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

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 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

Most studies of respiratory disease from dust exposure in the agricultural workplace have focused on allergic diseases caused by inorganic dusts, specifically occupational asthma and hypersensitivity pneumonitis. Exposures to inorganic (mineral) dusts among farmers and farm workers may be substantial. Such exposures are most frequent in dry-climate farming regions. In such locations farming activities that perturb the soil (e.g., plowing, tilling) commonly result in exposures to farm operators of 1-5 mg/m(3) respirable dust and >= 20 mg/m(3) total dust. The composition of inorganic dust in agriculture generally reflects the soil composition. Crystalline silica may represent up to 20% of particles, and silicates represent up to 80%. These very high concentrations of inorganic dust are likely to explain some of the increase in chronic bronchitis reported in many studies of farmers. Pulmonary fibrosis (mixed dust pneumoconiosis) has been reported in agricultural workers, and dust samples from the lungs in these cases reflect the composition of agricultural soils, strongly suggesting an etiologic role for inorganic agricultural dusts. However, the prevalence and clinical severity of these cases are unknown, and many exposures are to mixed organic and inorganic dusts. Epidemiologic studies of farmers in diverse geographic settings also have observed an increase in chronic obstructive pulmonary disease morbidity and mortality. It is plausible that agricultural exposure to inorganic dusts is causally associated with chronic bronchitis, interstitial fibrosis, and chronic obstructive pulmonary disease, but the independent contribution of mineral dusts beyond the effects of organic dusts remains to be determined.
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PMID:Exposures and health effects from inorganic agricultural dusts. 1093 84

Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; d) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.
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PMID:Silicosis and coal workers' pneumoconiosis. 1093 86

The authors determined pneumoconiosis as a chronic diffuse or diffuse and granulomatous pneumonitis with pulmonary fibrosis. The article deals with identification of lymphocytes subpopulations through monoclonal antibodies, details peculiarities of cellular immunity in pneumoconiosis patients, contains new data on LgE-dependent inflammatory mechanisms including specific response to industrial dust allergens. Discussion covers ways of immune correction therapy and immune prophylactics in accordance with phases of body response to homotoxins produced due to exogenous dust load.
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PMID:[Immunological aspects of modern forms of pneumoconioses]. 1093 46

Chronic interstitial lung diseases including pneumoconiosis have pathological characteristics which alter the lung structure and function consequent to the accumulation and activation of inflammatory cells in the lower respiratory tract. These activated cells usually secrete the inflammatory and fibrogenic mediators. Of the diffuse parenchymal lung diseases, the majority have no known etiology and idiopathic pulmonary fibrosis (IPF) is the diagnosis most frequently encountered by clinicians. Pathogenic similarities between pneumoconiosis and IPF provide a strong basis for hypothesizing that environmental agents may cause IPF. Many case-control studies have been published that provide further evidence for a number of associations between occupational and environmental exposures and IPF. Such reports support a strong evidence that IPF may be a heterogenous disorder associated with a number of environmental exposures. As a model of lung fibrosis, experimental pneumoconiosis is giving us a great information because crystalline silica is probably one of the most typical agent producing pulmonary fibrosis and the severity of its health effects and the widespread nature of exposure have been long recognized. Many papers provide evidence that particles have the potential to cause stimulation of phagocytes to release oxidants and such oxidative stress is believed to be a major factor in pulmonary inflammation followed by fibrotic change. Many kinds of cellular mediators are recognized as a implicating factor in this process including cell-to-cell interaction, enzymes, cytokines, arachidonic acid derivatives et al. Treatment of pneumoconiosis is an attractive and interesting topic. But, the mechanism of pathogenesis of pneumoconiosis is not thoroughly understood yet. Also, whether the process of fibrosis formation be retarded or not is questionable with some therapeutic trial. Therefore, a sensitive biomarker which is possible to estimate the pathological pathway in pneumoconiosis is needed. Our laboratory has studied particulate-induced pulmonary reaction for two decades consistently. This review will focus on signal transduction pathway involved in oxidative stress and some inhibitory agents with pleiotropic mechanism in pulmonary fibrosis. I will also introduce some data of animal studies with multidrug regimen as well.
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PMID:Recent advances in particulate-induced pulmonary fibrosis; for the application of possible strategy experimentally and clinically. 1146 77

Inhalation of dusts is an important cause of interstitial lung disease in the tropical countries such as India. While dusts of organic origin, such as the cotton dust causing byssinosis, generally cause bronchial or bronchiolar involvement and hypersensitivity pneumonitis, inorganic metallic dusts cause progressive pulmonary fibrosis. Silicosis, coal workers' pneumoconiosis, and asbestosis are the three most commonly recognized forms of pneumoconiotic pulmonary fibrosis. Pulmonary tuberculosis is an important complication seen in up to 50% of patients of silicosis in some reports from India. The presentation is generally chronic, although acute and accelerated forms of silicosis are known when the exposures are heavy. Breathlessness, dry cough, and general constitutional symptoms are commonly seen. Patients with silicotuberculosis or other forms of infection may also have significant expectoration, hemoptysis, fever, and rapid progression. Respiratory failure and chronic cor pulmonale occur in the later stages. The diagnosis is easily established if the occupational history is available. Dense nodular opacities on chest roentgenograms, which may be large in patients with massive pulmonary fibrosis, are characteristic. Emphysematous changes generally appear in advanced stages or in patients who smoke. Bronchoalveolar lavage and/or lung biopsy may occasionally be required to establish or exclude other causes of interstitial lung disease. Treatment is largely palliative, although a variety of drugs including corticosteroids and procedures such as whole lung lavage have been tried. None of these methods has yet been found successful in the treatment. Preventive safety steps, including removal of the patient from the site of exposure, are the only effective strategies to control disease progression.
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PMID:Dust-induced interstitial lung disease in the tropics. 1158 75

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

Welders with radiographic pneumoconiosis abnormalities have exhibited a gradual clearing of the X-ray identified effects following removal from exposure. In some cases, the pulmonary fibrosis associated with welding fumes appears in a more severe form in welders. Accordingly, to investigate the disease and recovery process of pneumoconiosis induced by welding-fume exposure, rats were exposed to welding fumes with concentrations of 63.6+/-4.1 mg/m(3) (low dose) and 107.1+/-6.3 mg/m(3) (high dose) of total suspended particulate for 2 h per day in an inhalation chamber for a total of 2 h or 15, 30, 60 or 90 days. Thereafter, the rats were no longer exposed and allowed to recover from the welding fume-induced lung fibrosis for 90 days. When compared to the unexposed control group, the lung weights significantly increased in both the low- and high-dose rats from day 15 to 90. A histopathological examination combined with fibrosis-specific staining revealed that the lungs from the low-dose rats did not exhibit any significant progressive fibrotic changes. Whereas, the lungs from the high-dose rats exhibited early delicate fibrosis from day 15, which progressed into the perivascular and peribronchiolar regions by day 30. Interstitial fibrosis appeared at day 60 and became prominent by day 90, along with the additional appearance of pleural fibrosis. Recovery, evaluated based on the body and lung weights and a histopathological examination, was observed in both the high and low-dose rats that were exposed up to 30 days. The rats exposed for 60-90 days at the low dose also recovered from the fibrosis, yet the rats exposed for 60-90 days at the high dose did not fully recover. Consequently, recovery from pneumoconiosis induced by welding-fume exposure was observed when the degree of exposure was short-term and moderate.
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PMID:Recovery from manual metal arc-stainless steel welding-fume exposure induced lung fibrosis in Sprague-Dawley rats. 1284 85

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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