Study Syllabus for Classification of Radiographs of Pneumoconioses

Clinical Overview

Major Occupational Lung Diseases

Pneumoconioses

Asbestosis and Asbestos-Related Pleural Diseases

Asbestosis is a slowly progressive fibrotic lung disease caused by inhalation of asbestos fibers. Other lung manifestations of asbestos exposure include pleural abnormalities (pleural effusions, plaques, and diffuse thickening) and chest malignancies (bronchogenic carcinoma and mesothelioma). Asbestos fibers are composed of hydrated magnesium silicates characterized by tensile strength, weavability and fire resistance, leading to multiple industrial uses. Exposures occur in asbestos mining and milling, industrial applications (i.e., insulation, shipbuilding, friction products, textiles), and non-occupational settings (i.e., geogenic sources, building demolition, and residential uses). Asbestos-related lung diseases typically occur with long latencies (10-30 years) following initial exposure. Insidious onset of exertional dyspnea, often with dry cough, are usual symptoms of asbestosis. Characteristic pulmonary function abnormalities may include restrictive changes, diminished DLCO, and exertional hypoxemia with more advanced disease. Lung biopsy is rarely needed to confirm a diagnosis.

The chest radiograph may show subtle, lower lobe predominant, small irregular opacities, often accompanied by pleural abnormalities. Many of those exposed to significant amounts of asbestos develop pleural plaques that preferentially involve the parietal pleura along the 6th through 9th ribs as well as the diaphragm (Fig. 7; note calcified and noncalcified plaque on parietal pleura (white arrows) and diaphragms (black arrows) bilaterally). Calcifications are seen in around 20% of plaques on chest radiograph and in 50% on CT. Pleural plaques and pleural thickening must be distinguished from extrapleural fat, which is characterized by relatively low attenuation soft tissue thickening, extending symmetrically in undulating fashion along the lateral chest wall all the way to the lung apices [Sargent et al. 1984] (Fig. 8), while pleural plaques are usually more focal and asymmetric. However, focal extrapleural fat may be impossible to distinguish on imaging from noncalcified pleural plaques but can be identified on CT; note attenuation of pleural thickening (black arrows) similar to subcutaneous fat (white arrow) (Fig. 9). Rounded atelectasis, which can occur as a consequence of asbestos related pleural thickening or effusion, is characterized by a mass-like opacity adjacent to thickened pleura, with associated lobar volume loss, and curving of bronchi and vessels into the mass [Lynch et al. 1988; McHugh and Blaquiere 1989] (Fig. 10). Benign asbestos pleural effusions are usually small and unilateral, and are one of the earliest imaging manifestations of asbestos exposure. Characteristic HRCT findings of asbestosis include subpleural linear densities; interlobular septal thickening; centrilobular thickening; subpleural parenchymal bands (Fig. 11, arrow); and reticular opacity with traction bronchiectasis and honeycombing in severe disease similar in appearance to UIP. (Fig. 11)

As with the other pneumoconioses, there is no specific treatment for asbestosis. Management includes early disease detection and removal from exposure, supplemental oxygen for hypoxia, prompt treatment of lung infection, appropriate vaccinations, and smoking cessation when applicable (in part to diminish the synergistic effect of combined smoking and asbestos exposure on risk for lung malignancy).

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