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

Chronic inhalation of coal dust can cause several lung disorders, including simple coal workers pneumoconiosis (CWP), progressive massive fibrosis (PMF), chronic bronchitis, lung function loss, and emphysema. This review focuses on the cellular actions and interactions of key inflammatory cells and target cells in coal dust toxicity and related lung disorders, i.e. macrophages and neutrophils, epithelial cells, and fibroblasts. Factors released from or affecting these cells are outlined in separate sections, i.e. (1) reactive oxygen species (ROS) and related antioxidant protection mechanisms, and (2) cytokines, growth factors and related proteins. Furthermore, (3) components of the extracellular matrix (ECM), including the modifying role of ROS, cytokines, proteases and antiproteases are discussed in relation to tissue damage and remodelling in the respiratory tract. It is recognised that inhaled coal dust particles are important non-cellular and cellular sources of ROS in the lung, and may be significantly involved in the damage of lung target cells as well as important macromolecules including alpha-1-antitrypsin and DNA. In vitro and in vivo studies with coal dusts showed the up-regulation of important leukocyte recruiting factors, e.g. Leukotriene-B4 (LTB4), Platelet Derived Growth Factor (PDGF), Monocyte Chemotactic Protein-1 (MCP-1), and Tumor Necrosis Factor-alpha (TNF alpha), as well as the neutrophil adhesion factor Intercellular Adhesion Molecule-1 (ICAM-1). Coal dust particles are also known to stimulate the (macrophage) production of various factors with potential capacity to modulate lung cells and/or extracellular matrix, including O2-., H2O2, and NO, fibroblast chemoattractants (e.g. Transforming Growth Factor-beta (TGF beta), PDGF, and fibronectin) and a number of factors that have been shown to stimulate and/or inhibit fibroblast growth or collagen production such as (TNF alpha, TGF beta, PDGF, Insulin Like Growth Factor, and Prostaglandin-E2). Further studies are needed to clarify the in vivo kinetics and relative impact of these factors.
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PMID:Mechanisms and mediators in coal dust induced toxicity: a review. 1002 91

Histiocytosis X (HX), also referred as Langerhans cell granulomatosis is a disorder characterized by the presence of destructive granulomas containing Langerhans cells, lymphocytes, eosinophils and fibroblastes in the involved organs. Three presentations are commonly observed: 1) nonproductive cough or effort dyspnea, 2) spontaneous pneumothorax 3) incidental pulmonary infiltrates on chest X-ray in asymptomatic patients. HRCT may be helpful in the initial diagnosis of pulmonary HX. HRCT scans show nodules, cysts and estimate the extent of disease. But the final diagnosis of histiocytosis X requires the histologic demonstration of specific histiocytosis X cell in biopsy specimens of the lung. The aim of this study was to define the importance of the detection of Langerhans cells in bronchoalveolar lavage fluid (BALF) for the diagnosis of HX. The searched cells express a specific CD1 antigen, recognized by the monoclonal antibody OKT-6. In our study the demonstration of more than 5% of CD1 positive cells was defined to confirm HX. We have studied the BALF in 21 patients with suspected histiocytosis X. In BALF of 4 patients more than 5% of CD1 positive cells were found. In 1 of them HX was confirmed with open lung biopsy. Two patients displayed 5% of CD1 positive cells. The final diagnosis of the first patient was hypersensitivity pneumonitis and of the second one was bronchitis chronica. In 5 patients out of 15 patients in whom less than 5% of CD1 positive cells were found histiocytosis X was histologically proven. In other 10 patients the following disorders were histologically recognised: pulmonary emphysema 3 cases, pneumoconiosis-3, LMA-BOOP-1, sarcoidosis-1 and pleuritis eosinophilica-1. The estimation of Langerhans cells in BALF can be a useful method among the diagnostic procedures for histiocytosis X. It is necessary to remember that demonstration of less than 5% of CD1 positive cells do not exclude histiocytosis X.
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PMID:[Usefulness of CD1 expression on surfaces of cells in bronchoalveolar fluid for diagnosis of histiocytosis X--our experience]. 1064 82

One of the issues concerning harmonization in the development of pharmaceutical products, especially antimicrobials, is discrepancy in the indications to be studied clinically. In particular, it has been very much questioned whether the underlying disease in Western patients diagnosed with acute exacerbation of chronic bronchitis (AECB) is identical with chronic bronchitis in Japan. We assessed chest X-ray films from 105 AECB patients enrolled in a clinical study of SB265805 (a fluoroquinolone antibacterial agent under development) conducted in Europe, and then compared their clinical signs/symptoms and laboratory data with Japanese historical data. Five of the 105 patients did not meet the criteria of AECB; i.e., 2 of them were diagnosed with pneumonia, 1 with bronchiectasis, 1 with pneumoconiosis, and 1 with bronchiectasis plus pulmonary emphysema. In the remaining 100 patients, chest X-ray findings and laboratory test results were consistent with the concept of chronic bronchitis, although 23 of them had other cardiac or pulmonary diseases as well. There were significant imbalances in distribution between Western patients and Japanese historical data in terms of age, cough, WBC counts, and C-reactive protein (CRP) levels. Compared with Japanese historical data, Western patients were younger and had a more severe cough, although increases in WBC and CRP were less remarkable. For other variables, i.e., sex, fever, and volume of sputum, no significant difference was detected in distribution. Overall, there was no significant difference between the two groups in regard to disease severity, as assessed by fever, WBC, and CRP.
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PMID:Comparison of chest X-ray findings and other parameters in acute exacerbation of chronic bronchitis in Japan and the West. 1140 55

Occupational exposure to crystalline silica dust is associated with an increased risk for pulmonary diseases such as silicosis, tuberculosis, chronic bronchitis, chronic obstructive pulmonary disease (COPD) and lung cancer. This review summarizes the current knowledge about the health effects of amorphous (non-crystalline) forms of silica. The major problem in the assessment of health effects of amorphous silica is its contamination with crystalline silica. This applies particularly to well-documented pneumoconiosis among diatomaceous earth workers. Intentionally manufactured synthetic amorphous silicas are without contamination of crystalline silica. These synthetic forms may be classified as (1) wet process silica, (2) pyrogenic ("thermal" or "fumed") silica, and (3) chemically or physically modified silica. According to the different physicochemical properties, the major classes of synthetic amorphous silica are used in a variety of products, e.g. as fillers in the rubber industry, in tyre compounds, as free-flow and anti-caking agents in powder materials, and as liquid carriers, particularly in the manufacture of animal feed and agrochemicals; other uses are found in toothpaste additives, paints, silicon rubber, insulation material, liquid systems in coatings, adhesives, printing inks, plastisol car undercoats, and cosmetics. Animal inhalation studies with intentionally manufactured synthetic amorphous silica showed at least partially reversible inflammation, granuloma formation and emphysema, but no progressive fibrosis of the lungs. Epidemiological studies do not support the hypothesis that amorphous silicas have any relevant potential to induce fibrosis in workers with high occupational exposure to these substances, although one study disclosed four cases with silicosis among subjects exposed to apparently non-contaminated amorphous silica. Since the data have been limited, a risk of chronic bronchitis, COPD or emphysema cannot be excluded. There is no study that allows the classification of amorphous silica with regard to its carcinogenicity in humans. Further work is necessary in order to define the effects of amorphous silica on morbidity and mortality of workers with exposure to these substances.
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PMID:Health hazards due to the inhalation of amorphous silica. 1187 95

A 72-year-old male painter, who complained of his "lungs burning" for 2 weeks, died suddenly. Autopsy examination revealed severe coronary atherosclerosis with plaque rupture as the cause of death. Examination of the lungs revealed emphysema, interstitial fibrosis, and multinucleated giant cells with intra- and extracellular brown-black, crystalline, polarizable foreign material. Energy-dispersive X-ray microanalysis showed the material to contain titanium, aluminum, silicon, and iron. An increased incidence of respiratory disease has been reported in professional painters. Titanium is widely used as a pigment in the manufacturing of commercial paints. Cases of pneumoconiosis and alveolar proteinosis have been described in painters in which analysis of lung tissue revealed increased levels of titanium. This case is presented as an example of a rarely reported phenomenon, which may have clinical implications for evaluation and management of lung disease in painters.
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PMID:Titanium particles identified by energy-dispersive X-ray microanalysis within the lungs of a painter at autopsy. 1274 5

Cysts and cavities are commonly encountered abnormalities on chest radiography and chest computed tomography. Occasionally, the underlying nature of the lesions can be readily apparent as in bullae associated with emphysema. Other times, cystic and cavitary lung lesions can be a diagnostic challenge. In such circumstances, distinguishing cysts (wall thickness < or = 4 mm) from cavities (wall thickness > 4 mm or a surrounding infiltrate or mass) and focal or multifocal disease from diffuse involvement facilitates the diagnostic process. Other radiological characteristics, including size, inner wall contour, nature of contents, and location, when correlated with the clinical context and tempo of the disease process provide the most helpful diagnostic clues. Focal or multifocal cystic lesions include blebs, bullae, pneumatoceles, congenital cystic lesions, traumatic lesions, and several infectious processes, including coccidioidomycosis, Pneumocystis carinii pneumonia, and hydatid disease. Malignant lesions including metastatic lesions may rarely present as cystic lesions. Focal or multifocal cavitary lesions include neoplasms such as bronchogenic carcinomas and lymphomas, many types of infections or abscesses, immunologic disorders such as Wegener granulomatosis and rheumatoid nodule, pulmonary infarct, septic embolism, progressive massive fibrosis with pneumoconiosis, lymphocytic interstitial pneumonia, localized bronchiectasis, and some congenital lesions. Diffuse involvement with cystic or cavitary lesions may be seen in pulmonary lymphangioleiomyomatosis, pulmonary Langerhans cell histiocytosis, honeycomb lung associated with advanced fibrosis, diffuse bronchiectasis, and, rarely, metastatic disease. High-resolution computed tomography of the chest frequently helps define morphologic features that may serve as important clues regarding the nature of cystic and cavitary lesions in the lung.
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PMID:Cystic and cavitary lung diseases: focal and diffuse. 1293 86

In the program of research into the natural history of coalworkers' pneumoconiosis now being carried out in Great Britain, emphasis is being put upon the importance of sharpening and validating means for early diagnosis, and upon the need for follow-up studies upon properly selected population samples. Existing information from morbidity and mortality figures from chronic bronchitis and emphysema in Great Britain suggests that atmosphere pollutants are important etiological factors. A parallel is drawn between the course of events in pneumoconiosis, in which dust retention in the lungs does not greatly disable until complicated by tuberculous infection, and a hypothesis that bronchitis is a hypersecretion of bronchial mucus caused by atmospheric irritants and does not disable but encourages secondary infection which may cause emphysema. This hypothesis requires testing by follow-up studies of population samples exposed to various environmental influences. It is suggested that in order to bring this common and disabling disease under control, clinicians must widen their interests beyond the confines of the hospital walls.
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PMID:Chronic disabling respiratory disease; ends and means of study. 1348 5

Industrial pleuropulmonary disorders may result from exposure of the human respiratory tract to diverse types of dusts and fumes, visible and invisible, benign and toxic, organic and inorganic. Meticulous radiological examination, combined with history and physical examination, appropriate laboratory tests, and the exclusion of other disorders which could produce similar changes, is essential for correct diagnosis. Criteria for the radiological diagnosis of pulmonary fibrosis, of generalized emphysema, and of cor pulmonale are outlined. The commoner types of pneumoconiosis are discussed in some detail, and the possible relationship of various inhaled noxa to primary bronchial carcinoma is considered.
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PMID:INDUSTRIAL PLEUROPULMONARY DISORDERS: RADIOLOGICAL CONSIDERATIONS. 1428 43

The activity of neutrophilic elastase and the level of its major inhibitor--an alpha 1-inhibitor of proteinases were studied to evaluate the protease-antiprotease system in the bronchoalveolar lavage fluid (BALF) of patients with chronic dust-induced bronchitis (CDB) and pneumoconiosis (PC). It was found that CDB, as compared with PC, was characterized by a higher elastase activity in the BALF (70%) and that there were a larger number of patients with elastase activity (40%), which correlated with the detection rate of emphysema. Free elastase activity and relative proteinase alpha 1-inhibitor deficiency suggest that the BALF protease-antiprotease system is impaired in patients with CDB and PC, which is more pronounced in patients with CDB.
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PMID:[Impaired balance of the lung proteolytic system in patients with pneumoconiosis and chronic dust-induced bronchitis]. 1452

The long-term exposure to dust in the hard coal mining industry can lead to various pathological lung changes, especially to chronic bronchitis without and with obstructive ventilation disorder, lung emphysema, pneumoconiosis (coal miner's pneumoconiosis, in Germany categorized as silicosis) and silicotuberculosis. These health disorders show a close pathogenetic and pathophysiological association and should not necessarily be regarded as individual entities. Most exposed subjects demonstrate more or less all of these pathological disorders. On account of individual (genetic?) susceptibility, their degree differs greatly. Some individuals are largely resistent, other subjects show severe effects like emphysema, progressive massive pneumoconiosis, or the Caplan syndrome. Several studies showed that the pathologically verified degree of lung fibrosis is associated with lung crystalline SiO(2) content whereas the emphysema score is inversely correlated with the coal content. With regard to diagnostics and medical expert opinion, it is important that conventional radiology has a low sensitivity. Further, health impairments of miners engaged for longtime which are insurance relevant (MdE) exist in cases without (BK 4111 if beginning after 12/31/1992) or with coalworkers' pneumoconiosis even for categories < 2/3.
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PMID:[Effects on the lung due to underground coal mining work]. 1496 33


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