INTRODUCTION — Asbestos is the general term for a group of naturally occurring fibers composed of hydrated magnesium silicates. The spectrum of pleuropulmonary disorders associated with asbestos exposure includes [1,2]:
●Pleural disease (benign asbestos effusion, focal and diffuse benign pleural plaques)
●Malignancies (non-small cell and small cell carcinoma of the lung as well as malignant mesothelioma)
Asbestosis specifically refers to the pneumoconiosis caused by inhalation of asbestos fibers. The disease is characterized by slowly progressive, diffuse pulmonary fibrosis. Asbestosis remains a significant clinical problem despite substantial reductions in occupational asbestos exposure, due to occupational exposure that occurred years earlier [3,4].
The pathophysiologic mechanisms and clinical manifestations of asbestos-related pleuropulmonary disease will be reviewed here [1,5-7]. The approach to the patient with suspected interstitial lung disease is presented separately. (See "Approach to the adult with interstitial lung disease: Clinical evaluation" and "Approach to the adult with interstitial lung disease: Diagnostic testing".)
ASBESTOS EXPOSURE — Asbestos is the general term for a group of naturally occurring fibers composed of hydrated magnesium silicates used for a variety of construction and insulating purposes.
Asbestos fibers are divided into two categories based on their shape. Serpentine fibers, of which chrysotile is the main commercial variety, are long, curly strands, whereas amphibole fibers (crocidolite, amosite, tremolite, and others) are long, straight, rod-like structures. Chrysotile accounts for over 90 percent of the asbestos in commercial use in the United States and is generally considered less toxic than the amphibole fibers [5,8,9].
When the use of asbestos was widespread, exposure occurred in a variety of occupational and non-occupational settings (table 1). As examples, exposure to asbestos resulted from involvement with the following [7,10]:
●Mining and milling of the fibers
●Industrial and occupational applications of asbestos (eg, work with textiles, cement, friction materials, insulation, shipbuilding)
●Nonoccupational exposure to airborne asbestos (eg, regular exposure to soiled work clothes brought home by an asbestos worker, renovation or demolition of asbestos-containing buildings, environmental exposure in the neighborhood of industrial sources, and natural environmental exposure to geological sources)
Commercial use of asbestos is banned in many countries. In the United States, asbestos use has been limited since the 1970s, but is still permitted in automotive brake pads and gaskets, roofing products, and fireproof clothing. Mining of asbestos is ongoing in several countries, most prominently Russia, China, Brazil, and Kazakhstan .
Environmental exposure to low levels of asbestos from naturally occurring sources or industrial emissions may increase the risk of malignant mesothelioma, but not asbestosis [12-15]. The health risk to occupants of a building in which asbestos is in good repair and undisturbed (ie, not respirable) is not considered significant .
ASBESTOSIS — Asbestosis specifically refers to the slowly progressive, diffuse pulmonary fibrosis caused by inhalation of asbestos fibers.
Pathology — The gross anatomic features of asbestosis include the presence of small, stiff lungs with fibrosis in the subpleural regions of the lower lobes. The adjacent visceral pleura may also be fibrotic and associated with parietal pleural plaques, while the central portions of the lung are relatively spared (picture 1) .
The histopathologic diagnosis of asbestosis requires the presence of uncoated or coated asbestos fibers (asbestos bodies) in association with interstitial pulmonary fibrosis that is similar in appearance to usual interstitial pneumonitis (UIP) (picture 2A-E and picture 3) [17,18]. Pulmonary fibrosis in asbestosis differs from that of UIP in two important ways . Fibroblast foci, which are characteristic of UIP, are infrequent in asbestosis. In addition, asbestosis is typically associated with mild fibrosis of the visceral pleura. (See "Idiopathic interstitial pneumonias: Classification and pathology", section on 'Pathology'.)
●Asbestos bodies — Asbestos bodies are composed of transparent asbestos fibers surrounded by a coating of iron and protein. Such a coating may surround a number of other mineral particles, such as glass, talc, iron, or carbon; the resulting structures are generically called ferruginous bodies. Asbestos bodies are differentiated from other ferruginous bodies by their transparent core . Light microscopy does not allow accurate determination of the mineral at the core of a ferruginous body, and definitive identification may require scanning electron microscopy with energy dispersive x-ray analysis of lung specimens. Amphibole fibers form asbestos bodies more readily than do chrysotile fibers, in part due to the less efficient pulmonary clearance of amphiboles [5,6].
Two or more asbestos bodies per square centimeter of a 5-mu thick lung section, in combination with interstitial fibrosis, are indicative of asbestosis . The quantity of asbestos fibers in the lungs (both coated and uncoated) is generally 10 to 20-fold higher in patients with asbestosis compared with unexposed individuals and correlates with the severity of fibrosis . Quantification of asbestos bodies by light microscopy significantly underestimates the total lung fiber burden. The number of asbestos bodies in digested lung is generally 10 to 10,000-fold less than the total number of uncoated fibers determined by electron microscopy .
Pathogenesis — Asbestos-induced diseases are probably caused by the direct toxic effects of the fibers on pulmonary parenchymal cells as well as the release of various mediators (reactive oxygen species, proteases, cytokines, and growth factors) by inflammatory cells [20-22]. Deleterious reactive oxygen and nitrogen free radicals may be formed either via reactions catalyzed by iron molecules within asbestos bodies or as a consequence of the activation of inflammatory cells. Free radicals can react with and damage a variety of cellular macromolecules and may disrupt DNA to give rise to malignancy .
Animal models suggest that inhaled asbestos fibers deposit at respiratory bronchiole and alveolar duct bifurcations [23-25]. This triggers the accumulation of alveolar macrophages and the development of an inflammatory reaction that extends centrifugally into the terminal respiratory bronchioles and adjacent alveolar interstitium [23-25]. The majority of fibers are removed from the lungs by mucociliary mechanisms, but some are taken up by alveolar macrophages and alveolar type I cells .
Amphibole fibers may be more toxic than chrysotile because their structure allows them to deposit more efficiently in the distal lung parenchyma and reduces their rate of clearance . Smoking increases the attack and/or progression rate of asbestosis, probably by interfering with the mucociliary clearance of inhaled fibers [26,27].
Over time, there is more diffuse pulmonary involvement characterized by loss of alveolar type I and II cells and expansion of the numbers of alveolar and interstitial macrophages, neutrophils, lymphocytes, and eosinophils. Fibroblast proliferation and collagen accumulation ultimately result [25,28,29].
Clinical findings — Most patients who develop asbestosis are asymptomatic for at least 20 to 30 years after the initial exposure; the latency period between exposure and symptoms is inversely proportional to the intensity of asbestos exposure [5,6,16,30].
●Symptoms – The earliest symptom of asbestosis is usually the insidious onset of breathlessness with exertion. Dyspnea commonly progresses even in the absence of further asbestos exposure. Cough, sputum production, and wheezing are unusual; if present, these symptoms tend to be a consequence of cigarette smoking rather than asbestos-induced lung disease .
●Physical examination – As asbestosis progresses, patients may develop bibasilar, fine end-inspiratory crackles (32 to 64 percent) and clubbing (32 to 42 percent) [31,32]. Cor pulmonale may ensue in advanced cases and may cause peripheral edema, jugular venous distension, hepatojugular reflux, and/or a right ventricular heave or gallop. (See "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary hypertension): Epidemiology, pathogenesis, and diagnostic evaluation in adults".)
●Laboratory studies – Laboratory studies are generally nonspecific and not useful clinically. Antinuclear antibodies, rheumatoid factor, and an elevated erythrocyte sedimentation rate may be present but do not correlate with disease severity or activity .
Evaluation — The evaluation of suspected asbestosis in a patient with a history of asbestos exposure generally includes pulmonary function testing to assess the severity and pattern of lung impairment and imaging to look for characteristic features of asbestosis. Bronchoalveolar lavage (BAL) has a limited role.
Pulmonary function tests — In the evaluation of dyspnea in a patient with possible asbestosis, pulmonary function testing should include spirometry, lung volumes, and diffusing capacity for carbon monoxide (DLCO). (See "Overview of pulmonary function testing in adults".)
The characteristic lung function abnormalities in patients with asbestosis include:
●Reduced lung volumes, particularly the vital capacity and total lung capacity
●Decreased pulmonary compliance
●Absence of airflow obstruction by spirometry (normal ratio of the forced expiratory volume in one second to forced vital capacity)
The earliest physiologic abnormalities detected in asbestos-exposed patients are reductions in the DLCO and pulmonary compliance and the presence of exertional hypoxemia [31,34]. Although hypoxemia early in the course of disease occurs only with exercise, more advanced disease can be associated with hypoxemia at rest.
Airways obstruction generally reflects concomitant exposure to cigarette smoke, but rarely occurs in the absence of tobacco exposure . Airflow limitation in these patients may be due to airway inflammation resulting from asbestos deposition along the respiratory bronchioles and alveolar duct bifurcations (picture 4).
Imaging — Imaging studies are an integral part of the evaluation of adult-onset dyspnea and of suspected asbestosis. (See "Imaging of occupational lung diseases", section on 'Asbestos-related thoracic diseases'.)
●Chest radiograph – The chest radiograph in patients with asbestosis usually reveals small bilateral parenchymal opacities with a multinodular or reticular pattern, often with associated pleural abnormalities [36,37]. These findings may be subtle. In one study, for example, 15 to 20 percent of individuals with histopathologic evidence of pulmonary fibrosis had no interstitial abnormalities on their chest radiographs .
The interstitial process typically begins in the lower lung zones and is associated with bilateral mid-lung zone plaques on the parietal pleura. In the early stages of asbestosis, combined interstitial and pleural involvement may cause a hazy, "ground glass" appearance to the chest radiograph that may blur the diaphragm and heart border, giving rise to the "shaggy heart" sign (image 1) . Honeycombing and upper lobe involvement develop in advanced stages of disease (image 2). Hilar and mediastinal lymphadenopathy are not seen with asbestosis and should suggest the presence of another process.
●High resolution computed tomography — High resolution computed tomography (HRCT) is more sensitive than plain films in detecting parenchymal abnormalities in asbestos-exposed individuals [39-43]. Up to 30 percent of asbestos-exposed individuals demonstrate an abnormal HRCT in spite of a normal chest radiograph . However, HRCT may still appear normal or near normal in cases of histopathologically proven asbestosis .
•Subpleural linear densities of varying length parallel to the pleura
•Basilar and dorsal lung parenchymal fibrosis, with peribronchiolar, intralobular, and interlobular septal fibrosis
•Coarse parenchymal bands (2 to 5 cm in length), often contiguous with the pleura
•Coarse honeycombing in advanced disease
•Pleural plaques, which help differentiate asbestos-induced parenchymal disease from other interstitial lung diseases (see 'Pleural plaques and diffuse pleural thickening' below)
The significance of abnormal HRCT scans in asymptomatic asbestos-exposed persons as well as the proper role of HRCT in detection of asbestos-induced lung disease need further study.
Bronchoalveolar lavage — While quantification of asbestos bodies in BAL fluid roughly correlates with the burden of lung parenchymal asbestos bodies, the clinical utility of BAL for evaluation of possible asbestosis is limited. We reserve BAL for patients in whom the HRCT is not sufficiently diagnostic, and malignancy, infection, or hypersensitivity pneumonitis are in the differential diagnosis. (See "Role of bronchoalveolar lavage in diagnosis of interstitial lung disease".)
Studies have shown that increased numbers of asbestos bodies are found in sputum and BAL fluid of asbestos workers with asbestosis compared with asbestos workers with a normal chest radiograph and also in those with more intense asbestos exposure [48,49]. Greater than one asbestos body/mL of BAL fluid correlates with more than 1000 asbestos bodies/gram of lung tissue in patients with suspected asbestos-related disease ; such levels are associated with significant exposure. However, interpretation of the results is difficult because of marked interpatient variation and the fact that a significant number of asbestos fibers may be present in exposed individuals without disease [19,51].
Diagnosis — For the majority of patients, a confident clinical diagnosis of asbestosis can be made on the basis of the exposure history and the HRCT findings (see 'Imaging' above). Examination of lung tissue is rarely needed to establish a diagnosis (table 2) [17,28,34,52]. There are three key findings that support the diagnosis of asbestosis (table 3A-B):
●A reliable history of exposure to asbestos with a proper latency period from the onset of exposure to the time of presentation, and/or presence of markers of exposure (eg, pleural plaques, which are virtually pathognomonic of previous exposure, or recovery of sufficient quantities of asbestos fibers/bodies in bronchoalveolar lavage or lung tissue) .
●Definite evidence of interstitial fibrosis, as manifested by one or more of the following: end-inspiratory crackles on chest examination; reduced lung volumes and/or DLCO; presence of typical chest radiograph or HRCT findings of interstitial lung disease; or histologic evidence of interstitial fibrosis.
●Absence of other causes of diffuse parenchymal lung disease. (See "Approach to the adult with interstitial lung disease: Diagnostic testing", section on 'Causes of ILD'.)
Differential diagnosis — The differential diagnosis of asbestosis includes idiopathic pulmonary fibrosis and diseases that are associated with usual interstitial pneumonia or fibrotic nonspecific interstitial pneumonia, such as rheumatoid arthritis and other rheumatic diseases, chronic hypersensitivity pneumonitis, drug-induced pneumonitis, combined pulmonary fibrosis and emphysema, and pleuropulmonary fibroelastosis, although chronic hypersensitivity pneumonitis and pleuropulmonary fibroelastosis tend to be upper lobe predominant. The characteristics of these diseases are described separately. (See 'Diagnosis' above and "Clinical manifestations and diagnosis of idiopathic pulmonary fibrosis", section on 'Differential diagnosis'.)
Management — There is currently no specific treatment for asbestosis. There have been no prospective studies of patients with asbestosis utilizing antiinflammatory or immunosuppressive agents, such as glucocorticoids or cytotoxic therapy, or antifibrotic agents . The absence of inflammation on histopathologic examination makes it unlikely that anti-inflammatory or immunosuppressive agents would be of benefit.
●Early detection of physiologic and radiographic abnormalities to aid prevention of further airborne asbestos exposure
●Supplemental oxygen when there is resting hypoxemia or exercise-induced oxygen desaturation
●Prompt treatment of respiratory infections
●Pneumococcal and influenza vaccination (table 5)
Whole lung lavage has been investigated as a means for removing retained dust in some pneumoconioses, but has not been applied to patients with asbestosis .
Complications — The two main complications of asbestosis are respiratory failure and malignancy.
Respiratory failure — Asbestosis is a slowly progressive process that culminates in respiratory failure in a minority of patients. Risk factors for progression of lung function abnormalities in asbestos-exposed individuals include [30,56,57]:
●Cumulative asbestos exposure
●Duration of exposure
●Fiber type (crocidolite exposure is associated with the most frequent progression)
●Symptoms of dyspnea
●Diffuse pleural thickening (see 'Pleural plaques and diffuse pleural thickening' below)
●Honeycombing on HRCT (see 'Imaging' above)
●Radiographic pattern consistent with typical or probable UIP (table 6) other than the presence of pleural plaques
Cigarette smoke may accelerate the progression of pulmonary fibrosis after asbestos exposure . Although the mechanisms for this synergistic interaction are unknown, reactive oxygen species have been implicated as having a prominent role [5,6,62].
Malignancy — Although some investigators have questioned the causal relationship between asbestosis and bronchogenic carcinoma, most studies have demonstrated a clear association between the two entities [43,63-65]. As an example, a Dutch cohort study of 58,279 men, in which 524 cases of lung cancer developed, found that asbestos exposure was associated with a relative risk of lung cancer of 3.5 (95 percent CI 1.7 to 7.2) after adjustment for age, smoking habits, and intake of vitamin C, beta-carotene, and retinol . A systematic review and meta-analysis found an increased risk of lung cancer associated with environmental exposure to asbestos, especially in neighborhoods near asbestos mines and factories .
The risk of lung cancer associated with asbestos is greatly magnified by coexisting exposure to tobacco smoke. A meta-analysis examined the risk of lung cancer in asbestos exposed smokers and nonsmokers: Compared with nonsmokers without asbestos exposure, the odds ratios for developing lung cancer were 1.70 (95% CI 1.31–2.21) among asbestos-exposed nonsmokers, 5.65 (95% CI 3.38–9.42) among smokers without asbestos exposure, and 8.70 (95% CI 5.8–13.10) among asbestos-exposed smokers .
In an earlier series of asbestos workers, the risk of dying of lung cancer increased 16-fold if they smoked more than 20 cigarettes per day and 9-fold if they smoked fewer than 20 cigarettes per day, compared with asbestos workers without a regular smoking history . (See "Cigarette smoking and other possible risk factors for lung cancer".)
For any given individual, the relative risk depends upon the magnitude of the exposure both to cigarette smoke and to asbestos. The type of asbestos fiber affects the risk of lung cancer as well; the risk appears to be considerably higher for workers exposed to amphibole fibers than for those exposed to chrysotile fibers [8,70]. However, an analysis of 35-year prospective cohort data suggested a significant exposure-response relationship between exposure to chrysotile asbestos and increased risk for lung cancer mortality .
Asbestos exposure increases the incidence of other neoplasms as well [5,6,72]. Other malignancies that have been linked to asbestos include cancers of the larynx, oropharynx, kidney, esophagus, and biliary system . Asbestos is the only known risk factor for malignant mesothelioma. (See 'Malignant mesothelioma' below and "Presentation, initial evaluation, and prognosis of malignant pleural mesothelioma".)
PLEURAL DISEASE — Pleural involvement is a hallmark of asbestos exposure but is unusual in other interstitial lung disorders.
Benign asbestos pleural effusion — Benign asbestos pleural effusions (BAPEs) are usually small and unilateral and occur years before the onset of interstitial disease [7,73,74]. The duration of asbestos exposure prior to BAPE is variably reported as a mean of 5.5 years  to a mean of 28 years , while the interval between exposure and onset of BAPE is reported as 15 years  to 46 years . The correlation between the exposure amount and development of BAPE is unclear; however, earlier onset appears associated with moderate-to-high levels of exposure to asbestos . (See 'Clinical findings' above.)
●Clinical manifestations – Symptoms of BAPE are nonspecific and include pleuritic chest pain, dyspnea, chronic cough, and less commonly fever [73,78]. In asbestos-exposed workers being monitored by interval chest radiographs, BAPEs were asymptomatic in 66 percent .
●Imaging – BAPEs are usually unilateral and may be associated with other evidence of asbestos-related pleural disease (image 5 and image 6). In a series of 36 patients with BAPE, CT imaging identified concomitant pleural plaques in 92 percent, rounded atelectasis in 44 percent, pleural calcification in 25 percent, and diffuse pleural thickening in 25 percent .
Pleural adhesions due to the inflammatory process of BAPE can cause atelectasis of a part of the peripheral lung, and this often takes on a rounded appearance on chest radiograph (ie, "rounded atelectasis") (image 7A-B). Rounded atelectasis can occur as a result of any type of pleural inflammation, but is most often associated with asbestos exposure (picture 5) [76,79-81]. (See "Imaging of occupational lung diseases", section on 'Pleural disease'.)
●Pleural fluid – The pleural fluid is exudative and can be serous, serosanguinous, or overtly bloody. Approximately one-third of BAPEs have increased pleural eosinophils, sometimes up to 50 percent of the total nucleated cell count .
●Diagnosis – BAPE may be suspected on the basis of a compatible history and timing of asbestos exposure, but the diagnosis of BAPE is based on exclusion of other causes of exudative effusion (eg, infection, rheumatoid pleuritis, and malignancy) and spontaneous resolution of the effusion. The likelihood of BAPE is increased by the presence of pleural plaques with linear calcification . However, exclusion of pleural malignancy may require closed pleural biopsy or thoracoscopic evaluation. (See "Pleural fluid analysis in adults with a pleural effusion" and "Diagnostic evaluation of the hemodynamically stable adult with a pleural effusion" and "Medical thoracoscopy (pleuroscopy): Diagnostic and therapeutic applications".)
As lung cancer and mesothelioma occur with increased frequency among asbestos-exposed workers, pleural effusions due to mesothelioma or spread of lung cancer are prominent in the differential diagnosis. When reviewing the CT scan in a patient with suspected BAPE, the presence of mediastinal pleural plaques increases the likelihood of mesothelioma, as mediastinal plaques were noted in 22 percent of patients with BAPE compared with 74 percent of patients with mesothelioma . Irregularity or nodularity of the interlobular septa is substantially more common in mesothelioma than BAPE , as are chest wall and rib involvement. (See 'Malignant mesothelioma' below and "Imaging of pleural plaques, thickening, and tumors", section on 'Malignant mesothelioma'.)
●Course – BAPEs typically resolve spontaneously over the course of several weeks to months (mean 4.3 months ), but can persist for up to a year. BAPEs can recur on the same or opposite side in approximately 30 percent of affected individuals [73,75]. As the pleural fluid of BAPE regresses, it may leave visible blunting of the costophrenic angle and/or diffuse pleural thickening of the visceral pleura. BAPEs do not predict an increased risk of mesothelioma beyond that of individuals with similar asbestos exposure without BAPE. (See 'Pleural plaques and diffuse pleural thickening' below.)
Pleural plaques and diffuse pleural thickening — Pleural plaques and diffuse pleural thickening are benign consequences of asbestos exposure.
Pleural plaques are circumscribed areas of pleural thickening with a linear, band-like, or nodular appearance. They are composed of deposits of collagen in the parietal pleura. Approximately 60 percent of persons with work-related asbestos exposure manifest pleural plaques when screened by low dose CT .
The plaques preferentially involve the parietal pleura adjacent to ribs, are less extensive in the intercostal spaces, and only rarely occur on the visceral pleura. Plaques are most commonly found along the sixth through ninth ribs and along the diaphragm and are typically bilateral (image 8 and image 9 and image 10 and picture 3). They are conspicuously absent in the region of the costophrenic sulci and at the lung apices. Calcifications are identified by chest radiography in 20 percent, on CT scanning in 50 percent, and at morphologic examination in 80 percent. (See "Imaging of pleural plaques, thickening, and tumors".)
Diffuse pleural thickening is defined based on the CT appearance: the pleural thickness is >3 mm, extends craniocaudad >8 cm, and extends axially >5 cm. It typically obliterates the costophrenic sulci. (See "Imaging of pleural plaques, thickening, and tumors", section on 'Diffuse pleural thickening'.)
One area of controversy has been whether circumscribed pleural plaques can contribute to respiratory impairment and a restrictive pattern on lung function testing (reduced forced vital capacity [FVC]) in the absence of asbestosis . This has been difficult to ascertain due to confounders such as age, lung parenchymal disease, and cigarette smoking. In one study, pleural plaques were associated with a small decrement in FVC (140 mL, p = 0.02), but less than that associated with diffuse pleural thickening (270 mL, p = 0.005) .
Rounded atelectasis may develop in patients with pleural plaques without known presence of BAPE. As with BAPE, pleural inflammation is thought to cause adherence of the pleura to a portion of peripheral lung, causing a small, rounded area of collapsed lung (image 7A-B). Rounded atelectasis can occur as a result of any type of pleural inflammation, but is most often associated with asbestos exposure (picture 5) [79-81]. (See 'Benign asbestos pleural effusion' above.)
Malignant mesothelioma — Malignant mesothelioma, which is highly associated with asbestos exposure, is a rare neoplasm that arises from mesothelial surface of the pleural cavity, peritoneal cavity, tunica vaginalis, or pericardium [85,86]. Malignant pleural mesothelioma (MPM) is the most common type. In one study of 66 patients with MPM, the mean duration of asbestos exposure was 17 years and a mean latency from exposure to disease presentation of 24 years . Symptoms are nonspecific and include chest pain, dyspnea, cough, and night sweats. Invasion of local structures can cause additional symptoms. (See "Presentation, initial evaluation, and prognosis of malignant pleural mesothelioma".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pneumoconiosis".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topic (see "Patient education: Asbestos exposure (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Asbestosis specifically refers to the pneumoconiosis caused by inhalation of asbestos fibers. The disease is characterized by slowly progressive, diffuse pulmonary fibrosis. (See 'Introduction' above.)
●Exposure to asbestos occurs during the mining and milling of the fibers, in industrial applications of asbestos (eg, work with cement, friction materials, insulation, shipbuilding), and in nonoccupational settings with airborne asbestos (eg, regular exposure to soiled work clothes brought home by an asbestos worker, renovation or demolition of asbestos-containing buildings). (See 'Asbestos exposure' above.)
●Most patients who develop asbestosis are asymptomatic for at least 20 to 30 years after the initial exposure; the latency period between exposure and symptoms is inversely proportional to the intensity of asbestos exposure. (See 'Clinical findings' above.)
●The earliest symptom of asbestosis is usually the insidious onset of breathlessness with exertion, which progresses even in the absence of further asbestos exposure. Cough, sputum production, and wheezing are unusual. (See 'Clinical findings' above.)
●Typical high resolution computed tomography (HRCT) scan findings of asbestosis include: subpleural linear densities of varying length parallel to the pleura, basilar and dorsal lung parenchymal fibrosis, with peribronchiolar, intralobular, and interlobular septal fibrosis, coarse parenchymal bands (2 to 5 cm in length), often contiguous with the pleura, coarse honeycombing in advanced disease, and pleural plaques (image 10 and image 9). (See 'Imaging' above.)
●The diagnosis of asbestosis is based on a reliable history of exposure to asbestos with a proper latency period, and/or presence of markers of exposure (eg, pleural plaques or recovery of sufficient quantities of asbestos fibers/bodies in bronchoalveolar lavage or lung tissue); definite evidence of interstitial fibrosis (eg, end-inspiratory crackles, reduced lung volumes and/or diffusing capacity, typical radiographic findings, or histologic evidence of interstitial fibrosis); and absence of other causes of diffuse parenchymal lung disease. (See 'Diagnosis' above.)
●No specific treatment has been identified for asbestosis. Management includes supportive care with an emphasis on smoking cessation, avoidance of further asbestos exposure, pneumococcal and influenza vaccination, and supplemental oxygen as needed to maintain adequate oxygenation. (See 'Management' above.)
●Benign asbestos pleural effusions (BAPEs) are usually small and unilateral and occur years before the onset of interstitial disease. Typically, BAPEs resolve spontaneously over several months, but may recur. (See 'Benign asbestos pleural effusion' above.)
●Pleural plaques and diffuse pleural thickening are benign consequences of asbestos exposure. Pleural plaques are circumscribed areas of pleural thickening with a linear, band-like, or nodular appearance, which may have areas of calcification. Diffuse pleural thickening, which may follow BAPE, is characterized by a pleural thickness >3 mm, extension craniocaudad >8 cm, and extension axially >5 cm. (See 'Pleural plaques and diffuse pleural thickening' above.)
●Malignant mesothelioma, which is highly associated with asbestos exposure, is a rare neoplasm that arises from mesothelial surface of the pleural cavity, peritoneal cavity, tunica vaginalis, or pericardium. (See 'Malignant mesothelioma' above.)
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