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PubMed1992

Exposures of older adults with chronic respiratory illness to nitrogen dioxide. A combined laboratory and field study.

We combined field and laboratory experimentation to evaluate the effects of nitrogen dioxide in a panel of Los Angeles area residents with chronic respiratory illness, 15 men and 11 women aged 47 to 69. All had heavy smoking history, chronic symptoms, and low FEV1; some also had low FVC. During the fall-winter high-NO2 season, they monitored themselves for 2-wk periods using spirometers in the home, passive NO2 sampling badges, and diaries to record time and activity patterns and clinical status. In the middle of each self-monitoring week they were exposed in a chamber, once to clean air and once to 0.3 ppm NO2. Chamber exposures were double blind, lasted 4 h, and included four 7-min exercise sessions with average ventilation rates near 25 L/min. Symptom reports and hourly forced expiratory function tests showed no statistically significant differences between clean air and NO2 chamber exposures, although peak flow showed a approximately 3% loss with NO2 relative to clean air during the first 2 h of exposure only (p = 0.056). No significant overall differences were found between field self-measurements and measurements of lung function in the chamber or between field measurements in clean air and NO2 exposure weeks. Field data showed that group average lung function and symptom levels were worse in the morning than later in the day (p < 0.005) but otherwise were stable over 2 wk. Even though most subjects smoked and stayed indoors 80 to 90% of the time, personal NO2 exposures correlated significantly with outdoor NO2 concentrations as reported by local monitoring stations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed2004

Spatial variation in nitrogen dioxide in three European areas.

In order to estimate the spatial variation within well-defined study areas, nitrogen dioxide was measured with diffusion samplers (Palmes tube) in 40-42 sites each in Germany (Munich), the Netherlands and Sweden (Stockholm County). Each site was measured over four 2-week periods during 1 year (spring 1999 to summer 2000). In each country, one reference site was measured during all periods and the results were used to adjust for seasonal variability, to improve the estimates of the annual average. Comparisons between the chemiluminescence method (European reference method) and Palmes tube measurement indicated a good agreement in Germany (with a ratio of 1.0 for Palmes tube/chemiluminescence) but underestimation for Palmes tube measurement in the Netherlands and Sweden (0.8 for both countries). The r2 values were between 0.86 and 0.90 for all three countries. The annual average values for NO2 for different sampling sites were between 15.9 and 50.6 (mean 28.8 microg/m3) in Germany, between 12.1 and 50.8 (mean 28.9 microg/m3) in the Netherlands and between 6.1 and 44.7 (mean 18.5 microg/m3) in Sweden. Comparing spatial variation between similar sites in the three countries, we did not find any significant differences between annual average levels for urban traffic sites. In Sweden, annual average levels in urban background and suburban backgrounds sites were about 8 microg/m3 lower than comparable sites in Germany and the Netherlands. Comparing site types within each country only urban traffic sites and suburban background sites differed in Germany. In the Netherlands and Sweden, the urban traffic sites differed from all other sites and in Sweden also the urban background sites differed from the other background sites. The observed contribution from local traffic was similar in the Netherlands and Sweden (10 and 8 microg/m3, corresponding to 26-27% of the NO2 concentration found in the urban traffic sites). In Germany, the contribution from local traffic was only 3 microg/m3, corresponding to 9% of the NO2 concentration found in the urban traffic sites. The spatial variation was substantially larger for NO2 than the variation for PM2.5 and similar to PM2.5 absorbance, measured in the same locations.

Air Pollutants↗

PubMed1980

Effect of acute nitrogen dioxide exposure on the free amino acids of rat serum.

Female Wistar rats were acutely exposed to 20 ppm nitrogen dioxide (NO2). After 20 h exposure, the concentrations of valine, leucine, isoleucine and phenylalanine in serum significantly increased. Significant decreases were observed for aspartic acid, threonine, serine, glutamic acid, glycine alanine, cystine, methionine, tyrosine, lysine, arginine and proline. The concentrations of free amino acids of rats exposed to NO2 for 40 h were close to the values for rats starved for 40 h.

Amino Acids↗

PubMed1995

Release of aldehydes from rat alveolar macrophages exposed in vitro to low concentrations of nitrogen dioxide.

This study demonstrated that aldehydes are released into the extracellular medium when alveolar macrophages (AM) are exposed to nitrogen dioxide (NO2) at concentrations that impair cell function but do not cause cell death. Butanal, glycolaldehyde, 4-hydroxynonenal, pentanal, pentenal, and hexanal were found. Dinitrophenylhydrazine (DNP) derivitization, thin layer chromatography, high performance liquid chromatography, and gas chromatography-mass spectrometry were used to identify the products. Some of the aldehydes have potential toxicity and may be responsible, in part, for altered AM function observed following NO2 exposure.

Aldehydes↗

PubMed1990

[Hematotoxic and immunotoxic effects of nitrogen dioxide].

The aim of the paper is to review hematological and immunological effects of experimental and occupational exposure to nitrogen dioxide (NO2). The NO2 exposure diminishes erythrocyte count, hemoglobin concentration and produces increased nitrosyl hemoglobin (NOHb) and methemoglobin (MetHb) concentrations in peripheral blood. The gas affects the activity of the membrane and glycolytic enzymes in erythrocytes. Experimental inhalation of NO2 results in an increased susceptibility to viral or bacterial infections. Moreover, the gas impairs phagocytic and bacteriocidal functions of alveolar macrophages. NO2 also causes lymphoid tissue damage reducing the thymus and spleen weight; it also diminishes specific antibody production and lymphocyte transformation in in vitro cultures with plant mitogens.

Animals↗

PubMed1988

Measurements of nitrogen dioxide concentrations at rural sites in the United Kingdom using diffusion tubes.

Nitrogen dioxide concentrations have been measured at rural sites in the United Kingdom and have revealed a marked spatial variation. The annual mean NO2 concentration varies from approximately 1 microg Nm-3 in Northern Ireland to approximately 7 microg Nm-3 in East Anglia. Though the temporal resolution of the diffusion tube method is limited by exposure periods of 2-4 weeks, it was possible to detect a marked seasonal variation in NO2 concentration at all sites, with higher values in the winter than in the summer. This is in contrast to the small seasonal variation previously observed at sites in London. Sulphur dioxide concentrations were measured daily using a bubbler method and, if expressed in terms of mass of sulphur and nitrogen, the SO2 and NO2 annual mean concentrations were similar. This is in contrast to an S/N ratio of greater than 3 in total UK emissions of SO2 and NOx. It seems likely that this difference is due to a combination of the different spatial distributions and heights of emissions of SO2 and NOx, the influence of local sources of NOx, and the smaller S/N ratio in Continental European emissions.

Journal Article↗

PubMedDate not supplied

Acute respiratory effects of short-term exposures to nitrogen dioxide.

Eleven study subjects with asthma and 12 normal controls were monitored for 5 days with a portable continuous nitrogen dioxide (NO2) monitoring instrument held at breathing level before, during, and after cooking dinner on a gas cooking range. Forced expiratory volume in 1 sec (FEV1.0), forced expiratory volume (FEV25-75), peak expiratory flow, and a tracing of the entire flow curve was monitored before the gas stove was turned on, during a break in cooking, immediately after, and 1 hr after cooking was completed. Study design for detection of health effects of the acute exposures to NO2 described above and a method of validating findings in an exposure chamber are discussed in this paper.

Adult↗

PubMed1977

A solid sorbent personal sampling method for the simultaneous collection of nitrogen dioxide and nitric oxide in air.

A sampling method is described for the collection of air samples containing both nitrogen dioxide (NO2) and nitric oxide (NO) in the range of 0.5 to 5 ppm NO2 and 9 to 50 ppm NO. These two gases are trapped on a solid sorbent sampling tube which employs the collection of the NO2 on a triethanol-amine (TEA)-impregnated molecular sieve surface; the oxidation of NO to NO2 by a solid oxidizer; and the collection of the converted NO on another section of TEA sorbent. The trapped NO/NO2 on each TEA section is desorbed and the concentrations are determined spectrophotometrically. At all concentrations tested, the collection efficiency for NO2 averaged approximately 96%. The collection efficiencies for NO were as follows: at 9 ppm, 97%; at 11 ppm, 106%; at 24 ppm, 84%; and at 50 ppm, 67%.

Air Pollutants↗

PubMed1984

A comparison of biochemical effects of nitrogen dioxide, ozone, and their combination in mouse lung.

Swiss Webster mice were exposed to either 4.8 ppm (9024 microgram/m3) nitrogen dioxide (NO2), 0.45 ppm (882 microgram/m3) ozone (O3), or their combination intermittently (8 hr daily) for 7 days, and the effects were studied in the lung by a series of physical and biochemical parameters, including lung weight, DNA and protein contents, oxygen consumption, sulfhydryl metabolism, and activities of NADPH generating enzymes. The results show that exposure to NO2 caused relatively smaller changes than O3, and that the effect of each gas alone under the conditions of exposure was not significant for most of the parameters tested. However, when the two gases were combined, the exposure caused changes that were greater and significant. Statistical analysis of the data shows that the effects of combined exposure were more than additive, i.e., they might be synergistic. The observations suggest that intermittent exposure to NO2 or O3 alone at the concentration used may not cause significant alterations in lung metabolism, but when the two gases are combined the alterations may become significant.

Animals↗

PubMedDate not supplied

Dose-response study of asthmatic volunteers exposed to nitrogen dioxide during intermittent exercise.

Twenty-one mildly asthmatic volunteers were exposed to 0, 0.3, 1.0, and 3.0 ppm nitrogen dioxide (NO2) in purified background air in an environmental control chamber. Exposures were separated by 1-wk periods and occurred in random order. Each lasted 1 hr and included three 10-min bouts of moderately heavy exercise (mean ventilation rate 41 L/min). Exposure temperature was near 22 degrees C and relative humidity near 50%. Specific airway resistance and maximal forced expiratory performance were measured preexposure, after the initial exercise, and near the end of exposure. Bronchial reactivity was assessed immediately following exposure, by normocapnic hyperventilation with subfreezing air. Symptoms were recorded on questionnaires before, during, and for 1-wk after each exposure. Exercise induced significant bronchoconstriction regardless of NO2 level. No statistically significant untoward response to NO2 was observed at any exposure concentration. This negative finding agrees with our previous results, but contrasts with findings elsewhere of respiratory dysfunction after exposure to 0.3 ppm. The discrepancy is presently unexplained, but it may relate to different severity of asthma in different subject groups.

Adult↗

PubMed1991

The nitric oxide/heme protein complex as a biologic marker of exposure to nitrogen dioxide in humans, rats, and in vitro models.

In an effort to develop a biologic marker of exposure to nitrogen dioxide (NO2), we investigated the in vivo formation of a complex between heme proteins and nitric oxide (NO). In aqueous solution, NO2 disproportionates to NO and nitrate. The NO binds to the iron of heme proteins to form an electron spin resonance (ESR)-detectable complex. We have shown that when rat liver, lung, or nasal microsomes are exposed to 20 ppm NO2 in vitro, an ESR signal attributable to an NO/heme protein complex is detected. After inhalation exposure of rats to 20 ppm NO2 for 6 h, this same ESR signal was detected in microsomes prepared from the exposed rats' lungs or liver; microsomes prepared from the nasal tissue failed to yield any detectable signal. When we lavaged the lungs of rats exposed for 6 h to 0, 5, 10, 20, or 30 ppm NO2 and isolated the bronchoalveolar cell pellets, the NO/heme protein complex was detected in the cell pellets. We were able to demonstrate a dose-dependent relationship between the ESR signal intensity of the NO/heme protein complex and the NO2 exposure concentration. Finally, we used ESR to examine bronchoalveolar lavage cell pellets obtained from human volunteers exposed to either 1.5 or 4 ppm NO2, for 20 min every other day, for six exposures. No signal was found in any of the samples taken 3 wk prior to NO2 exposure, but an ESR signal attributable to the NO/heme protein complex was detected in every sample obtained after the 4 ppm NO2 exposure and in five of eight samples obtained after the 1.5 ppm NO2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2007

Effects of nitrogen dioxide on the expression of intercellular adhesion molecule-1, neutrophil adhesion, and cytotoxicity: studies in human bronchial epithelial cells.

Nitrogen Dioxide (NO2) is a product of high-temperature combustion and an environmental oxidant of concern. We have recently reported that early changes in NO2-exposed human bronchial epithelial cells are causally linked to increased generation of proinflammatory mediators, such as nitric oxide/nitrite and cytokines like interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and IL-8. The objective of the present in vitro study was to further delineate the cellular mechanisms of NO2-mediated toxicity, and to define the nature of cell death that ensues upon exposure of normal human bronchial epithelial (NHBE) cells to a brief high dose of NO2. Our results demonstrate that the NHBE cells undergo apoptotic cell death during the early post-NO2 period, but this is independent of any significant increase in caspase-3 activity. However, necrotic cell death was more prevalent at later time intervals. Interestingly, an increased expression of HO-1, a redox-sensitive stress protein, was observed in NO2-exposed NHBE cells at 24 h. Since neutrophils (PMNs) play an active role in acute lung inflammation and resultant oxidative injury, we also investigated changes in human PMN-NHBE cell interactions. As compared to normal cells, increased adhesion of PMNs to NO2-exposed cells was observed, which resulted in an increased NHBE cell death. The latter was also increased in the presence of IL-8 and TNF-alpha + interferon (IFN)-gamma, which correlated with upregulation of intercellular adhesion molecule-1 (ICAM-1). Our results confirmed an involvement of nitric oxide (NO) in NO2-induced cytotoxicity. By using NO synthase inhibitors such as L-NAME and 3-aminoguanidine (AG), a significant decrease in cell death, PMN adhesion, and ICAM-1 expression was observed. These findings indicate a role for the L-arginine/NO synthase pathway in the observed NO2-mediated toxicity in NHBE cells. Therapeutic strategies aimed at controlling excess generation of NO and/or inflammatory cytokines may be useful in alleviating NO2-mediated adverse effects on the bronchial epithelium.

Apoptosis↗

PubMed1996

Extraction of nitric oxide and nitrogen dioxide from an oxygen carrier using molecular sieve 5A.

Nitric oxide (NO) is effective in the management of pulmonary hypertension and shunt-related hypoxia. Nitrogen dioxide (NO2) is formed when the gas is delivered with oxygen. Both oxides of nitrogen have well recognized adverse effects. The scavenging properties of several forms of soda lime have been investigated. A gas flow containing NO 70 ppm and NO2 5 ppm in oxygen was introduced into a vertically mounted Waters' canister containing: (i) 125 g of molecular sieve 5A (a calcium aluminosilicate zeolite) and (ii) 135 g of soda lime containing a potassium permanganate marker. NO and NO2 concentrations were measured at hourly intervals at the entry and exit points using an electrochemical analyser. Extraction ratios (gradient/ inlet x 100) were calculated for a 24-h period. High extraction ratios (in excess of 90%) of NO and NO2 were observed with both compounds for up to 1 h but these declined rapidly after this time with soda lime. In contrast, the molecular sieve produced extraction ratios in excess of 98% for both gases over the 24-h period. We conclude that the molecular seive 5A is a highly effective scavenger of NO and NO2.

Absorption↗

PubMed1979

Dysfunction of small airways following pulmonary injury due to nitrogen dioxide.

Serial physiologic studies were performed to characterize both the immediate and delayed effects of a single occupational exposure to nitrogen dioxide in a nonsmoker. During the initial acute stage of pulmonary edema, the abnormal static pressure-volume curve and decreased static compliance corresponded to a reduction in pulmonary volume. During the delayed acute stage, elastic recoil and properties of resistance to flow were normal, but dynamic compliance was reduced and dependent on respiratory frequency, and oxygen transport was abnormal during exercise, which is consistent with dysfunction of the small airways.

Forced Expiratory Flow Rates↗

PubMed1984

Combined effect of nitrogen dioxide and cold stress on the activity of the hepatic cytochrome P-450 system in rats.

The combined effects of nitrogen dioxide (NO2) and cold stress were assessed on the cytochrome P-450 system by measuring microsomal protein content, cytochrome P-450 content, aminopyrine N-demethylase activity, and aniline hydroxylase activity in the liver of male Wistar rats exposed to 4 ppm NO2 and/or cold environment (4 degrees C) for 24 h, 14 days, and 30 days. Exposure to cold alone changed the activity of the cytochrome P-450 system during the exposure up to 30 days, and exposure to NO2 alone also influenced it after 14 days and 30 days of exposure. Interactions were observed in the effect on the cytochrome P-450 system when rats were exposed to NO2 and cold simultaneously. There was a tendency that NO2 suppressed the increases in activities of the cytochrome P-450 system caused by cold of 24-h and 30-day exposure.

Aminopyrine N-Demethylase↗

PubMedDate not supplied

Comparison of effects of in vivo nitrogen dioxide exposure starting from different periods on alveolar macrophage activity, assessed by a chemiluminescence technique in Brown-Norway rats.

Nitrogen dioxide (NO2) has been extensively studied for its immune modulating effects on pulmonary cells. Alveolar macrophages (AMs) play an important role in pulmonary immunity. The Brown-Norway (BN) rat has been studied as a high-risk model of allergic diseases. In this study, BN rats were exposed to NO2 from the embryonic or weanling period (EP or WP, respectively). To evaluate the effects of NO2 exposure on pulmonary immunity, the activity levels of rat AMs were assessed as reactive oxygen species-generating capacity, measured by a chemiluminescence (CL) technique, and as cytokine-producing ability. Except for 0.2 ppm of NO2 exposure, the CL responses of AMs obtained from the WP group at 12 weeks old were suppressed significantly. Changes of the cytokine-producing levels suggest that inflammatory reactions are terminated at 12 weeks in the EP group. Correlations between the CL responses and the cytokine levels reveal that NO2 exposure may modulate the direction of AM activation. The CL technique is thought to be useful to evaluate changes in AM activity. In this study, the results suggest that, using the high-risk model of allergic diseases, NO2 exposure from the weanling period has stronger effects on AM activity.

Animals↗

PubMed1976

Effect of short-term, low-level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients.

Our purpose was to determine whether exposure to a realistic concentration of nitrogen dioxide (NO2) could increase the bronchial sensitivity of asthmatic patients to bronchoconstrictor agents. We established dose-response curves for changes in specific airway resistance (SRaw) in response to aerosolized carbachol in 20 asthmatics after each had spent 1 h in an exposure chamber breathing on one occasion unpolluted air and on a separate occasion 0.1 ppm NO2: sequence of exposures to unpolluted air and to low levels of NO2 were randomized in a single-blind fashion. NO2 induced a slight but significant increase in initial SRaw and enhanced the bronchoconstrictor effect of carbachol in 13 subjects: curves were shifted to the left and the mean dose of carbachol producing a twofold increase in initial SRaw was decreased from 0.66 mg to 0.36 mg (P less than 0.001). In contrast, NO2 neither modified the initial SRaw nor the bronchoconstrictor effect of carbachol in seven subjects. In 4 out of the 20 subjects, exposure to a higher concentration of NO2 (0.2 ppm) yielded variable results. Potentiation of the carbachol bronchoconstrictor response by NO2 could not be related to any physical or clinical characteristics of the subjects tested. Although the mechanisms underlying the NO2 effect remain controversial, the present results demonstrate that very low levels of NO2 can adversely affect some asthmatics.

Adolescent↗

PubMed1988

The pulmonary effects of ozone and nitrogen dioxide alone and combined in healthy and asthmatic adolescent subjects.

Separate exposures to 0.12 ppm ozone (O3) or 0.18 ppm nitrogen dioxide (NO2) have not demonstrated consistent changes in pulmonary function in adolescent subjects. However, in polluted urban air, O3 and NO2 occur in combination. Therefore, this project was designed to investigate the pulmonary effects of combined O3 and NO2 exposures during intermittent exercise in adolescent subjects. Twelve healthy and twelve well-characterized asthmatic adolescent subjects were exposed randomly to clean air or 0.12 ppm O3 and 0.30 ppm NO2 alone or in combination during 60 minutes of intermittent moderate exercise (32.5 1/min). The inhalation exposures were carried out while the subjects breathed on a rubber mouthpiece with nose clips in place. The following pulmonary functional values were measured before and after exposure: peak flow, total respiratory resistance, maximal flow at 50 and 75 percent of expired vital capacity, forced expiratory volume in one second and forced vital capacity (FVC). Statistical significance of pulmonary function changes was tested by analysis of covariance for repeated measures. After exposure to 0.12 ppm O3 a significant decrease was seen in maximal flow at 50% of FVC in asthmatic subjects. After exposure to 0.30 ppm NO2 a significant decrease was seen in FVC also in the asthmatic subjects. One possible explanation for these changes is the multiple comparison effect. No significant changes in any parameters were seen in the asthmatic subjects after the combined O3-NO2 exposure or in the healthy subjects after any of the exposures.

Adolescent↗