Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Rats was exposed to white smoke generated from mixtures of titanium dioxide-hexachloroethane (TiO2-HC) and zinc-hexachloroethane (Zn-HC), respectively, in an inhalation chamber operated in the static mode. The dose was varied by varying the amount of smoke mixture and/or the exposure time. The acute inhalation toxicity of TiO2-HC smoke was much lower than the Zn-HC smoke. Thus, the animals survived exposure to TiO2-HC smoke, even at relatively high smoke concentrations. This smoke was irritating to the animals and minor, acute inflammatory changes were seen in lung tissue. In contrast, Zn-HC smoke was very toxic and caused lethal injuries to the experimental animals, even at relatively low concentrations. Pulmonary injuries were extensive and death was due to blood congestion with pulmonary oedema. Since the TiO2-HC and Zn-HC mixtures form TiCl4 and ZnCl2, respectively, a separate study was performed in which rats were exposed to TiCl4 gas or ZnCl2 aerosol. No animals died from exposure to TiCl4 at concentrations between 370 and 2900 mg/m3 for 10 min. The LC50 of ZnCl2 was found to be around 2000 mg/m3 during a 10-min exposure period. The difference between the two types of smoke is explained by the difference in toxicity between TiCl4 and ZnCl2.
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PMID:A comparative study of the acute inhalation toxicity of smoke from TiO2-hexachloroethane and Zn-hexachloroethane pyrotechnic mixtures. 381 83

When Teflon is heated the developing fumes produce in exposed human an influenza-like syndrome (polymer fume fever) or also severe toxic effects like pulmonary edema, pneumonitis and death. The decomposition products and the resulting health effects are temperature-dependent. The toxic effects seem to be related to the ultrafine particulate fraction of the fume. To test the hypothesis that exposure to ultrafine particles results in an increased interstitialization of the particles which is accompanied by an acute pathological inflammation, rats were exposed to titanium dioxide (TiO2) particles by intratracheal instillation and by inhalation. Both acute intratracheal instillation and subchronic inhalation studies on rats show that ultrafine TiO2 particles (approximately 20 nm diameter) access the pulmonary interstitium to a larger extent than fine particles (approximately 250 nm diameter) and that they elicit an inflammatory response as indicated by PMN increase in lavaged cells. The release of ultrafine particles into the air of an enclosed environment from a thermodegradation event or from other sources is a potential hazard for astronauts. Knowing the mechanisms of action is a prerequisite for technical or medical countermeasures.
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PMID:Polymer degradation and ultrafine particles: potential inhalation hazards for astronauts. 1153 70

Exposure to titanium dioxide nanoparticles (TiO(2) NPs) elicits an adverse response such as oxidative damage. The molecular targets of TiO(2) NPs remain largely unidentified. In the present study, the function and signal pathway of nuclear factor erythroid 2 related factor 2 (Nrf2) in protection against TiO(2) NPs-induced oxidative stress in the mouse lung were investigated. Mice were exposed to 10 mg/kg body weight by an intratracheal administration for 15-90 days. With increasing exposed terms, TiO(2) NPs were significantly accumulated and increased the reactive oxygen species (ROS) production in lung, which resulted in severe pulmonary edema, inflammatory response and pneumonocyte apoptosis for 90 days. Furthermore, TiO(2) NPs exposure could greatly induce expression of Nrf2, heme oxygenase 1 (HO-1), and glutamate-cysteine ligase catalytic subunit (GCLC) from 15-day to 75-day exposure, whereas 90-day exposure caused significant decreases of three factors expression levels in lung. Our findings imply that the induction of Nrf2 expression is an adaptive intracellular response to TiO(2) NPs-induced oxidative stress in the mouse lung, and that Nrf2 is protective against TiO(2) NPs-induced pulmonary damages during certain exposure terms.
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PMID:Oxidative damage of lung and its protective mechanism in mice caused by long-term exposure to titanium dioxide nanoparticles. 2252 60