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PubMedDate not supplied

Experimental studies on human health effects of air pollutants. IV. Short-term physiological and clinical effects of nitrogen dioxide exposure.

Adult male volunteers were exposed to nitrogen dioxide (NO2) at 1.0 ppm in purified air under conditions simulating ambient photochemical smog exposures (2-hr exposure with intermittent light exercise at 31 degrees C and 35% relative humidity). Sham exposures to purified air alone served as controls. Exposure effects were assessed by pulmonary physiological tests and by a standardized clinical evaluation. No statistically physiological changes attributable to NO2 exposure were found except for a marginal loss in forced vital capacity after exposure on two successive days (1.5% mean decrease, P less than .05). Reported respiratory and other symptoms were slightly increased with exposure as compared to control, but the change was not significant. Short-term toxicity of NO2 at peak ambient concentrations appears to be substantially less than that of ozone in healthy people, but adverse NO2 effects in diseased people or in long-term exposures cannot be ruled out at present.

Adult↗

PubMed1990

Sequential changes in canine pulmonary epithelial and endothelial cell functions after nitrogen dioxide.

Through its ability to cause lipid peroxidation, nitrogen dioxide (NO2) may affect the functional properties of both the pulmonary epithelium and endothelium. We evaluated this possibility in 13 mongrel dogs by exposing these animals to 200 or 400 ppm NO2 for 1 h. The changes in pulmonary epithelial permeability (using a radioaerosol technique), FRC, and endothelial function (the removal of radiolabeled serotonin, [14C]5-HT, and prostaglandin E1, [3H]PGE1, from the pulmonary circulation) were measured at 1 h and at 2, 7, or 14 days after NO2 exposure. In another six dogs, we evaluated changes in cell population and albumin in bronchoalveolar lavage (BAL) fluid caused by NO2. In the first two days after NO2 exposure, focal pulmonary edema was documented on microscopy, radioaerosol clearance was delayed, and FRC decreased slightly. BAL showed a marked increase in albumin, but the removal of trace amounts of 5-HT and PGE1 by the endothelium was not altered. All physiologic abnormalities returned to normal with time.

Albumins↗

PubMed1998

Impact of residential nitrogen dioxide exposure on personal exposure: an international study.

Nitrogen dioxide (NO2) concentrations were measured during two-day winter periods in indoor and outdoor environments, and these concentrations were compared with simultaneously measured personal exposures in 18 cities in 15 countries around the world. Information was also gathered on activity patterns and household characteristics in order to determine the influences of these factors on personal exposures. All NO2 measurements were taken using passive filter badges. Personal exposures were found to vary greatly among the array of cities, with mean concentrations ranging between 11.0 ppb and 51.5 ppb. Personal NO2 exposures were more strongly correlated with indoor concentrations (r = 0.75) than with outdoor concentrations (r = 0.57) when all countries were considered simultaneously. Use of a gas stove in the home was the dominant activity influencing NO2 concentrations, with a 67% increase in mean personal NO2 exposure and an increase in indoor-outdoor ratios from 0.7 to 1.2 for participants using gas stoves, although preliminary evidence indicates the importance of combustion space heaters as well. These associations indicate the global nature of the correlation between personal NO2 exposures and indoor NO2 sources such as gas stoves or space heaters, demonstrating that this relationship is not dependent on country-specific parameters.

Air Pollution, Indoor↗

PubMed1989

Effects of nitrogen dioxide exposure on bronchoalveolar lavage proteins in humans.

Nitrogen dioxide (NO2) is a pollutant of both outdoor and indoor atmospheres that has the potential to alter alveolar epithelial permeability. In order to assess alterations in the protein content of alveolar lining fluid induced by brief (3-h) exposures to low-level NO2, normal volunteers were exposed sequentially to air and NO2, separated by at least 2 wk, in an environmental chamber. Bronchoalveolar lavage (BAL) was performed after exposure. Four experimental protocols were used: (1) continuous 0.60 ppm NO2 with BAL performed 3.5 h after exposure (n = 8), (2) background 0.05 ppm NO2 with three 15-min peaks of 2.0 ppm followed by BAL 3.5 h after exposure (n = 15), (3) continuous 0.60 ppm NO2 with BAL performed 18 h after exposure (n = 8), and (4) continuous 1.5 ppm NO2 with BAL 3.5 h after exposure (n = 15). No changes in lavage fluid levels of total protein or albumin were observed in response to NO2. However, exposure to continuous 0.60 ppm NO2 was associated with increases in lavage fluid levels of the antiprotease alpha-2-macroglobulin (alpha 2M) when assessed 3.5 h after exposure (air versus NO2: 20 +/- 1 versus 29 +/- 2 ng/ml, P = 0.01). No significant changes in levels of alpha 2M in BAL fluid were observed in the other exposure protocols. Lavaged cell numbers, differential counts, and viability were not altered by exposure to the pollutant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

[Changes of alveolar macrophage plasminogen activator in rats exposed to nitrogen dioxide].

In order to clarify the role of nitrogen dioxide (NO2) in the development of lung injury, male Wistar rats were exposed continuously to 0.3 or 5.0 ppm NO2 for 10, 20, 30, 60 and 90 days, and alveolar macrophages and lavage fluid obtained by bronchoalveolar lavage were examined. The results were as follows: 1) The number of alveolar macrophages increased significantly in response to NO2 exposure. Throughout the whole test period, the largest number was obtained in the group exposed to 5.0 ppm, followed by the group exposed to 0.3 ppm, and then by the control group. 2) The plasminogen activator (PA) released from alveolar macrophages was increased dose-dependently by NO2 exposure. The activities were significantly high in the groups exposed for 10 to 20 days at each concentration, and then slightly decreased at 30 days. Thereafter, activity showed a tendency to increase, reaching the maximum level on the 60th day of exposure. 3) Similarly, the fibrinolytic activity in the lavage fluid was increased dose-dependently by NO2 exposure. The maximum activity was noted on the 10th day of exposure, followed by a rapid decrease up to the 30th day, and a slight rise again between the 60th and 90th day. 4) In the group exposed to 5.0 ppm NO2, total protein in the lavage fluid increased, and the elastase inhibitory capacity (EIC) per milligram of protein decreased. In the group exposed to 0.3 ppm NO2, however, no difference from the control group was noted. These results revealed that the alveolar macrophages were affected and increased PA activity as a result of exposure to as little as 0.3 ppm NO2. This was shown to result in an increase of the fibrinolytic activity in the alveoli, leading to damage to the lung tissue. This evidence may explain the morphological findings of the appearance of emphysematous change in the lungs of rats exposed to low levels of NO2. For the detection of the effect of NO2 on the lung tissue, PA appears to be a more sensitive indicator than EIC.

Animals↗

PubMed2005

Differential assimilation of nitrogen dioxide by 70 taxa of roadside trees at an urban pollution level.

In order to screen for the best species for mitigating nitrogen dioxide (NO2) by plants at urban levels, we investigated assimilation of nitrogen dioxide by 70 taxa of woody plants that are mostly utilized as roadside trees. They were fumigated with 15N-labeled NO2 at 0.1 microl l(-1) for 8h, and the amount of reduced nitrogen derived from NO2 (in mg Ng(-1) dry weight) in the leaves (designated NO2 assimilation capability hereafter) were determined. Data were analyzed in the comparison with the previously reported ones obtained at 4 microl l(-1) NO2. Among the 70 taxa, the value of NO2 assimilation capability differed by a factor of 122 between the highest (Prunus yedoensis; 0.061) and the lowest (Cryptomeria japonica; 0.0005). Based on the analysis of NO2 assimilation capability values at 0.1 and 4 micro l(-1) NO2, the 70 taxa of woody plants appeared to be classified into four types; those of high NO2 assimilation and high NO2 resistance, those of high NO2 assimilation but low NO2 resistance, those of low NO2 assimilation and low NO2 resistance, and those of low NO2 assimilation but high NO2 resistance. The first, second, third and fourth types include 13, 11, 35 and 11 taxa, respectively. The broad-leaf deciduous trees may have advantages of high biomass and fast growth as compared with woody plants of other habits. Thus, four broad-leaf deciduous species, Robinia pseudo-acacia, Sophora japonica, Populus nigra and Prunus lannesiana, were concluded here to be the best phytoremediators for the urban air.

Air Pollutants↗

PubMed2005

Nitration of benzo[a]pyrene adsorbed on coal fly ash particles by nitrogen dioxide: role of thermal activation.

Nitration of benzo[a]pyrene (BaP) by nitrogen dioxide (NO2) adsorbed on the surface of thermally activated coal fly ash and model aluminosilicate particles led to the formation of nitrobenzo[a]pyrenes as verified by extraction and gas chromatography/mass spectrometry (GC/MS). In situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) was utilized to follow the nitration reaction on the surface of zeolite Y. Nitrobenzo[a]pyrene formation was observed along with the formation of nitrous acid and nitrate species. The formation of the BaP radical cation was also observed on thermally activated aluminosilicate particles by electron spin resonance (ESR) spectroscopy. On the basis of GC/MS, DRIFTS, and ESR spectroscopy results, a mechanism of nitration involving intermediate BaP radical cations generated on thermally activated aluminosilicate particles is proposed. These observations have led to the hypothesis that nitration of adsorbed polyaromatic hydrocarbons on coal fly ash by reaction with nitrogen oxides can occur in the smokestack, but with the aging of the fly ash particles, the extent of the nitration reaction will be diminished.

Adsorption↗

PubMedDate not supplied

An air pollution model for use in epidemiological studies: evaluation with measured levels of nitrogen dioxide and benzene.

The aim of the study was to evaluate the predictions derived from the Danish Operational Street Pollution Model (OSPM) when the input data are obtained by simple methods that could be used in large-scale epidemiological studies. The model calculations were thus compared with passive sampler measurements of nitrogen dioxide and benzene at 103 street locations in Copenhagen, Denmark, and at 101 locations in rural areas. Data on traffic and street configuration were collected by means of a simple registration scheme in which forms were filled out by local municipal authorities. Meteorological data were derived from routine measurements at Copenhagen airport, and data on background air pollution were based on a simple empirical model. Differences in air pollution levels between rural areas and Copenhagen and differences in nitrogen dioxide concentrations at various locations in Copenhagen were well reproduced by the OSPM. The correlation coefficients (r) between the measured and the predicted half-year average concentrations of nitrogen dioxide in Copenhagen were between 0.75 and 0.80 for various degrees of precision of the input data for the model. The results indicate that the OSPM used with the presented methods for generation of input data might be useful in assessing long-term exposure to air pollutants in epidemiological studies.

Air Pollution↗

PubMed2003

Dopamine prevents nitration of tyrosine hydroxylase by peroxynitrite and nitrogen dioxide: is nitrotyrosine formation an early step in dopamine neuronal damage?

Peroxynitrite and nitrogen dioxide (NO2) are reactive nitrogen species that have been implicated as causal factors in neurodegenerative conditions. Peroxynitrite-induced nitration of tyrosine residues in tyrosine hydroxylase (TH) may even be one of the earliest biochemical events associated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced damage to dopamine neurons. Exposure of TH to peroxynitrite or NO2 results in nitration of tyrosine residues and modification of cysteines in the enzyme as well as inactivation of catalytic activity. Dopamine (DA), its precursor 3,4-dihydroxyphenylalanine, and metabolite 3,4-dihydroxyphenylacetic acid completely block the nitrating effects of peroxynitrite and NO2 on TH but do not relieve the enzyme from inhibition. o-Quinones formed in the reaction of catechols with either peroxynitrite or NO2 react with cysteine residues in TH and inhibit catalytic function. Using direct, real-time evaluation of tyrosine nitration with a green fluorescent protein-TH fusion protein stably expressed in intact cells (also stably expressing the human DA transporter), DA was also found to prevent NO2-induced nitration while leaving TH activity inhibited. These results show that peroxynitrite and NO2 react with DA to form quinones at the expense of tyrosine nitration. Endogenous DA may therefore play an important role in determining how DA neurons are affected by reactive nitrogen species by shifting the balance of their effects away from tyrosine nitration and toward o-quinone formation.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Effects of ozone and nitrogen dioxide on drinking and eating behaviors in mice.

Male ICR mice were exposed continuously to ozone (O3) and nitrogen dioxide (NO2) for 7 days to examine the effects on drinking and eating behaviors. Ozone at 0.1 ppm did not affect drinking and eating activities, whereas drinking activity decreased in a concentration-dependent manner to 47.7, 12.8, and 3.0% of the control value with 2-day exposures to 0.2, 0.4, and 0.8 ppm O3, respectively, and eating activity decreased to 35.2 and 8.7% of the control value at 0.4 and 0.8 ppm O3, respectively. Body weight also decreased markedly by 2.0, 4.6, and 7.5 g at 0.2, 0.4, and 0.8 ppm O3, respectively. These decrements reached a maximum on the second day of exposure. However, alterations in drinking and eating activities and body weight were transient, leading to recovery during the continuous O3 exposures. The recovery processes were dependent on the concentrations of O3. Nitrogen dioxide at 4 ppm did not affect drinking and eating activities, whereas drinking activity decreased in a concentration-dependent manner to 56.8, 8.3, and 18.7% of the control value with 2-day exposures to 6, 8, and 12 ppm NO2, respectively, and eating activity decreased markedly to 21.8 and 16.4% at 8 and 12 ppm NO2, respectively. Body weight also decreased by 2.5, 5.5, and 6.1 g at 6, 8, and 12 ppm NO2, respectively. These decrements reached a maximum on the second day of exposure. As in the O3 exposures, the decrements in drinking and eating activities and body weight were transient and recovered during the continuous exposures to NO2 depending on the concentrations of NO2. Drinking and eating activities and body weights of mice that had been previously exposed to 12 ppm NO2 for 7 days did not show changes when the mice were exposed to 0.4 ppm O3 9 days after NO2 exposure. The present study demonstrates that photochemical oxidants suppress drinking and eating behaviors in mice and that they recover thereafter under the continuous exposure conditions.

Animals↗

PubMed1977

Fate and distribution of inhaled nitrogen dioxide in rhesus monkeys.

The intra- and extrapulmonary distributions of inspired nitrogen dioxide (NO2) were studied by exposing rhesus monkeys to air mixtures containing concentrations slightly greater than ambient (0.56 to 1.71 mg per m3, or 0.30 to 0.91 ppm) of NO2 labeled with tracer quantities of NO2 containing nitrogen-13 dioxide (13NO2). The 13NO2 (half-time, 10 min) was synthesized by the oxygen-16 (P, alpha)13N nuclear reaction in an isochronous cyclotron. The intrapulmonary location and concentration of the inspired 13NO2 was detected continuously by external monitoring of the annihilation radiation consequent to positron emissions from disintegrating 13N. The 13N concentration of arterial blood was also measured at intervals, and the blood values were correlated with those from the lung. Chemical measurements of NO2 concentration in inspired and expired air were performed by the Saltman method. Control studies were performed with xenon-125 (125Xe) (halftime, 17 hours). The results demonstrated that 50 to 60% of the inspired pollutant was retained by the primate during quiet respiration; the gas was distributed throughout the lungs. Once absorbed, NO2 or chemical intermediates remained within the lungs for prolonged periods after cessation of exposure, and dissemination of the pollutant or its derivatives to extrapulmonary sites occurred via the blood stream. Indirect evidence indicated the probable reaction of NO2 with water in the nasopharynx and lungs to form nitric and nitrous acids. The reaction of these acids with pulmonary and extrapulmonary tissues probably accounts for the biologic toxicity of NO2.

Animals↗

PubMed2005

Reactivity of 2',7'-dichlorodihydrofluorescein and dihydrorhodamine 123 and their oxidized forms toward carbonate, nitrogen dioxide, and hydroxyl radicals.

The aim of this study was to investigate the oxidation of two common fluorescent probes, dichlorodihydrofluorescein (DCFH2) and dihydrorhodamine (DHR), and their oxidized forms, dichlorofluorescein and rhodamine, by the radical products of peroxynitrite chemistry, *OH, NO2*, and CO3*-. At pH 8.0-8.2, rate constants for the interaction of carbonate radical with probes were estimated to be 2.6 x 10(8) x M(-1) s(-1) for DCFH2 and 6.7 x 10(8) M(-1) s(-1) for DHR. Nitrogen dioxide interacted more slowly than carbonate radical with these probes: the rate constant for the interaction between NO2* and DCFH2 was estimated as 1.3 x 10(7) M(-1) s(-1). Oxidation of DHR by nitrogen dioxide led to the production of rhodamine, but the kinetics of these reactions were complex. Hydroxyl radical interacted with both probes with rate constants close to the diffusion-controlled limit. We also found that oxidized forms of these fluorescent probes reacted rapidly with carbonate, nitrogen dioxide, and hydroxyl radicals. These data suggest that probe oxidation may often be in competition with reaction of the radicals with cellular antioxidants.

Antioxidants↗

PubMed1987

Lipidic nitrosating agents produced from atmospheric nitrogen dioxide and a nitrosamine produced in vivo from amyl nitrite.

In studies on nitrosating agent(s) formed in skin of mice exposed to nitrogen dioxide, we showed that: (i) N-nitrosomethylaniline was produced in skin of mice exposed to nitrogen dioxide and then painted with N-methylaniline; (ii) a nitrosating precursor in methyl linoleate is associated with peroxidation products; (iii) cholesterol is a major nitrosating precursor in mouse skin, probably because it produces the nitrosating agent, cholesteryl nitrite; (iv) cholesteryl nitrite enhances autoxidation of lipids in vivo and on mouse skin and, like sodium nitrite, catalyses the autoxidation of iodide; (v) N-nitrosomethylaniline was produced in mice injected intraperitoneally with methylaniline and gavaged with amyl nitrite; and (vi) nitrosating agents may occur normally in human skin lipids.

Amyl Nitrite↗

PubMed2005

Increase in tropospheric nitrogen dioxide over China observed from space.

Emissions from fossil fuel combustion and biomass burning reduce local air quality and affect global tropospheric chemistry. Nitrogen oxides are emitted by all combustion processes and play a key part in the photochemically induced catalytic production of ozone, which results in summer smog and has increased levels of tropospheric ozone globally. Release of nitrogen oxide also results in nitric acid deposition, and--at least locally--increases radiative forcing effects due to the absorption of downward propagating visible light. Nitrogen oxide concentrations in many industrialized countries are expected to decrease, but rapid economic development has the potential to increase significantly the emissions of nitrogen oxides in parts of Asia. Here we present the tropospheric column amounts of nitrogen dioxide retrieved from two satellite instruments GOME and SCIAMACHY over the years 1996-2004. We find substantial reductions in nitrogen dioxide concentrations over some areas of Europe and the USA, but a highly significant increase of about 50 per cent-with an accelerating trend in annual growth rate-over the industrial areas of China, more than recent bottom-up inventories suggest.

Air Pollutants↗

PubMed2004

Exposure to urban nitrogen dioxide pollution and the risk of myocardial infarction.

OBJECTIVES: This study attempted to determine whether long-term exposure to nitrogen dioxide (NO2), an indicator of motor vehicle exhaust, increases the risk of myocardial infarction (MI). METHODS: A population-based case-control study was conducted among men aged 25-64 years and residing in Kaunas, Lithuania. The study included all cases of first-time myocardial infarction in 1997-2000. Interviews with patients treated in hospitals elicited information on smoking and other risk factors, including residential histories. A high response rate (77.4%) resulted in 448 cases and 1777 controls. Nitrogen dioxide (NO2) was selected for analysis as an indicator of traffic-related air pollution. The annual air pollution levels were estimated for the residential districts; thereafter the data were linked to the home addresses of the cases and controls. RESULTS: After adjustment for age, education, smoking, blood pressure, body mass index, marital status, and psychological stress, the risk of myocardial infarction was higher for the men exposed to medium [odds ratio (OR) 1.43, 95% confidence interval (95% CI) 1.04-1.96] and high (OR 1.43, 95% CI 1.07-1.92) NO2 levels. The data suggested a stronger association among 55- to 64-year-old men. The risk of myocardial infarction increased by 17% among the 25- to 64-year-old men (OR 1.17, 95% CI 1.01-1.35) and by 34% among those aged 55-64 years (OR 1.34, 95% CI 1.08-1.67) from the first to the third tertile of NO2 exposure. CONCLUSIONS: The results indicate that urban NO2 pollution may increase the risk of myocardial infarction and that vehicle emissions may be of particular importance.

Adult↗

PubMed1992

Interaction of nitrogen dioxide with human plasma. Antioxidant depletion and oxidative damage.

Nitrogen dioxide (NO2.) is often present in inhaled air and may be generated in vivo from nitric oxide. Exposure of human blood plasma to NO2. caused rapid losses of ascorbic acid, uric acid and protein thiol groups, as well as lipid peroxidation and depletions of alpha-tocopherol, bilirubin and ubiquinol-10. No increase in protein carbonyls was detected. Supplementation of plasma with ascorbate decreased the rates of lipid peroxidation, alpha-tocopherol depletion and loss of uric acid. Uric acid supplementation decreased rates of lipid peroxidation but not the loss of alpha-tocopherol. We conclude that ascorbic acid, protein -SH groups, uric acid and alpha-tocopherol may be important agents protecting against NO2. in vivo. If these antioxidants are depleted, peroxidation of lipids occurs and might contribute to the toxicity of NO2..

Adult↗

PubMed2003

Sources and concentrations of indoor nitrogen dioxide in Barcelona, Spain.

Sources and concentrations of indoor nitrogen dioxide (NO2) were examined in Barcelona, Spain, during 1996-1999. A total of 340 dwellings of infants participating in a hospital-based cohort study were selected from different areas of the city. Passive filter badges were used for indoor NO2 measurement over 7-30 days. Dwelling inhabitants completed a questionnaire on housing characteristics and smoking habits. Data on outdoor NO2 concentrations were available for the entire period of the study in the areas of the city where indoor concentrations were determined. Bivariate analysis was performed to investigate relationships between indoor NO2 concentrations on one hand and outdoor NO2 concentrations, housing, and occupant characteristics on the other. Stepwise multiple linear regression was performed with variables that were found to have a significant bivariate relationship. Indoor NO2 mean values ranged between 23.57 ppb in 1996 and 27.02 ppb in 1999, with the highest yearly value of 27.82 ppb in 1997. In the same time period, mean outdoor NO2 concentration ranged between 25.26 and 25.78 ppb with a peak of 30.5 ppb in 1998. Multiple regression analysis showed that principal sources of indoor NO2 concentrations were the use of a gas cooker, the absence of an extractor fan when cooking, and cigarette smoking. The absence of central heating was also associated with higher NO2 concentrations. Finally, each ppb increase in outdoor NO2 was associated with a 1% increase in indoor concentrations.

Air Pollution, Indoor↗

PubMed1986

Activation and increment of alveolar macrophages induced by nitrogen dioxide.

Male Wistar rats were exposed to 4 ppm nitrogen dioxide (NO2) for 10 d, and at intervals alveolar macrophages were collected by pulmonary lavage. A metabolic enhancement of alveolar macrophages was observed on d 4 of exposure. The specific activities of glucose-6-phosphate dehydrogenase and glutathione peroxidase of the peroxidative metabolic pathway increased to 1.29-fold (p less than 0.001) and 1.17-fold (p less than 0.05) those of the control values, respectively. The specific activities of succinate-cytochrome c reductase of the mitochondrial respiratory system and pyruvate kinase of the glycolytic pathway also increased to 1.17-fold (p less than 0.01) and 1.20-fold (p less than 0.01) those of the control values, respectively. In addition, the incorporation of [3H]leucine and [14C]thymidine into alveolar macrophages were elevated to 1.77-fold (p less than 0.001) and 1.84-fold (p less than 0.01) those of the control values, respectively. The activities of all enzymes tested decreased to control levels by d 10. The number of alveolar macrophages collected from exposed animals increased to 1.24-fold (p less than 0.01) that of the control value on d 7 and was maintained at a significantly higher level until d 10. Alveolar macrophages were heterogeneous in size (7-21 micron in diameter), and most of them were distributed between 11 and 17 micron in diameter. Exposures to 4 ppm NO2 increased significantly the cells of 9-13 micron in diameter on the seventh day. These results show that exposures to 4 ppm NO2 cause a metabolic enhancement and subsequent increase in alveolar macrophages.

Animals↗