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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A laborer who worked in a steel mill and in a shipyard developed a nonspecific pulmonary interstitial fibrosis. Postmortem samples of his lung were digested, and the inorganic material present was extracted and examined using transmission electron microscopy, electron diffraction, and electron microprobe analysis. Uncoated asbestos fibers were present (1.4 X 10(5)/g wet lung), but the surprising finding was the presence of a large number of fly ash particles (6 X 10(6)/g wet lung). Fly ash, the particulate material produced during coal combustion, has not previously been reported to be present in human lung tissue. Although the contribution of the asbestos to this man's lung disease is uncertain, we believe, based on previous studies implicating aluminum silicates in pneumoconiosis, that the fly ash, an aluminum silicate, may be a contributing factor.
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PMID:Fly ash lung: a new pneumoconiosis? 706

Based on personal clinical observations in over one hundred cases and the data in the literature, a brief general review of the clinical and biological characteristics of chronic idiopathic fibrogenous interstitial pneumopathy (diffuse idiopathic interstitial fibrosis) is presented. Chief emphasis is placed on functional characteristics (inadequacy of the ventilation/perfusion ratio and disease of the small airways and of the interstitium per se), morphologic considerations, and analysis of bronchoalveolar lavage fluid. Typically the disease runs its course within about 4 years following diagnosis, the evolution being marked by episodes of infection complicating the concurrent respiratory insufficiency. Complications stemming from pre-existing coronary insufficiency or neoplastic transformation can occur in elderly patients. Recent advances have been the result of experimental data, of a better understanding of the biochemical structure of the lung (particularly with respect to the metabolism of collagen) and of cytologic and isotopic investigations, especially iterative bronchoalveolar lavage and gallium scintigraphy. Treatment remains disappointing, however, and principally symptomatic (corticotherapy and azathioprine). In relation to acquired fibrosis (common pneumoconiosis, extrinsic allergic alveolitis, iatrogenic pneumopathy, pulmonary fibrosis secondary to systemic disease) this syndrome represents a distinct, if not unequivocal or specific entity.
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PMID:[Idiopathic fibrogenous interstitial pneumopathy]. 745 55

Reactive oxygen species are important mediators of both mineral dust-induced (malignant) lung disease and in vitro DNA damage. Therefore, we studied in vivo oxidative DNA damage in coal workers who had been chronically exposed to silica-containing dust. In peripheral blood lymphocytes of 38 retired coal miners (eight with coal workers pneumoconiosis, 30 references) and 24 age-matched, non-dust-exposed controls 7-hydro-8-oxo-2'-deoxyguanosine (8-oxodG) was determined by reversed phase high-performance liquid chromatography with electrochemical detection. The ratio of 8-oxodG residues to deoxyguanosine (dG) was related to individual cumulative dust exposure estimates and pneumoconiotic stage as established by chest radiography. The ratio of 8-oxodG to dG(x 10(-5)) in lymphocytes did not differ between miners with coal workers' pneumoconiosis (2.61 +/- 0.44) and miners without coal workers' pneumoconiosis (2.96 +/- 1.86). However, oxidative DNA damage in all miners was higher than in the non-dust-exposed controls (1.67 +/- 1.31). 8-oxodG/dG ratio was not related to individual cumulative coal dust exposure, age or smoking (pack years) when evaluated by multiple linear regression. We suggest that oxidative damage to the DNA of peripheral blood lymphocytes may be introduced by increased oxidative stress responses in subjects chronically exposed to mineral dusts. Whether this is an important pathway in the suggested carcinogenicity of silica is still an open question.
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PMID:Oxidative DNA damage in peripheral blood lymphocytes of coal workers. 759 Nov 72

Animal studies show that antimony may cause lung cancer and heart and lung disease in rodents. In exposed humans, ECG abnormalities and heart and lung disease have been reported. This mortality study of 1,014 men employed between 1937 and 1971 in a Texas antimony smelter consisted primarily of workers of Spanish ancestry (n = 928, 91.5%). Hispanics are known to smoke at much lower rates than non-Hispanics, and their lung cancer and heart disease mortality is generally low. When ethnic-specific Texas lung cancer death rates were used for comparison, mortality from lung cancer among antimony workers was elevated (SMR) 1.39, 90% CI 1.01-1.88), and we observed a significant positive trend in mortality with increasing duration of employment. When ischemic heart disease death rates from three different Spanish-surnamed populations were used for comparison, the rate ratios for mortality from ischemic heart disease were 0.91 (90% CI 0.84-1.09), 1.22 (90% CI 0.78-1.89), and 1.49 (90% CI 0.84-2.63). Pneumoconiosis/ other lung disease death rates for Spanish-surnamed men were unavailable and so calculation of rate ratios used white males as a comparison population (SMR 1.22; 90% CI 0.80-1.80). These data suggest some increased mortality from lung cancer and perhaps nonmalignant respiratory heart disease in workers exposed to antimony. However, conclusions are limited by possible confounders and the difficulty of identifying appropriate referent groups.
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PMID:Mortality in a cohort of antimony smelter workers. 761 10

Several studies have suggested the use of serum type III procollagen peptide (PIIIP) as a marker in fibrotic lung disease. To test serum PIIIP as a biomarker for progression of coal workers' pneumoconiosis (CWP), a follow-up study was conducted among 156 coal miners. A five-year progression of simple CWP was determined from paired chest X-ray readings and related to serum PIIIP measured in 1987 (n = 73) and in 1992 (n = 104). Although in eight subjects CWP had progressed, none of these subjects had abnormal levels of serum PIIIP, nor were they different from nonprogressed miners with regard to exposure, age, or smoking habits. The results suggest that the use of serum PIIIP as a biomarker to screen for coal workers' pneumoconiosis is limited.
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PMID:Serum procollagen type III peptide in coal workers' pneumoconiosis: a five-year follow-up study. 784 78

Hospital discharge data from Michigan for the years 1990 and 1991 were used to examine potential associations between pneumoconiosis and pulmonary hypertension, lung cancer, obstructive lung disease, and connective tissue disease among both men and women. Lung cancer, pulmonary hypertension, and obstructive lung disease were associated with coal workers' pneumoconiosis. Pulmonary hypertension and obstructive lung disease were associated with asbestosis and silicosis. Rheumatoid arthritis was associated with silicosis. The potential is suggested that misdiagnosis is the cause of the association between lung cancer and coal workers' pneumoconiosis.
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PMID:Pneumoconiosis and associated medical conditions. 790 Jul 28

Hard metal lung disease is usually easy to diagnose, on the basis of occupational history, chest X-ray appearance of interstitial lung disease and, if necessary, by bronchoalveolar lavage (BAL). However, other interstitial lung diseases may affect patients with an occupational history of exposure to cobalt. In hard metal disease, the hylar lymphnodes may enlarge due to high draining of hard metals from the lung tissue via lymphatic vessels. Also, the presence of Giant Cells (even if Langhan's type) in the BAL fluid of sarcoid patients may be high. We present four patients with a history of exposure to hard metals and whose chest X-rays suggest sarcoidosis, stage II; in each, a pulmonary biopsy was necessary to confirm the diagnosis. Final diagnosis was sarcoidosis in one (showing typical granulomata in the lung tissue), and hard metal disease in three: two of these had foreign body-type granulomata in the lung tissue. Neutron activation analysis (NAA) study was carried out on these four patients using specimens of BAL fluid, blood, urine, toenails, pubic hair and sperm. In the light of available data, the concentration of elements may not be useful in differentiating between sarcoidosis and hard metal pneumoconiosis. However, NAA on BAL fluid or other specimens may be helpful in confirming the presence of the offending agent in suspected cases when the occupational history is not clear.
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PMID:The differential diagnosis of hard metal lung disease. 793 13

Coal Workers' Pneumoconiosis has been a compensable disease since the 1960s. In 1987 the Kentucky Workers' Compensation Law was changed to provide reduced benefits for coal miners with radiographic evidence of Black Lung Disease, but little or no respiratory impairment. This but little or no respiratory impairment. This paper reports a typical case of Black Lung today and discusses the status of workers' compensation for this disease in Kentucky.
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PMID:Coal workers' pneumoconiosis and compensation in Kentucky. 832 Apr 97

High-resolution computed tomography (HRCT) may show parenchymal abnormalities in patients with normal or questionable findings on the chest radiograph; and because it provides an accurate assessment of the pattern and distribution of lung disease, it also improves the accuracy of the differential diagnosis. HRCT may be able to distinguish areas of potentially reversible disease from irreversible fibrosis and be a helpful guide to the optimal type and site of lung biopsy. This review summarizes the current indications for HRCT of the chest in the assessment of patients with acute lung disease, chronic infiltrative lung disease, pneumoconiosis, bronchiectasis, and emphysema.
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PMID:High-resolution computed tomography of the chest: current indications. 832 Jul 62

Tungsten has been implicated as a cause of a severe form of pneumoconiosis in humans, the so-called "hard metal" lung disease. We have investigated the effect of intratracheal instillation of a powder of calcium tungstate on the pulmonary tissue of CD-1 mice. The tungsten-induced alterations were studied using 3 microanatomical methods: cytologic study of exudates obtained by bronchoalveolar lavage (BAL); histologic examination of paraffin-embedded sections of the lung; and scanning electron microscopic (SEM) examination of lung samples using x-ray microanalysis to detect tungsten in situ. The animals were sacrificed 1, 3, 7, 14 and 21 days after a single intratracheal instillation of 250 micrograms calcium tungstate particles suspended in 100 microliters of saline. We found that the metal particles induced a marked inflammatory response in the bronchoalveolar space characterized by a biphasic attraction of leukocytes with cellular peaks observed at day 1 and 14. More than 50% of the BAL macrophages showed ingested tungsten. In the lung parenchyma, the inflammatory infiltrates were predominantly located at the periphery of the bronchiolar walls. From 7 days on after the tungsten deposition, large inflammatory exudates were seen invading focal areas of the alveolar domain of the lung. SEM views revealed that the tungsten particles could be inside alveolar macrophages, in cells making up the alveolar wall, or inside periacinar lymphatics. Our data document that tungsten particles cause a marked inflammatory response in the lung tissue and that the leukocyte exudates may invade alveolar areas of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inflammatory response of the lung to tungsten particles: an experimental study in mice submitted to intratracheal instillation of a calcium tungstate powder. 834 Oct 86


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