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Figure 17.26 Pathogenesis of three common forms of pneumoconiosis. A, Coal-workers’ pneumoconiosis. The macrophages phagocytose CHAPTER 17
large amount of coal dust particles which are then passed into the interstitial tissue of the lung and aggregate around respiratory bronchiole and The Respiratory System
cause focal dust emphysema. B, Silicosis. The tiny silica particles are toxic to macrophages. The dead macrophages release fibrogenic factor and
eventually result in silicotic nodule. C, Asbestosis. Asbestos fibres initiate lot of interstitial fibrosis and also form asbestos bodies.

2. There is some increase in the network of reticulin and 2. The wall of respiratory bronchioles and pulmonary
collagen in the coal macules. vessels included in the massive scars are thickened and
3. Respiratory bronchioles and alveoli surrounding the their lumina obliterated.
macules are distended without significant destruction of
the alveolar walls.
PROGRESSIVE MASSIVE FIBROSIS. Grossly, besides
the coal macules and nodules of simple pneumoconiosis,
there are larger, hard, black scattered areas measuring
more than 2 cm in diameter and sometimes massive. They
are usually bilateral and located more often in the upper
parts of the lungs posteriorly. Sometimes, these masses
break down centrally due to ischaemic necrosis or due to
tuberculosis forming cavities filled with black semifluid
resembling India ink. The pleura and the regional lymph
nodes are also blackened and fibrotic (Fig. 17.27).
Histologically, the following features are present:
1. The fibrous lesions are composed almost entirely of
dense collagen and carbon pigment. Figure 17.27 Gross appearance of the lungs in simple coal-workers’
pneumoconiosis (A) and progressive massive fibrosis (B).