SEARCH · PubMed Health

Results for “NITROGEN DIOXIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources

PubMed1984

Modulation of nitrogen dioxide toxicity by lithium.

The effect of short-term intake of LiCl in drinking fluid on NO2 toxicity was studied in mice as a function of mortality and of specific activities of mouse liver alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenases (L-ALDH). Pretreatment with LiCl for 10 days decreased mortality in mice exposed to 60 to 70 PPM NO2 for 6 hr compared to controls. Pretreatment with LiCl for 10 days under continued exposure to 5 PPM NO2 resulted in a decrease in liver weight compared to control. Lithium treated mice exposed to NO2 showed less gain in body weight than the controls treated with LiCl and exposed to air. The latter group showed an induction of mitochondrial but not cytoplasmic L-ALDH and the NO2 exposure did not alter endogenous L-ALDH from corresponding controls. This induction of mitochondrial ALDH was associated with an increase in both Vmax and the apparent Km. Exposure to NO2 for 10 consecutive days resulted in inhibition of cytoplasmic L-ALDH. The data suggest that Li+ antagonized NO2 toxicity. A possible mechanism for reduction of NO2 toxicity by LiCl may be due to Li+ action on stabilizing cell membranes and/or modifying intercellular pulmonary response to NO2 injury.

Acetaldehyde↗

PubMed1987

Morphological effects of nitrogen dioxide on the rat lung.

Morphological studies of the rat lung exposed to 20 ppm NO2 for 20 hr (experiment 1), to 0.5 ppm for 19 months (experiment 2), and to 10 ppm for 14 days (experiment 3) were conducted. Changes in the mast cells of the tracheas and main bronchi of rats exposed to 0.5 ppm (experiment 4) were also observed. In the alveolus, cytoplasmic blebbing occurred in a small number of type I cells immediately after exposure to 20 ppm NO2 for 20 hr, and remarkable vacuolar change was observed 3 days after 10 ppm exposure. Exposure to 0.5 ppm did not cause degeneration. Swelling and hyperplasia of type II cells were observed. The cells gradually became flat and began a transition from type II to type I cells. These intermediate-type cells were noticed in experiments 1 and 2, but no intermediate-type cells were found in experiment 3. In each experiment, pinocytotic vesicles of endothelial cells in capillaries, followed by interstitial edema in the alveolar walls, were observed. In addition to these changes, desquamation of endothelium and widening of the endothelial junction of endothelial cells occurred in experiment 3. The early changes observed in the animals exposed to 0.5 ppm NO2 were the numerical and histochemical changes of mast cells in the trachea and main bronchus.

Animals↗

PubMed1993

Personal exposure to nitrogen dioxide from indoor heaters and cooking stoves.

The personal exposure to NO2 generated from various heaters and cooking stoves were studied, using 85 university students. The students attached NO2 filter badges to their chests or collars and wrote down the period of time for heating and cooking for 1 week. Types of heaters and smoking habits were described through a questionnaire. The urinary hydroxyproline/creatinine ratio (HOP/C) was examined as a biomarker for health effects. The outdoor NO2 concentration during the study period was 13.5-13.7 micrograms/m3. Smoking and the usage of electric heaters did not affect the exposure to NO2. Exposure increased according to the length of time kerosene heaters or oil fan heaters were used. The NO2 concentration during the heating by a kerosene heater and an oil fan heater was calculated to be 219 and 474 micrograms/m3, respectively. The correlation between the period of cooking and personal exposure was also observed. The NO2 levels during cooking were calculated to be 290 micrograms/m3. Using these calculated values of NO2 concentration, it is possible to presume the personal exposure levels from the length of time heaters and cooking stoves are used even if the subjects do not attach the filter badges. Neither smoking nor exposure to NO2 were associated with the increase of urinary HOP/C.

Adult↗

PubMed1986

Changes in early alveolar particle clearance due to single and repeated nitrogen dioxide exposures in the rabbit.

To better understand the potential health risks associated with short-term NO2 exposures, a study was conducted to examine the effects of single and repeated NO2 exposures on the clearance of inert tracer particles from the alveolar region of rabbit lungs. Single 2-h exposures to 0.3, 1.0, 3.0, and 10.0 ppm produced a concentration-related acceleration in alveolar particle clearance, which resulted in greater particle removal when compared to control. The greatest response was produced at the lower NO2 levels, where as much as 40% more particles were cleared when compared to control. Fewer particles were cleared following a 10.0-ppm NO2 exposure when compared to the lower NO2 levels, and there were indications from the clearance pattern that the higher level was beginning to slow clearance, although an actual retardation was not found. Repeated 14-d exposures (2 h/d) to 1.0 or 10.0 ppm NO2 produced a response similar to a single exposure at the same concentration, suggesting a certain degree of adaptation was produced after the initial exposures. Possible mechanisms for these differences in clearance patterns are discussed. The results of this study demonstrated altered alveolar clearance following short-term NO2 exposure at environmentally relevant concentrations; changes in this important host defense mechanism may be indicative of some underlying pathologic condition.

Animals↗

PubMed1992

Reductions in lymphocyte subpopulations after repeated exposure to 1.5 ppm nitrogen dioxide.

In this investigation the effects of repeated exposure to 1.5 ppm NO2 on immune competent cells in bronchoalveolar lavage (BAL) fluid was studied. Special attention was focused on effects on lymphocyte subpopulations. Eight healthy subjects were exposed to 1.5 ppm NO2 every second day on six occasions. Bronchoalveolar lavage fluid was collected at least three weeks before the exposure series as reference and 24 hours after the last exposure. The results obtained were analysed using a non-parametric test for paired observations, with each subject as his own control. Significant reductions were found in the total number and percentage of T cytotoxic-suppressor cells in BAL fluid; this caused an increase in the ratio of T helper-inducer: cytotoxic-suppressor cells. The total number of natural killer cells in the BAL fluid was also reduced. The numbers of all other cell types were unchanged after exposure. No reduction of phagocytosis of opsonised yeast particles by alveolar macrophages in vitro was detected. It is concluded that repeated short term exposures to 1.5 ppm NO2, a moderate occupational concentration, induces significant effects on immune competent bronchoalveolar lymphocytes. This indicates that previous findings of changes in the lymphoid immune system induced by NO2 in animals may well be applicable to humans.

Adult↗

PubMed1988

Nitrosamine formation from amines applied to the skin of mice after and before exposure to nitrogen dioxide.

Skin lipids of mice exposed to NO2 contain lipid-soluble nitrosating agent(s) (NSA) that react in vitro with amines to produce nitrosamines. To test whether this reaction occurs in skin, we exposed mice to 50 ppm NO2 for 4 h and, 20 h later, applied 25 mg morpholine or N-methylaniline to the skin, which was then analyzed for the corresponding nitrosamine. When morpholine was applied, mean N-nitrosomorpholine yield was only 0.3 nmol/mouse (not significant). When N-methylaniline was applied and mice were killed after 10-40 min, N-nitroso-N-methylaniline yield in the skin was 13-21 nmol/mouse of which 87% occurred in the hair. NSA formation when mice were exposed to 6.5 ppm NO2 was only 0.15% of that for exposure to 50 ppm NO2. NSA occurred mostly in surface lipids of the skin and its in vitro reaction to give nitrosamines was not inhibited by alpha-tocopherol. When morpholine was painted and mice were then exposed to 55 ppm NO2 for 30 min, the skins contained 19 nmol N-nitrosomorpholine/mouse, attributed to a direct reaction between NO2 and the amine. We concluded that nitrosamine formation in skin by this direct reaction may be more important than the reaction of amines with NO2-derived NSA.

Aniline Compounds↗

PubMed2005

Laboratory and field comparison of measurements obtained using the available diffusive samplers for ozone and nitrogen dioxide in ambient air.

This study presents an evaluation of the extent of differences between measurements performed by O(3) and NO(2) diffusive samplers and by the reference methods for diffusive samplers commercially available. The tests were performed in an exposure chamber under extreme conditions of controlling factors and under field conditions. For NO(2), the results of the laboratory experiments showed that most of the diffusive samplers were affected by extreme exposure conditions. The agreement between the samplers and the reference method was better for the field tests than for the laboratory ones. The estimate of the uptake rate for the exposure conditions using a model equation improved the agreement between the diffusive samplers and the reference methods. The agreement between O(3) measured by the diffusive samplers and by the reference method was satisfactory for 1-week exposure. For 8-hour exposures, the diffusive samplers with high uptake rates quantified better the O(3) concentration than the samplers with low uptake rates. As for NO(2), the results of the O(3) field tests were in better agreement with the reference method than the ones of the laboratory tests. The field tests showed that the majority of diffusive samplers fulfils the 25% uncertainty requirement of the NO(2) European Directive and the 30% uncertainty requirement of the O(3) European Directive for 1-week exposure.

Air Pollutants↗

PubMed1983

The nitrosating agent in mice exposed to nitrogen dioxide: improved extraction method and localization in the skin.

We reported previously that mice exposed to atmospheric NO2 contained a nitrosating agent (NSA) that reacted with morpholine in aqueous methanol homogenates of the mice to give N-nitrosomorpholine. We have now found that N-nitrosomorpholine was also produced by reacting morpholine with ether extracts of aqueous homogenates prepared from NO2-exposed mice. After exposure to NO2 for 4 hr, mice contained NSA (5.0 nmol/g tissue, corrected to 50 ppm NO2 and assuming that 1 mol NSA yields 1 mol N-nitrosomorpholine). This is 3.6 times the concentration observed by our previous method. Some NSA (0.6 nmol/g tissue) was also detected in untreated mice. The NSA in ether extracts was nonvolatile and stable on storage at -15 degrees or for short periods in the presence of water at pH 1 to 10, but it was decomposed by a pH 1 solution of nitrite scavengers. It reacted to similar extents with three different secondary amines. Eighty-eight % of the NSA occurred in the skin, one-third of which was in the hair. The high skin concentration occurred when the bodies but not the heads of mice were exposed to NO2, indicating that the major exposure route was the skin. The NSA might consist of alpha-nitro or other activated nitrite esters derived from unsaturated lipids.

Animals↗

PubMed1985

In vivo effects of nitrogen dioxide on the blood nitrate level and the Na+,K+-ATPase activity of red blood cells of rats.

Male Wistar rats were exposed to 0.4, 1.2 and 4.0 ppm NO2 for 13 weeks to examine the effects of NO2 on the blood nitrate concentration and the Na+,K+-ATPase activity of red blood cells. Exposures to 1.2 and 4.0 ppm NO2 caused an elevation of the blood nitrate level at the first, third and eighth week. The maximum concentration attained was 148% (P less than 0.001, at the third week) and 201% (P less than 0.001, at the eighth week) of the controls at 1.2 and 4.0 ppm NO2, respectively. On the other hand, the nitrate concentration was decreased to the control level at the second, fourth and thirteenth weeks. 0.4 ppm NO2 caused a progressive but slight increase in the blood nitrate concentration from the third week and reached the maximum (122% of the control, P less than 0.001) at the eighth week. The Na+,K+-ATPase activity decreased slightly from the first week upon exposure to 4.0 ppm NO2 and reached the minimum (72% of the control, P less than 0.05) at the third week. Subsequently, the activity was increased to 159% (P less than 0.001) of the control at the eighth week. Exposure to 0.4 and 1.2 ppm NO2 caused fundamentally similar but less significant alterations of the Na+,K+-ATPase activity.

Animals↗

PubMed2002

Performances and application of a passive sampling method for the simultaneous determination of nitrogen dioxide and sulfur dioxide in ambient air.

The performances and applicability of a diffusion tube sampler for the simultaneous measurements of NO2 and SO2 in ambient air were evaluated. SO2 and NO2 are collected by the passive sampler using triethanolamine as trapping agent and are determined as sulphate and nitrite with ion chromatography. The detection limit (2.3 microg m(-3) of NO2 and 4.2 microg m(-3) of SO2 for two weeks sampling) is adequate for the determination of concentrations in urban and industrial areas. Precision of the method as RSD is in mean 5% for NO2 and 12% for SO2 at the concentration levels in urban areas. Calibration of the method was performed in the field conditions by comparison between the responses of sampler and the concentrations measured by the continuous monitors. High degree of linearity (correlation coefficients > 0.8) is found between the passive sampler tube and the continuous monitor data for both NO2 and SO2. To reduce the wind velocity influence on passive sampling of diffusion tubes, a protective shelter was tested in this study. The overall uncertainty of one measure for the optimised method is estimated at 5 microg m(-3) for NO2 and 6 microg m(-3) for SO2. Suitability of this passive sampling method for air pollution monitoring in urban areas was demonstrated by the results shown in this paper on a campaign carried out in the French agglomeration.

Air Pollutants↗

PubMed1995

The cytoprotective roles of ascorbate and glutathione against nitrogen dioxide toxicity in human endothelial cells.

The depletion of human umbilical vein endothelial (HUVE) cell glutathione with buthionine sulfoximine or with sulfur amino acid-free medium potentiated the sub-lethal (3H-deoxyglucose release) and lethal (lactate dehydrogenase release) cytotoxicity responses of the cells to direct exposure to NO2 over the range 2-20 ppm. When control cells, or glutathione-depleted cells, were either pre-loaded with ascorbate (intracellular ascorbate), or washed with ascorbate-containing medium just before exposure (extracellular ascorbate), the cells were fully protected from NO2-dependent toxicity. Concomitant with these exposures, NO2 caused dose-dependent depletions of both glutathione and ascorbate. Further, it was noted that the depletion of the intracellular ascorbate pool was accelerated in these glutathione depleted cells. Conversely, loading ascorbate into the cells significantly diminished NO2-dependent depletion of intracellular GSH. In contrast to affecting the acute cytotoxicity response of the HUVE cells to NO2, ascorbate supplementation of the medium of cells exposed to NO2 at clonal density facilitated considerable protection to the colony-forming efficiency of the cells. We conclude that both ascorbate and glutathione play important protective roles in defending HUVE cells from the toxicity of NO2 under direct exposure conditions. The results also strengthen the premise that ascorbate and glutathione co-operate in the antioxidative protection of cellular viability.

Antioxidants↗

PubMed1992

Pulmonary performance of elderly normal subjects and subjects with chronic obstructive pulmonary disease exposed to 0.3 ppm nitrogen dioxide.

Symptoms and changes in pulmonary function of subjects with chronic obstructive pulmonary disease (COPD) and elderly normal subjects, induced by a 4-h exposure to 0.3 ppm NO2, were investigated using a double-blind, crossover design with purified air. The 5-day experimental protocol required approximately 2 wk with at least a 5-day separation between randomized 4-h exposures to either NO2 or air which included several periods of exercise. Over a 2-yr period, COPD subjects, all with a history of smoking, consisting of 13 men and 7 women (mean age of 60.0 yr) and 20 elderly normal subjects of comparable age and sex were evaluated. During intermittent light exercise, COPD subjects demonstrated progressive decrements in FVC and FEV1 compared with baseline with 0.3 ppm NO2, but not with air. Differences in percent changes from baseline data (air-NO2) showed an equivocal reduction in FVC by repeated measures of analysis of variance and cross-over t tests (p less than 0.10). Subgroup analyses suggested that responsiveness to NO2 decreased with severity of COPD; in elderly normal subjects, NO2-induced reduction in FEV1 was greater among smokers than never-smokers. A comparison of COPD and elderly normal subjects also revealed distinctions in NO2-induced responsiveness.

Aged↗

PubMed1998

In vitro effects of nitrogen dioxide on the release of nitric oxide by bovine alveolar macrophages.

Bovine alveolar macrophages (BAM) were assessed for nitric oxide-production after exposure to synthetic air or NO2 [0.2 ppm] for 2 h and subsequent treatment with lipopolysaccharide (LPS) [1 microg/ml]. Nitric oxide (NO) release, measured as nitrite in the supernatant, was quantified at different time points. LPS-stimulated BAM showed elevated nitrite levels after 24 h. Pre-treatment with NO2 resulted in higher nitrite levels in comparison to air exposed BAM. Some of the BAM preparations resulted in pre-activated macrophages that produce high amounts of NO without LPS treatment. Within these cells LPS treatment reduced the nitrite levels in comparison to untreated control incubations from the same preparation. These pre-activated BAM exhibited no uniform effect after NO2-exposure. In some experiments nitrite levels of pre-activated control BAM were decreased, while in others no influence could be observed. NO-production by pre-activated BAM or after LPS-treatment could be inhibited by N(G)-monomethyl-L-arginine (L-NMMA) [1 mM]. In order to investigate, whether NO2-exposure alters inducible NO-synthase mRNA expression, we now perform reverse transcription polymerase chain reaction (RT-PCR) of iNOS mRNA. This method will be a good tool to elucidate whether NO2-exposure can modulate iNOS mRNA expression.

Animals↗

PubMed1987

Intermittent inhalation of nitrogen dioxide: effects on rabbit alveolar macrophages.

Rabbits were exposed to 0.3 or 1 ppm NO2 for 2 h/d and the effects on alveolar macrophages recovered by bronchopulmonary lavage at 3 time points during the exposure series were assessed. Cells were examined 24 h after 2, 6, or 13 exposures, i.e., on d 3, 7, and 14. There was no change in the viability or numbers of macrophages recovered at any time, nor was an inflammatory response produced. The ability of macrophages to attach to a surface was not affected by exposure. Random mobility was reduced at d 3 in the 0.3 ppm exposure series, but was not different from control after any of the 1 ppm exposures. The phagocytic index, i.e., the fraction of viable cells able to phagocytize latex particles, was not affected by NO2 exposure. However, phagocytic capacity--i.e., the numbers of phagocytizing cells that internalized specific numbers of particles--was different from control on d 3 with both levels of NO2. At 0.3 ppm, particle uptake was reduced, while at 1 ppm it was enhanced in that a greater fraction of cells contained a large number of latex particles. The results show that phagocytic capacity and random mobility are sensitive indices of response to NO2 and that adaptation to the exposures apparently occurred in that both phagocytosis and mobility returned to control levels by d 7 and remained there through the duration of the exposure series.

Administration, Inhalation↗

PubMed1994

Development of a rabbit model to investigate the effects of acute nitrogen dioxide intoxication.

1. In previous studies a rat inhalation model was developed to investigate the effects of intervention after acute NO2 exposure. The object of the present study was to investigate whether acute NO2 intoxication induced comparable effects in rabbits as it does in rats. Where the effects of intervention in both species are similar, then the conclusions drawn from these studies may have more relevance for the treatment of man. 2. Biochemical variables in bronchoalveolar lavage and supernatant from lung homogenate, which may be relevant for the evaluation of lung injury and repair, were investigated and compared with histology. 3. After NO2 exposure for 10 min, the pulmonary effects observed became more pronounced with increasing NO2 concentrations (0, 125, 175, 250, 400, 600 or 800 ppm) [1 ppm NO2 is 1.88 mg m-3]. The effects in rabbits were found to be broadly comparable with those in rats. 4. To achieve severe lung injury in rabbits without mortality, enabling investigations of the effects of intervention over several days, exposure to a NO2 concentration of 600 ppm for 10 min was most appropriate, while a concentration of 175 ppm NO2 was needed to attain comparable effects in rats. 5. The repair phase starts later, namely at 3 days after exposure in rats, compared to 5 days in rabbits.

Animals↗

PubMed1994

Diffuse alveolar damage in the rat lung after short and long term exposure to nitrogen dioxide.

In order to quantify parenchymal, vascular and epithelial changes occurring in the exudative and organizing phase of diffuse alveolar damage (DAD) induced by inhaled NO2 groups of 7 rats were continuously exposed to 5, 10 or 20 ppm NO2 for 3 and 25 days alternatively. AgNOR analysis revealed the highest proliferative activity in the epithelium of the respiratory bronchioles. In this region already after 3d exposure to 5 ppm the maximum AgNOR number was reached. In contrast to long-term exposure after 3d exposure to 5 and 10 ppm NO2 the AgNOR number in the respiratory bronchioles was significantly higher than in central airway epithelia. After long-term exposure to 5 and 10 ppm AgNOR number decreased to normal values or showed no further significant increase, long-term exposure to 20 ppm resulted in a further increase of the AgNOR number. A significant increase of the alveolar circumference and decrease of alveolar surface density was found after an exposure to 20 ppm for 3d and long-term exposure to 10 and 20 ppm NO2, whereas the 5 ppm exposure groups disclosed no significant change of these values. Medial hypertrophy was detected after exposure to 10 and 20 ppm NO2 for 25 days, after the exposure to 5 ppm for 3d and 25d medial thickness was significantly decreased due to vasodilation induced by NO, one of the major reaction products of NO2.

Animals↗

PubMed1982

Effects of acute nitrogen dioxide exposure on swimming performance of mice.

To evaluate the acute effects of NO2 on the physical performance of experimental animals, male mice 15-16 wk old were exposed to 5, 10, 20, or 40 ppm NO2 for 24 h, and forced swimming endurance time (FSET), the changes in FSET during the postexposure days, lung wet weight, lung water content, and blood lactate level were examined. FSET of mice exposed to NO2 at 10, 20, and 40 ppm decreased immediately after exposure, FSET of mice exposed to 5 ppm NO2 did not change immediately after exposure, but a significant decrease was observed from d 1 to d 4 after exposure. FSET recovered to the initial control level after 5-6 d, 7-8 d, and over 9 d in mice exposed to NO2 at 5, 10, and 20 ppm, respectively. Lung wet weight of mice exposed to 20 and 40 ppm NO2 and lung water content of mice exposed to 10, 20, and 40 ppm NO2 increased with dose. A negative relation was demonstrated between FSET and lung wet weight and between FSET and lung water content. Without forced swimming exercise, the blood lactate level of mice exposed to 5 ppm NO2 was almost equivalent to that of control mice, but the blood lactate level of the exposed mice significantly increased immediately and 24 h after forced swimming exercise for 4 min.

Animals↗

PubMed1995

Nitrogen dioxide exposure impairs the frequency of the mucociliary activity in healthy subjects.

In previous studies, we have reported bronchoalveolar lavage (BAL) findings following single and repeated exposures to NO2. Here, we present the first data on measurements of the frequency of the mucociliary activity in healthy subjects following exposure to NO2. Twenty four healthy nonsmoking volunteers underwent fibreoptic bronchoscopy, during which mucociliary activity was measured using an in vivo method based on a two-way fibreoptic system, to obtain baseline data. Two weeks later, the subjects were reinvestigated following NO2 exposure. Eight volunteers were investigated 45 min after a 20 min exposure to 1.5 ppm NO2 (Group A); eight subjects 45 min after a 20 min exposure to 3.5 ppm NO2 (Group B); and eight subjects 24 h after a 4 h exposure to 3.5 ppm NO2 (Group C). No activity was detected in Group A or B 45 min after exposure, in contrast to the easily identifiable mucociliary activity waves at the reference bronchoscopy. In group C, a significant elevation of the frequency of the mucociliary activity waves was seen at 24 h. It is concluded that short-term exposure to NO2 in man produces a significant reduction in the mucociliary activity 45 min after exposure. The effect ceases within 24 h. Further studies are needed to evaluate the effects of repeated exposures with NO2 on mucociliary activity in man.

Adult↗