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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mice were injected intratracheally with silica or Mt. St. Helens volcanic ash (0.2 mg/g body weight) and examined 6 mo later for changes in pulmonary function, histology, and hydroxyproline content. Results were compared with a similar study using rats. Mice injected with volcanic ash showed significant changes only in wet lung weights. Those injected with silica showed an approximate doubling of lung wet weight and dry weight and hydroxyproline content. Larger increases in lung weight were seen if lymph nodes were left attached. Lung compliance, total lung capacity, and the shape of the pressure-volume curve of the lung were changed as much as 22% in the silica-treated mice. A mild degree of fibrosis with no dense lung consolidation was noted microscopically in silica-treated mice. In contrast, silica-treated rats showed dense lung consolidation, threefold to fivefold increases in both wet and dry lung weights and hydroxyproline content, and up to 40% reductions in pulmonary function measurements. It is concluded that Swiss albino mice develop a milder degree of fibrosis than similarly treated Sprague-Dawley rats and that both biochemical and functional indicators are effective in detecting pneumoconiosis in these species.
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PMID:Functional and biochemical indicators of pneumoconiosis in mice: comparison with rats. 649 83

A laborer who worked in a steel mill and in a shipyard developed a nonspecific pulmonary interstitial fibrosis. Postmortem samples of his lung were digested, and the inorganic material present was extracted and examined using transmission electron microscopy, electron diffraction, and electron microprobe analysis. Uncoated asbestos fibers were present (1.4 X 10(5)/g wet lung), but the surprising finding was the presence of a large number of fly ash particles (6 X 10(6)/g wet lung). Fly ash, the particulate material produced during coal combustion, has not previously been reported to be present in human lung tissue. Although the contribution of the asbestos to this man's lung disease is uncertain, we believe, based on previous studies implicating aluminum silicates in pneumoconiosis, that the fly ash, an aluminum silicate, may be a contributing factor.
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PMID:Fly ash lung: a new pneumoconiosis? 706

Fibrosis is a disorder characterized by a qualitative and quantitative alteration of the deposition of extracellular matrix with accumulation of mesenchymal cells in replacement of normal tissue. The sequence of events leading to fibrosis of an organ involves the subsequent processes of injury with inflammation and disruption of the normal tissue architecture, followed by tissue repair with accumulation of mesenchymal cells in this area. A similar sequence of events occurs in wound healing with formation of normal, limited and transient granulation tissue, while in fibrosis, a maladaptive repair leads to an extensive, exaggerated process with functional impairment. Inflammatory cells (mainly mononuclear phagocytes), platelets, endothelial cells, and type II pneumocytes play a direct and indirect role in tissue injury and repair. The evaluation of several human fibrotic lung diseases, five diffuse (idiopathic pulmonary fibrosis (IPF); adult respiratory distress syndrome (ARDS); coal workers' pneumoconiosis (CWP); Hermansky-Pudlak syndrome (HPS); systemic sclerosis (SS)) and two focal (tumour stroma in lung cancer; and obliterative bronchiolitis (OB) after lung transplantation), has shown that several cytokines participate in the local injury and inflammatory reaction (interleukin-1 (IL-1), interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1), and tumour necrosis factor-alpha (TNF-alpha)), while other cytokines are involved in tissue repair and fibrosis (platelet-derived growth factor (PDGF), insulin-like growth factor-1 (IGF-1), transforming growth factor-beta (TGF-beta), and basic-fibroblast growth factor (b-FGF)). A better understanding of the cytokines and cytokine networks involved in lung fibrosis leads to the possibility of new therapeutic approaches.
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PMID:The role of cytokines in human lung fibrosis. 868 Mar 82

Exposures in the workplace result in a diverse set of diseases ranging from the pneumoconiosis to other interstitial lung diseases to acute lung injury. Physician awareness of the potential disease manifestations associated with specific exposures is important in defining these diseases and in preventing additional disease. Most occupational diseases mimic other forms of lung disease, including pulmonary fibrosis, sarcoidosis, adult respiratory distress syndrome (ARDS), and bronchiolitis. A "sarcoidosis"-like syndrome, usually limited to the lungs, may result from exposure to bioaerosols and a number of metals. Exposure to beryllium in the workplace produces a granulomatous lung disease clinically indistinguishable from sarcoidosis, chronic beryllium disease (CBD). Beryllium's ability to produce a beryllium-specific immune response is used in the beryllium lymphocyte proliferation tests to confirm a diagnosis of CBD and exclude sarcoidosis. Exposure to other metals must also be considered in the differential diagnosis of sarcoidosis. When an individual presents acutely with ARDS or acute lung injury, an acute inhalational exposure must be considered. Exposure to a number of irritant substances at high levels may cause a "chemical pneumonitis" or acute lung injury, depending on the solubility and physicochemical properties of the substance. Some of the most notable agents include nitrogen and sulfur oxides, phosgene, and smoke breakdown products. Ingestion of paraquat may also result in an ARDS syndrome, with pulmonary fibrosis eventually resulting. Bronchiolitis is a rare manifestation of inhalational exposures but must also be considered in the clinical evaluation of inhalational exposure.
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PMID:Clinical approach to chronic beryllium disease and other nonpneumoconiotic interstitial lung diseases. 1236 66