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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In world industry and agriculture as a whole, the number of people with asthma and complex pneumopathies related to chemical and organic pollution seems important. Indeed, subjects with an atopic inclination are often the first to be jeoparized. However, it must be stressed that occurrence of asthma in relation with work should always lead to investigate an anomaly in professional hygiene. For other workers this latter eventuality constitutes in the long run a threat of precipitin pneumopathy, chronic bronchitis, pulmonary fibrosis, or even cancer (in the case of nickel). Selection upon hiring is an unsatisfactory measure. The improvement of the atmospheric conditions at work should always be sought for. In some professional asthma cases, we were able to confirm that medication provides efficient protection. This solution, however, seems only slightly satisfactory since the subject is still left in contact with substances which have harmful effects other than asthma. It is therefore important that doctors track down and explore the cases of professional asthma, declaring their existence to social security and work inspection organizations, in order to establish an epidemiological knowledge, regularly updated, which would provide an indispensable basis for any prevention through improvement of working conditions.
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PMID:[Asthma and professional life (author's transl)]. 49 90

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 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

After a brief mention of history and world use the authors review the major hazards to health associated with nickel and its compounds. These include pulmonary and sino-nasal cancer from exposure to the dusts involved in certain, now obsolete, processes, dermatitis and nickel carbonyl poisoning. Brief mention is also made of other less well established or hypothetical health risks mentioned in the nickel context including asthma, pulmonary fibrosis and acute poisoning. In conclusion the authors mention some current work being undertaken in the occupational health field and give sources of further information.
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PMID:Health problems associated with nickel refining and use. 821 83

Cobalt is a relatively rare magnetic element with properties similar to iron and nickel. The two valance states are cobaltous (II) and cobaltic (III) and the former is the most common valance used in the chemical industry. Cobalt occurs in nature primarily as arsenides, oxides, and sulfides. Most of the production of cobalt involves the metallic form used in the formation of cobalt superalloys. The term "hard metal" refers to compounds containing tungsten carbide (80-95%) combined with matrices formed from cobalt (5-20%) and nickel (0-5%). For the general population, the diet is the main source of exposure to cobalt. In the occupational setting, exposure to cobalt alone occurs primarily during the production of cobalt powders. In other industrial exposures (e.g., hard metal, diamond polishing), additional agents (tungsten) modulate the toxicity of cobalt. Cobalt is an essential element necessary for the formation of vitamin B12 (hydroxocobalamin); however, excessive administration of this trace element produces goiter and reduced thyroid activity. In 1966, the syndrome "beer drinker's cardiomyopathy" appeared in Quebec City, Canada, and was characterized by pericardial effusion, elevated hemoglobin concentrations, and congestive heart failure. An interstitial pulmonary fibrosis has been associated with industrial exposure to hard metal dust (tungsten and cobalt), but not to cobalt alone. Exposure to cobalt alone produces an allergic contact dermatitis and occupational asthma. Treatment of cobalt toxicity is primarily supportive.
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PMID:Cobalt. 1038 56

We report a case of pulmonary fibrosis in a 32-year-old man, who had worked at a steel mill and who died of respiratory failure due to interstitial fibrosis despite vigorous treatment. He showed SLE-associated symptoms, such as pleural effusion, malar rashes, discoid rashes, arthritis, leukopenia, and positive antinuclear antibody and anti-histone antibody. However, he did not present anti-DNA antibody. A thoracoscopic lung biopsy showed interstitial fibrosis, chronic inflammation and a small non-caseating granuloma in lung tissues, which could be induced by external agents such as metals. The manganese concentration in the lung tissue was 4.64 microg/g compared to 0.42-0.7 microg/g in the controls. The levels of other metals, such as iron, nickel, cobalt and zinc in patient's lung tissue were higher than those in the controls. The patient was probably exposed to Si and various metal dusts, and the lung fibrosis was related to these exposures. Exposure to Si and metal dusts should be sought in the history of any patient with SLE, especially in a male with pulmonary signs, and if present, exposure should be stopped. In the meantime, steps should be taken to ensure that workers exposure to Si and metal dusts in all environments have adequate protection.
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PMID:Pulmonary fibrosis in a steel mill worker. 1080 2

An intratracheal (IT) screening assay was performed in rats on a series of aluminosilicate catalysts (synthetic zeolites) and alumina binders to compare their relative ability to cause pulmonary fibrosis and related changes. Before initiation of IT screens, both the uniformity of deposition and residence time of a prototype catalyst in the lung were determined. Subsequently, the test materials were instilled and animals were evaluated 6 mo later for lung volumes, pulmonary pressure-volume curves, pulmonary hydroxyproline (OHPro) content, lung weights, and histopathology. Negative controls were saline and glass beads; the positive control was quartz. The test materials were organic-free ZSM-5 crystals, organic form of ZSM-5 crystals, alumina-bound ZSM-5, nickel/ZSM-5/ Al2O3 binder, used nickel/ZSM-5/Al2O3 binder, nickel-tungsten/ZSM-5/Al2O3 binder, and Bayer pseudoboehmite. For each, groups of 12 male rats were dosed once with either 25 or 50 mg of ground particles (> or =95% less than 2.4 microm). Second to quartz, the sample of alumina caused the most pronounced pulmonary reactions at 6 mo after dosing. Therefore, the effects of four aluminas were subsequently compared (Bayer pseudoboehmite, Bayer gammaAl2O3, Ziegler pseudoboehmite, and Ziegler gammaAl2O3). The results support the idea of a lack of long-term effects from exposure to normal concentrations of these materials in the workplace. Also, the IT assay proved to be a very useful tool for ranking the relative effects of this series of zeolites and aluminas.
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PMID:Comparison of synthetic zeolite catalysts and alumina binders administered intratracheally to rats. 1091 88

One cause of debilitating pulmonary fibrosis is inhalation of insoluble metals. Human epidemiological and animal studies have associated inhalation of nickel dusts with increased incidence of pulmonary fibrosis. However, specific mechanisms for nickel-induced pulmonary fibrosis have yet to be elucidated. The current studies examine the hypothesis that particulate nickel promotes pulmonary fibrosis by inhibiting the fibrinolytic cascade. Since the urokinase-type plasminogen activator (uPA) initiates this cascade, this hypothesis was tested by investigating the effects of noncytotoxic levels of nickel subsulfide on the balance of uPA expression relative to expression of its inhibitor, PAI-1, in cultured human bronchial epithelial cells (BEAS-2B). Exposure to the metal decreased secreted uPA protein levels and activity without affecting uPA mRNA levels. In contrast, these same exposures stimulated transcription of PAI-1, causing prolonged increases in both mRNA and protein levels. Despite partial recovery of uPA protein levels, uPA activity remained depressed for more than 48 h after exposure to nickel due to the continued increase in PAI-1 expression. These data indicate that particulate nickel inhibits the fibrinolytic cascade by increasing the ratio of plasminogen inhibitor to activator. Sustained loss of uPA activity may contribute to nickel-induced pulmonary fibrosis in exposed populations.
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PMID:Nickel-induced plasminogen activator inhibitor-1 expression inhibits the fibrinolytic activity of human airway epithelial cells. 1100 99

Human epidemiological and animal studies have associated inhalation of nickel dusts with an increased incidence of pulmonary fibrosis. At the cellular level, particulate nickel subsulfide inhibits fibrinolysis by transcriptionally inducing expression of plasminogen activator inhibitor (PAI)-1, an inhibitor of the urokinase-type plasminogen activator. Because nickel is known to mimic hypoxia, the present study examined whether nickel transcriptionally activates PAI-1 through the hypoxia-inducible factor (HIF)-1 alpha signaling pathway. The involvement of the NADPH oxidase complex, reactive oxygen species, and kinases in mediating nickel-induced HIF-1 alpha signaling was also investigated. Addition of nickel to BEAS-2B human airway epithelial cells increased HIF-1 alpha protein levels and elevated PAI-1 mRNA levels. Pretreatment of cells with the extracellular signal-regulated kinase inhibitor U-0126 partially blocked HIF-1 alpha protein and PAI-1 mRNA levels induced by nickel, whereas antioxidants and NADPH oxidase inhibitors had no effect. Pretreating cells with antisense, but not sense, oligonucleotides to HIF-1 alpha mRNA abolished nickel-stimulated increases in PAI-1 mRNA. These data indicate that signaling through extracellular signal-regulated kinase and HIF-1 alpha is required for nickel-induced transcriptional activation of PAI-1.
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PMID:Nickel requires hypoxia-inducible factor-1 alpha, not redox signaling, to induce plasminogen activator inhibitor-1. 1150 87

Inhalation of nickel dust has been associated with an increased incidence of pulmonary fibrosis. Nickel may promote fibrosis by transcriptionally activating plasminogen activator inhibitor (PAI)-1 and inhibiting fibrinolysis. The current studies examined whether nickel stimulated the PAI-1 promoter though an oxidant-sensitive activator protein (AP)-1 signaling pathway. Addition of nickel to BEAS-2B human airway epithelial cells stimulated intracellular oxidation, induced c-Jun and c-Fos mRNA levels, increased phospho- and total c-Jun protein levels, and elevated PAI-1 mRNA levels over a 24-h time course. Pretreatment of the cells with antioxidants did not affect increased c-Jun protein or PAI-1 mRNA levels. Expression of the dominant negative inhibitor of AP-1, TAM67, prevented nickel-stimulated AP-1 DNA binding, AP-1-luciferase reporter construct activity, and PAI-1 mRNA levels. Overexpression of c-Jun, however, failed to induce the AP-1 luciferase reporter construct or PAI-1 mRNA levels. These data indicated that nickel activated AP-1 through an oxidant-independent pathway and that basal AP-1 is necessary for nickel-induced expression of PAI-1.
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PMID:AP-1-dependent induction of plasminogen activator inhibitor-1 by nickel does not require reactive oxygen. 1150 88


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