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

Iron is a vital element in life. Because of the insolubility of iron oxides and sulfides the implication is that dissolved iron was fairly abundant and that oxygen and sulfide were rare in the atmosphere and ocean. Iron and its compounds present as pollutants in the atmosphere can cause deleterious effects to humans, animals, and materials. Analyses of urban air samples show that the iron content averages 1.6 microg/m(3), with the iron and steel industry probably the most likely source of emission. Iron is a natural component of soils and its concentration can be influenced by some industries. Iron concentration in surface water varies greatly, from 61 ppm to 2680 ppm. The disposition of iron in the human body is regulated by a complex mechanism to maintain homeostasis. Iron concentrations in body tissues must be tightly regulated because excessive iron leads to tissue damage, as a result of formation of free radicals. Iron has the capacity to accept and donate electrons readily. The content of body iron is regulated primarily by absorption since humans have no physiological mechanism by which excess iron is excreted. Iron has been identified as a component of asbestos and other mineral and synthetic fibers. Inhalation of iron oxide fumes or dust by workers in the metal industries may result in deposition of iron particles in lungs, producing an X-ray appearance resembling silicosis. During the last decades efforts regarding dietary iron supply focused mostly on the prevention of deficiencies, especially during growth and pregnancy. The chemical form of the iron influences absorption, as do interrelationships with other dietary components.
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PMID:Essential metals--case study on iron. 1291 52

We defined mixed-dust pneumoconiosis (MDP) pathologically as a pneumoconiosis showing dust macules or mixed-dust fibrotic nodules (MDF), with or without silicotic nodules (SN), in an individual with a history of exposure to mixed dust. We defined the latter arbitrarily as a mixture of crystalline silica and nonfibrous silicates. According to our definition of MDP, therefore, MDF should outnumber SN in the lung to make a pathologic diagnosis of MDP. In the absence of confirmation of exposure, mineralogic analyses can be used to support the pathologic diagnosis. The clinical diagnosis of MDP requires the exclusion of other well-defined pneumoconioses, including asbestosis, coal workers' pneumoconiosis, silicosis, hematite miners' pneumoconiosis, welders' pneumoconiosis, berylliosis, hard metal disease, silicate pneumoconiosis, diatomaceous earth pneumoconiosis, carborundum pneumoconiosis, and corundum pneumoconiosis. Typical occupations associated with the diagnosis of MDP include metal miners, quarry workers, foundry workers, pottery and ceramics workers, and stonemasons. Irregular opacities are the major radiographic findings in MDP (ILO 1980), in contrast to silicosis, in which small rounded opacities predominate. Clinical symptoms of MDP are nonspecific. MDP must be distinguished from a variety of nonoccupational interstitial pulmonary disorders.
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PMID:Proposed criteria for mixed-dust pneumoconiosis: definition, descriptions, and guidelines for pathologic diagnosis and clinical correlation. 1561 11

The workers of an iron foundry were exposed to air pollution, which after some time of exposure results in lung fibrosis among some workers. The diagnosis of pneumoconiosis in workers of an iron foundry is based mainly on the radiological findings among workers exposed to the dust causing lung fibrosis. However, on radiograms many parenchymal structures overlap, which limits sensitivity and specificity to the method. Difficulties in accurate interpretation of conventional radiograms in silicosis also result from their relatively low resolution. The purpose of the present study was to assess the value and usefulness of high resolution computed tomography in the diagnostics of nodular changes in foundry workers' pneumoconiosis, compared to conventional radiography. The study group consisted of 64 iron foundry workers in whom silicosis had been recognized. The average age of the group was 51 years and the mean silica exposure time was 23 years. Chest radiograms with hard X-rays were taken at the maximal inspiration phase. For the HRCT examination the Siemens Somatom ART apparatus was used, equipped with a 512 x 512 pixels reconstruction matrix and a special programme for high resolution algorithm image reconstruction. In our material, consistency of results for conventional radiography and HRCT in revealing the presence of nodules was high. A statistically significant increase in detectability of intralobular nodules and peripheral nodules localized under the pleura was observed. The increase in detectability of cavernous, calcified nodules and those in the upper pulmonary fields obtained from computed tomography, however, was not statistically significant. High resolution computed tomography provides significant additional information in patients with foundry workers' pneumoconiosis.
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PMID:Diagnostic value of high resolution computed tomography in the assessment of nodular changes in pneumoconiosis in foundry workers in Lublin. 1562 37

Pneumoconiosis may be classified as either fibrotic or nonfibrotic, according to the presence or absence of fibrosis. Silicosis, coal worker pneumoconiosis, asbestosis, berylliosis, and talcosis are examples of fibrotic pneumoconiosis. Siderosis, stannosis, and baritosis are nonfibrotic forms of pneumoconiosis that result from inhalation of iron oxide, tin oxide, and barium sulfate particles, respectively. In an individual who has a history of exposure to silica or coal dust, a finding of nodular or reticulonodular lesions at chest radiography or small nodules with a perilymphatic distribution at thin-section computed tomography (CT), with or without eggshell calcifications, is suggestive of silicosis or coal worker pneumoconiosis. Magnetic resonance imaging is helpful for distinguishing between progressive massive fibrosis and lung cancer. CT and histopathologic findings in asbestosis are similar to those in idiopathic pulmonary fibrosis, but the presence of asbestos bodies in histopathologic specimens is specific for the diagnosis of asbestosis. Giant cell interstitial pneumonia due to exposure to hard metals is classified as a fibrotic form of pneumoconiosis and appears on CT images as mixed ground-glass opacities and reticulation. Berylliosis simulates pulmonary sarcoidosis on CT images. CT findings in talcosis include small centrilobular and subpleural nodules or heterogeneous conglomerate masses that contain foci of high attenuation indicating talc deposition. Siderosis is nonfibrotic and is indicated by a CT finding of poorly defined centrilobular nodules or ground-glass opacities.
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PMID:Pneumoconiosis: comparison of imaging and pathologic findings. 1641 44

Alveolar macrophages (AMs) play a prominent role in influencing the development of lung inflammation and injury. The aim of this study is to investigate the roles of AMs response-related genes TNF-alpha, iNOS, and NRAMP1 (SLC11A1) in susceptibility to silicosis and pulmonary tuberculosis (PTB), and to analyze the interaction of dust exposure and genetic susceptibility to silicosis, interactions of TNF-alpha-308 and Natural Resistance-associated Macrophage Protein 1 (NRAMP1) INT4, D543N polymorphisms to PTB. Several epidemiological designs were used: retrospective investigations on dust exposure, case-control studies of 184 silicosis cases and 111 miners occupationally exposed to silica dust, and 1:2 matched case-control studies of 61 PTB cases and 122 PTB-free miners. The miners and controls were recruited from an iron mining operation in Anhui province, China. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique was applied to detect single nucleotide polymorphisms. Despite the recruitment of high dust exposure among the controls, silicosis patients still had significantly higher dust exposure than controls (242.6 +/- 98.8 vs. 217.6 +/- 100.7 mg a/m(3)). The mutation of iNOS Ser608Leu is associated with protection against silicosis and against severity of silicosis in the miners. There is a 0.47-fold (95% CI: 0.28-0.79) decrease in risk of silicosis for individuals with C/T, T/T genotype compared with the wild-type homozygous (C/C) individuals after adjustment for occupational exposure, smoking, and drinking. The protection effect of the iNOS polymorphism was particularly detected in the > or = 150 mg a/m(3) exposure group (OR: 0.44, 95% CI: 0.22-0.91). However, no interaction of dust exposure with the iNOS polymorphism was observed. Furthermore, the variant NRAMP1 INT4 genotype is significantly associated with PTB in miners. No association of other polymorphisms (NRAMP1 D543N, TNF-alpha-308) and susceptibility to silicosis or PTB in Chinese miners was found. Our data showed a 3.26-fold (95% CI: 1.47-7.23) increased risk of PTB for miners carrying both the NRAMP1 D543N G/G and NRAMP1 INT4 G/C+C/C genotypes. Additionally, in miners with TNF-alpha-308 G/G genotype, the risk of PTB increased 2.38-fold if they carry the NRAMP1 INT4 G/C+C/C genotype (95% CI: 1.14-4.98). In conclusion, the C>T mutation of iNOS Ser608Leu may be an important protective factor to miners. On the other hand, the variant NRAMP1 INT4 may play a role in the development of PTB in Chinese miners. Therefore, the novel information can be used as guideline for further mechanistic investigations and for strengthening specific protection protocols for workers.
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PMID:Genetic polymorphisms in alveolar macrophage response-related genes, and risk of silicosis and pulmonary tuberculosis in Chinese iron miners. 1722 86

Prolonged exposure to high levels of silica has long been known to cause silicosis This paper evaluates the evidence for an increased risk of chronic obstructive pulmonary disease (COPD) in occupations and industries in which exposure to crystalline silica is the primary exposure, with a focus on the magnitude of risks and levels of exposure causing disabling health effects. The literature suggests consistently elevated risks of developing COPD associated with silica exposure in several occupations, including the construction industry; tunneling; cement industry; brick manufacturing; pottery and ceramic work; silica sand, granite and diatomaceous earth industries; gold mining; and iron and steel founding, with risk estimates being high in some, even after taking into account the effect of confounders like smoking. Average dust levels vary from about 0.5 mg.m3 to over 10 mg.m3 and average silica levels from 0.04 to over 5 mg.m3, often well above occupational standards. Factors influencing the variation from industry to industry in risks associated with exposure to silica-containing dusts include (a) the presence of other minerals in the dust, particularly when associated with clay minerals; (b) the size of the particles and percentage of quartz; (c) the physicochemical characteristics, such as whether the dust is freshly fractured. Longitudinal studies suggest that loss of lung function occurs with exposure to silica dust at concentrations of between 0.1 and 0.2 mg.m3, and that the effect of cumulative silica dust exposure on airflow obstruction is independent of silicosis. Nevertheless, a disabling loss of lung function in the absence of silicosis would not occur until between 30 and 40 years exposure.
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PMID:Chronic obstructive pulmonary disease and occupational exposure to silica. 1835 Dec 26

Historical studies report that cellular injury and silicosis are related to cytosolic free calcium (Ca2+). Moreover, reactive oxygen species (ROS) have been linked to cellular injury. However, the detail mechanism of the increase in [Ca2+]i and the relationship between [Ca2+]i and ROS production remains unknown. Quartz particle has been found to increase [Ca2+]i and activate the generation of ROS. Our hypothesis is that [Ca2+]i increase induced by quartz particle is from extracellular Ca2+ through the Ca2+ channel, and [Ca2+]i increase is believed to activate ROS production. In order to examine this hypothesis, we treated rat alveolar macrophages with quartz (SiO2) particles and used laser scanning confocal microscopy to measure [Ca2+]i and the fluorescence intensity of ROS. Time- and dose-dependent increases in [Ca2+]I and ROS in macrophages as well as cell viability were observed. Through chelating extracellular Ca2+ with ethylene glycol tetraacetic acid and releasing intracellular Ca2+ with thapsigargin, we found that 72.7% of the [Ca2+]i increase was due to the influx of Ca2+ from the extracellular environment, via Ca2+ channels in the plasma membrane. By adding mannitol to scavenge hydroxyl radicals (OH(.)), and removing surface iron from the quartz particles to reduce OH(.) generation, we observed a reduced level of ROS generation, whereas the increase in [Ca2+]i was unaffected. When using EGTA to reduce [Ca2+]i, we observed a decrease in ROS production. This study suggests that the [Ca2+]i influx was independent of OH(.) production, and the [Ca2+]i increase resulted in ROS production. These results further indicate that there is a strong relationship between cytosolic free Ca2+ content and cellular injury as well as silica exposure.
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PMID:Intracellular influx of calcium induced by quartz particles in alveolar macrophages. 1983

The authors revealed features of clinical course and outcomes in patients with silicosis and silicotuberculosis, who worked on iron industry enterprise. The article covers comparative analysis of survival rate and mortality among silicosis patients over 14 years of observation.
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PMID:[Prospective analysis of clinical course and outcomes in silicosis patients]. 2063 42

The study covers comparative analysis of silicosis course in males and females engaged into iron industry. Findings are more frequent combination of silicosis and chronic bronchitis in the females, without smoking habit. Some other differences in silicosis course and development were seen dependent on sex.
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PMID:[Peculiarities of silicosis course in women engaged into metallurgy]. 2218 Sep 69

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


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