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

Natural SiO2 particles of 0--4, 0--5 and 5--10 micron of size were investigated by the aid of transmission and scanning electron microscope. Silicosis in rats was induced with SiO2 particles of 0--5 micron of size. After 18 month SiO2 was isolated from the silicotic lung and investigated by the aid of transmission and scanning electron microscopy and with electronmicroscopic diffraction technique. Natural and isolated from silcotic lung SiO granules were divided into different groups according to their planimetrycally measured area, and excentricity calculated from their diameter. It was established, that division of silica particles isolated from lungs became different as compared to the natural silica-dust. Among the silicadust isolated from silicotic lungs of rats proportion of finer granules is much higher than in natural silica-dust-fraction. Granules isolated from lung have rounded edges and part of them shows a decrease of electrondensity. Majority of particules of 0,01 micron of size appears to be isolated in the material got from the silicotic lung.
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PMID:[Electron microscopic study of natural SiO2 particles and SiO2 particles isolated from rat lung]. 18 72

There is a positive relation with significant differences in mean values between the severity of silicosis of hilar lymph noeds and their SiO2 contents. The average SiO2 values in silicosis I amount to 2.03 g %; in silicosis II: 2.86 g%, and in silicosis III: 3.89 g%. The average values in exposed miners without silicosis (= 1.70 g%) show no significant differences in comparison with those of silicose I cases and those of nonexposed male persons (= 0.82 g%). The results justify the attempt of a morphological classification of the severity of silicosis in the hilar lymph nodes encouraging the use of chemical examinations of dust for the evaluation of pneumoconioses, for instance, in the material of mediastinoscopies.
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PMID:[The relation between the morphological stage of silicosis and the SiO2 content in hilar lymph nodes (author's transl)]. 19 Aug 7

A high concentration of silica dust in the air many workstands in ceramic plants is a serious risk for the health of exposed workers. It can cause the development of silicosis. The aim of this paper is to evaluate a fibrogenic activity of dusts containing 98% crystalline silica. The ceramic masses have about 25% of Quartz. The samples of 2 lode quartz and 4 sand quartz originated from different mines in Poland were used for the experiment. Their physical properties were analysed by X-ray diffraction and SiO2 content was determined by colorimetry. Their biological aggresiveness was characterised by wet weight, hydroxyproline content, lipid level in the lungs and wet weight of mediastinal lymph nodes of rats which were intratracheally given of the dusts. The results show that the tested dusts have a moderated fibrogenic activity. At short time (3 months) after their administration the fibrogenic changes in lungs were different depending on the kind of dusts, but at the 6th month of the experiment they did not differ at all. The exposition of workers to silica dusts is a great occupational hazard.
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PMID:[Experimental silicosis. I. Fibrogenic activity of quartz material used in the ceramic industry]. 22 82

The contribution of the type II pneumocyte to the pathogenesis of silicosis is largely unknown. Prominent features of silicosis are hyperplasia and hypertrophy of type II epithelial cells, often accompanied by phospholipid accumulation in the lung. The biologic regulation of these events is poorly understood. This study addresses the question of a direct effect of silica on type II pneumocytes, since direct contact of the inhaled silica dust can occur in vivo. Type II cells were isolated from fetal rat lungs and their epithelial specificity was verified. Experiments were performed on 2nd passage monolayers in 2% serum. Repair, replication, and growth activity was evaluated by the incorporation of [3H]thymidine. Cytotoxicity was measured by quantitating the release of [14C]adenine and expressed as a cytotoxicity index (CI). Type II cell proliferation and cytotoxicity were evaluated for the mineral dusts silica (SiO2), aluminum-treated silica (SiO2AlK), and titanium (TiO2). Of these mineral dusts, only low concentrations of silica increased type II cell [3H]thymidine incorporation (silica 2.5 micrograms/mL: 52% above control, P less than .05; silica 20 micrograms/mL: 57% above control, P less than .02). In addition, silica increased the cell number significantly, although to a lesser degree. Exposure of the type II epithelial cells to silica dust for 24 h resulted in dose-dependent cytotoxicity (silica 10 micrograms/mL, CI = 9.1%, P less than .0002; 250 micrograms/mL, CI = 45.1%, P less than .0001). SiO2Al completely suppressed these proliferation and cytotoxicity effects, which were then similar to those of the inert dust, TiO2. These data suggest that direct exposure and contact of the type II pneumocytes to low-dose silica dust initiated repair, replication, and growth activity, while exposure to higher silica concentrations resulted in marked cytotoxicity. Both the repair, replication, and growth and the cytotoxic responses of the type II epithelial cells to silica exposure are related to the surface properties of silica.
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PMID:Silica exposure induces cytotoxicity and proliferative activity of type II pneumocytes. 131 66

The inhalation toxicity of three amorphous silicas (Aerosil 200, Aerosil R 974 and Sipernat 22S) was compared with that of quartz dust. Rats were exposed to 1, 6 or 30 mg Aerosil 200/m3, 30 mg Aerosil R 974/m3, 30 mg Sipernat 22S/m3 or 60 mg quartz/m3 for 6 hr/day, 5 days/wk for 13 wk. Some rats were killed at the end of the exposure period and some were killed 13, 26, 39 or 52 wk after the end of exposure. Clinical signs, body weight, haematology, biochemistry, urinalyses, organ weights, retention of test material in the lungs and regional lymph nodes, collagen content of the lungs, and gross and microscopic pathology were determined in order to disclose possible adverse effects and to study the reversibility, stability or progression of the effects. All test materials induced increases in lung weight, and pulmonary lesions such as accumulation of alveolar macrophages, inflammation, alveolar bronchiolization and fibrosis. In addition, rats exposed to Aerosil 200, Aerosil R 974 or quartz developed granulomatous lesions. Silicosis was observed only in quartz-exposed animals. At the end of the exposure period, Aerosil 200 and quartz had induced the most severe changes. Quartz dust was hardly cleared from the lungs and the changes in the lungs progressed during the post-treatment period, and eventually resulted in lesions resembling silicotic nodules and in one squamous cell carcinoma. Although Aerosil 200 was very quickly cleared from the lungs and regional lymph nodes, the changes in these organs were only partly reversed during the post-exposure period in rats exposed to 30 mg/m3. Aerosil R 974 and the lower levels of Aerosil 200 resulted in less severe, and mostly reversible, changes. The slightest changes were found after exposure to Sipernat 22S, notwithstanding the persistence of this silica in the lungs during the major part of the post-treatment period. The results of this study revealed that only quartz induced progressive lesions in the lungs resembling silicotic nodules. Of the amorphous silicas examined Aerosil 200 induced the most severe changes in the lungs, which only partly recovered, whereas Sipernat 22S induced the least severe, completely reversible lung changes.
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PMID:Subchronic inhalation toxicity of amorphous silicas and quartz dust in rats. 164 30

Rat alveolar macrophages were exposed to silica dust (quartz) suspended in culture medium (SiO2, dry particle size less than 5 microns in diameter) and fluctuation in their cytosolic free calcium content ([Ca2+]i) was detected in cell monolayers with a fluorescent calcium probe (Indo-1AM). Cytosolic free calcium content was correlated with lactate dehydrogenase (LDH) release, an index of cell damage. SiO2 induced a concentration- and time-dependent increase of cytosolic free Ca2+ ion concentration and LDH release. [Ca2+]i was increased about fivefold when cells were exposed to 200 micrograms of SiO2 per milliliter (3 ml per dish) for 2 hr. [Ca2+]i changed within 15 min of SiO2 treatment, whereas LDH release was measurably increased only after 30 min. Chelation of extracellular Ca2+ by 2 mM ethylene glycol bis(beta-aminoethyl ether) N,N'-tetraacetate did not prevent SiO2-induced fluctuation of macrophage [Ca2+]i, but did partially prevent the SiO2-induced increase in LDH release (p less than 0.01). We conclude that a very early event in SiO2-induced damage of alveolar macrophages involves mobilization of intracellular calcium pools to increase [Ca2+]i. These results suggest that SiO2-induced macrophage damage, a key event in the development of silicosis, may involve perturbation of intracellular calcium homeostasis.
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PMID:Silica increases cytosolic free calcium ion concentration of alveolar macrophages in vitro. 165 54

In a sample of 186 stone workers who performed granite "tearing" and "stone work" (either manual or mechanical) we have found silicosis in 50.5% (simple silicosis 47.3%, and complicated silicosis 3.2%). The most commonly found radiologic manifestation was a round opacity type "p" and a 1/1 to 1/3 profusion. From a functional respiratory perspective, a mild reduction of FVC, DLco (SB) and pO2 similar to that described in coal miners' pneumoconiosis was observed. It seems that "stone workers" had a higher incidence of suffering severe silicosis than stone "tearing" workers. Surprisingly, in the analysis of inhaled dust of such an activity which is performed in the open air the rates of dust and SiO2 are much higher than those found in coal workers. We believe that this is the first time that these measurements are performed, and published, in a group of stone workers.
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PMID:[The epidemiology of silicosis in the El Escorial region]. 196 38

Reactive radicals at the surface of quartz or other SiO2 polymorphs have been studied by EPR in relation to their possible role in pathogenicity. All the examined dusts bear the characteristic radicals of silica ground in air: Si, SiO., SiO.2 (peroxyradical) and O2.- (superoxide ion), but some also show additional spectral lines belonging to other radical forms. Comparison of standard quartz dusts (DQ-12, Min-u-sil 5) with a natural quartz and with what obtained by grinding a very pure quartz crystal indicates that to a higher purity corresponds a higher radical population. Cristobalite and vitreous silica exhibit similar spectra, with larger proportion by respect to quartz, of partially reduced oxygen forms. The reactivity of the silica surface towards O2 and NaClO aqueous solutions are investigated by examining the modification in the EPR spectra induced by these treatments. A possible mechanism for fibrogenicity is proposed whereby, within the activated macrophage, a catalytic reaction occurs between surface functionalities and macrophage oxygen metabolites. This reaction would trigger the abnormal production of fibroblast stimulating factors, ending up with silicosis.
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PMID:Chemical functionalities at the silica surface determining its reactivity when inhaled. Formation and reactivity of surface radicals. 196 71

Quartz but not titanium dioxide (TiO2) induced the production of reactive oxygen metabolites (ROM) by human monocyte-derived macrophages, as measured by lucigenin dependent chemiluminescence. Activation of the macrophages with BCG, bacterial lipopolysaccharide and macrophage-activating factor (MAF) caused a prominent increase of quartz-induced ROM production, MAF having the strongest effect. The activation did not affect the TiO2 responses to the same extent. Assuming that ROM have a role in the pathogenesis of silica-induced disease in man, we suggest that enhancement of quartz-induced production of ROM by activated pulmonary macrophages may at least partly explain the experimental and epidemiological data indicating that activation of the immune system during infection promotes the development of silicosis.
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PMID:Quartz-induced production of reactive oxygen metabolites by activated human monocyte-derived macrophages. 222 36

The activation of collagen synthesis during development of silicotic fibrosis was studied in rats exposed, in dusting chambers, to respirable SiO2 for periods of 2, 4, 6 or 12 months. Control animals were exposed similarly to clean air or TiO2. Development of fibrosis was followed by histological examination, measurement of lung weight and determination of lung collagen content (as hydroxyproline). A steady increase in lung weight and collagen content together with changes in cellularity and metabolic activity of the lungs, as ascertained by chemical determination of DNA and RNA, were measured in the lungs of the SiO2-exposed animals. Hybridization of total lung RNA, extracted at each time point, with cDNA probes specific for type I and type III procollagen mRNA levels showed that the development of fibrosis was associated with increased levels, as compared to age matched controls, of pulmonary procollagen mRNAs. Interestingly, the highest levels of procollagen mRNAs were observed in young (pretreatment control) animals, suggesting that during pulmonary development collagen metabolism in lungs is even greater than during development of fibrosis. In rats exposed to SiO2 the increase in type III procollagen mRNA occurred earlier than the increase in type I procollagen mRNAs. These observations demonstrate both age-dependent and silicosis-related changes in pulmonary procollagen mRNA levels. The results suggest that development of silicosis is associated with an altered capacity of the lungs to regulate collagen accumulation.
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PMID:Characterization of excessive collagen production during development of pulmonary fibrosis induced by chronic silica inhalation in rats. 247 54


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