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PubMed1995

Effect of six-hour exposure to nitrogen dioxide on early-phase nasal response to allergen challenge in patients with a history of seasonal allergic rhinitis.

BACKGROUND: Recent studies have suggested that exposure to air pollutants may enhance the airway responsiveness of susceptible individuals to inhaled allergen. METHODS: To investigate the effect of exposure to nitrogen dioxide (NO2) on nasal airways resistance (NAR) and inflammatory mediators in nasal lavage fluid, eight subjects with a history of seasonal allergic rhinitis, who were tested out of season, were exposed in a randomized single-blind, crossover study to either air or 400 ppb NO2 for 6 hours. The changes in NAR and eosinophil cationic protein (ECP), mast cell tryptase (MCT), neutrophil myeloperoxidase (MPO), and interleukin-8 (IL-8) in nasal lavage fluid before and after exposure were evaluated. Another group of eight subjects with a history of seasonal allergic rhinitis were also randomized to exposure to air or 400 ppb NO2 for 6 hours and then challenged with allergen, before evaluation for changes in NAR and changes in ECP, MCT, MPO, and IL-8 in nasal lavage fluid. RESULTS: Exposure to air or NO2 did not alter either NAR or the levels of ECP, MCT, MPO, or IL-8 in nasal lavage fluid. Allergen challenge after exposure to both air and NO2 significantly (p < 0.05) increased levels of MCT, but not MPO and IL-8 in the nasal lavage fluid. In addition, allergen challenge after exposure to NO2 but not air, significantly increased levels of only ECP in nasal lavage fluid (p < 0.05). CONCLUSIONS: These results suggest that acute exposure to NO2 at concentrations found at the curbside in heavy traffic during episodes of pollution, may "prime" eosinophils for subsequent activation by allergen in individuals with a history of seasonal allergic rhinitis.

Adolescent↗

PubMed1984

Studies on the biochemical effects of nitrogen dioxide. IV. Relation between the change of lipid peroxidation and the antioxidative protective system in rat lungs upon life span exposure to low levels of NO2.

This study examined the relation between lipid peroxidation and the antioxidative protective system in lungs of rats exposed to low levels of nitrogen dioxide (NO2). JCL:male Wistar rats were exposed to 0, 0.04, 0.4, and 4 ppm NO2 for 9, 18, and 27 months. Lipid peroxidation measured by TBA method, increased significantly in the 4 ppm NO2 group of the 9-month exposure and in the 0.4 and 4 ppm NO2 groups of the 18-month exposure. The activity of glutathione peroxidase measured with hydrogen peroxide as substrate decreased significantly in the 4 ppm NO2 group of the 9-month exposure and in the 0.4 and 4 ppm NO2 groups of the 18-month exposure. Furthermore, the activities of two glutathione S-transferases, aryl and aralkyl S-transferase, also decreased in the 0.4 and 4 ppm NO2 groups of the 18-month exposure, but not in any groups of the 9-month exposure. The activity of glutathione peroxidase measured with cumene hydroperoxide as substrate did not show any significant changes in any NO2 group. The activities of glucose-6-phosphate dehydrogenase and glutathione reductase were significantly higher than those in the control group for the 9-month exposure. In the 18-month exposure, however, they showed a tendency to return to control level. The activities of superoxide dismutase and disulfide reductase upon NO2 exposure for 9 and 18 months were not different from control values. To confirm that lipid peroxidation was increased with greater NO2 concentrations and exposure times, ethane and pentane exhalation in breath as an index of lipid peroxidation was examined. Ethane exhalation increased significantly following 0.04, 0.4, and 4 ppm NO2 exposure for 9 and 18 months. Furthermore, ethane formation of rats exposed to 0.04 and 0.4 ppm NO2 for 27 months also increased to twice the control level. On the other hand, after exposure to 4 ppm NO2 for 27 months, ethane levels returned to control level. Pentane formation increased significantly only in the 0.04 and 0.4 ppm groups in the 18-month exposure. Ethane exhalation in rats exposed to 0.04, 0.12, and 0.4 ppm NO2 for 9 and 18 months was similar. These results suggested that the antioxidative protective ability was decreased with prolonged exposure, while formation of cytotoxic lipid peroxides was increased.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2005

Variation of inspired nitric oxide and nitrogen dioxide concentrations during mechanical ventilation.

Inhaled Nitric oxide is a selective and potent pulmonary vasodilator with minimal influence on systemic vascular resistance. Due to these properties NO becomes widespread treatment for pulmonary hypertension of different etiologies. However, during inhalation via inspiratory limb of breathing circuit NO reacts with oxygen, producing nitrogen dioxide (NO2) which is known to be a toxic agent. Therefore, the exact measurements of NO and NO2 concentrations is very important during NO therapy, as was previously described by several authors. The aim of this study was to measure NO and NO2 concentrations at different sites of inspiratory limb of breathing circuit. Significant changes were found between different sites of circuit: Highest NO and lowest NO2 concentrations were detected at the distal points of circuit. We conclude, that NO delivery system should be connected with inspiratory limb of breathing circuit as distally as possible, to minimize contact of NO air with oxygen and to achieve maximal NO and minimal NO2 concentrations during inspiration.

Humans↗

PubMed1997

Evaluation of electrochemical nitric oxide and nitrogen dioxide analyzers suitable for use during mechanical ventilation.

OBJECTIVE: Inhaled nitric oxide (NO) is increasingly being used in the treatment of diseases characterized by hypoxemia and pulmonary hypertension. To avoid complications, accurate quantitative analysis of NO and NO2 is necessary during this therapy. We evaluated the accuracy of electrochemical NO and nitrogen dioxide (NO2) analyzers suitable for use during mechanical ventilation. METHODS: We evaluated six electrochemical NO analyzer brands (Bedfont, B & W, Dräger, EIT, Pulmonox, Saan). All were calibrated and used per manufacturer's specifications. An adult mechanical ventilator was used to produce serial dilutions of NO with O2 for [NO] of 0-80 ppm. F1O2 settings of 0.90, 0.70, 0.50, 0.30, and 0.21 were used. Settings of low, moderate, and high ventilation pressures were evaluated. Gas was sampled from the inspiratory limb of the ventilator circuit using either a sidestream or mainstream technique. [NO] was also measured using a calibrated chemiluminescence analyzer. For the analyzers that measured NO2, serial dilutions of 8.5 ppm NO2 with O2 were analyzed using chemiluminescence and the electrochemical analyzers. RESULTS: Bias +/- precision for [NO] by individual devices ranged from 1.8 +/- 1.9 ppm to -1.0 +/- 0.7 ppm. There were significant differences in the bias between analyzers (P < 0.001), pressure settings (P < 0.001), and NO level (P < 0.017). The difference in bias between levels of F1O2 was not significant (P = 0.062). Bias +/- precision for NO2 ranged from 0.18 +/- 0.12 ppm to -0.14 +/- 0.13 ppm, with a significant difference between analyzers (P < 0.001). CONCLUSIONS: The bias and precision of these analyzers was acceptable for clinical use. The devices tended to be most accurate at [NO] < or = 20 ppm-the clinical conditions at which NO is most commonly used.

Administration, Inhalation↗

PubMed1989

Impairment of humoral immune responses in mice exposed to nitrogen dioxide and ozone mixtures.

The relationship between immune defense mechanisms and environmental pollutants remains unknown because of uncertainty about the effects of combined or mixed pollutants. To investigate whether exposure to toxic gas mixtures change the effect of a single gas exposure on immune function, BALB/c mice were continuously exposed to 4.0 ppm nitrogen dioxide (NO2), 0.8 ppm ozone (O3), or the mixture of NO2 plus O3 for 3, 7, 14, and 56 days. Organ weights (lung, thymus, and spleen) and antibody responses to sheep red blood cells (SRBC), and to DNP-Ficoll were measured immediately after the exposure. Lung weights in mice exposed to O3 or the mixture were increased significantly in all exposure periods. The weights of thymus and spleen in mice exposed for 3, 7, and 14 days to the mixture were decreased. O3 exposure for 56 days showed significant decreases of the weights of both organs. Antibody response to SRBC in mice exposed for 3, 7, and 14 days to O3 or the mixture was markedly suppressed, but exposure to the mixture for 56 days did not show the suppression of anti-SRBC antibody response. No differences in anti-DNP antibody response between exposed and control mice were observed, except those exposed to O3 or the mixture for 14 days. These results suggest that mixed gas exposures variously modify the effects of a single gas exposure on antibody production in mice.

Air Pollutants↗

PubMed1985

Acute effects of 0.12 ppm ozone or 0.12 ppm nitrogen dioxide on pulmonary function in healthy and asthmatic adolescents.

Adolescent asthmatic subjects have been shown to be much more sensitive than healthy adolescents to the inhaled effects of sulfur dioxide. To test whether similar adolescent asthmatics are more sensitive to other common ambient air pollutants, 10 healthy and 10 asthmatic adolescent subjects were exposed for 60 min to filtered air, 0.12 ppm ozone (O3), and 0.12 ppm nitrogen dioxide (NO2) on separate days at rest. The following pulmonary functional values were measured before, at 30 min, and after 60 min of exposure: peak flow, total pulmonary resistance (RT), thoracic gas volume at functional residual capacity (FRC), maximal flow at 50 and 75% of expired vital capacity (Vmax50 and Vmax75), and forced expiratory volume in one second (FEV1). Following 60 min of exposure at rest to low concentrations of O3 or NO2, there were no consistent significant functional changes in either healthy or asthmatic adolescent subjects. There also were no measurable differences between the 2 groups.

Adolescent↗

PubMed1999

Influence of ozone and nitrogen dioxide on histamine and interleukin formation in a human nasal mucosa culture system.

There is evidence that asthma and other allergic diseases are increasing and air pollution has been considered an important contributing factor to this observation. Using a specially designed organ culture system, we examined the influence of ozone (0.06 to 0. 2 ppm) and nitrogen dioxide (NO2, 200 and 800 micrograms/m3) on nasal mucosa exposed for 24 h. Tissue was obtained from 105 patients undergoing surgical therapy (septoplasty and reduction of the inferior turbinates) for chronic nasal obstruction. The histamine content in the culture medium of ozone- and NO2-exposed samples was significantly elevated compared with the control cultures. This elevation was correlated with the number of degranulated mast cells in the tissue determined by histomorphometry (P < 0.001). Moreover, the cytokines interleukin (IL)-1beta (P < 0.05), IL-6 (P < 0.01), IL-8 (P < 0.001), and tumor necrosis factor-alpha (TNF-alpha, P < 0. 001) were significantly increased (ozone 0.1 ppm). Furthermore, we found significant increases in the release of IL-4, IL-6, IL-8, and TNF-alpha of ozone-exposed (0.1 ppm) samples of atopic versus nonatopic patients and to a lesser extent for histamine following exposure to 0.15 ppm ozone. These results indicate that low ozone concentrations and NO2 lead to an inflammation of human nasal mucosa in vitro and that priming factors such as atopy or preexisting inflammation do increase the sensitivity to ozone and NO2. This organ culture system proved to be a good experimental design for studying pathophysiologic alterations of human nasal mucosa under different experimental conditions (e.g., air pollutants).

Culture Media↗

PubMed1997

Appearance of electron spin resonance signals in the interaction of dithiocarbamate-Fe(II) with nitrogen dioxide and nitrite.

Whether dithiocarbamate-Fe(II) complexes used in the electron spin resonance (ESR) studies are specific for the detection of NO was investigated. It was found that the typical ESR signals of dithiocarbamate-Fe(II)-NO spin adducts appeared in the interaction of N-methyl-D-glucaminedithiocarbamate (MGD)-, bis(hydroxyethyl) dithiocarbamate (HED)- and diethyldithiocarbamate (DED)-Fe(II) complexes with the NO-derived nitrogen oxides, nitrogen dioxide (NO2) and nitrite ion (NO2-) in a prolonged incubation. Under the conditions of prolonged incubation, appearance of the ESR signals of the dithiocarbamate-Fe(II)-NO spin adducts may indicate the presence of not only NO but NO2 and NO2-.

Chelating Agents↗

PubMed1987

The effects of ozone and nitrogen dioxide on pulmonary function in healthy and in asthmatic adolescents.

The aim of this project was to investigate whether well-characterized asthmatic adolescent subjects were more sensitive to the inhaled effects of oxidant pollutants than were well-characterized healthy adolescent subjects. Ten healthy and 10 asthmatic subjects inhaled via a mouth-piece 0.12 or 0.18 ppm of ozone (O3) or nitrogen dioxide (NO2) or clean air for 30 min at rest followed by 10 min during moderate exercise (32.5 L/min) on a treadmill. The following pulmonary functional values were measured before and after exposure: peak flow, total respiratory resistance (RT), maximal flow at 50 and 75% of expired VC, and FEV1. After exercise exposure to 0.18 ppm O3, statistically significant increases were seen in RT in asthmatic and healthy adolescent subjects. No consistent changes were seen in either group after NO2 exposure. Also, no significant differences in response to oxidant pollutants between the 2 groups could be demonstrated. It was concluded that neither group was consistently sensitive to these pollutants.

Adolescent↗

PubMed2000

A demand valve device decreases exhaust nitric oxide and nitrogen dioxide by nitric oxide inhalation with a nasal cannula in the human.

To improve patients' quality of life and decrease pollution risks to medical personnel, we tested the usefulness of a nitric oxide (NO) inhalation system consisting of a nasal cannula and a demand valve in an open circuit system. To estimate the content of NO entering the lung with the open system, concentrations of NO and nitrogen dioxide (NO2) were measured in a mechanical lung model, and then nitrocylhaemoglobin (NO-Hb), methaemoglobin (Met-Hb), and nitrite (NO2-) + nitrate (NO3-) concentrations in venous blood were measured in eight healthy subjects. Exhaust NO and NO2 in the open system were also observed in 14 healthy subjects. In the lung model, NO concentration delivered with the open system was approximately 1/11 of that in the gas tank. Increases in Met-Hb and NO2- + NO3- with the open system showed that the concentration of delivered NO was approximately 1/9 of that in the gas tank. The open system reduced exhaust NO to 1/10 in human subjects. These data suggest that this NO inhalation system delivers sufficient NO to spontaneously breathing patients. In addition, these findings indicate that there is little environmental toxicity associated with the open circuit system.

Adult↗

PubMed2000

Quantitation and localization of pulmonary manganese superoxide dismutase and tumor necrosis factor alpha following exposure to ozone and nitrogen dioxide.

Tumor necrosis factor a (TNFalpha) and manganese superoxide dismutase (MnSOD) are thought to play critical roles in the process of lung injury, repair, and disease. The induction of TNFalpha and MnSOD were examined in a model of progressive pulmonary fibrosis along the length of the alveolar duct in rats exposed for 1, 5, and 8 weeks to a combination of 0.8 ppm ozone and 14.4 ppm nitrogen dioxide. This oxidant injury model results in a triphasic response with an initial inflammatory stage during weeks 1-3, followed by a partial resolution at weeks 4-5, and a final stage of rapidly progressive fibrosis during weeks 6-8. Changes in TNFalpha and MnSOD labeling for the proximal and distal alveolar ducts of the lungs were quantified using immunohistochemistry and morphometric techniques at 1, 5, and 8 weeks of exposure. A significant elevation in MnSOD was noted in alveolar macrophages and interstitial cells of the proximal and distal portions of the alveolar duct following 8 weeks of exposure. Labeling for TNFalpha only in the proximal region of the alveolar duct, was significantly increased in alveolar macrophages after 1 and 8 weeks of exposure, while a significant increase in TNFalpha labeling of interstitial cells in proximal regions was noted at all time points. We conclude that MnSOD is elevated in areas of focal injury as well as the more distal protected areas of the lungs, while TNFalpha correlates strongly with both the temporal and spatial aspects of greatest cellular injury in the lungs.

Administration, Inhalation↗

PubMed1993

Gamma-tocopherol detoxification of nitrogen dioxide: superiority to alpha-tocopherol.

In the vitamin E group, alpha-tocopherol is generally considered to be the most potent antioxidant with the highest vitamin bioactivity, yet gamma-tocopherol is produced in greater amounts by many plants and is the principal tocopherol in the United States diet. This report describes a fundamental difference in the chemical reactivities of alpha-tocopherol and gamma-tocopherol with nitrogen dioxide (NO2), which leads to the formation of a nitrosating agent from alpha-tocopherol, but not from gamma-tocopherol. Nitric oxide (NO) is a major product of the reaction of gamma-tocopherol with NO2, while alpha-tocopherol reacts with NO2 to form an intermediate tocopheroxide analogue. The biological significance of gamma-tocopherol is suggested by limited epidemiological data as well as the observation that it is a more potent inhibitor than alpha-tocopherol of neoplastic transformation during the postinitiation phase in 3-methylcholanthrene-treated C3H/10T1/2 murine fibroblasts. This latter property suggests the superiority of gamma-tocopherol in a mammalian biological assay and a role for endogenous NO production in promotion of neoplastic transformation.

Animals↗

PubMed1998

Carbon Monoxide, Nitric Oxide, and Nitrogen Dioxide Levels in Gas Ovens Related to Surface Pinking of Cooked Beef and Turkey.

Carbon monoxide (CO) and total nitrogen oxide (NO(x)()) levels were monitored during meat cookery with a standard Ovenpak and a new ultralow-NO(x)() (ULN) cyclonic gas burner. With the standard burner, CO varied from 103 to 152 ppm, NO(x)() was 1.3-10.7 ppm, and surface pinking was observed on both beef and turkey. The ULN burner at optimal efficiency produced only 6.7 ppm of CO and 1 ppm of NO(x)(), insufficient to cause surface pinking. To determine the relative contribution of CO and NO(x)() to pinking, trials were also conducted in an electric oven with various pure gases. Pinking was not observed with up to 149 ppm of CO or 5 ppm of NO. However, as little as 0.4 ppm of nitrogen dioxide (NO(2)) caused pinking of turkey rolls. Beef roasts were pink at >2.5 ppm of NO(2). Thus, pinking previously attributed to CO and NO in gas ovens is instead due to NO(2), which has much greater reactivity than NO with moisture at meat surfaces.

Journal Article↗

PubMed2006

Concurrent multiaxis differential optical absorption spectroscopy system for the measurement of tropospheric nitrogen dioxide.

The development of a new concurrent multiaxis (CMAX) sky viewing spectrometer to monitor rapidly changing urban concentrations of nitrogen dioxide is detailed. The CMAX differential optical absorption spectroscopy (DOAS) technique involves simultaneous spectral imaging of the zenith and off-axis measurements of spatially resolved scattered sunlight. Trace-gas amounts are retrieved from the measured spectra using the established DOAS technique. The potential of the CMAX DOAS technique to derive information on rapidly changing concentrations and the spatial distribution of NO2 in an urban environment is demonstrated. Three example data sets are presented from measurements during 2004 of tropospheric NO2 over Leicester, UK (52.62 degrees N, 1.12 degrees W). The data demonstrate the current capabilities and future potential of the CMAX DOAS method in terms of the ability to measure real-time spatially disaggregated urban NO2.

Journal Article↗

PubMed2004

Interpersonal and daily variability of personal exposures to nitrogen dioxide and sulfur dioxide.

Chronic exposure is often assessed using a single measurement per individual or group. However, daily levels of personal exposure can vary greatly. Chronic exposure classification by a single measurement could be significantly affected by the interpersonal and daily variations of exposures. The purpose of this study is to determine the effect of using a single personal exposure measurement on estimating long-term exposure. This study used measurements of consecutive 14 daily personal exposures to nitrogen dioxide (NO(2)) and sulfur dioxide (SO(2)) of 50 individuals in Yeochun, Korea. The daily personal exposures were measured by passive samplers. Personal exposure to NO(2) was associated with gas cooking, and personal exposure to SO(2) was associated with ambient air pollution. Mixed effects models indicated that daily variability was greater than interpersonal variability for both the pollutants. Effectiveness of using single-day personal measurements for long-term population mean exposure was supported by relatively consistent daily population averages, but multiple-day measurements might be warranted for characterizing individual exposures or high-end population exposures such as the 95th percentile. Although classification of high and low exposure groups by 1-day exposure and by 14-day exposure produced similar group totals, 20% of individual NO(2) exposures and 31% of individual SO(2) exposures were misclassified using 1-day exposures. Average values of 1-day exposure and 14-day exposure were significantly different, but the difference decreased by an increase in the number of measurements for the short-term exposure. The findings were similar for both NO(2) and SO(2), although the two air pollutants have different sources and behaviors.

Air Pollutants↗

PubMed1987

Effect of nitrogen dioxide, ozone, and peroxyacetyl nitrate on metabolic and pulmonary function.

The metabolic and pulmonary function responses were investigated in 32 non-smoking men and women (8 men and 8 women 18-26 years of age, and 8 men and 8 women 51-76 years of age) who were exposed for 2 hours to each of 8 conditions: 1) filtered air (FA), 2) 0.13 ppm peroxyacetyl nitrate (PAN), 3) 0.45 ppm ozone (O3), 4) 0.60 ppm nitrogen dioxide (NO2), 5) 0.13 ppm PAN + 0.45 ppm O3 (PAN/O3), 6) 0.13 ppm PAN + 0.60 ppm NO2 (PAN/NO2), 7) 0.60 ppm NO2 + 0.45 ppm O3 (NO2/O3), and 8) 0.13 ppm PAN + 0.60 ppm NO2 + 0.45 ppm O3 (PAN/NO2/O3). The subjects alternated 20-min periods of rest (n = 3) and cycle ergometer exercise (n = 3) at a work load predetermined to elicit a ventilatory minute volume (VE) of approximately 25 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and post-exposure. Forced vital capacity (FVC) was determined before and after exposure, and 5 min after each exercise period. Heart rate was monitored throughout each exposure, and VE was measured during the last 2 min of each exercise period. Exposure to FA, PAN, NO2, and PAN/NO2 had no effect on any measure of pulmonary or metabolic function. Ozone was primarily responsible for the pulmonary function effects observed. There was no significant difference between the responses to O3 exposure and the responses to the three O3 mixtures, indicating no interactions between the pollutants. The results suggest that women may be somewhat more responsive to O3 exposure than men, and that older people (51-76 years of age) may be less responsive to O3 than younger people (18-26 years of age).

Acetates↗

PubMed1988

Ozone, nitrogen dioxide and lung cancer: a review of some recent issues and problems.

Lung cancer in man is a common disease. There is some recent concern that oxidant air pollutants might be a contributing risk factor. Experimental data show that ozone and NO2 increase incidence and multiplicity of lung tumors in strain A mice; however, the data are not always statistically significant. Also it depends on experimental design whether ozone enhances or inhibits the development of lung tumors in mice. Similarly, ozone and nitrogen dioxide enhance lung colonization by cancer cells injected intravenously following exposure to the air pollutants, whereas NO2 kills lung metastases if cells are injected prior to exposure. Both ozone and NO2 modulate the proliferation of pulmonary neuroendocrine cells, the precursor cells for small cell lung cancer. It is concluded that there is little evidence to implicate ozone or NO2 directly as pulmonary carcinogens, but that they might modify and influence the carcinogenic process in the lung.

Animals↗

PubMed2005

Childhood asthma and exposure to traffic and nitrogen dioxide.

BACKGROUND: Evidence for a causal relationship between traffic-related air pollution and asthma has not been consistent across studies, and comparisons among studies have been difficult because of the use of different indicators of exposure. METHODS: We examined the association between traffic-related pollution and childhood asthma in 208 children from 10 southern California communities using multiple indicators of exposure. Study subjects were randomly selected from participants in the Children's Health Study. Outdoor nitrogen dioxide (NO2) was measured in summer and winter outside the home of each child. We also determined residential distance to the nearest freeway, traffic volumes on roadways within 150 meters, and model-based estimates of pollution from nearby roadways. RESULTS: Lifetime history of doctor-diagnosed asthma was associated with outdoor NO2; the odds ratio (OR) was 1.83 (95% confidence interval=1.04-3.22) per increase of 1 interquartile range (IQR=5.7 ppb) in exposure. We also observed increased asthma associated with closer residential distance to a freeway (1.89 per IQR; 1.19-3.02) and with model-based estimates of outdoor pollution from a freeway (2.22 per IQR; 1.36-3.63). These 2 indicators of freeway exposure and measured NO2 concentrations were also associated with wheezing and use of asthma medication. Asthma was not associated with traffic volumes on roadways within 150 meters of homes or with model-based estimates of pollution from nonfreeway roads. CONCLUSIONS: These results indicate that respiratory health in children is adversely affected by local exposures to outdoor NO2 or other freeway-related pollutants.

Air Pollutants↗