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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Asbestosis and silicosis are chronic, fibrosing lung diseases due to prolonged inhalation of asbestos fibers or silica particles. However, little is known about the implication of these toxic dusts on cell-mediated cytotoxicity. Among the first types of cells that are in contact with the dusts are the alveolar macrophages (AM). We studied the effect of different concentrations of UICC chrysotile asbestos and silica on 18-h cytotoxicity of AM against tumor necrosis factor (TNF)-resistant P815 target cells or TNF-sensitive L929 target cells. Rat AM, obtained by bronchoalveolar lavage, were incubated for 2 h with 20, 50, or 100 micrograms/ml chrysotile or silica before the addition of target cells. AM cytotoxicity was significantly inhibited at greater than 20 micrograms/ml of chrysotile. In contrast, silica did not inhibit AM-mediated cytotoxicity at any concentration used. Asbestos, but not silica, caused significant production of PGE2 by macrophages and target cells. Addition of the cyclooxygenase inhibitor indomethacin to our system abolished all inhibition by asbestos. These results suggest that the inhibition of AM-mediated cytotoxicity by chrysotile was caused by prostaglandins, and that fibrogenic particles differ in their capacity to modulate AM function.
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PMID:Inhibition of alveolar macrophage cytotoxicity by asbestos: possible role of prostaglandins. 215 23

Prolonged asbestos and silica inhalation is associated with pulmonary inflammation and fibrosis. Several studies suggest that TNF may play a role in the development of inflammation and fibrosis. We studied TNF production in a murine model of asbestosis and silicosis. Asbestos fibers caused a significant inflammatory response at two weeks and pulmonary fibrosis beginning at one month. Pulmonary inflammation was principally caused by an accumulation of neutrophils (0.88 x 10(5) neutrophils/compared to 0.05 x 10(5) in controls). TNF production by bronchoalveolar cells was higher in asbestos-instilled mice at two weeks, but was significantly diminished in older mice. Pulmonary inflammation was observed until six months in silica-instilled mice. Neutrophils were also the principal protagonists of the inflammation. In this group, severe fibrosis was observed at two weeks. TNF production in silica-instilled mice was similar to controls, possibly due to the presence of large numbers of neutrophils (3.3 x 10(5)/lavage) that could adsorb TNF. In vitro experiments showed an augmentation of TNF production by bronchoalveolar cells in the presence of silica. Taken together, our data suggest that asbestos and silica stimulate alveolar macrophages to produce TNF, which can be involved in pulmonary inflammation and fibrosis.
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PMID:Pulmonary inflammation and fibrosis in a murine model of asbestosis and silicosis. Possible role of tumor necrosis factor. 275 23

Cohorts of Finnish asbestos sprayers and of asbestosis and silicosis patients were followed for cancer with the aid of the Finnish Cancer Registry in the period 1967-1994. Compared with the cancer incidence of the total Finnish population, asbestos sprayers had an increased risk for total cancer (standardized incidence ratio [SIR] 6.7, 95% confidence interval [95% CI] 4.2-10); lung cancer (SIR 17.95% CI 8.2-31); and mesothelioma (SIR 263, 95% CI 85-614). The SIR of the asbestosis patients was 3.7 (95% CI 2.8-5.0) for all sites, 10 (95% CI 6.9-14) for lung cancer, and 65 (95% CI 13-188) for mesothelioma. The silicosis patients also had significantly high SIR values for all sites (1.5, 95% CI 1.0-2.1) and lung cancer (2.7, 95% CI 1.5-4.5). The values for the SIR and the standardized mortality ratio for all sites and lung cancer were very similar, and therefore it seems that both are reliable indicators of the occurrence of occupational cancer. It was concluded that pneumoconioses patients and asbestos-exposed workers have a markedly elevated risk for cancer. Asbestos-induced occupational cancers are not only diseases of the elderly, since the relative risk is high also for middle-aged people.
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PMID:Cancer incidence and mortality among Finnish asbestos sprayers and in asbestosis and silicosis patients. 913 Dec 23

Michigan has a statewide mandatory occupational disease reporting system. As part of that system, reports are received from hospital, physicians, death certificates, the worker's compensation bureau, and company medical departments. Based on this reporting, the State of Michigan has a special emphasis program for the surveillance of silicosis, a known disease outcome among foundry workers. From 1985-1996, 115 cases reported to the State Surveillance System as silicosis, pneumoconiosis not specified, or pulmonary fibrosis were reclassified as having asbestos related x-ray changes after a B-reader interpretation of each case's chest x-ray. During this same period there were an additional 697 reports confirmed as silicosis and 6,724 cases reported to the surveillance system as asbestosis. Among the 115 reports reclassified as having asbestos-related x-ray changes without evidence of silicosis-related x-ray changes, 54 had worked in foundries. Only 7 (14.8%) of these individuals had their primary work in maintenance in the foundry; 40 (85.1%) had their primary foundry work in a production job; and for 10 individuals the occupation was not known. Asbestos has been used in foundries on pipe laggings, boiler coverings, as insulation in fan housings, in gloves, aprons and curtains, as insulation in cupolas, and in ladles and insulation in sand molds. Clinicians caring for foundry workers need to be aware that asbestos-related x-ray changes are not uncommon in this population and asbestos exposure should be considered as one of the carcinogens contributing to the known increased risk of lung cancer among foundry workers.
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PMID:Asbestos-related x-ray changes in foundry workers. 1227 84

The clinical observation, the work history, the analysis of pulmonary function tests and, mainly, the conventional x-ray chest radiograms have represented, til now, the diagnostic basis for pneumoconiosis (silicosis, mixed dust pneumoconiosis, asbestosis). Recently, the high resolution chest tomography (HRCT) has been introduced into the diagnostic procedures: such method seems to have its main application in the assessment of incipient clinical pictures of pneumoconiosis, particularly when characterized by normal pulmonary function tests. Asbestos fibers exposed workers were submitted to both radiologic methods. The great majority of them had already been recognized to be affected by asbestosis. A considerable statistical agreement (Cohen K) was observed between radiographic and tomographic I.L.O. classes. In conclusion, high resolution chest tomography doesn't appear to be an indispensable test for the diagnosis in admitted subjects, but we underline its importance in the evaluation of pleural thickenings.
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PMID:[High resolution computerized tomography in the diagnosis of asbestosis]. 1077 40

India being a developing nation is faced with traditional public health problems like communicable diseases, malnutrition, poor environmental sanitation and inadequate medical care. However, globalization and rapid industrial growth in the last few years has resulted in emergence of occupational health related issues. Agriculture (cultivators i.e. land owners + agriculture labourers) is the main occupation in India giving employment to about 58% of the people. The major occupational diseases/morbidity of concern in India are silicosis, musculo-skeletal injuries, coal workers' pneumoconiosis, chronic obstructive lung diseases, asbestosis, byssinosis, pesticide poisoning and noise induced hearing loss. There are many agencies like National Institute of Occupational Health, Industrial Toxicology Research Centre, Central Labour Institute, etc. are working on researchable issues like Asbestos and asbestos related diseases, Pesticide poisoning, Silica related diseases other than silicosis and Musculoskeletal disorders. Still much more is to be done for improving the occupational health research. The measures such as creation of advanced research facilities, human resources development, creation of environmental and occupational health cells and development of database and information system should be taken.
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PMID:Occupational health research in India. 1512 63

Particulates refer to particles, dust, dirt, soot and aerosol mists that has suspended in the surrounding air. They may consist of solids of various forms including fibres or liquids. Long term exposure to silicon dioxide containing dusts (crystalline silica: quartz, tridymite, cristobalite, coesite, stishovite) may cause pneumoconiosis in the form of acute or/either chronic silicosis. Asbestos refers to a divers family of crystalline hydrated fibrous siliates typically exhibiting a greater tha 3:1 length ot diameter ratio. It is subdivided into serpentine (Chrysotile) and amphibole (crocidolite, amosite, anthophyllite, tremolite, actinolite). Exposure to asbestos fibres may cause lung fibrosis and promote cancer of the lung or the pleura. Besides the induction of malignant diseases dust exposure may result in obstructive as well as restrictive lung diseases which may be compensate in case of the recognition as a occupational diseases. Other occupational exposures leading to pneumoconiosis are caused be talc, or metals including aluminium containing dusts. Also the group of man-made mineral (MMMFs) or vitreous fibres (MMVFs), including glass wool, rock wool, slag wool, glass filaments, microfibres, refractory ceramic fibres are bioactive under certain experimental conditions. Although it has been shown that MMMFs may cause malignancies when injected intraperitoneally in high quantities in rodents, inhalation trials and human studies could not reproduce these results in the same precision. Fine particles (particulate matter = PM) comprise one of the most widespread and harmful air pollutants in the industrialized world. PM may cause worsening of asthma and other respiratory diseases, reduce lung function development in children, potentially increased the risk of premature death in the elderly and enhance mortality from cardiac diseases. Because of the small size PM2.5 is seen to be even more hazardous than PM10.
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PMID:[Health significance of inhaled particles]. 1654 43

Asbestosis, silicosis and Coal Worker's Pneumoconiosis (CWP) represent three of the most important occupationally-related dust diseases in Australia. To gain a clear picture of pneumoconiosis trends over time, a 24-yr retrospective analysis of national mortality data was performed for the period 1979 to 2002. Over 1,000 pneumoconiosis-related fatalities occurred during this time, 56% of which were caused by asbestosis, 38% by silicosis and 6% by CWP. Between 1979 and 1981, silicosis accounted for 60% of all pneumoconiosis-related fatalities in Australia, followed by asbestosis (31%). By 2002 however, asbestosis was causing 78% of all fatalities, while silicosis accounted for only 19%. Asbestos-related mortality increased three-fold between 1979 and 2002, with a clear excess risk demonstrated among males. On the other hand, mortality rates for silicosis and CWP declined significantly during the same time period. Overall, this study suggests that pneumoconiosis, particularly asbestosis, continues to be an important occupational disease in Australia. Although progress has been made in reducing deaths due to occupational silicosis and CWP, asbestosis rates continue to rise, reflecting the long latency between dust exposure and clinical disease. Countries which continue to use asbestos products in the workplace should note the tragic legacy of this material within contemporary Australia.
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PMID:24 years of pneumoconiosis mortality surveillance in Australia. 1705 96

Asbestos causes lung fibrosis known as asbestosis as well as cancers such as malignant mesothelioma and lung cancer. Asbestos is a mineral silicate containing iron, magnesium, and calcium with a core of SiO(2). The immunological effect of silica, SiO(2), involves the dysregulation of autoimmunity because of the complications of autoimmune diseases found in silicosis. Asbestos can therefore cause alteration of immunocompetent cells to result in a decline of tumor immunity. Additionally, due to its physical characteristics, asbestos fibers remain in the lung, regional lymph nodes, and the pleural cavity, particularly at the opening sites of lymphatic vessels. Asbestos can induce chronic inflammation in these areas due to the production of reactive oxygen/nitrogen species. As a consequence, immunocompetent cells can have their cellular and molecular features altered by chronic and recurrent encounters with asbestos fibers, and there may be modification by the surrounding inflammation, all of which eventually lead to decreased tumor immunity. In this paper, the brief results of our investigation regarding reduction of tumor immunity of immunocompetent cells exposed to asbestos in vitro are discussed, as are our findings concerned with an investigation of chronic inflammation and analyses of peripheral blood samples derived from patients with pleural plaque and mesothelioma that have been exposed to asbestos.
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PMID:Asbestos-induced cellular and molecular alteration of immunocompetent cells and their relationship with chronic inflammation and carcinogenesis. 2250 91

Occupational and environmental exposures to airborne asbestos and silica are associated with the development of lung fibrosis in the forms of asbestosis and silicosis, respectively. However, both diseases display distinct pathologic presentations, likely associated with differences in gene expression induced by different mineral structures, composition and bio-persistent properties. We hypothesized that effects of mineral exposure in the airway epithelium may dictate deviating molecular events that may explain the different pathologies of asbestosis versus silicosis. Using robust gene expression-profiling in conjunction with in-depth pathway analysis, we assessed early (24 h) alterations in gene expression associated with crocidolite asbestos or cristobalite silica exposures in primary human bronchial epithelial cells (NHBEs). Observations were confirmed in an immortalized line (BEAS-2B) by QRT-PCR and protein assays. Utilization of overall gene expression, unsupervised hierarchical cluster analysis and integrated pathway analysis revealed gene alterations that were common to both minerals or unique to either mineral. Our findings reveal that both minerals had potent effects on genes governing cell adhesion/migration, inflammation, and cellular stress, key features of fibrosis. Asbestos exposure was most specifically associated with aberrant cell proliferation and carcinogenesis, whereas silica exposure was highly associated with additional inflammatory responses, as well as pattern recognition, and fibrogenesis. These findings illustrate the use of gene-profiling as a means to determine early molecular events that may dictate pathological processes induced by exogenous cellular insults. In addition, it is a useful approach for predicting the pathogenicity of potentially harmful materials.
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PMID:Indications for distinct pathogenic mechanisms of asbestos and silica through gene expression profiling of the response of lung epithelial cells. 2535 96


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