Lecture Notes: Asbestosis

Introduction to Asbestosis
Asbestosis specifically refers to the pneumoconiosis caused by inhalation of asbestos fibers. The disease is characterized by slowly progressive, diffuse pulmonary fibrosis. Asbestosis remains a significant clinical problem despite substantial reductions in occupational asbestos exposure.

Pathogenesis of Asbestosis
Asbestos-induced diseases are probably caused by the direct toxic effects of the fibers on pulmonary parenchymal cells as well as the release of various mediators (reactive oxygen species, proteases, cytokines, and growth factors) by inflammatory cells. Deleterious reactive oxygen and nitrogen free radicals may be formed either via reactions catalyzed by iron molecules within asbestos fibers or as a consequence of the activation of inflammatory cells. Free radicals can react with and damage a variety of cellular macromolecules and may disrupt DNA to give rise to malignancy.

Clinical Findings of Asbestosis
Most patients who develop asbestosis are asymptomatic for at least 20 to 30 years after the initial exposure; the latency period between exposure and symptoms is inversely proportional to the intensity of asbestos exposure. In contrast, pleural disease is often present earlier. As an example, benign asbestos pleural effusions (BAPEs) usually occur within 15 years of first exposure to asbestos (range less than 1 year to up to 50 years).
  • Symptoms - The earliest symptom of asbestosis is usually the insidious onset of breathlessness with exertion. Dyspnea commonly progresses inexorably even in the absence of further asbestos exposure. Cough, sputum production, and wheezing are unusual; if present, these symptoms tend to be a consequence of cigarette smoking rather than asbestos-induced lung disease.
  • Physical examination - As asbestosis progresses, patients may develop bibasilar, fine end-inspiratory crackles (32 to 64 percent) and clubbing (32 to 42 percent). Cor pulmonale may ensue in advanced cases and may cause peripheral edema, jugular venous distension, hepatojugular reflux, and/or a right ventricular heave or gallop.
  • Laboratory test - Laboratory test are generally nonspecific and not useful clinically. Antinuclear antibodies, rheumatoid factor, and an elevated erythrocyte sedimentation rate may be present but do not correlate with disease severity or activity.
  • Pulmonary function tests - The characteristic lung function abnormalities in patients with asbestosis include:
    • Reduced lung volumes, particularly the vital capacity and total lung capacity.
    • Diminished single breath DLCO.
    • Decreased pulmonary compliance.
    • Absence of airflow obstruction by spirometry (normal ratio of the forced expiratory volume in one second to forced vital capacity).

Imaging of Asbestosis
  • Chest radiograph -  The chest radiograph in patients with asbestosis usually reveals small bilateral parenchymal opacities with a multinodular or reticular pattern, often with associated pleural abnormalities.
  • Computed tomographic scanning - High resolution computed tomography (HRCT) is more sensitive than plain films in detecting parenchymal abnormalities in asbestos-exposed individuals. The characteristic HRCT findings of asbestosis include:
    • Subpleural linear densities of varying length parallel to the pleura.
    • Basilar and dorsal lung parenchymal fibrosis, with peribronchiolar, intralobular, and interlobular septal fibrosis.
    • Coarse parenchymal bands (2 to 5 cm in length), often contiguous with the pleura.
    • Coarse honeycombing in advanced disease.
    • Pleural plaques, which, as noted above, help differentiate asbestos-induced parenchymal disease from other interstitial lung diseases.

Diagnosis of Asbestosis
There are three key findings that support the diagnosis of asbestosis:
  • A reliable history of exposure to asbestos with a proper latency period from the onset of exposure to the time of presentation, and/or presence of markers of exposure (eg, pleural plaques, which are virtually pathognomonic of previous exposure, or recovery of sufficient quantities of asbestos fibers/bodies in bronchoalveolar lavage or lung tissue).
  • Definite evidence of interstitial fibrosis, as manifested by one or more of the following: 
    • end-inspiratory crackles on chest examination; 
    • reduced lung volumes and/or DLCO; 
    • presence of typical chest radiograph or HRCT findings of interstitial lung disease; or 
    • histologic evidence of interstitial fibrosis.
  • Absence of other causes of diffuse parenchymal lung disease.

Treatment of Asbestosis
There is currently no specific treatment for asbestosis. There have been no prospective studies of patients with asbestosis utilizing antiinflammatory or immunosuppressive agents such as glucocorticoids or cytotoxic therapy. Thus, management of patients with asbestosis should focus on preventive measures, including:
  • Smoking cessation.
  • Early detection of physiologic and radiographic abnormalities.
  • Prevention of further airborne asbestos exposure.
  • Supplemental oxygen when there is resting hypoxemia or exercise-induced oxygen desaturation.
  • Prompt treatment of respiratory infections.
  • Pneumococcal and influenza vaccination. 

Medical Lecture Note Copyright © 2011