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PubMed2006

Short-term effects of nitrogen dioxide on mortality: an analysis within the APHEA project.

The short-term effects of nitrogen dioxide (NO(2)) on total, cardiovascular and respiratory mortality in 30 European cities participating in the Air Pollution on Health: a European Approach (APHEA)-2 project were investigated. The association was examined using hierarchical models implemented in two stages. In the first stage, data from each city were analysed separately, whereas in the second stage, the city-specific air pollution estimates were regressed on city-specific covariates to obtain overall estimates and to explore sources of possible heterogeneity. A significant association of NO(2) with total, cardiovascular and respiratory mortality was found, with stronger effects on cause-specific mortality. There was evidence of confounding in respiratory mortality with black smoke and sulphur dioxide. The effect of NO(2) on total and cardiovascular mortality was observed mainly in western and southern European cities, and was larger when smoking prevalence was lower and household gas consumption was higher. The effect of NO(2) on respiratory mortality was higher in cities with a larger proportion of elderly persons in the population and higher levels of particulate matter with a 50% cut-off aerodynamic diameter of 10 mum. The results of this large study are consistent with an independent effect of nitrogen dioxide on mortality, but the role of nitrogen dioxide as a surrogate of other unmeasured pollutants cannot be completely ruled out.

Air Pollutants↗
PubMed2006

Housing characteristics and indoor concentrations of nitrogen dioxide and formaldehyde in Quebec City, Canada.

Concentrations of nitrogen dioxide and formaldehyde were determined in a study of 96 homes in Quebec City, Canada, between January and April 2005. In addition, relative humidity, temperature, and air change rates were measured in homes, and housing characteristics were documented through a questionnaire to occupants. Half of the homes had ventilation rates below 7.5 L/s person. Nitrogen dioxide (NO2) and formaldehyde concentrations ranged from 3.3 to 29.1 microg/m3 (geometric mean 8.3 microg/m3) and from 9.6 to 90.0 microg/m3 (geometric mean of 29.5 microg/m3), respectively. The housing characteristics documented in the study explained approximately half of the variance of NO2 and formaldehyde. NO2 concentrations in homes were positively correlated with air change rates (indicating a significant contribution of outdoor sources to indoor levels) and were significantly elevated in homes equipped with gas stoves and, to a lesser extent, in homes with gas heating systems. Formaldehyde concentrations were negatively correlated with air change rates and were significantly elevated in homes heated by electrical systems, in those with new wooden or melamine furniture purchased in the previous 12 months, and in those where painting or varnishing had been done in the sampled room in the previous 12 months. Results did not indicate any significant contribution of indoor combustion sources, including wood-burning appliances, to indoor levels of formaldehyde. These results suggest that formaldehyde concentrations in Quebec City homes are caused primarily by off-gassing, and that increasing air change rates in homes could reduce exposure to this compound. More generally, our findings confirm the influence of housing characteristics on indoor concentrations of NO2 and formaldehyde.

Air Movements↗
PubMed1993

Failure of ozone and nitrogen dioxide to enhance lung tumor development in hamsters.

We tested the hypothesis that the two common oxidant air pollutants, ozone and nitrogen dioxide, modulate the development of respiratory tract tumors in Syrian golden hamsters. The animals received subcutaneous injections of the carcinogen diethylnitrosamine (20 mg/kg) twice a week while being exposed continuously to an atmosphere of 0.8 parts per million (ppm)* of ozone or 15 ppm of nitrogen dioxide. Animals were killed 16 weeks or 24 to 32 weeks after the beginning of the treatment. Ozone delayed the appearance of tracheal tumors and reduced the incidence of tumors in the lung periphery. A suspected neuroendocrine differentiation of those lung tumors could not be established by immunocytochemistry due to overfixation of tissues. On the other hand, ozone seemed to mitigate development of hepatotoxic lesions mediated by diethylnitrosamine. In animals treated with diethylnitrosamine and exposed to nitrogen dioxide, fewer tracheal tumors and no lung tumors were found. Only a few lung tumors were produced in animals treated with diethylnitrosamine and kept in an atmosphere of 65% oxygen. The previously observed neuroendocrine nature of tumors induced by simultaneous exposure to diethylnitrosamine and hyperoxia could not be established because the long fixation of tissues precluded immunocytochemical stains. Animals treated with diethylnitrosamine and kept in filtered air while being housed in wire-mesh cages developed fewer lung tumors than animals given the same treatment and kept on conventional bedding in shoebox cages. Although all inhalants tested are known to produce substantial cell proliferation in the respiratory tract, it was not possible to document whether this would enhance lung tumor development. The role of the two common air pollutants, ozone and nitrogen dioxide, as possible additional risks in the pathogenesis of lung cancer in animals continues to remain uncertain.

Animals↗
PubMed2000

Effect of serial-day exposure to nitrogen dioxide on airway and blood leukocytes and lymphocyte subsets.

Nitrogen dioxide (NO2) is a free radical-producing oxidant gas. Inhalation of NO2 could cause airway inflammation, and decrease immune function. This experiment tested the hypothesis that exposure to NO2 would: 1) increase leukocytes in bronchoalveolar lavage (BAL); and 2) change the distribution of lymphocyte subsets and activation in BAL and peripheral blood (PB). Using a counter-balanced, repeated-measures design, 15 healthy volunteers were exposed to filtered air (FA) or 2.0 parts per million NO2 for 4 h x day(-1) (4 x 30 min of exercise), for three consecutive days. Bronchoscopy was performed 18 h following each exposure set, and PB was drawn pre-exposure and pre-bronchoscopy. Flow cytometry was used to enumerate lymphocyte subsets and activation makers in BAL and PB. In the bronchial fraction, there was an increase in the percentage of neutrophils following NO2 exposure compared to FA (median (interquartile range): 10.6 (4.8-17.2)% versus 5.3 (2.5-8.3)%; p=0.005). In the BAL, there was a decrease in the percentage of T-helper cells following NO2 exposure compared to FA (55.9 (40.8-62.7)% versus 61.6 (52.6-65.2)%; p=0.022). For PB, there were no between-condition differences in any leukocyte or lymphocyte subsets, or activation. In conclusion exposure to nitrogen dioxide results in bronchial inflammation and a minimal change in bronchoalveolar lavage T-helper cells, and no changes in peripheral blood cells.

Adult↗
PubMed2006

Theoretical mechanistic study on the radical-radical reaction of ketenyl with nitrogen dioxide.

The radical-radical reaction between the ketenyl radical (HCCO) and nitrogen dioxide (NO(2)) played a very important role in atmospheric and combustion chemistry. Motivated by recent laboratory characterization about the reaction kinetics of ketenyl radical with nitrogen dioxide, in this contribution, we applied the coupled cluster and density functional theory to explore the mechanism of the title reaction. These calculations indicate that the title reaction proceeds mostly through singlet pathways, less go through triplet pathways. It is found that the HCCO + NO(2) reaction initially favors formation of adduct OCCHNO(2) (1) with no barrier. Subsequently, starting from isomer 1, the most feasible pathway is ring closure of 1 to isomer O-cCCHN(O)O (2) followed by CO(2) extrusion to product HCNO + CO(2) (P(1)), which is the major product with predominant yields. Much less competitively, 1 can take the successive 1,3-H- and 1,3-OH-shift interconversion to isomer OCCNOHO (3(a), 3(b), 3(c)) and then to isomer OCOHCNO (4(a), 4(b)), which can finally take a concerted H-shift and C-C bond fission to give HCNO + CO(2) (P(1)). The least competitive pathway is the ring-closure of isomer 3(a) to form isomer O-cCCN(OH)O (5(a), 5(b)) followed by dissociation to HONC + CO(2) (P(2)) through the direct side CO(2) elimination. Because the intermediates and transition states involved in the most favorable channel all lie below the reactants, the title reaction is expected to be rapid, as is confirmed by experiment. Therefore, it can be significant for elimination of nitrogen dioxide pollutants. The present results can lead us to a deep understanding of the mechanism of the title reaction and can be helpful for understanding NO(x)-combustion chemistry.

Journal Article↗
PubMed1980

Role of nitrogen dioxide in the biosynthesis of nitraosamines in mice.

Groups of three to four mice were gavaged with aqueous solutions of 2 milligrams of morpholine, after which they were exposed to nitrogen dioxide in inhalation chambers at concentrations of 0.2 to 50 parts per million for up to 4 hours. At sequential intervals during the exposure, mice were frozen and pulverized in liquid nitrogen, and the mice powder was extracted with ice-cold 35 percent aqueous methanol and dichloromethane; organic-phase concentrates were analyzed for N-nitrosomorpholine with a thermal energy analyzer interfaced to a gas chromatograph. The N-nitrosomorpholine yields, ranging up to about 2.3 micrograms per mouse, were time-dependent relative to the duration of exposure to nitrogen dioxide and dose-dependent relative to the concentrations of nitrogen dioxide; control levels (in mice that were gavaged with morpholine or distilled water and then exposed to air instead of nitrogen dioxide) were less than 5 nanograms per mouse. These preliminary studies demonstrate the in vivo nitrosating potential of nitrogen oxides.

Amines↗
PubMed1993

Further studies on the effect of nitrogen dioxide on mast cells: the effect of the metabolite, nitrite.

To evaluate the relationship between atmospheric nitrogen dioxide exposure and the development of allergic diseases, the effects of nitrite as a chemical product of inhaled nitrogen dioxide on mast cell functions were investigated. We have studied nitrite-induced histamine release from two functionally distinct mast cell populations, namely peritoneal mast cells (PMC) and intestinal mucosal mast cells (IMMC) of Nippostrongylus brasiliensis-infected rats. High concentrations of nitrite alone (10, 20, and 50 mM) induced histamine release from IMMC, but not from PMC. Moreover, histamine release from PMC and IMMC stimulated with sensitizing antigen was significantly enhanced by pretreatment with 50 mM nitrite or nitrate. No differences in histamine release from nitrite-treated and control PMC were seen below 1 mM. To investigate the effect of nitrite on tumor cell cytotoxic activity, PMC were incubated with various concentrations of nitrite. Pretreatment with 5 and 50 mM nitrite markedly depressed tumor necrosis factor (TNF)-alpha-dependent natural cytotoxicity of PMC for the tumor target WEHI-164. Thus, high concentrations of nitrite enhanced mast cell histamine release, but depressed TNF-alpha-dependent cytotoxicity. However, low concentrations of nitrite (< 1 mM) that would normally be produced by short-term atmospheric exposure to nitrogen dioxide may have no significant effects on mast cell functions.

Animals↗
PubMed2005

Exploration of gas sensing possibilities with edge plane pyrolytic graphite electrodes: nitrogen dioxide detection.

The voltammetric response of nitrogen dioxide in aqueous sulfuric acid using an edge plane pyrolytic graphite electrode has been explored and contrasted with that from basal plane pyrolytic graphite, glassy carbon or boron-doped diamond electrodes. Edge plane graphite electrode is found to produce an excellent voltammetric signal in comparison with other carbon-based electrodes exhibiting a well-defined analytically useful voltammetric redox couple in 2.5 M sulfuric acid which is absent on the alternative electrodes.

Electrochemistry↗
PubMed1989

Responses of susceptible subpopulations to nitrogen dioxide.

This project was undertaken to investigate symptom responses and changes in the pulmonary function of two susceptible groups--people with asthma and people with chronic obstructive pulmonary disease (COPD)--when exposed to 0.3 parts per million (ppm) (560 micrograms/m3) nitrogen dioxide. In these controlled clinical studies, a double-blind crossover design with purified air in a 45-m3 environmental chamber was used. Groups of non-respiratory-impaired (normal) subjects of a comparable age range and of both genders constituted controls for the asthmatic and COPD groups. The exposure protocol required five days: day 1, training and base-line preexposure measurements; day 2, a first exposure to 0.3 ppm nitrogen dioxide or air in a randomized sequence; day 3, 24-hour follow-up measurements of possible delayed effects; day 4, a second exposure; and day 5, a second 24-hour postexposure follow-up. All four-hour exposures included several predetermined periods of exercise and pulmonary function measurements. To examine changes in bronchial responsiveness and to aid in subject selection, bronchial challenges with carbachol and isoproterenol aerosol were used. The project was undertaken in four phases, each lasting approximately one year. In the first year, 20 normal non-smoking volunteers (10 women and 10 men) with an average age of 31.0 years were assessed. The second year, 20 non-smoking subjects with mild to moderate asthma were evaluated. This group was comparable in gender and age to the control group of normal volunteers. The third year, 20 subjects with COPD were studied. This group had a mean age of 60.0 years and consisted of 13 men and seven women. All subjects had a history of smoking. During the fourth and final year of the study, a group of 20 elderly normal volunteers similar in age and gender to the COPD group were evaluated. The main findings of the study were as follows. No significant symptomatic or physiologic responses to nitrogen dioxide could be detected in either the young or the elderly control group. Prior studies of asthmatic subjects had led us to hypothesize that 0.3 ppm nitrogen dioxide is close to the minimum level needed to produce significant functional deficits during moderate activity in this susceptible group. However, in this study the asthmatic group as a whole did not manifest significant reductions in lung function after exposure to 0.3 ppm nitrogen dioxide compared to their preexposure base-line data or to their responses after a comparable four-hour exposure to air.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

Nitrogen dioxide and respiratory illnesses in infants.

Nitrogen dioxide is an oxidant gas that contaminates outdoor air and indoor air in homes with unvented gas appliances. A prospective cohort study was carried out to test the hypothesis that residential exposure to NO2 increases incidence and severity of respiratory illnesses during the first 18 months of life. A cohort of 1,205 healthy infants from homes without smokers was enrolled. The daily occurrence of respiratory symptoms and illnesses was reported by the mothers every 2 wk. Illnesses with wheezing or wet cough were classified as lower respiratory tract. Indoor NO2 concentrations were serially measured with passive samplers place in the subjects' bedrooms. In stratified analyses, illness incidence rates did not consistently increase with exposure to NO2 or stove type. In multivariate analyses that adjusted for potential confounding factors, odds ratios were not significantly elevated for current or lagged NO2 exposures, or stove type. Illness duration, a measure of illness severity, was not associated with NO2 exposure. The findings can be extended to homes with gas stoves in regions of the United States where the outdoor air is not heavily polluted by NO2.

Air Pollutants↗
PubMed1988

The pathophysiology of enhanced susceptibility to murine cytomegalovirus respiratory infection during short-term exposure to 5 ppm nitrogen dioxide.

To determine whether exposure to nitrogen dioxide (NO2) affects respiratory tract susceptibility to viral infection, CD-1 mice were inoculated intratracheally with murine cytomegalovirus (MCMV) during exposure to varying concentrations of NO2. Exposure lasted for 6 h per day; it began 2 consecutive days prior to instillation of MCMV and continued for 4 days after virus inoculation. Exposure to 5 ppm NO2 resulted in MCMV proliferation and a mild bronchopneumonia in some animals inoculated with 10(2) plaque-forming units of virus. Importantly, this inoculum was too low to produce either viral replication or histologic abnormalities in the lungs of air-exposed animals. We also found that the amount of virus required to infect animals exposed to 5 ppm of NO2 was 100-fold lower than that needed to consistently produce infection in air-exposed animals. Animals exposed to 5 ppm NO2 also exhibited depressed phagocytosis of colloidal Au198 in vivo as well as diminished macrophage destruction of instilled MCMV compared to air-exposed animals. These results demonstrate that exposure to 5 ppm NO2, although not associated with evidence of overt lung injury per se, is nevertheless capable of predisposing the lower respiratory tract to viral infection.

Animals↗
PubMed1991

Plasma membrane-specific phospholipase A1 activation by nitrogen dioxide in pulmonary artery endothelial cells.

Nitrogen dioxide (NO2), an environmental oxidant, alters the plasma membrane structure and function of pulmonary artery endothelial cells through peroxidative injury. Because perioxidative injury can activate membrane phospholipases and alter phospholipid composition of membranes, we evaluated the effects of NO2 exposure on phospholipase A1 (PLA1), phospholipase A2 (PLA2), and diacylglycerol lipase (DG lipase) activities in pulmonary artery endothelial cell plasma, mitochondrial, and microsomal membranes. We also evaluated the effect of NO2 exposure on the phospholipid composition of plasma membranes of these cells. Exposure to 5 ppm NO2 for 48 hr resulted in a significant (p less than 0.01) increase in PLA1 activity in plasma membranes but not in mitochondrial or microsomal membranes of pulmonary artery endothelial cells, whereas PLA2 and DG lipase activities were comparable to controls in all membranes. As a result of PLA1 activation, the total phospholipid content of the plasma membranes of NO2-exposed cells was significantly (p less than 0.01) reduced compared to controls. Phosphatidylethanolamine (PE) content was reduced (p less than 0.05), whereas lyso-PE (LPE), a product of PLA1 hydrolysis of PE, as well as phosphatidylserine (PS) contents were increased (p less than 0.01 for both LPE and PS) in the plasma membranes of NO2-exposed cells. Incorporation of exogenous PS into pulmonary artery endothelial cells mimicked the stimulatory effect of NO2 on PLA1 activity. These results demonstrate that NO2 specifically reacts with the plasma membrane component of pulmonary artery endothelial cells, causing specific activation of PLA1. The NO2-induced increase of PS in the plasma membranes appears to be responsible for the specific activation of PLA1 in pulmonary artery endothelial cells.

Animals↗
PubMed2005

Nitrogen dioxide increases cardiorespiratory admissions in Torrelavega (Spain).

The objective of the study reported here was to analyze relationships between levels of air pollutants and emergency admissions for cardiorespiratory disease. Admission data from January 1, 1992, to December 31, 1995, were obtained from the Marques de Valdecilla University Hospital Admission Service; meteorological data (rainfall, temperatures wind speed, wind direction) were obtained from the National Meteorology Institute in Santander. Pollutant data on sulfur dioxide (SO2), hydrogen sulfide (H2S), total suspended particles (TSP), nitrogen oxide (NO), and nitrogen dioxide (NO2) were provided by the secretary of environment for the Cantabrian Regional Government. Rate ratios were estimated for each pollutant by Poisson regression; they were adjusted for meteorological variables. It was found that elevated NO2 increased by 20 percent the risk of having an admission for cardiorespiratory diseases; this effect was mainly due to respiratory diseases (rate ratio = 1.7, p < .001) and was negligible for cardiac diseases (rate ratio = 1.1, p = .28). In the one-pollutant model, elevated particulates and nitrogen monoxide were also related to admissions, but this effect disappeared when a five-pollutant model was used (p = .21 and p = 0.36, respectively. SO2 and SH2 did not show any relationship with admissions. Thus, nitrogen dioxide was the only pollutant the authors found to be related to emergency admissions for cardiorespiratory diseases. It is difficult to generalize from these results because of the small number of daily admissions and the variability in pollutant levels; therefore, more studies are necessary to improve knowledge about the relationship between air pollution and health in small towns.

Air Pollutants↗
PubMedDate not supplied

Studies on the effect of long-term exposure to nitrogen dioxide on serum and liver proteins level and enzyme activity in guinea pigs.

Forty male guinea pigs were exposed to nitrogen dioxide in a concentration of 2 mg/m3, 8 hours daily for a period of 180 days. Forty male animals were used as a control group. The following changes were found in intoxicated animals: the decrease of total protein and seromucoid concentration in blood serum and the decrease of total protein, perchloric acid-soluble proteins, protein-bound hexosamines and sialic acids content, in liver tissue. Electrophoretic examination of the serum proteins showed the increase of alpha 1- and beta 2-globulins and the decrease of albumin concentration. Changes in the level of glycoproteins fractions and protein-bound carbohydrates in blood serum were described also. Estimation of enzymes activity showed the decrease of alanine and aspartate transaminase activity in blood serum caused by the strong decrease of the cytoplasmic fraction of these enzymes. However the simultaneous increase of the mitochondrial fraction of transaminases activity was observed. The decrease of the activity of choline esterase was found also. Similar changes of enzymes activity were found in liver tissue. Histopathological studies were done for the further clearing the influenze of nitrogen dioxide on serum and liver proteins concentration and enzymes activity. It was found that after long-term exposure to nitrogen dioxide the destruction processes may be observed in the liver. The possible mechanism of the nitrogen dioxide-induced damage of protein metabolism is discussed.

Alanine Transaminase↗
PubMed1965

Nitrogen dioxide fixation in bacterial chromatin studies.

Eller, Charles (St. John's University, Jamaica, N.Y.), and William H. Beckert. Nitrogen dioxide fixation in bacterial chromatin studies. J. Bacteriol. 90:1710-1712. 1965.-Satisfactory chromatin staining was obtained with two Bacillus species when nitrogen dioxide was used for fixation in conjunction with either the acid Giemsa or Feulgen staining methods. An impression method was employed for the transfer of bacilli to a new environment as well as for smears. Advantages of nitrogen dioxide fixation are discussed.

Bacillus↗
PubMed1986

Inhalation of 0.30 ppm nitrogen dioxide potentiates exercise-induced bronchospasm in asthmatics.

Epidemiologic studies support an association among elevated levels of nitrogen dioxide (NO2), increased respiratory symptoms, and alterations in lung function. To determine if low level NO2 inhalation potentiates exercise-induced bronchospasm, 15 asthmatic subjects, defined by airway constriction with cold air provocation, inhaled 0.30 ppm (560 micrograms/m3) NO2 for 30 min. All asthmatics inhaled either air or 0.30 ppm NO2 via a mouthpiece for 20 min at rest followed by 10 min of exercise on a bicycle ergometer at a workload of 300 kpm/min, producing a 3-fold or greater increase in minute ventilation. Our studies showed 72 +/- 2 (SE)% deposition of inhaled NO2 at rest and 87 +/- 1% deposition with exercise (p less than 0.001). Nitrogen dioxide inhalation at rest resulted in no significant change in pulmonary function. Nitrogen dioxide inhalation plus exercise compared to control (air) exposure plus exercise produced significantly greater reductions in FEV (p less than 0.01) and partial expiratory flow rates at 60% of total lung capacity (p less than 0.05). One hour after completion of NO2 exposure and exercise, pulmonary function had returned to baseline values. To determine if NO2 exposure caused increased reactivity to a known bronchoconstrictor, asthmatic subjects inhaled cold air (range: -11 +/- 2 degrees C) at 3 successive rates of isocapnic ventilation. The response to cold air was expressed as the respiratory heat exchange required to reduce the FEV by 10% (PD10RHE). Prior NO2 exposure potentiated the fall in FEV, PD10RHE, and specific airway conductance (p less than 0.05) after isocapnic cold air hyperventilation, compared to the control exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Nitrogen dioxide and carbonate radical anion: two emerging radicals in biology.

Nitrogen dioxide and carbonate radical anion have received sporadic attention thus far from biological investigators. However, accumulating data on the biochemical reactions of nitric oxide and its derived oxidants suggest that these radicals may play a role in various pathophysiological processes. These potential roles are also indicated by recent studies on the high efficiency of urate and nitroxides in protecting cells and whole animals against the injury associated with conditions of excessive nitric oxide production. The high protective effects of these antioxidants are incompletely defined at the mechanistic level but some of them can be explained by their efficiency in scavenging peroxynitrite-derived radicals, particularly nitrogen dioxide and carbonate radical anion. In this review, we provide a framework for this hypothesis and discuss the potential sources and properties of these radicals that are likely to become increasingly recognized as important mediators of biological processes.

Carbonates↗