A comparative study of mesothelioma and asbestosis using computed tomography and conventional chest radiography.
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Alveolar macrophage-derived plasminogen activator (PA) activity is decreased in some chronic interstitial lung diseases such as idiopathic pulmonary fibrosis and sarcoidosis but increased in experimental models of acute alveolitis. Although asbestos fibers can stimulate alveolar macrophages (AM) to release PA in vitro, the effect of chronic asbestos exposure of the lower respiratory tract on lung PA activity remains unknown. The present study was designed to evaluate PA activity of alveolar macrophages and bronchoalveolar lavage (BAL) fluid in asbestos-exposed sheep and asbestos workers. Forty-three sheep were exposed to either 100 mg UICC chrysotile B asbestos in 100 ml phosphate-buffered saline (PBS) or to 100 ml PBS by tracheal infusion every 2 wk for 18 months. At Month 18, chest roentgenograms were analyzed and alveolar macrophage and extracellular fluid PA activity were measured in samples obtained by BAL. Alveolar macrophage PA activity was increased in the asbestos-exposed sheep compared to control sheep (87.2 +/- 17.3 versus 41.1 +/- 7.2 U/10(5) AM-24 h, p less than 0.05) as was the BAL fluid PA activity (674.9 +/- 168.4 versus 81.3 +/- 19.7 U/mg alb-24 h, p less than 0.01). Among the asbestos-exposed sheep, 10 had normal chest roentgenograms (Group SA) and 15 had irregular interstitial opacities (Group SB). Strikingly, whereas Group SA did not differ from the control group in BAL cellularity or PA activity, Group SB had marked increases in alveolar macrophages (p less than 0.005), AM PA activity (p less than 0.02), and BAL PA activity (p less than 0.001) compared to the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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The diagnosis of asbestos-associated pulmonary fibrosis was established in 3 patients by finding ferruginous bodies in transbronchial lung biopsies. Ferruginous bodies may be difficult to identify in histologic preparations when they are not oriented parallel to the plane of tissue section or when camouflaged by anthracotic pigment. We describe a simple method to enhance diagnostic sensitivity by digesting biopsy tissue and examining the filtered residue for ferruginous bodies.
Analysis of bronchoalveolar cell types and structure was performed during the development of asbestos-induced lung injury in the rat. Animals received single intratracheal injections of one of the following: saline (control), UICC chrysotile B asbestos (5 mg), or very short 4T30 chrysotile fibers (5 mg). Bronchoalveolar lavage (BAL) was performed at various intervals after instillation. Analysis of BAL fluid showed significant increase in inflammatory cells in response to asbestos, which persisted longer in animals treated with chrysotile B. Presence of numerous mitotic figures in BAL fluid of treated animals suggests that macrophage replication may contribute in part to this response. Differential cellular analysis indicated that after injection of long chrysotile fibers, which causes fibrotic lesions within 7 days, polymorphonuclear leukocytes (PMN) appear as early as Day 1 in significant concentration (40%) in the bronchoalveolar compartment and persist through Day 7 after treatment. From Day 7 to Day 21, multinucleated cells (MGC) were found in lavage fluid (5 to 8%). Most of these cells were binucleated, and none had more than 3 nuclei. By contrast, exposure to very short chrysotile fibers caused only a very transient influx of PMN on Day 1. By Day 7, there was a significant increase in MGC, which persisted through Day 21, at which time no fibrosis was apparent. Although most of these cells were binucleated, many cells had 3 or more nuclei. The giant cells were predominantly of the foreign body type, with MGC of the Langhans type also present.(ABSTRACT TRUNCATED AT 250 WORDS)
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Progression of asbestos-related disease was assessed in a group of 253 dockyard workers examined in 1966 and 1975. Despite the almost complete protection from exposure to asbestos since 1966, radiographic parenchymal abnormalities increased and occurred more frequently during the next 9 years in those men who had been more heavily exposed to asbestos. Lung function values were lower in those most heavily exposed and were declining at a faster rate than in those with less dust exposure. The most sensitive lung function index was the transfer factor.Those men with persistent crackles in 1966 exhibited a restrictive pattern of lung function, whereas an obstructive pattern was seen in men with wheezes in 1966. The men with irregular small opacities of category 1/1 or more or with diffuse pleural change in 1966 and who survived to 1975 had worse lung functions than any other groups.Progression of disease was greater for smokers than non-smokers, with those who gave up smoking between 1966 and 1975 suffering the greatest changes. This latter group showed most increase in small opacities and included almost all new cases of diffuse pleural changes. They also showed the greatest declines in forced expiratory volume and forced vital capacity.
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