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Asbestosis is characterized by diffuse interstitial pulmonary fibrosis resulting from prolonged exposure to airborne asbestos particles. Asbestosis may develop many years (about 15 to 20) after regular exposure to asbestos ceases. Asbestos exposure also causes pleural plaques and mesotheliomas of the pleura and the peritoneum. A potent cocarcinogen, asbestos heightens a cigarette smoker's risk for lung cancer. In fact, an asbestos worker who smokes is 90 times more likely to develop lung cancer than a smoker who never worked with asbestos.


Asbestosis is a form of pneumonoconiosis. It follows prolonged inhalation of respirable asbestos fibers (about 50 microns long and 0.5 microns wide). Sources of exposure include asbestos mining and milling, the construction industry (where asbestos is used in a prefabricated form), and the fireproofing and textile industries. Asbestos is also used in the production of paints, plastics, and brake and clutch linings. Asbestosrelated diseases develop in families of asbestos workers as a result of exposure to fibrous dust shaken off workers' clothing at home. Such diseases develop in the general public as a result of exposure to fibrous dust or waste piles from nearby asbestos plants.

Signs and Symptoms

The main symptoms of asbestosis are:

  • increasing breathlessness, especially when exercising,
  • coughing, 
  • chest pain
  • a feeling of tightness in the chest.

Asbestosis may damage the function of the lungs so much that the condition progresses to respiratory (breathing) failure. At this stage the oxygen supply to the body is so poor that the patient is always breathless and has blue-tinged skin even when at rest in bed.

Diagnostic tests

Chest X-rays may show fine, irregular, and linear diffuse infiltrates. If the patient has extensive fibrosis, X-rays may disclose lungs with a honeycomb or ground­glass appearance. Films may also show pleural thickening and pleural calcification, bilateral obliteration of costophrenic angles and, in later disease stages, an enlarged heart with a classic "shaggy" border.

Pulmonary function tests may identify decreased vital capacity, forced vital capacity (FVC), and total lung capacity; decreased or normal forced expiratory volume in 1 second (FEV1); a normal ratio of FEV1 to FVC; and reduced diffusing capacity for carbon monoxide when fibrosis destroys alveolar walls and thickens the alveolocapillary membrane.

Arterial blood gas analysis may reveal decreased partial pressures of arterial oxygen and carbon dioxide from hyperventilation.


Chest physiotherapy techniques, such as controlled coughing and postural drainage with chest percussion and vibration, may be implemented to relieve respiratory signs and symptoms and, in advanced disease manage hypoxia and cor pulmonale.

Aerosol therapy, inhaled mucolytics, and increasec: fluid intake (at least 3 L [3.2 qt] daily) may also help relieve respiratory symptoms. Hypoxia requires oxygen administration by cannula or mask (up to 2 L/minute) or by mechanical ventilation if the patients arterial oxygen level can't be maintained above 40 mm Hg.

Diuretic agents, digitalis preparations, and salt restriction may be necessary for patients with cor pulmonale. Respiratory tract infections require prompt antibiotic therapy.


Early screening by chest x-ray of people who are exposed to asbestos may help prevent asbestosis.

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