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

Silicosis is a preventable occupational lung disease caused by inhaling dust containing crystalline silica; no effective treatment for silicosis is available. Deaths from inhalation of silica-containing dust can occur after a few months' exposure (1). Crystalline silica exposure and silicosis have been associated with work in mining, quarrying, tunneling, sandblasting, masonry, foundry work, glass manufacture, ceramic and pottery production, cement and concrete production, and work with certain materials in dental laboratories. To describe patterns of silicosis mortality in the United States, CDC analyzed data from the National Institute for Occupational Safety and Health (NIOSH) National Occupational Respiratory Mortality System (NORMS) for 1968-2002. This report summarizes the results of that analysis, which indicated a decline in silicosis mortality during 1968-2002 and suggested that progress has been made in reducing the incidence of silicosis in the United States. However, silicosis deaths and new cases still occur, even in young workers. Because no effective treatment for silicosis is available, effective control of exposure to crystalline silica in the workplace is crucial.
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PMID:Silicosis mortality, prevention, and control--United States, 1968-2002. 1585 59

Silicosis is an occupational lung disease resulting from the inhalation of silica particles over prolonged periods of time, which causes chronic inflammation and progressive pulmonary fibrosis. Alveolar macrophages (AM) are critical effector cells, while less is known about the role and function of pulmonary dendritic cells (DC) in silicosis. We hypothesize that a balance exists between the suppressive nature of AM and the stimulatory capacity of DC to regulate lung immunity, and that this equilibrium may be overcome by silica exposure in vivo. Our results demonstrate that in response to silica exposure, both the percent and absolute number of AM significantly decreased over time, with a concomitant significant increase in DC. Both AM and DC exhibited cellular activation in response to silica, indicated by increased expression of cell surface markers. In the absence of silica-induced AM apoptosis (TNFR 1/2-null and Gld mice), no change was observed in the percent or absolute number of either cell type. Furthermore, bone marrow-derived DC, but not bone marrow-derived macrophages, migrated from the alveoli into the lung parenchyma in response to silica, resulting in significantly increased numbers of activated T lymphocytes. Collectively, the results demonstrate that AM and DC are distinct antigen-presenting cells within the respiratory tract that respond to silica exposure in vivo in unique ways, with significant implications for immune reactivity of the lung in response to environmental pathogens.
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PMID:Antigen-presenting cell population dynamics during murine silicosis. 1764 Dec 96

Since 1939, it has been known that, silicosis and extrinsic allergic alveolitis can be seen among dental technicians. The interstitial disease caused by the exposure to complex substances used by dental technicians is classified as a special group called dental technician's pneumoconiosis. A 36-year-old man, who has no smoking history, presented with severe dyspnea. He had worked in different dental laboratories for 22 years, but he did not have respiratory symptoms until five years ago. After that date, he had hospitalized and had been examined for respiratory pathologies for many times. He had came to our clinic, because of the progression of his dyspnea. Diffuse pulmonary parenchymal infiltrates which can be related with pneumoconiosis and chronic type 1 respiratory deficiency had been diagnosed as the result of the examinations. While he has no history of smoking or any other risk factors or diseases in his medical history, the case was accepted as dental technician's pneumoconiosis. The factors related with the pathogenesis of dental technician's pneumoconiosis are; the complex compound of the substances (metal dusts, silica, plaster, wax and resins, chemical liquids, methyl methacrylate) used in this sector and their effects on the lung parenchyma. Extrinsic allergic alveolitis related with methyl methacrylate has been reported. The most important factor to acquire an occupational lung disease is a complex occupational exposure. The insufficient workplace airing and the lack of preventive measures added on this exposure, the risks become much more greater.
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PMID:[Dental technician's pneumoconiosis; a case report]. 1870 82

Despite federally mandated safety standards, occupational lung disease remains one of the most common work-related injuries. Inhaled dust can result in a range of tissue injury in the lung and can lead to significant respiratory insufficiency causing death. Although silicosis and coal worker's pneumoconiosis are becoming less common, hypersensitivity pneumonitis is increasingly recognized as an occupational lung disease with new antigens being introduced annually. Imaging, particularly high-resolution computed tomography, is central to the management of occupational lung disease and is useful in diagnosis, assessment of disease activity, and evaluating response to therapy.
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PMID:Occupational lung disease. 1993 27

Silicosis is the most common occupational lung disease worldwide. It leads to respiratory impairment and may have associated infections that decrease pulmonary function. We describe the case of a 55-year-old man with chronic silicosis who presented with hemoptysis and a cavitated conglomerate mass. The final diagnosis was silicotuberculosis.
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PMID:Cavitated conglomerate mass in silicosis indicating associated tuberculosis. 2081 60

Sandblasting is one of the occupational causes of silicosis. This report details three cases diagnosed as silicosis caused by sandblasting in Teflon-coated pan manufacturing: Case 1--A 24-year-old man admitted with dyspnea and cough; Case 2--An 18-year-old man admitted with shortness of breath and fever; and Case 3--A 25-year-old man admitted with dyspnea and weight loss. Chest examinations of the first and second cases revealed crackles in both lungs, but the third case was normal, no crackles. Chest x-rays showed bilateral reticulonodular densities and hilar enlargement in all cases. They were clinically and radiologically diagnosed as silicosis due to occupational exposure. All cases had worked in the sandblasting unit at a Teflon-coated pan manufacturing factory for one to three years. Silicosis is a preventable occupational lung disease, but no effective treatment is available for the disease yet. Improving workplace conditions is the most effective way to prevent silicosis.
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PMID:Acute silicosis in teflon-coated pan manufacturing due to metal sandblasting. 2190 88

Silicosis is the most common occupational lung disease in Egypt where its prevalence rate ranges from 18.5 % to 45.8% among workers exposed to free crystalline silica dust. Despite its high prevalence, there is a lack of enforcement of exposure limits, availability and use of personal protective equipment, and occupational health education programs. These factors led the authors to study this unique working population; to the best of our knowledge, this is the first work that investigates the effect of exposure to crystalline silica on select immune response of exposed Egyptian phosphate miners. The main aims of this study were to investigate the effect of exposure to free crystalline silica on pulmonary function parameters and select immune response of exposed Egyptian phosphate miners. The study involved of three groups: 50 silica-exposed workers with radiological evidence of silicosis, 50 silica-exposed workers without evidence of silicosis, and 50 healthy unexposed subjects. There were significant differences between pulmonary function parameters in exposed groups with and without silicosis, and healthy unexposed control subjects (p<.001) and pulmonary function was significantly correlated with duration of silica exposure. Smoking had an additive effect on reduction of pulmonary function. Average values of C-reactive protein, rheumatoid factor, complement component C3, IgA, IgG, and IgM were significantly higher in the exposed group with silicosis than in the exposed group without silicosis and in healthy unexposed control subjects (p<.001).
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PMID:Immune response due to silica exposure in Egyptian phosphate mines. 2210 8

Coal workers' pneumoconiosis (CWP) is a chronic occupational lung disease caused by long-term inhalation of dust, which triggers inflammation of the alveoli, eventually resulting in irreversible lung damage. CWP ranges in severity from simple to advanced; the most severe form is progressive massive fibrosis (PMF). Advanced CWP is debilitating and often fatal. To prevent CWP, the Coal Mine Health and Safety Act of 1969 established the current federal exposure limit for respirable dust in underground and surface coal mines. The Act also established a surveillance system for assessing prevalence of pneumoconiosis among underground coal miners, but this surveillance does not extend to surface coal miners. With enforcement of the exposure limit, the prevalence of CWP among underground coal miners declined from 11.2% during 1970-1974 to 2.0% during 1995-1999, before increasing unexpectedly in the last decade, particularly in Central Appalachia. Exposure to respirable dust is thought to be less in surface than underground coal miners. Although they comprise 48% of the coal mining workforce, surface coal miners have not been studied since 2002. To assess the prevalence, severity, and geographic distribution of pneumoconiosis among current surface coal miners, CDC obtained chest radiographs of 2,328 miners during 2010-2011 through the Coal Workers' Health Surveillance Program of the National Institute for Occupational Safety and Health (NIOSH). Forty-six (2.0%) of 2,257 miners with >1 year of surface mining experience had CWP, including 37 who had never worked underground. Twelve (0.5%) had PMF, including nine who had never worked underground. A high proportion of the radiographs suggested silicosis, a disease caused by inhalation of crystalline silica. Surface coal mine operators should monitor worker exposures closely to ensure that both respirable dust and silica are below recommended levels to prevent CWP. Clinicians should be aware of the risk for advanced pneumoconiosis among surface coal miners, in addition to underground coal miners, to facilitate prompt disease identification and intervention.
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PMID:Pneumoconiosis and advanced occupational lung disease among surface coal miners--16 states, 2010-2011. 2269 82

Silicosis is an occupational lung disease, which is caused by the inhalation of silica and affects a wide range of jobs. There are many clinical forms of silicosis: acute silicosis, results from exposure to very large amounts of silica dust over a period of less than 2 years. Simple chronic silicosis, the most common type that we see today, results from exposure to low amounts of silica between 2 and 10 years. Chronic silicosis complicated, with silicotic conglomerates. In many cases the diagnosis of silicosis is made according to epidemiological and radiological data, without a histological confirmation. It is important to know the various radiological manifestations of silicosis to differentiate it from other lung diseases and to recognize their complications. The objective of this work is to describe typical and atypical radiological findings of silicosis and their complications in helical and high resolution (HRCT) thorax CT.
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PMID:[Silicosis: computed tomography findings]. 2288 89

Granuloma formation occurs in the human body if there is a particle which persists in phagocytes and which the immune system cannot eliminate. The immune reaction of granuloma formation evolved in order to combat mycobacteria with the aim of localizing mycobacteria and to avoid spreading of mycobacteria throughout the body. Granulomatous lung diseases are often accompanied by severe, systemic inflammation. However, acute phase proteins may be only slightly elevated. The spectrum of granulomatous lung diseases is broad. Sarcoidosis is the most common granulomatous lung disease. To diagnose sarcoidosis, other infectious granulomatous lung diseases such as tuberculosis, atypical mycobacterial and fungal infection have to be ruled out. Pulmonary granuloma also evolve in the context of autoimmune diseases such as rheumatoid arthritis, granulomatosis with polyangiitis (GBA, Wegener's) and eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss syndrome). Furthermore, immunodeficiencies such as common variable immunodeficiency (CVID) and immune reconstitution syndrome in HIV can be associated with systemic granulomatous inflammation. Finally, occupational lung disease, particularly hypersensitivity pneumonitis, silicosis, hard metal lung, and chronic berylliosis are associated with pulmonary granuloma formation.
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PMID:[Granulomatous lung and systemic diseases]. 2346 60


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