In cases 3, 7, and 8, there was radiographic evidence of bilateral interstitial disease, in addition to new bilateral nodular densities in case 3, and a “new” patchy infiltrate in the left lower lobe in case 7. Hyaline pleural plaques characteristic of those caused by asbestos were observed radiographically in cases 3, 4, and 8.
The pathologic and mineralogic findings in the eight cases are listed in Table 2. In cases 1, 2, and 3, there was intraluminal fibrosis and inflammation of distal air spaces (IFDA), a pattern of change frequently referred to as “bronchiolitis obliterans organizing pneumonitis” (BOOP) (Fig 1). Ferruginous bodies with cores characteristic of asbestos bodies were easily identified in the tissue, although in case 1, it was sometimes difficult to tell if some ferruginous bodies were asbestos bodies because their cores could not be seen. In case 2, the IFDA was associated with marked pleural thickening, but did not show the macroscopic or histologic features of rounded atelectasis. In these cases, the asbestos bodies were most prevalent in the regions of IFDA. The subpleural nodule from case 4 had an unusual appearance, showing localized alveolar edema with an intense eosinophil inflammatory infiltrate admixed with a few histiocytes and other inflammatory cells with early organization of the alveolar exudate in a few areas (Fig 2). Asbestos bodies were easily identified in this tissue, and again were localized to the area of inflammation and fibrosis.
Figure 1. Region of organizing pneumonitis (case 1) showing ferruginous body near center of fibroinflammatory tissue (arrow, hematoxylin and eosin, X330). In this instance, the core of the ferruginous body was thin and nearly transparent, characteristic of an asbestos body (insert, hematoxylin and eosin, x 1Д00).
Figure 2. In some regions of the mass in case 4, there was “early” organization of the infiltrate with intra-alveolar fibroblast proliferation (hematoxylin and eosin, X 110). Ferruginous bodies consistent with asbestos bodies were observed admixed with the inflammatory exudate in the alveoli (insert, iron stain, hematoxylin and eosin, X330).
Table 2—Fathobgic and Mineralogic Findings
|Histologic Features of Lesion||OtherPathologic
|1||Surgical||2 nodular grayish-tan masses, RUL||IFDA (BOOP) with numerous ab||Hyaline pleural plaques||11,200 ab/g wit|
|2||Surgical||Subpleural 4 x 3 x 5-cm LUL grayish-white mass||IFDA (BOOP) with ab||Hyaline pleural plaques||10,500 ab/g wit|
|3||Surgical||Grayish-tan nodular regions in association with difluse scarring, LLL||IFDA (BOOP) with ab||Hyaline pleural plaques; difluse interstitial fibrosis||8,500 ab/g wit|
|4||Autopsy||2 x 2 x 1-cm grayish-tan mass, RUL||Localized intra-alveolar eosinophil-macrophage infiltrate with focal organization and ab||Calcified hyaline pleural plaques, visceral pleural fibrosis||3,400-10,600 ab/g wit|
|5||Surgical||3 x 2 X 2-cm grayish-white mass, posterior segment RUL||Fibroinflammatory changes with localized desquamative interstitial pneumonitis and ab|
|Autopsy||10 x 10 x 8-cm region of gray-whiteconsolidation with cystic change||Fibroinflammatory changes with bronchiectasis and necrotizing granulomata containing ab||Bilateral calcified hyaline pleural plaques; grade 4 asbestosis in lower lobes||1,700-8,300 ab/g wit|
|6||Surgical||Grayish-tan nodular mass with necrosis||Fibrosis; inflammation; necrotizing granulomata containing degenerating fungal hyphae (Aspergillus) with birefiringent crystals (probably calcium oxalate)||6,600 ab/g wit|
|7||Autopsy||Difluse fibrosis w/ vague nodular regions in lower lobes||Granulomatous inflammation resembling sarcoidosis; ab in granulomata||Grade 4 asbestosis; calcified hyaline pleural plaques||30,000-70,000 ab/g wit|
|8||Surgical||Pink-tan tissue||Lymphocyte-plasma cell interstitial inflammatory cell infiltrate; small nonnecrotizing granulomata||Focal interstitial and intra-alveolar fibrosis||1.380.000 amosite fibers/g dlt5.520.000 chrysotile fibers/g dlt|