Exposure to nitrogen dioxide and the occurrence of bronchial obstruction in children below 2 years.
(1/562)
BACKGROUND: The objective of the investigation was to test the hypothesis that exposure to nitrogen dioxide (NO2) has a causal influence on the occurrence of bronchial obstruction in children below 2 years of age. METHODS: A nested case-control study with 153 one-to-one matched pairs was conducted within a cohort of 3754 children born in Oslo in 1992/93. Cases were children who developed > or = 2 episodes of bronchial obstruction or one episode lasting >4 weeks. Controls were matched for date of birth. Exposure measurements were performed in the same 14-day period within matched pairs. The NO2 exposure was measured with personal samplers carried close to each child and by stationary samplers outdoors and indoors. RESULTS: Few children (4.6%) were exposed to levels of NO2 > or = 30 microg/m3 (average concentration during a 14-day period). In the 153 matched pairs, the mean level of NO2 was 15.65 microg/m3 (+/-0.60, SE) among cases and 15.37 (+/-0.54) among controls (paired t = 0.38, P = 0.71). CONCLUSIONS: The results suggest that NO2 exposure at levels observed in this study has no detectable effect on the risk of developing bronchial obstruction in children below 2 years of age. (+info)
Nitrogen dioxide formation during inhaled nitric oxide therapy.
(2/562)
BACKGROUND: Nitrogen dioxide (NO2) is a toxic by-product of inhalation therapy with nitric oxide (NO). The rate of NO2 formation during NO therapy is controversial. METHODS: The formation of NO2 was studied under dynamic flows emulating a base case NO ventilator mixture containing 80 ppm NO in a 90% oxygen matrix. The difficulty in measuring NO2 concentrations below 2 ppm accurately was overcome by the use of tunable diode laser absorption spectroscopy. RESULTS: Using a second-order model, the rate constant, k, for NO2 formation was determined to be (1.19 +/- 0.11) x 10(-11) ppm-2s-1, which is in basic agreement with evaluated data from atmospheric literature. CONCLUSIONS: Inhaled NO can be delivered safely in a well-designed, continuous flow neonatal ventilatory circuit, and NO2 formation can be calculated reliably using the rate constant and circuit dwell time. (+info)
Air pollution, pollens, and daily admissions for asthma in London 1987-92.
(3/562)
BACKGROUND: A study was undertaken to investigate the relationship between daily hospital admissions for asthma and air pollution in London in 1987-92 and the possible confounding and modifying effects of airborne pollen. METHODS: For all ages together and the age groups 0-14, 15-64 and 65+ years, Poisson regression was used to estimate the relative risk of daily asthma admissions associated with changes in ozone, sulphur dioxide, nitrogen dioxide and particles (black smoke), controlling for time trends, seasonal factors, calendar effects, influenza epidemics, temperature, humidity, and autocorrelation. Independent effects of individual pollutants and interactions with aeroallergens were explored using two pollutant models and models including pollen counts (grass, oak and birch). RESULTS: In all-year analyses ozone was significantly associated with admissions in the 15-64 age group (10 ppb eight hour ozone, 3.93% increase), nitrogen dioxide in the 0-14 and 65+ age groups (10 ppb 24 hour nitrogen dioxide, 1.25% and 2.96%, respectively), sulphur dioxide in the 0-14 age group (10 micrograms/m3 24 hour sulphur dioxide, 1.64%), and black smoke in the 65% age group (10 micrograms/m3 black smoke, 5.60%). Significant seasonal differences were observed for ozone in the 0-14 and 15-64 age groups, and in the 0-14 age group there were negative associations with ozone in the cool season. In general, cumulative lags of up to three days tended to show stronger and more significant effects than single day lags. In two-pollutant models these associations were most robust for ozone and least for nitrogen dioxide. There was no evidence that the associations with air pollutants were due to confounding by any of the pollens, and little evidence of an interaction between pollens and pollution except for synergism of sulphur dioxide and grass pollen in children (p < 0.01). CONCLUSIONS: Ozone, sulphur dioxide, nitrogen dioxide, and particles were all found to have significant associations with daily hospital admissions for asthma, but there was a lack of consistency across the age groups in the specific pollutant. These associations were not explained by confounding by airborne pollens nor was there convincing evidence that the effects of air pollutants and airborne pollens interact in causing hospital admissions for asthma. (+info)
Nitrogen dioxide induces cis-trans-isomerization of arachidonic acid within cellular phospholipids. Detection of trans-arachidonic acids in vivo.
(4/562)
Oxygen free radicals oxidize arachidonic acid to a complex mixture of metabolites termed isoeicosanoids that share structural similarity to enzymatically derived eicosanoids. However, little is known about oxidations of arachidonic acid mediated by reactive radical nitrogen oxides. We have studied the reaction of arachidonic acid with NO2, a free radical generated by nitric oxide and nitrite oxidations. A major group of products appeared to be a mixture of arachidonic acid isomers having one trans-bond and three cis-double bonds. We have termed these new products trans-arachidonic acids. These isomers were chromatographically distinct from arachidonic acid and produced mass spectra that were nearly identical with mass spectra of arachidonic acid. The lack of ultraviolet absorbance above 205 nm and the similarity of mass spectra of dimethyloxazoline derivatives suggested that the trans-bond was not conjugated with any of the cis-bonds, and the C=C bonds were located at carbons 5, 8, 11, and 14. Further identification was based on comparison of chromatographic properties with synthetic standards and revealed that NO2 generated 14-trans-eicosatetraenoic acid and a mixture containing 11-trans-, 8-trans-, and 5-trans-eicosatetraenoic acids. Exposure of human platelets to submicromolar levels of NO2 resulted in a dose-dependent formation of 14-trans-eicosatetraenoic acid and other isomers within platelet glycerophospholipids. Using a sensitive isotopic dilution assay we detected trans-arachidonic acids in human plasma (50.3 +/- 10 ng/ml) and urine (122 +/- 50 pg/ml). We proposed a mechanism of arachidonic acid isomerization that involves a reversible attachment of NO2 to a double bond with formation of a nitroarachidonyl radical. Thus, free radical processes mediated by NO2 lead to generation of trans-arachidonic acid isomers, including biologically active 14-trans-eicosatetraenoic acid, within membrane phospholipids from which they can be released and excreted into urine. (+info)
Myeloperoxidase-generated reactive nitrogen species convert LDL into an atherogenic form in vitro.
(5/562)
Oxidized LDL is implicated in atherosclerosis; however, the pathways that convert LDL into an atherogenic form in vivo are not established. Production of reactive nitrogen species may be one important pathway, since LDL recovered from human atherosclerotic aorta is enriched in nitrotyrosine. We now report that reactive nitrogen species generated by the MPO-H2O2-NO2- system of monocytes convert LDL into a form (NO2-LDL) that is avidly taken up and degraded by macrophages, leading to massive cholesterol deposition and foam cell formation, essential steps in lesion development. Incubation of LDL with isolated MPO, an H2O2-generating system, and nitrite (NO2-)-- a major end-product of NO metabolism--resulted in nitration of apolipoprotein B 100 tyrosyl residues and initiation of LDL lipid peroxidation. The time course of LDL protein nitration and lipid peroxidation paralleled the acquisition of high-affinity, concentration-dependent, and saturable binding of NO2-LDL to human monocyte-derived macrophages and mouse peritoneal macrophages. LDL modification and conversion into a high-uptake form occurred in the absence of free metal ions, required NO2-, occurred at physiological levels of Cl-, and was inhibited by heme poisons, catalase, and BHT. Macrophage binding of NO2-LDL was specific and mediated by neither the LDL receptor nor the scavenger receptor class A type I. Exposure of macrophages to NO2-LDL promoted cholesteryl ester synthesis, intracellular cholesterol and cholesteryl ester accumulation, and foam cell formation. Collectively, these results identify MPO-generated reactive nitrogen species as a physiologically plausible pathway for converting LDL into an atherogenic form. (+info)
Formation of nitrogen dioxide from nitric oxide and their measurement in clinically relevant circumstances.
(6/562)
Therapy with inhaled nitric oxide in oxygen requires adequate monitoring of nitric oxide and nitrogen dioxide. The characteristics of chemiluminescence and electrochemical measurement techniques were determined by analysis of continuously flowing gas mixtures and comparisons with traceable gas standards. Gas mixtures were also diluted with mass flow controllers and in addition created in ventilator breathing systems. Factors influencing the formation of nitrogen dioxide were defined. Both techniques accurately measured nitric oxide (10-80 parts per million, ppm) and nitrogen dioxide (0.5-5 ppm) in normoxic and hyperoxic (90% oxygen) gas in the studied ranges. Nitrogen dioxide in hyperoxic gas had three origins: (1) from the premixing point of nitric oxide in nitrogen, (2) as a result of the mixing process, and (3) from post-mixing and time-dependent continuous formation of nitrogen dioxide in oxygen. We conclude that adequate monitoring is possible and that factors affecting nitrogen dioxide generation can be defined. (+info)
Association of air pollution with daily GP consultations for asthma and other lower respiratory conditions in London.
(7/562)
BACKGROUND: Very few published studies have looked at the effects of air pollution on health in the primary care setting. As part of a large study to examine the association between air pollution and a number of health outcomes, the relationship between daily GP consultations for asthma and other lower respiratory diseases (LRD) and air pollution in London was investigated. METHODS: Time-series analysis of daily numbers of GP consultations controlling for time trends, seasonal factors, day of week cycles, influenza, weather, pollen levels, and serial correlation was performed. Consultation data were available from between 268 718 and 295 740 registered patients from 45-47 London practices contributing to the General Practice Research Database during 1992-4. RESULTS: Positive associations, weakly significant and consistent across lags, were observed between asthma consultations and nitrogen dioxide (NO2) and carbon monoxide (CO) in children and particulate matter of less than 10 microm in diameter (PM10) in adults, and between other LRD consultations and sulphur dioxide (SO2) in children. A consistently negative association with ozone in children was observed in both disease categories. The effect estimates of most pollutants were much larger when analysed separately by season, particularly in the children: percentage change in asthma consultations during the warm season (April-September) for a 10-90th percentile increase in 24 hour NO2 lagged by one day = 13.2% (95% CI 5.6 to 21.3), with CO = 11.4% (95% CI 3.3 to 20.0), and with SO2 = 9.0% (95% CI 2.2 to 16.2). In adults the only association consistent over different lag periods was with PM10 = 9.2% (3.7 to 15.1). The associations of pollution and consultations for LRD were increased mainly in the winter months: percentage change in consultations by children in winter with NO2 = 7.2% (95% CI 2.8 to 11.6), CO = 6.2% (95% CI 2.3 to 10.2), and SO2 = 5.8% (95% CI 1.6 to 10.2). CONCLUSIONS: There are associations between air pollution and daily consultations for asthma and other lower respiratory disease in London. The most significant associations were observed in children and the most important pollutants were NO2, CO, and SO2. In adults the only consistent association was with PM10. (+info)
Chloramphenicol inhibition of denitrifying enzyme activity in two agricultural soils.
(8/562)
Chloramphenicol, at concentrations greater than 0.1 g/liter (0.3 mM), inhibited the denitrifying enzyme activity (DEA) of slurries of humisol and sandy loam soils by disrupting the activity of existing nitrate reductase enzymes. When the concentration of chloramphenicol was increased from 0.1 to 2.0 g/liter (6.0 mM), the rate of nitrite production from nitrate decreased by 25 to 46%. The rate of NO production from nitrate decreased by 20 to 39%, and the rate of N(2)O production from nitrate, in the presence of acetylene (DEA), decreased by 21 to 61%. The predicted values of DEA at 0 g of chloramphenicol/liter computed from linear regressions of DEA versus chloramphenicol concentration were 18 to 43% lower than DEA measurements made in the absence of chloramphenicol and within a few per cent of DEA rates measured in the presence of 0.1 g of chloramphenicol/liter. We conclude that DEA assays should be carried out with a single (0.1-g/liter) chloramphenicol concentration. Chloramphenicol at concentrations greater than 0.1 g/liter inhibits the activity of existing denitrifying enzymes and should not be used in DEA assays. (+info)