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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although nickel is an essential element for animal nutrition, the physiological role of nickel is not yet established. Pathological alterations of nickel metabolism are recognized in several human diseases. The diverse clinical manifestations of nickel toxicology include: (1) acute pneumonitis from inhalation of nickel carbonyl, (2) chronic rhinitis and sinusitis from inhalation of nickel aerosols, (3) cancers of nasal cavities and lungs in nickel workers, and (4) dermatitis and other hypersensitive reactions from cutaneous and parenteral exposures to nickel alloys. The toxicity, carcinogenicity and embryotoxicity of nickel compounds in experimental animals are reviewed in this article, and consideration is given to the therapeutic use of chelating drugs in nickel poisoning.
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PMID:A review of the metabolism and toxicology of nickel. 33 46

Selenium concentrations in the serums of 17 acutely ill Legionnaires' disease patients were significantly lower than in their matching convalescent-phase serums. This trend was not observed in ten similarly paired samples of serum from control patients with pneumonia. There were no significant differences in the concentrations of nickel, copper, bromine, rubidium, lead, barium, or titanium in the serums of Legionnaires' disease and control patients.
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PMID:Legionnaires' disease: concentrations of selenium and other elements. 50 18

The histopathologic findings in lung tissue are reported from five cases of Philadelphia Legionnaire's Disease and the results are compared to pneumonias caused by other microbial and chemical agents. Histopathology of lung tissue was similar in all cases, despite the fact that death occurred between the fourth and 14th day of clinical illness. The inflammatory response was almost totally limited to the lower respiratory tract and primarily involved respiratory bronchioles, alveolar ducts and alveoli. Major bronchial branches and pulmonary interstices showed little or no involvement. There was considerable variation in the extent and nature of the consolidation, but the overall reaction pattern was highly characteristic of diffuse alveolar damage. Most involved areas showed intra-alveolar, fibrinocellular mononuclear cell predominant exudates, associated with pneumonocytic hyperplasia and slough. These findings plus the presence of erythroleucophagocytosis by macrophages and paucity of polymorphonuclear leucocytes are commonly associated with psittacine pneumonia, and much less so with classic patterns of bacterial, viral, fungal or rickettsial pneumonias. Of the toxic inhalants, nickel carbonyl, phosgene, nitrous oxide, cadmium oxide and some halogenated hydrocarbons have been associated with this tissue reaction pattern. Bacteria were notably absent in lung tissue stained by methods used to demonstrate the Legionnaires' Disease agent.
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PMID:Legionnaires' disease pneumonia: histopathologic features and comparison with microbial and chemical pneumonias. 53 30

Air quality correlates of chronic disease mortality in 180 census tracts of Harris County, Texas, were studied using 3 years mortality for 1969--1971. This study was designed to test with a different data base the universality of several study results which have reported significant correlations between heart disease and air pollutants. Air quality data (suspended particulates, benzene solubles, sulfur dioxide, and metals associated with particulates: copper, mercury, manganese, lead, nickel, zinc, chromium, and cadmium) were related to both sex and age adjusted crude death rates, and cause-specific death rates for age cohorts for 7 categories of heart disease, and pneumonia, asthma, cancer, tuberculosis, and accident deaths. The results of the study were in agreement with the findings of the other researchers who used national data. Suspended particulates and cadmium concentrations were found to be correlated (r=.38, .36; P less than .001) with ischemic heart disease (IHD). Many other significant correlations are reported but are not cause-specific. Socio-economic indicators were also correlated with IHD, thus confounding the issue. Further work is planned using more sophisticated statistical techniques to disentangle the relative contribution of each of these highly intercorrelated factors. No causality can be assigned at this stage, although this study, with the other cited, points to possible risk factors for IHD which need further evaluation.
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PMID:Air quality correlates of chronic disease mortality: Harris County, Texas 1969--1971. 72 89

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

To elucidate the subacute toxic reactions to parenteral administration of Ni2+, male F-344 rats were given daily injections of NiCl2 (62.5 or 125 mumol/kg, sc) for 3 to 6 weeks. Nickel accumulation was greater in lung than in the other major organs, based upon tissue analyses by electrothermal atomic absorption spectrometry. After 5 or 6 weeks of NiCl2 treatment, severe pathological changes developed in the lungs, including a) prominent hydropic and degenerative changes of the endothelium of pulmonary arteries and veins; b) marked proliferation of alveolar lining cells, affecting Type II (granular)pneumocytes; c) thickening of alveolar walls, with proteinaceous alveolar exudate; d) hyperplasia of bronchial epithelium, with cellular atypia and mitoses; and e) focal bronchial pneumonia with intrabronchial exudates. These pulmonary responses to repeated daily injections of NiCl2 were substantially different from the pathological lesions seen 24 to 72 hours after a single sc injection of NiCl2 (500 or 750 mumol/kg), which included perivascular edema, karyorrhexis and pyknosis of mononuclear cells in focal perivascular infiltrates, and mild pulmonary congestion. This study shows that the lung is a primary site of toxicity in rats following parenteral administration of NiCl2; vascular endothelial cells, Type II pneumocytes, bronchial epithelial cells, and mononuclear cells constitute the principal cellular targets for pulmonary toxicity of Ni2+.
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PMID:Pulmonary histopathology of rats following parenteral injections of nickel chloride. 319 57

Groups of F344/N rats and B6C3F1 mice were exposed to aerosols of nickel subsulfide (Ni3S2) 6 hr/day for 12 days not including weekends. Actual exposure concentrations were within 3% of target (target = 10.0, 5.0, 2.5, 1.2, 0.6, and 0.0 mg Ni3S2/m3). Nickel lung burdens of exposed rats and mice increased linearly with exposure concentration. Two male rats and all mice exposed to 10.0 mg Ni3S2/m3 died before the end of the exposures. Exposure to Ni3S2 had no effect on the natural killer cell activity of mouse spleen cells. Lesions in rats and mice related to inhalation of Ni3S2 were found in the nasal epithelium, lung, and bronchial lymph nodes. The most extensive lesions were found in the lung and included necrotizing pneumonia. Emphysema developed in rats exposed to 5.0 or 10.0 mg Ni3S2/m3, while fibrosis developed in mice exposed to 5.0 mg Ni3S2/m3. Degeneration of the respiratory epithelium and atrophy of the olfactory epithelium of the nose occurred in rats exposed to as low as 0.6 mg Ni3S2/m3 and mice exposed to 1.2 mg/m3. Results indicate that inhalation exposure of rats and mice to Ni3S2 aerosol concentrations near the current threshold limit value (TLV) for nickel compounds (1 mg/m3 for Ni metal and roasting fume and dust and 0.1 mg/m3 as Ni for soluble compounds) can produce lesions in the respiratory tract. Atrophy of lymphoid tissues (spleen, thymus, and bronchial lymph nodes) was found in animals of the highest exposure concentration. Degeneration of the testicular germinal epithelium was also observed in mice and rats that survived 5.0 or 10.0 mg/m3 exposure concentrations.
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PMID:Comparative inhalation toxicity of nickel subsulfide to F344/N rats and B6C3F1 mice exposed for 12 days. 365 67

Rats were exposed to single periods of inhalation of fumes generated by arc welding. Two processes were compared: either manual metal arc (MMA) using flux-coated mild steel (MS) electrodes or metal inert-gas (MIG) welding with stainless steel (SS). Widespread but small deposits of fume particles were cleared effectively from alveoli and airways. Peribronchial and subpleural aggregates of particle-laden macrophages remained. More massive and persistent lung-burdens were established by intratracheal administration of suspensions of fume-particles (10 mg and 50 mg, single doses). Initial pneumonitis was attributed to irritant gases or soluble toxic components of particles. MIG-SS particle deposits were more persistent and lesions more severe, inhibition of phagocytosis or clearance and damage to epithelial cells being associated with possible toxic effects in macrophages. Both types of particle caused alveolar epithelial thickening, with proliferation of granular pneumocytes and exudation of lamellar material. Foam cells appeared in alveoli. Long-term effects (80-300 days) involved formation of nodular aggregates of particle-laden macrophages. Giant cells were formed. Nodules containing MIG-SS material were irregular and surrounded by collapsed and thickened epithelium. Soluble chromium or nickel constituents are cited as probable active agents producing effects resembling those of cytotoxic non-fibrogenic dusts, e.g., soluble silicas . MMA-MS particles produced low-grade fibrotic ( collagenised ) changes.
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PMID:Pneumoconiotic effects of welding-fume particles from mild and stainless steel deposited in the lung of the rat. 673

A man was taken ill suddenly while spraying nickel using a thermal arc process. He was relieved of his duties and sent home. His condition deteriorated and he was admitted to hospital with a diagnosis of pneumonia. Thirteen days after exposure he died. At post mortem examination the cause of death was determined to be shock lung or Adult Respiratory Distress Syndrome (ARDS). Reproduction of the conditions under which the man had operated the metal arc process produced nickel concentrations of 382.1 mg m-3 in the air next to the operator. Of this nickel, 64.6% was in the form of particles less than 1.4 microns in diameter; the majority being 50 nm in diameter. The total amount of nickel inhaled by the man, who operated the process for 90 min, was estimated to be nearly 1 g. The toxicity of the nickel is thought to be associated with the very fine particulate nature of the metal fume and the large amount inhaled. The importance of wearing adequate protective equipment while operating this metal arc process is stressed.
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PMID:Death following exposure to fine particulate nickel from a metal arc process. 782 32

Though metals represent the largest group of elements they rather rarely cause respiratory diseases. This article will therefore review the most important ones caused by inhaled dusts of metals and some of their inorganic compounds, but leaving aside silicosis and silicatosis as well as iatrogenically induced metal pneumopathies. Among toxic inflammatory diseases metal fume fever, an influenza-like condition caused by zinc oxide, ranks as the commonest. Activities such as oxi-acetylene cutting and welding of zinc covered metal pieces account for about 90% of all cases compensated in Switzerland. Due to the non-recurrent character of this type of work, the typical waning of symptoms while exposure is going on has become seldom. Toxic pneumonia caused by inhaled metal fumes occurs rather seldom. However, serious cases have been reported where soldiers were exposed to zinc chloride from smoke bombs. The existence and extent of chronic airflow limitation due to occupational exposure to metallic dusts have not been widely examined but are to be assumed when there is poor occupational hygiene. Concerning asthma, there are at least four metals and several of their compounds which have been proven to cause variable airway narrowing, namely chromium, nickel, platinum and cobalt (the latter as hardmetal). Platinum complex salts (chloro-compounds) are very potent sensitizers leading to a notable prevalence of asthma among exposed workforces. Nevertheless, there have been no such cases in Switzerland for more than ten years. Hard-metal not only causes asthma but also an alveolitis-like interstitial lung disease progressing to fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lung disorders due to metals]. 789 59


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