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PubMed1998

Does beta-carotene protect membrane lipids from nitrogen dioxide?

Lipid peroxidation in rat liver microsomes, induced by nitrogen dioxide (NO2), a free radical toxin, was examined in the absence and in the presence of varying concentrations of beta-carotene. The extent of peroxidation was assayed by determining the malonaldehyde formed as thiobarbituric acid reactive substances (TBARS). When the concentration of beta-carotene was 13.8 and 43.1 nmol/mg protein, no protection was seen, rather an increase of 10% and 30%, respectively, in TBARS was observed as compared with the normal microsomes containing no beta-carotene. However, at beta-carotene concentrations of 66.5 and 89.4 nmol/mg protein, only a marginal increase of 9% and 4% in TBARS, respectively, was observed. The amount of beta-carotene consumed during peroxidation, determined by following the absorbance at 450 nm, was found to increase linearly with increased exposure to NO2. The direct reaction of NO2 with beta-carotene was studied in an inert organic solvent, acetonitrile, by following the absorption spectrum of beta-carotene in the wavelength region 220-600 nm. The rate of loss of beta-carotene was found to be much faster than that in microsomes. The results suggest that in in vitro systems, the reaction of secondary lipid-derived radicals with beta-carotene and their relative competition for NO2 plays an important role in the actual function of beta-carotene as a prooxidant or an antioxidant. Another lipid soluble antioxidant, alpha-tocopherol (vitamin-E), showed significant protection against NO2-induced lipid peroxidation at a concentration of 45 nmol/mg protein under these conditions.

Animals↗
PubMed1982

Biochemical studies on strain differences of mice in the susceptibility to nitrogen dioxide.

Strain differences of mice in their susceptibility to nitrogen dioxide (NO2) were examined by measuring the activities of antioxidative protective enzymes, and the amounts of antioxidants and lipid peroxides in lungs. Four strains of mice: ICR, BALB/c, ddy and C57BL/6 were used in this study and their LC50 values after exposure to NO2 for 16 hr were: 38, 49, 51 and 64 ppm, respectively (1). Genetic strain differences were observed in the enzyme activities, the antioxidant contents and lipid peroxide contents among these four different strains. The activities of glutathione peroxidase (GPX), glutathione S-transferase, and superoxide dismutase (SOD), and the contents of non-protein sulfhydryls (NPSH), alpha-tocopherol (alpha-Toc) and total lipids in lungs of the four strains were related to their LC50, while TBA reactants in lungs of the four strains were inversely related to their LC50. After exposure to 20 ppm NO2 for 16 hr, the activities of the protective enzymes and the contents of NPSH decreased, while the level of alpha-Toc increased markedly. The activities of GPX, 6-phosphogluconate dehydrogenase, SOD and disulfide reductase, and the contents of NPSH, alpha-Toc and total lipids were also related to their LC50. On the other hand, TBA reactants increased higher than those of the control groups and were inversely related to their LC50. These results suggest that the protective enzymes and the antioxidants are important factors at defence mechanism in lungs to NO2 and that the intensity of the protective systems in pigmented strains is generally greater than that in albino strains.

Animals↗
PubMed1999

Effect of nitrogen dioxide on respiratory viral infection in airway epithelial cells.

Nitrogen dioxide (NO(2)) is a common air pollutant outdoors and indoors in homes with unvented combustion sources. It is also a constituent of tobacco smoke. Epidemiological studies suggest that children exposed to NO(2), or living with smoking parents, have an increased incidence of respiratory viral infections. The most common virus causing severe respiratory symptoms in infants and young children is respiratory syncytial virus (RSV). In the present study we investigated whether NO(2) exposure affects RSV infection in airway epithelial cells, the host cells for viral replication and virus-induced cytokine production. Cultures of the bronchial epithelial cell line BEAS-2B exposed to 0.5, 1.0, and 1.5 ppm NO(2) for 60 min were infected with RSV. Viral replication, as well as RSV-induced interleukin (IL)-6 and IL-8, was assessed at various times postinfection. The NO(2) doses used were not toxic to the BEAS-2B cells as measured by release of lactic dehydrogenase (LDH). The internalization of RSV was increased by exposure to 0.5 ppm NO(2) and decreased by exposure to 1.5 ppm NO(2). On the other hand, the release of infectious virus 48 h postexposure was not affected by the two lower doses of NO(2), but was significantly reduced in cells exposed to 1.5 ppm NO(2). Virus-induced cytokine production was also significantly reduced in cells exposed to 1.5 ppm NO(2), and not affected by 0.5 and 1.0 ppm. It is likely that the decrease in cytokine production is related to the decrease in viral burden. These data suggest that possible increases in viral clinical symptoms associated with NO(2) may not be caused by increased susceptibility of the epithelial cells to infection but may result from effects of NO(2) on host defenses that prevent the spread of virus.

Air Pollutants↗
PubMed1988

Effects of nitrogen dioxide and ozone on blood-borne cancer cell colonization of the lungs.

In this article we report inhalation effects of nitrogen dioxide (NO2) and ozone (O3) mixture as well as O3 alone on blood-borne cancer cell colonization of lungs. The findings are discussed in light of our earlier studies with NO2 exposure alone. In all of these studies the mouse B16 melanoma model was used. Animals were exposed to ambient concentrations of pollutants before melanoma-cell infusion. The results have indicated that inhalation of NO2 played a significant role in facilitation of blood-borne cancer cell spread, while O3 inhalation did not. With respect to mechanisms involved, the role of natural immunity was investigated and its was postulated that nitrogen dioxide may affect cells of the immune system and may in part account for the results. These findings may have direct bearing on dissemination of human cancer cells, since many cancer patients have circulating cancer cells and are exposed daily to noxious air pollutants. Most importantly, this effect may be preventable by reducing air pollution in urban areas.

Air Pollutants↗
PubMed1975

Effects of nitrogen dioxide and 3-methylcholanthrene on pulmonary enzymes.

Guinea pig lung phenol-O-methyltransferase, catechol-O-methyltransferase, and benzpyrene hydroxylase activities were examined after nitrogen dioxide and 3-methylcholanthrene treatment. While benzypyrene hydroxylase activity was enhanced by 3-methylcholanthrene, none of the pulmonary enzyme activities was altered after exposure to either 40 or 70 ppm of nitrogen dioxide for 2 hr.

Benzopyrene Hydroxylase↗
PubMed2006

Relation between concentration of air pollution and cause-specific mortality: four-year exposures to nitrogen dioxide and particulate matter pollutants in 470 neighborhoods in Oslo, Norway.

This study investigated the concentration-response relation between air pollution (nitrogen dioxide and particulate matter pollutants PM(10) and PM(2.5)) and cause-specific mortality. The population included all inhabitants of Oslo, Norway, aged 51-90 years on January 1, 1992 (n = 143,842) with follow-up of deaths from 1992 to 1998. An air dispersion model (AirQUIS; Norwegian Institute for Air Research (NILU), Oslo, Norway) was used to estimate levels of exposure in 1992-1995 in all 470 administrative neighborhoods. These data were linked to census, education, and death registries. A consistent effect on all causes of death was found for both sexes and age groups by all indicators of air pollution. The effects appeared to increase at nitrogen dioxide levels higher than 40 micro g/m(3) in the youngest age group and with a linear effect in the interval 20-60 micro g/m(3) for the oldest. An effect of all indicators on cardiovascular causes, lung cancer, and chronic obstructive pulmonary disease was also found in both age groups and sexes. The effects were particularly strong for chronic obstructive pulmonary disease, which appeared to have linear effects, whereas cardiovascular causes and lung cancer seemed to have threshold effects. Results show that vulnerable persons with chronic obstructive pulmonary disease and the elderly seem to be susceptible to air pollution at lower levels than the general population.

Aged↗
PubMed2002

Exposure to carbon monoxide and nitrogen dioxide in enclosed ice arenas.

This article summarises the latest information on the adverse cardiorespiratory effects of exposure to carbon monoxide (CO) and nitrogen dioxide (NO(2)) in enclosed ice rinks. Sources of CO and NO(2) emissions are identified, current standards for these agents, as well as methods of controlling the emissions, dispersion, and evacuation of these toxic gases are presented. A detailed literature search involving 72 references in English and French from research conducted in North America and Europe was used. Material was from peer reviewed journals and other appropriate sources. Air pollutants such as carbon monoxide (CO), and nitrogen dioxide (NO(2)) which are present in enclosed skating facilities, may exacerbate a pre-existing pathogenic condition in those people who spend considerable time in these environments. Considering the popularity of ice hockey, short track speed skating, and figure skating, and the hundreds of hours that a sensitive person may spend each year in these environments, it would seem appropriate to seek more definitive answers to this important health problem. From the findings and conclusions of the research reviewed in this paper, 10 recommendations are listed.

Air Pollution, Indoor↗
PubMed1995

Nitrogen dioxide production during mechanical ventilation with nitric oxide in adults. Effects of ventilator internal volume, air versus nitrogen dilution, minute ventilation, and inspired oxygen fraction.

BACKGROUND: Inhaled nitric oxide (NO) may be useful in the treatment of adult respiratory distress syndrome and other diseases characterized by pulmonary hypertension and hypoxemia. NO is rapidly converted to nitrogen dioxide (NO2) in oxygen (O2) environments. We hypothesized that in patients whose lungs are mechanically ventilated and in those with a long residence time for NO in the lungs, a clinically important [NO2] may be present. We therefore determined the rate constants for NO conversion in adult mechanical ventilators and in a test lung simulating prolonged intrapulmonary residence of NO. METHODS: NO (800 ppm) was blended with nitrogen (N2), delivered to the high-pressure air inlet of a Puritan-Bennett 7200ae or Siemens Servo 900C ventilator, and used to ventilate a test lung. The ventilator settings were varied: minute ventilation (VE) from 5 to 25 l/min, inspired O2 fraction (FIO2) from 0.24 to 0.87, and [NO] from 10 to 80 ppm. The experiment was then repeated with air instead of N2 as the dilution gas. The effect of pulmonary residence time on NO2 production was examined at test lung volumes of 0.5-4.0 l, VE of 5-25 l/min, FIO2 of 0.24-0.87, and [NO] of 10-80 ppm. The inspiratory gas mixture was sampled 20 cm from the Y-piece and from within the test lung. NO and NO2 were measured by chemiluminescence. The rate constant (k) for the conversion of NO to NO2 was determined from the relation 1/[NO]t-1/[NO]o = k x [O2] x t, where t = residence time. RESULTS: No NO2 was detected during any trial with VE 20 or 25 l/min. With N2 dilution and the Puritan-Bennett 7200ae, NO2 (< or = 1 ppm) was detected only at a VE of 5 l/min with an FIO2 of 0.87 and [NO] > or = 70 ppm. In contrast, [NO2] values were greater with the Servo 900C ventilator than with the Puritan-Bennett 7200ae at similar settings. When NO was diluted with air, clinically important [NO2] values were measured with both ventilators at high [NO] and FIO2. Rate constants were 1.46 x 10(-9) ppm-2.min-1 when NO was mixed with N2, 1.17 x 10(-8) ppm-2.min-1 when NO was blended with air, and 1.44 x 10(-9) ppm-2.min-1 in the test lung. CONCLUSIONS: [NO2] increased with increased FIO2 and [NO], decreased VE, blending with air, and increased lung volumes. Higher [NO2] was produced with the Servo 900C ventilator than the Puritan-Bennett 7200ae because of the greater residence time. With long intrapulmonary residence times for NO, there is a potential for NO2 production within the lungs. The rate constants determined can be used to estimate [NO2] in adult mechanical ventilation systems.

Adult↗
PubMed1995

Increasing concentrations of nitrogen dioxide pollution in rural Wales.

Monitoring of nitrogen dioxide pollution was carried out in rural environments throughout Wales during a 1-year survey to quantify any changes in background concentrations and distribution of the pollutant since an earlier survey in 1986. There were 23 sites in the present survey of which 16 had been monitored during the 1986 survey. The remaining 7 sites were based on moorland in mid-Wales within map squares for which critical loads for soil acidification are expected to be exceeded by the year 2005. All sites were chosen so as to be remote from major local sources of NO(2) and the values obtained were deemed to be minimum concentrations for the different regions. Measurements were made using diffusion tubes which aimed to provide mean concentrations of NO(2) for 2-week exposure periods. Concentrations of NO(2) were found to be higher in the winter months for most sites and this is probably related to a greater use of fossil fuels for heating buildings at this time of year. The exception was the high concentrations of NO(2) in May and June for several sites in North Wales, and in July and August for a site on Mount Snowdon. These high summer concentrations in North Wales are thought to be related to increased traffic associated with tourism. It is apparent that there has been a substantial increase in rural concentrations of NO(2) throughout Wales since the earlier survey of 1986. As an average of all 16 sites used in both surveys, there was a 53% increase in the annual mean concentration of NO(2). Also, it is evident that, since 1986, there has been a substantial increase in the area of south-eastern Wales which has a background level in excess of 10 ppb NO(2) and a notable reduction in land area with concentrations below 6 ppb NO(2) as an annual mean concentration. The possible future impact of increasing rural concentrations of NO(2) on Welsh vegetation is discussed with references to estimates of critical levels of NO(2) for adverse effects on plants.

Journal Article↗
PubMedDate not supplied

Acute respiratory distress syndrome following nitrogen dioxide exposure.

A young laborer was accidentally exposed to toxic nitrogen dioxide fumes following an accidental explosion at work place. He developed acute respiratory distress within few hours of exposure and manifested with severe hypoxemia and permeability edema. Assistance with mechanical ventilation and corticosteroid therapy could be instituted only after 24 hours of exposure. He had shown remarkable recovery and could be weaned off after seven days. At three weeks after discharge, his lung function tests were normal.

Adult↗
PubMed1998

Mechanism of reaction of nitrogen dioxide radical with hydroxycinnamic acid derivatives: a pulse radiolysis study.

Nitrogen dioxide radical (NO2.) is known as a toxic agent produced in the metabolism of nitrates and nitrites. By the use of the pulse radiolysis technique, the mechanism of the reaction of NO2. radical with hydroxycinnamic acid derivatives (HCA) was studied and the rate constants have been measured. The rate constants were found to be 7.4 x 10(8), 7.2 x 10(8), 8.6 x 10(8) dm3 mol(-1) s(-1) for ferulic acid, sinapic acid and caffeic acid, respectively. The reactions produce the corresponding phenoxyl radical.

Caffeic Acids↗
PubMed1994

Alterations in the ontogeny of rat pup ultrasonic vocalization produced by prenatal exposure to nitrogen dioxide.

Wistar female rats were exposed to low concentrations of nitrogen dioxide, NO2 (1.5 and 3 ppm) from day 0 to day 20 of pregnancy. The results show that prenatal exposure to this oxidant gas produced significant changes in the duration pattern of ultrasonic vocalizations emitted by male pups removed from their nest. In particular, a significant decrease in the length of ultrasonic calls was found in both 10- and 15-day-old rats exposed to NO2 (3 ppm) during gestation. These alterations were found at dose levels which did not significantly affect reproduction parameters, body weight gain and motor activity development. These findings suggest that gestational exposure to NO2, at concentrations below those associated with overt signs of toxicity, induces in rat offspring subtle behavioral changes characterized by altered ontogeny of ultrasonic emission.

Aging↗
PubMedDate not supplied

Measurement of background urban nitrogen dioxide pollution levels with passive samplers in Montpellier, France.

Background nitrogen dioxide (NO2) pollution levels in Montpellier were measured in the context of an assessment operation carried out by the local monitoring network (AMPADI-LR), using Palmes passive samplers. The equipment was validated by continuous measurement with automatic chemiluminescence analyzers. Measurements from representative background pollution sites and the ensuing cartographic representation provide information about local pollution data, a description of seasonal evolution and an assessment of the influence of various sources. The study may be used to define parameters for establishing an exposure index, taking into account roads with heavy traffic, which affects the distribution of NO2 over Montpellier, and meteorological factors. This is a pilot study which will subsequently be used for a more precise assessment measuring the personal exposure of inhabitants, for the purposes of a study on effects on health.

Analysis of Variance↗
PubMed1990

The risk of nitrogen dioxide: what have we learned from epidemiological and clinical studies?

Nitrogen dioxide (NO2) is an oxidant gas which contaminates ambient air in many urban and industrial locations, and indoor air in homes with combustion appliances. The Environmental Protection Agency presently regulates NO2 in ambient air as a "criteria" pollutant. In spite of decades of laboratory, clinical, and epidemiological research, the health effects of NO2 exposure on humans are not well understood. The toxicological evidence suggests that increased susceptibility to infection, functional deficits from effects on airways, and deterioration of the status of persons with chronic respiratory conditions, including asthmatics, are of potential concern. This paper provides a perspective on the present evidence related to human health effects of NO2. It addresses methodological barriers that limit the available data; assesses the adequacy of the data for risk assessment; and proposes a research agenda to obtain needed information on the health effects of NO2.

Air Pollutants↗
PubMed1999

Bronchopulmonary inflammation and airway smooth muscle hyperresponsiveness induced by nitrogen dioxide in guinea pigs.

We investigated whether acute exposure to nitrogen dioxide (NO2) causes major inflammatory responses (inflammatory cell recruitment, oedema and smooth muscle hyperresponsiveness) in guinea pig airways. Anaesthetised guinea pigs were exposed to 18 ppm NO2 or air for 4 h through a tracheal cannula. Bronchoalveolar lavage was performed and airway microvascular permeability and in vitro bronchial smooth muscle responsiveness were measured. Exposure to NO2 induced a significant increase in eosinophils and neutrophils in bronchoalveolar lavage fluid, microvascular leakage in the trachea and main bronchi (but not in peripheral airways), and a significant in vitro hyperresponsiveness to acetylcholine, electrical field stimulation, and neurokinin A, but not to histamine. Thus, this study shows that in vivo exposure to high concentrations of NO2 induces major inflammatory responses in guinea pig airways that mimic acute bronchitis induced by exposure to irritant gases in man.

Acetylcholine↗
PubMed1992

Rat model to investigate the treatment of acute nitrogen dioxide intoxication.

1. The pulmonary toxic events induced by acute nitrogen dioxide (NO)2 exposure were studied in the rat to develop an inhalation model to investigate therapeutic measures. 2. A good correlation was observed between the lung weights and severity of the atypical pneumonitis. The pulmonary effects observed, became more pronounced with increasing NO2 concentrations (0, 25, 75, 125, 175 or 200 ppm, 1 ppm NO2 = 1.88 mg m-3 NO2) and exposure times (5, 10, 20 or 30 min). 3. An adequate NO2 concentration is 175 ppm, because it can induce a severe lung injury without mortality. This makes it possible to investigate suitable therapeutic interventions for several days. 4. Following acute inhalatory NO2 intoxication, transformation of NO2 to nitrate is presumably more notable than transformation to nitrite. 5. The transformation of NO2 to nitrate in lung tissue causes a slight increase in the serum nitrite concentration, which does not induce measurable formation of methaemoglobin. 6. Presumably, methaemoglobin does not contribute to the toxicity of NO2 intoxication.

Administration, Inhalation↗
PubMed2004

Acousto-optic differential optical absorption spectroscopy for atmospheric measurement of nitrogen dioxide in Hong Kong.

Measurement of the atmospheric concentration of nitrogen dioxide (NO(2)) pollutant was demonstrated by differential optical absorption spectroscopy (DOAS) using a visible acousto-optic tunable filter. In a traditional spectral scanning DOAS system for atmospheric concentration monitoring, a highly stable light source is required. When the light intensity fluctuates during scanning, the concentration retrieval will be inaccurate. In order to reduce the error due to intensity fluctuations, a modified DOAS system has been developed by introducing a broadband light intensity monitoring channel. Using the measured intensity of the broadband channel as the intensity of the light source, the spectrum can be de-biased and the residual intensity variation will primarily result from atmospheric extinction. In addition, by employing the lock-in detection technique, the background light interference is also removed in the modified DOAS system. The atmospheric NO(2) concentration measurement was performed at the campus of City University of Hong Kong, and the results were compared with the concentration reported from a nearby monitoring station in Sham Shui Po, operated by the Hong Kong Environmental Protection Department.

Absorption↗