A single asbestos body was identified in the frozen section specimen, and asbestos digestion analysis of the lung tissue showed 4,666 asbestos bodies per gram of wet lung tissue, 819 X 10^ chrysotile fibers per gram of dry lung tissue, and 20 X 106 tremolite fibers per gram of dry lung tissue. The authors discussed the experimental and clinical studies, suggesting that asbestos could cause such a lesion, but they did not comment on the association of desquamative interstitial pneumonitis with cigarette smoking.
In case 5, at postmortem examination, approximately one third of the right upper lobe was involved by a fibrotic process with associated cystic changes in which necrotic material was present in the dilated cystic spaces. Histologically, there was necrotizing granulomatous inflammation (culture and microorganism special stain negative), in which asbestos bodies were easily identified and seemed to be concentrated in the areas of necrosis. The pathogenesis and morphogenesis of this change is uncertain, although the pathologic changes suggested a fungal or mycobacterial infection.
Continue reading
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (10)
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (9)
The pathologic changes observed in case 4 were unusual, with focal organization of the intra-alveolar inflammatory infiltrate and easily identifiable asbestos bodies in the tissue. Because of the numerous eosinophils and macrophages within the alveoli, the diagnosis of chronic eosinophilic pneumonia was considered, although chronic eosinophilic pneumonia is usually not described as a localized disease. Also, eosinophils are reported to be a common inflammatory cell in pleural eflusions caused by asbestos and are a frequent cell type in bronchoalveolar lavage fluid specimens from persons with asbestosis.
Continue reading
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (8)
Lynch et al studied 260 asbestos-exposed individuals by computed tomography (CT) and identified 43 unsuspected pulmonary masses in 27 individuals. These masses included 10 examples of fissural pleural plaques, 3 cases of fibrotic bands, 11 cases of rounded atelectasis, 3 carcinomas, and 16 cases of presumed benign masses. Of these presumed benign masses, 9 were intraparenchymal and 7 were subpleural without features of rounded atelectasis. All of the subpleural masses were “stable” on serial radiographs or CT scans for at least one year, and all were less than 2 cm in diameter. Of the intraparenchymal masses, two were stable for at least one year as determined by chest radiograph and three masses were stable for more than two years. In one patient, no change was identified in three nodules evaluated by CT and chest radiograph over a nine-month period. One 3-cm ill-defined mass resolved without therapy over a six-month period of observation. The subpleural and intraparenchymal masses were not resected, and therefore no comments could be made concerning their pathologic features.
Continue reading
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (7)
In his description of the pathologic features of asbestosis, Spencer states the following: “Accompanying these changes there is an outpouring of inflammatory oedema fluid accompanied by a histiocytic and giant-cell formation in the walls of the terminal and respiratory bronchioles. Later reticulin and collagen fibers are laid down in increasing numbers in the interstitium of the alveolar walls and many of the alveoli, alveolar ducts and respiratory bronchioles become obliterated by fibrosis, but the elastic framework still remains.” The photograph of asbestosis shown by Spencer displays an organizing pneumonitis characterized by extensive intraluminal fibrosis of the distal airways. In addition, Roggli reported observing several cases of organizing pneumonia in patients with asbestos exposure who underwent thoracotomy for suspected malignancy.
Continue reading
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (6)
The main pathologic changes in cases 1, 2, and 3, and to a lesser degree in case 4, of intraluminal fibrosis and inflammation involving the distal air spaces, ie, alveoli, alveolar ducts, and terminal and respiratory bronchioles, show a pathologic change that is considered to be a response to injury that occurs in a variety of disorders,’ and is therefore not a specific disease. This entity has been referred to as “cryptogenic organizing pneumonitis,’ “organizing pneumonia like process,” and most frequently BOOP. That asbestos can potentially produce a localized BOOP-like pulmonary lesion in humans was first suggested in 1961 in a New England Journal CPC. In that case, a 61-year-old man developed a localized consolidation in the left upper lobe that histologically showed organizing pneumonitis in which there were numerous asbestos bodies.
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (5)
Sections of autopsy lung tissue in case 7 showed extensive granulomatous inflammation and fibrosis involving the peripheral lung tissue. The granulomata were not located in any specific distribution within the lung, and autopsy sections of regional lymph nodes and other tissue did not show granulomata. Numerous asbestos bodies were scattered throughout the region of granulomatous inflammation, and asbestos bodies were identified in the cytoplasm of many histiocytic giant cells, some of which were components of the granulomata (Fig 6). Cultures and special stains of lung tissue in case 7 were negative for microorganisms.
In case 8, the peripheral lung tissue macroscopically appeared relatively normal, although microscopically showed a diffuse lymphocyte-plasma cell interstitial inflammatory cell infiltrate (Fig 7) with a few widely scattered nonnecrotizing granulomata. The histologic changes were nonspecific, although they resembled those seen in extrinsic allergic alveolitis.
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (4)
The right upper lobe nodule in case 5 showed a localized desquamative interstitial pneumonitis pattern in association with focal dense scarring (Fig 3). Asbestos bodies were frequently seen admixed with the alveolar macrophages. This man died nine years after his right upper lobe biopsy, and postmortem examination of the right lung showed extensive fibrosis and cystic cavitary change involving approximately one third of the right upper lobe. Microscopically, there were structures that had the appearance of necrotizing granulomata, although special stains and cultures for routine bacteria, fungi, and mycobacteria were negative, and in the areas of necrosis there were frequent asbestos bodies (Fig 4).
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (3)
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.
Continue reading
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (2)
In all patients, lung tissue was available for asbestos digestion analysis. This was performed using a slight modification of the Smith and Naylor technique. In cases 1, 2, and 4, lung tissue showing the pathologic changes described herein was removed from the paraffin block. In our experience, lung tissue processed from paraffin for asbestos quantitation typically shows a 10 to 25 percent decrease in asbestos body content compared with nonprocessed, paraffin-embedded tissue. The asbestos fiber analysis in case 6 was performed in the laboratory of Dr. Ronald F. Dodson, according to his procedure.
Sections of lung tissue were routinely stained with hematoxylin-eosin, Movat pentachrome, Ziehl-Neelsen, Gomori methenamine silver, and Brown-and-Brenn tissue Cram stain. Portions of lung tissue from cases 1, 2, 5, 6, and 7 were cultured for routine bacteria, mycobacteria, and fungi. The histologic sections were carefully examined for the presence of intranuclear and cytoplasmic viral inclusions.
Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (1)
Asbestos is recognized as causing five forms of L nonneoplastic pleuropulmonary disease (pleural efiusion, hyaline pleural plaques, visceral pleural fibrosis, rounded atelectasis, and asbestosis), the pathogenesis of which is poorly understood. Whereas parietal pleural plaques and rounded atelectasis are characteristically localized lesions, asbestosis is often considered a diffuse disease, even though it may begin as localized peribronchiolar fibrosis. Asbestos is usually not thought of as producing localized parenchymal lung masses, although Hillerdal and Hem-mingsson described ten patients with localized visceral pleural fibrosis and fibrosis of the underlying lung parenchyma that caused a pseudotumor. More recently, Lynch et al identified 16 localized masses (9 intraparenchymal, 7 subpleural) in 260 asbestos-exposed individuals who were evaluated radiographi-cally.
The purpose of this article is to present the clinical and pathologic features of eight patients, occupationally exposed to asbestos, who developed localized pulmonary nodules or unusual pulmonary pathologic reactions. The localized disease processes were clinically thought to represent neoplasms and were resected for that reason. The data suggesting that these pathologic changes were caused by asbestos are discussed.
Continue reading