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PubMed1995

Effects of prolonged exposure to low doses of nitric oxide or nitrogen dioxide on the alveolar septa of the adult rat lung.

BACKGROUND: Nitric oxide (NO) and nitrogen dioxide (NO2) are common copollutants resulting from combustion processes such as the burning of fossil fuels and tobacco smoke. The relative toxicity of these two pollutants has not been adequately addressed. Separate low level exposures to each of these two pollutants were carried out to allow comparisons of relative health risks. EXPERIMENTAL DESIGN: Male rats were exposed to either NO or NO2 for 9 weeks at 0.5 ppm with twice daily, 1-hour spikes to 1.5 ppm. Lungs from five rats in each exposed group and from rats from a clean air control group were preserved by vascular perfusion of fixative and were embedded for sectioning. The number of fenestrations in alveolar septa of the lung was determined by using serial sections to directly count the number of fenestrae in a known volume of lung. RESULTS: The average number of fenestrae was 328 +/- 156 x 10(3) (mean +/- SE, n = 5) per lung in the NO group. In the NO2 exposure group, there were 99 +/- 42 x 10(3) fenestrae per lung. The number of fenestrae per lung in the controls (9 +/- 9 x 10(3)) was not statistically different from zero. The number of fenestrae in the NO group was significantly greater than that in the control or NO2 groups. Analyses of total parenchymal cells per lung demonstrated a statistically significant 29% reduction in the number of interstitial cells in the NO group. There were no significant differences in the numbers of other types of cells between the control and exposed groups. The thickness of the interstitial space was reduced in the NO group (0.24 +/- 0.02 microns versus 0.32 +/- 0.02 microns in controls) but not in the NO2 group (0.29 +/- 0.02 microns). Epithelial cell thickness did not differ between groups. CONCLUSIONS: Focal degeneration of interstitial cells, interstitial matrix, and connective tissue fibers is the principal injury resulting from low level NO exposure. NO is significantly more potent than NO2 in the production of these defects in the interstitial spaces of alveolar septa. Although limited in number and size, the formation of fenestrae by atrophy of the interstitial spaces is similar to the initial steps in an emphysema-like destruction of alveolar septa.

Animals↗

PubMed1989

Mutagenicity of the reaction products of carbazole in the presence of nitrogen dioxide and nitrocarbazole.

The mutagenicity of the photochemical reaction products of carbazole in the presence of nitrogen dioxide (NO2) and nitrocarbazole was investigated using a high-pressure mercury lamp (100 W). Samples extracted from the photochemical reaction products of carbazole with NO2 were more mutagenic than those of acridine and phenazine with NO2 for Salmonella typhimurium strain TA98 in the absence of S9 mix with a trend toward detoxification in the presence of the metabolic system. The mutagenicity of the photochemical reaction products of carbazole with NO2 were higher than those of the reaction products of carbazole with a mixture of NO2 and sulfur dioxide (SO2) and no irradiation. Mononitro- and dinitro-carbazole in the samples extracted from the reaction products were analyzed by mass spectrometry. It was suggested that mononitrocarbazole, which seemed to be weakly mutagenic, and dinitrocarbazole were readily formed by the reaction of carbazole with NO2, and that the other high-potency mutagens were formed by the photochemical reaction of carbazole with NO2 with irradiation by light.

Acridines↗

PubMed1999

Effect of nitric oxide predilution on inhaled nitrogen dioxide concentrations.

We examined the possibility that predilution of a concentrated nitric oxide (NO) source with nitrogen, before contact with oxygen, can reduce the inspired nitrogen dioxide (NO2) concentration during administration of nitric oxide. A Manley Blease and a Siemens Servo 900 C ventilator delivered 10, 20, 40, 60 and 80 parts per million (ppm) NO using an NO source of 1000, 400 and 200 ppm. With the Manley Blease system, predilution from 1000 to 200 ppm NO reduced the inhaled NO2 concentration from 0.14 to 0.05 ppm (p < 0.01) at 10 ppm inhaled NO, and from 1.20 to 1.00 ppm (p < 0.01) at 40 ppm inhaled NO. With the Siemens Servo 900 C ventilator, inspiratory NO2 concentrations decreased from 0.21 to 0.11 ppm (p < 0.01) at 10 ppm inhaled NO, and from 1.49 to 1.16 ppm (p < 0.01) at 40 ppm NO. Predilution from 1000 to 400 ppm NO reduced the inspired NO2 concentrations by < 3% using either ventilator when the inspirated NO concentration was 80 ppm. Predilution of NO with nitrogen significantly reduced the inspired NO2 concentrations for nitric oxide concentrations between 10 and 40 ppm, but offered no clinically relevant advantage at higher NO concentrations.

Drug Administration Schedule↗

PubMed1982

Effect of nitrogen dioxide exposure on cyclic GMP in rat lung.

In vivo exposure of rats to 10 ppm nitrogen dioxide (NO2) for 6 h caused approx. 5-fold increase in the content of cyclic GMP in lung tissue. This increased cyclic GMP level lasted up to 24 h but returned to the normal level within 2 days, even when the NO2 exposure continued. This increase in the content of cyclic GMP of lung tissue by NO2 exposure was observed in both young and aged rats. There were no statistically significant changes in the content of cyclic AMP in lung tissue.

Animals↗

PubMed1982

Lung function and morphology of dogs after sublethal exposure to nitrogen dioxide.

The relationship between respiratory function and morphological changes in 10 dogs exposed for 6 h to 69 ppm nitrogen dioxide was studied. Two additional dogs served as controls. Functional assessments included breathing pattern, breathing mechanics, forced expiration, gas exchange, and acid-base status. Gross, microscopic, and ultrastructural evaluations were made of lung tissues from dogs killed at 0.1, 1.0, 2.0, 3.0, 7.0 and 14.0 d after exposure. Functional changes were similar to those reported for man. The principal dysfunction was gas-exchange impairment, apparently resulting from foam in the airways. Breathing-pattern alterations appeared to result from stimulation of neural receptors. Gas-exchange measurements provided the most useful indicators of the pulmonary damage observed in this study.

Animals↗

PubMed2000

Nitrogen dioxide and particle pollution near trunk roads and in towns of the south Midlands in England.

Nitrogen dioxide (NO2) and particulate emissions play an important role in atmospheric pollution and might be a major cause of human respiratory problems in urban areas. This report provides an overview of traffic-related emissions monitored on several trunk roads and towns of the South Midlands of England between 1996 and 1999. NO2 pollution on major trunk roads frequently exceeded British and European Union air quality standards, while particle pollution was lower. The possible effects of traffic diversion activities in the research area are discussed. Bypasses of busy trunk roads might reduce NO2 pollution between 30 and 40% in urban centres and improve air quality for inhabitants in those areas.

Air Pollutants↗

PubMedDate not supplied

Hyperplasia of Type 2 pneumocytes following 0.34 ppm nitrogen dioxide exposure: quantitation by image analysis.

Swiss Webster male mice were exposed to intermittent 0.34 ppm nitrogen dioxide for 6 wk. Quantitative image analysis showed increased Type 2 cell numbers in each of the three lobes measured, with and without adjustment to alveolar wall measurements for lung volume normalization (e.g., P less than .037 for Type 2 cell number adjusted to alveolar wall perimeters, combined lobe analysis of variance). The exposed animals dominated the upper quartile ranking of the cell number/alveolar area ratio computations (P less than .025), which implied the presence of an especially susceptible subpopulation of animals. The Type 2 cell increase is believed to result from damage and loss of Type 1 cells, the reversibility and progression of which are presently unknown. The data also suggest an increased size of the Type 2 cell, and possibly slight atelectasis and/or edema of the alveolar walls.

Animals↗

PubMed2004

A 5-year follow-up of airway symptoms after nitrogen dioxide exposure in an indoor ice arena.

The authors investigated whether exposure to high levels of nitrogen dioxide (NO2) in an indoor ice hockey arena might be associated with airway symptoms 5 yr later. A follow-up questionnaire was answered by 71 subjects who had experienced such an exposure, accompanied by acute respiratory illness, in Stockholm in 1994. The same questionnaire was answered by 40 reference subjects. The overall response rate for both groups was 71%. Information was obtained regarding various background factors, such as smoking and respiratory symptoms since 1994. For those who had stopped playing ice hockey during the follow-up period, the exposure to high NO2 levels appeared to be associated with an increase in upper airways symptoms (i.e., nasal blockage or rhinitis) (odds ratio = 3.1, 95% confidence interval = 1.1, 8.8), after adjustment for age, smoking, and family history of allergy. These data suggest that exposure to high NO2 levels in an indoor ice arena may be associated with increased airway symptoms several years later.

Adolescent↗

PubMed1983

In vivo formation of N-nitrosomorpholine in CD-1 mice exposed by inhalation to nitrogen dioxide and by gavage to morpholine.

Male CD-1 mice were exposed to approximately 20 ppm nitrogen dioxide (NO2) for 5-6 hours, to 1 g morpholine/kg body weight by gavage, or to both. Treatments were repeated daily for 5 consecutive days. N-nitrosomorpholine (NMOR) was found in whole carcasses (16-146 ng NMOR/mouse) in all animals that had been exposed to both NO2 and to morpholine, but NMOR was not found in tissues from animals that had been exposed to either chemical alone. Approximately one-third of the NMOR was found in the gastrointestinal tract, mainly in the stomach. The coadministration of 2 g sodium ascorbate/kg body weight or 1 g alpha-tocopheryl acetate/kg body weight had no effect on the amount of NMOR that was found in any tissue. Another possible product of the interaction of NO2 and morpholine, N-nitromorpholine, was not detected in any tissue. We concluded that the repeated, concurrent exposures of mice to NO2 by inhalation and to morpholine by gavage resulted in the in vivo formation of significant quantities of NMOR. The biological significance of the observation remains unknown.

Animals↗

PubMedDate not supplied

Effects of 0.2 ppm nitrogen dioxide on pulmonary function and response to bronchoprovocation in asthmatics.

To study the respiratory effects of nitrogen dioxide (NO2) at ambient concentrations, we exposed 31 asthmatic volunteers to purified air (control) and to 0.2 ppm NO2 for 2-h periods with light intermittent exercise. Bronchial reactivity (loss of forced expiratory performance in response to graded doses of methacholine chloride aerosol) was determined postexposure, using a newly developed apparatus that allowed accurate quantitation of methacholine dose. Forced expiratory performance, total respiratory resistance, and symptoms were also recorded immediately pre- and postexposure (prior to methacholine challenges). No significant direct effect of NO2 exposure on forced expiratory function or total respiratory resistance was observed. Symptoms showed a small significant (p less than 0.05) excess in purified air relative to NO2 exposures. Individual responses to methacholine varied greatly. About two-thirds of the subjects showed greater response after NO2 than after purified air, but the mean excess response was small. Mean changes attained significance in some but not all applicable statistical tests. Thus we cannot conclude unequivocally that NO2 exposure increased bronchial reactivity in this group, although there was some tendency in that direction.

Adolescent↗

PubMed1985

Measurements of carbon monoxide and nitrogen dioxide in British homes using unflued heating or cooking appliances.

Measurements of Carbon Monoxide (CO) and Nitrogen Dioxide (NO2) were made in three kitchens, two with gas cookers and one all electric, and two living rooms, one heated by a portable butane heater and the other by a paraffin stove. The measurements were taken whilst the homes were in normal use and the occupants kept a diary of when specific appliances were used. Measurements of NO2 were made simultaneously by chemiluminescence and by diffusion tubes. The accuracy of the diffusion tube measurements relative to the chemiluminescent standard was estimated as +/- 10% and the precision less than or equal to 300 ppb. hr. Results from diffusion tubes were used to indicate the distribution of NO2 throughout other rooms in the house. At the all electric house the CO and NO2 concentrations were very similar to the expected outdoor levels. In all the other houses NO2 levels exceeded typical outdoor concentrations measured in Central London and in the paraffin heated house and one gas cooking house median CO concentrations exceeded these measured at the curbside of a very busy road in Central London. The living room concentrations of NO2 where the paraffin heater was in use were elevated for long periods. Analysis of the decay of pollutant concentration in one kitchen yielded an effective deposition velocity for NO2 of 3 X 10(-5) m s-1. The magnitude of the CO and NO2 concentrations measured in this survey confirms that indoor air pollution should be taken into account when assessing overall public exposure to air pollution.

Carbon Monoxide↗

PubMed1995

The effect of nitrogen dioxide exposure on the release of surfactant isolated from neonatal rabbit type II pneumocytes in culture.

Nitrogen dioxide (NO2) is a well-known environmental air toxin, produced from a variety of sources, including cigarette smoke. Because of the growing knowledge of the harmful effects of passive smoking on children, we decided to study the effect of NO2 exposure on the release of surfactant from isolated neonatal type II pulmonary epithelial cells. After isolation from 1 to 4 day old rabbits, type II epithelial cells were allowed to adhere for 18 hours, washed, media changed, and were exposed to either 5% CO2 in room air or NO2, 5 ppm, for 2 hours (all results mean +/- sd; comparisons, paired t-test). There was no difference in cell number or viability prior to exposure. Cells exposed to NO2 had an increase in LDH release [LDH activity in media/(LDH in media+cells) x 100], air 12.6 +/- 2.2%, NO2 21.7 +/- 3.7%, (p < 0.05). NO2-exposed cells also had an increase in total phospholipid (microgram/cell culture dish) in media compared to air exposed, air 170.13 +/- 7.54, NO2 195.15 +/- 11.2, (p < 0.05). 3H-choline incorporation as a precursor to disaturated phosphatidylcholine (DSPC) was also conducted during exposure to either air or NO2. Incorporation of 3H-choline into surfactant lipid was increased in media from cells after NO2 exposure compared to air, 58.23 +/- 15.16 air, 76.81 +/- 19.86 NO2 (cpm/microgram protein; p < 0.05). These results show that 2 hours of 5 ppm NO2 exposure is associated with an increase in release of surfactant from neonatal type II cells in culture.

Animals↗

PubMed1998

Indoor nitrogen dioxide in homes along trunk roads with heavy traffic.

OBJECTIVES: To assess the distribution of indoor nitrogen dioxide (NO2) concentrations in homes located in differing environments, and to investigate the influence of factors such as automobile exhaust on the indoor environment. METHODS: The concentrations of indoor NO2 over 24 hours were measured in both the heating and non-heating periods in homes of pupils from nine elementary schools in Chiba, Japan. Information on factors that could influence indoor environments was collected by questionnaire. RESULTS: Indoor NO2 concentrations during the heating period were higher in homes with unvented heaters than in homes with vented heaters, although the concentrations varied greatly among homes primarily because of the type of heating device used. During the non-heating period, indoor NO2 concentrations were significantly higher in homes adjacent to trunk roads than in homes located in other areas. Multiple regression analysis showed that indoor NO2 concentrations were associated with atmospheric NO2 in homes with vented heaters during the heating period, and in homes in areas other than on the roadside during the non-heating period. In areas other than the roadside, cigarette smoking in indoor environments also significantly contributed to indoor NO2. The average concentrations of indoor NO2 in the homes of pupils attending each school were significantly related to the atmospheric NO2 in areas other than the roadside. However, the relation between indoor and atmospheric NO2 concentrations was not significant in roadside areas. CONCLUSIONS: These findings suggest that indoor NO2 concentrations are related to the atmospheric NO2 and type of heating appliances, and are also affected by automobile exhaust in homes located in roadside areas.

Air Pollution↗

PubMed1996

[Nitric oxide delivery through ventilator and its toxic oxidative product nitrogen dioxide].

OBJECTIVE: To observe nitric oxide(NO) delivery through mechanically ventilator. NO is rapidly converted to nitrogen dioxide(NO2)in oxygen(O2) environments. METHODS: NO(800 ppm)was blended with compressed air, delivered to the high-pressure air inlet of a Siemens Servo 900C or VIP BIRD ventilator, and used to ventilator as a test lung. The ventilator settings were varied, minute ventilation (VE)from 2 to 6 L/min, inspired O2 fraction(FiO2)from 0.25 to 0.65, and NO concentration from 10 to 80 ppm. The inspiratory gas mixture was sampled just at the outlet port of ventilator. NO and NO2 were measured both by hemiluminescence and electro-chemical fuel cell technique. RESULTS: No NO was detected during any trial with VE 5 or 6 L/min., with FiO2 0.35 or 0.25, with NO 20 or 10 ppm. Low VE and low NO, NO2 values were greater with Servo 900C ventilator than with VIP BIRD ventilator at similar settings High VE and low NO or low VE and high NO, NO2 values were similar with both ventilators. High VE and high NO, NO2 values were greater with VIP BIRD ventilator than with Servo 900C ventilator. At same VE, NO2 values increased with increased FiO2 and NO. (NO2) = 0.0607 (NO)- 0.6604 VE + 7.004 FiO2, R2 = 0.7649 with Servo 900C ventilator,(NO2) = 0.0929(NO)- 0.1296 VE + 7.9360 FiO2, R2 = 0.8687 with VIP BIRD ventilator. CONCLUSIONS: NO(800 ppm) was blended with compressed air, delivered to the high-pressure air inlet of a Siemens Servo 900C or VIP BIRD ventilator is a portable, accurate, and adaptable system to deliver NO. During NO inhalation, VIP BIRD ventilator is more adaptable while low VE. Servo 900C ventilator is more adaptable while high VE.

Humans↗

PubMed1995

DNA damage in lung cells in vivo and in vitro by 1,3-butadiene and nitrogen dioxide and their photochemical reaction products.

A UV-irradiated mixture of 1,3-butadiene and nitrogen dioxide (NO2) was tested for its potency to induce DNA damage measured as single-strand breaks (SSB) in lungs of mice. Both gases were also tested separately. After 16 h exposure a UV-irradiated mixture of 40 ppm butadiene + 20 ppm NO2, but not 20 ppm butadiene + 10 ppm NO2 + UV, induced a significant increase in SSB as measured by the alkaline unwinding technique. There was no increase in the level of SSB using the alkaline elution technique during the same testing conditions. However, after 5 h exposure to 60 ppm butadiene + 30 ppm NO2 + UV both methods demonstrated a significant increase in SSB. Mice were also exposed to butadiene at 80 and 200 ppm for 16 h and at 500 ppm for 5 h. DNA damage was demonstrated in both liver and lung after 5 and 16 h (only at 200 ppm) of exposure using the unwinding technique. Using the alkaline elution assay, a significant increase in the level of SSB in lung and liver was found only after 5 h of exposure. When mice were exposed to 30 ppm NO2 for 16 h or 50 ppm for 5 h, a significant increase in SSB was found with the unwinding technique. Alveolar macrophages from mice were also exposed in vitro to the gas mixture and to butadiene and NO2 separately. In these experiments, the DNA damage was studied with the unwinding technique. A significant effect was demonstrated with 40 ppm butadiene + 20 ppm NO2 + UV. NO2 itself contributed to some extent to the increase. Reasons for the discrepancies between the unwinding and the alkaline elution techniques are discussed.

Air Pollutants↗

PubMed2006

Associations between personal exposures and fixed-site ambient measurements of fine particulate matter, nitrogen dioxide, and carbon monoxide in Toronto, Canada.

A longitudinal study investigating personal exposures to PM(2.5), nitrogen dioxide (NO(2)), and carbon monoxide (CO) for cardiac compromised individuals was conducted in Toronto, Canada. The aim of the study was (1) to examine the distribution of exposures to PM(2.5), NO(2), and CO; and (2) to investigate the relationship between personal exposures and fixed-site ambient measurements of PM(2.5), NO(2), and CO. In total, 28 subjects with coronary artery disease wore the Rupprecht & Patashnick ChemPass Personal Sampling System one day a week for a maximum of 10 weeks. The mean (SD) personal exposures were 22 microg m(-3) (42), 14 p.p.b. (6), and 1.4 p.p.m (0.5) for PM(2.5), NO(2), and CO, respectively. PM(2.5) and CO personal exposures were greater than central fixed-site ambient measurements, while the reverse pattern was observed for NO(2). Ambient PM(2.5) and NO(2) were correlated with personal exposures to PM(2.5) and NO(2) with median Spearman's correlation coefficients of 0.69 and 0.57, respectively. The correlations between personal exposures and ambient measurements made closest to the subjects' homes or the average of all stations within the study were not stronger than the correlation between personal exposures and central fixed-site measurements. Personal exposures to PM(2.5) were correlated with personal exposures to NO(2) (median Spearman's correlation coefficient of 0.43). This study suggests that central fixed-site measurements of PM(2.5) and NO(2) may be treated as surrogates for personal exposures to PM(2.5) and NO(2) in epidemiological studies, and that NO(2) is a potential confounder of PM(2.5).

Aged↗

PubMed1999

Effect of fluticasone propionate aqueous nasal spray on allergen-induced inflammatory changes in the nasal airways of allergic rhinitics following exposure to nitrogen dioxide.

BACKGROUND: The authors have recently demonstrated that prior exposure for 6 h to 400 p.p.b. nitrogen dioxide significantly enhances the early phase response of eosinophils in the nasal airways of allergic rhinitics to subsequent allergen provocation. OBJECTIVE: To investigate whether treatment with fluticasone propionate aqueous nasal spray (FP) can alter the inflammatory response in the nasal airways under these conditions. METHODS: Sixteen allergic, rhinitic patients were recruited for this double-blind, randomized, cross-over study and received either topical FP 200 microg once daily or matched placebo for 4 weeks. At the end of treatment, all underwent nasal lavage followed by a 6 h exposure to 400 p.p.b. NO2. Following exposure to NO2, nasal allergen challenge was performed and nasal lavage repeated. After a 4 week washout period, patients were given alternate treatment and tested as above. RESULTS: Analysis of eosinophil cationic protein (ECP) in lavage samples from patients treated with placebo, demonstrated that this was significantly increased from a median value of 2.3 ng/mL (range: 1.0-7.1) to 15.1 ng/mL (range: 1.5-40.0; P = 0.001) following exposure to NO2 and allergen challenge. However, in patients treated with FP, ECP concentrations only increased from 3.3 ng/mL (range: 0.2-9.2) to 5.1 ng/mL (range: 0.3-20.0; P = 0.034) following exposure to NO2 and allergen challenge. The difference of the changes in ECP concentration between the placebo and the FP-treated group was significant (P = 0.003). Similarly, there was a significant increase in the number of eosinophils in nasal lavage after exposure to NO2 and allergen challenge in the placebo group, and this increase was inhibited in FP group (P = 0.002). CONCLUSION: These results suggest that FP influences NO2- and allergen-induced changes in eosinophil function, as well as eosinophil number in the nasal airway of allergic rhinitics.

Adult↗

PubMed1997

[Nitrogen dioxide]

In order to assess level of human exposure to nitrogen dioxide, 22 traffic police from the city of Rio de Janeiro were monitored during their working hours for 3 consecutive days. Samples were taken by using a passive sampler (badge) and analyzed spectrophotometrically after reacting with sulphanilic acid followed by coupling with N-naphtilethylenediamine dihydrochloride. Results ranged from 13.3 to 193.6 mg/m3. According to the literature, these levels are not associated with any acute damage to human health but care should be taken to avoid long-term problems.

Journal Article↗