Disease relevance of Asbestosis

• Preliminary observations indicate that fibronectin is also present in the lesions of silicosis and asbestosis [1].
• There was increased immunolocalization of all three TGF-beta isoforms in the fibrotic lesions of asbestosis and pleural fibrosis [2].
• According to the standards proposed by the Pneumoconiosis Committee of the College of American Pathologists, features consistent with asbestosis grade 1 (AG1) include findings of bilateral pleural plaques, high concentrations of asbestos bodies (ABs) in digested lung tissue, and a history of occupational risk [3].
• Slides of sputum samples from 201 former uranium miners with silicosis, 100 patients with asbestosis, 103 workers resected for lung cancer, and 200 controls (50% smokers), were stained using the Papanicolaou (Pap) method and the Feulgen reaction with thionin [4].
• The P(A-a)O2/VO2(mm Hg)/L of O2 was the most discriminatory measurement of gas transport between groups, with mean values of 14.45 +/- 9.24 for normal, 19.04 +/- 10.52 for CAO, 16.85 +/- 8.94 for CAO and pleural disease and 34.07 +/- 21.54 for asbestosis with or without CAO [5].

High impact information on Asbestosis

• Inhalation models of crocidolite- and chrysotile-induced inflammation and asbestosis were used to study the localization of p65, a protein subunit of the NF-kappa B transcription factor, in sham control rats and those exposed to asbestos [6].
• We found significant increases for TNF-alpha release in both diseases (p < 0.01) and a significant increase for IL-1 beta release in asbestosis compared to normal controls (p < 0.01) [7].
• The antioxidant enzyme extracellular superoxide dismutase (EC-SOD) can protect the lung against a variety of insults; however, its role in asbestosis is unknown [8].
• In humans, genetic hemochromatosis and asbestosis are two major diseases associated with iron-induced carcinogenesis [9].
• The percentage of individuals in these three groups with increased serum concentrations of TGF-alpha, erbB-2 ECD, and mutant p53, respectively, were: asbestosis patients with cancer, 36%, 16%, 19%; asbestosis patients without cancer, 38%, 19%, 6%; control subjects, 0%, 5%, 10% [10].

Chemical compound and disease context of Asbestosis

• Spirometry was completed successfully in 214 workers without known asbestosis and 207 underwent methacholine bronchoprovocation testing [11].
• In both samples, those who quit were more likely to have had lower alveolar carbon monoxide (COa) levels, to be older, and to have had asbestosis [12].
• Special emphasis is given to the hypothesis that iron-catalyzed hydroxyl radicals (HO.-) have a pivotal role in causing asbestosis [13].
• The involvement of microsomal enzymes in asbestosis was indicated by alterations in glucose-6-phosphatase and tyrosine transaminase and aniline hydroxylase [14].
• The authors counted the asbestos bodies in multiple paraffin-embedded sections of lung tissues stained for iron, and compared those numbers with the asbestos body counts determined by hypochlorite digestion of wet formalin-fixed lung tissue in six cases of asbestosis or asbestos-associated neoplasia [15].

Biological context of Asbestosis

• However, when rales and a low diffusing capacity of the lung for carbon monoxide are also present, the diagnosis of asbestosis on clinical grounds can be made with reasonable confidence [16].
• Transgenic mouse models to determine the role of epidermal growth factor receptor in epithelial cell proliferation, apoptosis, and asbestosis [17].
• Pi*S and Pi*Z alpha 1 antitrypsin polymorphism and the risk for asbestosis in occupational exposure to asbestos [18].
• The asbestosis cases had lower total lymphocyte count as well as proportions and absolute number of E-RFC as compared to asbestos workers without asbestosis and/or ANA [19].

Anatomical context of Asbestosis

• To evaluate a possible role for release of neutrophil chemotactic factor (NCF) in the pathogenesis of asbestosis, spontaneous NCF release from alveolar macrophages obtained by bronchoalveolar lavage (BAL) in eight individuals with asbestosis, 13 asbestos-exposed individuals without asbestosis, and five control subjects has been studied [20].
• Alveolar macrophages from subjects with asbestosis released more NCF (97 +/- 19 neutrophils per high-power field [N/HPF]) than controls (3 +/- 1 N/HPF; p less than 0.01) [20].
• After 20 hr of culture in concanavalin A, monocytes from normal subjects expressed the gene for the B chain of PDGF while, under the same culture conditions, none of the monocyte preparations from patients with asbestosis produced mRNA for this growth factor [21].
• In all cases of pleural mesothelioma, the quantity of hyaluronic acid in mg/g of dry tissue was at least 0.10 mg, whereas carcinomatous pleural tissue and pleura in asbestosis contained 0.02 to 0.03 mg/g of dry tissue [22].

Gene context of Asbestosis

• Hybridization of total AM RNA to a 32P-labeled IGF-I receptor riboprobe using solution hybridization demonstrated IGF-I receptor mRNA transcripts in AM from an individual with asbestosis, consistent with active expression of the IGF-I receptor gene [23].
• Our results suggest that the alpha 1 antitrypsin polymorphisms, especially Pi*Z, could help to predict asbestosis risk and confirm the high prevalence of the Pi*S allele in Spain [18].
• Tumour necrosis factor-alpha (TNF-alpha) in patients who have asbestosis and develop cancer [24].
• They did not have asbestosis or cancer and their EGFR values were higher in those without plaques [25].
• This research allows us to hypothesise that IL-10 may have a pathogenetic role in the evolution of asbestosis [26].

Analytical, diagnostic and therapeutic context of Asbestosis

• Bronchoalveolar lavage (BAL) findings in 27 individuals with crocidolite- or chrysotile-induced asbestosis were compared to BAL findings in 29 unexposed control subjects [27].
• All patients with early asbestosis had isolated reduction of diffusing lung capacity to carbon monoxide (DLCO), whereas all patients with advanced asbestosis had reduced DLCO and restrictive disease; two of them also had an obstruction pattern [28].

References