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

The relation of chronic bronchitis and respiratory dysfunction to age, tobacco smoking, and occupational exposure to surface and underground mining operations were examined in a cross sectional survey of 1363 men employed in the Kalgoorlie mining industry in 1985. Overall, the prevalence of chronic bronchitis was 14%. Eleven per cent of the workers had obstructive lung disorder (FEV1/FVC less than 0.70) and 9% had restrictive lung disorder (FVC less than 0.80 of predicted for height and age). There was little change in the prevalence of chronic bronchitis from that observed in a survey of the same industry in 1961-2. Only 1% of the workers in 1985 had radiographic signs of silicosis compared with 22% in 1961-2. Age, smoking, and underground mining experience all exerted strong effects on the development of chronic bronchitis with or without associated respiratory function abnormalities. After control of confounding by age and smoking, it was estimated that compared with a lifetime non-miner, the odds ratio (OR) of chronic bronchitis was 1.8 (95% confidence interval, 1.0-3.3) for one to nine years underground mining gold, 2.5 (1.2-5.2) for 10-19 years, and 5.1 (2.4-10.9) for 20 or more years. Underground mining of minerals other than gold was also associated with chronic bronchitis (OR = 5.1; 95% CI, 1.1-25.0) whereas exclusive surface mining had only a small empirical effect (OR = 1.3; 95% CI, 0.6-2.5). It is estimated that the proportion of cases of chronic bronchitis in working underground miners due to occupational factors is 50%. The results support the existence of an industrial cause of chronic bronchitis, although caution must be exercised in generalising the results to miners with progressive and sever respiratory impairment.
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PMID:Determinants of chronic bronchitis and lung dysfunction in Western Australian gold miners. 368 16

The computed tomographic (CT) appearance of interstitial lung disease was assessed in 23 patients with known interstitial disease. These included seven patients with fibrosing alveolitis, six with silicosis, two with hypersensitivity pneumonitis, three with lymphangitic spread of tumor, two with sarcoidosis, one with rheumatoid lung disease, and two with neurofibromatosis. The CT appearance of the interstitial changes in the different disease entities was assessed. Nodules were a prominent CT feature in silicosis, sarcoidosis, and lymphangitic spread of malignancy. Distribution of nodules and associated interlobular septal thickening provided further distinguishing features in these diseases. Reticular densities were the predominant CT change in fibrosing alveolitis, rheumatoid lung disease, and extrinsic allergic alveolitis. A marked peripheral predominance of the interstitial densities was seen in all seven cases of fibrosing alveolitis and in the patient with rheumatoid lung, in marked contrast with the two cases of hypersensitivity pneumonitis in whom a central distribution of the changes was seen. The observed patterns correlate with the pathologic findings and provide information that at times cannot be obtained from the chest radiograph. CT can be useful in the investigation of selected instances of interstitial pulmonary disease.
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PMID:CT in the diagnosis of interstitial lung disease. 392 66

The retrospective evaluation of 472 judgements of professional disease in persons exposed to dusts showed that all observed restrictions of cardio-pulmonary function (obstructive lung disease, increase of residual volume, respiratory failure, pulmonary hypertension) occurred almost independently from the presence and stage of silicosis, but correlated first of all with the duration of exposure. Frequency and degree of functional disorders in exposed persons without radiologically demonstrable silicosis indicate that the fraction of nonspecific dusts, which is by far larger than the SiO2-fraction, produces chronic obstructive lung disease and its sequelae (emphysema, pulmonary hypertension). The term "pneumoconiosis" should therefore be used in a much broader sense than hitherto. This leads to considerations of the present practice of judgement on silicosis which are presented and discussed in detail.
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PMID:[Interpretation of pneumoconiosis--results of cardiopulmonary function tests in dust-exposed patients with and without silicosis]. 401 1

Between 1972 and 1981, 38 patients suffering from lung disease by atypical mycobacteria were admitted to our institute. 36 out of them were males and 2 females with an average age of 55 years. In 10 patients silicosis was present. The patients received chemotherapy at special combinations using Rifampicin, Ethambutol and one or two additional drugs. 2 patients could be healed by lung lobe resection. In 12 patients x-ray regression could be observed. In the remaining patients, stabilization of the lung lesions and sputum conversion--at least temporarily--could be obtained. Because of multiple drug resistance, the therapy of mycobacteriosis is complicated, and permanent conversion of sputum cannot always be obtained, especially in diseases caused by M. intracellulare-avium. Bacteriological relapses are to be expected in 30 to 40 percent.
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PMID:[Therapeutic results in lung diseases caused by atypical mycobacteria]. 620 70

72 cases of diffuse interstitial lung diseases were observed from 1969 to 1976. Specimens removed from 47 patients were subjected to the whole spectrum of reactions. According to variation of both elastin and collagen, the following groups were outlined: group A: mycobacteriosis, farmer's lung, sarcoidosis and silicosis; group B: chronic eosinophilic pneumonia, lymphocytic interstitial pneumonia, post-tuberculous pulmonary fibrosis, and group C: X-ray pneumopathy, desquamative interstitial pneumonia, sclerodermic pneumopathy and chronic pulmonary fibrosis (primary chronic fibroadenomyosis). Each of these groups presents a close relationship between histochemical, radiological, clinical and functional findings.
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PMID:Diffuse interstitial lung diseases: a histochemical approach. 623 29

Silicosis and asbestosis are two forms of fibrotic lung disease resulting from the inhalation of inert materials indigestible by pulmonary alveolar macrophages. Results of studies of the host response to these particulates have not always been consistent. It is clear, however, that after phagocytosis, both cause alveolar macrophage damage, with resultant release of macrophage products, including fibrogenic factors and chemotactic factors for neutrophils. The latter cells also release lysosomal enzymes and free radicals when exposed to silica and asbestos. The net effect of these observations suggests that the combination of tissue damage and fibroblast stimulation results in the pulmonary fibrosis characterizing these diseases. Patients with silicosis and asbestosis have normal or decreased cell-mediated and increased humoral immunity with a high incidence of circulating immune complexes and autoantibodies. Whether these abnormalities are related to the pathogenesis of pulmonary fibrosis or are epiphenomena remains to be determined.
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PMID:Current concepts about the pathogenesis of silicosis and asbestosis. 628 50

The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response, appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. The insidious and probably most important human lung disease due to particles is bronchiolar obstruction and obliteration, producing progressive impairment of air flow. The responsible particle is the complex combination of poorly digestive lipids and complex carbohydrates with active chemicals which we call cigarette smoke. More research is needed to perfect, correct and quantify our preliminary picture of the pathogenesis of lung disease by particles, but a useful start has been made.
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PMID:Particles causing lung disease. 637 14

Epidemiological data show that chronic diseases of the respiratory apparatus have constantly increased over the last 20 years or so, often involving relatively young age classes. The increased survival rates due to chemotherapy also increase the importance of rehabilitation in such diseases. The officially accepted concept of a "global" rehabilitation is particularly significant in the case of patients of working age. The main rehabilitation procedures include chest physiotherapy, aerosol therapy, oxygen therapy (where selection criteria have been established and where there are new prospects related to long-term oxygen therapy), intermittent positive pressure breathing and physical retraining. Details on the methods of assessment and training and data concerning three groups of patients suffering from respectively chronic obstructive lung disease, silicosis and asbestosis, are given. The data show a general pattern of a decrease in ventilation (for an unchanged level of O2 uptake and CO2 output) and reflect a rise in muscular efficiency (exercising and respiratory) enabling the body to perform the same work load at a lower energy cost. The authors discuss the vocational rehabilitation of the patient with lung disease and illustrate the most useful procedures in the assessment of the subject, the environment and the place of work, including guidelines to achieve this. Rehabilitation treatment is also summarized into a number of stages, with the goals at different therapeutic levels and the ways to reach them.
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PMID:[Rehabilitation of the worker with bronchopneumopathy]. 648 73

Pulmonary blood volume (PBV) was measured by double injection (pulmonary artery trunk and wedged pulmonary artery) in 43 patients with chronic lung disease, at rest supine, with the legs raised, and during light exercise. At rest, PBV was reduced slightly in group 1 (eight with silicosis), but notably in groups 2 (16 bronchitis patients) and 3 (19 patients! with pulmonary vascular restriction). With the legs raised, PBV increased by 14 percent in group 1, 7 per cent in group 2, and 5 percent in group 3. From rest to exercise, the pressure increase was much greater in groups 2 and 3 than in group 1. The slope of the pressure-volume curve, delta V/delta P, was lower in groups 2 and 3, which could mean that lung vessel distensibility was reduced in these groups, or that, despite its low value, PBV was near its maximum capacity already at rest.
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PMID:Pulmonary blood volume in chronic lung disease: changes with legs raised and during exercise. 707 74

Male CFY rats were injected into their trachea with a suspension of dust of ore mine dead rock of high quartz content and mixed composition (particle size: 0-60 micrometers). Three and six months after treatment, foreign body granulation and after twelve months a non-fibrotic diffuse lung disease was seen in the animals. After twelve months of exposure, non-specific, mature sinus histiocytosis and small focal epitheloid cell reaction were found to develop in the cervical, lung-hilar and retroperitoneal lymph nodes. The histopathological changes were compared with those seen in experimental silicosis induced by DQ12 quartz. It is concluded that the hazardous effect of industrial dusts is not identical with their fibrogenic effect.
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PMID:Experimental pneumoconiosis due to dusts of ore mines, I. 709 Aug 62


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