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

An autopsy case of cemented tungsten carbide pneumoconiosis, the first lethal case in our country, is presented. A 28-year-old woman, who had been engaged in grinding presintered metallic matrix for four years, developed respiratory symptoms. X-ray examinations were indicative of interstitial pulmonary fibrosis. Corticosteroid therapy revealed only little effect. She expired five years after the onset of the symptoms. Postmortem examination showed nonspecific interstitial pneumonitis resulting in marked lung fibrosis. Ultrastructurally, crystals were observed in cytoplasm of presumable macrophages in the fibrotic lung tissue. Electron probe microanalysis of the lung tissue showed the presence of tungsten and other constituents of tungsten carbide except for cobalt. Metal analysis demonstrated a large amount of tungsten in the lung. Cobalt was detected tenfold of the normal value in the bone. In pathogenesis of the pneumoconiosis in the cemented tungsten carbide workers, toxicity of cobalt is most suspectable, and in addition, individual susceptibility may be also important.
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PMID:Cemented tungsten carbide pneumoconiosis. 73 23

In order to shed light on the histological changes occurring in the lungs of patients with rheumatoid arthritis (RA), we scrutinized an open lung biopsy file of 199 patients and selected the patients with RA. The histopathological patterns observed were: pulmonary rheumatoid nodules (4 cases, including one with rheumatoid pneumoconiosis); usual interstitial pneumonia (UIP) (2 cases); desquamative interstitial pneumonia (2 cases); bronchiolitis obliterans with patchy organizing pneumonia (2 cases); follicular bronchiolitis (1 case); organizing pneumonia always associated with bronchiolitis (3 cases); granulomatous reaction (3 cases); obliterating vasculitis (3 cases); granulomatous vasculitis (1 case); lymphoid hyperplasia (2 cases); and localized pulmonary fibrosis (1 case). The clinical data and laboratory findings for the histopathological groups overlapped and did not properly predict the anatomical picture. Both patients with UIP died of lung disease. Otherwise the prognosis in the series was good.
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PMID:Open lung biopsy of patients with rheumatoid arthritis. 208 43

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

A 62-year-old male, was admitted on Oct. 7, 1987 because of productive cough and dyspnea. He worked for an iron factory, where pneumoconiosis was regarded as an occupational disease, for 40 years. No abnormal finding had been noted on his mass screening chest roentgenograms. He was well until three years ago when hypertension and Parkinsonism were noted. Since then he was treated with beta blockers, L-DOPA, amantadine and bromocriptine. Two weeks before admission, he suddenly complained of dyspnea and productive cough. His chest roentgenograms showed diffuse reticulonodular infiltration in both lung fields. The partial pressure of oxygen of the arterial blood was 65.9 Torr. The first transbronchial lung biopsy obtained from right B8 on Sept. 29, 1987 (before the admission) revealed some epithelioid granulomas and the second biopsy obtained from right B10 on Oct. 14, 1987 demonstrated bronchiolar edema and infiltration of inflammatory cells. Fibrotic changes associated with carbon dust between airways and vessels were also noted. Lymphocyte stimulation index by bromocriptine was 362%, and that by amantadine, 139%, L-DOPA, 150%, respectively. After ceasing the administration of bromocriptine, productive cough, dyspnea and the reticulonodular shadows diminished gradually. These findings strongly suggest that the interstitial pulmonary lesions are bromocriptine-induced interstitial pneumonitis. His occupational exposure to inorganic dust may be a predisposing factor.
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PMID:[A case of bromocriptine-induced interstitial pneumonitis in an iron factory worker exposed to sand dust]. 261 76

Pneumoconiosis in dental laboratory workers has been associated with exposure to metal alloys and silica used in the manufacturing of dental prosthetics. In this report, we describe a 27-yr-old dental student who was found to have bilateral basal pulmonary interstitial infiltrates and nodules on a chest roentgenogram after a brief episode of upper respiratory infection. An open lung biopsy revealed interstitial pneumonitis with an abundance of vacuolated macrophages in the alveolar spaces. Ultrastructural analysis showed in the alveolar and interstitial spaces the accumulation of macrophages laden with electron-lucent bodies resembling plastic beads. An inhalation exposure history, taken subsequent to these findings, revealed exposure to high levels of acrylic plastic in a dental school laboratory. Removal from the site of exposure has resulted in the gradual resolution of the roentgenographic abnormalities.
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PMID:Acrylic resin pneumoconiosis: report of a case in a dental student. 264 10

We report four cases of giant-cell interstitial pneumonia that occurred in association with exposure to hard metals. All patients presented with chronic interstitial lung disease and had open-lung biopsies that revealed marked interstitial fibrosis, cellular interstitial infiltrates, and prominent intraalveolar macrophages as well as giant cells displaying cellular cannibalism. We also review the literature to determine the sensitivity and specificity of giant-cell interstitial pneumonia for hard-metal pneumoconiosis. Although hard-metal pneumoconiosis may take the form of usual interstitial pneumonia, desquamative interstitial pneumonia, and giant-cell interstitial pneumonia, the finding of giant-cell interstitial pneumonia is almost pathognomonic of hard-metal disease and should provoke an investigation of occupational exposure.
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PMID:Giant-cell interstitial pneumonia and hard-metal pneumoconiosis. A clinicopathologic study of four cases and review of the literature. 266 Jun 10

A hygiene study of a hard metal factory was conducted from 1981 to 1984. All workers exposed to hard metal were medically examined and their exposure to cobalt measured. Eighteen employees had occupational asthma related to exposure to hard metal, a prevalence rate of 5.6%. Nine had a positive bronchial provocation test to cobalt and reactions of the immediate, late, or dual type were elicited. Exposure measurements suggest that asthma may be caused by cobalt at a mean time weighted average concentration below 0.05 mg/m3. Only two of the nine individuals with cobalt asthma had a positive patch test to cobalt. Chest radiographs of three workers showed diffuse shadows of category 1 or over. X ray microanalysis of lung biopsy specimens from two of these three workers showed the presence of tungsten, titanium, cobalt, nickel, and some minerals. One of the two was diagnosed as having pneumoconiosis due to exposure to silica in a steel industry and the other was suspected of having pulmonary fibrosis caused by dust generated from the carborundum wheels used to grind hard metal. There were no cases with interstitial pneumonitis in the factory.
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PMID:Respiratory diseases in hard metal workers: an occupational hygiene study in a factory. 371 95

Pulmonary blue bodies are intra-alveolar laminated basophilic concretions of uncertain etiology. Blue bodies were studied in lung biopsy specimens from 10 patients. The patients ranged in age from 47 to 69 years and were predominantly men. Three had a history of overt exposure to environmental dusts such as sawdust and asbestos, and two showed occasional ferruginous bodies in the lung, raising the possibility of pneumoconiosis. In eight cases there was interstitial pneumonitis, which resembled desquamative interstitial pneumonia by light microscopy but which was often seen to be patchy and asymmetrically distributed in the lung by chest x-ray examination. Of two other patients, one had xanthogranulomatous inflammation and the other, necrotizing granulomatous inflammation. Light and electron microscopic, histochemical, microchemical, and x-ray diffraction studies of blue bodies were also performed. Calcium carbonate is a major component of blue bodies and is responsible for their birefringence in unstained sections and ready solubility in acid solutions. Blue bodies also contain a mucopolysaccharide matrix and iron. We offer the hypothesis that blue bodies (calcium carbonate) are a product of histiocytic catabolism.
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PMID:Pulmonary blue bodies. 616 27

Viruses and other possible causative agents should be sought light and electron microscopically in all cases of ill-defined diseases including "sarcoid." Ideally, tissue should be prepared for electron microscopic examination as soon as a specimen is obtained; however, when this has not been done, tissue preserved in formalin solution can be used. Viruses, some bacteria, and other agents suspected on the basis of light microscopic findings can be verified electron microscopically by reprocessing paraffin-embedded tissue from areas that show smudge cells, focal necrosis with atypical cellular proliferation, and nuclear inclusions. Electron microscopically, all dying cells show swelling and rupture of cellular organelles and membranes; reactive changes include proliferation of branching tubules and paracrystalline and other types of proteinaceous precipitates (inclusions) in both the nucleus and cytoplasm. Qualitative and quantitative changes of cellular organelles, fibrils, microvilli, and intercellular junctions reflect hyperplasia, metaplasia, or dysplasia of the cell and may enable identification of the diseases, e.g., desquamative interstitial pneumonia. In various conditions, basal laminae become irregular, disruptive, or reduplicated following epithelial necrosis and regeneration. Electron microscopic evidence of immunologic damage to basal lamina and cells and immuno-electron-microscopic features of the lung in general require further studies. Electron microscopic features of transbronchial biopsy specimens may be diagnostic in cases of alveolar proteinosis, histiocytosis X, and amyloidosis. Ultrastructural abnormalities of cilia are common; primary ciliary defects are rare. Finally, light microscopic, scanning electron microscopic, and x-ray energy-dispersive spectrometric examinations of paraffin-embedded sections appear most practical for the pathologic evaluation of cases of pneumoconiosis.
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PMID:Applications of electron microscopy to diagnostic pulmonary pathology. 635 60

Interstitial pneumonia and recurrent pneumothorax developed in a 48-year-old man who had worked as a metal grinder. He died of respiratory failure despite having received antibiotics and steroids, and despite having undergone pleural sclerosis therapy. Giant cell interstitial pneumonia was diagnosed; innumerable bizarre giant cells engulfing black granules were found within the alveoli. The results of high-energy dispersion X-ray microanalysis indicated that the patient had hard metal pneumoconiosis associated with tungsten in the black granules. When he was admitted to the hospital, his serum CA19-9 and SLEX concentrations were abnormally high (2600 and 200 ng/ml, respectively). Immunohistochemical analysis of lung tissue was done with anti-CA19-9 and SLEX antibodies. CA19-9 staining revealed strong bronchialization and squamous metaplasia in contrast to type II hyperplasia. SLEX staining showed strong type II hyperplasia. Further investigations will be needed to determine the mechanism of elevated tumor-associated carbohydrate antigens in serum.
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PMID:[Giant cell interstitial pneumonia in a metal grinder with an abnormally high level of serum CA19-9]. 747 73


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