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 Asbestosis or Pneumoconiosis

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inhalation disease,Pneumoconiosis,asbestosis,Pneumoconiosis
,lung disesase,Pneumoconiosis,asbestosis,asbestos,


Pneumoconiosis is the general term for lung disease caused by inhalation and deposition of mineral dust.Pneumoconiosis
caused by asbestos inhalation is called asbestosis. The word asbestos
is derived from Greek and means inextinguishable, and asbestos is a
group of naturally occurring, heat-resistant fibrous silicates. Asbestos
fibers are long and thin (length-to-diameter ratio >3) and may be
either curved or straight. The curved fibers are called serpentine
(chrysotile is the prime example), and the straight fibers are
amphiboles. 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.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.Also see Asbestos-Related Disease and Asbestosis for a radiological focus. Note the image below.

Asbestos pleural plaques.

cumulative dose of fibers inhaled over a period of time and the type,
durability, and dimensions of the fiber influence carcinogenicity and
fibrogenicity. The incidence of asbestosis varies with the cumulative
dose of inhaled fibers; the greater the cumulative dose, the higher the
incidence of asbestosis. 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]
Next Section: Pathophysiology


United States

Asbestos consumption (per capita) peaked in 1951, declined gradually until 1971, and declined rapidly thereafter.No
reliable information exists regarding the number of people presently at
risk 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 in the level of asbestos
fibers in the air) has drastically reduced the risk of developing
asbestosis. However, those who have been previously exposed continue to
be at risk for asbestosis and other asbestos-related diseases.[2]

in usage of asbestos and observational studies suggest that asbestosis
and other asbestos-related diseases are likely to be continuing problems
in developing countries.

Study of
mortality trends in the United States show that while deaths from other
pneumoconioses are declining, deaths from asbestosis are increasing.
Further, they are not expected to decrease in the next 15 years. One
model predicts 29,667 deaths from 2005 to 2027.[3] 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.[4] People
who smoke are likely to develop chronic bronchitis and obstructive
airway disease and are prone to respiratory tract infections. 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 developing lung carcinoma than individuals who have
neither exposure.[5] Some
studies show that asbestos exposure alone, without a smoking history,
increases the risk of lung carcinoma 6-fold. Asbestos exposure increases
the risk of developing malignant mesothelioma and cancers of upper
respiratory tract, esophagus, kidney, and biliary system. 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.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.[6] No significant correlation was shown between pulmonary function parameters and cumulative asbestos exposure.
Asbestosis Clinical Presentation


the development of asbestosis is dose dependent, symptoms appear only
after a latent period of 20 years or longer. This latent period may be
shorter after intense exposure.Dyspnea upon exertion is the most
common symptom and worsens as the disease progresses. Patients may have a
dry (ie, nonproductive) cough. A productive cough suggests concomitant
bronchitis or a respiratory infection. Patients may report nonspecific
chest discomfort, especially in advanced cases.
Next Section: Physical


(ie, end-inspiratory crackles) are the most important finding during
examination. The rales are persistent and dry and are described as fine
cellophane rales or coarse Velcro rales. The rales are best auscultated
at the bases of the lungs posteriorly and in the lower lateral areas.
Initially, physicians hear the rales in the end-inspiratory phase.
However, in advanced disease, rales may be heard during the entire
inspiratory phase. Occasionally, the presence of rales precedes
radiographic finding abnormalities and pulmonary function test
abnormalities. Rales are not to be expected in all patients; one third
of patients may not have them. Finger clubbing is observed in
32-42% of cases. This finding is not necessarily related to the severity
of disease. Reduced chest expansion in advanced disease correlates with
restrictive ventilatory impairment and reduced vital capacity. In
advanced disease, patients may show the following signs associated with
cor pulmonale: cyanosis, jugular venous distention, hepatojugular
reflux, and pedal edema.
Next Section: Physical

Pathophysiology for a discussion of various factors that cause
asbestosis. Among them, the level of asbestos fiber exposure is of prime
importance. Experts estimate a 1% risk of developing asbestosis after a
cumulative dose of 10 fiber-year/m3. In modern times,
the risk to persons 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 acoustical, thermal, and fireproofing purposes
Examples of occupations associated with asbestosis include the following:

  • Insulation workers
  • Boilermakers
  • Pipefitters
  • Plumbers
  • Steamfitters
  • Welders
  • Janitors
  • Asbestosis Differential Diagnoses
  • Differentials
  • Coal Worker's Pneumoconiosis
  • Dermatomyositis
  • Hypersensitivity Pneumonitis
  • Pulmonary Fibrosis, Idiopathic
  • Sarcoidosis
  • Silicosis
  • Asbestosis Workup
  • Laboratory Studies

    the diagnosis of asbestosis is built upon 3 features: (1) reliable
    exposure history with an appropriate latency period; (2) evidence of
    fibrosis by radiographs (eg, chest radiographs, high-resolution computed
    tomography [HRCT]), consistent physical examination findings, and
    pulmonary function findings with or without histologic evidence
    (asbestos bodies in bronchoalveolar lavage [BAL] fluid[8] or fibrosis in biopsy samples of lung tissue); and (3) absence of other causes for interstitial fibrosis. The diagnosis is based on the following:

    • A
      reliable and significant (ie, dose x time) history of asbestos exposure
      and an appropriate latency period between exposure and detection of
    • 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
    tests for antinuclear antibodies, rheumatoid factor, and erythrocyte
    sedimentation rate lack diagnostic specificity and are not useful in
    diagnosis or in activity assessment.
    Next Section: Imaging Studies
    Imaging Studies

    Radiography findings are as follows:

    • Chest radiographs (ie, posteroanterior and lateral views) are basic and required diagnostic imaging studies.
    • 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.
    • The
      diagnosis of asbestosis requires multiple elements; a chest radiograph
      alone has only a modest positive predictive value for diagnosis.
      However, when it is combined with abnormal signs (rales) and pulmonary
      function test results, the positive predictive value is markedly
    • 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 affected by tuberculosis and the lower third damaged by
      empyema, trauma, or past pleurodesis therapy.
    • A
      calcified pleural plaque located in the diaphragmatic pleura is a
      reliable indicator of asbestos exposure but is not a required element
      for 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.
    • Rarely,
      pleural adhesions may cause peripheral atelectasis with a rounded border
      (rounded atelectasis) that may simulate a lung tumor.[10]
    • 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.
    • The
      International Labor Office standardized classification of radiographic
      abnormalities is useful in grading the extent of disease in asbestosis
      and in other pneumoconioses.
    • An oblique-view radiograph may be helpful in recognizing pleura-based abnormalities.
    Computed tomography scanning[11] findings are as follows:

    • CT
      scan is useful in delineation of pleural or pleura-based abnormalities
      (eg, effusion, thickening, plaque, malignant mesothelioma, rounded
      atelectasis) and in delineation of a parenchymal density that is
      suggestive of bronchogenic carcinoma.
    • An HRCT scan allows better definition of interstitial infiltrates and may be helpful in diagnosing early stages of asbestosis.
    • In a minority of cases, HRCT abnormalities may be seen in individuals with normal chest radiograph findings.
    • Typical
      HRCT findings of asbestosis include subpleural linear opacities seen
      parallel to the pleura, basilar lung fibrosis and peribronchiolar,
      intralobular and interlobular septal fibrosis, honeycombing, and pleural

    Next Section: Imaging Studies
    Other Tests

    Pulmonary function test findings are as follows:

    • Diffusing
      capacity reduction precedes lung volume changes, but findings from a
      diffusing capacity measurement are not specific. Besides diffusing
      capacity reduction, the earliest physiologic abnormality is exertional
    • Total lung capacity is reduced in asbestosis as in other restrictive disorders.
    • Using
      spirometry, vital capacity typically appears reduced, without a
      reduction in the ratio of forced expiratory volume in 1 second to forced
      vital capacity (FEV1 -to-FVC).
    • Small airway flow rates (eg, midexpiratory forced expiratory flow, FEF25-75) are reduced but are nonspecific for a diagnosis of small airway obstructive disease.
    Oximetry findings are as follows:

    • Evaluation
      of oxygenation is important because uncorrected hypoxemia causes
      pulmonary hypertension and may lead to cor pulmonale.
    • Physicians
      can use a noninvasive test of pulse oximetry as a screening test,
      especially if oximetry is performed during rest and during exercise (eg,
      6-minute walk test).
    • Obtain
      accurate information through measurement of arterial blood gases, which
      requires an arterial puncture. In selected cases, an exercise study may
      demonstrate desaturation during exercise.
    A lung scan
    with gallium citrate Ga 67 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.
    Next Section: Imaging Studies

    lavage has only limited application in the diagnosis and management of
    asbestosis. BAL is helpful in diagnosing infections that may present
    with diffuse infiltrates, which simulate asbestosis, and BAL may aid in
    the diagnosis of a coexisting bronchogenic carcinoma. In workers who are
    exposed to asbestos, BAL can provide quantitative information by
    asbestos fiber counts. More than 1 asbestos body (ie, coated asbestos
    fiber) per milliliter of lavage effluent suggests significant exposure. Fiberoptic
    bronchoscopy is performed to facilitate BAL. In addition, bronchoscopy
    is indicated for airway examination when radiologic studies are
    suggestive of bronchogenic carcinoma. Transbronchoscopic lung biopsy is
    not recommended for diagnosis of asbestosis. This procedure yields
    inadequate tissue and may cause crush alterations to the tissue. Open-lung
    biopsy is not indicated in most cases. However, this procedure provides
    sufficient tissue for the pathologist to make a definitive diagnosis.
    Next Section: Imaging Studies

    Histologic Findings

    often, physicians diagnose asbestosis without histopathological
    examination of lung tissue. A pathologic diagnosis of asbestosis
    requires visualization of both fibrosis and asbestos bodies through
    light microscopy or a significant quantity of asbestos fibers observed
    through electron microscopy. The American College of
    Pathologists' scheme for assessing the severity of asbestosis grades
    fibrosis in 4 categories. Grade 1 is fibrosis in the wall of a
    respiratory bronchiole without extension to distant alveoli. Grades 2
    and 3 define more extensive disease, and Grade 4 is 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 occasionally examiners find asbestos
    bodies in people without known exposure.
  • Asbestosis Treatment & Management
  • Medical Care

    of asbestos in the workplace is the most effective method for
    preventing asbestosis. Cessation of further exposure to asbestos once
    the diagnosis of asbestosis is made is imperative because further
    exposure increases the rate of progression. However, the disease may
    progress even after cessation of exposure. Additionally, note the

    • Advise smokers to quit smoking, and provide referral to a smoking cessation clinic.
    • Inform
      patients on the work-related causation of the disease (potentially
      compensable) and report it to appropriate state or federal agencies.
    • Assessment
      of disease severity and functional impairment are important in
      tailoring a treatment and follow-up plan (ie, frequency of clinic
      visits, chest radiographs, pulmonary function testing).
    • Treatment requires prompt attention to respiratory infections and immunizations against influenza and pneumococcal pneumonia.
    • Perform prompt antimicrobial treatment of respiratory infections.
    • Assess
      oxygenation status at rest and with exercise. If testing detects
      hypoxemia at rest or with exercise, prescribe supplemental oxygen.
    • Remain aware of the complications of asbestosis to expedite detection and treatment.
    • Provide palliative care for the relief of distressing symptoms in advanced disease.

    Next Section: Consultations

    a pulmonologist to assess the need for long-term oxygen therapy and for
    the management of advanced cases and complications (see
    Mortality/Morbidity). If patients smoke, refer them to a smoking
    cessation clinic. Because of the likelihood of bronchogenic carcinoma,
    consult a thoracic surgeon if a solitary pulmonary nodule develops in a
    patient with asbestosis. Provide hospice referral (preferably at home)
    when disease reaches the terminal phase.
    Asbestosis Medication

Medication Summary

Drugs are
not effective in the treatment of asbestosis. Corticosteroids and
immunosuppressive drugs do not alter the course of the disease.
Asbestosis Follow-up


Control of asbestos in the workplace is the most effective method for preventing asbestosis.
Next Section: Complications

The following complications may be observed:

  • Pulmonary hypertension
  • Cor pulmonale
  • Right-sided heart failure
  • Progressive
    respiratory insufficiency: The risk factors for developing this
    complication are cumulative amount of asbestos inhaled; degree of
    dyspnea; cigarette smoking; combined pulmonary and pleural involvement;
    honeycombing visible on radiographs; and a high number of neutrophils,
    eosinophils, and fibronectin in 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 upper respiratory tract, esophagus,
    biliary system, and kidney.

Next Section: Complications

Patient Education

patients of the work-related causes of asbestosis (see Medical Care).
For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article Bronchoscopy

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