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Asbestosis

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

Background

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

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

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

The production and use of asbestos increased greatly between 1877 and 1967. In the 1930s and 1940s, scientists recognized a causal link between asbestos exposure and asbestosis. In the 1950s and 1960s, researchers established asbestos as a predisposing factor for bronchogenic carcinoma and malignant mesothelioma. (See Epidemiology and Prognosis.)

Patient education

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

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Etiology

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

All types of asbestos fibers are fibrogenic to the lungs. Amphiboles, particularly crocidolite fibers, are markedly more carcinogenic to the pleura. Fibers with diameters smaller than 3 micrometers are fibrogenic because they penetrate cell membranes. Long fibers (ie, >5 micrometers) are incompletely phagocytosed and stay in the lungs, setting up cycles of cellular events and the release of cytokines.

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

Oxygen free radicals (eg, superoxide anion, hydrogen peroxide, hydroxy radicals) that are released by the macrophages damage proteins and lipid membranes and sustain the inflammatory process. A plasminogen activator, which is also released by macrophages, further damages the interstitium of the lung by degrading matrix glycoproteins.

Individuals probably differ in their susceptibility to asbestosis based on respiratory clearance and other unidentified host factors. People who smoke have an increased rate of asbestosis progression, likely due to impaired mucociliary clearance of asbestos fibers.[1]

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

Antinuclear antibodies

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

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

Sources of asbestos exposure

The risk of asbestos exposure in the United States occurs mainly through the processing, manufacturing, and end-use of asbestos.

Manufacturers commonly use asbestos in the following products:

  • Products containing asbestos cement - Pipes, shingles, clapboards, sheets
  • Vinyl-asbestos floor tiles
  • Asbestos paper in filtering and insulating products
  • Material in brake linings and clutch facings
  • Textile products - Yarn, felt, tape, cord, rope
  • Spray products used for acoustic, thermal, and fireproofing purposes

Occupations associated with asbestosis include the following:

  • Insulation workers
  • Boilermakers
  • Pipefitters
  • Plumbers
  • Steamfitters
  • Welders
  • Janitors

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

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

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Epidemiology

Occurrence in the United States

Asbestos consumption (per capita) peaked in 1951, declined gradually until 1971, and fell rapidly thereafter. No reliable information exists regarding the number of people presently at risk of asbestos exposure in the United States and in other countries. Since the early 1940s, as many as 10 million workers in the United States may have been exposed to asbestos. In 1972, reports estimated that 250,000 persons were at risk. By the 1980s, the number of active asbestos miners and millers had fallen to a few hundred.

Strict regulation (eg, prohibition of asbestos sprays in buildings, controls on the level of asbestos fibers in the air) has drastically reduced the risk of asbestosis development. However, persons who have been previously exposed to asbestos continue to be at risk for asbestosis and other asbestos-related diseases.[9]

International occurrence

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

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Prognosis

The following complications can result from asbestos exposure:

  • Pulmonary hypertension
  • Cor pulmonale
  • Right-sided heart failure
  • Progressive respiratory insufficiency
  • Malignancy

Progressive respiratory insufficiency

See the list below:

  • The risk factors for developing this complication are as follows:
  • Cumulative amount of asbestos inhaled
  • Degree of dyspnea
  • Cigarette smoking
  • Combined pulmonary and pleural involvement
  • Honeycombing visible on radiographs
  • High number of neutrophils, eosinophils, and fibronectin in bronchoalveolar lavage (BAL) fluid

Malignancy

A higher risk of lung carcinoma has been found in patients with asbestosis. Patients with asbestosis are also at risk for malignant mesothelioma and carcinomas of the upper respiratory tract, esophagus, biliary system, and kidney.

People who smoke are likely to develop chronic bronchitis and obstructive airway disease and are prone to respiratory tract infections. Moreover, people who smoke are at high risk for the development of bronchogenic carcinoma because asbestos and tobacco smoke are synergistic in carcinogenicity. Individuals who both smoke and are exposed to asbestos are several times more susceptible to the development of lung carcinoma than are individuals who have neither exposure.[14]

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

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

Concomitant diseases

Asbestosis may coexist with other asbestos-related diseases, including calcified and noncalcified pleural plaques, pleural thickening, benign exudative pleural effusion, rounded atelectasis, and malignant mesothelioma of the pleura.

Airway obstruction

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

Asbestosis-related mortality

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

Estimated annual years of potential life lost before age 65 years attributable to asbestosis totaled 7267 in the years 2001-2005 and represented a significant increase from 1968-1972.[18]

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Contributor Information and Disclosures
Author

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

Basil Varkey, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Coauthor(s)

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

Anita B Varkey, MD is a member of the following medical societies: American College of Physicians, Society of General Internal Medicine

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

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

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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