Histopathologic Changes

CWP lesions are focal. Simple CWP is associated with macular and nodular lesions, whereas complicated CWP is associated with PMF and lesions of rheumatoid pneumoconiosis (Caplan syndrome, discussed later on).

The pleural surfaces of a coal worker's lung show an irregular pattern of bluish-black pigmentation that corresponds to the junction sites of septal-lymphatic vessels and the pleura. Peribronchial, hilar, and paratracheal lymph nodes are enlarged, black, and firm. The initial lesions in the lung are the coal dust macules, which correspond macroscopically to focal areas of black pigmentation. On microscopic examination, the macule is seen to be composed of coal dust–laden macrophages within the walls of the respiratory bronchioles and adjacent alveoli (Figure 51-2). Focal emphysema around the coal dust macule is common and is considered an integral part of the lesion of simple CWP.

The histopathologic hallmark of simple CWP is the nodule. The nodules are rounded lesions with collagenous centers. On microscopic examination, the nodule can be divided into three zones: a central zone composed of whorls of dense, hyalinized fibrous tissue; a middle zone made up of concentrically arranged collagen fibers (onion-skinning); and a peripheral zone of more randomly oriented collagen fibers mixed with dust-laden macrophages and lymphoid cells (Figure 51-3). “Old” inactive nodules often are relatively acellular. Particles of silica may be demonstrated in the nodules as birefringent particles under polarized light. Nodules represent a form of mixed-dust fibrosis (i.e., coal dust plus silica exposure), usually are found in association with macules, and in some instances may develop from preexisting macules. They are not confined to the respiratory bronchioles but also are seen in the subpleural and peribronchial connective tissues. Nodules tend to cluster and eventually coalesce to produce PMF. Degenerative changes commonly are observed in the nodular lesions, including calcification, cholesterol clefts, and cavitation. In severe silicosis, structural alterations of the pulmonary vasculature may result from the accumulation of dust in the adventitia of large vessels, and involvement of the smaller blood vessels by silicotic nodules also may be seen.

Progressive massive fibrosis is defined as an opacity or fibrotic pneumoconiotic lesion of 1 cm in diameter or greater. These lesions appear as black fibrotic masses that may be round, oval, or irregular in shape. The lung and bronchovascular rays become markedly distorted. Microscopically, the lesions are composed of bundles of haphazardly arranged hyalinized collagen fibers and/or reticulin fibers and coal dust. Dust particles near the periphery of the lesion are found mainly within macrophages, whereas in the center, the dust tends to lie free in clefts and cavities. The nodules are confluent, emphysematous bullae often surrounding the areas of massive fibrosis. Focal interstitial fibrosis can be observed in the lungs of workers exposed to dust containing a combination of silica and silicates, with sometimes sufficiently advanced lesions to result in honeycombing-type changes. Areas of liquefactive necrosis containing fragments of degenerating collagen as well as cholesterol crystals are frequently observed.

The histopathologic pattern in acute silicosis is quite different from that in the chronic form. Infiltration of the alveolar walls with plasma cells, lymphocytes, and fibroblasts, with some collagenation, is typical. The alveoli are filled with an eosinophilic coagulum (Figure 51-4). Electron microscopy shows widening of alveolar walls, with some collagen and clusters of type II cells; the alveolar spaces contain degenerating cells that probably are type II alveolar cells and macrophages. Silica particles may be demonstrated in the lungs and lymph nodes; silicotic nodules are few or absent.