Asbestosis is a process of diffuse interstitial fibrosis of the lung due to exposure to asbestos dust.[1, 2] 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 since the 1970s.
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.
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.[3]
All types of asbestos fibers are fibrogenic to the lungs. Amphiboles, particularly crocidolite fibers, are markedly more carcinogenic to the pleura.[3] The dimensions of the fibers are also important.[4, 5] 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, 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, insulinlike growth factor, and fibroblast growth factor, which interact to induce fibroblast proliferation.
Oxygen free radicals (eg, superoxide anion, hydrogen peroxide, 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 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.[6] In addition, although data regarding the association between MUC5B promoter polymorphism and idiopathic pulmonary fibrosis appear to be clear, the data are mixed about the MUC5B promoter variant being a potential genetic risk factor for asbestosis.[7, 8, 9]
Uncertainty remains about the mode(s) of action of asbestos in the genesis of diseases; therefore, an expert group has previously proposed cooperative action by diverse scientific disciplines to address such issues as terminology, mineralogy, test materials, and experimental models.[10]
Antinuclear antibodies
Exposure to amphibole asbestos fibers is linked to the production of autoantibodies. Moreover, studies indicate 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. These studies were conducted on the population of Libby, Montana, where mining, transportation, and processing of asbestos-contaminated vermiculite caused an increased risk of asbestos-related pleural and lung diseases.[11] Serum samples in the study showed that the majority of persons sampled were positive for ANAs.[12, 13] In addition, the risk of developing pleural or interstitial abnormalities was more than triple in the ANA-positive individuals than it was in persons who were ANA negative.[12]
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 in which there is an association with the development of autoimmune disorders.[14, 15, 16]
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. Manufacturers commonly use asbestos in the following products:
Asbestos paper in filtration and insulation 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 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.[17, 18] A separate study provided a detailed assessment of the health hazards of exposure to asbestos-containing drywall accessory products.[19]
The World Health Organization (WHO) estimates 125 million people worldwide are exposed to asbestos in the workplace and over 100,000 people die each year from asbestos-related lung cancer, mesothelioma, and asbestosis.[3] In addition, nearly 400 deaths have been attributed to non-occupational exposure to asbestos.[3] According to 1999-2010 mortality data from the National Center for Health Statistics (NCHS), 6,290 deaths were attributed to asbestosis in this period, of which the majority of deaths were in white males (95%) with a median age of 79 years.[20] The most recent US mortality data due to asbestosis span 2005–2014 (posted May 2017), in which 13,024 deaths were related to asbestosis, again predominantly in white males but with a slightly older median age (80.8 years).[21]
The World Trade Center Health Registry estimates about 410,000 people were exposed to asbestos when up to 400 tons of it was released following the collapse of the the Twin Towers on September 11, 2001 ("9/11").[22] Those at highest risk for developing 9/11-related illnesses are workers who participated in the rescue, recovery, and clean-up efforts at the sites of the towers, and those living and working in lower Manhattan during the clean-up.
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 are potentially exposed to asbestos during maintenance activities or remediation of buildings containing asbestos.[20] In the United States, vermiculite mined in Libby, Montana, was found to be contaminated with asbestos; this Libby vermiculite was used in 70% of vermiculite insulation in the United States from 1919 to 1990. In a study of 128 Libby miners, 119 had asbestos-related findings on high-resolution computed tomography scans.[23]
Asbestos has not been mined in the United States since 2002, but approximately 340 metric tons were imported in 2016 for use in the chloralkali industry to manufacture semi-permeable 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.[24]
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 due to long latency periods following exposure.[25, 26] In addition, trends in developing countries and countries that are emerging as economic powers indicate an increasing problem with asbestos-related diseases.[27]
The following complications can result from asbestos exposure:
Pulmonary hypertension
Cor pulmonale
Right-sided heart failure
Progressive respiratory insufficiency
Malignancy
Progressive respiratory insufficiency
The risk factors for developing progressive respiratory insufficiency 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
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. Findings from a mortality study published in 2018 that followed 3984 Genoa Italian shipyard workers between 1960 and 1981 to 2014 found an 83.6% mortality (n = 3331), with excess mortality for all cancers, pleural mesothelioma, and cancers of the larynx and lung, as well as for respiratory diseases, including asbestosis.[28] Of 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.[29] Individuals who both smoke and are exposed to asbestos are several times more susceptible to the development of lung carcinoma than are individuals without either exposure.[30]
Some studies show that asbestos exposure alone, without a smoking history, increases the risk of lung carcinoma six-fold.
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.[31] This association should be interpreted with caution as some cohort studies included in prior meta-analyses reported disease misclassification for peritoneal mesothelioma.[32]
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=3,660) with previous occupational exposure to asbestos.[33] No significant correlation was shown between pulmonary function parameters and cumulative asbestos exposure.
Inform patients of the work-related causes of asbestosis (see Medical Care). For patient education information, see Bronchoscopy.
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 theiri work. Occupations at high risk include construction workers, roofers, welders, insulation workers, etc. As absestos can linger on articles of clothing, family members of people who work in these occupations can be exposed if not careful.
What health problems can result from exposure to asbestos?
Asbestos can causes many health problems. The mnemonic CAP can help you remember the health problems associated with asbestos exposure. C stands for cancer. Asbestos exposure has been associated with lung cancer and rarely mesothelioma. A stands for asbestosis. Asbestosis is when asbestos causing damage to parts of the lung, which can make it diffiicult to breathe. P stands for pleural disease. The pleura is the thin outer coveriing of your lungs. When asbestos causes disease in the pleura, it can cause fluid to accumulate in that space. This fluid accumulation can cause difficulty breathing.
Symptoms of asbestos exposure do not occur immediately after contact with the mineral. Some people may not have symptoms for 15 to 30 years. Most patients who develop asbestosis or other related disease due to asbestos exposure will have shortness of breath. Other symptoms include coughinig up blood or chest pain. If you experience any of these systems. you should seek medical attention.
A detailed occupational and potential exposure history is essential. Obtain the following information[2] :
Employment
Exposure: Year, duration, and end; type (occupational, domestic, environmental)
Intensity: Direct contact for longer than 6 months (8 hours daily, 40 hours per week) or a high concentration of asbestos in the air breathed is considered intense exposure. Exposure risk covers an area within a 300-2200 meter radius (dependent on wind direction).
Asbestos type
Smoking history
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 upon 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.
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 finding abnormalities and pulmonary function test abnormalities. However, note that up to one of patients may not have rales at al.
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.
The diagnosis of asbestosis is based on the following[35] :
A reliable and significant (ie, dose × 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
In general, laboratory studies are nonspecific and rarely useful. Blood tests for antinuclear antibodies (ANAs), rheumatoid factor, and erythrocyte sedimentation rate (ESR) lack diagnostic sensitivity or specificity and are not useful in diagnosis, disease severity, or activity assessment.
A lung scan with gallium citrate (67Ga) 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 of asbestosis 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 the 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 examiners occasionally 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 of less than 50% for the condition, but when it is combined with abnormal signs (rales) and pulmonary function test results, the positive predictive value is markedly increased.[36]
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, making it an important diagnostic consideration.
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.)
View Image
Asbestosis. Asbestos pleural plaques.
Rarely, pleural adhesions may cause peripheral atelectasis with a rounded border (rounded atelectasis) that may simulate a lung tumor.[37]
The International Labor Office standardized classification of radiographic abnormalities is useful in grading the extent of disease in asbestosis and in other pneumoconioses.[2, 38]
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.[39]
A review of chest CT images for 35 individuals exposed to asbestos found a high incidence of pleural plaque (94%) and pulmonary fibrosis (77%y). The findings of lung parenchymal lesions were as follows: centrilobular opacities (94%), subpleural dot-like or branching opacities (80%), interlobular septal thickening (57%), intralobular interstitial thickening (46%), parenchymal bands (43%), and subpleural curvilinear line (29%).[40]
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.
Radiation delivered during repeated screening of asbestos-exposed workers is a major concern. Low dose or ultra-low dose CT scans can reduce radiation doses up to 87%, but image noise increases and may diminish image quality. Tekath et al compared ultra-low dose CT with standard CT scanning for detecting asbestos-related diseases and found that ultra-low dose CT scanning compares favorably with standard CT in detecting pleural plaques, diffuse pleural thickening, and pulmonary modules. However sensitivity for interstitial pulmonary abnormalities was poor in ultra-low dose CT.[41] Because early findings of asbestosis on CT scans are very subtle, it may be unsuitable to scan the patient with low dose or ultra-low dose CT scan.
In asbestosis, a reduction in diffusing capacity precedes lung volume changes, but findings from a diffusing capacity measurement are not specific.[2] 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 they 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.
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).
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 (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 (mL) of lavage effluent suggests significant exposure.[18]
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.
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 a significant quantity of asbestos fibers observed through electron microscopy.
The American College of Pathologists uses a scheme for assessing the severity of asbestosis by grading fibrosis in the following four categories[42] :
Grade 1: Fibrosis in the wall of a respiratory bronchiole without extension to distant alveoli
Grade 2: Fibrosis extends to alveolar ducts and/or at least two tiers of alveoli adjacent to the respiratory bronchiole, with sparing of at least some alveoli between adjacent bronchioles
Grade 3: Fibrotic thickening of the walls of all alveoli between two or more adjacent respiratory bronchioles
Grade 4: Alveolar and septal fibrosis with spaces larger than alveoli, ranging up to 1 cm (ie, honeycombing)
Asbestos bodies (ie, ferruginous bodies) are asbestos fibers that develop a ferritin-protein coat and have a characteristic long-beaded appearance. Asbestos bodies alone are not diagnostic for disease, because examinersoccasionally find asbestos bodies in people without known exposure.
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.
Remain aware of the complications of asbestosis 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 for 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.[1]
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 the disease reaches the terminal phase.
Medications
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 is made is imperative because additional exposure increases the rate of progression. However, the disease may progress even after exposure has stopped.
Consultations
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.
In 2014, an update to the 1997 consensus Helsinki guidelines for the diagnosis of asbestos-related disorders was published. The guidelines define asbestosis 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] :
Over 0.1 million amphibole fibers (>5 μm) per gram of dry lung tissue, or
Over 1 million amphibole fibers (>1 μm) per gram of dry tissue, as measured by electron microscopy in a qualified laboratory, or
Over 1,000 asbestos bodies per gram of dry tissue (100 asbestos bodies per gram of wet tissue), or
Over 1 asbestos body per milliliter of bronchoalveolar lavage fluid, as measured by light microscopy in a qualified laboratory.
The guidelines recommend the use of computed tomography (CT) imaging in the diagnosis of asbestos-related diseases under the following circumstances:
A borderline finding of lung fibrosis (International Labor Office [ILO] 0/1-1/0) is detected;
There is a discrepancy between a lung function finding of restriction and radiographs interpreted as normal;
Widespread pleural changes severely hamper the radiographic visibility of the lung parenchyma.
The criteria for diagnosis of asbestosis on CT scans include:
Sum grade of ≥2–3 bilateral irregular opacities in the lower zones according to the reference film, or
Bilateral honeycombing (sum grade ≥2) would be sufficient to represent fibrosis, according to the ICOERD system (International Classification of high-resolution CT [HRCT] for Occupational and Environmental Respiratory diseases classification).
The guidelines further note that in histopathology, bronchiolar wall fibrosis has been associated with asbestos exposure and other exposures including smoking. Subpleural curvilinear lines or dots in HRCT are findings of bronchiolar fibrosis.[1]
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.
Additional Contributors
Anita B Varkey, MD, Assistant Professor, Department of Medicine, Loyola University Medical Center; Associate Program Director, Internal Medicine Residency; Medical Director, General Internal Medicine Clinic, Loyola Outpatient Center
Disclosure: Nothing to disclose.
Basil Varkey, MD, FCCP, Professor Emeritus, Department of Internal Medicine, Division of Pulmonary and Critical Care, Medical College of Wisconsin; Consulting Pulmonologist, Froedtert Memorial Lutheran Hospital
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
The National Institute for Occupational Safety and Health (NIOSH). Asbestosis. Available at http://wwwn.cdc.gov/eWorld/Grouping/Asbestosis/92. May 2017; Accessed: March 4, 2020.
U.S. Department of the Interior-United States Geological Survey. Mineral Commodity Summaries: Asbestos. United States Geological Survey. Available at https://minerals.usgs.gov/minerals/pubs/commodity/asbestos/. January 2017; Accessed: December 2, 2017.
International Labor Office. Guidelines for the use of the ILO international classification of radiographs of pneumoconioses, revised edition 2011. 2011 Nov 11.
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