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PubMed2001

Effect of exposure to nitrogen dioxide on alveolar macrophage-mediated immunosuppressive activity in rats.

Nitrogen dioxide (NO2), a major component of air pollutants, induces inflammatory responses in the lungs. Resident alveolar macrophages (AM) play an immunosuppressive role in the lungs via suppression of lymphocyte proliferation, and nitric oxide (NO) plays a crucial role in this immunosuppressive activity. Microenvironmental changes within the alveoli during inflammatory responses, however, can inhibit this immunosuppressive activity of AM. The present study was designed to clarify the effect of NO2 exposure on the immunosuppressive activity of and NO production by AM in rats. Wistar rats were exposed to 10 ppm NO2 for 3, 14 or 28 days, after which bronchoalveolar lavage fluid (BALF) was taken as a sample of the alveolar microenvironment. Suppression of concanavalin A-induced lymphocyte proliferation and NO production by AM were markedly inhibited by BALF from NO2-exposed rats (NO2-BALF). The inhibitory effect of NO2-BALF at 28-days exposure was stronger than that of NO2-BALF at 3 or 14 days exposure. In conclusion, AM-mediated immunosuppressive activity was inhibited by the NO2-induced changes of the alveolar microenvironment through the inhibition of NO production.

Animals↗

PubMed1990

Indoor nitrogen dioxide exposure and children's pulmonary function.

Elevated concentrations of nitrogen dioxide (NO2) are produced in the home by the use of unvented gas appliances. In studies on potential health effects of indoor exposure to NO2, exposure has mostly been estimated from the presence or absence of sources like gas cookers in the home. This leads to misclassification of exposure, as NO2 concentrations in the home depend also on source use, ventilation habits, time budgets, etc. The availability of cheap, passive monitoring devices has made it possible to measure indoor concentrations of NO2 directly in health effects studies, albeit with averaging times of one to several days. So far, it has not been evaluated whether this increases the sensitivity of a study to detect health effects of NO2. In this paper, a comparison is made between NO2 sources and weekly average indoor NO2 measurements, as predictors of pulmonary function in a study among children aged 6-12 years. The relationship between exposure and lung functions was found to be generally non-significant in this study. The results further suggested that in this study, measuring indoor NO2 concentrations with passive monitors offered no advantage over the simple use of source presence as exposure variable.

Air Pollutants↗

PubMed1994

Localization of increased collagen in ferret lung tissue after chronic exposure to nitrogen dioxide.

Chronic exposure of experimental animals to moderate levels of nitrogen dioxide (NO2) leads to increased collagen deposition in the lung parenchyma. To localize this increased collagen, lung sections from ferrets exposed to 0.5 or 10 ppm of NO2 4 h daily for 8 or 15 weeks were stained with Sirius red under conditions in which the stain is specific for collagen. Stained areas of respiratory bronchiolar submucosa were compared between NO2-exposed and air-exposed control animals using computer-aided image analysis. The stained areas, relative to the total respiratory epithelium, were increased in the sections from NO2-exposed ferrets as compared to air-exposed controls after 8 or 15 weeks. Removal from exposure after 8 weeks and allowing a 7-week recovery did not result in a decrease in stained areas. In the 10 ppm group, but not in the 0.5 ppm group, the increase was statistically significant. Measurement of total collagen in lung tissue by chemical means showed no differences among the various treatment groups. This study showed that increases in collagen deposition can be readily localized in order to identify the site(s) of potentially adverse effects of air pollutants. It is suggested that the use of Sirius red staining may offer a sensitive method for detection of early fibrotic changes in the lung.

Analysis of Variance↗

PubMed1994

Overview of nitrogen dioxide effects on the lung with emphasis on military relevance.

Nitrogen dioxide exposure occurs in many civilian occupations as well as during military combat. Little interaction has occurred between the two communities in regards to the exchange of information about NO2 research. This presentation provides an overview of NO2 related epidemiology; available research models and issues of particular interest to both the civilian and military sectors; clinical presentations, prophylaxis and treatment; and pathophysiology and mechanisms of injury. Throughout the presentation civilian and military issues are contrasted when pertinent. The most significant difference between the civilian and military research requirements is the need for information on chronic (with and without intermittent peaks) for the former, and information on acute high-level NO2 research for the latter. Another military requirement is predicting not only injury but incapacitation. This requirement can be compared to the need of clinicians to measure impairment for patients seeking disability. Both communities are faced with the same challenges of selecting appropriate models, understanding dosimetry and its many variables, clarifying the fate of inhaled NO2, developing specific markers of injury, and elucidating the mechanisms of NO2 injury for the development of prophylactic and therapeutic agents. Further research is required in these areas and it is hoped that this symposium will be the first attempt to join civilian and military resources and expertise for future research cooperation and collaboration.

Animals↗

PubMed2000

Health effects of daily indoor nitrogen dioxide exposure in people with asthma.

Household gas appliances produce nitrogen dioxide (NO2), which may be associated with an increase in symptoms in asthmatics. The relationship between indoor NO2 exposure, and respiratory symptoms in people with asthma was evaluated. Self-reported asthmatics (n=125) wore lapel badges that measured NO2 daily over 6 weeks at home. Outdoor pollutants, spores and meteorological parameters were measured daily, in addition to smoking status and demographic factors. Seven asthma symptoms were recorded in diaries, for analysis by same day and also with 1 day lag exposures, using a generalized estimating equation. Significant interactions were demonstrated between NO2 at age < or =14 yrs, with respect to the symptoms of chest tightness on the same day (odds ratio (OR): 1.29, 95% confidence interval (CI): 1.16-1.43) and with a 1 day lag (OR: 1.29, 95% CI: 1.14-1.46), breathlessness on exertion with a 1 day lag (OR: 1.13, 95% CI: 1.00-1.28), daytime asthma attacks on the same day (OR: 1.13, 95% CI: 1.02-1.26) night asthma attacks on the same day (OR: 1.16, 95% CI:1.03-1.30) and with a 1 day lag (OR: 1.15, 95% CI; 1.03-1.29) after adjustment for potential confounders. A significant interaction between NO2 and age 35-49 yrs was demonstrated for coughs with a 1 day lag (OR: 1.15, 95% CI: 1.01-1.31). Daily personal exposures to NO2 are associated with asthmatic symptoms in children.

Adolescent↗

PubMed2002

Kinetics of the reactions of nitrogen dioxide with glutathione, cysteine, and uric acid at physiological pH.

Nitrogen dioxide (NO(2)(*)) is a key biological oxidant. It can be derived from peroxynitrite via the interaction of nitric oxide with superoxide, from nitrite with peroxidases, or from autoxidation of nitric oxide. In this study, submicromolar concentrations of NO(2)(*) were generated in < 1 micros using pulse radiolysis, and the kinetics of scavenging NO(2)(*) by glutathione, cysteine, or uric acid were monitored by spectrophotometry. The formation of the urate radical was observed directly, while the production of the oxidizing radical obtained on reaction of NO(2)(*) with the thiols (the thiyl radical) was monitored via oxidation of 2,2'-azino-bis-(3-ethylthiazoline-6-sulfonic acid). At pH 7.4, rate constants for reaction of NO(2)(*) with glutathione, cysteine, and urate were estimated as approximately 2 x 10(7), 5 x 10(7), and 2 x 10(7) M(-1) s(-1), respectively. The variation of these rate constants with pH indicated that thiolate reacted much faster than undissociated thiol. The dissociation of urate also accelerated reaction with NO(2)(*) at pH > 8. The thiyl radical from GSH reacted with urate with a rate constant of approximately 3 x 10(7) M(-1) s(-1). The implications of these values are: (i) the lifetime of NO(2)(*) in cytosol is < 10 micros; (ii) thiols are the dominant 'sink' for NO(2)(*) in cells/tissue, whereas urate is also a major scavenger in plasma; (iii) the diffusion distance of NO(2)(*) is approximately 0.2 microm in the cytoplasm and < 0.8 microm in plasma; (iv) urate protects GSH against depletion on oxidative challenge from NO(2)(*); and (v) reactions between NO(2)(*) and thiols/urate severely limit the likelihood of reaction of NO(2)(*) with NO* to form N(2)O(3) in the cytoplasm.

Cysteine↗

PubMed2002

Significant pulmonary response to a brief high-level, nose-only nitrogen dioxide exposure: an interspecies dosimetry perspective.

Brief, high-level nitrogen dioxide (NO(2)) exposures are major hazards during fires and heat-generating explosions. To characterize the lung response to a brief high-level NO(2) exposure, we exposed two groups (n = 5) of 325-375 g, male, Sprague-Dawley rats to either 200 +/- 5 ppm (376 +/- 9 mg/m(3)) NO(2) or room air for 15 min. The rats were nose-only exposed in a multiport exposure chamber fitted with pressure transducers to monitor their respiration during exposure. One hour after exposure, we euthanized the rats, collected blood samples, lavaged the lungs with warm saline, and then excised them. One lung lobe was cooled to -196 degrees C and used for low-temperature electron paramagentic resonance (EPR) analysis. The remainder was homogenized and used for biochemical analyses. Inspired minute ventilation (V(i)) during exposure decreased 59% (p < 0.05). Calculated total inspired dose was 0.880 mg NO(2). In lung lavage, both total and alveolar macrophage cell counts declined (approximately 75%, p < 0.05), but epithelial cell count increased 8.5-fold. Lung weight increased 40% (p < 0.05) after exposure. In the blood, potassium and methemoglobin increased 45 and 18% (p < 0.05), respectively; glucose, lactate, and total hemoglobin were not altered significantly. EPR analysis of lung tissue revealed hemoglobin oxidation and carbon-centered radical formation. Vitamins E and C and uric acid were depleted, and lipid peroxidation measured by three different methods (TBARS, conjugated dienes, and fluorescent peroxidation end products) was elevated, but total protein, DNA, and lipid contents were unchanged. These observations combined demonstrate that a brief (15 min) high-level (200 ppm) NO(2) exposure of rats was sufficient to cause significant damage. However, comparison of the exposure dose normalized to rat body weight with previously reported sheep and estimated human values revealed significant differences. This raises a question about interspecies dosimetry and species-specific responses when animal data are extrapolated to humans and used for safety standard setting, particularly with high-level brief exposures.

Administration, Inhalation↗

PubMed2000

Biochemical and morphological changes in lung tissue and isolated lung cells of rats induced by short-term nitrogen dioxide exposure.

To investigate the effects of repeated exposure to nitrogen dioxide (NO2) on antioxidant enzymes in lung tissue and isolated lung cells, rats were continuously exposed to 20 mg/m3 NO2 (10.6 ppm) for 4 days. The activities of glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), and glutathione peroxidase (GSHPx) were measured in the cytosolic fraction of lung tissue of both control and NO2-exposed rats as well as in isolated alveolar macrophages (AMs) and type II cells. Qualitative and quantitative changes in AM and type II cells were studied by electron microscopy and by morphometric analyses using enzyme and immunohistochemistry. NO2 exposure resulted in significantly increased pulmonary activities of G6PDH, GR, and GSHPx, both expressed per lung and per gram of lung weight. Morphometric data show that NO2 exposure significantly increased the number of type II cells, predominantly in the centriacinar region, indicating proliferation of epithelium following cellular injury. Type II cells in lungs of NO2-exposed rats had a squamous, less cuboidal appearance with more lamellar bodies compared to type II cells in lungs of control rats. Compared to control lungs, a higher number of macrophages could be isolated from NO2-exposed lungs, while numbers of type II cells isolated from lungs of control and NO2-exposed rats were the same. Isolated type II cells from control and NO2-exposed rats were polymorphic, with a small number of lamellar bodies and without polarity. Isolated macrophages were rounded and contained many filopodia. NO2 exposure caused increases in the activities of G6PDH and GSHPx in isolated type II cells and of GSHPx in isolated macrophages, when expressed per number of cells. Macrophages and type II cells isolated from control and NO2-exposed rats and re-exposed in vitro to NO2, showed no differences in phagocytosis and viability features. Our results indicate that NO2-induced increases in pulmonary antioxidant enzymes are also reflected in isolated AM and type II cells. Since these lung cells do not display a decreased sensitivities toward an in vitro NO2 exposure, overall increase in antioxidant enzyme activities do not seem to play the most pivotal role in controlling cellular NO2 sensitivity and oxidant defence. Combined data from biochemical, morphological, and morphometric analyses of lungs and lung cells suggest that lung cell and tissue oxidant sensitivity and defence largely depends on the cell and tissue organisation, i.e., cell numbers and morphology as well as the ratio of surface area to cytoplasmic volume.

Animals↗

PubMed1990

Genotoxic activity of 1,3-butadiene and nitrogen dioxide and their photochemical reaction products in Drosophila and in the mouse bone marrow micronucleus assay.

The genotoxic activity of a photochemical reaction mixture of 1,3-butadiene and nitrogen dioxide was investigated in vivo in the mouse bone marrow micronucleus assay and the somatic mutation and recombination test in Drosophila (the wing spot test). Butadiene alone was not mutagenic in Drosophila, but induced micronuclei in mice at 10 ppm after 23 h of exposure. Nitrogen dioxide was not genotoxic in either test system. The photochemical reaction products were toxic but probably not mutagenic in Drosophila and not genotoxic in mouse bone marrow. The in vivo results do not confirm earlier in vitro results that demonstrated a strong direct-acting mutagenic activity of the photochemical products in Salmonella.

Animals↗

PubMed1980

Respiratory pentane: a measure of in vivo lipid peroxidation applied to rats fed diets varying in polyunsaturated fats, vitamin E, and selenium and exposed to nitrogen dioxide.

Pentane is one decomposition product of omega 6-unsaturated lipid hydroperoxides. The measurement of respiratory pentane is one of the most sensitive in vivo tests of lipid peroxidation. This measurement was applied to test the ability of a low level, short-term exposure of rats of nitrogen dioxide to induce lipid peroxidation. When exposed to 4.48 ppm nitrogen dioxide for 60 min, no increase in pentane production was detected. For 10 weeks prior to exposure, the rats were fed Torula yeast-based diets with 10% stripped lard or 10% stripped corn oil. The ratios of basal pentane production by rats fed the following antioxidants were for corn oil- and lard-fed rats, respectively: 40 I.U. vitamin E/kg and 0 selenium: 0 vitamin E and 0.1 ppm selenium: 0 vitamin E and 0 selenium, 1:2.2:5.8 and 1:1.9:3.5. Pentane production was significantly (P<0.05) greater by corn oil-fed rats than by lard-fed rats only when both vitamin E and selenium were absent from the diet.

Animals↗

PubMed1984

The relationship between indoor nitrogen dioxide concentration levels and personal exposure: a pilot study.

A small, personal monitoring study was performed in a subpopulation (14 families) of a case-control study on the relationship between indoor nitrogen-dioxide exposure and respiratory diseases of schoolchildren. Mothers, schoolchildren and pre-schoolchildren were asked to carry duplicate Palmes diffusion tubes during one week. Simultaneously nitrogen-dioxide concentrations were measured in the kitchen, living room, bedroom, outdoors and--for a few participants--at school and at work. Information on time activity patterns was gathered by means of a self administered diary. Several models for estimating exposure were constructed and tested against measured exposure. The personal exposure of the participants could well be explained by models containing indoor concentrations. Models with time-weighted average concentrations did not explain personal exposure better than models containing indoor concentrations. A calculated time-weighted average exposure was found to underestimate measured personal exposure by an average 20%, probably because the average concentration in a location does not necessarily reflect the actual exposure in that location. Personal exposure of mothers and children was very similar and highly correlated, indicating that the personal exposure of the mother might be a reasonable estimate for the exposure of the child.

Adult↗

PubMed1992

Nitrogen dioxide induced changes in level of free fatty acids, triglyceride, esterified fatty acid, ganglioside and lipase activity in the guinea pig brain.

The biochemical response to controlled inhalation of nitrogen dioxide (NO2) was studied in 18 male guinea pigs. Animals were exposed to 2.5, 5.0, and 10 ppm NO2 for 2h daily for 35 consecutive days, and the results compared with six control animals exposed to filtered air for 2h daily for same period. Five biochemical parameters, including triglyceride, free fatty acids, esterified fatty acid, ganglioside and lipase activity were measured immediately after the last day of exposure. At 2.5 ppm NO2 inhalation no significant changes occurred in any region of the central nervous system (CNS). While as the dose concentration was increased to 5 and 10 ppm nitrogen dioxide, significant dose-related alteration were observed in the levels of triglyceride, free fatty acid, esterified fatty acid, ganglioside and lipase activity in the different regions of the guinea pig CNS.

Administration, Inhalation↗

PubMed2005

Ground-based zenith sky abundances and in situ gas cross sections for ozone and nitrogen dioxide with the Earth Observing System Aura Ozone Monitoring Instrument.

High-accuracy spectral-slit-function calibration measurements, in situ ambient absorption gas cell measurements for ozone and nitrogen dioxide, and ground-based zenith sky measurements with the Earth Observing System Aura Ozone Monitoring Instrument (OMI) flight instrument are reported and the results discussed. For use of high-spectral-resolution gas absorption cross sections from the literature in trace gas retrieval algorithms, accurate determination of the instrument's spectral slit function is essential. Ground-based measurements of the zenith sky provide a geophysical determination of atmospheric trace gas abundances. When compared with other measurements, they can be used to verify the performance of the OMI flight instrument. We show that the approach of using published high-resolution absolute absorption cross sections convolved with accurately calibrated spectral slit functions for OMI compares well with in situ gas absorption cell measurements made with the flight instrument and that use of these convolved cross sections works well for reduction of zenith sky data taken with the OMI flight instrument for ozone and nitrogen dioxide that are retrieved from measured spectra of the zenith sky with the differential optical absorption spectroscopy technique, the same method to be used for the generation of in-flight data products. Finally, it is demonstrated that the spectral stability and signal-to-noise ratio performance of the OMI flight instrument, as determined from preflight component and full instrument tests, are sufficient to meet OMI mission objectives.

Air Pollutants↗

PubMed1981

Interaction of glutathione and ascorbic acid in guinea pig lungs exposed to nitrogen dioxide.

The interaction of two important water-soluble antioxidants, glutathione and ascorbic acid, was studied. The perfused guinea pig lung was found to contain about twice as much reduced glutathione as ascorbic acid. Nitrogen dioxide exposure decreased the levels of the two antioxidants both in vitro and in vivo. Ascorbic acid concentration was lowered to a greater extent than glutathione. The pulmonary ascorbic acid level was identical in both control and glutathione-deficient guinea pigs exposed to nitrogen dioxide, suggesting that there was little interaction between the two antioxidants in the lungs during oxidant stress.

Animals↗

PubMed1996

Effect of nitrogen dioxide and other combustion products on asthmatic subjects in a home-like environment.

Nitrogen dioxide (NO2) is one of a number of nitrogen compounds that are by-products of combustion and occur in domestic environments following the use of gas or other fuels for heating and cooking. In this study, we examined the effect of two levels of NO2 on symptoms, lung function and airway hyperresponsiveness (AHR) in asthmatic adults and children. In addition, in the same subjects, we examined the effects of the same levels of NO2 mixed with combustion by-products from a gas space heater. The subjects were nine adults, aged 19-65 yrs, and 11 children, aged 7-15 yrs, with diagnosed asthma which was severe enough to require daily medication. All subjects had demonstrable AHR to histamine. Exposures were for 1 h on five separate occasions, 1 week apart, to: 1) ambient air, drawn from outside the building; 2) 0.3 parts per million (ppm) NO2 in ambient air; 3) 0.6 ppm NO2 in ambient air; 4) ambient air+combustion by-products+NO2 to give a total of 0.3 ppm; and 5) ambient air+combustion by-products+NO2 to give a total of 0.6 ppm. Effects were measured as changes in lung function and symptoms during and 1 h after exposure, in AHR 1 h and 1 week after exposure, and in lung function and symptoms during the week following exposure. Exposure to NO2 either in ambient air or mixed with combustion by-products from a gas heater, had no significant effect on symptoms or lung function in adults or in children. There was a small, but statistically significant, increase in AHR after exposure to 0.6 ppm NO2 in ambient air. However, there was no effect of 0.6 ppm NO2 on AHR when the combustion by-products were included in the test atmosphere nor of 0.3 ppm NO2 under either exposure condition. We conclude that a 1 h exposure to 0.3 or 0.6 ppm NO2 has no clinically important effect on the airways of asthmatic adults or children, but that 0.6 ppm may cause a slight increase in airway hyperresponsiveness.

Adolescent↗

PubMedDate not supplied

Protein leakage in the lungs of mice exposed to 0.5 ppm nitrogen dioxide.

Forty-four mice were continuously exposed to 0.47 ppm nitrogen dioxide for ten, 12, and 14 days. The protein content of homogenized lung tissue was assayed fluorometrically after the animals had received intravenous injections of fluorescamine, a new reagent for protein assay. The mean protein value of all exposed animals was higher than that of the control animals (P less than .025). No correlation was noted between serum fluorophor levels and those in the lung homogenate.

Animals↗

PubMed2004

Concentrations of ammonia and nitrogen dioxide at roadside verges, and their contribution to nitrogen deposition.

Bimonthly integrated measurements of NO2 and NH3 have been made over one year at distances up to 10 m away from the edges of roads across Scotland, using a stratified sampling scheme in terms of road traffic density and background N deposition. The rate of decrease in gas concentrations away from the edge of the roads was rapid, with concentrations falling by 90% within the first 10 m for NH3 and the first 15 m for NO2. The longer transport distance for NO2 reflects the production of secondary NO2 from reaction of emitted NO and O3. Concentrations above the background, estimated at the edge of the traffic lane, were linearly proportional to traffic density for NH3 (microg NH3 m(-3) = 1 x 10(-4) x numbers of cars per day), reflecting emissions from three-way catalysts. For NO2, where emissions depend strongly on vehicle type and fuel, traffic density was calculated in terms of 'car equivalents'; NO2 concentrations at the edge of the traffic lane were proportional to the number of car equivalents (microg NO2 m(-3) = 1 x 10(-4) x numbers of car equivalents per day). Although absolute concentrations (microg m(-3)) of NH3 were five times smaller than for NO2, the greater deposition velocity for NH3 to vegetation means that approximately equivalent amounts of dry N deposition to road side vegetation from vehicle emissions comes from NH3 and NO2. Depending on traffic density, the additional N deposition attributable to vehicle exhaust gases is between 1 and 15 kg N ha(-1) y(-1) at the edge of the vehicle lane, falling to 0.2-10 kg N ha(-1) y(-1) at 10 m from the edge of the road.

Air Pollutants↗

PubMed1991

Reactions of dinitrogen pentoxide and nitrogen dioxide with 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine.

The reactions of gaseous dinitrogen pentoxide (N2O5) and nitrogen dioxide (NO2) with 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine (POPC) coated on the inside surface of a glass reaction cell were studied at 298 K. Unsaturated phosphatidylcholines are significant components of pulmonary surfactant in the alveolar region of the lung and hence serve as a simple model to examine reactions of pulmonary surfactant with these oxidant air pollutants. Using high-performance liquid chromatography (HPLC), Fourier transform infrared and fast atom bombardment mass spectroscopy, the major products of reactions of POPC with N2O5 and NO2 were separated and identified. In the POPC-N2O5 reaction using either air or helium as a buffer gas, the nitronitrate, vinyl nitro and allylic nitro derivatives, as well as a small amount of the trans-isomer of the starting material, were obtained. The nature of the products obtained from the POPC-NO2 reaction depends on the concentration of NO2 as well as whether air is present. At low NO2 concentrations (PNO2/N2O4 less than or equal to 3.8 Torr) in air or in helium, the trans-isomer of POPC was formed almost exclusively. At higher NO2 concentrations (PNO2/N2O4 greater than or equal to 20 Torr) in helium, the dinitro, vinyl nitro and nitro alcohol derivatives were formed. In the presence of air (or 24% 18O2 in helium), a nitronitrate and a dinitronitrate were additional products. Mechanisms for the formation of the observed products and implications for the inhalation of oxides of nitrogen are discussed.

Chromatography, High Pressure Liquid↗