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PubMed1977

Diffuse alveolar damage in cats induced by nitrogen dioxide or feline calicivirus.

The ultrastructural morphogenesis of pulmonary lesions was studied in cats exposed to either aerosols of feline calicivirus (FCV) or high concentrations of NO2. Both directly injured alveolar lining cells, particularly type I cells. Necrosis of pneumocytes attended by an acute exudative response in the air exchange tissues was evident from 0 through 24 hours after exposure of cats to NO2 and from 12 through 96 hours after infection with FCV. The reparative process following alveolar injury was characterized by regenerative hyperplasia of type II pneumocytes, proliferation of stromal cells, and infiltration of mononuclear cells. Differences in the lesions produced by NO2 and FCV also were encountered. Endothelial necrosis was detected only after NO2 injury, whereas a marked infiltration of neutrophils and immunocytes was observed only after FCV injury. The FCV/NO2 experimental system in cats is well suited for studies of diffuse alveolar damage of toxic and viral etiology.

Animals↗

PubMed1987

Effect of repeated exposures to nitrogen dioxide and sulfuric acid mist alone or in combination on mucociliary clearance from the lungs of rabbits.

The biological response to ambient air pollution may be a function of specific combinations of pollutants. Groups of rabbits were exposed to NO2 (0.3 ppm or 1 ppm) with and without H2SO4 (0.5 mg/m3) for 2 hr/day for up to 14 days for assessment of effects upon mucociliary clearance of tracer particles from the tracheobronchial tree. Exposure to NO2 did not alter clearance, while exposure to H2SO4 produced a retardation toward the middle of the exposure series. The combination of 0.3 ppm NO2 with H2SO4 resulted in a speeding of clearance, while no change from control was seen with the mixture employing 1 ppm NO2 with acid. These results emphasize the importance of performing studies with pollutant mixtures, since it is not always possible to extrapolate responses from studies examining effects of individual pollutants.

Administration, Intranasal↗

PubMedDate not supplied

Effects of vitamin E deficiency and nitrogen dioxide exposure on lung lipid peroxidation: use of lipid epoxides and malonaldehyde as measures of peroxidation.

The effect of vitamin E deficiency in male Sprague-Dawley rats upon lipid peroxidation in lung tissue was examined by measuring malonaldehyde and lipid epoxide production. In addition to controls, some animals were also exposed to 3 +/- 0.1 ppm NO2 continuously for 7 d in order to study the effects of oxidant stress on lung lipid peroxidation and vitamin E content. The observed changes in malonaldehyde and epoxide content could serve as good indices of lipid peroxidation, particularly under conditions of vitamin E deprivation. The responses measured indicated an inverse relation in the lung between tissue vitamin E content and quantity of lipid peroxidation products. Measurement of lipid epoxides served as a reliable indicator of lung tissue lipid peroxidation. Finally, NO2 inhalation appeared to elicit a response characterized by increased assimilation of vitamin E into lung tissue.

Animals↗

PubMed1984

In vivo effect of nitrogen dioxide on the activities of glycolytic enzymes in red blood cells of rats.

The effects of short-term exposure to NO2 on the glycolytic enzymes of rat red cells were examined. Exposure to 10 ppm NO2 resulted in decrease in activities of pyruvate kinase (PK) and phosphofructokinase (PFK) at day 1 and then increased progressively. Exposure to 4 ppm NO2 caused progressive increases in these enzyme activities from the first day. At day 5, the PK and PFK activities of exposed animals became higher than those of controls followed by decreasing to the control level at day 10. Red blood cells were fractionated according to their ages. The specific activities of PK and PFK decreased as red cells became older. 7-day exposure to 4 ppm NO2 resulted in elevation of PK and PFK activities in all red cell subfractions. In addition, the amount of youngest cells decreased concomitant with increases in those of older cells. These findings suggest that NO2 inhalation enhances red cell turnover.

Animals↗

PubMed2000

Levels of nitrogen dioxide in the Zagreb air.

Surveillance of NO2 in Zagreb started in 1994 at five measuring sites. This paper presents the levels and trends of NO2 annual mean values for the period between 1994 and 1998. The obtained data are compared with the recommended and limit values according to the Law on Air Quality Protection in Croatia and the Ordinance on Recommended and Limit Air Quality Values. For the past five years, ever since the measurement commenced, the concentration levels of NO2 in Zagreb have kept between the national recommended and limit values at all measuring sites, indicating that the air has been moderately polluted. This paper also shows the variations of monthly mean values through 1998 at all sites. The levels of NO2 in the northern part of Zagreb were measured at two distances from traffic. Daily variations in the levels were measured near the road and presented as hourly averages for workdays and weekends in winter and in summer reflecting the activity pattern of emission sources.

Air Pollutants↗

PubMed1991

Acute pulmonary effects of nitrogen dioxide exposure during exercise in competitive athletes.

The acute pulmonary responses of athletes after short-term exposure to ambient concentrations of NO2 during heavy exercise have been examined. Intercollegiate male athletes were screened for history of cardiac disease, respiratory disease, allergic conditions and extensive exposure to pollutants. After completion of serum IgE level determination, exercise tolerance test and methacholine challenge test with normal results, nine healthy subjects 18 to 23 years of age were exposed to filtered air and to 0.18 and 0.30 ppm NO2 for 30 min on different days while exercising on a treadmill. Pulmonary function parameters were measured before and after each exposure. In this study, no statistically significant changes were observed in FEV1, RT PEFR, and Vmax50% after exposure to 0.18 and 0.30 ppm NO2. For these selected healthy athletes, short-term exposure to ambient NO2 levels during heavy exercise does not affect adversely the pulmonary function.

Adult↗

PubMed1985

A review of urinary hydroxyproline as a biochemical marker on health effects of smoking and air pollution with nitrogen dioxide.

A series of epidemiologic studies on the health effects caused by smoking and air pollution with NO2 were carried out. Urinary hydroxyproline (HOP) which is excreted into the urine by catabolism of lung collagen was used as a biochemical marker. Urinary HOP of smokers increased dose-dependently with increasing numbers of cigarettes smoked and this result was accepted under blind conditions. Urinary HOP of nonsmokers also increased with increasing the amounts of involuntary smoking caused by smokers in their families although the increases in HOP by passive smoking were less than those by active smoking. Health effects caused by indoor air pollution with NO2 in winter and automobile exhaust in summer were also demonstrated using urinary HOP. The effects of cessation of smoking were followed up for 14 weeks by the decrease in urinary HOP. In practice, the HOP to creatinine ratio (HOP ratio) in random urine samples was used as representative of the 24-hour urine samples. Some confounding factors for urinary HOP were taken into consideration in these studies.

Air Pollution↗

PubMed1981

Mutagenic effects of nitrogen dioxide combined with methylurea and ethylurea in Drosophila melanogaster.

The standard sex-linked recessive lethal test was used to test whether NO2 induces lethal mutations in male germ cells of Drosophila in the presence or absence of alkylureas. Methylurea, ethylurea and NO2 alone did not enhance the mutation frequency significantly. However, highly significant enhancement in the mutation frequency was observed when adult flies were exposed to NO2 (150--280 ppm) for 3 h after ingestion of methylurea (0.1 M) or ethylurea (0.1 M) for 2 days. Oral administration of ethylnitrosourea and also of methylurea or ethylurea that had been exposed to NO2 in vitro were more effective in increasing the mutation frequency than methylurea or ethylurea combined in vivo with NO2. These results suggest that ingested alkylurea is converted in vivo by inhaled NO2 to highly mutagenic nitrosoalkylurea and/or other mutagens. No significant enhancement of the mutation frequency was observed when flies were fed on methylurea solution after they had been exposed to NO2.

Animals↗

PubMed1980

Reaction of hemoglobin with nitric oxide and nitrogen dioxide in mice.

The reaction of hemoglobin with NO and NO2 was compared in mice exposed to these cases. Nitrosyl hemoglobin (NOHb) and methemoglobin (MetHb) were determined simultaneously by electron spin resonance spectrometry at -140 degrees C. In mice exposed to 40 ppm NO, NOHb became constant (0.7%) in 30 min and declined rapidly with a half-life of several minutes when the mice were removed to room air. An increase of MetHb (5%) was also caused by exposure to NO and the time course was almost the same as that of NOHb. Exposure to 40 ppm NO2 produced only NOHb (0.2%); MetHb did not increase. The time course of NOHb was identical to that observed with NO exposure. Dose-effect relationships were determined with both gases at concentrations ranging from 20 to 80 ppm. A linear relationship could be observed between the concentrations of the gases and NOHb, but NO produced more NOHb than did NO2. There was an exponential increase of MetHb, particularly at high concentrations of NO.

Animals↗

PubMed1981

Combined effects of ozone and nitrogen dioxide on respiratory function in man.

Ten young adult males were exposed to either filtered air or 0.50 ppm ozone plus 0.50 ppm NO2 in filtered air under four environmental conditions: 25 degree C, 45 % rh; 30 degrees C, 85% rh; 35 degrees C, 40% rh; and 40 degrees C, 50% rh. There were eight 2-hour exposures per subject. After 1 hour of sitting exposure the subjects exercised for 30 minutes (35-40% predicted maximum capacity) which increased ventilatory exchange to approximately 40 L/min (BTPS). Pulmonary function tests were performed before, during, and after exposure. Metabolism and ventilation were determined during the last 15 minutes of exercise. A symptom questionnaire was completed at the termination of each exposure following reexamination by a physician. There was a decrease in vital capacity, inspiratory capacity, and several flow-related measures of lung function during exposure. The response to exposure to the combined pollutants (O3 and NO2) was similar to that observed in ozone exposures alone. No synergism was observed.

Adult↗

PubMed1977

Stimulation of DNA synthesis in the lungs of hamsters exposed intermittently to nitrogen dioxide.

Stimulation of [3H] thymidine incorporation in the lungs of hamsters exposed singly and repeatedly to 10 ppm NO2 was studied. Within 24 hr of the first exposure to NO2, the response was characterized by a marked increase in [3H] thymidine labeling in the bronchi, bronchioles, and alveolar ducts, but not in the trachea or the peripheral alveoli. If, after the first NO2 exposure, subsequent exposures were repeated daily, no further stimulation of [3H] thymidine incorporation was observed in any part of the respiratory tract. However, if the interval between the first and subsequent exposures was 2-3 days rather than 1 day, stimulation of [3H] thymidine incorporation was observed in the bronchi, bronchioles, and alveolar ducts for up to 21 NO2 exposures. A significantly greater increase in [3H] thymidine incorporation was observed when the interval between subsequent exposures was extended to 7 days. However, no repeated exposure, whether at 2-3 or 7 day intervals, was as effective as the first NO2 exposure in stimulating incorporation of [3H] thymidine.

Animals↗

PubMed1988

Ambient nitrogen dioxide concentrations increase bronchial responsiveness in subjects with mild asthma.

Twenty subjects with mild asthma were exposed at rest in a body plethysmograph, to NO2 at 0, 260, 510 and 1,000 micrograms.m3, for 30 min on four separate days. Bronchial responsiveness (histamine inhalation test) was measured after each exposure session. Airway resistance (Raw), thoracic gas volume (TGV) and specific airway resistance (sRaw) were measured before, during and after exposure, and the breathing pattern was monitored during the whole session. Bronchial responsiveness increased significantly after 30 min exposure to 510 micrograms.m3 NO2 (p less than 0.01). There were also tendencies to an increased bronchial responsiveness after exposure to 260 and 1,000 micron.m3 NO2, but these changes were not statistically significant. Effects on airway resistance and breathing pattern were not demonstrated by exposure to 0-1,000 micrograms.m3 NO2. We conclude that short-term NO2 exposure at about 500 micrograms.m3 slightly affects human bronchial responsiveness in subjects with mild asthma.

Adult↗

PubMed2003

Reaction of cyclic nitroxides with nitrogen dioxide: the intermediacy of the oxoammonium cations.

Piperidine and pyrrolidine nitroxides, such as 2,2,6,6-tetramethylpiperidinoxyl (TPO) and 3-carbamoylproxyl (3-CP), respectively, are cell-permeable stable radicals, which effectively protect cells, tissues, isolated organs, and laboratory animals from radical-induced damage. The kinetics and mechanism of their reactions with .OH, superoxide, and carbon-centered radicals have been extensively studied, but not with .NO2, although the latter is a key intermediate in cellular nitrosative stress. In this research, .NO2 was generated by pulse radiolysis, and its reactions with TPO, 4-OH-TPO, 4-oxo-TPO, and 3-CP were studied by fast kinetic spectroscopy, either directly or by using ferrocyanide or 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonate), which effectively scavenge the product of this reaction, the oxoammonium cation. The rate constants for the reactions of .NO2 with these nitroxides were determined to be (7-8) x 10(8) M(-)(1) s(-)(1), independent of the pH over the range 3.9-10.2. These are among the highest rate constants measured for .NO2 and are close to that of the reaction of .NO2 with .NO, that is, 1.1 x 10(9) M(-1) s(-1). The hydroxylamines TPO-H and 4-OH-TPO-H are less reactive toward .NO2, and an upper limit for the rate constant for these reactions was estimated to be 1 x 10(5) M(-1) s(-1). The kinetics results demonstrate that the reaction of nitroxides with .NO2 proceeds via an inner-sphere electron-transfer mechanism to form the respective oxoammonium cation, which is reduced back to the nitroxide through the oxidation of nitrite to .NO2. Hence, the nitroxide slows down the decomposition of .NO2 into nitrite and nitrate and could serve as a reservoir of .NO2 unless the respective oxoammonium is rapidly scavenged by other reductant. This mechanism can contribute toward the protective effect of nitroxides against reactive nitrogen-derived species, although the oxoammonium cations themselves might oxidize essential cellular targets if they are not scavenged by common biological reductants, such as thiols.

Benzothiazoles↗

PubMed1983

Effects of acute nitrogen dioxide exposure on cellular immunity after lung immunization.

The effects of acute NO2 exposure on antigen-specific cell-mediated lung immunity in Fischer 344 rats were evaluated. Animals were exposed for 24 hr to either room air or 5, 10, or 26 ppm NO2 before intratracheal immunization with 10(8) sheep red blood cells (SRBC). Cellular immunity was evaluated by antigen-specific lymphocyte stimulation assays of pooled lymphoid cell suspensions from either the thoracic lymph nodes or spleens. Elevated cellular immunity was observed after exposure to NO2. The ability of the 26 ppm NO2 exposure to increase cellular immunity seemed to parallel, and in some cases even exceed, that seen in control animals immunized with SRBC mixed with 2 X 10(7) heat-killed Bacillus Calmette-Guerin. These results support the theory that lung damage, and/or alterations of regulatory populations of immune cells, induced by agents such as NO2 can be responsible for the production of abnormally elevated immune responses to antigens deposited in the damaged lung.

Animals↗

PubMedDate not supplied

[Preliminary analysis of indoor pollution from nitrogen dioxide in an area of Northern Italy].

OBJECTIVE: The aims of this work are to describe the annual mean concentration of NO2 and to identify the home features and "habits" of its occupants related to NO2 levels. Both indoor and outdoor NO2 concentrations were measured in 114 dwellings in Pavia (Northern Italy). DESIGN: The study is in the frame of European Community Respiratory Health Survey II. Data were collected in the period 2001-2002 during home visits by trained fieldworkers. PARTICIPANTS: 116 subjects gave the consent to home visits. MAIN OUTCOME MEASURE: NO2 concentration measured using passive samplers. RESULTS: Indoor NO2 concentration is in average 47.1 microg/m3 (+/- 24.5 microg/m3) and outdoor NO2 concentration is 44.3 microg/m3 (+/- 14.5 microg/m3). The gas oven is the only domestic gas appliance associate with high levels of NO2 when measuring in homes. The outdoor pollution affects NO2 indoor concentrations and contribute to store NO2 in homes. CONCLUSION: the study is the first step in the evaluation of NO2 exposure effect on respiratory health.

Adult↗

PubMed1985

Personal exposure to nitrogen dioxide and its relation to indoor and outdoor air quality.

An estimating equation of annual geometric average of personal NO2 exposure was proposed. The average could be calculated from three variables, that is, personal NO2 exposures in one winter and one summer month and ratio of winter period in a year. Ten housewives living in Suginami Ward, a residential area in Tokyo, were chosen as subjects of this study. They were asked to measure daily averages of the personal NO2 exposures with a filter badge. Measurements were performed on consecutive seven days in every month from January to December of 1982 for a total of 84 samples per person. Their activities, the amount of fuel consumption and other living conditions were recorded at the same time. Outdoor NO2 concentrations and maximum, minimum and average temperatures were also measured at the center of their living area. The personal NO2 exposure and its seasonal variation were found to depend mainly on the type of space heaters, frequency of ventilation fan usage in a kitchen, and the amount of fuel consumption.

Air Pollutants↗

PubMed1986

Inhibitory effect of alpha-tocopherol on the formation of nitrosomorpholine in mice treated with morpholine and exposed to nitrogen dioxide.

The possibility that alpha-tocopherol (vitamin E) inhibits the formation of nitrosomorpholine (NMOR) in vivo was investigated in mice orally pretreated with alpha-tocopherol (2.5-100 mg/kg body wt) once daily for 6 days. Twenty-four hours later, the animals were injected i.p. with 2 mg of morpholine (MOR) per animal followed by exposure to 47 p.p.m. of NO2 for 2 h. Under these conditions, low oral doses of alpha-tocopherol (2.5-5 mg/kg body wt) significantly decreased NMOR formation in vivo. As total body alpha-tocopherol levels increased, in vivo NMOR formation decreased, and a maximal 50-70% inhibition of NMOR formation occurred at alpha-tocopherol levels of 5 micrograms/g body wt. Additional results showed that NMOR was rapidly eliminated in mice, so that studies which measure the levels of NMOR found in animals treated with MOR and then exposed to NO2 may underestimate the amount of NMOR that is actually formed. Finally, oral pretreatment of up to 100 mg of alpha-tocopherol/kg body wt had no effect on NMOR elimination.

Animals↗

PubMed1985

[Effect of chronic exposure to nitrogen dioxide on biogenic amine levels in the brain of guinea pigs].

The experiment was carried out on male guinea pigs exposed to NO2 at a constant concentration of 0.1 ppm 24 h daily for 1, 2.5 and 6 months, or NO2 concentration was increased to 0.5 ppm twice daily, between 7:00 and 8:00 AM and 4:00 and 5:00 PM. After the exposure to NO2 was over the animals were killed by decapitation. The cranium was opened and the brain removed, and afterwards at 0 degrees C the left hemisphere was dissected into discrete areas which were then frozen on dry ice and weighed. The tissues were kept for 2-3 days at -20 degrees C, and afterwards the content of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindole-acetic acid was estimated spectrofluorometrically in examined parts of the brain (thalamus--hypothalamus pons + medulla oblongata hippocampus, cortex frontalis). It was shown that the applied NO2 concentrations brought about slight and nonspecific alterations in the content of the investigated amines in guinea pigs' brain.

Air Pollutants↗