nitrogen-dioxide and Pulmonary-Edema

Acute toxic inhalation by irritant, and particularly oxidant, gases has until recently been considered to be no more complicated conceptually than a chemical burn of the epithelial surface. More recently, however, toxic inhalation has been appreciated to be a complex process involving biochemical, morphological and functional changes which are quantitatively similar, although inducible by different agents. Recent advances in pulmonary pathophysiology, inhalation toxicology, and particularly endothelial biology have clarified the events occurring at the moment of, and immediately following, exposure to oxidant gases. Studies of the pathophysiologic mechanisms associated with toxic inhalation by oxidant gases have been relatively static, however. Implications of recent findings in related fields illuminate the pathophysiology of toxic inhalation. Several principal speakers in this workshop are collaborating in an effort to develop a research facility for the study of toxic inhalation injury. This would be an international registry to serve as a teaching and research facility for documentation of cases of occupational and environmental toxic inhalation, considered as lung injury resulting from the inhalation of a toxic substance in a workplace setting or an uncontrolled release affecting residents of a community. The registry, as proposed, would encourage submissions by clinicians and institutions of a data set on each patient and on each incident; the registry would further encourage long-term follow-up of subjects and documentation of residual effects.

Topics: Administration, Inhalation; Air Pollutants; Humans; International Cooperation; Models, Theoretical; Nitrogen Dioxide; Pulmonary Edema; Registries; Research Design; Sentinel Surveillance

Topics: Environmental Exposure; Equipment Failure; Hockey; Humans; Nitrogen Dioxide; Pulmonary Edema; Respiratory Tract Diseases; Time Factors

Topics: Adult; Age Factors; alpha 1-Antitrypsin; alpha 1-Antitrypsin Deficiency; Alpha-Globulins; Animals; Antigen-Antibody Reactions; Cadmium; Collagen; Elastin; Environmental Exposure; Humans; Infant; Leukocytes; Lung; Lung Diseases; Macrophages; Microbial Collagenase; Nitrogen Dioxide; Ozone; Pancreatic Elastase; Peptide Hydrolases; Pulmonary Alveoli; Pulmonary Edema; Pulmonary Emphysema; Smoking

Topics: Animals; Capillary Permeability; Dimethyl Sulfoxide; Environmental Exposure; Humans; Lung; Lymphatic System; Nitrogen Dioxide; Occupational Diseases; Pulmonary Artery; Pulmonary Circulation; Pulmonary Edema; Rats; Sulfur Dioxide

Topics: Aged; Ammonia; Humans; Male; Middle Aged; Nitric Oxide; Nitrogen; Nitrogen Dioxide; Nitrous Oxide; Occupational Diseases; Pulmonary Edema

Topics: Air Pollution; Airway Resistance; Alkaline Phosphatase; Animals; Bronchi; Bronchitis; Constriction; Cricetinae; Guinea Pigs; Humans; Lung Neoplasms; Mice; Nitrogen Dioxide; Ozone; Pulmonary Edema; Rabbits; Rats; Respiratory System; Spirometry; Sulfur Dioxide; Vehicle Emissions

Topics: Air Pollution; Animals; Blood Circulation; Bronchial Diseases; Lung Diseases; Nasal Mucosa; Nitrogen Dioxide; Nose Diseases; Ozone; Pulmonary Circulation; Pulmonary Edema; Respiratory Tract Diseases; Sulfoxides; Sulfur; Sulfur Dioxide

To establish the rats model of acute pulmonary edema induced by inhalation of high concentrations of nitrogen dioxide (NO2).. 38 SD rats were divided into the experimental group (n = 30) and the control group (n = 8). 30 rats in the experimental group were exposed to (6747.47 ± 25.24) mg/m(3) NO2 in the exposure system. At the time point of 6, 12, 18, 24 h, chest X-ray examination was taken for the experimental group. And at each time point, 6 rats were sacrificed after taking blood samples. After sacrificing, the lung of rats was taken for pathological examination and calculated lung wet/dry weight ratio. Erythrocyte superoxide dismutase (SOD) activity and plasma atrial natriuretic peptide (ANP) concentration of blood samples were detected.. Acute pulmonary edema was successfully induced by exposure to NO2 in 30 rats within 24 hours. There were some cloudy shadows without clear edge on the chest X-ray. To the time point of 12 hours, shadows combined with each other, and to the time point of 18 hours, the whole lung became "white" on the X-ray. The situation stabilized but not improved at the time point of 24 hours. HE staining of the lung tissue showed that to the time point of 6 hours, the alveolar gap increased and small amount of eosinophilic liquid leaked into alveolar. To the time point of 12 hours, alveolar combined with each other and eosinophilic liquid increased in amount. To the time point of 18 hours, the whole alveolar was filled with eosinophilic liquid and the situation stabilized till the time point of 24 hours. Wet/dry weight ratio of the experimental group at each time point were 5.6 ± 0.20, 6.89 ± 0.25, 8.03 ± 0.47, 7.81 ± 0.45. There was significant difference compared with the control group which was 4.72 ± 0.06 (P < 0.01). There was statistical difference between 12, 18, 24 h and 6 h time points (P < 0.01). Moreover, statistical difference was observed between 18, 24 h and 12 h time points for wet/dry weight ratio (P < 0.01). The erythrocyte SOD activity reduced significantly. Compared with the control group, there was a statistical difference (P < 0.01) at each time point. After exposure of 18 and 24 hours, plasma ANP concentration (136.66 ± 35.37) and (134.10 ± 60.41) ng/ml respectively, which were higher than (31.31 ± 13.06) ng/ml of control group and (34.71 ± 13.42) ng/ml of 6 hours time point and (47.98 ± 7.86) ng/ml. The differences were significant (P < 0.01).. High concentrations of NO2 can induce acute pulmonary edema model successfully in SD rats.

Topics: Animals; Disease Models, Animal; Female; Nitrogen Dioxide; Pulmonary Edema; Rats; Rats, Sprague-Dawley

To investigate the therapeutic effect of glucocorticoids on the acute pulmonary edema in rats induced by nitrogen dioxide (NO₂).. Thirty SD female rats were randomly equally divided into 5 groups: normal control group, NO₂ exposed group, high-, middle- and low-dose of glucocorticoids treated group (6 rats per group). 6 rats in the normal control group were exposed to room air for 30 min, and the other rats to NO₂. 18 rats in the glucocorticoids group were treated with different doses of dexamethasone (6.0, 3.0, 1.0 mg/kg), while the rats in the NO₂ poisoning group were treated with normal saline (2.5 mg/kg). The lung wet/dry (W/D) weight ratio was calculated, and plasma atrial natriuretic peptide (ANP) levels, superoxide dismutase (SOD) activity from whole blood, plasma interleukin 6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor-α (TNF-α) and Interferon-γ (IFN-γ) were detected by enzyme-linked immunosorbent assay (ELISA).. The lung W/D ratios were increased significantly in glucocorticoids treated group and NO₂-exposed group compared with normal control group (P < 0.05), while they were significantly reduced in glucocorticoids treated group as compared with NO₂-exposed group (P < 0.05). SOD activity in whole blood in glucocorticoids treated group and NO₂-exposed group was significantly lower than that of normal control group (P < 0.05), while it was no significant difference between that of glucocorticoids treated group and NO₂-exposed group (P > 0.05). Plasma ANP was significantly increased in NO₂-exposed group compared with normal control group (P < 0.05), while it was significantly decreased in glucocorticoids treated group compared with NO₂-exposed group (P > 0.05). Plasma TNF-α of high-, middle- and low-dose of glucocorticoids treated group [(27.04 ± 8.19), (40.10 ± 9.09), (39.76 ± 9.60) pg/ml] was decreased significantly as compared with NO₂-exposed group (68.55 ± 27.84 pg/ml) (P < 0.05). Plasma IL-6 in high- and middle-dose of glucocorticoids treated group [(15.97 ± 6.18), (19.69 ± 5.52) pg/ml] was significantly decreased as compared to NO₂-exposed group [(29.29 ± 9.31) pg/ml] (P < 0.05). Plasma IL-10 in high-, middle- and low-dose of glucocorticoids treated group [(23.24 ± 5.14), (27.78 ± 8.17), (33.29 ± 10.42) pg/ml] was significantly reduced compared with NO₂-exposed group [(44.38 ± 9.19) pg/ml] (P < 0.05). Plasma IFN-γ in high- and middle-dose of glucocorticoids treated group [(7.21 ± 4.55), (19.23 ± 4.35) pg/ml] was reduced compared with NO₂-exposed group [(30.83 ± 6.82) pg/ml] (P < 0.05).. High-, middle-, low-dose glucocorticoids all can improve the permeability of alveolar wall and capillary, and have nonspecific anti-inflammatory effects. The therapeutic effects on pulmonary edema are significant. High and middle dose of glucocorticoids treated group are more useful for decreased inflammatory factors.

Topics: Animals; Disease Models, Animal; Female; Glucocorticoids; Nitrogen Dioxide; Pulmonary Edema; Rats; Rats, Sprague-Dawley

Topics: Humans; Male; Middle Aged; Nitrogen Dioxide; Pulmonary Edema

Human inhalation exposures to relatively high mass concentrations of the oxidant gas nitrogen dioxide (NO2) can result in a variety of pulmonary disorders, including life-threatening pulmonary edema, pneumonia, and bronchiolitis obliterans. Inasmuch as most experimental studies to date have examined NO2-induced lung injury following exposures to near ambient or supra-ambient concentrations of NO2, e.g., < or = 50 ppm, little detailed information about the pulmonary injurious responses following the acute inhalation of higher NO2 concentrations that are more commensurate with some actual human exposure conditions is currently available. Described in this report are the results from a series of investigations in which various aspects of the inhalation toxicity of high concentrations of NO2 have been examined in laboratory rats. In the first component of our study, we characterized the kinetic course of development of lung injury following acute exposures to high concentrations of NO2 delivered over varying durations, and we assessed the relative importance of NO2 exposure concentration versus exposure time in producing lung injury. For a given exposure duration, the resulting severity of lung injury was found to generally scale proportionately with inhaled mass concentration, whereas for a given concentration of inhaled NO2, the magnitude of resulting injury was not directly proportional to exposure duration. Moreover, evidence was obtained that indicated exposure concentration is more important than exposure time when high concentrations of NO2 are inhaled. In a second component of our investigation, we assessed the pulmonary injurious response that occurs when NO2 is inhaled during very brief, 'high burst' exposures to very high concentrations of NO2. Such exposures resulted in significant lung injury, with the magnitude of such injury being directly proportional to exposure concentration. Comparisons of results obtained from this and the first component studies additionally revealed that brief exposures to the very high concentrations of NO2 are more hazardous than longer duration exposures to lower concentrations. In a third study series, we examined pre-exposure, exposure, and post-exposure modifiers of NO2-induced lung injury, including dietary taurine, minute ventilation, and post-exposure exercise. Results from these studies indicated: (i) dietary taurine does not protect the rat lung against high concentration NO2 exposure, (ii) the severity of acu

Topics: Administration, Inhalation; Animals; Disease Models, Animal; Dose-Response Relationship, Drug; Lung Diseases; Male; Nitrogen Dioxide; Permeability; Physical Conditioning, Animal; Pneumonia; Pulmonary Alveoli; Pulmonary Edema; Rats; Rats, Inbred F344; Respiration; Taurine; Time Factors

Exposure protocols were designed to ask whether lung damage in rats exposed to either ozone or nitrogen dioxide is proportional to dose rate or to cumulative dose. Thus, the response of rats to a constant product of concentration of oxidant air pollutant and time of exposure (C x T) was evaluated for 3-day exposures over a fourfold range of concentrations of ozone (0.2-0.8 ppm) or of nitrogen dioxide (3.6-14.4 ppm) for exposure durations of 6-24 hr per day. The response of rat lungs was quantified by changes in total protein content of lung lavage supernatants or by changes in content of specific cell types in lung lavage pellets. The results of these experiments clearly demonstrate that acute lung damage is a function of cumulative dose (that is, C x T product) for the three highest dose rates tested. However, when exposure duration is extended to include the entire 24-hr period (the lowest dose rate tested), there is a marked attenuation of pulmonary response. Rats were also exposed to mixtures of ozone and nitrogen dioxide with the C x T product held constant. Our results clearly demonstrate that when rats are exposed to combinations of ozone and nitrogen dioxide, lung damage is a function of peak concentration rather than a function of cumulative dose. This deviation from Haber's Law is attributed to a concentration-dependent, synergistic (greater than additive) response to this specific mixture of oxidant air pollutants.

Topics: Administration, Inhalation; Air Pollutants; Animals; Dose-Response Relationship, Drug; Drug Synergism; Lung; Male; Nitrogen Dioxide; Oxidants; Ozone; Pulmonary Edema; Rats; Rats, Inbred Strains

The treatment of nitrogen dioxide (NO2)-induced lung edema is controversial. In addition, mechanisms and patterns of interstitial edema formation in this form of increased permeability edema are unclear. To ascertain if methylprednisolone (MP) is effective in the therapy of NO2-induced edema, we exposed 108 unaesthetized guinea pigs, in groups of 12, to 277-448 ppm.hr NO2: in 60, we administered MP just before, and in 48 immediately after exposure. In each group, half the animals were randomly assigned to receive 30 mg/kg MP ip, and the other half saline. Mortality rates and lung water with wet weight/dry weight (W/D) ratios were calculated. Alveolar edema, periarterial interstitial edema, and NO2-induced bronchiolitis were graded semiquantitatively by light microscopy from freeze-substituted middle (ML) and lower lobes (LL). We found NO2 produced an exposure-dependent increase in lung water (R = 0.70, p less than 0.01). Treatment with MP preexposure produced a fourfold reduction mortality, and and a significant fall in W/D ratios and in alveolar and interstitial edema. No difference in the degree of acute bronchiolitis was found between treated and untreated animals, although ML had significantly more inflammation than LL. Treatment with MP immediately after NO2 was ineffective since mortality rates, W/D ratios, and alveolar and interstitial edema were not lower in the treated animals; there was significantly more intestitial edema in the middle lobes of the latter. Both LL and ML had equally abundant alveolar edema, but LL had significantly more interstitial edema, supporting our previous findings that in NO2-induced edema interstitial fluid accumulation follows alveolar flooding, with interlobar discrepancies probably due to differences in lung volume or in ventilation.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Capillary Permeability; Female; Guinea Pigs; Male; Methylprednisolone; Nitrogen Dioxide; Pulmonary Edema; Respiration; Species Specificity

Topics: Adrenal Cortex Hormones; Bronchiolitis Obliterans; Death, Sudden; Humans; Lung Diseases; Male; Nitrogen Dioxide; Pulmonary Edema; Silo Filler's Disease

Previous investigations have indicated that postexposure exercise (E) can can potentiate nitrogen dioxide (NO2)-induced lung injury. In this report, we (1) further characterize the potentiation of expression of NO2-induced lung injury in the rat by E; (2) characterize the postexposure period during which such potentiation by E can occur, i.e., "window of susceptibility"; (3) assess whether two E bouts performed during the "window of susceptibility" have even greater potentiating effects; and (4) determine if early postexposure E can extend the window of susceptibility. Groups of Fischer-344 rats were exposed to 100 ppm NO2 for 15 min, exercised at times ranging from 30 min to 24 hr thereafter, and sacrificed during a 24-hr postexposure period. Other exposed rats were exercised 30 min to 24 hr thereafter and sacrificed for lung studies 30 min following the E runs. Still other exposed animals were exercised immediately and at 8 or 24 hr postexposure and sacrificed 30 min after the last E run. NO2-exposed but rested rats, and sham-air-exposed and rested or exercised rats served as controls. E immediately or at 8 hr post-NO2 exposure caused marked increases in lung wet weight (LWW) and right cranial lobe dry weights (RCLDW) and more pronounced histopathologic disturbances beyond those following NO2 exposure and rest only. Potentiation of injury was not observed in rats exercised 24 hr after exposure. The pattern of subsidence of the LWW and RCLDW increases after immediate or 8 hr E differed with the increases in the former being more persistent. Two E bouts (30 min and 8 hr postexposure) caused lung changes consistent with an additive effect. E performed immediately after NO2 exposure extended the window of susceptibility to E beyond 24 hr.

Topics: Animals; Lung; Male; Nitrogen Dioxide; Organ Size; Physical Exertion; Pulmonary Edema; Rats; Rats, Inbred F344

To ascertain whether the pattern of fluid accumulation could be altered by an agent introduced through the airways, the authors studied the physiology and morphology of 11 dogs exposed to 150-494 ppm.hr NO2 and compared them with 3 new and 5 previously reported control dogs. NO2 caused a partly reversible decrease in systemic arterial pressure and cardiac output, a fall in arterial PO2, and rapid shallow breathing, while pulmonary arterial and wedge pressures remained normal. Post mortem, lower (LL) and middle (ML) lobes were frozen, sections fixed for light microscopy by freeze-substitution, and wet weight/dry weight (W/D) ratios were measured. Alveolar edema was graded, and the distribution of interstitial edema around arteries and veins and within bronchovascular bundles was studied with morphometry: edema ratios (ER) were calculated as area of interstitium/area of vessel or airway. We found that NO2 produced an exposure-dependent increase in lung water (r = 0.73), and that both LL and ML had similar W/D ratios (7.77 and 8.39, respectively) and percent alveolar edema (30% and 34%). Morphometry of interstitial edema showed that the ER for vessels and airways of edematous LL were essentially similar to controls, while those of the ML were markedly increased. It is concluded that NO2 produces exposure-related lung edema and preferential alveolar flooding with probable secondary interstitial accumulation. The discrepancies in interstitial edema between middle and lower lobes may be due to differences in lung volume or in ventilation.

Topics: Animals; Body Water; Dogs; Female; Hemodynamics; Lung; Male; Nitrogen Dioxide; Pulmonary Edema; Respiration

The effects of the cytochrome P450 inducer beta-naphthoflavone (BNF) on NO2 toxicity were studied in two strains of mice. In one strain (C57B1/6J), cytochrome P450 could be induced by the aromatic hydrocarbon, while in the other strain (DBA/2J) cytochrome P450 was not inducible by this compound. Mice were treated with BNF before and during 4 days of exposure to 20 ppm NO2. The body growth of NO2-exposed mice improved only in BNF-treated C57B1/6J mice. In this strain, BNF reduced both pulmonary edema (as measured by wet and dry lung weights or as assessed by histological studies) and lung peroxidation (as measured by malondialdehyde). This protective effect of BNF on NO2 toxicity in C57B1/6J mice was associated with an increase in the components of the cytochrome P450 system (cytochrome P450 and cytochrome b5), whereas the activities of pulmonary antioxidant enzymes (superoxide dismutase, glutathione peroxidase, and glutathione reductase) were not significantly increased. These data suggest that the induction of the cytochrome P450 system may be important in promoting NO2 tolerance in those strains of mice in which the cytochrome P450 system is genetically inducible.

Topics: Animals; Antioxidants; Benzoflavones; beta-Naphthoflavone; Body Weight; Cytochrome P-450 Enzyme System; Enzyme Induction; Female; Flavonoids; Lipid Peroxides; Lung; Malondialdehyde; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; Nitrogen Dioxide; Pulmonary Edema; Species Specificity

Various corticoid derivatives administered by inhalation or intraperitoneally were investigated for a preventive effect on the pulmonary oedema of the rat induced by the 30-min inhalation of 100-105 ppm NO2. After inhalational administration in the form of an aqueous aerosol, dexamethasone-21-isonicotinate showed a considerably greater efficacy than beclomethasone-17,21-dipropionate or dexamethasone-21-dihydrogen phosphate. With prophylactic intraperitoneal administration dexamethasone (free alcohol), dexamethasone-21-dihydrogen phosphate and 6 alpha-methylprednisolone-21-dihydrogen succinate had to be given in much higher doses than dexamethasone-21-isonicotinate to achieve the same effects on the toxic pulmonary oedema.

Topics: Adrenal Cortex Hormones; Aerosols; Animals; Female; Injections, Intraperitoneal; Nitrogen Dioxide; Pulmonary Edema; Rats; Rats, Inbred Strains

Topics: Animals; Drug Interactions; Glucocorticoids; Histamine; Lung; Male; Nitrogen Dioxide; Pulmonary Edema; Rats; Rats, Inbred Strains; Sodium Salicylate

Topics: Animal Feed; Humans; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Pulmonary Edema; Silage

The histopathology of rat lung after exposure to high concentrations of mixed oxides of nitrogen (NOx) has been studied. Considerable damage was observed, which initially took the form of 'thickening' and 'blebbing' of the alveolar epithelium and disruption of type II pneumocytes. These early changes were attributed to the direct effect of the oxidant action of NOx. There then followed a latent period of approximately 6 h after which the development of oedema of the interstitium and alveolar septum was observed. Clinical observations and the results from light and electron microscopical examination suggested that the lung damage caused by exposure to 518 parts/10(6) NOx for 5 min was greater than that caused by 1435 parts/10(6) for 1 min. This was not supported by the findings from light microscopy where similar damage was observed at both dose levels. These results suggest that such exposures might pose a risk of lung damage to man.

Topics: Animals; Dose-Response Relationship, Drug; Lung; Lung Diseases; Male; Microscopy, Electron; Nitric Oxide; Nitrogen Dioxide; Nitrogen Oxides; Pulmonary Edema; Rats; Rats, Inbred Strains

A collective nitrous fumes poisoning (five cases) is reported. Two patients (case 3 and case 4) were comatose, in severe respiratory distress. Shock and slate blue cyanosis were noted. Physical examination and chest X ray revealed acute pulmonary edema-Methemoglobin levels were 71,3% (case 3) and 58% (case 4). Despite treatment both of them died from severe hypoxia resulting in cardiorespiratory arrest. Post-mortem examination was performed upon these four men. On admission the last one (case 5) was conscious, and in good hemodynamic condition. Acute pulmonary edema and cyanosis were present. Methemoglobin level was 37,3%. This patient recovered appropriate therapy. For case 1 and 2 acute anoxia due to methemoglobinemia seems to be cause of death. For cases 3 and 4 death is due to hypoxemia associated with pulmonary edema.

Topics: Accidents, Occupational; Bronchi; Cyanosis; Hemodynamics; Humans; Lung; Methemoglobinemia; Nitrates; Nitrogen Dioxide; Nitrogen Oxides; Occupational Diseases; Pulmonary Edema; Radiography; Water-Electrolyte Imbalance

Topics: Animals; Animals, Newborn; Cell Survival; Lung; Nitrogen Dioxide; Pulmonary Edema; Rats; Rats, Inbred Strains

Pretreatment with cycloheximide or emetine provided significant protection against pulmonary edema in rats exposed to ozone or nitrogen dioxide. Other inhibitors of protein-synthesis, actinomycin D or puromycin, failed to show such effects. Possible actions of these agents as well as the doses and times that afforded the significant protection were investigated. These agents, by themselves, did not alter the water content of the lungs. In vitro study revealed that both cycloheximide and emetine hardly acted as scavengers of oxidant. Pretreatment with either agent was associated with a significant increase in the activity of glucose 6-phosphate dehydrogenase of the lungs, but the increase did not necessarily coincide with the protection. Activity levels of non-protein SH, glutathione-peroxidase and -reductase in the lungs of rats treated with either agent were scarcely altered. The effect of these agents administered in vivo or in vitro on the in vitro lipid peroxidation by air was also investigated. Other possible mechanisms of these agents responsible for the protective effect against pulmonary edema induced by oxidants were also discussed.

Topics: Animals; Cycloheximide; Emetine; Male; Nitrogen Dioxide; Ozone; Premedication; Pulmonary Edema; Rats; Rats, Inbred Strains

Topics: Animals; Blood Cell Count; Dogs; Lung Diseases; Nitrogen Dioxide; Pulmonary Diffusing Capacity; Pulmonary Edema; Ventilation-Perfusion Ratio

Topics: Airway Resistance; Animals; Bronchi; Bronchial Provocation Tests; Hemodynamics; Lung; Mucus; Nitrogen Dioxide; Pulmonary Circulation; Pulmonary Edema; Sheep; Trachea

Serial physiologic studies were performed to characterize both the immediate and delayed effects of a single occupational exposure to nitrogen dioxide in a nonsmoker. During the initial acute stage of pulmonary edema, the abnormal static pressure-volume curve and decreased static compliance corresponded to a reduction in pulmonary volume. During the delayed acute stage, elastic recoil and properties of resistance to flow were normal, but dynamic compliance was reduced and dependent on respiratory frequency, and oxygen transport was abnormal during exercise, which is consistent with dysfunction of the small airways.

Topics: Forced Expiratory Flow Rates; Forced Expiratory Volume; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Pulmonary Edema; Respiration Disorders; Total Lung Capacity; Vital Capacity

Twenty-three patients exposed to nitrogen dioxide in agriculture or industry were referred to the University of Wisconsin Medical Center. Eighteen experienced a transient upper respiratory tract syndrome; five developed pulmonary edema or bronchiolitis obliterans. This latter group responded to steroid therapy but all demonstrated evidence of persistent pulmonary dysfunction on follow-up studies. Combining our findings with those in the literature we concluded: (1) exposure to NO2 is more common than generally appreciated; (2) case fatality is high--29% for silo-filler's disease; (3) steroids are effective therapy and should be continued for at least eight weeks; (4) although the majority recover without significant sequelae, some individuals may develop persistent functional abnormalities; (5) there is no evidence that long-term exposure to low concentrations of NO2 leads to chronic airway obstruction; and, (6) NO2-induced pulmonary disease could be elminated with appropriate preventive measures.

Topics: Adult; Female; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Pneumonia; Prednisone; Pulmonary Edema; Radiography; Syndrome

Topics: Bronchitis; Environmental Exposure; Humans; Male; Middle Aged; Nitrates; Nitrogen Dioxide; Occupational Diseases; Pulmonary Edema

Topics: Adult; Animals; Dogs; Guinea Pigs; Humans; Male; Mice; Nitrogen Dioxide; Occupational Diseases; Pulmonary Edema; Rabbits; Rats

Topics: Adult; Humans; Male; Metallurgy; Mining; Nitrogen Dioxide; Occupational Diseases; Pulmonary Edema; Radiography

Topics: Aging; Animals; Bronchi; Lung; Male; Nitrogen Dioxide; Pulmonary Alveoli; Pulmonary Edema; Rats

Topics: Accidents, Occupational; Adult; Follow-Up Studies; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Phosgene; Poisoning; Pulmonary Edema; Respiratory Function Tests; Switzerland

Topics: Animals; Bronchi; Dogs; Environmental Exposure; France; History, 19th Century; Humans; Middle Aged; Nitrogen Dioxide; Poisoning; Pulmonary Edema; Time Factors

Topics: Animals; Drug Synergism; Environmental Exposure; Lung; Male; Mice; Nitrogen Dioxide; Ozone; Phagocytosis; Phosphorus Radioisotopes; Pulmonary Edema; Staphylococcus

Topics: Anti-Bacterial Agents; Carbon Monoxide Poisoning; Child; Child, Preschool; Dexamethasone; Humans; Hypoxia; Infant; Intubation, Intratracheal; Methylprednisolone; Nitrogen Dioxide; Oxygen Inhalation Therapy; Pneumonia; Positive-Pressure Respiration; Pulmonary Atelectasis; Pulmonary Edema; Respiration, Artificial; Respiratory Insufficiency; Shock; Smoke; Sulfur Dioxide; Time Factors; Tracheotomy

Topics: Animals; Capillaries; Hemorrhage; Hyperbaric Oxygenation; Lung; Male; Mice; Nitrogen Dioxide; Oxygen Inhalation Therapy; Pulmonary Alveoli; Pulmonary Edema

Topics: Agricultural Workers' Diseases; Fermentation; Humans; Lung Diseases; Male; Nitrogen Dioxide; Pulmonary Edema; Silage

Topics: Adult; Anti-Bacterial Agents; Autoimmune Diseases; Blood Viscosity; Capillaries; Cell Membrane; Fibrin; Gas Poisoning; Glucocorticoids; Humans; Hypoxia; Male; Nitrogen Dioxide; Pulmonary Edema; Shock

Topics: Animals; Antibodies; Antibody Formation; Body Temperature; Environmental Exposure; Haplorhini; Hemagglutination Inhibition Tests; Hemagglutination Tests; Hematocrit; Injections; Lung; Male; Neutralization Tests; Nitrogen Dioxide; Orthomyxoviridae; Pulmonary Edema; Species Specificity; Spirometry; Trachea

Topics: Air Pollution; Animals; Blood Pressure; Carbon Dioxide; Cardiac Output; Dogs; Environmental Exposure; Heart Rate; Lipids; Lung; Lung Compliance; Nitrogen Dioxide; Organ Size; Oxygen; Partial Pressure; Pulmonary Edema; Respiration; Surface Properties

Topics: Cadmium; Environmental Exposure; Fluorides; Humans; Nitrogen Dioxide; Occupational Diseases; Oxides; Pulmonary Edema; Respiratory Tract Diseases; Silver

Topics: Adult; Agricultural Workers' Diseases; Airway Resistance; Bronchial Diseases; Carbon Dioxide; Follow-Up Studies; Humans; Hydrogen-Ion Concentration; Leukocytosis; Lung Compliance; Lung Diseases; Male; Nitrogen Dioxide; Oxygen; Pulmonary Edema; Radiography; Respiratory Function Tests; Silo Filler's Disease; Spirometry

Topics: Adult; Environmental Exposure; Escherichia coli Infections; Fires; Humans; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Pulmonary Edema; Radiography; Respiratory Function Tests; Respiratory Insufficiency

Topics: Engineering; Humans; Male; Nitrogen Dioxide; Occupational Diseases; Pulmonary Edema

Topics: Air Pollution; Animals; Bronchi; Bronchitis; Environmental Exposure; Klebsiella Infections; Lung; Lymphocytes; Mice; Nitrogen Dioxide; Pneumonia; Pulmonary Alveoli; Pulmonary Edema; Time Factors

Topics: Animals; Animals, Newborn; Body Weight; Injections, Intraperitoneal; Mice; Nitrogen Dioxide; Organ Size; Pulmonary Edema; Rats; Thiourea

Topics: Animals; Bronchopneumonia; Dogs; Hemorrhage; Lung Diseases; Mucous Membrane; Nitric Oxide; Nitrogen Dioxide; Pulmonary Alveoli; Pulmonary Edema

Topics: Acidosis; Acidosis, Respiratory; Animals; Blood Pressure; Dogs; Electrocardiography; Heart Rate; Methemoglobinemia; Nitric Oxide; Nitrogen Dioxide; Oxygen; Polarography; Pulmonary Edema

Topics: Humans; Netherlands; Nitrogen Dioxide; Nitrous Oxide; Occupational Diseases; Pulmonary Edema; Ventilation

Topics: Animals; Biometry; Female; Mice; Microscopy, Electron; Nitrogen Dioxide; Pulmonary Alveoli; Pulmonary Edema

Topics: Animals; Body Weight; Corneal Opacity; Dogs; Guinea Pigs; Haplorhini; Nitrogen Dioxide; Pulmonary Edema; Rabbits; Rats; Respiratory System; Species Specificity

Topics: Anti-Bacterial Agents; Humans; Male; Nitrogen Dioxide; Occupational Diseases; Oxygen Inhalation Therapy; Pulmonary Edema; Radiography, Thoracic; Welding

Topics: Cadmium; Diagnosis; Fluorides; Humans; Nitrogen Dioxide; Occupational Diseases; Ozone; Pulmonary Edema; Sulfates; Sulfides; Therapeutics; Toxicology

Topics: Accidents; Accidents, Occupational; Industry; Nitrogen; Nitrogen Dioxide; Pathology; Poisoning; Pulmonary Edema; Sulfur; Sulfur Dioxide; Toxicology

Topics: Air Pollution; Animals; Bronchial Diseases; Bronchitis; Bronchopneumonia; Dogs; Guinea Pigs; Lung; Lung Diseases; Mice; Nitrogen Dioxide; Pathology; Poisoning; Pulmonary Edema; Pulmonary Fibrosis; Rabbits; Rats; Research; Toxicology; Tracheitis

Topics: Acclimatization; Adaptation, Physiological; Air Pollution; Gases; Irritants; Mice; Nitrogen Dioxide; Pulmonary Edema; Rats; Research; Toxicology