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

Although the risks connected with occupational exposure to asbestos and its numerous industrial uses are widely known, it still happens that instances of exposure with high potential risk are discovered. A detailed study of a worker suffering from silicosis and asbestosis who had worked for many years in a firm dealing with the recovery and re-use of used jute sacks also containing asbestos, revealed the existence of a real asbestosis risk in the firm, with the result that other workers in the same firm were studied. A total of 22 subjects were studied, 17 of whom also underwent bronchoalveolar lavage (BAL) and determination of the cellular composition of the recovery liquid in order to establish the presence of asbestous alveolitis. The age of the subjects ranged between 39 and 75 years (x = 56.36), length of service in the firm ranged between 2 and 18 years (x = 9.27), time between start of exposure and clinical examination varied between 29 and 50 years (x = 40.27). The 22 subjects were divided into 3 groups on the basis of the radiological examinations: 1) 8 cases were negative (36.36%); 2) 8 cases had pleural alterations only (36.36%); 3) 6 cases had interstitial lung disease (with and without pleural lesions) (27.27%). Of the 17 subjects who underwent BAL, 7 were in the first group, 7 in the second and 3 in the third. Among these 17 subjects BAL showed absence of alveolitis in all subjects of the first group, diagnosis of alveolitis in only some of the second group, and in all of the third group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An unusual exposure to asbestosis risk in a bag manufacturing plant: observations on 22 cases]. 207 27

The data on airborne dust and occupational disease in the main dust-related industries of the People's Republic of Bulgaria are generalized and analyzed for a period of 15 years. In the ore producing industry is established a stability in the concentration of total and respirable dust 1-2 TWA concentrations and decrease of silica content in dust. The highest occupational hazard is registered in diggers. The levels of TWA total and respirable dust and silica concentrations in the other underground mines as well as in the overground industries are strongly variable and high. Silicosis is still in the first place among dust-related diseases, but mainly among miners of advanced age. The newly detected other pneumoconiosis, asbestosis, mixed pneumoconiosis are already more than the cases of silicotuberculosis. An essential part is taken by the newly detected diffusive pneumosclerosis and dust bronchitis. The distribution of the newly detected occupational lung diseases is studied according to branches of industry.
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PMID:[Dust levels and dust-induced diseases in the main dust-producing industries]. 209 45

The authors have carried out a statistical analysis of cases of occupational asthma and other occupational lung diseases submitted to the Ministry of Labour in Quebec between 1986 and 1988. The total number of claims was 913, 993, and 866 respectively for the 3 years of which 61% to 71% were accepted. 41% to 55% were new assessments. Of 228 new claims accepted in 1988, 81 (36%) were for occupational asthma. This number surpassed the number of claims accepted for traditional pneumoconiosis (asbestos = 30, and silicose = 36). Isocyanates were the principle cause of occupational asthma (23% of cases were recognised in 1988) followed by flour, red and white cedar, snow crab process workers, and various pharmaceutical products and grains. In comparison with statistics in 1977, one noticed there was a large reversal of the frequency of certain occupational lung diseases that are recognised, because at that time asbestosis and silicosis were the principle causes of claims put forward and accepted. The authors discuss the statistical bias of occupational lung disease obtained by medico-legal agencies. Although occupational asthma has not been the object of the systematic screening program in the work place and although there is a tendency for workers to avoid or abandon their occupation more often than in the traditional pneumoconioses current protection is sufficient in Quebec to motivate individuals who are possibly suffering from occupational asthma to put in a claim for compensation.
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PMID:[Medico-legal statistics on occupational asthmna in Quebec between 1986 and 1988]. 214 54

Asbestosis and silicosis are chronic, fibrosing lung diseases due to prolonged inhalation of asbestos fibers or silica particles. However, little is known about the implication of these toxic dusts on cell-mediated cytotoxicity. Among the first types of cells that are in contact with the dusts are the alveolar macrophages (AM). We studied the effect of different concentrations of UICC chrysotile asbestos and silica on 18-h cytotoxicity of AM against tumor necrosis factor (TNF)-resistant P815 target cells or TNF-sensitive L929 target cells. Rat AM, obtained by bronchoalveolar lavage, were incubated for 2 h with 20, 50, or 100 micrograms/ml chrysotile or silica before the addition of target cells. AM cytotoxicity was significantly inhibited at greater than 20 micrograms/ml of chrysotile. In contrast, silica did not inhibit AM-mediated cytotoxicity at any concentration used. Asbestos, but not silica, caused significant production of PGE2 by macrophages and target cells. Addition of the cyclooxygenase inhibitor indomethacin to our system abolished all inhibition by asbestos. These results suggest that the inhibition of AM-mediated cytotoxicity by chrysotile was caused by prostaglandins, and that fibrogenic particles differ in their capacity to modulate AM function.
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PMID:Inhibition of alveolar macrophage cytotoxicity by asbestos: possible role of prostaglandins. 215 23

Epidemiologic surveys have indicated an excess of nonmalignant respiratory disease in workers exposed to aluminum oxide (Al2O3) during abrasives production. However, clinical, roentgenographic, histologic, and microanalytic description of these workers are lacking. This is a report of nine Al2O3-exposed workers with abnormal chest roentgenograms (profusion greater than or equal to 1/0, ILO/UC) from a plant engaged in the production of Al2O3 abrasives from alundum ore. Mean duration of exposure was 25 yr, and time since first exposure was 28 yr. in a subgroup of three, the severity of symptoms, reduction in the forced vital capacity (67% predicted) and diffusing capacity (51% predicted), and progressive roentgenographic changes (profusion greater than or equal to 2/2) prompted open lung biopsy. Lung tissue was analyzed by scanning electron microscopy and electron microprobe analysis. In each of the three biopsies, interstitial fibrosis with honeycombing was seen on routine section. In one biopsy, silica and asbestos fiber counts were at the low end of the range seen with silicosis and asbestosis; however, the absence of asbestos bodies and silicotic nodules suggested that the fibrosis was due to another cause. Metals occurred in amounts several orders of magnitude above background, and the majority was aluminum as Al2O3 and aluminum alloys. The findings in these nine workers suggests a common exposure as the possible cause. The nonspecific pathologic findings, absence of asbestos bodies and silicotic nodules, and the striking number of aluminum-containing particles suggest that Al2O3 is that common exposure. The possibility of "mixed dust" fibrosis should also be considered.
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PMID:Pulmonary fibrosis in aluminum oxide workers. Investigation of nine workers, with pathologic examination and microanalysis in three of them. 224 Aug 41

The history of class conflict in occupational health in the United States is illustrated by the current Pittston Company attack on coal miners' health benefits, the silicosis and asbestosis controversies, the corporate restrictions on state workers' compensation laws, and the unremitting management opposition to the federal Coal Mine Health and Safety Act of 1969 and the Occupational Health and Safety Act of 1970. A positive action program is presented as the basis for convening the long-overdue White House Conference on Occupational Health and Safety. Mining engineers are urged to support that action program to prevent unnecessary work-related death and disability.
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PMID:Occupational health: a classic example of class conflict. 233 90

A pilot study was performed to assess the prevalence of hyperreactive bronchial system (HBS) in various occupational lung diseases. 204 patient records were evaluated with the following diagnosis: Allergic rhinitis: (N = 25, 12%), allergic bronchial asthma (N = 70, 34%), toxic asthma (N = 22, 11%), silicosis (N = 12, 6%), asbestosis (N = 15, 7%), farmer's lung (N = 12, 6%), chronic unspecific respiratory syndrome (N = 48, 24%). In each case an inhalative methacholine test (MCHT) was performed. HBS was considered to be present whenever there was a resistance increase of more than 100% of the baseline values. The prevalence of HBS varied between 50% (asbestosis) and 77% (toxic asthma); the average was 68%. Allergic diseases showed a higher prevalence of 71% in comparison to nonallergic diseases with 65%. Patients with silicosis or asbestosis and without additional chronic bronchitis or emphysema demonstrate a "normal" prevalence of HBS of 11%. Age, gender, smoking, alcohol, family history of allergy and repeated bronchitis, the number of eosinophils in the blood. IgE concentration in serum showed no significant association with an increased prevalence of HBS. The coincidence of anamnestically affirmed or denied bronchial hypersensitivity to environmental factors, and the positive or negative result of the MCHT test, was relatively low, being only 43% in case of a "positive" test and 17% in case of a "negative" test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pilot study of the prevalence of a hyperreactive bronchial system in various occupationally-induced lung diseases]. 238 88

A survey of 762 New Jersey physicians showed that 35% reported seeing patients with either asbestosis, coal worker's pneumoconiosis, occupational asthma or silicosis. Three to four times as many patients with these diagnoses were seen as outpatients as were hospitalized. The implications of these results in using hospital discharge data for occupational disease surveillance are discussed.
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PMID:Surveillance of occupational lung disease: comparison of hospital discharge data to physician reporting. 240 39

Pathohistological findings are playing an important role in the advice of toxic organ damages. After presentation of some details about the frequency of toxic organ damages, the pathways of toxic agents in the organism are discussed. In cells toxic damage may induce cell necrosis, functional disturbance, inhibition of cell proliferation or malignant transformation; in extracellular structures it may lead to degradation phenomena in the connective tissue matrix. As demonstrated in example of calciphylaxis, a combination of different noxes may not only add but even potentiate the effects of the single noxes. In intracellular reparation processes the lysosomal system is involved. In case of necrosis regeneration is possible in most kinds of tissues, if connective tissue rails are preserved. Otherwise an irreversible reparative fibrotic alteration of organ structure is induced which develops according to particular general and schematic rules. As mostly character and course of the tissue reaction is unspecific, pathohistological findings do not enable conclusions on the type of inducing toxic agent. The following presentation of some examples of toxic damages with pathognomonic histological appearance deals with asbestosis, silicosis, chloroquine-induced cardiomyopathy, aluminum-induced osteopathy and a recently described liver cirrhosis in early childhood induced by copper-containing drinking water. Some limits of traditional pathohistological evaluation of toxic organ damages have been overcome by application of new morphological techniques. Own investigations revealed that the immunocytochemical demonstration of the C5b-9-complement complex enables a better and earlier detection of irreversibly damaged cells. Discrimination of toxic and virus-induced tissue damage is facilitated by the technique of in-situ-hybridization. Sometimes a specific recognition and localization of toxic agents is achieved by X-ray microanalysis, electron-spectroscopic imaging (= ESI) resp. laser microprobe mass spectrometry (= LAMMA); comparing these techniques X-Ray microanalysis and ESI, both, enable specific identification of chemical elements, while LAMMA, in addition, offers some information about the involved molecules and isotopes.
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PMID:[Toxic organic damage]. 265 Apr 56

Prolonged asbestos and silica inhalation is associated with pulmonary inflammation and fibrosis. Several studies suggest that TNF may play a role in the development of inflammation and fibrosis. We studied TNF production in a murine model of asbestosis and silicosis. Asbestos fibers caused a significant inflammatory response at two weeks and pulmonary fibrosis beginning at one month. Pulmonary inflammation was principally caused by an accumulation of neutrophils (0.88 x 10(5) neutrophils/compared to 0.05 x 10(5) in controls). TNF production by bronchoalveolar cells was higher in asbestos-instilled mice at two weeks, but was significantly diminished in older mice. Pulmonary inflammation was observed until six months in silica-instilled mice. Neutrophils were also the principal protagonists of the inflammation. In this group, severe fibrosis was observed at two weeks. TNF production in silica-instilled mice was similar to controls, possibly due to the presence of large numbers of neutrophils (3.3 x 10(5)/lavage) that could adsorb TNF. In vitro experiments showed an augmentation of TNF production by bronchoalveolar cells in the presence of silica. Taken together, our data suggest that asbestos and silica stimulate alveolar macrophages to produce TNF, which can be involved in pulmonary inflammation and fibrosis.
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PMID:Pulmonary inflammation and fibrosis in a murine model of asbestosis and silicosis. Possible role of tumor necrosis factor. 275 23


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