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At least 19 recordsLinked to original sources
PubMed1987

Induction of SOS functions in Escherichia coli and biosynthesis of nitrosamine in rabbits by nitrogen dioxide.

Nitrogen dioxide induced SOS functions in Salmonella typhimurium and Escherichia coli K-12 and was mutagenic in Escherichia coli WP2. When a rabbit was administered aminopyrine intravenously and administered nitrogen dioxide by inhalation, N-nitrosodimethylamine was detected in its blood. Analysis was conducted with 15N-nitrosodimethylamine as an internal standard by a combination of capillary gas chromatography and mass spectrometry. Accompanying administration of cystamine increased the blood concentration of N-nitrosodimethylamine in the rabbit, suggesting inhibition of its metabolism. Concurrent sulfur trioxide inhalation increased N-nitrosodimethylamine formation in the rabbit.

Aminopyrine↗
PubMedDate not supplied

The pathobiochemistry of nitrogen dioxide.

Nitrogen dioxide (*NO2) is an oxidizing free radical which can initiate a variety of destructive pathways in living systems, and several diseases are suspected to be connected with both exogenously and endogenously formed *NO2. Peroxynitrite (ONOO-/ONOOH) is believed to be an important endogenous source of *NO2 radicals, but other sources, among them enzymatically ones, have been identified recently. It also became clear during the last few years that in vivo formation of 3-nitrotyrosine strictly depends on the availability of *NO2 radicals. Since nitrogen dioxide is a very toxic compound an arsenal of antioxidants (e.g. vitamin C, glutathione, vitamin E, and beta-carotene) must eliminate this harmful radical in vivo. Here the recently identified superoxide (O2*-)-dependent formation of peroxynitrate (O2NOO-) and the central role of vitamin C are of special importance.

Animals↗
PubMed1999

[Monitoring and elimination of sulfur dioxide and nitrogen dioxide by passive sampling method].

The concentration of atmospheric pollutants, sulfur dioxide and nitrogen dioxide, were monitored by passive sampler with spectrophotometric determination method. The results were compared with active sampling method. It was found that the two methods got the same results. The adsorption of sulfur dioxide and nitrogen dioxide by sorbent-saturated filter paper was also studied.

Air Pollutants↗
PubMed1999

Inflammatory response in humans exposed to 2.0 ppm nitrogen dioxide.

Nitrogen dioxide (NO2) is a common indoor air pollutant, especially in homes with unvented combustion appliances. Epidemiological studies suggest that children living in homes with unvented heating sources are more prone to respiratory infections than children living in homes with lower levels of NO2. However, experimental studies in which human volunteers were exposed acutely to moderate levels of NO2 (0.5-2.0 ppm) have shown little evidence of lung inflammation or decreased host resistance capacity. In the study reported here, 8 healthy volunteers were exposed to 2.0 ppm NO2 and to filtered air for 4 h while undergoing intermittent moderate exercise. Bronchoalveolar lavage was performed the following morning. The lavage was divided into a predominantly bronchial washing (first 20 ml of lavage; BL) and a predominantly alveolar washing (BAL). In the BL, NO2 exposure caused increases in polymorphonuclear neutrophils (PMNs), interleukin 6 (IL-6), IL-8, alpha1-antitrypsin, and tissue plasminogen activator, and decreases in epithelial cells. In the BAL, there were no NO2-induced changes in either cell numbers or soluble mediators. On the other hand, alveolar macrophages from BAL showed a decrease in the ability to phagocytose unopsonized Candida albicans and a decrease in superoxide production. No difference in susceptibility to virus infection was found between the NO2- and air-exposed macrophages. No changes in lung function were observed, but the aerosol bolus recovery technique revealed a statistically significant (p <.05) decrease in the fraction of aerosol recovered following nitrogen dioxide exposure, which is suggestive of small obstructive changes induced by NO2.

Adolescent↗
PubMedDate not supplied

Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide.

Nitrogen dioxide (NO2) is both edematogenic and cytotoxic to the lung. Preexposure to NO2 protects against mortality from formation of excessive pulmonary edema (tolerance) and, depending on the preexposure schedule, may or may not protect against the cytotoxic effects of NO2 in the lung. Measurement of DNA synthesis in hamster lung was used to study the question of whether the more subtle cytological injury induced by NO2 is mediated by a system that also exhibits tolerance. It was found that when hamsters are preexposed daily to 10 ppm NO2, they develop tolerance for normally lethal concentrations of NO2, are protected against cytological injury from 10 ppm NO2, but are not protected from the cytotoxic effects of NO2 at concentrations greater than 10 ppm. Animals exposed weekly to 10 ppm NO2 are not protected from further cytological injury induced by weekly exposures to 10 ppm NO2, but do develop tolerance for lethal concentrations of NO2. Thus, the data indicate that induction of tolerance to NO2 does not necessarily protect the cell populations of the lung from the cytotoxic effects of NO2.

Animals↗
PubMed1993

Human bronchial epithelial cell dysfunction following in vitro exposure to nitrogen dioxide.

Nitrogen dioxide (NO2), is a major air pollutant, that causes bronchoconstriction and bronchial hyperreactivity, and may also lead to damage and inflammation of the airway epithelium. We have cultured human bronchial epithelial cells and investigated the effect of exposure to NO2, for 20 min on epithelial cell membrane integrity and function in vitro. Epithelial cell membrane damage and permeability were assessed by release of 51Cr from prelabelled cells, and movement of 14C-labelled bovine serum albumin (BSA) across the bronchial epithelial cell monolayers. Ciliary beat frequency (CBF) of the cells was monitored by the analogue contrast enhancement technique, and arachidonic acid (AA) metabolism was investigated by analysis of radiolabelled AA metabolites generated from cultures prelabelled by incubation with [3H]-arachidonic acid. Exposure to 400 and 800 parts per billion (ppb) NO2 significantly increased the release of 51Cr from 0.9 +/- 0.4%, in control cultures exposed to 5% CO2 in air, to 9.7 +/- 3.2% and 13.9 +/- 3.5%, respectively. Similarly, NO2 also significantly increased the movement of 14C-BSA across the epithelial monolayers from 1.3 +/- 0.2%, in control cultures, to 2.7 +/- 0.2%, 3.8 +/- 0.4% and 5.1 +/- 0.5%, respectively, in cultures exposed to 100, 400 and 800 ppb NO2. Although NO2 attenuated the CBF of the cells at all concentrations investigated, this was significant only at the concentration of 2,000 ppb NO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1999

Persistent airway inflammation but accommodated antioxidant and lung function responses after repeated daily exposure to nitrogen dioxide.

Nitrogen dioxide (NO2) is a common indoor and outdoor air pollutant that may induce deterioration of respiratory health. In this study the effects of repeated daily exposure to NO2 on airway antioxidant status, inflammatory cell and mediator responses, and lung function were examined. Healthy nonsmoking subjects were exposed under controlled conditions to air (once) and to 2 ppm of NO2 for 4 h on four consecutive days. Lung function measurements were made before and immediately after the end of each exposure. Bronchoscopy with endobronchial biopsies, bronchial wash (BW), and bronchoalveolar lavage (BAL) was carried out 1.5 h after the air exposure and after the last exposure to NO2. Repeated NO2 exposure resulted in a decrease in neutrophil numbers in the bronchial epithelium. The BW revealed a twofold increase in content of neutrophils (p < 0.05) and a 1.5-fold increase in myeloperoxidase (MPO) (p < 0.01) indicative of both migration and activation of neutrophils in the airways. After the fourth NO2 exposure, antioxidant status of the airway fluid was unchanged. Significant decrements in FEV1 and FVC were found after the first exposure to NO2, but these attenuated with repeated exposures. Together, these data indicate that four sequential exposures to NO2 result in a persistent neutrophilic inflammation in the airways, whereas changes in pulmonary function and airway antioxidants are resolved. We conclude that NO2 is a proinflammatory air pollutant under conditions of repeated exposure.

Adult↗
PubMed1996

Combined exposures of human ciliated cells to different concentrations of sulfur dioxide and nitrogen dioxide.

In the present study we investigated the influence of two common air pollutants, sulfur dioxide (SO2) and nitrogen dioxide (NO2) on ciliary beat frequency (CBF). Ciliated cells were obtained by nose brush from 12 healthy volunteers and placed on a polycarbonate membrane which was in contact with Ringer's electrolyte solution. This allowed the supply of the cells by capillarity in parallel to the reaction of the pollutants with the cell surfaces. In an exposure chamber the cells were exposed for 30 min. at 37 degrees C either to SO2 (2.5-12.5 ppm) or to NO2 (3.0-15.0 ppm), or to a mixture of NO2 (12.0 ppm) and SO2 (2.5 or 5.0 ppm). CBF was measured by video-interference-microscopy. With SO2 we observed a dose-dependent decrease in CBF with Ringer's solution. 2.5 ppm SO2 caused a 42.8% decrease and 12.5 ppm a decline of approximately 100% (8.10 +/- 0.24 Hz vs. 0.28 +/- 0.20 Hz). In parallel, we observed a decrease in the pH-value from 7.4 to 3.6. 30 min. NO2 exposure (3.0-15.0 ppm) induced a significant dose dependent increase in CBF from 8.4 +/- 0.34 Hz to 9.4 +/- 0.44 Hz. Exposure to a mixture of SO2 and NO2 with Ringer's solution revealed that SO2 exerts a stronger influence on CBF than NO2. Exposure to both pollutants resulted in the same as exposure to SO2 alone. Our findings demonstrate a strong correlation between SO2-modified pH values and CBF. Exposure to a combination of two pollutants revealed the dominant influence of SO2 on CBF while the augmented effect of exposure to NO2 alone might be due to the oxidative potential of this gas.

Adult↗
PubMed1987

Effects of sulphur dioxide and nitrogen dioxide, singly and in mixture, on the macroscopic growth of three birch clones.

An investigation of some aspects of the effects of low concentrations of the gases, sulphur dioxide and nitrogen dioxide, singly and in mixture, was made on the growth of three birch clones, two of Betula pendula Roth. (silver birch) and one of Betula pubescens Ehr. (downy birch). Comparative measurements of the growth form and dry mass increment were made over one year in glasshouses supplied with charcoal-filtered ambient air, and SO(2) and NO(2), singly or in mixture, at mean concentrations of 62 ppb (nl litre (-1)) of one or both gases. The main effects were found in those plants that were fumigated with SO(2) singly, and SO(2) and NO(2) together. Both treatments induced premature leaf loss and reduction in mass, especially of roots, the effects increasing over time. The heights and initial leaf areas were maintained, apparently at the expense of other parameters. NO(2), if present singly, had little or no effect, but it tended to enhance the damaging effect of SO(2) when the two were applied together. The different clones showed different degrees of response to the pollutants, but these differences became less marked during the second season of fumigation. The effects found are discussed in relation to the annual growth of trees, particularly birch.

Journal Article↗
PubMed1998

Simultaneous sulfur dioxide and nitrogen dioxide removal by calcium hydroxide and calcium silicate solids.

At conditions typical of a bag filter exposed to a coal-fired flue gas that has been adiabatically cooled with water, calcium hydroxide and calcium silicate solids were exposed to a dilute, humidified gas stream of nitrogen dioxide (NO2) and sulfur dioxide (SO2) in a packed-bed reactor. A prior study found that NO2 reacted readily with surface water of alkaline and non-alkaline solids to produce nitrate, nitrite, and nitric oxide (NO). With SO2 present in the gas stream, NO2 also reacted with S(IV), a product of SO2 removal, on the exterior of an alkaline solid. The oxidation of S(IV) to S(VI) by oxygen reduced the availability of S(IV) and lowered removal of NO2. Subsequent acidification of the sorbent by the removal of NO2 and SO2 facilitated the production of NO. However, the conversion of nitrous acid to sulfur-nitrogen compounds reduced NO production and enhanced SO2 removal. A reactor model based on empirical and semi-empirical rate expressions predicted rates of SO2 removal, NO2 removal, and NO production by calcium silicate solids. Rate expressions from the reactor model were inserted into a second program, which predicted the removal of SO2 and NOx by a continuous process, such as the collection of alkaline solids in a baghouse. The continuous process model, depending upon inlet conditions, predicted 30-40% removal for NOx and 50-90% removal for SO2. These results are relevant to dry scrubbing technology for combined SO2 and NOx removal that first oxidizes NO to NO2 by the addition of methanol into the flue duct.

Air Pollutants, Occupational↗
PubMedDate not supplied

Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide.

Nitrogen idoxide (NO2) is both edematogenic and cytotoxic to the lung. Preexposure to NO2 protects against mortality from formation of excessive pulmonary edema (tolerance) and, depending on the preexposure schedule, may or may not protect against the cytotoxic effects of NO2 in the lung. Measurement of DNA synthesis in hamster lung was used to study the question of whether the more subtle cytological injury induced by NO2 is mediated by a system which also exhibits tolerance. It was found that when hamsters are preexposured daily to 10 ppm NO2, they develop tolerance against normally lethal concentrations of NO2; are protected against further cytological injury from 10 ppmNO2; but are not protected from the cytotoxic effects of NO2 greater than 10 ppm. Animals exposed weekly to 10 ppm NO2 are not protected from further cytotological injury induced byweekly exposures to 10 ppm NO2, but do develop tolerance against lethal concentrations of NO2. Thus the data indicate that induction of tolerance to NO2 does not necessarily protect the cell populations of the lung from the cytotoxic effects of NO2.

Animals↗
PubMed1983

Respiratory effects of two-hour exposure with intermittent exercise to ozone, sulfur dioxide and nitrogen dioxide alone and in combination in normal subjects.

Seven adult male healthy volunteer subjects were exposed to 0.15 ppm each of O3, SO2 and NO2 alone and in combination, with intermittent light exercise for two hours. Three of the 7 subjects developed cough during deep inspiration and one subject had chest pain during exposure to O3 alone. Among the various indices of pulmonary function tests, specific airway conductane (Gaw/Vtg) was the most sensitive index to examine the changes produced by the exposure to O3 and other pollutants. Significant decrease of Gaw/Vtg in comparison with control measurements was observed in 6 of 7 subjects during exposure to O3 alone, and in all subjects during exposures to the mixture of O3 and other pollutants. However, no significant enhancement of effect was observed in the mixture of O3 and other pollutants, although a slightly greater decrease of Gaw/Vtg was observed for the mixture of O3 and other pollutants than for O3 alone.

Adult↗