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

Pulmonary specimens obtained from ten normal subjects and 53 patients with various pulmonary diseases were studied with energy-dispersive x-ray analysis. The amount of silicon in the pulmonary tissue was determined and expressed as a silicon/sulfur (Si/S) ratio. This Si/S ratio was below 0.2 in the ten normal subjects and in 14 patients who had various interstitial pulmonary diseases but had no previous history of exposure to silica or other dusts known to cause pulmonary fibrosis. The Si/S ratio was greater than 0.3 in 19 of 22 patients who had a history of exposure to silica dust and had clear-cut histologic evidence of silicosis. The Si/S ratio was less than 0.2 in 12 and between 0.2 and 0.3 in two of the 14 patients who had a history of exposure to silica dusts but no clinical or histologic evidence of silicosis. We conclude that the determination of the silicon content of tissue by energy-dispersive x-ray analysis is useful in separating the fibrosis due to silicosis from the other causes of pulmonary fibrosis.
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PMID:Value of in situ elemental microanalysis in the histologic diagnosis of silicosis. 670 80

Studies were undertaken by the Departments of Otolaryngology-Head and Neck Surgery and Anesthesiology at Northwestern University Medical School and the Medical College of Wisconsin (Milwaukee) to compare the potential for tissue injury to the trachea and lungs of canines. Polyvinylchloride (PVC), Rusch red rubber, and silicone tubes were tested. The effects of an intraluminal tube fire on the larynx and trachea were documented with laryngeal and bronchoscopic photographs taken immediately postburn and at the time of sacrifice six hours later. The most severe burns were associated with the PVC tube. Silica ash was seen in the airway after the silicone tube fires and raises the possibility of future problems with silicosis. Histological examination of the trachea showed acute injury in all of the animals; specimens from the dogs with the PVC tube fires demonstrated the most severe cellular damage.
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PMID:Comparison of tracheal damage from laser-ignited endotracheal tube fires. 688 33

Although most were unknown a few years ago, present evidence indicates that at least 25 trace elements have some pertinence to health. Unlike vitamins, they cannot be synthesized. Some trace elements are now considered important only because of their harmful effects but traces of them may be essential. Zinc is especially important during puberty, pregnancy and menopause and is related to protein metabolism. Both fluoride and cadmium accumulate in the body year after year. Cadmium is positively correlated with several chronic diseases, especially hypertension. It is obtained from smoking and drinking soft water. Silicon, generally associated with silicosis, may be necessary for healthy bone and connective tissue. Chromium, believed to be the glucose tolerance factor, is obtained from brewer's yeast, spices, and whole wheat products. Copper deficiency may be implicated in a wide range of cardiovascular and blood related disorders. Either marginal deficiencies or slight excesses of most trace elements are harmful. Nurses should instruct patients to avoid highly refined foods, fad diets, or synthetic and fabricated foods. A well balanced and varied diet is the best safeguard against trace element excesses or deficiencies.
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PMID:Trace elements: implications for nursing. 689 39

Type II cell hypertrophy with surfactant accumulation in the lung is a common observation in silicosis. Mechanisms leading to these alterations are poorly understood. By using silica dusts and alveolar fluids from saline and silica exposed sheep, we explored four different pathways of surfactant turnover in vitro: (1) synthesis and (2) secretion of lipids by rat type II cells; and dipalmitoylphosphatidylcholine (DPPC) uptake/reuptake by (3) type II cells and (4) alveolar macrophages. Silica had no direct specific effect on type II cell lipid metabolism. Alveolar fluids from both saline and silica exposed animals induced several alterations compared to control medium: (a) an increase in lipid synthesis (60 to 130%, P < 0.05); (b) a decrease in lipid secretion (25 to 70%, P < 0.05); (c) a 50 to 75% increase in DPPC reuptake by type II cells (P < 0.05); (d) a 65 to 75% decrease in DPPC uptake by alveolar macrophages (P < 0.05). DPPC uptake by in vivo silica exposed alveolar macrophages was reduced. Alterations of surfactant lipid metabolism induced by alveolar fluids from silicotic animals was more pronounced than in those treated with control fluids. Anti SP-A antibodies significantly suppressed most of the alveolar fluid induced effects on surfactant turnover. From these in vitro data, silica-induced type II cell hypertrophy seems to result from an increase in lipid synthesis activity and an imbalance in the lipid secretion/reuptake ratio.
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PMID:Alterations of surfactant lipid turnover in silicosis: evidence of a role for surfactant-associated protein A (SP-A). 754 43

Two cases of extrathoracic silicosis in buffaloes raised near a quartz quarry and suffering from clinically severe silicosis are described. The extrapulmonary changes were characterized by silicoconiotic nodules in the tonsils, mesenteric lymph nodes and spleen. A combination of energy dispersive X-ray microanalysis and scanning electron microscopy revealed that the mineral component of these lesions consisted mainly of silicon, aluminium, iron, calcium, magnesium, zinc, sulphur and potassium. It is concluded that domestic animals raised in polluted environmental conditions represent an important biological source from which helpful data may be obtained for assessing risks to human health and gaining new insight into pathogenetic mechanisms.
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PMID:Extrapulmonary silicosis in two water buffaloes. 772 11

The question whether silica is carcinogenic is not new, but there has been a resurgence of research over the last two decades with the use of more powerful epidemiological methodologies. There is sufficient evidence for the carcinogenicity of crystalline silica in animals. A large number of cohort and case-control studies consistently suggest a modest excess of lung cancer in workers with occupational silica exposure (relative risk less than 2). However, in many studies, the association is confounded by exposures to cigarette smoke, and environmental cocarcinogens like radon daughters, polyaromatic hydrocarbons and asbestos. The excess risk of lung cancer is more pronounced in workers with silicosis (relative risk of 2 to 4). Silica may act as a direct carcinogen or indirectly by the adsorption of cocarcinogens such as polyaromatic hydrocarbons from cigarette smoke or industrial pyrolysis products, and/or by impairing pulmonary clearance, thereby increasing the effective dose and duration of exposure to these carcinogens. Pulmonary fibrosis itself may be a precursor to the development of lung cancer.
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PMID:Silica and lung cancer: a continuing controversy. 784 60

Silica and ferric oxide are common industrial exposures. Studies have indicated that all commonly occurring forms of crystalline silica can cause fibrotic lung disease. There is evidence to indicate that crystalline silica is carcinogenic in humans who have not developed silicosis, while amorphous silica is not carcinogenic in humans. An important biological response to particles deposited deep in the lung is their engulfment by pulmonary alveolar macrophages (AM). To assess the role of AM in silica-induced lung disease, particle size distribution and surface area of crystalline, gelled, precipitated, and fumed silica, ferric oxide, and aluminum oxide were characterized; the cytotoxicity of the particles to hamster and rat AM in vitro was measured at 0.0-0.5 mg/1 x 10(6) cells at 24 and 48 h using dye exclusion procedures. The count medium diameter for aluminum oxide, ferric oxide, and amorphous silica was equal to or less than 0.38 microns, while for crystalline silica the value was 0.83 microns. The surface areas for the amorphous silicas and the aluminum oxide ranged from 253 to 125 m2/g with gelled silica having the highest value; the values for crystalline silica and ferric oxide were 4.3 and 10.8 m2/g, respectively. Crystalline silica (1.6%) was detected in the fumed silica, while none was detected in precipitated or gelled silica. With gelled silica, based on the dose of the particle, the viability of the hamster AM decreased to 27% at 0.05 mg and to zero at 0.1 mg at 24 h. At doses of 0.05 and 0.1 mg of crystalline, precipitated, or fumed silica, the percent viability decreased significantly to 76-67% and 51-42%, respectively, and to zero at 0.5 mg. Macrophages viable at 24 h decreased further at 48 h compared with the control culture. The ferric oxide and the aluminum oxide showed minimal to no changes in viability. Similar results for the particles were obtained with rat AM. The results indicate that precipitated and fumed amorphous silica tested at equivalent doses are equally as toxic to AM lavaged from two species of rodents as crystalline silica; gelled silica is more toxic than crystalline. Ferric oxide and aluminum oxide are noncytotoxic in this system. The results of this study indicate that the dose as well as the surface area and surface characterization are important determinants in the cytotoxicity of hamster and rat AM to these particles.
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PMID:Influence of particle dose on the cytotoxicity of hamster and rat pulmonary alveolar macrophage in vitro. 805 15

Transforming growth factor-alpha (TGF-alpha) a cytokine having potent mitogenic activity for epithelial and mesenchymal cells, may play a role in the lung remodeling of silicosis. Lung macrophages are among the major cells producing TGF-alpha in a lung tissue. A pivotal event in the cascade of pathologic events leading to pulmonary silicosis is the interaction between inhaled silica and macrophages. TGF-alpha may be critical in directing the proliferation of type II pneumocytes that characterize silicosis. An inhalation model of brief exposure of pathogen-restricted male rats to 25 mg/M3 cristobalite, a highly reactive form of silicon dioxide was used to study experimental silicosis. This model is characterized by a rapid, intense, and sustained increase in macrophages, neutrophils, and lymphocytes in both alveolar and interstitial compartments of the lung. TGF-alpha was measured in an A431 cell proliferation assay made specific with the use of anti-TGF-alpha neutralizing antiserum in epithelial lining fluid (ELF) and conditioned media harvested from cultured alveolar and interstitial macrophages. Soluble TGF-alpha levels found in ELF were slightly elevated above control values during the exposure period, then increased 5-fold during the 20 weeks after the 8-day exposure period. Secretion of TGF-alpha by macrophages was elevated during exposure to cristobalite but then fell during the early post exposure period. Marked elevations in TGF-alpha secretion from both interstitial and alveolar macrophages (10- and 12-fold, respectively) occurred 8-16 weeks after cessation of exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Patterns of secretion of transforming growth factor-alpha (TGF-alpha) in experimental silicosis. Acute and subacute effects of cristobalite exposure in the rat. 824 Sep 39

Silica particles cause considerable damage to macrophages resulting in their eventual breakdown. At the same time, the development of silicosis involves a number of mechanisms associated with the activation of macrophages. In suggesting schemes for the pathogenesis of this disease many authors associate the central part with activation, completely neglecting damage to cells. Our experiments have shown, however, that much of the activation phenomena could be reproduced in vitro or in vivo by exposing macrophages to macrophage breakdown products. Alternatively, the secondary character of activation is demonstrated by the fact that it reveals itself only at silica doses which cause part of the cells to lose their viability in the same culture. Our data show that the range of macrophage activation phenomena which could be considered as secondary with respect to the breakdown of cells includes the production of neutrophil attractants, enhanced co-operation with T lymphocytes, increase in phagocytic activity, enhancement of cellular O2 consumption and peroxidation, an increase in the activity of dehydrogenases, reduction in the activity of 5'-nucleotidase, and some other effects. Although not denying that small silica doses may be able to exert a direct activating influence upon the macrophage we do, however, believe that the most important and primary role in the pathogenesis of silicosis is played by the damage to and the breakdown of this cell.
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PMID:On the relationship between activation and breakdown of macrophages in the pathogenesis of silicosis (an overview). 881 62

A combination of risk factors are involved in susceptibility to a primary or secondary form of vasculitis. Most forms of vasculitis are probably genetically based but environmentally triggered. This review discusses currently available evidence for a pathophysiologic role of one possible environmental trigger, silica. Since 1960, several patients with pulmonary silicosis have been described that developed pauci-immune necrotizing crescentic glomerulonephritis, i.e., with either completely negative immunofluorescence findings or nonspecific granular IgM or C3 deposits along the capillary wall. Recently it was reported that these patients have antineutrophil cytoplasmic antibodies (ANCAs) that are in most cases directed to myeloperoxidase. Further, patients with pulmonary silicosis may develop microscopic polyangiitis, the syndrome of lung hemorrhage and nephritis, or Wegener's granulomatosis. To further substantiate the relation between silicon exposure and renal failure or vasculitis, several case-control studies have been reported. Exposure to silicon-containing compounds was found to be related to chronic renal failure (odds ratio, 1.7:2.5) or vasculitis (odds ratio, 6.5:14.0). The mechanisms by which silica may induce ANCA-associated glomerulonephritis or vasculitis are not well known. Silicon-containing compounds have a pronounced adjuvant effect on immune responses, and silica particles are potent stimulators of lymphocytes and monocytes or macrophages. Further, silica may induce apoptosis of monocytes or macrophages and possibly neutrophils. In conclusion, at present there is ample evidence that occupational exposure to silicon-containing compounds is related to the development of ANCA-associated glomerulonephritis and vasculitis, and silica is one of the first well-documented environmental triggers in these diseases.
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PMID:Silicon exposure and vasculitis. 944 85


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