Asbestosis

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Asbestosis
Chest X-ray in asbestosis shows plaques above diaphragm
ICD-10	J61
ICD-9	501
DiseasesDB	928
MedlinePlus	000118
MeSH	D001195

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Introduction

Asbestosis is a chronic inflammatory medical condition affecting the parenchymal tissue of the lungs. It occurs after long-term, heavy exposure to asbestos, e.g. in mining, and is therefore regarded as an occupational lung disease. Sufferers have severe dyspnea (shortness of breath) and are at an increased risk regarding several different types of lung cancer.

As clear explanations are not always stressed in non-technical literature, care should be taken to distinguish between several forms of relevant diseases. According to the World Health Organisation (WHO), these may defined as; asbestosis (the subject of this article), lung cancer, and mesothelioma (generally a very rare form of cancer, but increasing in frequency as people exposed to asbestos age).

As a summary; Asbestosis is a chronic non-malignant pneumoconiosis caused by inhalation of asbestos fibers, characterized by slowly, progressive pulmonary fibrosis. Asbestos exposure is also associated with the development of benign pleural disease and malignancy.

Signs and symptoms

The primary symptom of asbestosis is generally the slow onset of shortness of breath on exertion. In severe, advanced cases, this may lead to respiratory failure. Coughing is not usually a typical symptom, unless the patient has other, concomitant respiratory tract diseases.

People with extensive occupational exposure to the mining, manufacturing, handling or removal of asbestos are at risk of developing asbestosis. There is also an increased risk of lung cancer and mesothelioma. Asbestosis and lung cancer require prolonged exposure to asbestos. However, cases of mesothelioma have been documented with even 1-3 months of exposure, and only indirect exposure (through air ventilation system.) Most cases of asbestosis do not present until 5-10 years after exposure to the material.

Risk Factors

• Asbestos exposure occurs most commonly in the workplace.

  • Miners and millers of asbestos are at risk, but at even greater risk are people exposed during manufacturing and construction.
  • Maintenance, repair, and removal of asbestos-containing material can also result in significant exposures.
  • The health risk to building occupants where asbestos is in good repair and undisturbed is thought to be insignificant.
  • Occupational Safety & Health Administration (OSHA) regulations require special precautions in areas where the concentration is > 0.2 fibers per cubic milliliter of air.
  • About 8% of asbestos workers will die of respiratory failure secondary to asbestosis, and asbestos workers have a 50% chance of dying from malignancy (versus 18% chance for the average American).

• Asbestosis is a slowly progresive disease, so only a subset of patients progress on to respiratory failure.

  • Risk factors for progression include:

    • Cumulative exposure
    • Duration of exposure
    • Degree of symptoms
    • Cigaretter smoking
    • Diffuse pleural thickening
    • Honeycombing on high-resolution computed tomography (HRCT)
    • High concentrations of inflammatory cells on BAL

Pathogenesis

Asbestosis is the scarring of lung tissue (around terminal bronchioles and alveolar ducts) resulting from the inhalation of asbestos fibers. There are two types of fibers, amphibole (thin and straight) and serpentine (curved). The former are primarily responsible for human disease as they are able to penetrate deeply into the lungs. When such fibers reach the alveoli (air sacs) in the lung, where oxygen is transferred into the blood, the foreign bodies (asbestos fibers) cause the activation of the lung's local immune system and provoke an inflammatory reaction. This inflammatory reaction can be described as chronic rather than acute, with a slow ongoing progression of the immune system in an attempt to eliminate the foreign fibres. Macrophages phagocytose (ingest) the fibers and stimulate fibroblasts to deposit connective tissue. Due to the asbestos fibres' natural resistance to digestion, the macrophage will die off, releasing certain cytokines and attracting further lung macrophages and fibrolastic cells to lay down fibrous tissue, which eventually forms a fibrous mass. The result is interstitial fibrosis. The fibrotic scar tissue causes alveolar walls to thicken, which reduces elasticity and gas diffusion, reducing oxygen transfer to the blood as well as the removal of carbon dioxide.

Asbestos presents as a restrictive lung disease. The total lung capacity (TLC) may be reduced through alveolar wall thickening. In the more severe cases, the drastic reduction in lung function due to the stiffening of the lungs and reduced TLC may induce right-sided heart failure (cor pulmonale).

More than 50% of people affected with asbestos develop plaques in the parietal pleura, in the space between the chest wall and lungs. Clinically, patients present with dry inspiratory crackles, clubbing of the fingers, and a diffuse fibrotic pattern in the lower lung lobes (where asbestosis is most prevalent).

In general;

• Asbestos is a useful product because of its thermal, electric and sound-insulating qualities, and has been used in many settings for these reasons.

  • Asbestos refers to a group of naturally-occurring fibers composed of hydrated magnesium silicates.
  • World production and consumption peaked in the mid-1970s around 5.0 million tons, and has fallen thereafter to about 2.5 million tons today. Use has fallen in Europe and America, but has risen in countries with rapidly growing economies.
  • As many as 8 million persons living in the U.S. have been occupationally exposed in the last 50 years.

• Asbestosis is a fibrotic interstitial lung disease.

  • The asbestos fibers are inhaled into the pulmonary tree.
  • The fibers tend to deposit at the level of the respiratory bronchiole and alveolar duct bifurcans. Most are removed by mucociliary clearance, but some are taken up by alveolar macrophages and alveolar cells.
  • Alveolar macrophages accumulate and inflammation develops, and there is movement of other inflammatory cells into the lung.
  • Various mediators including proteases, cytokines, growth factors and reactive oxygen species are released by inflammatory cells in response to the fibers. As alveolar and interstitial macrophages, neutrophils, lymphocytes, and eosinophils accumulate, normal alveolar cells are lost.
  • The asbestos fibers probably have a direct toxic effect on the lung as well.
  • Fibroblast proliferation and collagen accumulation eventually develop resulting in pulmonary fibrosis.

• Onset of fibrosis occurs 15-30 years after first exposure.

Risk Stratification and Prognosis

• Malignancy is associated with asbestos exposure:

  • Mesothelioma

    • Mesotheiloma is an insidious neoplasm arising from the mesothelial surfaces of the pleural and peritoneal cavities or pericardium. 80% are pleural.
    • The tumor forms on the visceral and parietal pleura in discrete plaques and nodules, and can grow to several centimeters with minimal lung penetration. Adjacent structures including the pericardium, chest wall, and diaphragm are commonly involved. Local lymph nodes may be involved, and distant hematogenous metastases in the liver, lung, bone and adrenals may develop.
    • Asbestos exposure is the only known risk factor for mesothelioma, involved in >70% of cases. Lifetime risk of mesothelioma among asbestos workers is 8-13%.
    • Annual U.S. incidence is 2200 cases per year. It is increasingly common in non-Western countries where there is increasing asbestos exposure.
    • Tobacco use does not increase risk
    • Patients present with increasing dyspnea, often in the 5th-7th decades of life.
    • CXR usually initially shows a large unilateral pleural effusion. Chest CT more clearly shows extent of disease.
    • Video-assisted thorascopy or open biopsy are often required to make the diagnosis.
    • Median survival is 6-18 months and is ‘’not particularly amenable to treatment.’’ Death is from respiratory failure, or due to complications of invasion of involved organs.

  • Lung cancer

    • Lung cancer is more common in patients with asbestosis
    • In one study, asbestos exposure increased relative risk of lung cancer 6-fold
    • Tobacco use increases risk of developing lung cancer in a multiplicative fashion
    • Cigarette smoking alone increased relative risk of lung cancer 11-fold.
    • Cigarette smoking and asbestos exposure increased relative risk of cancer 59-fold
    • Furthermore, a dose-response curve exists for cigarettes
    • The risk of asbestos workers dying of lung cancer increases 9-fold if they smoked 1-20 cigarettes a day, and 16-fold if they smoke >20 cigarettes a day

  • Other cancers

    • Risk may be increased for gastrointestinal, larynx, oropharynx, and kidney and other cancers. Associations have been noted in some studies.

Diagnosis

• Clinical diagnosis typically made on the basis of an appropriate exposure history, an appropriate delay between exposure and clinical manifestations, and appropriate clinical, spirometry and radiographic findings.

History and Symptoms

• Asbestosis presents with insidious onset of gradually progressive dyspnea, initially only noticeable with exertion, usually 15-30 years after initial exposure. Manifestations generally progress even if further exposure does not occur.
• Cough, sputum production, and wheezing may be present in a subset, but are probably more associated with smoking or other pulmonary disease than with asbestosis.

Lungs

• Pulmonary function tests are not diagnostic, but provide a measure of pulmonary function.

  • Most patients demonstrate a restrictive pattern with reduced lung volumes, particularly with reduced vital capacity and reduced total lung capacity, and reduced pulmonary compliance.
  • Reductions in diffusing capacity are common.
  • Some patients may show obstructive patterns, but rarely without associated tobacco exposure. Airflow limitation in these patients may be due to inflammation of large airways, resulting from asbestos deposition along the respiratory bronchioles.

• Exudative pleural effusions may develop. These usually occur within 15 years of exposure. These may resolve spontaneously, and may leave visceral pleural thickening and blunting of the costophrenic angle, and can even impair pulmonary function in some cases.
• Hyaline plaques may form on the parietal pleura, and may calcify. These may develop after less exposure than required for asbestosis, and are therefore more common, occurring in up to 50% of patients with asbestos exposure.

Chest X Ray

• Patients may be asymptomatic, with diagnosis made during chest x-ray (CXR) examination performed for other reasons
• Exam often shows persistent bibasilar fine ‘’crackles’’, often at end-expiration, in one to two-thirds of patients.

  • In advanced disease, markers of severe pulmonary dysfunction may be present, such as clubbing (32-42%), cyanosis, and cor pulmonale. Patients with cor pulmonale may show peripheral edema, jugular venous distension, hepatojugular reflux, and/or a right ventricular heave or gallop.

• Chest radiograph shows irregular linear or nodular opacities

  • These are most commonly seen initially at the bases and the periphery, and they often gradually become visible in the mid and occasionally upper zones of the lung.
  • If seen in conjunction with pleural plaques, the diaphragm and heart border may lose definition, giving rise to the “shaggy heart” sign.
  • Hilar and mediastinal adenopathy is not typical, and suggests another process.

• Chest radiograph is about 80% sensitive for asbestosis, but chest CT is more sensitive, showing abnormalities in 30% of asbestos-exposed individuals with normal CXRs.

  • HRCT typically shows:

    • Basilar and dorsal lung parenchymal fibrosis, with peribronchiolar, intralobular, and interlobular septal fibrosis.
    • Subpleural linear densities parallel to the pleura
    • Coarse parenchymal bands, often contiguous with the pleura
    • Honeycombing in advanced disease
    • Pleural plaques may be present

Biopsy

• Bronchoalveolar lavage or biopsy may be necessary for diagnosis in some cases.

  • Path shows coated or uncoated asbestos fibers in association with pulmonary fibrosis
  • Asbestos bodies are asbestos fibers surrounded by a coating of iron and protein. Other fibers such as talc, glass, carbon, etc, may also be coated in such a manner, producing “ferruginous bodies”. Electron, but not light, microscopy can differentiate the central fiber.
  • Quantity of asbestos fibers correlates with the degree of fibrosis

Differential Diagnosis

• Pleural disease is common in patients with asbestos exposure, occurring in up to 50%, but does not necessarily indicate asbestosis. Pleural disease includes circumscribed pleural plaques, with or without calcification, or diffuse pleural thickening, including blunting of the costrophrenic angle, and rarely rounded atelectasis secondary to pleural adhesions.

  • The plaques are most commonly on the parietal pleura, particularly adjacent to ribs, most commonly along the 6th-9th ribs and along the diagphragm. They are typically absent from the apices and costrophrenic angle. Calicification is found on CXR in 20%, on CT scanning in 50%, and at post in 80%.
  • Parenchymal fibrosis from asbestos exposure can occur with or without pleural plaques
  • Pleural disease is not common in other causes of interstitial lung diseases

Treatment

There is no curative treatment . Oxygen therapy at home is often necessary to relieve the shortness of breath. Supportive treatment of symptoms includes respiratory physiotherapy to remove secretions from the lungs by postural drainage, chest percussion, and vibration. Nebulized medications to thin secretions may be prescribed.

• The management approach for affected patients include amelioration of symptoms, withdrawal from any persistent exposure, and reduction of risk of associated conditions.
• Risk of disease correlates with quantity of exposure, so it seems prudent to limit any further exposure in affected patients, though there is not direct data to prove this.
• Management might include:

  • Vaccination against pneumococcus and influenza
  • Mobilization of secretions
  • Oxygen supplementation as needed
  • Bronchodilator treatment as needed
  • Pulmonary rehabilitation
  • Cessation of smoking
  • Monitoring for associated malignancy

Primary Prevention

• The only effective treatment for asbestosis is prevention.

  • Workers exposed to asbestos should wear appropriate fitting masks and must be monitored, and the workplace itself must be monitored.

Legal issues

Main article: Asbestos and the law

The first lawsuits against asbestos manufacturers were in 1929. Since then, many lawsuits have been filed against asbestos manufacturers and employers , for neglecting to implement safety measures after the link between asbestos, asbestosis and mesothelioma became known (some reports seem to place this as early as 1898). The liability resulting from the sheer number of lawsuits and people affected has reached billions of dollars. The amounts and method of allocating compensation have been the source of many court cases, and government attempts at resolution of existing and future cases.

See also

• Pneumoconiosis

External links

• World Health Organization report
• British Government Health and Safety Executive
• Asbestos Exposure - National Cancer Institute, USA
• Public Health Guidance: Asbestos, Queensland Govt., Australia
• Integrated Risk Information System: Asbestos
• Information on Asbestos Induced Conditions