Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SILICOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed2001

Lung tissue mechanics and extracellular matrix composition in a murine model of silicosis.

The dynamic mechanical properties of lung tissue and its contents of collagen and elastic fibers were studied in strips prepared from mice instilled intratracheally with saline (C) or silica [15 (S15) and 30 days (S30) after instillation]. Resistance, elastance, and hysteresivity were studied during oscillations at different frequencies on S15 and S30. Elastance increased from C to silica groups but was similar between S15 and S30. Resistance was augmented from C to S15 and S30 and was greater in S30 than in S15 at higher frequencies. Hysteresivity was higher in S30 than in C and S15. Silica groups presented a greater amount of collagen than did C. Elastic fiber content increased progressively along time. This increment was related to the higher amount of oxytalan fibers at 15 and 30 days, whereas elaunin and fully developed elastic fibers were augmented only at 30 days. Silicosis led not only to pulmonary fibrosis but also to fibroelastosis, thus assigning a major role to the elastic system in the silicotic lung.

Algorithms↗
PubMed1989

Polyarteritis nodosa and necrotizing glomerulonephritis associated with long-standing silicosis.

A 55-year-old white male, with silicosis diagnosed 10 years earlier, presented massive proteinuria with microscopic hematuria, moderate renal failure and distal polyneuropathy. Bilateral renal angiography showed multiple intraparenchymal saccular aneurysms. Renal biopsy disclosed a focal segmental necrotizing glomerulonephritis and arteriolitis. After combined corticosteroid and immunosuppressive treatment, renal function improved and remained stable 6 months later.

Glomerulonephritis↗
PubMed1975

[Mechanics of breathing and exertion dyspnea in silicosis (author's transl)].

Mechanics of breathing as studied in patients with different stages of silicosis in rest and during exercise show the following: dynamic compliance and work against elastic and viscous resistances could not be found to be decisive indices of exertion dyspnea. Evidence of exertion dyspnea could only be achieved by means of the ration VT/PT (VT equals tidal volume, PT equals tidal esophageal pressure). Exertion dyspnea was observed at less than 0,081 VT per cm H20 PT. In accordance with Campbell and Howell, dyspnea is seen as an inappropriateness between ventilation and pressure needed.

Dyspnea↗
PubMed1995

Alveolar fibrosis and capillary alteration in experimental pulmonary silicosis in rats.

To analyze the evolution of fibrotic and vascular changes in pulmonary silicosis, ultrastructural and immunohistochemical studies were made of the lungs of rats given a single intratracheal injection of silica particles. Early lesions were characterized by accumulations of macrophages and neutrophils in alveolar lumina and interstitium and by damage to alveolar capillaries and epithelial cells. The intraluminal masses of inflammatory cells developed into granulomas and became associated with myofibroblasts that migrated from the interstitium through the damaged epithelial lining. Type II epithelial cells and bronchiolar cuboidal cells proliferated rapidly to line the intraluminal granulomas, incorporating them into the interstitium. This process mediated the transition from intraalveolar fibrosis to interstitial fibrosis. Vascular damage was repaired by proliferation and migration of endothelial cells. Some endothelial cells in alveolar capillaries expressed Factor VIII-related antigen at 2 wk after silica infusion. In normal animals, this feature was present in peribronchiolar but not in alveolar capillaries. Two patterns of endothelial cell migration were shown by staining for proliferating-cell nuclear antigen. The first pattern was characterized by endothelial cells that extended their cytoplasm over preexisting, denuded basement membranes and replaced necrotic cells in alveolar capillaries. At 4 mo after injury, some of these cells had developed fenestrations. The second pattern consisted of budlike sproutings that developed only in peribronchiolar connective tissue. These observations indicate that peribronchiolar vessels are sources for renewal of alveolar capillary endothelium as well as for neovascularization.

Animals↗
PubMed1998

Radiographic evidence of silicosis risk in the diatomaceous earth industry.

There is limited and conflicting evidence regarding the exposure-response relationship between exposure to crystalline silica and silicosis; the level of risk to current workers remains uncertain. We conducted an epidemiologic investigation of 1,809 workers in the diatomaceous earth industry, where exposures to crystalline silica are primarily to the cristobalite form. On the basis of the median of three independent readings, 81 (4.5%) workers were judged to have opacities on chest radiographs (small opacities, profusion >= 1/0, and/or large opacities). Age-adjusted relative risk of opacities increased significantly with cumulative exposure to crystalline silica. The concentration of respirable crystalline silica to which workers were exposed (highly correlated with period of hire) was an important determinant of risk after accounting for cumulative exposure. For workers with an average exposure to crystalline silica of <= 0.50 mg/m3 (or hired >= 1950), the cumulative risk of opacities for a cumulative exposure to crystalline silica of 2.0 mg/m3-yr was approximately 1.1%; for an average exposure > 0.50 mg/m3 (or hired < 1950), the corresponding cumulative risk was 3.7%. These findings indicate an exposure-response relationship between cumulative exposure to crystalline silica and radiographic opacities; moreover, the relationship was substantially steeper among workers exposed at the highest average concentrations of crystalline silica.

Adult↗
PubMed1989

Lymphocyte populations in lung tissue, bronchoalveolar lavage fluid, and peripheral blood in rats at various times during the development of silicosis.

Inflammatory cells and lymphocyte populations were examined in the bronchoalveolar lavage (BAL) fluid, lung tissues, and peripheral blood from rats at various times after the intratracheal instillation of silica. In lavage fluid, there was a rapid initial increase in the percentage and number of polymorphonuclear leukocytes (PMN), which slowly decreased during the course of the experiment. In addition, compared to controls, there was an increased number and percentage of lymphocytes throughout the 75 days of the experiment. The lymphocytic populations, which were determined by an indirect immunofluorescence method with monoclonal antibodies to lymphocyte surface markers, showed a predominance of the T-helper phenotype from Day 14 through the end of the experiment (Day 75). The number of PMNs obtained from collagenase digest of the lung was increased over control levels up to Day 7 after silica administration and remained at a relatively constant level until Day 14, after which time they decreased slightly in number. The total number of lymphocytes peaked on Day 14, with cells of the T-helper phenotype predominating after this time. In the peripheral blood, T-helper cells from silicotic rats were significantly increased over control rats on Days 7 and 14 but returned to normal control values after this time. The lymphocyte subsets in the BAL, but not in the peripheral blood, more closely reflect the lymphocyte patterns in the lung. The results of these experiments suggest that T-helper cells may play an important role in the inflammatory-fibrotic events in the lungs of rats with silicosis.

Animals↗
PubMed1989

The utility of bronchoalveolar lavage and transbronchial lung biopsy combined with energy-dispersive X-ray analysis in the diagnosis of silicosis.

We used analytical electron microscopic techniques, including energy-dispersive X-ray analysis, to evaluate a patient with diffuse infiltrates and a history of silica exposure. We identified silica particles in digested bronchoalveolar lavage fluid, sectioned alveolar macrophages recovered by lavage, and parenchymal specimens obtained by transbronchial biopsy. This analysis confirmed our clinical suspicion (a sporadic case of accelerated silicosis) and eliminated the need for additional, more complicated, diagnostic procedures.

Adult↗
PubMed1991

Acute silicosis due to inhalation of a domestic product.

A 20-yr-old woman with no history of pulmonary disease presented with acute dyspnea and fever. After various investigations and treatments the symptoms persisted and a lung biopsy was performed. Pathologic analysis disclosed the presence of silicotic crystals within lung tissue and mediastinal lymph nodes. The patient admitted having repeatedly inhaled a domestic scouring powder rich in silica during the preceding 6 months. This is the first report of acute pulmonary silicosis developing after exposure to a common household product.

Acute Disease↗
PubMed1991

Computed tomography scan in the early detection of silicosis.

We evaluated the ability of both the conventional and high resolution computed tomography (CCT and HRCT, respectively) scans of the thorax to detect early silicosis in subjects exposed to silica dust in the mines and foundries of Québec for an average of 29 +/- 2 yr. The study was limited to subjects with chest radiograph (CR) of the International Labor Organization (ILO) Categories 0 or 1 as determined independently a priori. All subjects had a standard high-kilovoltage posteroanterior and lateral CR, a set of 10 to 15 1 cm collimation CCT scans, and a set of three to five 2 mm collimation HRCT scans in the upper, middle, and lower lung fields. For each CR and sets of CT scans, readings were done independently by four experienced readers. For small opacities of the lung parenchyma on CR, 32 of the 51 subjects were normal (Group A), six were indeterminate (Group B), and 13 were abnormal (Group C). By the combined readings of HRCT and CCT, 13 of the subjects (40%) in Group A were abnormal (p less than 0.001); four of the subjects in Group B were abnormal, and in Group C, one subject was normal, one indeterminate, and 11 (84%) abnormal. For confluence of small opacities, 48 of the 51 subjects were negative (Group 0), and three were positive (Group 1) on the CR. By the CT scan, 42 of the 48 subjects in Group 0 were negative, and the three subjects in Group 1 were positive; thus the CT scan added six positive cases with confluence of small opacities (six of 48, 12.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1977

Acute silicosis in tombstone sandblasters.

Four men developed silicosis after sandblasting tombstones for an average of 35 months; 3 of them died an average of 59 months after their first exposure to sandblasting. Lung tissue demonstrated noncaseating granulomas and silicotic nodules involving small arteries and veins in 3 patients and alveolar proteinosis in 2. X-ray energy spectrometry showed primarily elemental silicon in the lung parenchyma. One patient developed lupus erythematosus and another focal glomerulonephritis. Two developed pneumothorax. None had cultural or morphologic evidence of tuberculosis. Pulmonary function studies in all 4 patients revealed a restrictive pattern. Industrial investigations revealed that the patients wore inadequate personal protection equipment and were exposed to 5 times the threshold limit value for respirable silica.

Acute Disease↗
PubMed1977

Cell-mediated immunity in silicosis.

Selected parameters of cell-mediated immunity were determined in a group of 16 patients with silicosis. The results were compared with those of a control group of 13 subjects without silica exposure. There were no group differences in the mean number of delayed hypersensitivity skin tests to a battery of recall antigens (purified protein derivative, candida, streptokinase-streptodornase, and trichophyton) or in the mean number of peripheral blood lymphocytes. Lymphocyte responsiveness to phytohemagglutinin, pokeweed mitogen, and the antigens listed, and the percentage of lymphocytes that formed sheep red blood cell rosettes (t cells) and complement rosettes (B cells) were also similar in both groups; however, the silica-exposed group demonstrated depressed lymphocyte stimulation in response to low concentrations of concanavalin A.

Humans↗
PubMed2002

Apoptosis underlies immunopathogenic mechanisms in acute silicosis.

We investigated immunopathogenic roles for apoptosis in acute murine silicosis. Intratracheal silica instillation induced pulmonary inflammation and enlarged thoracic lymph nodes. Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and markedly increased activation-induced cell death, compared with control lymphocytes from saline-exposed lymph nodes. CD4(+) T cell death was mediated by Fas ligand, because CD4(+) T cells from Fas ligand-deficient gld mice did not undergo activation-induced apoptosis. Silica deposition also resulted in increased apoptosis associated with inflammatory infiltrates in lung parenchyma. In vivo treatment with caspase inhibitors reduced neutrophil accumulation, and alleviated inflammation in the lungs of silica-treated mice. These results suggest that silica-induced apoptosis plays an inflammatory role in the lung parenchyma, and creates immunologic abnormalities in regional lymph nodes, with pathogenic implications for the host.

Acute Disease↗
PubMed1984

Silica-stimulated monocytes release fibroblast proliferation factors identical to interleukin 1. A potential role for interleukin 1 in the pathogenesis of silicosis.

Previous study strongly suggests that silicotic fibrosis is mediated by macrophages and their soluble mediators. The biochemical properties of the mediators involved in silicotic fibrosis, however, are as yet ill defined. The current study, therefore, determined whether human monocyte-macrophages treated with fibrogenic silica dust released factors capable of activating fibroblasts as measured by an increase in fibroblast proliferation. Silica, but not nonfibrogenic diamond dust, stimulated the release of fibroblast proliferation factors. Moreover, the level of fibroblast proliferation activity was comparable with the level of thymocyte proliferation (interleukin-1) activity in the same culture supernatants. The factors responsible for these seemingly diverse activities were found to behave identically when analyzed by gel filtration chromatography, size exclusion chromatography, isoelectrofocusing, ion exchange chromatography, and hydrophobic chromatography. Moreover, the response of these factors to four different proteases and heat (56 degrees C) was also identical, which shows that their comigration on various separation media could not be explained by noncovalent interaction between otherwise unrelated species. The data demonstrate that a monocyte-derived thymocyte proliferation factor having the molecular properties of interleukin 1 is capable of regulating fibroblast proliferation. In silicosis and other fibrotic diseases, the local release of interleukin 1 may contribute to abnormal connective tissue deposition by stimulating fibroblast proliferation, and thereby, amplifying other signals stimulating the synthesis of connective tissue components.

Cells, Cultured↗
PubMed2002

Broncholithiasis and lithoptysis associated with silicosis.

A case of broncholithiasis associated with massive silicosis is reported, showing a rare aspect of parenchymal lesions generating broncholiths as well as the presence of recurrent lithoptysis, with subsequent regression of radiological lesions. Aetiological, clinical, physiopathological, and radiological aspects of the disease are discussed, demonstrating the importance of the use of computed tomography in diagnosis. The mineralogical analysis of expectorated fragments is also shown.

Adult↗
PubMed1989

Trends and perspectives of the biological prophylaxis of silicosis.

Based on earlier paper in this journal, as well as on new data concerning factors predetermining individual susceptibility to silicosis, we propose a comprehensive system of recommendations aimed at increasing the working population's resistance against the harmful action of silica dust. These recommendations consider, on one hand, the criteria of possible selection for employment in dusty industries of individuals who do not possess characteristics making them especially sensitive to this harmful action (collective biological prophylaxis), and on the other hand, the influences that could diminish such sensitivity (individual biological prophylaxis). Some ethical and practical problems of the biological prophylaxis of occupational diseases and a mathematical approach to predicting its effectiveness are also discussed.

Age Factors↗
PubMed1994

"Souvenir" casting silicosis.

A case of silicosis in a 47-year-old worker who was employed for many years in a small souvenir casting shop is described. This work site demonstrates many unfavorable characteristics of small industries, such as lack of awareness of the need for safety measures, exposure control, protection of workers, and lack of compliance with environmental and medical-legal standards.

Humans↗
PubMed1977

Silicosis in workers dealing with tonoko: case reports and analyses of tonoko.

We found three cases of pneumoconiosis among those workers who had been dealing with tonoko (a mineral powder) for more than ten years at a shop making wooden furniture in Sendai, Japan. In the factory the workers were exposed to tonoko dust and had been inhaling it for a long time. Until now, this disease has not been found in employees of furniture factories; and, furthermore, tonoko has not been regarded as a harmful material. Tonoko is a very fine mineral powder used widely in Japan for filling the grains of surfaces of wooden products. The three workers had scanty clinical symptoms; however, their chest x-ray films revealed disseminated nodulations throughout both pulmonary fields. One of the workers suffered from the complication of active pulmonary tuberculosis. Some of the analyses revealed that tonoko contained about 50% quartz. Accordingly, the disease is strongly suspected to be a sort of silicosis caused by inhalation of tonoko dust.

Airway Resistance↗
PubMed1979

Mixed pneumoconiosis: silicosis, asbestosis, talcosis, and berylliosis.

Mixed pneumoconiosis is pulmonary disease due to two or more inhaled mineral irritants. Chronic disease due to beryllium has not been a component of any described mixed pneumoconiosis. A man with occupational exposure to a combination of dusts developed severe pulmonary disease. Silicosis, talcosis, asbestosis, and berylliosis were all documented by an open biopsy of the lung. The varieties of mixed pneumoconiosis are summarized.

Asbestosis↗