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

Lipid peroxidation parameters, such as malonic dialdehyde and antioxidant defense (superoxide dismutase and catalase activities) were studied in healthy individuals, miners of different occupations, working at mines of different altitudes. The studies showed that increased lipid peroxidation and decreased antioxidant defense are connected with the altitude of work and exposure to the quartz-containing dust combined with hypobaric hypoxia. Malonic dialdehyde, the final toxic product of peroxidation, is accumulated as a result of it. Increased membranous lipid peroxidation results in death and lysis of cells. It becomes the principal pathogenetic component of pneumoconiosis formation and clarifies the mechanism of its early development, comparatively fast progressing, frequency of nodular forms in miners from the high and middle altitudes. That testifies the ability of hypobaric hypoxia to produce silicosis.
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PMID:[The mechanisms of the formation of pneumoconiosis under high-altitude conditions]. 142 41

Activity of purine metabolism enzyme, adenosine deaminase (ADA) in lymphocytes and erythrocytes from patients with pneumoconiosis and chronic bronchitis was determined. ADA activity decrease was found in lymphocytes and erythrocytes for both decreases. The observed decrease of ADA activity indicates that after the long term work in mineral dust industry damage of purine metabolism takes place, that is similar to the disturbance observed under secondary immunodeficiency. Changes in activity of superoxide dismutase and catalase show some decrease of functional activity of anti-radical protection. Therefore the results obtained can be used for the selection of a group with highest risk of predisposition to these diseases.
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PMID:[Changes in adenosine deaminase and antioxidative enzyme activity in patients with lung diseases of dust etiology]. 179 56

Electron spin resonance (ESR) measurements show that grinding of quartz particles in air produces silicon-based (Si. and SiO.) radicals which decay with aging in air. ESR spin trapping measurements provide evidence for the generation of hydroxyl and possibly superoxide radicals from a suspension of fresh quartz particles. The hydroxyl radical generation potential of the fresh quartz particles decreases on storing in ambient air and on the addition of catalase, superoxide dismutase, desferroxamine, or DMSO. Silica-induced lipid peroxidation also decreases on storing the fresh particles in ambient air. These findings suggest that oxygenated radicals play a role in the biochemical mechanism of pneumoconiosis in general and acute silicosis in particular.
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PMID:ESR spin trapping and cytotoxicity investigations of freshly fractured quartz: mechanism of acute silicosis. 216 64

The pneumoconioses are associated with chronic inflammatory processes during which increased amounts of reactive oxygen species are formed in the lower respiratory tract. To characterize the effect(s) of these processes on the defense system against free radicals, we studied 91 individuals with long-term occupational exposure to coal mine dust. Thirty-one subjects were classified with radiological evidence to be pneumoconiotics, while 58 control miners had no pulmonary disorders. We measured antioxidant parameters in red blood cells, considering the latter to reflect the oxidative stress in the lung. Glutathione levels were significantly decreased (p = 0.04) in red blood cells of miners with coal workers' pneumoconiosis with radiograph classification 0/1 to 2/1, while in miners with classification 3/2 to 3/3, the plasma iron concentrations were significantly decreased (p = 0.04). Moreover, some factors of the anti-oxidant system (superoxide dismutase, catalase, glutathione peroxidase) were correlated in the diseased but not in the control miners. Taken together, all data support the role of the erythrocyte as a circulating anti-oxidant carrier and also that changes in red blood cell anti-oxidant factors reflect the oxidative stress imposed by the pneumoconiotic (inflammatory) processes in the lung.
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PMID:Blood anti-oxidant parameters at different stages of pneumoconiosis in coal workers. 235 Nov 20

Occupational exposure to coal mine dust causes coal workers' pneumoconiosis (CWP) and other pulmonary diseases by mechanisms that remain unclear. Because the hydroxyl radicals (.OH) may play an important role in the pathogenesis of CWP, we studied the potential role of bituminous coal mine dust samples for catalyzing the generation of .OH from hydrogen peroxide (H2O2). These coal mine dusts evaluated represented two geographic areas with diversity in CWP prevalence. Electron spin resonance (ESR), with the aid of spin trapping techniques, was used to measure the .OH radical generation. Bituminous coal mine dusts representing the Pittsburgh seam in the eastern United States and Blind Canyon seam in the mid-western United States were used together with a standard coal dust obtained from the National Institute of Standards and Technology, Gaithersburg, MD. All the coal mine dust samples generated varying levels of .OH radicals from H2O2 in the presence of a .OH spin trap 5,5-dimethyl-l-pyrroline-N-oxide (DMPO). .OH radical generation by the coal from H2O2 was effectively inhibited by deferoxamine and catalase, but only partially inhibited by superoxide dismutase. Metal chelators DETAPAC and EDTA enhanced the radical generation. These results indicated that the Fenton reaction is predominantly involved in the generation of .OH radicals from H2O2. The .OH-generating potential of all the coal dusts showed a positive correlation with the surface iron content of coal mine dusts. In addition, the potential to induce lipid peroxidation by the coal samples exhibited a good correlation with the available surface iron. Based on the results presented here, we propose that higher concentrations of surface iron in coal mine dust may be involved in the generation of increased levels of .OH radicals and may play an important role in the development of CWP in different coal mining areas.
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PMID:Hydroxyl radical generation by coal mine dust: possible implication to coal workers' pneumoconiosis (CWP). 789 64

This study investigated whether differences in the prevalence and severity of coal workers' pneumoconiosis (CWP) between three coal mines could be related to differences in oxidative stress exposure as evaluated in vivo through red-blood-cell antioxidant enzyme activities. Blood samples were obtained from 229 miners selected according to their occupation and their pneumoconiotic status. The following biomarkers were evaluated: erythrocyte catalase, Cu2+/Zn2+ superoxide dismutase (Cu2+/Zn2+ SOD), and glutathione peroxidase activities. Antioxidant enzyme activities did not differ significantly between the group of surface workers in Lorraine and the group of underground miners without CWP in Lorraine and in the other coal mines. Erythrocyte Cu2+/Zn2+ SOD activity was slightly decreased in the group of active underground miners with simple pneumoconiosis as compared with the group of miners without CWP in Nord/Pas-de-Calais. No effect was seen between retired miners at different stages of CWP. Our findings indicate that differences in the prevalence and severity of CWP do not seem to be related to various oxidative activities of coal dust particles, at least as reflected by measurements of antioxidant enzyme activities in circulating erythrocytes in this study.
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PMID:Erythrocyte antioxidant enzyme activities in coal miners from three French regions. 963 82

The studies covered metabolism of serum phospholipids during lipids peroxidation and hydrolysis by phospholipase A2. Metabolism of serum phospholipids appeared to depend on duration of exposure to mine dust and on coal pneumoconiosis stage. Lipids peroxidation becomes activated after 20 and more years of service, intensifies with anthracosilicosis development on background of higher catalase activity that is low on early stages of the disease. Activity of phospholi pase A2 increases with pulmonary fibrosis progression.
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PMID:[Metabolism of serum phospholipids in coal miners]. 1051 90

Previous studies on symptomatic coal miners have shown that alveolar macrophages, recovered by bronchoalveolar lavage (BAL), release excessive amounts of reactive oxygen species (ROS) and inflammatory cytokines. It has been proposed that these secretions may mediate cell injury and initiate the disease process. We hypothesized that acellular bronchoalveolar lavage fluid (BALF) indices in coal miners chronically exposed to coal dust may reflect the status of important homeostatic modulations in the lung that lead to the development of coal workers' pneumoconiosis (CWP). To test this hypothesis, we measured inflammatory status, oxidant burden, antioxidant defenses, cytokines, growth factors, fibronectin, and alpha(1)-antitrypsin (alpha(1)-AT) in the BALF of healthy never-smoker control subjects, never-smoker underground coal miners with negative radiographs (ILO 0/0-1/0), and two miners with moderate changes in the chest radiographs (ILO 2/2). Interestingly, indices of injury and inflammation increased with the progression of disease in coal miners. Antioxidant enzymes, such as catalase, glutathione peroxidase, and superoxide dismutase, showed a 19-fold, 22-fold, and 6-fold increase above control, respectively, in coal miners with category 2/2 CWP. Significant increases in the secretion of IL-1, IL-6, TNF-alpha, TGF-beta, fibronectin, and alpha(1)-AT also were evident in coal miners with disease. This up-regulation of antioxidant defenses and cytokines was not evident in coal miners in the absence of clinically evident radiographic disease. In addition, the concentration of lipid peroxidation by products in the BALF of coal miners without evidence of radiographic disease showed a moderate 3-fold increase, whereas, in coal miners with category 2/2 CWP it showed a 59-fold increase compared to control subjects. These results are in good agreement with our hypothesis that development of CWP and its progression may be correlated with an oxidative stress and up-regulation of cytokines and mediators of growth.
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PMID:Changes in bronchoalveolar lavage indices associated with radiographic classification in coal miners. 1098 13

Coal mining causes health problems, such as pneumoconiosis. We have previously shown that prevalence of pneumoconiosis in workers from various coalmine regions positively correlates with levels of bioavailable iron (BAI) in the coals from that region. In the present study, the nature of reactive oxygen species formed by BAI in the coals and its mechanisms of the induction of biological responses were investigated. Human lung epithelial cell line, A549 cells, were used to examine the induction of interleukin-6 (IL-6), a pro-inflammatory cytokine, which is known to play a crucial role in the development of pneumoconiosis. We found that levels of IL-6 protein as well as its mRNA were significantly increased in the cells treated for 24 h with 20 microg/cm2 of the BAI-containing Pennsylvania (PA) coal; for example we observed 6.7-fold increase in IL-6 protein. Levels of IL-6 protein in cells treated with the Utah (UT) coal containing low-BAI were only 1.9-fold of the control levels. The enhancing effect on the IL-6 by the PA coal was similar to that caused by hydrogen peroxide. Superoxide dismutase (SOD), catalase (CAT), and N-acetyl-L-cysteine (NAC) all had inhibitory effects on the PA coal-induced IL-6 formation. However, CAT had the least protective effect as compared to SOD and NAC. Our results indicate that BAI in the PA coal may induce IL-6 through both ferryl species (via iron autoxidation) and hydroxyl radicals (via the Fenton/Haber Weiss reactions).
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PMID:Induction of interleukin-6 by coal containing bioavailable iron is through both hydroxyl radical and ferryl species. 1268 31

Fibroproliferative response of rat heart and lung fibroblasts to the lanthanide cerium was examined, as the element has been implicated in the causation of cardiac and pulmonary fibrosis. Fibroblasts from both of the organs were morphologically identical, and the response to fetal bovine serum, a nonspecific mitogen, was also comparable. The oxygen radical generator (hypoxanthine + xanthine oxidase [Hyp. + XO]) induced a proliferative response that was neutralized in both cardiac and lung fibroblasts by free-radical scavengers. Superoxide dismutase was more effective than catalase in reducing the mitogenic effect of Hyp. + XO. The free-radical scavenger N-acetyl-L-cysteine neutralized the free-radical-mediated changes in pulmonary fibroblasts but had a negative effect in cardiac fibroblasts, indicating a tissue-dependent variation. Reactive oxygen species are known to act as biological mediators of tissue fibrosis induced by metallic compounds. Exposure to low levels of cerium (0.5 microM) stimulated a mitogenic response in cardiac fibroblasts, but the pulmonary fibroblasts were not sensitized by the element. Tissue-dependent variation in proliferative response to cerium shows a positive association with intracellular generation of reactive oxygen species. Fibrotic changes in cerium pneumoconiosis may either be replacement fibrosis following tissue damage or mediated by nonfibroblastic cells. The study confirms that cardiac and pulmonary fibroblasts are dissimilar cellular subtypes.
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PMID:Variation in mitogenic response of cardiac and pulmonary fibroblasts to cerium. 1297 91


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