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PubMedDate not supplied

Nitrogen dioxide increases eosinophil activation in the early-phase response to nasal allergen provocation.

Recent studies have suggested that exposure to air pollutants may sensitise susceptible individuals to allergen. We have investigated the effect of exposure for 6 h to 400 ppb NO2 on nasal airways resistance (NAR) and changes in inflammatory mediators (IMs) in nasal lavage in subjects with a history of seasonal allergic rhinitis. In this single blind crossover study, 8 patients were randomised to exposure to either air or 400 ppb NO2 in air and evaluated for changes in NAR and IM, before and after exposure. Another 8 patients were further challenged with allergen after similar exposure regimes and then evaluated for changes in NAR and IMs. Exposure to air or NO2 did not alter either NAR or the levels of eosinophil cationic protein (ECP), mast cell tryptase (MCT), myeloperoxidase (MPO) or interleukin (IL)-8 in nasal lavage. MCT was significantly increased after allergen challenge following exposure to both air and NO2. In contrast, ECP was significantly increased by allergen challenge only after exposure to NO2. Neither MPO nor IL-8 were altered after allergen challenge. These results suggest that NO2 may increase eosinophil activation in the early-phase response to nasal allergen provocation in allergic rhinitis.

Adolescent↗

PubMed2006

Structure-activity relationship of cyclic nitroxides as SOD mimics and scavengers of nitrogen dioxide and carbonate radicals.

Synthetic nitroxide antioxidants attenuate oxidative damage in various experimental models. Their protective effect reportedly depends on ring size and ring substituents and is greater for nitroxides having lower oxidation potential. The present study focuses on the kinetics and mechanisms of the reactions of piperidine, pyrrolidine and oxazolidine nitroxides with HO2*/O2*-, *NO2 and CO3*- radicals, which are key intermediates in many inflammatory and degenerative diseases. It is demonstrated that nitroxides are the most efficient scavengers of *NO2 at physiological pH (k = (3-9) x 10(8) M(-1) s(-1)) and among the most effective metal-independent scavengers of CO3*- radicals (k = (2 - 6) x 10(8) M(-1) s(-1)). Their reactivity toward HO2*, though not toward *NO2 and CO3*-, depends on the nature of the ring side-chain and particularly on the ring-size. All nitroxide derivatives react slowly with O2*- and are relatively inefficient SOD mimics at physiological pH. Even piperidine nitroxides, having the highest SOD-like activity, demonstrate a catalytic activity of about 1000-fold lower than that of native SOD at pH 7.4. The present results do not indicate any correlation between the kinetics of HO2*/O2*-, *NO2 and CO3*- removal by nitroxides and their protective activity against biological oxidative stress and emphasize the importance of target-oriented nitroxides, i.e., interaction between the biological target and specific nitroxides.

Antioxidants↗

PubMed1994

Random-effects linear regression meta-analysis models with application to the nitrogen dioxide health effects studies.

As the field of epidemiology grows and multiple studies of the same topic are more frequently available, increased focus is placed on quantitative methods for synthesis of results to yield an overall conclusion. A major difficulty encountered in practice has been the lack of convenient methodology for addressing groups of studies which are similar, but not exactly alike, in features which may affect study results. The age group from which subjects were selected, the general health of subjects when selected, and the specific health endpoint examined are examples of such features. Some previous investigators have addressed the problem using iterative techniques, although most have opted for simpler models which assume that differences in the studies do not appreciably affect the outcome under investigation. That is, he studies are taken to be homogeneous in that the underlying effect being investigated is the same in each study. This paper presents a random-effects linear regression technique which allows differences in the individual study features. The proposed methodology does not require iterative or other complicated procedures, making it more readily accessible to the applied researcher. We demonstrate this technique on a set of studies of the health effects of indoor NO2 exposure in children. It is seen that odds ratios from these studies vary considerably according to subject age, the study location, and the health endpoint considered. A simple synthesis which does not account for these differences may be misleading.

Air Pollutants, Occupational↗

PubMed1979

Inhibition of pulmonary prostaglandin metabolism by exposure of animals to oxygen or nitrogen dioxide.

The effects of exposure of animals to 100% O2 and NO2 on the rate of prostaglandin metabolism by lung and kidney were studied in vitro. Exposure of guinea pigs to 100% O2 for 48 h inhibited the metabolism of prostaglandin F2 alpha by both NAD+- and NADP+-dependent prostaglandin dehydrogenase in lung, but had no effect on the metabolism in kidney. Succinate dehydrogenase, but not glucose 6-phosphate dehydrogenase, in guinea-pig lung was inhibited by exposure to 100% O2. Exposure to 46 p.p.m. but not 16 or 29 p.p.m. NO2 for 6 h inhibited guinea-pig lung prostaglandin dehydrogenase in vitro. The inhibition of pulmonary prostaglandin dehydrogenase by exposure to 100% O2 or to 49 p.p.m. NO2 was dependent on the duration of exposure, but returned to control values within 7 days after cessation of the exposure. The pulmonary transport system responsible for removing circulating prostaglandins from the blood was not affected by exposure to 100% O2 as measured by using the isolated perfused lung. Kinetic analysis of the inhibition of pulmonary prostaglandin dehydrogenase activity in guinea pig exposed to 100% O2 showed non-competitive inhibition with respect to both prostaglandin F2 alpha and NAD+, which suggests destruction or inactivation of the enzyme. Pulmonary prostaglandin dehydrogenase appears to be inhibited by exposure to oxidant gases, which may lead to elevated prostaglandin concentrations in the lungs or in the systemic circulation.

15-Oxoprostaglandin 13-Reductase↗

PubMed1987

Modulation of pulmonary defense mechanisms by acute exposures to nitrogen dioxide.

The effect of acute exposures to NO2 on the antibacterial defenses of the murine lung was assessed following inhalation challenges with Staphylococcus aureus, Proteus mirabilis, and Pasteurella pneumotropica. Animals were challenged with the bacteria and exposed for 4 hr to increasing concentrations of NO2 after which pulmonary bactericidal activity was quantitated. With S. aureus pulmonary antibacterial defenses were suppressed at NO2 levels of 4.0 ppm and greater. Exposure to 10.0 ppm enhanced the intrapulmonary killing of P. mirabilis which correlated with an increase in the phagocytic cell populations lavaged from the lungs; at 20.0 ppm bactericidal activity against P. mirabilis was impaired. Pulmonary antibacterial defenses against P. pneumotropica were impaired at 10.0 ppm which correlated with a decrease in the retrieved phagocytic lung cell population. Reversing the order of treatment (ie., NO2 exposure prior to bacterial challenge) raised the threshold concentration for NO2-induced impairment of intrapulmonary bacterial killing. With S. aureus the effect was not observed at 5.0 ppm but at 10.0 ppm and with P. mirabilis not at 20.0 ppm but at 30.0 ppm intrapulmonary killing was enhanced. Exposures up to 20.0 ppm of NO2 did not effect the physical translocation mechanisms of the lung as quantitated by declines in pulmonary radiotracer activity following aerogenic challenge with 32P-labeled staphylococci. These studies demonstrate that NO2 modulates pulmonary antibacterial defenses and points to the importance of the challenge organism and the exposure protocol in establishing a threshold dose for the adverse effect.

Animals↗

PubMed1983

Pulmonary effects of intermittent subacute exposure to low-level nitrogen dioxide.

The pulmonary biochemical and morphological changes resulting from the inhalation of relatively low levels of NO2 for up to 15 wk were investigated. Specific pathogen-free Fischer 344 rats were exposed to 0, 1, or 5 ppm NO2 or 1 ppm with two spikes to 5 ppm NO2 for 7 h/d, 5 d/wk for up to 15 wk. These exposures produced a mild concentration-related pulmonary injury, with the 5-ppm group sustaining the most damage. The other NO2-exposed animals showed similar types of damage, although the extent was less than that observed in the 5-ppm-exposed group. After 15 wk of exposure, histopathological examination revealed focal areas of hyperinflation and alveolar macrophage accumulation in some of the 5-ppm- and 1-5-ppm-exposed-exposed animals. These changes were preceded by a series of biochemical changes in the bronchoalveolar lavage fluid. Cell necrosis was indicated by elevated lavage fluid concentrations of lactate dehydrogenase after 1.7 to 2.7 wk of exposure. Also elevated were alkaline phosphatase and glutathione peroxidase. Lung tissue levels of glutathione reductase and glucose-6-phosphate dehydrogenase were also increased, indicating a possible protective response to the oxidant gas. After 15 wk of exposure, all biochemical indicators of injury has resolved. These data suggest that intermittent exposure to relatively low levels of NO2 with spike concentrations produces biochemical changes that resolve with continued exposure but produce histopathological changes that may persist with continued exposure.

Animals↗

PubMed2000

Reliability of nitrogen dioxide passive diffusion tubes for ambient measurement: in situ properties of the triethanolamine absorbent.

Factors concerning NO2 uptake by the absorbent triethanolamine (TEA) in NO2 diffusion tubes are examined. Although the nominal freezing point of TEA is 17.9-21.2 degrees C, we show that, for a range of aqueous TEA solutions (0-20%, H2O), no freezing occurs even at -10 degrees C. Therefore NO2 collection efficiency is unlikely to be impaired by low temperature exposure. The recovery of TEA from the meshes of exposed samplers is determined as approximately 98%, even after 42 days, showing that the stability in situ of TEA is unaffected by long-term exposure. A model of a diffusion tube sampling array for simultaneous exposures, with a 0.1 m sampler spacing, shows that NO2 uptake by individual samplers is not affected by the presence of neighbouring tubes in the array. This is confirmed by sampler precision at two Cambridge sites. Four sampler preparation methods are compared for differences in NO2 uptake of exposed samplers. All methods employ TEA as absorbent, transferred by either dipping meshes in a TEA-acetone solution or pipetting aliquots of a TEA-H2O solution onto the meshes. For samplers prepared by three of the methods, no difference in NO2 uptake is found, but for samplers prepared using a 50% v/v TEA-H2O solution, a mean reduction of 18% is found. Student's t-tests show that the difference is highly significant (P < or = 0.001). Reasons for the difference are discussed.

Absorption↗

PubMed2003

Repeated daily exposure to 2 ppm nitrogen dioxide upregulates the expression of IL-5, IL-10, IL-13, and ICAM-1 in the bronchial epithelium of healthy human airways.

BACKGROUND: Repeated daily exposure of healthy human subjects to NO2 induces an acute airway inflammatory response characterised by neutrophil influx in the bronchial mucosa AIMS: To assess the expression of NF-kappaB, cytokines, and ICAM-1 in the bronchial epithelium. METHODS: Twelve healthy, young non-smoking volunteers were exposed to 2 ppm of NO2/filtered air (four hours/day) for four successive days on separate occasions. Fibreoptic bronchoscopy was performed one hour after air and final NO2 exposures. Bronchial biopsy specimens were immunostained for NF-kappaB, TNF-alpha, eotaxin, Gro-alpha, GM-CSF, IL-5, -6, -8, -10, -13, and ICAM-1 and their expression was quantified using computerised image analysis. RESULTS: Expression of IL-5, IL-10, IL-13, and ICAM-1 increased following NO2 exposure. CONCLUSION: Upregulation of the Th2 cytokines suggests that repeated exposure to NO2 has the potential to exert a "pro-allergic" effect on the bronchial epithelium. Upregulation of ICAM-1 highlights an underlying mechanism for leucocyte influx, and could also explain the predisposition to respiratory tract viral infections following NO2 exposure since ICAM-1 is a major receptor for rhino and respiratory syncytial viruses.

Adult↗

PubMed1987

Biochemical effects on combined gases of nitrogen dioxide and ozone. I. Species differences of lipid peroxides and phospholipids in lungs.

In the present study, changes of lipid peroxides, phospholipids and antioxidant levels in lungs of 4 animal species exposed to the combined gases of NO2 and O3 were compared. Male mice, hamsters, rats and guinea pigs were used. Lipid peroxides were increased significantly in the lungs of mice and guinea pigs exposed to the combined gases, but not in hamsters and rats. Changes of alpha-tocopherol (VE) contents were slight. On the other hand, non-protein sulfhydryl (NPSH) contents were increased strikingly, especially in hamsters, but were not increased in guinea pigs. Phosphatidylcholine (PC) contents were increased and phosphatidylethanolamine (PE) contents were decreased by the exposure to the combined gases, with the order guinea pig greater than mouse greater than rat. In hamsters no changes were seen. The changes of fatty acid composition in guinea pigs and mice were marked, the increases of palmitate and palmitolate and the decreases of polyunsaturated fatty acid were especially characteristic. These changes in phospholipid class and fatty acid composition may be a "a kind of adaptation phenomenon" to avoid further lipid peroxidation. On the other hand, the changes in hamsters and rats were small. The results show the existence of species differences in lipid peroxide formation by exposure to the combined gases of NO2 and O3. They were found to be related to the contents of antioxidants and the compositions of phospholipids and their fatty acids.

Animals↗

PubMed1989

Structural changes in airways of rats exposed to nitrogen dioxide intermittently for seven days. Comparison between major bronchi and terminal bronchioles.

Structural changes caused by exposure to NO2 were compared between the largest intrapulmonary bronchi (major bronchi) and the terminal bronchioles. Rats were exposed to 50 ppm NO2 for 5 h a day for 7 consecutive days, and microscopic findings were assessed subjectively and quantitatively. Destruction of airway epithelium was present on Day 1, and the reparative phase was observed between Days 3 and 7. Light microscopy showed that on Day 1, loss of cilia and disintegration of epithelium occurred, and that the latter was worse in major bronchi than in terminal bronchioles; apical projections of Clara cells in terminal bronchioles were lost almost totally. Recovery of epithelium began by Day 3 and cilia by Day 5, and ciliogenesis progressed less promptly in terminal bronchioles. Clara cells did not return to normal during the experiment. Furthermore, a decrease in the airway diameter occurred in peripheral airways along with an increase in mural thickness in terminal bronchioles. Mural inflammation was also seen more conspicuously in terminal bronchioles. Electron microscopy revealed that epithelial cells lost secretory granules on Day 1 and began to repair them by Day 5 in major bronchi and by Day 7 in terminal bronchioles. It is likely that epithelium in terminal bronchioles is not particularly sensitive to NO2 compared with that in major bronchi, but that recovery occurs more promptly in major bronchi than in terminal bronchioles. Mechanisms underlying bronchoconstriction occurring preferentially in peripheral airways are also discussed.

Animals↗

PubMed1985

Certain aspects of the responses of laboratory rats to exposure to (a) nitrogen dioxide and (b) tobacco smoke.

Exposure of rats to 150 ppm NO2 for 2 hours causes death from pulmonary oedema. Continuous exposure to 25 ppm for 150 days causes gross enlargement with loss of elastic recoil and proliferative and metaplastic epithelial changes in the vicinity of the terminal bronchioles. Continuous exposure to 2 ppm results in an initial loss of cilia and focal hyperplasia of the terminal bronchiolar epithelium, but these changes, for the most part, quickly subside. Chronic daily exposure of rats to tobacco smoke results in proliferative and metaplastic epithelial changes in the vicinity of the terminal and respiratory bronchioles. Also, both at this site and elsewhere, aggregates of golden-brown pigment-laden macrophages accumulate in the lungs. The proliferative/metaplastic changes are similar to those seen in response to NO2, asbestos and other irritant gases and particles. The aggregates of golden-brown macrophages are seemingly a special feature of the response to tobacco smoke. Some rats exposed for over two years to tobacco smoke, develop foci of squamous metaplasia, firstly in the region of terminal bronchioles, but later at points scattered throughout the lung parenchyma. Comparable changes have not been reported in rats exposed to NO2. Although no strictly comparable data for NO2 and tobacco smoke exposure are available, it is reasonable to conclude that, whereas the NO2 in tobacco smoke may contribute to the production of cuboidal/columnar metaplasia in the vicinity of terminal bronchioles, it otherwise plays little part in the aetiology of lesions in the lungs of smoke-exposed rats.

Animals↗

PubMed2000

Ozone, but not nitrogen dioxide, exposure decreases glutathione peroxidases in epithelial lining fluid of human lung.

Antioxidants, such as glutathione peroxidases (GPxs), in epithelial lining fluid (ELF) protect against health effects of oxidant pollutants, which includes O(3) or NO(2). We hypothesized that GPxs concentration in ELF is responsive to O(3) or NO(2) exposure. Subjects underwent two 4-h exposures to O(3) (0.22 ppm) and one to air. In another experiment, subjects underwent 3-h exposures to air and NO(2) (0.6 and 1.5 ppm). Bronchoalveolar lavage (BAL) was performed immediately or 18 h after O(3) exposure and 3.5 h after each NO(2) exposure. GPx activity and extracellular GPx (eGPx) protein concentrations were determined in ELF, and their relationships to markers of lung function, inflammation, and epithelial permeability were examined. Although the total amounts were not changed, basal (air) GPx activity (223.6 +/- 24.4 mU/ml), basal eGPx protein concentration (2.62 +/- 0.25 microg/ml), and basal ELF dilution factor (152.3 +/- 8.4) decreased 40% immediately after O(3) exposure and remained 30% decreased 18 h after exposure (p = 0.0001). No effect of NO(2) exposure on GPxs concentration was detected. There was an inverse correlation between baseline ELF eGPx protein concentration and the change in PMN 18 h after O(3) exposure (p = 0.04). Thus, O(3), a strong oxidant, decreases both GPx activity and eGPx protein in ELF, whereas NO(2), a weaker oxidant, does not. eGPx in ELF may protect against O(3)-induced airway inflammation.

Adolescent↗

PubMed1990

Reactive uptake governs the pulmonary air space removal of inhaled nitrogen dioxide.

With the use of an isolated rat lung model, we investigated pulmonary air space absorption kinetics of the reactive gas NO2 in an effort to determine the contributory role of chemical reaction(s) vs. physical solubility. Unperfused lungs were employed, because vascular perfusion had no effect on acute (0- to 60-min) NO2 absorption rates. We additionally found the following: 1) Uptake was proportional to exposure rates (2-14 micrograms NO2/min; 10-63 ppm; 37 degrees C) but saturated with exposures greater than or equal to 14 micrograms NO2/min. 2) Uptake was temperature (22-48 degrees C) dependent but, regardless of temperature, attained apparent saturation at 10.6 micrograms NO2/min. 3) Lung surface area (SA) was altered by increasing functional residual capacity (FRC). Expanded SA (8 ml FRC) and temperature (48 degrees C) both raised fractional uptakes (greater than or equal to 0.81) relative to 4 ml FRC, 37 degrees C (0.67). Uptake rates normalized per unit estimated SA revealed no independent effect of FRC on fractional uptake. However, temperature produced a profound effect (48 degrees C = 0.93; 4 and 8 ml FRC = 0.54). 4) Arrhenius plots (ln k' vs. 1/T), which utilized derived reactive uptake coefficients (k'), showed linearity (r2 = 0.94) and yielded an activation energy of 7,536 kcal.g-1.mol-1 and Q10 of 1.43, all consistent with a reaction-mediated process. These findings, particularly the effects of temperature, suggest that acute NO2 uptake in pulmonary air spaces is, in part, rate limited by chemical reaction of NO2 with epithelial surface constituents rather than by direct physical solubility.

Air Pollutants↗

PubMed1985

What interaction does indoor nitrogen dioxide have on the effect of the automobile exhaust.

An attempt was made to investigate the effects of automobile exhaust to the people living alongside major traffic arterial in Tokyo. Several hundreds of housewives aged from 40 to 59 who lived more than 3 years were sampled both from the area A; within 20 m from road side, and from the area B which extended from 20 m to 150 m along the road next to the area A. ATS-DLD questionnaire was used to check the prevalence of respiratory symptom, its results was analysed with a deliberate consideration on smoking habits and using status of unvented kerosene space heater. Among each symptom prevalence, difference between the area A and the B was observed significantly in symptom rate related persistent cough and phlegm. These differences became much distinguished in non-smoking group and people not using unvented heater. For about one tenth of sample subject, joined the study of measurement of personal exposure to NO2 for 24 hr using NO2 filter badge. The average concentration of exposure depends largely on heater using status but does not on the study area, even though the atmospheric concentration of NO2 in the area A was higher than that of the area B. The difference of symptom prevalence between the study area becomes not significant compared with the group of using unvented heater. This means that, we suppose, the substantial higher symptom prevalence which observed in the area along the roadside is masked by repeated exposure to elevated indoor concentration of NO2 resulted from using kerosene space heater.

Climate↗

PubMed1987

Effects of long-term nitrogen dioxide exposure on rat lung: morphological observations.

Rats continuously exposed to NO2 at 0.04, 0.4, and 4.0 ppm for as long as 27 months were submitted to morphological observation and electronmicroscopic morphometry of the lung. At 4 ppm exposure for 9 months, bronchial epithelium showed typical proliferation, which progressed further at 18 months. At this stage, proliferation of type II alveolar epithelium and edematous extension of interstitial tissue were evident and yielded fibrosis at 27 months. At 0.4 ppm, morphological changes in 18-month specimens were still ambiguous, although a tendency toward epithelial changes, as well as interstitial edema of the alveolar wall, was noticed under the electron microscope. Slight but definite alteration of the epithelium became evident after 27 months. At 0.04 ppm there were no remarkable changes throughout the entire exposure period. The morphometry revealed concentration- and duration-dependent increases in arithmetic mean thickness (AMT) of the alveolar wall. At 4 ppm, increase of AMT started as early as 9 months, became significant at 18 months, and showed a slight decrease at 27 months. This decrease was interpreted as a recovery of alveolar epithelium and decreased amount of septal edema, which in turn led to fibrosis. At 0.4 ppm, a slight increase of AMT started at 18 months and extended significantly in 27 months. A similar but insignificant tendency was found even at 0.04 ppm. The morphological alterations were parallel to the concentration and duration of exposure. These findings suggested that an intensive study should be conducted to confirm whether alterations were due to prolonged exposure and/or due to elevated sensitivity of the aged lung.

Animals↗

PubMed1994

In vitro exposure to nitrogen dioxide (NO2) does not alter bronchial smooth muscle responsiveness in ovalbumin-sensitized guinea-pigs.

The aim of this study was to investigate whether in vitro exposure to NO2 affects responsiveness in ovalbumin-sensitized guinea-pig bronchi. Twenty-three animals were sensitized by three weekly intraperitoneal injections of 1 mg ovalbumin in saline with Freund's adjuvant; twenty-one control guinea-pigs received the diluent alone. From each animal, the two main bronchi were obtained and cannulated, then exposed in vitro to a constant intraluminal flow of: (i) either air or 2.5 ppm NO2 with four spikes of 10 ppm NO2 for 2 h; (ii) either air or 10 ppm NO2 for 4 h. A bronchial ring obtained from each animal before exposure was kept in aerated Krebs-Henseleit solution. Rings from bronchi exposed to air, NO2, or kept in Krebs solution were studied isometrically. We performed overall and non-adrenergic non-cholinergic voltage-response curves to electrical field stimulation, concentration-response curves to acetylcholine and to neurokinin A, followed by administration of 10 mg/ml ovalbumin. We did not find any significant difference in bronchial smooth muscle responsiveness between nonexposed, air-exposed and NO2-exposed bronchi, as well as between bronchi from control and sensitized animals. We conclude that in vitro exposure to NO2 does not alter bronchial smooth muscle responsiveness to either specific or non-specific stimuli.

Acetylcholine↗

PubMed2000

Sources and concentrations of indoor nitrogen dioxide in Hamburg (west Germany) and Erfurt (east Germany).

Here we report indoor and outdoor concentrations of NO2 for Erfurt and Hamburg and assess the contribution of the most important indoor sources (e.g. the presence of gas cooking ranges, smoking) and outdoor sources (traffic exhaust emissions). We examined the relative contribution of the different sources of NO2 to the total indoor NO2 levels in Erfurt and Hamburg. NO2 indoor concentrations in Hamburg were slightly higher than those in Erfurt (i.e. living room: 15 microg m(-3) for Erfurt and 17 microg m(-3) for Hamburg). A linear regression model including the variables, place of residence, season and outdoor NO2 levels, location of the home within the city, housing and occupant characteristics accounted for 38% of the NO2 variance. The most important predictors of indoor NO2 concentrations were gas in cooking followed by other characteristics, such as ventilation or outdoor NO2 level. Residences in which gas was used for cooking, or in which occupants smoked, had substantially higher indoor NO2 concentrations (41 or 18% increase, respectively). An increase in the outdoor NO2 concentration from the 25th to the 75th-percentile (17 microg m(-3)) was associated with a 33% increase in the living room NO2 concentration. Multiple regression analysis for both cities separately illustrated that use of gas for cooking was the major indoor source of NO2. This variable caused a similar increase in the indoor NO2 levels in each city (43% in Erfurt and 47% in Hamburg). However, outdoor sources of NO2 (motor vehicle traffic) contributed more to indoor NO2 levels in Hamburg than in Erfurt.

Air Pollution, Indoor↗

PubMed2002

Effect of nitrogen dioxide on ovalbumin-induced allergic airway disease in a murine model.

The effect of exposure to irritant air pollutants on the development of allergic airway disease is poorly understood. This study examines the effects of the lower respiratory tract irritant, NO(2), on the outcome of ovalbumin (OVA)-induced allergic airway disease. Male and female C57Bl/6 mice were sensitized by weekly intraperitoneal (ip) OVA injections for 3 wk followed by daily 1-h OVA aerosol inhalation challenge for 3 or 10 d. Initially, mice were exposed daily for 3 d to air or 0.7 or 5 ppm NO(2) for 2 h following each OVA aerosol challenge. OVA exposure resulted in pronounced lower airway inflammation, as evidenced by a significant increase in bronchoalveolar lavage (BAL) total cellularity and eosinophil levels. BAL eosinophil levels were significantly lower in OVA-NO(2) compared to OVA-air animals. The reduction was similar at both NO(2) exposure concentrations. In a subsequent study, sensitized animals were exposed for 3 or 10 d to aerosolized OVA followed by air or 0.7 ppm NO(2). BAL eosinophils were again reduced at 3 d by OVA-NO(2) exposure compared to OVA-air mice. At 10 d the eosinophilia was virtually abolished. This reduction in OVA-induced cellular inflammation by NO(2) was confirmed by histopathological analysis. Contrary to expectations, exposure to NO(2) during the aerosol challenge to OVA dramatically diminished the outcome of allergic disease in lungs as measured by airway cellular inflammation.

Aerosols↗