Study Syllabus for Classification of Radiographs of Pneumoconioses
Pathology Basis of Occupational Lung Disease
Pulmonary silicosis is caused by the inhalation of free crystalline silica (SiO2). It is important to make the distinction between silica and silicates, in which silicon is combined with various cations and anions in a crystalline matrix. Silicates, including asbestos, are common in the industrial setting, are generally less fibrogenic than free crystalline silica, and, when present in combination with silica, may alter the tissue reaction, producing a mixed-dust fibrotic nodule [Silicosis and Silicate Disease Committee 1988].
Chronic Nodular Silicosis
The anatomic hallmark of pulmonary silicosis is the silicotic nodule, a well-demarcated, rounded fibrotic lesion that tends to concentrate in the upper lung lobes. Macroscopically, nodules range in color from gray to black depending on the amount of associated carbonaceous dust or other black pigments incorporated into the lesion. In its mature form, the silicotic nodule is microscopically composed of concentrically arranged coarse collagen bundles of low cellularity (Fig. 19). In younger lesions, the central fibrotic core is cuffed by a rim of fibroblasts and dust-laden macrophages. Cellular nodules composed of histiocytes, resembling granulomas, are a notable feature of accelerated silicosis due to very heavy silica exposure [Silicosis and Silicate Disease Committee 1988; Gibbs and Wagner 1998]. Under polarized light microscopy, silica canbe recognized within the nodules as weakly birefringent polyhedral particles, approximately 1 to 2 microns in maximal dimension, typically interspersed with pigment and brightly birefringent needle-like silicate crystals (Fig. 20).
Focal calcification and central necrosis and breakdown are variable features of silicotic nodules. Chronic nodular pulmonary silicosis is classified pathologically as simple or complicated according to the size of the nodules. Large radiographic opacities 1 cm or greater in diameter are designated as complicated silicosis (PMF) [Silicosis and Silicate Disease Committee 1988]. The minimum size criterion for the diagnosis of complicated silicotic nodules in tissue specimens varies between 1 and 2 cm, with the majority of references advocating a 1-cm tissue standard [Silicosis and Silicate Disease Committee 1988; Gibbs and Wagner 1998]. Growth of silicotic nodules may occur by expansion of individual lesions or more often by fusion of multiple nodules, forming a conglomerate nodule (Fig. 19). Thus, complicated silicosis occurs in a background of simple silicosis. Large silicotic nodules may be associated with paracicatricial emphysema with or without emphysematous bullae. As they enlarge, conglomerate lesions not only replace lung parenchyma but also may cross interlobar fissures and obliterate pulmonary arteries, leading to pulmonary hypertension. Ischemia of large nodules may result in central necrosis and cavitation. Inhalational silica exposure also increases the risk for mycobacterial infections. Consequently, mycobacterial granulomas can modify the morphology of silicotic nodules, introducing Langhans giant cells, caseation necrosis, cavitation, and acid-fast bacilli into the histological picture.
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