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

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

A 45 yr old male developed pulmonary fibrosis after 29 yrs of employment as a dental technician. He subsequently developed adenocarcinoma of the lung. Diffuse interstitial fibrosis was seen using light microscopy. Neutron activation analysis of non-neoplastic lung tissue demonstrated high levels of chromium and cobalt suggesting the possibility of a chromium-cobalt alloy pneumoconiosis.
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PMID:A dental technician with pulmonary fibrosis: a case of chromium-cobalt alloy pneumoconiosis? 209 Apr 88

Communication between cells determines the steady-state composition of the lung in health and becomes a critical determinant of outcome in pathologic processes resulting in anatomic remodeling. This review presents the evolving concepts of the biology of cytokines (also known as peptide growth factors or biological response modifiers) in maintaining normal tissue growth and homeostasis. How these extracellular signaling proteins are involved in such pathologic disorders as spontaneous pulmonary fibrosis, sarcoidosis, pneumoconiosis, and the evolution and recovery from acute lung injury is also discussed. During the past decade the cytokines have come to the fore as important multifunctional mediators of cell behavior and cell-cell communication. A wide range of cellular responses are influenced or triggered when cytokines interact with cells. These include mitosis, chemotaxis, angiogenesis, cytoskeleton arrangement, immunomodulation, and extracellular matrix production. Cytokines influence cell behavior by binding to specific high affinity surface receptors on target cells. These receptors are linked in turn at the cell membrane to a complex array of intracellular signaling pathways. Individual cytokines may inhibit as well as promote cellular functions such as mitosis and thereby play a critical role in homeostasis of normal tissue elements. Hence, cytokines are intimately involved in normal tissue homeostasis as well as in processes eventuating in growth and remodeling. All cells produce and secrete cytokines at some time during their life. Each cytokine is capable of modulating more than one cellular function. Although produced by a variety of cell types, the triggers that induce a specific cytokine to be produced differ between cells. Many of the cytokines share regions of homologous nucleic acid sequences, suggesting that they are members of larger gene families. Given that tissues and cells are exposed to complex cytokine mixtures rather than to individual cytokines, recent attention has turned to understanding how cytokines interact. The combined effects of cytokine mixtures have proved to be both complex and unpredictable based on knowledge of the separate actions of the individual cytokines involved. In studies of the role of cytokines in lung disease, early research attention has focused on those cytokines released by alveolar macrophages (the so-called macrophage-derived growth factors). However, structural cells as well as immune effector cells of the lung are capable of cytokine production and release. The cytokines receiving the most attention to date in relation to pulmonary diseases include platelet-derived growth factor (PDGF), interleukin-1 (IL-1), transforming growth factor-beta (TGF-beta), tumor necrosis factor-alpha (TNF-alpha), insulinlike growth factor I (IGF-I), and, most recently, interleukin-6 (IL-6).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytokines of the lung. 224 Aug 51

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

Asbestosis is a pneumoconiosis that results from the inhalation of asbestos fibers. There is a body of evidence that implicates the alveolar macrophage in the pathogenesis of asbestosis because of its prominence in asbestos-related histologic lesions. Injury to the alveolar epithelium also may contribute to the pathogenesis of asbestosis. Evidence is presented to suggest that pulmonary fibrosis may result from the persistent release of inflammatory mediators (chemoattractants, lysosomal enzymes, toxic oxygen radicals, arachidonic acid metabolites, interleukins, and fibroblast growth factors) at sites of asbestos deposition. Histologic features of asbestosis can be detected within months after the initial contact with asbestos. In contrast, the stigmata of asbestos-related disease usually are not radiologically detectable, even by the most sensitive imaging techniques, until after a latency period of at least a decade, and often considerably longer. There is, therefore, a long diagnostic delay between the time when asbestosis is histologically detectable and when it is radiographically detectable.
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PMID:Current issues regarding the pathobiology of asbestosis: a chronologic perspective. 305 34

To clarify the clinical value of the International Labor Office (ILO) roentgenographic classification of pneumoconiosis in assessing asbestos-exposed persons, we determined the relationships among spirometric values, radiographic evidence of parenchymal pulmonary fibrosis and/or pleural thickening, and cigarette smoking history in 684 consecutively enrolled male plumbers and pipefitters participating in a larger cross-sectional prevalence study. The subjects were mainly marine pipefitters (35%), plumbers (24%), and steamfitters/welders (23%); 28% had never smoked, 39% were ex-smokers, and 33% currently smoked cigarettes. Mean values for FVC and FEV1 were 95.0 and 91.9% of predicted, respectively, with mean FEV1/FVC ratio 77.7%; by standard criteria, 7.8% had restrictive impairment, and 21.7%, obstructive defects. Chest radiographs were normal in 63% and showed pleural abnormalities only in 17%, parenchymal abnormalities only in 7%, and both pleural and parenchymal abnormalities in 12%. Both FVC and FEV1 correlated with the degree of small opacity profusion, as assessed by ILO grade. Pleural abnormalities were associated with lower FVC values, independently of ILO profusion grade for Grades less than or equal to 1/0, and were unexplained by smoking status. In addition, there was a positive association between smoking history and degree of ILO parenchymal abnormality, particularly in those with the heaviest cumulative smoking history. Our results suggest that the ILO classification of pneumoconiosis, although a useful epidemiologic tool, should be applied with caution in persons with asbestos exposure, and that pleural abnormalities may be associated with physiologic impairment in such persons.
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PMID:The relation among pulmonary function, chest roentgenographic abnormalities, and smoking status in an asbestos-exposed cohort. 319 27

Numerous dusts found commonly in the dental laboratory have been suggested as potential pulmonary hazards. We recently noted a case of severe interstitial pulmonary fibrosis with intraalveolar deposition of unique foreign body inclusions in an elderly dentist. The composition of these particles was shown to be consistent with that of alginate impression powder. This is in contrast to previously reported pneumoconioses in dental workers, which are usually induced by metallic alloys or silicates. Further studies are needed to identify the causes and prevalence of pneumoconiosis in the dental lab.
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PMID:Pneumoconiosis in an elderly dentist. 337 Nov 14

After a case of advanced pneumoconiosis occurred in a dental laboratory technician, 31 other dental technicians and 30 control subjects controlled for smoking habits, sex, and age were investigated. More technicians (55%) than controls (30%) had at least grade 1 dyspnoea (p greater than 0.05). Multiple regression analysis showed that 13 technicians who had produced dental prostheses for at least 15 years had consistently lower lung function (FVC, FEV1, FEV1/FVC, MEF50, and DCO single breath), although the differences were not statistically significant. All mean lung function values for technicians and controls were within normal limits. Increases in MEF50 after breathing 80% helium and 20% O2 failed to show small airways dysfunction among the technicians. Of the six with radiological pneumoconiosis (5 simple, 1 advanced) four had symptoms. All three biopsy specimens showed varying degrees of pulmonary fibrosis. DCO single breath was diminished in four of the six. One male dental technician had scleroderma and possibly Erasmus syndrome. Blind readings showed an increased number of suspicious chest x rays films (greater than or equal to category 0/1) among older smokers and ex-smokers (p = 0.013) regardless of occupation. Our results support other evidence that dental technicians are at risk of developing pneumoconiosis. Therefore, adequate hygienic control of dental laboratories is indicated.
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PMID:Small opacities among dental laboratory technicians in Copenhagen. 337 11

In a case control study of 122 ex-shale workers, half of whom had simple pneumoconiosis and half of whom did not, those with pneumoconiosis were found to have the poorer lung function. Significant reductions in forced expiratory capacity (FEV1), forced vital capacity (FVC), Vmax50, lung volumes, and carbon monoxide transfer were found in men with pneumoconiosis. It is suggested that these abnormalities may represent a mixture of pulmonary fibrosis and airways obstruction related to exposure to dust and fumes in shale mines and at shale retorts.
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PMID:Epidemiologic studies of Scottish oil shale workers: II. Lung function in shale workers' pneumoconiosis. 371 67

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


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