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PubMed1983

Effects of nitric oxide and nitrogen dioxide on bacterial growth.

The effects of low concentrations of nitric oxide (NO) and nitrogen dioxide (NO2) on actively dividing cultures of Staphylococcus aureus, Micrococcus luteus, Micrococcus roseus, Serratia marcescens, Bacillus subtilis, Bacillus circulans, Bacillus megaterium, and Bacillus cereus were studied. Fresh cultures of each organism were incubated for 24 h at 25 degrees C on both nutrient agar and mineral salts glucose agar plates under atmospheres containing various low concentrations of NO in air (0 to 1.9 ppm [0 to 2.0 micrograms/g of air]), NO2 in air (0 to 5.5 ppm [0 to 8.8 micrograms/g of air]), or NO and NO2 in air. Bacteria grown under air only were used as controls. After incubation, the colonies that developed on the plates were counted. None of the bacteria tested was affected by NO or NO2 at the indicated concentrations while growing on nutrient agar. Serratia marcescens, B. circulans, B. subtilis, B. megaterium, and B. cereus grown on mineral salts glucose agar were not significantly affected by NO or NO2. Low concentrations (0 to 1.9 ppm) of NO were bacteriostatic to log-phase cultures of M. roseus, M. luteus, and Staphylococcus aureus grown on mineral salts glucose agar. Bacteriostatic activity over a 24-h interval was maximal at an initial NO concentration of 1 ppm. Appreciable amounts of NO2 were produced in 24 h at initial NO concentrations greater than 1 ppm. These results suggest that NO2 may reduce the bacteriostatic activity of NO. Low concentrations (0 to 5.5 ppm) of NO2 in air did not affect any of the bacteria tested. At these low concentrations, NO affected bacterial growth, although NO2, NO2-, and NO3- did not. In addition, it was determined that the bacteriostatic activity observed in this study was not due to an increase in the acidity of the medium.

Bacillus↗

PubMed2005

Association of indoor nitrogen dioxide exposure with respiratory symptoms in children with asthma.

RATIONALE: Chronic exposure to indoor nitrogen dioxide (NO2) is a public health concern. Over half of U.S. households have a source of NO2, and experimental data suggest potential for adverse respiratory effects. OBJECTIVE: To examine associations of indoor NO2 exposure with respiratory symptoms among children with asthma. METHODS: NO2 was measured using Palmes tubes, and respiratory symptoms in the month before sampling were collected during home interviews of mothers of 728 children with active asthma. All were younger than 12 yr, lived at the sampled home for at least 2 mo, and had asthma symptoms or used maintenance medication within the previous year. MEASUREMENTS: Respiratory symptoms (wheeze, persistent cough, shortness of breath, chest tightness). RESULTS: Mean (SD) NO2 was 8.6 (9.1) ppb in homes with electric ranges and 25.9 (18.1) ppb in homes with gas stoves. In models stratified by housing type (a factor associated with socioeconomic status), gas stove presence and elevated NO2 were each significantly associated with respiratory symptoms, controlling for age, ethnicity, medication, mold/mildew, water leaks, and season of sampling. Among children in multifamily housing, exposure to gas stoves increased likelihood of wheeze (odds ratio [OR], 2.27; 95% confidence interval [95% CI], 1.15, 4.47), shortness of breath (OR, 2.33; 95% CI, 1.12, 5.06), and chest tightness (OR, 4.34; 95% CI, 1.76, 10.69), whereas each 20-ppb increase in NO2 increased both likelihood of any wheeze (OR, 1.52; 95% CI, 1.04, 2.21) or chest tightness (OR, 1.61; 95% CI, 1.04, 2.49), and days of wheeze (rate ratio (RR), 1.33; 95% CI, 1.05, 1.68) or chest tightness (RR, 1.51; 95% CI, 1.18, 1.91). CONCLUSION: Exposure to indoor NO2 at levels well below the Environmental Protection Agency outdoor standard (53 ppb) is associated with respiratory symptoms among children with asthma in multifamily housing.

Air Pollution, Indoor↗

PubMed2004

Nitrogen dioxide is not associated with respiratory infection during the first year of life.

BACKGROUND: Nitrogen dioxide (NO(2)) has been related to respiratory infections in experimental studies but its role remains controversial in general population studies of children. We aim to assess the association between indoor NO(2) and lower respiratory tract infections (LRTI) during the first year of life in a multicentre prospective cohort study. METHODS: Children (n = 1611) were recruited prior to birth for the Asthma Multicentre Infants Cohort Study (AMICS). Three concurrent cohorts (Ashford, Kent [UK]; Barcelona city, and Menorca Island [Spain]) followed the same research protocol. NO(2) was measured with passive diffusion tubes placed in the living room for 2 weeks when infants were approximately 3 months old. Doctor-diagnosed LRTI during the first year of life (as well as antibiotic use) were measured by questionnaire, and in Ashford validated by the examination of clinical records. In Barcelona, direct measurements using nasopharyngeal lavage and cultures within a continuous surveillance system were done. RESULTS: The cumulative rates of LRTI (39% in Ashford, 28% in Barcelona, and 45% in Menorca) were unrelated to NO(2) levels (corresponding medians 6, 46, and 12 ppb, respectively) in all three centres (all odds ratios being around 1). Similarly, the rates of LRTI in Barcelona measured with the continuous record showed no association with NO(2) (all rate ratios being below 1). In addition, there was no association between rate of antibiotics courses per year per child (2.4 in Ashford, 1.7 in Barcelona, 0.9 in Menorca) and NO(2) levels. CONCLUSIONS: Indoor NO(2) at current levels does not seem to be involved in increasing respiratory infections by itself in infants, suggesting that the effects observed in studies on outdoor air are probably due to other copollutants.

Air Pollutants↗

PubMed2002

Effect of nitrogen dioxide and ozone on the risk of dying in patients with severe asthma.

BACKGROUND: A study was performed to assess the acute association between air pollution, pollen and spores, and mortality in a population based cohort of subjects with asthma recruited from emergency room admissions for an asthma exacerbation using a case crossover design. METHODS: Patients in Barcelona aged over 14 years who died during the period 1985-95 who had visited the emergency department of one of the four largest hospitals in the city for asthma during 1985-9 were included in the study (a total of 467 men and 611 women). Deaths were identified by record linkage of the cohort individuals with the Catalonia mortality registry. Causes of death were based on the underlying cause on the death certificate. Air pollution, pollen and spore levels were measured at the city monitoring stations which provide an average for the entire city. RESULTS: Nitrogen dioxide was associated with mortality for all causes of death (adjusted odds ratio (OR) for an increase of the interquartile range = 1.50, 95% confidence interval (CI) 1.09 to 2.64) in asthmatic patients with more than one emergency room admission for asthma. The association was particularly strong for respiratory causes (OR 1.63, 95% CI 0.93 to 2.86). Ozone also increased the risk of death in asthmatic patients (OR 1.90, 95% CI 1.09 to 3.30) during spring and summer. The association with particles, pollen, and spores was not significant, and no interactions between air pollutants and pollen and spores were found. CONCLUSION: Nitrogen dioxide and ozone may exacerbate severe asthma and even cause death among asthmatic subjects.

Adult↗

PubMed1989

[Cell population and elastase activity in bronchoalveolar lavage fluid from rats exposed to high concentration of nitrogen dioxide].

The purpose of this study was to clarify what elastase acts primarily to injure the lung tissue when animals are exposed to nitrogen dioxide (NO2). Rats were exposed to 50 ppm NO2 for 5 hours a day on 7 consecutive days. Approximately six animals were sacrificed after the exposure of the 1st, 3rd, 5th and 7th days. On the 1st day, diffuse alveolar edema was seen accompanying deposits of fibrin nets, suggesting the increase of permeability. Inflammatory cell infiltration was seen in terminal bronchioles and alveolar ducts on the 3rd day, however these changes diminished gradually thereafter. The increase of total cell count was seen in bronchoalveolar lavage fluid on day 3 and thereafter. The number of neutrophils was raised markedly on the 3rd day, whereas that of macrophages showed a gradual increase thereafter. The protein concentration of bronchoalveolar lavage fluid increased markedly on the 1st day and was reduced rapidly thereafter. Elastase activity was measured in bronchoalveolar lavage fluid using succinyl-trialanyl-p-nitroanilide as substrate. Total elastase activity was significantly increased on the 1st and 3rd day. Inhibition studies using EDTA and DFP suggested that most of the elastase activity was due to a metaleoprotease. These data suggest that elastase from macrophage may be mainly related to nitrogen dioxide-induced lung injury.

Animals↗

PubMed1991

Mutagenic activity of photoreaction products formed from chlorinated ethenes and nitrogen dioxide.

The mutagenicity in Salmonella, strain TA 100, of photoreaction products from chlorinated alkenes and nitrogen dioxide, was studied after a mean reaction time of 40 min with UV-irradiation and an exposure time of 20 hr. Only vinyl chloride (monochloroethene) gave rise to significantly mutagenic photoreaction products. Of the other chloroethenes, 1,1-dichloroethene and tetrachloroethene, but not 1,2-dichloro- or trichloroethene, formed slightly mutagenic products. Bacteriotoxic effects occurred at low doses, especially with tri- and tetrachloroethene.

Dichloroethylenes↗

PubMed1976

Effect of chronic exposure to nitrogen dioxide on collagen fractions content in skin of guinea pigs.

Guinea pigs were exposed to nitrogen dioxide in concentration of 2 mg/m3 (8 hrs. daily, 180 days). Control group inspired fresh air. Collagen fractions were estimated in skin and assayed as hydroxyproline concentration. An increase of total collagen content, due to on increase of salt-soluble collagen fraction was found in the skin of the exposed animals, while a simultaneous decrease of insoluble collagen content was observed.

Animals↗

PubMed1959

Protection by sulfur compounds against the air pollutants ozone and nitrogen dioxide.

Two distinct but related pathways of protection against the lethal effects of ozone and nitrogen dioxide are shown by (i) simultaneous inhalation of compounds that furnish -SH or -SS-, or both, and (ii) by injection of thiourea derivatives several days prior to exposure to these oxidant gases. The mechanism of (i) is believed similar to that proposed for the action of radiation-protective compounds; that of (ii) involves the development of a tolerance initiated by the thiourea against the oxidants.

Administration, Inhalation↗

PubMed2004

Associations between short-term changes in nitrogen dioxide and mortality in Canadian cities.

The association between daily variations in ambient concentrations of nitrogen dioxide (NO2) and mortality was examined in 12 of Canada's largest cities, using a 19-yr time-series analysis (from 1981-1999). The authors employed parametric statistical methods that are not subject to the recently discovered convergence and error estimation problems of generalized additive models. An increase in the 3-d moving average of NO2 concentrations equivalent to the population-weighted study mean of 22.4 ppb was associated with a 2.25% (t = 4.45) increase in the daily nonaccidental mortality rate and was insensitive to adjustment for ozone, sulfur dioxide, carbon monoxide, coefficient of haze, size-fractionated particulate mass, and the sulfate ion measured on an every-6th-day sampling schedule. The 3-d moving average of NO2 was sensitive to adjustment for fine particulate matter measured daily during the 1998-2000 time period.

Aged↗

PubMed1985

The mortality rate from lung metastases in animals inhaling nitrogen dioxide (NO2).

A study was carried out to determine the interrelationship between the inhalation of nitrogen dioxide (0.4 +/- 0.50 ppm), lung metastases development from circulating cancer cells, and death rate from such metastases. C57 BL/6J mice were used in these experiments. Animals were divided into control and NO2-exposed groups, and were exposed to filtered air and 0.4 ppm of NO2, respectively. Following 12 weeks of exposure, all animals were infused intravenously with syngeneic, viable B16 melanoma cells. The results indicate that a subpopulation of NO2-exposed animals showed a significant increase in mortality rate during the early part of the experiment. The interpretation is that animals especially sensitive to the NO2 insult developed extensive metastases at an early stage. The question raised is whether or not the progression of human cancer is influenced by the inhalation of noxious pollutants in the ambient atmosphere.

Air Pollutants↗

PubMed1987

Intermittent exposures to mixed atmospheres of nitrogen dioxide and sulfuric acid: effect on particle clearance from the respiratory region of rabbit lungs.

Nitrogen dioxide (NO2) and sulfuric acid (H2SO4) are important constituents of the gas-particle complex in ambient air. The purpose of this study was to examine the effects of combined exposures upon the clearance of insoluble tracer particles from the respiratory region of the lungs. Rabbits were the animal model, and were exposed for 2 h/day for 14 days to either 0.3 ppm NO2, 1 ppm NO2, or 500 microgram/m3 H2SO4 alone, or to mixtures of the low and high NO2 concentrations with acid. Inhaled singly, both concentrations of NO2 accelerated clearance while H2SO4 retarded it, compared to control. Exposure to the combination of 0.3 ppm NO2 plus H2SO4 resulted in a response which was not different from that due to the acid alone. However, exposure to 1 ppm NO2 plus H2SO4 resulted in a clearance pattern which differed from that of both NO2 and H2SO4, but was more similar to that of the latter.

Aerosols↗

PubMed2005

Effects of nitrogen dioxide on allergic airway responses in subjects with asthma.

OBJECTIVE: We sought to determine whether nitrogen dioxide (NO2) can enhance airway inflammation after allergen challenge in asthmatic subjects. METHODS: Fifteen house-dust-mite (HDM)-sensitive asthmatic subjects were exposed for 3 hours to filtered air or 0.4 ppm NO2, followed by inhalational challenge with HDM allergen. Markers of inflammation were measured in sputum at 6 hours and 26 hours after allergen challenge. RESULTS: After exposure to NO2, eosinophil concentration decreased significantly in the 6-hour postallergen sputum. No significant NO2-related difference was observed for other variables. CONCLUSIONS: Our results suggest that, in most asthmatic individuals, multi-hour exposure to a high ambient concentration of NO2 does not enhance the inflammatory response to subsequent inhaled allergen as assessed by cell distribution in induced sputum. Because the decrease in airway eosinophils has been reported in previous animal studies, future research should be directed toward the mechanism of this effect.

Adult↗

PubMed1981

The UCLA population studies of chronic obstructive respiratory disease. IV. Respiratory effect of long-term exposure to photochemical oxidants, nitrogen dioxide, and sulfates on current and never smokers.

Questionnaires, spirometry, and the single-breath nitrogen test were administered to 3,192 participants 25 to 39 yr of age in area exposed to low concentrations of all pollutants (Lancaster, California) and to 2,369 similar participants living in an area exposed to high concentrations of photochemical oxidants, nitrogen dioxide, and sulfates (Glendora, California). The prevalence of symptoms and results in the majority of the tests were worse in the polluted area between current and never smokers and men and women. Those tests associated primarily with small airways (Vmax50, Vmax75, delta N 2(750-1250) showed little or no difference between areas. The difference in the prevalence of participants with a poor FEV1 and/or poor FEV1 and/or poor FVC and in the mean Vmax and closing volume was greater between areas than between smoking categories. These results suggest that long-term exposure to high concentrations of photochemical oxidants, NO2, and sulfates at place of residence may result in measurable impairment in both current smokers and never smokers. Firmer documentation of this effect will require following these populations for changes in lung function that correlate with pollutant exposures.

Adult↗

PubMedDate not supplied

Does nitrogen dioxide affect inflammatory markers after nasal allergen challenge?

BACKGROUND: Exposure to high ambient levels of nitrogen dioxide (NO2) enhances the bronchial inflammatory reaction to allergen in humans. We tested whether this NO2 effect occurs also in the upper airways. METHODS: Sixteen allergic subjects with rhinitis and mild asthma were exposed at rest to either purified air or 500 microg/m3 NO2 for 30 minutes, followed 4 hours later by a nasal allergen challenge. Nasal lavage was performed before air/NO2 exposure, before allergen challenge, and 1, 4 and 18 hours after allergen challenge. Symptoms were recorded. RESULTS: The percentage of eosinophils and neutrophils, eosinophil cationic protein, and myeloperoxidase were similar after exposure to air + allergen and to NO2 + allergen. We noticed a tendency to increased sneezing the day after exposure to NO2 + allergen. CONCLUSION: The priming effect of an ambient brief NO2 exposure on subsequent allergic response was not noticeable in activation of inflammatory cells and mediators in the upper airways.

Adult↗

PubMed1983

Synergistic effects on rat lungs of mixtures of oxidant air pollutants (ozone or nitrogen dioxide) and respirable aerosols.

A hitherto unexpected synergism between the oxidant air pollutants ozone or nitrogen dioxide and a respirable-sized aerosol of ammonium sulfate was observed during controlled exposures of rats to these substances. Response of rat lungs to these pollutants was quantitated by measurement of apparent collagen synthesis rates in vitro by lung minces from exposed animals. Dose-response curves to either O3 or NO2 were altered in the presence of 5 mg/m3 of (NH4)2SO4 aerosol. Morphometric and histologic observations of lungs from rats exposed to high levels of ozone, with and without concurrent exposure to the (NH4)2SO4 particles, confirmed such synergistic effects. In a separate set of experiments, rats were exposed at near ambient levels to mixtures of ozone and sulfuric acid aerosol (submicron-sized aerosol). Potentiation of ozone effects on lung collagen synthesis rates was also observed in these experiments. These observations may have broad implications for the appropriate evaluation of laboratory data in the setting of ambient air quality standards and/or threshold limit values for occupational safety.

Aerosols↗

PubMed1994

Ozone, but not nitrogen dioxide, fragments elastin and increases its susceptibility to proteolysis.

The effects of ozone (O3) and nitrogen dioxide (NO2) on the solubility and proteolytic susceptibility of elastin were examined to better understand how these oxidant air pollutants might damage the lung. In vitro O3 exposures at pH 7.4 resulted in the complete solubilization of elastin, but NO2 had no effect on solubility. The initial solubilization rate was 65 micrograms/mumol of O3, which increased to 150 micrograms/mumol in the midregion of a sigmoidal solubilization curve. Peptide fragments of the O3-solubilized elastin ranged in size from 5 to 20 kD. The conversion of insoluble elastin into soluble fragments by O3 was not due to the destruction of desmosine crosslinks. The effect of O3 on the proteolytic susceptibility of elastin was measured using insoluble elastin recovered from exposures that resulted in 5.3%, 12.8%, and 26.3% solubilization. Human neutrophil elastase (HNE) digested the remaining insoluble elastin samples 4.3, 6.0, and 9.8 times faster than unexposed elastin. In contrast, NO2-exposed elastin was no more susceptible to digestion by HNE. Ascorbate, EDTA, and uric acid reduced the proteolytic susceptibility of O3-exposed elastin, but mannitol afforded no protection. These findings indicate that the inhalation of O3 may contribute to lung disease by directly damaging elastin and by increasing its susceptibility to proteolysis, whereas NO2 probably damages lungs via alternative mechanisms.

Air Pollutants↗

PubMed1999

Centriacinar remodeling and sustained procollagen gene expression after exposure to ozone and nitrogen dioxide.

Sprague-Dawley rats were exposed to 0.8 ppm ozone (O3), to 14.4 ppm nitrogen dioxide (NO2), or to both gases simultaneously for 6 h per day for up to 90 d. The extent of histopathologic changes within the central acinus of the lungs was compared after 7 or 78 to 90 d of exposure using morphometric analysis by placement of concentric arcs radiating outward from a single reference point at the level of the bronchiole- alveolar duct junction. Lesions in the lungs of rats exposed to the mixture of gases extended approximately twice as far into the acinus as in those exposed to each individual gas. The extent of tissue involvement was the same at 78 to 90 d as noted at 7 d in all exposure groups. At the end of exposure, in situ hybridization for procollagen types I and III demonstrated high levels of messenger RNA within central acini in the lungs of animals exposed to the combination of O3 and NO2. In contrast, animals exposed to each individual gas had a similar pattern of message expression compared with that seen in control animals, although centriacinar histologic changes were still significantly different from control animals. We conclude that the progressive pulmonary fibrosis that occurs in rats exposed to the combination of O3 and NO2 is due to sustained, elevated expression of the genes for procollagen types I and III. This effect at the gene level is correlated with the more severe histologic lesions seen in animals exposed to both O3 and NO2 compared with those exposed to each individual gas. In contrast, the sustained expression of the procollagen genes is not associated with a shift in the distribution of the lesions because the area of change in each group after 7 d of exposure was the same as after 78 to 90 d of exposure.

Animals↗

PubMed1995

Dual effect of nitrogen dioxide on barrier properties of guinea pig tracheobronchial epithelial monolayers cultured in an air interface.

Nitrogen dioxide (NO2) is an oxidant gas that may injure the airway epithelial lining, leading to decrements in barrier and active ion transport properties. The present studies examined alterations of bioelectric properties and solute flux by guinea pig tracheobronchial epithelial (GPTE) monolayers exposed in vitro to NO2. Confluent GPTE monolayers were exposed to NO2 levels between 0.5 and 5 ppm, while controls were exposed to air. Following exposure, monolayers were mounted in Ussing chambers for measurement of transepithelial resistance (Rte) and short-circuit current (SCC). A 1-h exposure to 1 ppm NO2 significantly increased SCC to 131.3 +/- 8.7% of air controls, while Rte with a value of 109.3 +/- 13.8% was unchanged. In contrast, a 1-h exposure to 2 or 5 ppm NO2 significantly decreased Rte to 39.0 +/- 1.6 or 35.5 +/- 7.3% of air controls, respectively, while SCC values of 140.3 +/- 10.4 or 153.3 +/- 8.6%, respectively, were also significantly elevated. A 1-h exposure to 2 or 5 ppm NO2 significantly increased sucrose permeability across GPTE monolayers to 446.8 +/- 117 or 313.3 +/- 39.5% of air controls, respectively, while glycerol permeability was unchanged. In contrast, a 1-h exposure to 1 ppm NO2 produced no alterations of sucrose or glycerol flux. The SCC of control GPTE monolayers (1-h air exposure) consisted of 50% bumetanide-sensitive and 40% amiloride-sensitive current; exposure for 1 h to 2 ppm NO2 led to no changes in the corresponding SCC components. Active ion transport (i.e., SCC) across the airway epithelium was significantly increased after exposure to NO2 levels < or = 1 ppm with no change of paracellular pathways for diffusion, suggesting that this reactive gas alters cell membrane function. The increased SCC may lead to impairment of fluid balance and mucociliary clearance. NO2-mediated tissue injury with levels > or = 2 ppm primarily affects passive airway epithelial barrier functions, probably by altering tight junctions, which could result in increased transepithelial solute and fluid leakage in vivo.

Animals↗