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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The workforce of Alberta, a province rich in fossil fuel, faces an increasing risk of exposure to hydrogen sulfide (H2S). Basic knowledge of the population exposed during the years 1969 to 1973 inclusive was accumulated to identify the immediate medical and management problems. Data were recorded from three sources of records: the Workers' Compensation Board of Alberta, the Alberta Hospital Services Commission and the provincial coroner's office. There were 221 cases of exposure to H2S. The overall mortality was 6%; 5% of victims were dead on arrival at hospital. Admission to hospital was required for 65% of the victims arriving at a hospital emergency room (78% of the 221). Acute problems were coma, dysequilibrium and respiratory insufficiency with pulmonary edema. Increased attention to cardiopulmonary resuscitation at the exposure site and during transportation to hospital is necessary to reduce the mortality from H2S exposure. No long-term adverse effects were apparent in the survivors.
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PMID:Hydrogen sulfide poisoning: review of 5 years' experience. 14 53

Significant progress has been made in determining the action of sulfide on the primary target organs. It is reasonably clear that sulfide causes both K(+)-channel-mediated hyperpolarization of neurons and potentiation of other inhibitory mechanisms. It is not clear whether these processes are similar to those that occur in anoxia. Changes in perinatal and adult brain neurotransmitter content and release may be related to clinical impairment of cognition. H2S exposures at concentrations below the current occupational limits cause physiological changes in pulmonary function, thus suggesting that asthmatics are at risk. Studies of fetal and neonatal brain tissue have shown an abnormal development, and the long-term consequences of these neuronal changes have not yet been assessed. Finally, new approaches to therapy are required, such as the use of agents that actively remove sulfide from its sites of action. This may prove more useful in preventing some of the long-term adverse sequelae than the use of nitrites and hyperbaric O2, although the latter should be used in cases of pulmonary edema.
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PMID:Toxicology of hydrogen sulfide. 160 65

Hydrogen sulfide (H2S) poisoning involves a risk of hypoxic brain damage. Six patients who lost consciousness due to H2S poisoning are described. The symptoms varied from anosmia in the patient with the shortest but highest exposure to delayed neurological deterioration in the patient with the longest exposure. The two patients with the most serious symptoms developed pulmonary edema, which may have prolonged the hypoxia. The patients were reexaminated 5 years or more after the poisoning. The five patients who had been unconscious in H2S atmosphere for from 5 to 15-20 min showed persisting impairment at neurological and neuropsychological re-examination. Memory and motor function were most affected. One patient was seriously demented. Recent reports of large groups of H2S-poisoned workers probably underestimate the risk of sequelae, due to the inclusion of cases with exposure of short duration and lack of follow-up.
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PMID:Brain damage caused by hydrogen sulfide: a follow-up study of six patients. 186 21

This study was designed to test whether intraperitoneally injected sodium hydrosulfide (NaHS) would mimic the pulmonary alterations induced by lethal peracute exposure to an atmosphere containing hydrogen sulfide. Groups of five Sprague-Dawley rats were exposed to an atmosphere of either 2317.6 +/- 547.3 mg m-3 H2S (H2S group) or no H2S (air group), or were injected intraperitoneally with a solution containing 30 mg kg-1 sodium hydrosulfide (NaHS group) or saline solution (vehicle control). Rats of the air and saline groups were killed by cervical dislocation. All rats exposed to H2S or injected with NaHS died within 3 min; however, only rats exposed to H2S showed severe respiratory distress in the agonic phase preceding death. In addition, rats in the H2S group had a notable discharge of serous fluid from the mouth and nostrils. At necropsy, all rats in the H2S group had gross and histologic evidence of pulmonary edema characterized by massive extravasation of eosinophilic fluid into the bronchoalveolar space. In contrast, the lungs of rats injected with NaHS or saline or exposed to air were unaffected. It was concluded that the edematogenic effect of H2S in the lungs cannot be reproduced by injection of NaHS. The severity of lung edema induced by a peracute exposure to H2S was extensive enough to account for death.
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PMID:Peracute toxic effects of inhaled hydrogen sulfide and injected sodium hydrosulfide on the lungs of rats. 271 35

Fischer-344 rats were killed 1, 18, and 42 hr after a single 4-hr exposure to an atmosphere of 0, 116, or 615 mg m-3 of hydrogen sulfide (H2S). Lungs, fixed by the intratracheal route, were examined by light and electron microscopy. Histologic changes were transient and mainly present in rats exposed to 615 mg m-3 H2S. Lesions included severe but transitory pulmonary edema and fibrinocellular alveolitis which was restricted to the proximal alveolar region of the lung. Electron microscopically, ciliated bronchiolar cells were the only cells that developed necrosis; they were rapidly replaced by mitosis. Alveolar endothelium had cytoplasmic blebs, but alveolar epithelium had minor changes. No mast cell degranulation was detected in lungs with edema. A 4-hr exposure to 615 mg m-3 is markedly edematogenic for the lung but only moderately cytotoxic for pulmonary cells.
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PMID:Histologic and ultrastructural alterations in lungs of rats exposed to sub-lethal concentrations of hydrogen sulfide. 323 10

Occupational exposure to hydrogen sulfide (H2S) and the medical management of H2S-associated toxicity remains a problem in the sour gas industry and some other industrial settings. The acute effects of exposure to H2S are well recognized, but accurate exposure-response data are limited to acutely lethal effects, even in animal studies. Odor followed by olfactory paralysis and keratoconjunctivitis are the characteristics effects of H2S at lower concentrations. H2S-induced acute central toxicity leading to reversible unconsciousness is a "knockdown"; it is controversial whether repeated or prolonged knockdowns are associated with chronic neurologic sequelae but the evidence is suggestive. Knockdowns can be acutely fatal as a consequence of respiratory paralysis and cellular anoxia. Pulmonary edema is also a well-recognized acute effect of H2S toxicity. Human studies of sublethal exposure with satisfactory exposure assessment are almost nonexistent. There are indications, poorly documented at present, of other chronic health problems associated with H2S exposure, including neurotoxicity, cardiac arrhythmia, and chronic eye irritation but apparently not cancer. Rigorous and comprehensive studies in the sour gas industry are difficult, in part because of confounding exposures and uncertain end points.
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PMID:Occupational exposure to hydrogen sulfide in the sour gas industry: some unresolved issues. 781 93

Selenium is an essential trace element at lower concentrations and toxic at higher concentration. Animals can metabolize both inorganic and organic forms and convert non methylated Se to mono--or di--or tri--methylated forms, of which, mono-methylated forms are most toxic. Glutathione reductase converts selenoglutathione to H2S in liver and erythrocytes and is ultimately excreted. Se effects the toxicities of xenobiotic agents, provides antagonistic effect to Sulphur and co-administration with Zn increase Se retention in certain organs. At its toxic level (4-8 ppm) it increases Cu contents of heart, liver and kidney and has detoxifying or protecting effect against Cd and Hg. It is a prosthetic group of several seleno metalloenzymes. The concentration of the element is decreased in serum/plasma or erythrocytes of patients of AIDS, trisomy-21, Crohn's and Down's syndrome, phenylketonurea, Keshan's disease and cancer. Rather, the element has antiproliferative and cancer protecting effect. Se content of testes increases considerably during pubertal maturation and, during Se deficiency, the supply to the testes has priority over the other tissues. The element is localized in the mitochondrial capsule protein (MCP) and is involved in biosynthesis of testosterone. Neither the age of mother nor the concentration of Se during pregnancy has any effect on weight of baby or the length of pregnancy. Se levels in human milk is affected by maternal intake and its requirements by infants and young children are higher for their rapid growth. Clinical symptoms of its toxicity include severe irritations of respiratory system, metallic taste in mouth, formication of nose, signs of rhinitis, lung edema and brancho-pneumonia. The typical garlic odour of breath and sweat is due to dimethyl-selenide.
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PMID:Selenium--its biological perspectives. 823 95

Hydrogen sulphide (H2S) is the primary chemical hazard in natural gas production in 'sour' gas fields. It is also a hazard in sewage treatment and manure-containment operations, construction in wetlands, pelt processing, certain types of pulp and paper production, and any situation in which organic material decays or inorganic sulphides exist under reducing conditions. H2S dissociates into free sulphide in the circulation. Sulphide binds to many macromolecules, among them cytochrome oxidase. Although this is undoubtedly an important mechanism of toxicity due to H2S, there may be others H2S provides little opportunity for escape at high concentrations because of the olfactory paralysis it causes, the steep exposure-response relationships, and the characteristically sudden loss of consciousness it can cause which is colloquially termed 'knockdown.' Other effects may include mucosal irritation, which is associated at lower concentrations with a keratoconjunctivitis called 'gas eye' and at higher concentrations with risk of pulmonary oedema. Chronic central nervous system sequelae may possibly follow repeated knockdowns: this is controversial and the primary effects of H2S may be confounded by anoxia or head trauma. Treatment is currently empirical, with a combination of nitrite and hyperbaric oxygen preferred. The treatment regimen is not ideal and carries some risk.
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PMID:Hydrogen sulphide. 891 53

This paper deals with the problem of fatal accidents that occur repeatedly in "confined spaces", with particular attention to exposure to hydrogen sulfide (H2S). This, at high concentrations, appears to be the most compatible with the dynamics of many recent incidents with sudden death. H2S offers little chance to escape at high concentrations because of the smell that causes paralysis of olfactory nerves and sudden loss of consciousness. Besides the problem of acute exposure to high concentrations, health effects may also be caused by prolonged and repeated exposures to lower doses: at low concentrations can occur eyes irritation with keratoconjunctivitis and, at higher concentrations, the risk of pulmonary oedema or chronic central nervous system sequelae. In this paper several aspects are detailed, including an interpretative analysis of the content of Articles 66 and 121 of Legislative Decree 81/2008 and subsequent amendments, the work contexts where H2S is present as a raw material or product of the process and the effects on human health. Moreover, due to few epidemiological initiatives at national level, some aspects related to the accident dynamics are taken into account through the reconstruction of cases of fatal accidents occurred in Italy in recent years and comparing it with that reported in the literature of other Countries.
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PMID:[Fatal hydrogen sulphide (H2S) poisoning in "confined spaces"]. 2339 47

Oxygen (O2) sensing by the carotid body and its chemosensory reflex is critical for homeostatic regulation of breathing and blood pressure. Humans and animals exhibit substantial interindividual variation in this chemosensory reflex response, with profound effects on cardiorespiratory functions. However, the underlying mechanisms are not known. Here, we report that inherent variations in carotid body O2 sensing by carbon monoxide (CO)-sensitive hydrogen sulfide (H2S) signaling contribute to reflex variation in three genetically distinct rat strains. Compared with Sprague-Dawley (SD) rats, Brown-Norway (BN) rats exhibit impaired carotid body O2 sensing and develop pulmonary edema as a consequence of poor ventilatory adaptation to hypobaric hypoxia. Spontaneous Hypertensive (SH) rat carotid bodies display inherent hypersensitivity to hypoxia and develop hypertension. BN rat carotid bodies have naturally higher CO and lower H2S levels than SD rat, whereas SH carotid bodies have reduced CO and greater H2S generation. Higher CO levels in BN rats were associated with higher substrate affinity of the enzyme heme oxygenase 2, whereas SH rats present lower substrate affinity and, thus, reduced CO generation. Reducing CO levels in BN rat carotid bodies increased H2S generation, restoring O2 sensing and preventing hypoxia-induced pulmonary edema. Increasing CO levels in SH carotid bodies reduced H2S generation, preventing hypersensitivity to hypoxia and controlling hypertension in SH rats.
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PMID:Inherent variations in CO-H2S-mediated carotid body O2 sensing mediate hypertension and pulmonary edema. 2439 6


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