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

Silica granulomas are rare in the skin. Involvement of the regional lymph nodes seems to be unusual. The case of a 35-year-old man with massive diffuse fibrosis of the axilla with multiple foreign body granulomas and involvement of axillary lymph nodes is presented. The lymph nodes exhibit multiple epithelioid cell granulomas and silicotic nodules which are indistinguishable from similar nodules in mediastinal lymph nodes in pulmonary silicosis. It is assumed that the numerous silica particles which were identified by X-ray microanalysis under the scanning electron microscope and recovered from the mineral ash after incineration were accidentally implanted into the skin at the time of an injury 26 years previously. The long delay between silica exposure and granuloma development is a typical feature of these lesions. The possible mechanisms operative in this process are discussed.
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PMID:Unusual silica granulomas of the skin with massive involvement of axillary lymph nodes. 22 32

In recent years, with the aging of patients with pneumoconiosis, autoimmune diseases as a complication have been observed. One of the reasons for this may be that autoimmune diseases are prone to develop among the elderly. On the other hand, it has been reported that dust itself, such as silica for example, has adjuvant effect. A review of the recent literature published in Japan and abroad was made to clarify the relationship between pneumoconiosis and autoimmune diseases and the following results were obtained. 1) Disorders which accompany pneumoconiosis: Scleroderma, rheumatoid arthritis, systemic lupus erythematosus (SLE), and disorders of the kidney and liver have been reported. In Japan, about 30 cases of pneumoconiosis accompanied with autoimmune diseases have been reported. In many of the reports, patients with pneumoconiosis and scleroderma have a past history of exposure to silica. In both case studies and case control studies, patients with rheumatoid arthritis and history of silica exposure are prone to develop pneumoconiosis. 2) Immunological studies of patients with pneumoconiosis: As for humoral immunity, elevation of polyclonal gamma-globulin, especially IgG, has been often reported together with high positive rate of autoantibodies such as antinuclear antibodies. In cellular immunity, decreased delayed type skin reaction and decreased CD4/8 ratio have been reported. In human leukocyte antigen (HLA) typing the elevated frequency of DR4 has been reported. In the study of BAL increased production of superoxide anion O2- by alveolar macrophages has been observed. 3) EXPERIMENTAL STUDIES: Silica is well known for its toxicity to cells and also for its adjuvant effect. In the German Democratic Republic, patients with scleroderma and history of long term silica exposure are recognized as patients with occupational disease even though pneumoconiosis is not clearly demonstrated on X-ray film. It is difficult from this review to nrake a definite conclusion regarding the relation between silicosis and autoimmune diseases. There is a need to repeat this review of the literature on autoimmune diseases and pneumoconiosis in the near future.
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PMID:[Relationship between autoimmune diseases and pneumoconiosis]. 140 2

Scleroderma-like diseases can be induced by a number of chemical compounds, such as plastics, solvents and drugs. Contaminated rapeseed oil was the cause of the toxic oil syndrome and L-tryptophan induces the so-called eosinophilia-myalgia-syndrome. On the other hand, paraffin and silicon can trigger so-called adjuvant disease, while long-term exposure to silica can lead to idiopathic scleroderma (associated with silicosis in some cases). In addition to the clinical features, some pathogenetic data in the literature, such as genetic factors (HLA, chromosomal anomalies, enzyme deficiencies) and the metabolism of chlorinated ethylenes via reactive epoxide intermediate products, and our own findings are reported. Silica-induced scleroderma cannot be distinguished from the idiopathic form by epidemiological, clinical or immunological studies or by parameters referring to the blood vessels or collagen metabolism. In cell culture studies it has been shown that macrophages/monocytes release IL1, IL6 and TNF after ingestion of silica, which affects fibroblasts, T-helper cells and endothelial cells. Comparative results from the silicosis literature are reported. Finally, the possibly stimulating role of ionizing irradiation (uranium mining) in favouring the development of scleroderma is discussed.
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PMID:[Chemically-induced scleroderma]. 150 11

Alveolar epithelial cell injury and increased alveolar-capillary membrane permeability are important features of acute silicosis. To determine whether silica particles contribute directly to this increased permeability, we measured paracellular permeability of rat alveolar epithelium after exposure to silica, in vitro, using markers of the extracellular space. Silica (Minusil) markedly increased permeability in a dose- and time-dependent manner. This was not the result of cytolytic injury, because lactate dehydrogenase release from monolayers exposed to silica was not increased. Pretreatment of the silica with serum, charged dextrans, or aluminum sulfate blocked the increase in permeability. Scanning electron microscopy demonstrated adherence of the silica to the surface of the alveolar epithelial cells. Thus silica can directly increase permeability of alveolar epithelium.
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PMID:Silica directly increases permeability of alveolar epithelial cells. 169 64

In silicosis, alveolar macrophages (AM) are thought to induce chronic inflammation and fibrosis by release of cytokines. Rats were exposed to aerosols of alpha-quartz and examined 4 to 9 mo later for persistence of silica particles and release of tumor necrosis factor-alpha (TNF-alpha) from macrophages. Silica particles were detected in AM, lung parenchyma, and thoracic lymphoid organs, whereas extrathoracic lymphoid tissues and organs were free of the mineral. When AM were tested functionally, no spontaneous release of TNF-alpha was observed. However, upon in vitro stimulation of AM from silicotic rats with a low concentration of lipopolysaccharide (10 ng/ml), abundant TNF-alpha production was found that was higher and occurred more rapidly than with AM from sham-exposed animals. Peritoneal macrophages, which did not have contact with silica particles, displayed a similarly enhanced TNF-alpha release in response to low doses of lipopolysaccharide. These data demonstrate a state of systemic preactivation ("priming") of macrophages that supports the notion that silicosis is associated with a general immunostimulation.
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PMID:Systemic macrophage stimulation in rats with silicosis: enhanced release of tumor necrosis factor-alpha from alveolar and peritoneal macrophages. 191 Aug 24

Electron spin resonance (ESR) measurements show that grinding of quartz particles in air produces silicon-based (Si. and SiO.) radicals which decay with aging in air. ESR spin trapping measurements provide evidence for the generation of hydroxyl and possibly superoxide radicals from a suspension of fresh quartz particles. The hydroxyl radical generation potential of the fresh quartz particles decreases on storing in ambient air and on the addition of catalase, superoxide dismutase, desferroxamine, or DMSO. Silica-induced lipid peroxidation also decreases on storing the fresh particles in ambient air. These findings suggest that oxygenated radicals play a role in the biochemical mechanism of pneumoconiosis in general and acute silicosis in particular.
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PMID:ESR spin trapping and cytotoxicity investigations of freshly fractured quartz: mechanism of acute silicosis. 216 64

A single intratracheal injection of 50 mg crystalline silica (quartz) into rats produces silicosis. This animal model may be used to study collagen metabolism during the early, middle, and late phases of lung injury, corresponding respectively to the stages of lung injury, development of discrete granulomas, and development of mature silicotic nodules. The early phase is characterized by a rapid increase in the rate of synthesis of lung collagen (within one week of instillation) and increased deposition of excess lung collagen (significant increases within two weeks of instillation). Later phases are characterized by a continuing increase in deposition of excess lung collagen for at least one year after instillation. Silica-induced fibrosis is unique among all the animal models (and in most human fibrotic diseases) thus far examined, in that the excess collagen deposited in the lung contains normal ratios of the two major collagen types of the lung: types I and III. This collagen is nonetheless biochemically different from normal lung collagen. There are reproducible and characteristic differences in the intermolecular cross-links of the collagen in lungs from rats injected with silica. Within one month of silica instillation (the earliest time point examined thus far), an increased hydroxylysine content of collagen can be appreciated. The reducible dysfunctional cross-links are also more likely to be derived from hydroxylysine (i.e. the ratio of dihydroxylated to monohydroxylated cross-links increases). Within four months of silica instillation (and increasingly thereafter), increased amounts of the mature trifunctional cross-link hydroxypyridinium (derived from three residues of hydroxylysine) can also be appreciated, seemingly paralleling the evolution of mature silicotic nodules in these lungs. These changes in cross-linking of lung collagen seem to be common to all the animal models of pulmonary fibrosis examined, and are also consistent with changes occurring in human fibrotic lungs. Preliminary observations suggest that the locus of cross-linking remains the same: hydroxylysine replaces lysine in the primary structure of a specific collagen alpha chain to form the altered cross-links. Thus, there may be molecular markers for the collagen of fibrosis in diseased lungs.
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PMID:Effects of silica on lung collagen. 242 84

Several inhaled substances, from occupational or other environmental exposure, produce significant pulmonary disease and abnormalities demonstrated by pulmonary imaging. Areas of controversy and misconception relate principally to the extent and nature of both the clinical disease and the imaging abnormalities specific to each substance. The size and shape of the inhaled particles is an important determinant of the nature and severity of the disease produced, with fibrous shapes usually being the most pathogenetic. Fibrogenicity is another important pathogenetic characteristic of talc and kaolin, as well as asbestos. Talc produces four distinct forms of pulmonary disease, depending not only on the other substances with which it is inhaled, but also whether it is inhaled or injected intravenously. When inhaled alone, talc does not appear to produce significant pulmonary fibrosis or malignancy. Kaolin, mica, fuller's earth, zeolite, and fiberglass all vary in disease production according to their shape and fibrogenicity. Silica, diatomaceous earth, and other forms of silica are all highly fibrogenic and thus produce clinically obvious disease with sufficient inhalation. The largest particles usually produce nodular patterns in the upper pulmonary fields, as is typical of silicosis. The fibrous particles are more likely to manifest themselves as interstitial patterns in the lower pulmonary fields.
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PMID:Misconceptions regarding the pathogenicity of silicas and silicates. 253 43

A clinicopathological analysis was carried out on 50 cases of lung cancer with silicosis diagnosed from April 1975 to March 1988. All patients were males and the age distribution ranged from 47 to 85 years with a mean of 63.5 at diagnosis. They had been exposed to silica in tunneling for 3 to 42 years, with an average of 15.1. Forty eight cases smoked. Histologically, squamous cell carcinoma was the most common with 29 cases, followed by 10 small cell carcinomas, 6 adenocarcinomas, 4 large cell carcinomas and one adenosquamous carcinoma. Thirty seven tumors were located in peripheral regions, mostly upper lobe or S6, while 13 tumors were in large bronchi. As the most common histological types of lung cancer with silicosis were squamous cell carcinoma and small cell carcinoma, some carcinogens might be involved in tumorigenesis. Silica alone is not considered to be a carcinogen, however, silica containing adsorbed polycyclic aromatic hydrocarbons from cigarette smoking or from industrial pyrolysis can act as a carcinogen or promoter.
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PMID:[Silicosis and lung cancer]. 255 44

Silicosis is an interstitial lung disorder that is frequently associated with hypergammaglobulinemia and increased numbers of lymphocytes at sites of disease. To determine the effect of silica on the generation of immunoglobulin-secreting cells, mononuclear cells were stimulated with antigens or mitogens and placed into 1) high-density cultures (2.5 X 10(6) cells/ml) that were not exposed to silica, in which pokeweed mitogen (PWM)-induced generation of immunoglobulin-secreting cells was suppressed by the presence of monocytes; or 2) low-density cultures (0.5 X 10(6) cells/ml) that were not exposed to silica, in which PWM-induced generation of immunoglobulin-secreting cells was not suppressed. Silica added to PWM-stimulated high-density cultures significantly increased the numbers of immunoglobulin-secreting cells. Silica also significantly increased the numbers of immunoglobulin-secreting cells in high-density cultures stimulated with purified protein derivative and tetanus toxoid and augmented the proliferation of phytohemagglutinin-stimulated mononuclear cells (P less than 0.05). In contrast to high-density cultures, silica added with PWM to low-density cultures reduced the numbers of immunoglobulin-secreting cells. These studies suggest that silica can have potent regulatory effects on various cellular immune processes that are relevant to the lung.
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PMID:Divergent effects of silica on lymphocyte proliferation and immunoglobulin production. 284 Dec 79


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