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PubMed1987

In vivo nitrogen dioxide exposure depresses spleen cell in vitro mitogenic responses: effects of sulfur compounds.

The in vivo mitogenic responses to lipopolysaccharide or concanavalin A by spleen cells of mice exposed to 20 ppm nitrogen dioxide (NO2) for 96 hr, were evaluated. [3H]Thymidine incorporation after addition of either mitogen, was significantly lower in spleen cells from acutely NO2-exposed mice (NO2 SC) than from control mice, although cell viability was not affected. T- and B-cell mitogenic responses were inhibited to the same extent by NO2 exposure. NO2 SC responses were protected by the thiol compounds 2-mercaptoethanol, L-cysteine, and selenomethionine. No restoration of mitogenic response was observed after treatment with reduced glutathione. Mechanisms accounting for this in vivo NO2 immune toxicity, are discussed in terms of oxidative injury.

Animals↗

PubMed2005

Outdoor carbon monoxide, nitrogen dioxide, and sudden infant death syndrome.

AIMS: To investigate whether infants who died of SIDS were more likely to have higher acute and lifetime average exposures to outdoor carbon monoxide (CO) and nitrogen dioxide (NO2) than comparison healthy infants. METHODS: A total of 169 case and 169 matched control infants born between 1988 and 1992, were studied. CO and NO2 concentrations, averaged for all days within the infant's lifespan, and the last 30 days, 7 days, 3 days, and 1 day of life were obtained from air pollutant data provided by the California Air Resources Board. RESULTS: Based on monthly aggregated data, average CO and particularly NO2 were associated with SIDS count, even after adjustment for seasonal trends. SIDS outcome was not significantly associated with high average outdoor CO levels for any time period. However, high average outdoor NO2 levels on the last day of the infant's exposure period were significantly associated with SIDS; the adjusted odds ratio was 2.34 (95% CI 1.13 to 4.87). CONCLUSIONS: SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life. Further studies are needed to replicate this finding.

Air Pollutants↗

PubMed1993

Effect of nitrogen dioxide on human nasal epithelium.

The nasal epithelium of young adult white men in good health was evaluated by electron microscopy in a condition blind fashion relative to exposures of 2 ppm nitrogen dioxide (NO2) or clean air for 4 h. The exposure protocol involved two separate exposures of the same individuals to NO2 or clean air approximately 3 wk apart. We found qualitative and quantitative evidence that luminal border membranes of ciliated cells were ultrastructurally altered in six of seven samples of nasal epithelium obtained following NO2 exposures, although subsequent morphometric statistical analyses were not significant. This alteration was characterized by cilia containing excess matrix in which individual or, more commonly, multiple ciliary axonemes were embedded, and by vesiculations of luminal border ciliary membranes, a pattern less common in clean air-exposed control specimens. Although these patterns were not widespread, their morphology was consistent with findings of previous animal studies involving acute and chronic exposure to NO2. Our findings suggest that adverse effects on mucociliary function in normal humans due to acute exposure to low levels of NO2 are most likely minimal. However, in view of other reports of NO2 exposure in laboratory animals documenting ciliary injury, our observations support a view that similar patterns might appear more prominently with higher NO2 levels and/or more extended exposure intervals.

Adolescent↗

PubMed1979

The relation between respiratory illness in primary schoolchildren and the use of gas for cooking--III. Nitrogen dioxide, respiratory illness and lung infection.

We examined the relation between lung function and respiratory illness in a population of 808 primary school children aged 6-7 years and the levels of nitrogen dioxide (NO2) in the kitchens and bedrooms in their homes. Complete data were collected on about 66% of the population. The children lived in a defined 4 square km area in Middlesbrough, Cleveland, UK. One week average outdoor levels of NO2 varied little over the area (14-24 ppb); The prevalence of respiratory illness was higher in children from gas than electric cooking homes (p approximately or equal to 0.1). Although prevalence was not related to kitchen NO2 levels (range 5-317 ppb) it increased with increasing levels of NO2 in the children's bedrooms in gas cooking homes (range 4-169 ppb, p approximately or equal to 0.1). Symptoms in siblings and parents were not related to kitchen NO2 levels. Lung function was not related to NO2 levels in the kitchen or bedroom. Because of the very low levels of NO2 at which an association with illness was observed and the inconsistency between our results in the UK and those from several studies in the US, it is possible that the NO2 levels were a proxy for some other factor more directly related to respiratory disease such as temperature or humidity.

Air Pollutants↗

PubMed1994

Nitrogen dioxide and respiratory illness in children. Part III: Quality assurance in an epidemiologic study.

This report describes the quality assurance and quality control program developed for the previously reported epidemiologic study of nitrogen dioxide (NO2) and respiratory illness in children (Health Effects Institute Research Report 58, Parts I and II). The specific aims of the program were to make certain that data were sufficiently accurate, complete, verifiable, and retrievable. The quality assurance and quality control program consisted of: a written protocol, standard operating procedures, written records, a project management system, appropriate data processing, data verification, and data analysis planning, and was staffed by qualified and appropriately trained personnel. Within the activities of the overall program, two focused quality assurance studies were conducted. During the first of these focused studies, parents maintained a calendar-diary of their child's daily respiratory symptoms. Telephone interviews were conducted at intervals of two weeks, and parents used the calendars to report on symptom occurrence since the previous call. To assess the comparability of illness events based on symptom reports from the parents with usual clinical diagnostic methods, nurse practitioners examined children during illness, and office and clinic records of outpatient visits were reviewed. Using the parent reports, respiratory illnesses were defined as symptom episodes of at least two consecutive days; lower respiratory illnesses included at least one day of either wet cough or wheeze. Runny or stuffy nose was reported for 93% of illnesses; and wet cough for 33% and wheeze for 6% of illnesses. In comparison with the diagnoses made by a nurse practitioner, parent reports of wet cough or wheeze were sensitive (93.4%) for detecting lower respiratory illnesses, but nonspecific (with specificity of only 24.2%). The majority of the false-positive lower respiratory illnesses had the symptom of wet cough. The comparison of parent reports with outpatient records provided similar findings. These findings indicate that standardized reporting of respiratory illnesses can be achieved with regular telephone interviews, but the classification of specific illnesses from the observations of parents' information may differ from diagnoses made by clinicians. The second focused quality assurance study evaluated the measurement error associated with the parents' use of passive diffusion samplers for NO2. Midway through the study, technicians conducted home visits to assess compliance with stated procedures, and to make independent measurements of NO2. Based on criteria for placement and use of the samplers, conditions of noncompliance were observed on about 40% of visits.(ABSTRACT TRUNCATED AT 400 WORDS)

Data Collection↗

PubMed1999

Nitrogen dioxide radical generated by the myeloperoxidase-hydrogen peroxide-nitrite system promotes lipid peroxidation of low density lipoprotein.

Myeloperoxidase, a heme protein secreted by activated phagocytes, is present and enzymatically active in human atherosclerotic lesions. In the current studies, we explored the possibility that reactive nitrogen species generated by myeloperoxidase promote lipid peroxidation of low density lipoprotein (LDL) -- a modification that may render the lipoprotein atherogenic. We found that myeloperoxidase, an H2O2-generating system and nitrite (NO2-) peroxidized LDL lipids. The process required NO2- and each component of the enzymatic system; it was inhibited by catalase, cyanide and ascorbate, a potent scavenger of aqueous phase radicals. LDL peroxidation did not require chloride ion, and it was little affected by the hypochlorous acid scavenger taurine. Collectively, these results suggest that lipid peroxidation is promoted by a nitrogen dioxide radical-like species. These observations indicate that myeloperoxidase, by virtue of its ability to form reactive nitrogen intermediates, may promote lipid peroxidation and atherogenesis.

Antioxidants↗

PubMedDate not supplied

Chronic disease associated with long-term concentrations of nitrogen dioxide.

A prospective epidemiologic cohort study of 6,000 residentially stable and non-smoking Seventh-day Adventists (SDA) in California was conducted to evaluate long-term cumulative levels of ambient nitrogen dioxide (NO2) in association with several chronic diseases. These diseases included respiratory symptoms, cancer, myocardial infarction (MI), and all natural causes mortality. Cumulative ambient concentrations of NO2 were estimated for each study subject using monthly interpolations from fixed site monitoring stations and applying these estimates to the monthly residence and work place zip code histories of study participants. In addition, a personal NO2 exposure study on a randomly selected sample of 650 people in southern California was conducted to predict total personal NO2 exposure using household and lifestyle characteristics and ambient NO2 concentrations. It was found that good predictability could be obtained (correlation coefficient between predicted and observed values = 0.79) from a model predicting personal NO2. The resulting regression equations from the personal NO2 exposure study were applied to the epidemiologic study cohort to adjust ambient concentrations of NO2.

Adult↗

PubMed1995

Absorption of nitrogen dioxide and nitric oxide by soda lime.

Inhaled nitric oxide (NO) is used for the treatment of pulmonary hypertension as a selective pulmonary vasodilator. However, NO is oxidized rapidly to the more toxic nitrogen dioxide (NO2). Elimination of NO2 from inspired gas is essential for safe clinical use NO. We therefore investigated the efficacy of soda lime in absorbing NO2 from NO2-containing gases. Commercially available soda limes (Soda sorb and Wako lime-A), were exposed to the following six gas mixtures containing NO and NO2 in a hypoxic carrier gas for 20 min: No. 1: NO 40 ppm; No. 2: NO 35 ppm and NO2 5 ppm; No. 3: NO 30 ppm and NO2 10 ppm; No. 4: NO 20 ppm and NO2 20 ppm; No. 5: NO 10 ppm and NO2 30 ppm; and No. 6: NO2 40 ppm. Both types of soda lime completely absorbed the NO2 in all samples when it was present (Nos 2-6). NO concentration in these gas mixtures was reduced by an amount equal to the NO2 absorbed by soda lime. NO was absorbed minimally when NO2 was not present in the mixture. Nitrite was detected from the Wako lime-A granules exposed to the test gas by the chemical analysis. These findings suggest that soda lime completely absorbs NO2 by chemical neutralization, but NO is absorbed as simultaneously absorbed NO2 only where NO and NO2 coexist. Therefore, we conclude that soda lime is useful for NO2 absorption during NO inhalation therapy but NO monitoring from a point distal to the soda lime is required for precise control of inspired NO concentration.

Absorption↗

PubMed1989

Nitrogen dioxide exposure in vivo and human alveolar macrophage inactivation of influenza virus in vitro.

Epidemiologic studies have reported an increased incidence of respiratory infections and illness in association with elevated indoor levels of nitrogen dioxide (NO2). Animal exposure studies have found that brief exposures to peak levels of NO2 produce greater morbidity than continuous lower level exposure. In order to examine the effect of NO2 inhalation on human alveolar macrophages, normal volunteers were exposed sequentially to air or NO2, by double-blind randomization, in an environmental chamber. Two exposure protocols with comparable concentration x time products were used: (a) continuous 0.60 ppm NO2 (n = 9), and (b) background 0.05 ppm NO2 with three 15-min peaks of 2.0 ppm (n = 15). Inhalation of NO2 caused no significant changes in pulmonary function or airway reactivity in either exposure protocol. Alveolar macrophages obtained by bronchoalveolar lavage 3 1/2 hr after exposure to continuous 0.60 ppm NO2 tended to inactivate influenza virus in vitro less effectively than cells collected after air exposure (1.96 vs 1.25 log10 plaque-forming units on Day 2 of incubation, P less than 0.07). Four of nine subjects accounted for the observed impairment in virus inactivation; cells from these four subjects demonstrated an increase in interleukin-1 (IL-1) production after NO2 vs air, whereas the five remaining subjects decreased IL-1 production after NO2. In contrast, intermittent peak exposure did not alter the rate of viral inactivation or IL-1 production. This methodology has the potential to identify pollutant effects on mechanisms of respiratory defense in humans.

Adult↗

PubMedDate not supplied

Collagen breakdown and nitrogen dioxide inhalation.

Measurements of urinary hydroxylysine glycosides indicate that considerable collagen degradation occurred during the reentry into the earth's atmosphere of the American astronauts of the Apollo-Soyuz mission. Since the crew accidentally inhaled nitrogen dioxide, a recognized pulmonary irritant, and showed clinical and roentgenographic signs of diffuse chemical pneumonitis, it is likely that collagen degradation occurred in the pulmonary parenchyma.

Collagen↗

PubMed1989

Current nitrogen dioxide exposures among railroad workers.

As part of a series of epidemiologic studies of the mortality patterns of railroad workers, various air contaminants were measured to characterize the workers' current exposures to diesel exhaust. Nitrogen dioxide (NO2), which is a constituent of diesel exhaust, was examined as one possible marker of diesel exposure. An adaptation of the Palmes personal passive sampler was used to measure the NO2 exposures of 477 U.S. railroad workers at four railroads. The range of NO2 exposures expressed as the arithmetic average +/- two standard errors for the five career job groups were as follows: signal maintainers, 16-24 parts per billion (ppb); clerks/dispatchers/station agents, 23-43 ppb; engineers/firers, 26-38 ppb; brakers/conductors, 50-74 ppb; and locomotive shop workers, 95-127 ppb. Variations among railroads and across seasons were not significant for most job groups.

Air Pollutants, Occupational↗

PubMed1992

Wood stove effects on indoor air quality in Brazilian homes: carcinogens, suspended particulate matter, and nitrogen dioxide analysis.

The effects of wood burning stoves on indoor air quality was investigated in a rural community of southern Brazil, during the winter season of 1991. The concentrations of polycyclic aromatic hydrocarbons (PAHs), nitrogen dioxide (NO2) and suspended particulate matter (SPM) were assessed in houses with wood stoves and the results compared with levels found in houses with gas stoves. Strikingly higher (p < 0.01) levels of PAHs, and much higher (p = 0.07) levels of SPM were found in the kitchens with wood stoves. In contrast, NO2 concentrations in the kitchen as well in personal exposure, were found to be slightly higher in houses with gas stoves. All these differences were minimally affected by smoking, outdoor air pollution or other emissions from indoor combustion products. These findings appear to support the hypothesis that domestic wood burning stoves are risk factors for some upper digestive and respiratory tract cancers in Brazil.

Air Pollutants↗

PubMed2005

Assessing spatial variability of ambient nitrogen dioxide in Montréal, Canada, with a land-use regression model.

The purpose of this study was to derive a land-use regression model to estimate on a geographical basis ambient concentrations of nitrogen dioxide (NO2) in Montreal, Quebec, Canada. These estimates of concentrations of NO2 will be subsequently used to assess exposure in epidemiologic studies on the health effects of traffic-related air pollution. In May 2003, NO2 was measured for 14 consecutive days at 67 sites across the city using Ogawa passive diffusion samplers. Concentrations ranged from 4.9 to 21.2 ppb (median 11.8 ppb). Linear regression analysis was used to assess the association between logarithmic concentrations of NO2 and land-use variables derived using the ESRI Arc 8 geographic information system. In univariate analyses, NO2 was negatively associated with the area of open space and positively associated with traffic count on nearest highway, the length of highways within any radius from 100 to 750 m, the length of major roads within 750 m, and population density within 2000 m. Industrial land-use and the length of minor roads showed-no association with NO2. In multiple regression analyses, distance from the nearest highway, traffic count on the nearest highway, length of highways and major roads within 100 m, and population density showed significant associations with NO2; the best-fitting regression model had a R2 of 0.54. These analyses confirm the value of land-use regression modeling to assign exposures in large-scale epidemiologic studies.

Air Pollutants↗

PubMed1997

Nitrogen dioxide depletes uric acid and ascorbic acid but not glutathione from lung lining fluid.

The aim of this study was to determine the kinetics of the reactions between the gaseous free-radical pollutant, nitrogen dioxide (NO2), and the water-soluble antioxidants present in respiratory tract lining fluid (RTLF). Samples of RTLF, recovered from 12 subjects (mean age 54.1+/-16.3 years; eight male, four female) as bronchoalveolar lavage (BAL) fluid were exposed ex vivo to NO2 [50-1000 parts per billion (ppb)] for 4 h. For comparison, similar exposures were carried out with single and composite solutions with relevant RTLF antioxidant concentrations. Ascorbic acid (AA), uric acid (UA), GSH depletion, and GSSG and malondialdehyde (MDA) formation were determined with time. In the three models, UA and AA were consumed in a time- and NO2-concentration-related fashion. In addition, their rate of depletion correlated positively with their initial concentration (UA, r=0.92, P<0.05; AA, r=0.94, P<0.05). Little difference was found between the rate of loss of AA (2.2+/-0. 2; 1.9+/-0.5; 1.4+/-0.3 nmol.l-1.h-1.ppb-1), and that of UA (2.4+/-0. 2; 2.1+/-0.6; 1.3+/-0.2 nmol.l-1.h-1.ppb-1) in the three RTLF models examined (single, composite, BAL fluid respectively). GSH loss from BAL fluid (0.2+/-0.1) was significantly less than that seen in either single (1.4+/-0.3) or composite (1.2+/-0.5 nmol.l-1.h-1. ppb-1) antioxidant solutions. In all cases, GSH consumption was significantly less than AA or UA. As model complexity increased, the rate of individual antioxidant loss decreased, such that in BAL fluid, AA, UA and GSH consumption rates were significantly less (P<0. 05) than in the pure or composite antioxidant mixtures. In BAL fluid, little GSSG production was observed at any NO2 concentration. MDA concentration, determined as a measure of lipid peroxidation, did not change following exposure to 50, 150 or 400 ppb NO2, but increased MDA was seen in BAL fluid from 8/12 subjects following exposure to 1000 ppb NO2 for 1 h or more. In conclusion, NO2, at environmentally relevant concentrations, depletes BAL fluid of the antioxidant defences, UA and AA, but not GSH.

Antioxidants↗

PubMed1983

The microbial flora of herring fillets after storage in carbon dioxide, nitrogen or air at 2 degrees C.

Herring fillets from the Baltic Sea were stored in glass vessels in air, nitrogen or carbon dioxide (CO2) at 2 degrees C and the microbial development was studied. The microbiological shelf-life of the herring (the time to reach 10(7) organisms/g) was prolonged by a factor of 3.5 in CO2 as compared to air. The corresponding factor in nitrogen was 1.5. The microflora of fresh and spoiled herring was classified. The initial microflora was dominated by coryneforms, Flavobacterium spp., Moraxella-like organisms and Pseudomonas spp. The spoilage-flora in air (after 9 d) was dominated by Pseudomonas spp. and Moraxella-like organisms, and in nitrogen (14 d) Enterobacteriaceae, Vibrionaceae and Lactobacillus spp. were dominant. Homofermentative Lactobacillus spp. were the only organisms isolated from fillets stored in CO2 (28 d). It was concluded that storing fresh fish in pure CO2 at low refrigeration temperatures is a method with industrial potential. The method (1) improves the microbiological stability and (2) reduces the microbiological health hazards of the fish.

Air↗

PubMed1975

Dietary vitamin E and the effects of inhaled nitrogen dioxide on rat lungs.

Groups of rats were fed diets containing supplemented adequate, or deficient amounts of alpha-tocopherol. Some rats from each group were exposed for 2 h to high-level concentrations of nitrogen dioxide in their breathing air. A comparison of wet and dry lung weights did not indicate that exposure of the gas was a cause of edema. Proportion of lung weight to total body weight was increased in all animals with the lipid content diminishing according to the amount of dietary apha-tocopherol available. Dietary intake of the vitamin did not seem to protect the lipid content of lungs of the supplemented dietary group from oxidation. No difference in total peroxides was noted between any of the groups. Inflation and deflation compliance measurements were greater for both exposed and non-exposed supplemented animals when compared to the adequate and deficient groups.

Animals↗

PubMed1992

Structural and functional impairment of surfactant protein A after exposure to nitrogen dioxide in rats.

The major surfactant protein A (SP-A) determines the dynamics of surfactant metabolism and function. We now for the first time studied the in vivo exposure of the SP-A to nitrogen dioxide (NO2) and compared it to in vitro exposure effects. Several properties that are believed to possess physiological functions were investigated. Exposure of rat SP-A to NO2 showed 1) a higher alveolar pool size after in vivo exposure, 2) a slightly decreased mannose binding capacity for the in vivo exposed form but a highly decreased binding after in vitro exposure, 3) an affected protein-lipid aggregation that was impaired most by the in vitro exposed protein, 4) a low inhibition for the secretion of phosphatidylcholine in isolated type II pneumocytes, and 5) no difference in apparent molecular weight and immunological reactivity of the differently exposed SP-A. The NO2-induced alterations of the SP-A may contribute to the pulmonary toxicity of this oxidant. It is clear from this study that the extend of the effects from in vivo and in vitro exposure are different. Therefore both forms of exposure are necessary to assess the biological significance of NO2 exposure.

Animals↗

PubMed1990

Bronchoalveolar mastocytosis and lymphocytosis after nitrogen dioxide exposure in man: a time-kinetic study.

The combination of environmental chamber exposure and bronchoalveolar lavage (BAL) was used to study the time-course of the cell response in the human lung to nitrogen dioxide (NO2). Healthy subjects were exposed for 20 min to 7 mg NO2.m-3 (4 ppm), a concentration which occurs indoors in industries and is below the peak exposure limit for work places in most countries, 10 mg.m-3 (5.5 ppm). BAL was performed in all subjects several weeks before exposure and 4, 8, 24 and 72 h after exposure, in eight subjects at each time. Mastocytosis and lymphocytosis were found in BAL fluid 4-24 h after exposure, with normalization after 72 h. A mild increase in lysozyme positive macrophages was found 24-72 h after exposure. The time-course of the human pulmonary cell response to NO2, demonstrated in BAL fluid, represents a new and previously not reported finding after exposure to this common air pollutant. Our findings are diverging from results obtained in animal studies, using approximately the same NO2 concentrations, indicating that the results from the animal studies may not be transferable to man.

Adult↗