the most important finding during examination in a patient with suspected asbesosis. Persistent and dry, they are described as fine cellophane rales or coarse Velcro rales. The rales are best auscultated at the posterior lung bases and in the lower lateral areas.

Initially, rales may be heard 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 abnormalities and pulmonary function test abnormalities. It should be kept in mind, however, that some patients may not have rales at all.

Finger clubbing is observed in 32-42% of cases of asbestosis. 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 asbestosis, patients may show the signs associated with cor pulmonale, such as cyanosis, jugular venous distention, hepatojugular reflux, and pedal edema.

Approach Considerations

The diagnosis of asbestosis is based on the following[43] :

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.

In general, laboratory studies are nonspecific and rarely useful. Blood tests for antinuclear antibodies (ANAs), rheumatoid factor (RF), and erythrocyte sedimentation rate (ESR) lack diagnostic sensitivity or specificity and are not useful in the workup.

Imaging findings can facilitate differentiation of asbestosis from other asbestos-related diseases. Computed tomography (CT) is useful in the delineation of pleural or pleura-based abnormalities. High-resolution CT (HRCT) is playing an increasingly important role in the diagnosis of diffuse interstitial lung disease. However, chest radiography remains the initial modality for detection and characterization of pleural and parenchymal disease. Ultrasonography (US) plays a role in characterizing pleural effusions and in guiding pleural aspiration and biopsy.

Imaging of mesothelioma typically includes CT, magnetic resonance imaging (MRI), and positron emission tomography (PET); images may be acquired during initial tumor diagnosis and staging, treatment response assessment, or patient surveillance.

According to the 2016 Austrian Mesothelioma Interest Group (AMIG) consensus statement for the diagnosis and staging of malignant pleural mesothelioma, after initial imaging with CT and confirmation of disease via video-assisted thoracic surgery (VATS), a potential candidate for surgical treatment should undergo PET-CT to rule out distant metastases and involvement of the abdomen and mediastinal lymph nodes.[44] In some cases of unclear involvement of adjacent structures (eg, chest wall), MRI can be added to discern resectability.

Optical imaging using electromagnetic radiation in (or near) the visible light region of the spectrum has been applied in the intraoperative setting for mesothelioma. Early results have suggested that such imaging may aid surgeons in their attempt to achieve a macroscopic complete resection.[45]

In most cases, asbestosis is diagnosed without a histopathologic examination of lung tissue. A pathologic diagnosis of asbestosis requires visualization of both fibrosis and asbestos bodies through light microscopy or of a significant quantity of asbestos fibers observed through electron microscopy.

Helsinki guidelines for diagnosis

According to the 2014 Helsinki guidelines for the diagnosis of asbestos-related disorders, asbestosis is defined as diffuse interstitial fibrosis of the lung as a consequence of exposure to asbestos dust. The following criteria should be used to identify asbestos exposure[1] :

The guidelines recommended the use of CT imaging in the diagnosis of asbestos-related diseases in the following circumstances:

The criteria for diagnosis of asbestosis on CT were as follows:

The guidelines further noted that in histopathologic evaluation, bronchiole-wall fibrosis has been associated with asbestos exposure and other exposures, including smoking. Subpleural curvilinear lines or dots on HRCT are characteristic of bronchiolar fibrosis.[1]

Chest Radiography

Chest radiographs (posteroanterior [PA] and lateral views) are basic and required diagnostic imaging studies. However, the diagnosis of asbestosis requires multiple elements. By itself, a chest radiograph has only a modest (< 50%) positive predictive value (PPV) for asbestosis, but when it is combined with characteristic signs (rales) and abnormal pulmonary function test (PFT) results, the PPV is markedly increased.[46]

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. Honeycombing may also be seen with idiopathic pulmonary fibrosis (IPF), making IPF an important diagnostic consideration.

The International Labour Organization (ILO) standardized classification of radiographic abnormalities is useful for grading the extent of disease in asbestosis and in other pneumoconioses.[2, 47]

Pleural thickening

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.)

Pleural plaque

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 images below.)



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Asbestosis. Asbestos pleural plaques.



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Posteroanterior (PA) chest radiograph in 58-year-old man with history of occupational exposure to asbestos shows right diaphragmatic pleural plaque ca....

Rarely, pleural adhesions may cause peripheral atelectasis with a rounded border (rounded atelectasis) that may simulate a lung tumor.[48]

Benign effusion

Benign asbestos-related effusions have the same radiographic appearance as effusions due to other causes; the diagnosis is usually one of exclusion. (See the image below.) Effusions usually are small and may be unilateral or bilateral; they tend to resolve over a period ranging from 1 month to 1 year (commonly 3-4 mo), with residual blunting of costophrenic angles due to pleural thickening in 50% of patients. As many as 30% of effusions recur. Some effusions are associated with pleural plaques.



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Man (67 y) with decades-long history of occupational exposure to asbestos began experiencing nagging left-side chest pain. Posteroanterior chest radio....

Asbestosis

Asbestosis is characterized by interstitial pulmonary fibrosis secondary to the presence of intrapulmonary asbestos bodies or asbestos fibers. The fibrosis usually is most severe in the subpleural lower zones. Chest radiographic findings include fine reticular opacities and septal lines that progress toward a coarser linear pattern of honeycombing. With advanced disease, the heart border and diaphragmatic contours become ill defined—the so-called shaggy heart.

Rounded atelectasis

Rounded atelectasis appears as a well-defined, rounded, focal, subpleural soft tissue mass 2-7 cm in diameter that abuts an area of pleural thickening. Most atelectases are located in the posterolateral or posteromedial parts of the lower lobes. Occasionally, bilateral masses are seen. Mild volume loss may be associated with the condition. Appearances usually remain stable over time, but occasionally, masses may increase or decrease in size.

Malignancy

Appearances of bronchogenic carcinoma are those of non-asbestos-related lung cancers. The most common radiographic finding is a pulmonary mass with associated mediastinal lymphadenopathy.

Mesothelioma typically appears as irregular, nodular, diffuse pleural thickening, occasionally associated with pleural effusion. Less commonly, an isolated effusion or pleural mass is seen. The tumor progresses to encase the entire hemithorax, including the lung. The mediastinum usually is fixed or is shifted toward the side of the tumor.

Computed Tomography

CT is useful in the delineation of pleural or pleura-based abnormalities (eg, effusion, thickening, plaque, malignant mesothelioma, and rounded atelectasis) and in the delineation of a parenchymal density that is suggestive of bronchogenic carcinoma.[49] ​(See the image below.) It has been reported to be 50% more sensitive than chest radiography for the detection of pleural calcification.



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Contrast-enhanced CT scan of chest at level of pulmonary artery bifurcation shows calcified pleural plaques along posterior, lateral, and anterior ple....

A review of chest CT images for 35 individuals exposed to asbestos found a high incidence of pleural plaque (94%) and pulmonary fibrosis (77%).[50]  The findings of lung parenchymal lesions were as follows: centrilobular opacities (94%), subpleural dotlike or branching opacities (80%), interlobular septal thickening (57%), intralobular interstitial thickening (46%), parenchymal bands (43%), and subpleural curvilinear line (29%).

Plaques appear as discrete, well-defined areas of localized pleural thickening. They usually are multiple, bilateral, and located adjacent to rigid structures such as the ribs, the midportion of the chest, the aponeurotic portion of the diaphragm, the mediastinum, and paravertebral regions. Lung apices and costophrenic angles typically are spared. Rarely, the visceral pleura within fissures is involved, or plaques may be pedunculated.

Asbestosis

HRCT 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. (See the image below.)



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Former asbestos worker (55 y) complained of shortness of breath. High-resolution CT (HRCT) scan obtained at lung bases shows prominent interstitial se....

Ground-glass attenuation (increased lung attenuation without obscuration of the underlying pulmonary architecture) is a relatively unusual feature of asbestosis. When present, it may represent edema or fine intralobular fibrosis.

Ancillary findings of curvilinear subpleural lines and parenchymal bands, which are linear opacities 2-5 cm long extending from or paralleling the pleural surface, may be seen. These are characteristic (occurring in 60-80% of patients with asbestosis), though not specific (occurring in 10-20% of patients with non-asbestos-related diseases). The lines and bands represent contiguous, thickened interlobular septa, which are areas of subsegmental atelectasis or fibrosis along bronchovascular bundles.

Mild mediastinal lymphadenopathy, which is believed to represent a form of reactive hyperplasia, is found frequently in patients with uncomplicated asbestosis.

Pleural thickening

Diffuse pleural thickening is defined as an uninterrupted sheet at least 5 cm wide, 8-10 cm long craniocaudally, and 3 mm thick. Proliferation of extrapleural fat is a frequent finding; this presumably occurs as a response to pleural retraction. (See the image below.) Disease may be bilateral and tends to involve the posterolateral surfaces of the lower thorax. Differentiation of diffuse pleural thickening from discrete pleural plaques is important because the former may be associated with a significant reduction in pulmonary function.



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Pulmonary window setting of chest CT scan shows irregular nodular pleural surface, not lung parenchymal nodules. Nodularity is also present along fiss....

Pleural effusion

Effusions may be unilateral or bilateral and usually are small (typically < 500 mL if benign). They are associated with subsequent development of diffuse pleural thickening in slightly more than 50% of patients, and an association with subsequent development of round atelectasis has been noted.

Rounded atelectasis

On CT, as on chest radiographs, rounded atelectasis appears as a well-defined round or wedge-shaped mass forming an acute angle with the adjacent pleura, which is always thickened. The mass usually is separated from the diaphragm by interposed lung. (See the image below.) Additional features identifiable on CT may include crowding of air bronchograms and the presence of a comet-tail sign or a hurricane sign (a curvilinear bronchovascular bundle leading into the mass).[51]  Volume loss, focal emphysema, and calcification may be seen.



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Asymptomatic man (>50 y) was noted to have mass in left lower lobe after exposure to asbestos. High-resolution CT (HRCT) demonstrates round mass at si....

Because a rounded atelectasis represents a collapsed lung, it enhances significantly after intravenous (IV) administration of contrast material, usually with a minimum attenuation increase of 200%. Enhancement is usually uniform.

Pleuroparenchymal fibrous bands may be seen radiating from the thickened pleura. These crows' feet are believed to represent contiguous, thickened interlobular septa.

Malignancy

CT findings in malignant mesothelioma include irregular, nodular pleural thickening (92%), which may involve interlobar fissures (86%), pleural effusion (74%), loss of volume (42%), pleural calcification (20%), and chest-wall invasion (18%). Pleural thickening typically is nodular and usually measures more than 1 cm, circumferentially involving the parietal and visceral costal and mediastinal pleurae. (See the image below.)



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Soft-tissue window setting of chest CT scan shows envelopelike mass along pleural surface surrounding lung. This is mesothelioma.

Tumor often spreads to involve the underlying lung, causing thickening of interlobular septa and parenchymal nodules. Chest-wall and mediastinal invasion spreading to the contralateral hemithorax and through the diaphragm may be identified. Mediastinal lymphadenopathy occurs, though distant metastases, including hematogenous spread to the contralateral lung, are uncommon. Rarely, malignant mesotheliomas may present as localized masses.

Low-dose and ultralow-dose scanning

Radiation delivered during repeated screening of asbestos-exposed workers is a major concern. The use of low-dose or ultra-low dose CT can reduce radiation doses by as much as 87%, but image noise increases and may diminish image quality.

Tekath et al compared ultralow-dose CT with standard CT for detecting asbestos-related diseases and found that it compared favorably with standard CT for detecting pleural plaques, diffuse pleural thickening, and pulmonary modules, though its sensitivity for delineating interstitial pulmonary abnormalities was poor.[52]

Because early findings of asbestosis on CT are very subtle, low-dose or ultralow-dose scanning may be unsuitable.

Ultrasonography

US is helpful for characterizing pleural effusions and for evaluating pleural thickening or masses. It also facilitates image-guided pleural intervention.

US has been employed in the evaluation of rounded atelectasis and has been shown to reliably demonstrate the mass and adjacent pleural thickening. The presence of a highly echogenic line within the mass, which represents invaginated fibrotic pleura, is described as a useful ancillary finding and is seen in 86% of patients.

Magnetic Resonance Imaging

No consistent pattern of signal intensity has been described for rounded atelectasis on MRI.[53] However, mesothelioma typically shows high signal intensity on T1-weighted images and moderately high signal intensity on T2-weighted images.

MRI and CT have been shown to be comparably accurate in the diagnosis of malignant mesothelioma. MRI is superior to CT in depicting isolated foci of the chest wall and diaphragmatic invasion; however, this difference has not been shown to confer any benefit in terms of overall staging.

One advantage of MRI is that the thorax can be directly imaged in various planes. Normal pleural space cannot be depicted on MRI. T2-weighted sequences may offer tissue-specific information concerning pleural effusions and chest-wall invasion by malignant processes due to increased tumor-to-muscle contrast.

Nuclear Medicine

Nuclear medicine study has a limited role in the investigation of asbestos-related intrathoracic disease. Gallium-67 (67Ga) citrate testing has been used to differentiate benign from malignant asbestos-related pleural disease and to obtain a quantitative index of inflammatory activity in patients with asbestosis.[54]  However, its results do not always correlate with other measurements of inflammation, and it is no longer generally recommended.

Single photon-emission computed tomography (SPECT) improves sensitivity for detecting the presence and extent of interstitial occupational lung disease.

PET with [fluorine-18]-fluorodeoxy-glucose (18F-FDG) has been suggested to aid in the differentiation of rounded atelectasis from bronchogenic carcinoma. Some studies have found round atelectasis to be metabolically inactive.[55]

In a study conducted to evaluate the role of 18F-FDG PET-CT integrated imaging in differentiating malignant from benign pleural effusion, 18F-FDG PET-CT was found to be a more reliable modality than either 18F-FDG PET alone or CT alone.[56] The sensitivities of CT, 18F-FDG PET, and 18F-FDG PET-CT integrated imaging were 75.0%, 91.7%, and 93.5%, respectively, in detecting malignant effusion and were 69.8%, 91.9%, and 93.0%, respectively, in distinguishing metastatic effusion.

Other Tests

Pulmonary function testing

In asbestosis, a reduction in diffusing capacity precedes lung volume changes, but findings from a diffusing capacity measurement are not specific.[2]  Besides reduced diffusing capacity, the earliest physiologic abnormality is exertional hypoxemia. Total lung capacity is reduced in asbestosis, as in other restrictive disorders.

On spirometry, vital capacity on a pulmonary function test typically appears reduced, without a reduction in the ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC).

Small-airway flow rates (eg, midexpiratory forced expiratory flow [FEF25-75]) are reduced, but they are nonspecific for a diagnosis of small-airway obstructive disease.

Assessment of oxygenation

The evaluation of oxygenation is important because uncorrected hypoxemia causes pulmonary hypertension and may lead to cor pulmonale. Clinicians 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).

Accurate information can be obtained through measurement of arterial blood gas (ABG) values, which requires an arterial puncture.

In selected cases, an exercise study may demonstrate desaturation during exercise.

Procedures

Bronchoalveolar lavage

BAL has only limited application in the diagnosis and management of asbestosis. It is helpful in diagnosing infections that may present with diffuse infiltrates and simulate asbestosis, and it 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. The presence of more than one asbestos body (ie, coated asbestos fiber) per 1 mL of lavage effluent suggests significant exposure.[21]

Bronchoscopy

Fiberoptic bronchoscopy is performed to facilitate BAL. In addition, bronchoscopy is indicated for airway examination when findings from 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

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

Histologic Findings

Physicians often make the diagnosis of asbestosis without histopathologic confirmation. Errors may occur because other, more common, interstitial diseases (eg, IPF) can mimic the clinical, radiologic, and pulmonary functional features of asbestosis. The long latency period that exists between patient exposure and the manifestation of symptoms and signs of asbestosis should be borne in mind.

When lung tissue is available for histopathologic examination, confirmation of the diagnosis requires both fibrosis and accumulation of fibers or asbestos bodies. Asbestos bodies (ie, ferruginous bodies) are asbestos fibers that develop a ferritin-protein coat and have a characteristic long-beaded appearance. The presence of these bodies, by itself, is not diagnostic of the disease, because examiners occasionally find asbestos bodies in people without known exposure to asbestos.

The College of American Pathologists has published a scheme for assessing the severity of asbestosis by grading fibrosis in the following four categories[57] :

Medical Care

To expedite detection and treatment of asbestosis, it is important to remain aware of potential complications. Patients should be informed about the work-related causation of the disease (potentially compensable), and it should be reported to appropriate state or federal agencies. Additionally, smokers should be advised to quit smoking, and referral to a smoking cessation clinic should be provided.

Assessment of disease severity and functional impairment are important for tailoring a plan for treatment and follow-up (ie, clinic visits, chest radiographs, and pulmonary function testing).

Management of asbestosis requires prompt antimicrobial therapy for respiratory infections, as well as immunization against influenza and pneumococcal pneumonia.[1]  Drugs are not directly effective in the treatment of asbestosis. Corticosteroids and immunosuppressive drugs do not alter the course of the disease.

The patient’s oxygenation status should be assessed both at rest and with exercise. If hypoxemia at rest or with exercise is detected, supplemental oxygen should be prescribed.

In cases of advanced disease, palliative care should be provided for the relief of distressing symptoms. When the disease reaches the terminal phase, referral for hospice care (preferably at home) should be provided.

Prevention

Control of asbestos in the workplace is the most effective method for preventing asbestosis. Once the diagnosis of asbestosis is made, cessation of further exposure to asbestos is imperative because additional exposure increases the rate of progression. It should be noted, however, that the disease may progress even after exposure has stopped.

Consultations

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

Author

Christopher D Jackson, MD, Faculty, Department of Internal Medicine, University of Tennessee Health Science Center College of Medicine-Memphis; Staff Physician, Christ Community Health Services; Staff Physician, Baptist Memorial Hospital

Disclosure: Nothing to disclose.

Coauthor(s)

Muthiah P Muthiah, MD, FCCP, D-ABSM, Associate Professor of Medicine, Division of Pulmonary and Critical Care and Sleep Medicine, Vice Chair for Internal Medicine (VA Academic Affairs), University of Tennessee Health Science Center College of Medicine; Director of Medical Intensive Care Unit (MICU), Memphis Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP, Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Asbestosis. Asbestos pleural plaques.

Posteroanterior (PA) chest radiograph in 58-year-old man with history of occupational exposure to asbestos shows right diaphragmatic pleural plaque calcifications, linear calcification along left pericardium, and bilateral pleural plaques along upper ribs.

Man (67 y) with decades-long history of occupational exposure to asbestos began experiencing nagging left-side chest pain. Posteroanterior chest radiograph shows left pleural effusion and peripheral left-side nodules.

Contrast-enhanced CT scan of chest at level of pulmonary artery bifurcation shows calcified pleural plaques along posterior, lateral, and anterior pleural surfaces.

Former asbestos worker (55 y) complained of shortness of breath. High-resolution CT (HRCT) scan obtained at lung bases shows prominent interstitial septal lines, subpleural cysts, and pleural plaques. This has appearance of asbestosis.

Pulmonary window setting of chest CT scan shows irregular nodular pleural surface, not lung parenchymal nodules. Nodularity is also present along fissure.

Asymptomatic man (>50 y) was noted to have mass in left lower lobe after exposure to asbestos. High-resolution CT (HRCT) demonstrates round mass at site of pleural thickening, with comet-tail bronchovascular bundle. This has appearance of folded lung (round atelectasis). Soft-tissue window shows parenchymal enhancement.

Soft-tissue window setting of chest CT scan shows envelopelike mass along pleural surface surrounding lung. This is mesothelioma.

Asbestosis. Asbestos pleural plaques.

Posteroanterior (PA) chest radiograph in 58-year-old man with history of occupational exposure to asbestos shows right diaphragmatic pleural plaque calcifications, linear calcification along left pericardium, and bilateral pleural plaques along upper ribs.

Contrast-enhanced CT scan of chest at level of pulmonary artery bifurcation shows calcified pleural plaques along posterior, lateral, and anterior pleural surfaces.

Asymptomatic man (>50 y) was noted to have mass in left lower lobe after exposure to asbestos. High-resolution CT (HRCT) demonstrates round mass at site of pleural thickening, with comet-tail bronchovascular bundle. This has appearance of folded lung (round atelectasis). Soft-tissue window shows parenchymal enhancement.

Former asbestos worker (55 y) complained of shortness of breath. High-resolution CT (HRCT) scan obtained at lung bases shows prominent interstitial septal lines, subpleural cysts, and pleural plaques. This has appearance of asbestosis.

Man (67 y) with decades-long history of occupational exposure to asbestos began experiencing nagging left-side chest pain. Posteroanterior chest radiograph shows left pleural effusion and peripheral left-side nodules.

Pulmonary window setting of chest CT scan shows irregular nodular pleural surface, not lung parenchymal nodules. Nodularity is also present along fissure.

Soft-tissue window setting of chest CT scan shows envelopelike mass along pleural surface surrounding lung. This is mesothelioma.