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Study Syllabus for Classification of Radiographs of Pneumoconioses

Pathology Overview

Pathology Basis of Occupational Lung Disease

Asbestos Pleuropulmonary Disease

Unlike the compact mineral particles of silica and coal mine dust, asbestos represents a family of fibrous silicates presenting as thin filaments with a high aspect (length to width) ratio. The 2 mineralogic forms of asbestos are amphiboles (e.g., crocidolite and amosite) and serpentines, of which chrysotile is the only commercially important form. Although restrictions have been placed on the use of asbestos in developed countries, asbestos exposure still remains an important cause of lung and pleural disease in persons previously exposed to airborne asbestos fibers and in those who continue to be exposed in the processing, application or removal of asbestos or its products [“Diagnostic,” 2004].

Because of their irregular or long filamentous configurations, asbestos fibers tend to be deposited at the bifurcation of small airways and subsequently pass into and through bronchiolar walls. Smaller fibers reach the lung parenchyma via the airstream, where they can penetrate alveolar septa or the visceral pleura [Churg 1998a]. Amphibole asbestos is durable within the lung, whereas chrysotile degrades over time because of the leaching of magnesium ions. Short asbestos fibers may be phagocytized by alveolar macrophages and subsequently removed from the lung by means of airways or lymphatics [Churg 1998a]. A relatively minor proportion of larger fibers are coated with protein and iron by alveolar macrophages to form asbestos bodies [Roggli 2004]. Unlike uncoated fibers, asbestos bodies can be readily recognized by light microscopy in slides of lung tissue and serve as valuable markers of asbestos exposure (Fig. 32). Histochemical stains for iron enhance the recognition and detection of asbestos bodies in tissue. Asbestos is fibrogenic to the lung and pleura, is a recognized cause of lung carcinoma, and is the most important cause of pleural mesothelioma [Roggli et al. 2010].


Asbestosis is defined as lung parenchymal fibrosis due to inhaled asbestos fibers [“Diagnostic,” 2004; Churg 1998a; Roggli et al. 2010]. Macroscopically, the lung is remodeled by interstitial fibrosis and honeycombing, frequently with a lower-lobe distribution, imparting an appearance similar to that of idiopathic pulmonary fibrosis. Coarse gray fibrous trabeculae and fibrotic interlobular septa extend into the lung parenchyma, which often has a bronze discoloration in the fixed specimen (Fig. 33). Histologically, the extent (and progression) of fibrosis is graded from 1 (fibrosis confined to the walls of respiratory bronchioles and the first tier of adjacent alveoli) to 4 (honeycomb changes) [Roggli et al. 2010]. Fibrosis histologically has a chronic collagenous appearance with low cellularity and irregular effacement of alveolar architecture, which gives rise to small irregular opacities in the chest radiograph [Dick et al. 1992] (Fig. 34). Two or more asbestos bodies per square centimeter of a 5-mm thick lung section, in combination with interstitial fibrosis of the appropriate pattern, are indicative of asbestosis (Fig. 32). Fewer asbestos bodies do not necessarily exclude a diagnosis of asbestosis, but evidence of excess asbestos would then require quantitating fibers by electron microscopy following lung digestion and sediment extraction [Roggli et al. 2010; Roggli and Sharma 2004].