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PubMed1985

Induction of umuC gene expression by nitrogen dioxide in Salmonella typhimurium.

Gaseous nitrogen dioxide (NO2) was found to induce umuC gene expression in Salmonella typhimurium carrying the umuC-lacZ fusion plasmid. The induction level of the umu operon responsible for inducible mutagenesis was measured by the level of beta-galactosidase in the cell, encoded by the fusion gene. NO2 gas was bubbled into bacterial suspensions at 10, 30 and 90 microliters/l for 30 min at a flow rate of 100 ml/min. Expression of the umuC gene varied with the concentration, flow rate and bubbling time of the NO2 gas. Although NO2 gas induces SOS functions, mutagenesis due to it was not detectable in Salmonella typhimurium TA100 and TA102. Nitric oxide gas (NO) did not induce any umuC gene expression.

DNA Repair↗

PubMed2005

Nitration of the tyrosyl radical in ribonucleotide reductase by nitrogen dioxide: a gamma radiolysis study.

Nitrogen dioxide is a product of peroxynitrite homolysis and peroxidase-catalyzed oxidation of nitrite. It is of great importance in protein tyrosine nitration because most nitration pathways end with the addition of *NO2 to a one-electron-oxidized tyrosine. The rate constant of this radical addition reaction is high with free tyrosine-derived radicals. However, little is known of tyrosine radicals in proteins. In this paper, we have used *NO2 generated by gamma radiolysis to study the nitration of the R2 subunit of ribonucleotide reductase, which contains a long-lived tyrosyl radical on Tyr122. Most of the nitration occurred on Tyr122, but nonradical tyrosines were also modified. In addition, peptidic bonds close to nitrated Tyr122 could be broken. Nitration at Tyr122 was not observed with a radical-free metR2 protein. The estimated rate constant of the Tyr122 radical reaction with *NO2 was of 3 x 10(4) M(-1) s(-1), thus several orders of magnitude lower than that of a radical on free tyrosine. Nitration rate of other tyrosine residues in R2 was even lower, with an estimated value of 900 M(-1) s(-1). This study shows that protein environment can significantly reduce the reactivity of a tyrosyl radical. In ribonucleotide reductase, the catalytically active radical residue is very efficiently protected against nitrogen oxide attack and subsequent nitration.

Catalysis↗

PubMedDate not supplied

Nitrogen dioxide exposure assessment and cough among preschool children.

The association between exposure to ambient air nitrogen dioxide and cough was evaluated in a panel study among 162 children aged 3-6 y. The weekly average nitrogen dioxide exposure was assessed with Palmes-tube measurements in three ways: (1) personally, (2) outside day-care centers, and (3) inside day-care centers. Ambient air nitrogen dioxide concentrations were obtained from the local network that monitored air quality. The parents recorded cough episodes daily in a diary. The risk of cough increased significantly (relative risk = 3.63; 95% confidence interval = 1.41, 9.30) in the highest personal nitrogen dioxide exposure category in winter, and a nonsignificant positive trend was noted for the other assessment groups. In spring, risk increased nonsignificantly in all exposure-assessment groups, except for the fixed-site monitoring assessment. It is important that investigators select an exposure-assessment method sufficiently accurate to reflect the effective pollutant dose in subjects.

Child↗

PubMed1999

Production of nitrogen dioxide during nitric oxide therapy using the Servo Ventilator 300 during volume-controlled ventilation.

BACKGROUND: Inhaled nitric oxide may be useful in the treatment of pulmonary hypertension and hypoxaemia. Nitric oxide is rapidly oxidized to nitrogen dioxide, which is toxic and may adversely affect the airways of the patient. The aim of the present investigation was to examine factors that may affect the concentration of nitrogen dioxide, using the Servo Ventilator 300 nitric oxide delivery system, where nitric oxide is flow-proportionally mixed with the main ventilatory flow in the proximal part of the inspiratory limb. METHODS: In this experimental study nitric oxide and nitrogen dioxide levels were measured at the inspiratory site of a Y-piece with a chemiluminescence analyzer and electrochemical fuel cells. The effects of different concentrations of nitric oxide and oxygen, minute volume, different tube lengths, a soda lime absorber, and a humidifier placed in the inspiratory limb were evaluated. RESULTS: The concentration of nitrogen dioxide was dependent on the concentrations and residence time of nitric oxide with oxygen and the minute volume ventilation used. A soda lime absorber reduced concentrations of nitrogen dioxide at the expense of almost corresponding reductions in inhaled concentrations of nitric oxide. A humidifier increased the concentration of nitrogen dioxide, to an extent depending on the water volume and temperature used. CONCLUSION: Concentrations of nitric oxide and oxygen, minute volume ventilation, and residence time in the inspiratory part of the ventilatory circuit were factors that affected the generation of nitrogen dioxide. A soda lime absorber in this system is not recommended.

Administration, Inhalation↗

PubMed1983

Effect of nitrogen dioxide exposure on rat lung lipids.

Rats were exposed continuously to 40 ppm nitrogen dioxide for 4 hours. The phospholipid contents and fatty acid compositions were determined in homogenates and subcellular fractions of rat lungs immediately after exposure. There were no significant changes in the total phospholipid content or phospholipid concentration as a result of nitrogen dioxide exposure. In addition, nitrogen dioxide did not induce any significant changes in the fatty acid composition of the lung phospholipids, with the exception of arachidonic and docosapentanoic acids in the mitochondrial fraction, which showed a slight increase over the air-exposed control.

Animals↗

PubMed2005

Combination of nitrogen dioxide radicals with 8-oxo-7,8-dihydroguanine and guanine radicals in DNA: oxidation and nitration end-products.

The oxidation and nitration reactions in DNA associated with the combination of nitrogen dioxide radicals with 8-oxo-7,8-dihydroguanine (8-oxoGua) and guanine radicals were explored by kinetic laser spectroscopy and mass spectrometry methods. The oxidation/nitration processes were triggered by photoexcitation of 2-aminopurine (2AP) residues site-specifically positioned in the 2'-deoxyribooligonucleotide 5'-d(CC[2AP]TC[X]CTACC) sequences (X = 8-oxoGua or G), by intense 308 nm excimer laser pulses. The photoionization products, 2AP radicals, rapidly oxidize either 8-oxoGua or G residues positioned within the same oligonucleotide but separated by a TC dinucleotide step on the 3'-side of 2AP. The two-photon ionization of the 2AP residue also generates hydrated electrons that are trapped by nitrate anions thus forming nitrogen dioxide radicals. The combination of nitrogen dioxide radicals with the 8-oxoGua and G radicals occurs with similar rate constants (approximately 4.3 x 10(8) M(-1) s(-1)) in both single- and double-stranded DNA. In the case of 8-oxoGua, the major end-products of this bimolecular radical-radical addition are spiroiminodihydantoin lesions, the products of 8-oxoGua oxidation. Oxygen-18 isotope labeling experiments reveal that the O-atom in the spiroiminodihydantoin lesion originates from water molecules, not from nitrogen dioxide radicals. In contrast, combination of nitrogen dioxide and guanine neutral radicals generated under the same conditions results in the formation of the nitro products, 5-guanidino-4-nitroimidazole and 8-nitroguanine adducts. The mechanistic aspects of the oxidation/nitration processes and their biological implications are discussed.

2-Aminopurine↗

PubMed2002

Asthma in children exposed to nitrogen dioxide in ice arenas.

Very high concentrations of nitrogen dioxide (NO2) have been measured in arenas using combustion engine-powered resurfacing machines. This study was performed to compare the occurrence of asthma in children playing ice hockey in arenas using propane-powered machines and in children attending arenas using electric machines. Children regularly playing hockey in the arenas (nine propane, six electric) were sent a questionnaire, including questions on allergic disease and risk factors. Measurements of NO2 were performed with passive diffusion samplers during 3 consecutive days. The mean NO2 concentration in the propane arenas was 276 microg x m(-3) (range 28-1015 microg x m(-3)) and 11 microg x m(-3) (2-30) in the electric arenas. Questionnaires were answered by 1,536 children (78%), with an overall prevalence of asthma of 16%. The odds ratio (OR) for asthma was 0.9 (95% confidence interval (CI) 0.7-1.2) comparing propane arenas to electric. However, children in propane arenas with higher than median concentration of NO2 reported more wheezing (OR 1.4, 95% CI 1.0-1.9) and nasal symptoms (OR 1.7, 95% CI 1.3-2.3) than children in propane arenas with lower concentrations. In conclusion, children playing ice hockey in indoor arenas have a high prevalence of asthma, but it appears unlikely that increased exposure to combustion products, including nitrogen dioxide, is a major contributor to this excess risk.

Adolescent↗

PubMed2002

Personal exposure monitoring of particulate matter, nitrogen dioxide, and carbon monoxide, including susceptible groups.

AIMS: To investigate the relation between personal exposures to nitrogen dioxide, carbon monoxide, and PM(10), and exposures estimated from static concentrations of these pollutants measured within the same microenvironments, for healthy individuals and members of susceptible groups. METHODS: Eleven healthy adult subjects and 18 members of groups more susceptible to adverse health changes in response to a given level of exposure to nitrogen dioxide, carbon monoxide, and/or PM(10) than the general population (six schoolchildren, six elderly subjects, and six with pre-existing disease-two with chronic obstructive pulmonary disease (COPD), two with left ventricular failure (LVF), and two with severe asthma) were recruited. Daytime personal exposures were determined either directly or through shadowing. Relations between personal exposures and simultaneously measured microenvironment concentrations were examined. RESULTS: Correlations between personal exposures and microenvironment concentration were frequently weak for individual subjects because of the small range in measured concentrations. However, when all subjects were pooled, excellent relations between measured personal exposure and microenvironment concentration were found for both carbon monoxide and nitrogen dioxide, with slopes of close to one and near zero intercepts. For PM(10), a good correlation was also found with an intercept of personal exposure (personal cloud) of 16.7 (SD 10.4) micro g/m(3). Modelled and measured personal exposures were generally in reasonably good agreement, but modelling with generic mean microenvironment data was unable to represent the full range of measured concentrations. CONCLUSIONS: Microenvironment measurements of carbon monoxide and nitrogen dioxide can well represent the personal exposures of individuals within that microenvironment. The same is true for PM(10) with the addition of a personal cloud increment. Elderly subjects and those with pre-existing disease received generally lower PM(10) exposures than the healthy adult subjects and schoolchildren by virtue of their less active lifestyles.

Adult↗

PubMed1992

Concentration-response relationships of rat lungs to exposure to oxidant air pollutants: a critical test of Haber's Law for ozone and nitrogen dioxide.

Exposure protocols were designed to ask whether lung damage in rats exposed to either ozone or nitrogen dioxide is proportional to dose rate or to cumulative dose. Thus, the response of rats to a constant product of concentration of oxidant air pollutant and time of exposure (C x T) was evaluated for 3-day exposures over a fourfold range of concentrations of ozone (0.2-0.8 ppm) or of nitrogen dioxide (3.6-14.4 ppm) for exposure durations of 6-24 hr per day. The response of rat lungs was quantified by changes in total protein content of lung lavage supernatants or by changes in content of specific cell types in lung lavage pellets. The results of these experiments clearly demonstrate that acute lung damage is a function of cumulative dose (that is, C x T product) for the three highest dose rates tested. However, when exposure duration is extended to include the entire 24-hr period (the lowest dose rate tested), there is a marked attenuation of pulmonary response. Rats were also exposed to mixtures of ozone and nitrogen dioxide with the C x T product held constant. Our results clearly demonstrate that when rats are exposed to combinations of ozone and nitrogen dioxide, lung damage is a function of peak concentration rather than a function of cumulative dose. This deviation from Haber's Law is attributed to a concentration-dependent, synergistic (greater than additive) response to this specific mixture of oxidant air pollutants.

Administration, Inhalation↗

PubMed1996

Measurements of indoor and outdoor nitrogen dioxide concentrations using a diffusive sampler.

The Willems badge, a short-term diffusion sampler, was used to measure nitrogen dioxide concentrations inside and outside the homes of participants in the European study "PEACE' (Pollution Effects on Asthmatic Children in Europe). The main aim of the study was to determine levels of nitrogen dioxide concentrations both outside and inside children's homes, and to estimate the indoor/outdoor ratios for nitrogen dioxide in an urban area, in comparison with a less urbanized control area. We conducted measurements in 23 homes in Umeå, a city of about 100,000 inhabitants in the northern part of Sweden, in addition to 20 homes in a less urbanized control area situated about 20 km from Umeå. Measurements were made on two different occasions in each home during the period January-March, 1994. The houses were not equipped with any gas appliances. The mean outdoor 24-h concentration in Umeå was 28 micrograms m-3 and the mean indoor concentration was 11 micrograms m-3. The mean indoor: outdoor ratio was 0.44 (s = 0.23). The highest outdoor value, measured in the city centre of Umeå, was 54 micrograms m-3. In the control area the mean ambient 24-h concentration was 12 micrograms m-3, approximately half as high as in the urban area, and the mean indoor concentration was 6 micrograms m-3. The mean indoor: outdoor ratio was 0.67 (s = 0.55). The correlation coefficient between indoor and outdoor concentrations was higher in the control area, r = 0.79 (p < 0.001), in comparison with the urban area, r = 0.43 (p < 0.01). It is concluded that the outdoor as well as the indoor concentrations of nitrogen dioxide were approximately twice as high in Umeå as in the control area. This could be explained by heavier traffic density in Umeå. The mean 24-h concentration outside homes in Umeå was, however, below the 24-h national standard level of 75 micrograms m-3. The higher correlation between indoor and outdoor concentrations, combined with higher indoor: outdoor ratio, in the control area is interpreted as a sign of a lower level of penetration of outdoor air into the houses in the urban area. This was not explained by differences in types of buildings between the two areas, but possibly by differences in air-exchange rates and in habits of ventilating rooms with open windows.

Air Pollutants↗

PubMed1989

Influence of experimental pulmonary emphysema on the toxicological effects from inhaled nitrogen dioxide and diesel exhaust.

This project examined the influence of preexisting, experimentally induced pulmonary emphysema on the adverse health effects in rats of chronic inhalation exposure to either nitrogen dioxide or automotive diesel-engine exhaust. Previous reports indicated that humans with chronic lung disease were among those most severely affected by episodic exposures to high concentrations of airborne toxicants. There were no previous reports comparing the effects of chronic inhalation exposure to components of automotive emissions in emphysematous and normal animals. The hypothesis tested in this project was that rats with preexisting pulmonary emphysema were more susceptible than rats with normal lungs to the adverse effects of the toxicant exposures. Young adult rats were housed continuously in inhalation exposure chambers and exposed seven hours per day, five days per week, for 24 months to nitrogen dioxide at 9.5 parts per million (ppm)2, or to diesel exhaust at 3.5 mg soot/m3, or to clean air as control animals. These concentrations were selected to produce mild, but distinct, effects in rats with normal lungs. Pulmonary emphysema was induced in one-half of the rats by intratracheal instillation of the proteolytic enzyme elastase six weeks before the toxicant exposures began. Health effects were evaluated after 12, 18, and 24 months of exposure. The measurements included respiratory function, clearance of inhaled radiolabeled particles, pulmonary immune responses to instilled antigen, biochemistry and cytology of airway fluid, total lung collagen, histopathology, lung morphometry, and lung burdens of diesel soot. The significance of influences of emphysema and toxicant exposure, and interactions between influences of the two treatments, were evaluated by analysis of variance. The elastase treatment resulted in pulmonary emphysema that was manifested by enlarged alveoli and alveolar ducts, and by ruptured alveolar septa. There was no accompanying inflammation and no alterations of bronchioles. The emphysema persisted throughout the study period, with little evidence of progression. Lung weight was increased, physiological lung volumes were enlarged, lung compliance was increased, and airflow was obstructed. Nitrogen dioxide exposure of normal rats caused mild epithelial hyperplasia and a thickening of the walls of terminal bronchioles, an extension of bronchiolar epithelium into proximal alveoli, and inflammation in proximal alveoli. Lung volume and weight and the lung collagen content were increased. Airway fluid indicators of cell damage and oxidant protective mechanisms were increased. Similar effects of nitrogen dioxide exposure were superimposed over the effects of emphysema in emphysematous nitrogen dioxide-exposed rats. Several parameters were affected similarly by nitrogen dioxide exposure and emphysema (for example, increased lung volume), and the combined effects tended to be additive.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1985

Health effects of nitrogen dioxide and oxidants.

The document is an evaluation of the health effects of nitrogen dioxide (NO2) and ozone (O3) intended to serve as a basis for establishing Swedish air quality standards. The specific effects of nitrogen dioxide and ozone are reviewed on the basis of published studies on animals, tissues and cells, controlled studies on humans, and epidemiologic studies. The focus is on the importance of the gases in relation to sensitive groups, outdoor-indoor exposure relationships, the question of short- or long-term limit values, and their combined effects with other pollutants. The minimum adverse effect level for human short-term exposure is assessed to be 900 micrograms/m3 for nitrogen dioxide and 200 micrograms/m3 for ozone; for sensitive persons these values should possibly be even lower. Large safety factors should be added to these values before they are used for air pollution control purposes.

Air Pollutants↗

PubMed2004

A new method for atmospheric nitrogen dioxide measurements using the combination of a stripping coil and fluorescence detection.

A new stripping coil for the collection of nitrogen dioxide (NO2) has been developed to increase its versatility and efficiency. Nitrogen dioxide measurements based on quantitative collection through a reaction coil into an alkaline solution has been examined. Nitrogen dioxide is collected in a 0.1 N NaOH solution. This collection system has an efficiency of nearly 100%. The absorbed nitrogen dioxide has been measured by fluorescence detection with sub-ppbv detection limits. The excitation wavelength at 360 nm and the produced emission wavelength at 405 nm were suitable for nitrite ion measurements.

Journal Article↗

PubMed2006

Development and optimization of a lab-on-a-chip device for the measurement of trace nitrogen dioxide gas in the atmosphere.

We propose the use of lab-on-a-chip technology for measuring gaseous chemical pollutants, and describe the development of a microchip for the detection of nitrogen dioxide (NO2) in air. A microchip fabricated from quartz glass has been developed for handling the following three functions, gas absorption, chemical reaction and fluorescence detection. Channels constructed in the microchip were covered with porous glass plates, allowing nitrogen dioxide to penetrate into the triethanolamine (TEA) flowing within the microchannel beneath. The nitrogen dioxide was then mixed with TEA and reacted with a suitable fluorescence reagent in the chemical reaction chamber in the microchip. The reacted solution was then allowed to flow into the fluorescence detection area to be excited by an ultraviolet light-emitting diode (UV-LED), and the fluorescence was detected using a photomultiplier tube (PMT). The reaction time, reagent concentration, pH, flow rate and other measurement conditions were optimised for analysis of nitrogen dioxide in air. Preliminary studies with standardized test solutions revealed quantitative measurements of nitrite ion (NO2-), which corresponded to atmospheric nitrogen dioxide in the range of 10-80 ppbv.

Air Pollutants↗

PubMed1986

Nitrogen dioxide exposure and development of pulmonary emphysema.

This study assessed the relationship between nitrogen dioxide inhalation and the development of pulmonary emphysema and investigated how the severity of preexisting emphysema brought about by protease (elastase) instillation into the lung may be augmented by a subchronic exposure to a relatively high concentration of nitrogen dioxide. Lungs of adult Fischer-344 rats were evaluated for emphysematous changes after (1) a single intratracheal instillation of elastase (E), (2) a 25-d exposure to 35 ppm nitrogen dioxide (NO2), and (3) elastase instillation followed by 25-d exposure to 35 ppm NO2 (E + NO2). Rats instilled with sterile normal saline and subsequently exposed to filtered air served as a control group (NS). Residual volumes (RV) of the NO2 and NS groups were virtually identical, whereas the RV of the E and E + NO2 lungs (2.3 and 2.3 ml, respectively) were significantly greater than those of the NS and NO2 lungs (1.3 and 1.4 ml, respectively). Directionally similar changes in the excised lung volumes and total lung capacities were obtained with the E and E + NO2 groups; NO2 alone, however, did not alter these volumetric parameters. No differences in arterial blood gases and pH values, minute ventilation, or breathing frequencies were found among the experimental groups. The mean linear intercept values (MLI) obtained with the NS and NO2 exposed lungs were essentially identical with average values of approximately 62 micron. This morphometric parameter was substantially increased in the E- and E + NO2-exposed lungs; no significant differences, however, were found between the MLI values obtained with the E and E + NO2 lungs (approximately 95 and approximately 97 micron, respectively). From these data, as well as histologic examinations of lung sections for evidence of emphysema, we conclude that (1) a subchronic, moderately high level of NO2 exposure does not produce an irreversible emphysematous lesion in the rat model and (2) exposure of rats to 35 ppm for 25 d after elastase instillation into the lungs does not potentiate protease-induced emphysema or bring about a progression in preexisting emphysema.

Animals↗

PubMed1994

Nitrogen dioxide exposures inside ice skating rinks.

OBJECTIVES: The common operation of fuel-powered resurfacing equipment in enclosed ice skating rinks has the potential for producing high concentrations of carbon monoxide and nitrogen dioxide. Exposures to these gaseous combustion products may adversely affect the health of those inside the rink. Little information is available on pollutant concentrations under normal operating conditions. METHODS: One-week average nitrogen dioxide concentrations in 70 northeastern US rinks were measured with passive samplers during normal winter season conditions. RESULTS: The median nitrogen dioxide level inside rinks was 180 ppb, more than 10 times higher than the median outdoor concentration. One-week average nitrogen dioxide concentrations above 1000 ppb were measured in 10% of the rinks. CONCLUSIONS: Considering that short-term peak concentrations were likely to have reached two to five times the measured 1-week averages, our results suggest that nitrogen dioxide levels were well above short-term air quality guidelines and constitute a public health concern of considerable magnitude.

Air Pollutants↗

PubMed2003

Exposure of intensive care unit nurses to nitric oxide and nitrogen dioxide during therapeutic use of inhaled nitric oxide in adults with acute respiratory distress syndrome.

BACKGROUND: Although low concentrations of inhaled nitric oxide may by therapeutic, both nitric oxide and its oxidation product nitrogen dioxide are potentially toxic. The threshold limits for time-weighted average concentrations of nitric oxide and nitrogen dioxide issued by the American Conference of Governmental Industrial Hygienists are 25 and 3 ppm, respectively. The concentrations of these gases in the breathing space of hospital personnel during administration of nitric oxide to adult patients have not been reported. METHODS: Air was sampled from the breathing zone of intensive care unit nurses via collar-mounted tubes during the nurses' routine duties attending patients who were receiving inhaled nitric oxide at 5 or 20 ppm. The exhaust ports of the mechanical ventilators were left open to the room. Nitric oxide and nitrogen dioxide were chemically assayed as nitrite from sorbent tubes by using spectrophotometry. Ambient nitric oxide levels were measured at sequential distances from the ventilator by using chemiluminescence. RESULTS: The time-weighted average concentrations of inspired gas for nurses during inhaled nitric oxide treatment were 0.45 ppm or less for nitric oxide and less than 0.29 ppm for nitrogen dioxide. Nitric oxide levels at the ventilator during delivery at 20 ppm were 9.2 ppm, but dropped off markedly beyond 0.6 m (2 ft), to a mean of about 30 ppb. CONCLUSION: Inhaled nitric oxide therapy at doses up to 20 ppm does not appear to pose a risk of excessive occupational exposure to nitric oxide or nitrogen dioxide to nurses during routine delivery of critical care.

Administration, Inhalation↗

PubMedDate not supplied

Controlled exposure of volunteers with chronic obstructive pulmonary disease to nitrogen dioxide.

Twenty-two volunteers with chronic obstructive pulmonary disease were exposed to nitrogen dioxide at 0.0, 0.5, 1.0, and 2.0 ppm in a controlled environment chamber. Exposure lasted 1 hr and included two 15-min exercise periods, during which the mean ventilation rate was roughly 16 L/min. Pulmonary mechanical function was evaluated pre-exposure, after initial exercise, and at the end of exposure. Blood oxygenation was measured by ear oximetry pre-exposure and during the second exposure period. Symptoms were recorded during exposures and for 1-wk periods afterward. No statistically significant changes in symptom reporting could be attributed to nitrogen dioxide exposure at any concentration, compared to the 0.0 ppm control condition. Measures of pulmonary mechanics showed either no significant changes, or small and equivocal changes. Arterial oxygen saturation showed marginal improvement with exercise, regardless of nitrogen dioxide concentration.

Aged↗