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

An evaluation of the effects of dust prevention in the Jiangxi tungsten mines has been carried out. The rate of silicosis morbidity in most mines was under 1%. Up to 1983, the rate in individual mines is 1.95%. According to the data from those mines, the forecasting of cumulative probability of morbidity of mine workers having been in contact with dust for 30 years is up to 7.5%. From those data, the authors suggest that the maximum permissible concentration of dust should be 1.0 mg/m3 in the mines with concentration of silicon dioxide dust over 70%.
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PMID:[Evaluation of effects of dust prevention in the principal tungsten mines in Jiangxi]. 234 Jul 65

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

For the stimulation of research on scleroderma and the prophylaxis of occupational scleroderma-like diseases and the prevention of iatrogenic injuries, respect., it is important to know the inducing environmental substances. Plastics (vinyl chloride, epoxy resins), solvents (chlorinated, aromatic and aliphatic hydrocarbons), drugs (bleomycin, pentazocine), cocaine (abuse) and contaminated rapeseed oil are more or less able to induce scleroderma-like diseases. Vinyl chloride disease is the best known among these. The toxic oil syndrome represents the most inglorious example of the recent time. Paraffin and silicon can act as adjuvants and induce a progressive systemic sclerosis. In our studies it could be shown, that silica is able to induce not only a silicosis, but also a true progressive systemic sclerosis after long term exposure. Acknowledgment of such cases as an occupational disease is justified and regulated by law in the German Democratic Republic.
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PMID:[Scleroderma and scleroderma-like diseases caused by environmental pollutants]. 242 99

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

Inhalation of respirable crystalline silica dusts (sized between 0.5 and 5.0 micrograms) causes silicosis. Crystalline silica fillers are used in some composites and fine dusts/aerosols generated during high-speed finishing of these materials may be regularly inhaled by clinical dental personnel. Due to the widespread use of composites, the potential of these dusts/aerosols for causing silicosis warrants concern. Six composites were polymerized, then abraded with diamond and carbide finishing burs to produce dusts in a manner simulating the clinical finishing of esthetic veneers. Dusts were collected on 0.8 micron filters using an air sampling pump. Six hundred particles of each dust sample were counted and measured using a light microscope. The respirable fraction of dust particles ranged between 57.2 and 85.7%. The diamond bur created more respirable particles than the carbide bur for each composite tested. The elemental composition of particles of each composite was determined by energy dispersive x-ray analysis. Silicon was detected in amounts ranging from 71-100%. Based on the composition and particle size distribution only, dusts generated during simulated finishing of composite resins containing quartz filler have the potential for causing silicosis in dental personnel.
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PMID:Particle size and composition of composite dusts. 270 Jun 35

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

The recent finding of cases of silicosis among jade workers in Hong Kong points to this disease being an occupational hazard. The source was found to be the silica flour that was added in a polishing process. Five cases are described together with the results of environmental investigation in a workplace. In three cases the disease was of early onset, rapidly progressive, and presented the features of galloping silicosis noted in other occupational exposures to silica flour. One patient had massive fibrosis and severe glomerulonephropathy, an association that has also been previously noted. One case showed evidence of active tubercular infection in addition to silicosis and two had healed lesions. Silica concentrations in the workplace during the suepect process were well above accepted threshold limit values.
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PMID:Silicosis in jade workers. 299 34

A 54-year-old foundry worker with extensive silica exposure, but no pulmonary disease, developed the nephrotic syndrome and renal failure over a 3-month period. Renal biopsy demonstrated a proliferative glomerulonephritis; energy dispersive x-ray analysis detected silicon within the renal tubules. Measurements of respirable silica at the foundry revealed levels up to 2.5 times the current occupational standard. Similar glomerular disease has been reported in silica-exposed animals and workers with silicosis. This case suggests that clinicians should include silica exposure in the differential diagnosis of unexplained diffuse proliferative glomerulonephritis, renal disease may occur without clinically evident pulmonary disease in silica exposure, and silica-induced glomerulonephritis warrants further clinical and epidemiologic research.
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PMID:Silica and glomerulonephritis: case report and review of the literature. 303 97

To evaluate the biological effects of aluminum lactate therapy on nodular silicosis, we exposed the tracheal lobe of three groups of sheep containing eight sheep per group to either 11 mg of Al lactate in 100 ml saline (Al group), 100 mg of Minusil-5 in 100 ml saline (Si group), or 100 mg of Minusil-5 in 100 ml saline followed by 11 mg of Al lactate at monthly intervals 4 months after exposure (Si Al-treated group). The lung biological processes were evaluated by sequential lung lavage analyses of cellularity and biochemistry of supernatant and by autopsy analyses of cellularity and biochemistry of supernatant and by autopsy analyses of lung tissue histopathology and quartz content. Al lactate alone did not have any significant effect. Silica exposure produced the silicotic nodules and significant increases on lung lavage of cellularity, enzyme release, surfactant, and glycosaminoglycan accumulations. Al lactate therapy at month 4 after exposure did not decrease the pathological score of disease, but it significantly reduced all markers of cellular hyperactivity. This therapy was associated with a 65% reduction of the quartz retention in lung tissue and might help to prevent long-term progression of the disease process.
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PMID:Late aluminum therapy reduces the cellular activities of simple silicosis in the sheep model. 303 11


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