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

For a number of years we have observed six patients whose illness began after inhaling high concentrations of mercury vapor in a single exposure. They all had symptoms of acute mercury poisoning with fever, chills, chest pain, and weakness. Three men had diffuse pulmonary infiltrates on chest x-ray suggesting chemical pneumonitis. Two of the men excreted large amounts of mercury in their urine two days after exposure following BAL therapy. Their chronic symptoms differed somewhat, but many complained of nervousness, irritability, lack of ambition, and loss of sexual desire. Chronic mercury poisoning is generally felt to follow only long periods of exposure. Although thess patients had symptoms which are not pathognomonic of chronic mercury poisoning, we feel the events described strongly suggest their relationship to a single brief exposure and represent a form of chronic mercurialism.
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PMID:Chronic mercury poisoning from a single brief exposure. 69 Jul 36

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

A family of four was exposed to toxic levels of mercury vapor while attempting to extract silver from mercury amalgam. All four suffered respiratory failure and subsequent death despite chelation therapy with dimercaprol. Histologic findings at autopsy were similar in all four cases demonstrating a progression of acute lung injury that appeared related to postexposure day survival. There were no clinical signs of extrapulmonary manifestations despite toxic serum mercury levels. Although serum mercury levels decreased in response to the mercury chelating agent dimercaprol, serum levels remained in the toxic range and no clinical response was observed. Acute inhalational exposure to high concentrations of mercury vapor causes pneumonitis that can lead to respiratory failure and death. This continues to be a health hazard in both the workplace and the home environment.
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PMID:Respiratory failure and death following acute inhalation of mercury vapor. A clinical and histologic perspective. 198 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

In a group of six workers acutely exposed to metallic mercury vapour in a confined space, one patient had acute renal and respiratory failure which required daily haemodialysis and mechanical ventilation, another had acute bilateral pneumonitis with respiratory insufficiency, and the other four had corrosive oropharyngeal mucositis with a 'flu-like syndrome. Serum and urinary mercury showed an obvious correlation with the clinical picture. After removal from the source of exposure and the institution support measures (including chelant therapy in the first two patients), all recovered without evidence of residual damage.
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PMID:Acute mercury vapour intoxication: report of six cases. 249 55

A total of 5 Staphylococcus aureus strains from patients with postinfluenzal staphylococcal pneumonia, 7 from burn patients with staphylococcal pneumonia, and 21 from the nasopharynx of carriers were phenotypically characterized. All or most strains produced coagulase, clumping factor, DNase, thermostable DNase, protease, gelatinase, lipase, and pigment; the strains were low to moderate producers of extracellular protein A, fibrinolysin, and alpha-hemolysin. All strains were sensitive to mercury, half were sensitive to arsenate and cadmium, and 67 to 92% were resistant to penicillin. Differences between strains were not statistically significant. Cell surface hydrophobicity was determined by measuring percent adsorption to hexadecane. Hydrophobicity of postinfluenzal staphylococcal pneumonia strains was significantly lower than that of pneumonia strains from burn patients and carriers (P less than 0.005). Immunoblot experiments with sera immune to one clinical test strain allowed the separation of all strains into three groups based on probe-positive reactions with primarily four staphylococcal polypeptides (154,200, 130,000, 77,100, and 64,400 molecular weight). The difference in distribution of clinical and carrier strains was highly significant (P = 0.007).
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PMID:Characterization of clinical strains of Staphylococcus aureus associated with pneumonia. 301 27

A 3-year-old child with cricopharyngeal dysfunction is reported. Swallowing difficulties, nasal regurgitation, and gagging developed at 2 months of age. Repeated aspirations and over 40 episodes of pneumonia necessitating multiple hospitalizations occurred up to 2 years of age, along with pharyngeal pooling of saliva and inability to swallow solid food. Barium was held up at the cricopharyngeal level, and a prominent esophageal impression was seen at the same level. Symptoms were completely alleviated after two esophageal dilatations by mercury dilators, and the relief persisted for the 6 months of follow-up. The diagnosis of cricopharyngeal dysfunction is discussed, and the necessity for manometric studies, in the face of often misleading radiologic appearance, is emphasized. It is suggested that early use of esophageal dilatations might prevent prolonged morbidity and afford long-term symptomatic relief.
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PMID:Cricopharyngeal dysfunction in childhood: treatment by dilatations. 369 45

This report describes a patient who developed acute chemical pneumonitis following overexposure to metal mercury vapor. The exposure occurred in a gold extraction facility where a gold-mercury amalgam was heated in a confined area. Prompt treatment with penicillamine and corticosteroids was instituted; radiologic pulmonary infiltrates disappeared within a week, but there was little change in the pulmonary function abnormalities (restriction and diffusion impairment) over the period of 11 months of follow-up. This raises the possibility of persistent pulmonary function impairment after metal mercury vapor-induced chemical pneumonitis.
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PMID:Acute mercury poisoning with severe chronic pulmonary manifestations. 401 88

Seven cases of acute intoxications by inhalation of metallic vapors are reported. The metals involved were zinc in three cases, tin in one case and mercury in three cases. The severity of the respiratory symptoms was dependent from the inhalated metal. The inhalation of zinc or tin vapors produced an acute limited pneumonitis. A lesional pulmonary oedema and acute interstitial fibrosis with lethal outcome was observed in two cases of intoxication by mercury vapors. The treatment by dimercaptopropanol used in mercury intoxications, increased urinary mercury excretion, but did not improve the pulmonary symptoms.
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PMID:[Acute poisoning by inhalation of metallic vapors]. 667 9

An 8-month-old girl with acute mercury vapor intoxication experienced pneumonitis with respiratory failure, bilateral pneumothorax, pneumomediastinum, acute renal failure, hepatocellular dysfunction, and seizures. Treatment centered on intensive supportive care; her survival is exceptional among infants with severe mercury intoxication.
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PMID:Survival after acute mercury vapor poisoning. 686 32


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