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

From West Texas to West Virginia, from California to New York, in industries from oil refining to coal mining and work settings from foundries to shipyards, the United States is experiencing an epidemic of silicosis, a preventable disease. Silica sand has been linked to cancer, and the International Agency for Research on Cancer has named silica as a probable human carcinogen. This article analyzes the reawakening of national concern about silicosis and the social, economic, and epidemiologic factors that have led scientists, policy makers, industrial hygienist, and labor and industry representatives to reassess the danger that silica sand poses to the health of an estimated two million workers in this country.
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PMID:The reawakening of national concern about silicosis. 967 67

Exposure to silica has been associated with progressive pulmonary inflammation and fibrosis. While the fibroblasts play an important role in the pathogenesis of silicosis, the direct interaction between silica and fibroblasts is poorly understood. We observed that silica particles stimulated intracellular ROS generation in Rat2 fibroblast, evidenced by DCFH oxidation. Silica-induced DCFH oxidation was inhibited by catalase and DPI, a flavoenzyme inhibitor. Additionally, the time course of elevation of the intracellular ROS was paralleled by the increases of MEK and ERK phosphorylation. Silica-induced ERK phosphorylation was also effectively attenuated by catalase and DPI. However, SOD enhanced the silica-induced ERK phosphorylation, indicating a role for H(2)O(2) in ERK activation. Furthermore, ERK and MEK phosphorylation are reproduced by H(2)O(2) treatment. Taken together, these results demonstrate that silica stimulates ROS production via flavoenzyme-dependent mechanism in Rat2 fibroblasts and the H(2)O(2), in turn, serves as a signal transduction element in activating MEK-ERK pathway.
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PMID:Silica-induced generation of reactive oxygen species in Rat2 fibroblast: role in activation of mitogen-activated protein kinase. 1047 90

Silica exposure results in an initially acute inflammatory response followed by chronic fibrotic change. The mechanism for the maintenance of silica-induced inflammation has not been understood yet. In silica-induced acute inflammation and chronic fibrosis, various mediators such as reactive oxygen species, cytokines and growth factors are released. And these substances are suggested to have the regulatory role for the inflammation and fibrosis by possessing the potential to influence apoptosis. To demonstrate the apoptosis as an underlying mechanism for the development of silicosis, in vitro and in vivo models were designed. In in vitro study, we evaluated that apoptotic cell fraction in silica (10, 50 microg/cm2)-treated A549 cells was significantly increased in comparison with control by FACS (fluorescein activated cell sorter). Also genomic DNA from silica (10, 50 microg/cm2)-treated A549 showed DNA ladder formation while control and 1 microg/cm2 groups didn't. In in vivo study, total cell numbers and apoptotic cell numbers of BAL (bronchoalveolar lavage) fluid from silica (10, 20, 40 mg/kg)-instilled rats were significantly higher than control group from 1 week. From these results, we concluded acute and chronic presence of apoptosis may contributes to silica-induced acute inflammation and chronic fibrosis.
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PMID:Silica-induced apoptosis in vitro and in vivo. 1051 Dec 80

By measuring the activity of telomerase in a silica-instilled rat lung, the study found a significant increase in telomerase activity compared to that of the control. Pneumoconiosis displays the characteristics of fibroblast-proliferation and accumulation of collagen, which finally causes the pathologic changes of irreversible and progressive fibrosis of the lung. On the basis of the hypothesis that cellular proliferation may trigger telomerase-activity, the experiment was carried out with telomerase-activation in silicosis. Silica-instilled rat lungs showed increased activity of telomerase, which was measured by TRAP (telomeric repeat amplification protocol) assay, at the time of the 1st, 5th and 8th week after intratracheal instillation of silica in vivo. However, no activity was shown in silica-co-cultured fibroblast in vitro. By summarizing these results, the activity of telomerase is thought to be a very sensitive marker for the evaluation of pathogenicity, showing cellular immortalization in an experimental silicosis model.
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PMID:Activation of telomerase by silica in rat lung. 1064 71

The authors verify whether in silicosis the accumulation of silicon dioxide (SiO2) particles in the lung can induce changes of the activated T lymphocytes in the peripheral blood. The lymphoblastic transformation of lymphocytes stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), Mycobacterium tuberculosis (Mt) and purified protein derivative (PPD) was studied using the classical methods. It was observed that in patients exposed to SiO2 lymphocyte reactivity to the above stimulants decreases. Significant differences between patients and controls were observed only in the response to PHA (p < 0.001).
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PMID:Value of the lymphoblastic transformation in patients with silicosis. 1066 Sep 71

Silicosis is a serious occupational lung disease associated with irreversible pulmonary fibrosis. The interaction between inhaled crystalline silica and the alveolar macrophage (AM) is thought to be a key event in the development of silicosis and fibrosis. Silica can cause direct injury to AMs and can induce AMs to release various inflammatory mediators. Acute silicosis is also characterized by a marked elevation in surfactant apoprotein A (SP-A); however, the role of SP-A in silicosis is unknown. We investigated whether SP-A directly affects the response of AMs to silica. In this study, the degree of silica toxicity to cultured rat AMs as assessed by a (51)Cr cytotoxicity assay was shown to be dependent on the time of exposure and the concentration and size of the silica particles. Silica directly injured rat AMs as evidenced by a cytotoxic index of 32.9 +/- 2.5, whereas the addition of rat SP-A (5 microg/ml) significantly reduced the cytotoxic index to 16.6 +/- 1.2 (P < 0. 001). This effect was reversed when SP-A was incubated with either polyclonal rabbit anti-rat SP-A antibody or D-mannose. These data indicate that SP-A mitigates the effect of silica on AM viability, and this effect may involve the carbohydrate recognition domain of SP-A. The elevation of SP-A in acute silicosis may serve as a normal host response to prevent lung cell injury after exposure to silica.
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PMID:Surfactant protein A prevents silica-mediated toxicity to rat alveolar macrophages. 1074 48

This work presents the concentrations dynamics of dust in a cast iron foundry, in parallel with the frequency and gravity dynamics of the getting sick of silicosis. The knowing of the real risk of exposure to silicotic dust was possible through the data processing concerning the dusting degree (the average of working place), the content of silicon free-crystalline dioxide (SiO2 l.c.) for the calculation of the maximum admitted concentration (C.M.A.) and the dispersion degree of dust in a cast iron and steel foundry for the studied period (1982-1996). New cases of silicosis appeared in this period were studied and they were colligated with the age at declaration, the average length of service and the profession. The values of the dusting degree outrun the C.M.A. up to 168 times, especially at the preparation of mixture and grinding with a prevalence of particles under 3 micron (40-70%) and the Si02 l.c. content varies between 35.2% and 64.5%. From those 98 new cases of silicosis appeared in 15 years, 82.65% were traced out in the incipient phases of the disease. The average age in service and the average age increase (43.1 respective 19.8 years). The coefficients of correlation and regress (+0.286 respective +0.383) show a good correlation between the silicosis number and the age in service. The advanced stages of silicosis and age in service under 10 years were found at the foundry-workers and formators, occupations which imply a high silicotic risk. The foretelling calculations for the next 20 years show an increase of the silicosis incidence for foundry-workers.
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PMID:[The dynamics of exposure to silicotic dusts and silicosis in a foundry]. 1075 97

An accelerated silicosis case made our Occupational Health Unit focus on a pathology thought dropping so far to die out. Furthermore this event occurred in a manufacturing (lost-wax process in jewelry casting) regarded as a low-risk exposure. Besides unsuitable procedures, the user had underestimated the specific risk of that raw material (talcum-like powder at 60-80% silica crystalline level), commonly called "gypsum", inappropriately labelled since not yet adequately classified by the hazardous substances list. The widespreading of this manufacture in our area (Vicenza district) and the recent inclusion of Silica Crystalline in the Class 1 made by IARC (Jan 1997) have urged this Unit to take action in industrial hygiene investigations, instructions to the workers, mandatory directions to dealers concerning the proper hazard labelling for products containing silica crystalline and circulation of information among other Occupational Health Units involved.
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PMID:[Acute silicosis in jewelry casting]. 1077 39

Nuclear factor-kappaB (NF-kappaB) is a multiprotein complex that may regulate a variety of inflammatory cytokines involved in the initiation and progression of silicosis. The present study documents the ability of in vitro silica exposure to induce DNA-binding activity of NF-kappaB in a mouse peritoneal macrophage cell line (RAW264.7 cells) and investigates the role of reactive oxygen species (ROS) and/or protein tyrosine kinase in this activation. In vitro exposure of mouse macrophages to silica (100 microg/ml) resulted in a twofold increase in ROS production, measured as the generation of chemiluminescence (CL), and caused activation of NF-kappaB. Silica-induced CL was inhibited 100% by superoxide dismutase (SOD) and 75% by catalase, while NF-kappaB activation was inhibited by a variety of antioxidants (catalase, superoxide dismutase, alpha-tocopherol, pyrrolidine dithiocarbamate, or N-acetylcysteine). Further evidence for the involvement of ROS in NF-kappaB activation is that 1 mM H2O2 enhanced NF-kappaB/DNA binding and that this activation was inhibited by catalase. Specific inhibitors of protein tyrosine kinase, such as herbimycin A, genistein, and AG-494, prevented NF-kappaB activation in silica-treated cells. Genistein and AG-494 also reduced NF-kappaB activation in H2O2-treated cells. Results confirm that tyrosine phosphorylation of several cellular proteins (approximate molecular mass of 39, 58-70, and 103 kD) was increased in silica-exposed macrophages and that genistein inhibited this silica-induced phosphorylation. In contrast, inhibitors of protein kinase A or C, such as H89, staurosporin, calphostin C, and H7, had no marked inhibitory effect on silica-induced NF-kappaB activation. The results suggest that ROS may play a role in silica-induced NF-kappaB activation in macrophages and that phosphorylation events mediated by tyrosine kinase may be involved in this activation.
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PMID:Silica-induced nuclear factor-kappaB activation: involvement of reactive oxygen species and protein tyrosine kinase activation. 1083 16

The relationship between crystalline silica and lung cancer has been the subject of many recent publications, conferences, and regulatory considerations. An influential, international body has determined that there was sufficient evidence to conclude that quartz and cristobalite are carcinogenic in humans. The present authors believe that the results of these studies are inconsistent and, when positive, only weakly positive. Other, methodologically strong, negative studies have not been considered, and several studies viewed as providing evidence supporting the carcinogenicity of silica have significant methodological weaknesses. Silica is not directly genotoxic and is a pulmonary carcinogen only in the rat, a species that seems to be inappropriate for assessing particulate carcinogenesis in humans. Data on humans demonstrate a lack of association between lung cancer and exposure to crystalline silica. Exposure-response relationships have generally not been found. Studies in which silicotic patients were not identified from compensation registries and in which enumeration was complete did not support a causal association between silicosis and lung cancer, which further argues against the carcinogenicity of crystalline silica.
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PMID:Silica, silicosis, and lung cancer: a response to a recent working group report. 1128 67


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