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PubMed1992

Production of the Criegee ozonide during the ozonation of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine liposomes.

It is likely that Criegee ozonides are formed in small amounts in the lungs of animals breathing ozone-containing air. This makes these compounds potential candidates to act as secondary toxins which relay the toxic effects of ozone deeper into lung tissue than ozone itself could penetrate. Therefore, we have determined the yields of Criegee ozonides from unsaturated lipids in liposomal systems as a model of the types of yields of Criegee ozonides that might be expected both in the lung lining fluid layer and in biological membranes. Ozonation of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine liposomes produced both cis- and trans-Criegee ozonides. These ozonides have been isolated by solid phase extraction and high-performance liquid chromatography of the ozonized lipid, and the products have been identified by two-dimensional 1H nuclear magnetic resonance. The combined yield of the cis- and trans-Criegee ozonides is 10.7 +/- 2.8% (avg. +/- SD, n = 7) with small unilamellar liposomes and 10.6 +/- 2.7% (n = 3) with large multilamellar liposomes. We had previously reported (Chem. Res. Toxicol. 5, 505-511, 1992) that ozonation of methyl oleate in sodium dodecylsulfate micelles also produces an 11% yield of the Criegee ozonides. Thus, ozonation in a variety of models gives about 11% of the Criegee ozonide, suggesting that these products also would be formed in small but significant amounts in the lungs of animals breathing polluted air. Further research on the pharmacokinetics and possible toxicity of the Criegee ozonides of fatty acids is suggested.

Liposomes↗
PubMed1990

Guinea pig ozone-induced airway hyperreactivity is associated with increased N-acetyl-beta-D-glucosaminidase activity in bronchoalveolar lavage fluid.

High level ozone exposure is known to cause acute, neutrophil-independent airway hyperreactivity in the guinea pig. The precise biochemical mechanisms involved remain unclear. Because of its potential pathophysiologic importance, we examined whether a lysosomal hydrolase, N-acetyl-beta-D-glucosaminidase (NAGA) was released from the airways in vivo and from bronchoalveolar cells, specifically macrophages. Muscarinic reactivity was determined by measuring specific airway resistance (sRaw) in response to increasing doses of aerosolized acetylcholine in guinea pigs that were either exposed to air or to ozone (3.0 ppm, 2 h). The ozone-exposed animals showed substantial muscarinic hyperreactivity 30 min after exposure. In addition, both total and percent released NAGA in bronchoalveolar lavage fluid obtained immediately after reactivity testing were significantly greater in the ozone-exposed group. It was also found that substantially more NAGA was released from mixed bronchoalveolar lavage cells in response to 20 microM A23187. Moreover, bronchoalveolar macrophages of ozone-exposed animals secreted more NAGA upon stimulation in vitro by either 20 microM A23187 or 200 micrograms/ml opsonized zymosan. We conclude that ozone-induced airway hyperreactivity in guinea pigs is associated with the presence of increased NAGA activity in bronchoalveolar fluid. Our data suggest that bronchoalveolar macrophages may, at least in part, be responsible for release of this enzyme into the airways after ozone exposure.

Acetylglucosaminidase↗
PubMed2001

Basic examinations on chemical pre-oxidation by ozone for enhancing bioremediation of phenanthrene contaminated soils.

Biological treatment of polycyclic aromatic hydrocarbons (PAH) has been demonstrated to be a feasible and common remediation technology which has been successfully applied to the clean-up of contaminated soils. Because bioavailability of the contaminants is of great importance for a successful bioremediation, a chemical pre-oxidation step by ozone was tested to enhance the subsequent biodegradation steps. Oxidation of PAH by ozone should result in reaction products that have a better solubility in water and thus a better bioavailability. A major part of this work was done by examinations of the model substance phenanthrene as a typical compound of PAH. After initial ozonation of phenanthrene, analysis by GC-MS showed at least seven identified conversion-products of phenanthrene. In comparison with phenanthrene these conversion products were more efficiently biodegraded by Sphingomonas yanoikuyae or mixed cultures when the ozonation process resulted in monoaromatic compounds. Primary ozonation products with biphenylic structures were found not to be biodegradable. Investigations into the toxicity of contaminated and ozonated soils were carried out by well-established toxicity assays using Bacillus subtilis and garden cress. The ozonated soils surprisingly showed higher toxic or inhibitory effects towards different organisms than the phenanthrene or PAH itself. The microbial degradation of phenanthrene in slurry reactors by S. yanoikuyae was not enhanced significantly by preozonation of the contaminated soil.

Bacillus subtilis↗
PubMed2006

Control strategy optimization for attainment and exposure mitigation: case study for ozone in Macon, Georgia.

Implementation of more stringent 8-hour ozone standards has led the U.S. Environmental Protection Agency to designate nonattainment status to 474 counties nationwide, many of which had never previously violated air quality standards. As states select emission control measures to achieve attainment in these regions, their choices pose significant implications to local economies and the health of their citizens. Considering a case study of one such nonattainment region, Macon, Georgia, we develop a menu of potential controls that could be implemented locally or in neighboring parts of the state. The control menu offers the potential to control about 20-35% of ozone precursor emissions in most Georgia regions, but marginal costs increase rapidly beyond 15-20%. We link high-order ozone sensitivities with the control menu to identify cost-optimized strategies for achieving attainment and for alternative goals such as reducing spatially averaged or population-weighted ozone concentrations. Strategies targeted toward attainment of Macon ozone would prioritize local reductions of nitrogen oxides, whereas controls in the more densely populated Atlanta region are shown to be more effective for reducing statewide potential population exposure to ozone. A U.S. EPA-sanctioned approach for demonstrating ozone attainment with photochemical models is shown to be highly dependent on the choice of a baseline period and may not foster optimal strategies for assuring attainment and protecting human health.

Air Pollution↗
PubMed2002

Concepts in developing health-based indicators for ozone.

OBJECTIVES: The traditional manner to evaluate whether regulatory controls meet their public health goals of reducing adverse health effects associated with exposure to environmental pollutants is to compare measured concentrations of the target pollutant in the environment with a standard. A complementary approach is also to measure health-based indicators, e.g., changes in the prevalence of adverse health outcomes attributed to the pollutant. This manuscript presents the concepts of using asthma emergency room (ER) visits and hospital admission as potential health-based indicators for ozone. METHODS: The frequency of ER visits and hospital admissions for asthma in New Jersey in 1995 was compared with daily ozone concentrations, to establish the consistency of the relationship and the presence of potential confounders, and to establish whether routinely documented adverse outcomes in asthmatics could serve as health-based indicators. RESULTS: A mathematical model relating ER visits and hospital admissions of asthmatics to ozone concentration was developed for 1995, which was to be used as a baseline year within a health-based indicator program. A coherent relationship was found between same-day ambient air ozone concentrations and ER visits and 2-day time-lagged ambient ozone and hospital admissions during 1995; pollen was identified as a confounder and the association between ER visits and ozone concentration was similar to that determined for 1986 to 1990. CONCLUSIONS: Sufficient databases exist for ER visits by asthmatics in Northern and Central New Jersey, and throughout the state for hospital admissions, for these health outcomes to be used as health-based indicators, complementing air-monitoring data in assessing whether improvements in public health are occurring because of reduction in emissions of precursors of ozone.

Air Pollutants↗
PubMed1997

Long-term exposure to ozone alters peripheral and central catecholamine activity in rats.

In addition to its noxious influence on lung airways, ozone inhalation can induce extrapulmonary neural dysfunctions the mechanisms of which are poorly understood. This study was intended to characterize the effects of long-term exposure to ozone (0.5 ppm, 5 days) on catecholamine activity in rat sympathetic efferents and brain areas of prime importance to adaptation to environmental stressors. Catecholamine activity was assessed by estimating the turnover rate of catecholamines and in vivo tyrosine hydroxylase activity in peripheral and central structures, i.e., heart, lungs, superior cervical ganglia, cerebral cortex, hypothalamus and striatum, A2 cell group within the nucleus tractus solitarius (NTS), and locus ceruleus (A6). Ozone inhibited norepinephrine turnover in heart (-48% of the control level) but not in lungs. Ozone failed to modify the tyrosine hydroxylase activity in superior cervical ganglia, and the catecholamine content in the adrenal glands. In the central nervous system, ozone inhibited tyrosine hydroxylase activity in noradrenergic brainstem cell groups, including the locus ceruleus (-62%) and the caudal A2 subset (-57%). Catecholamine turnover was decreased by ozone in the cortex (-49%) and striatum (-18%) but not in the hypothalamus. The data show that ozone can produce marked neural disturbances in structures involved in the integration of chemosensory inputs, arousal, and motor control.

Adrenal Glands↗
PubMed2005

Measurements of ozone concentrations in Zagreb.

Ozone concentrations were measured in Zagreb at four sites from May 1999 to April 2001 in order to categorize the air quality with respect to ozone. In the summer of 2000, the ozone measurements were also extended to four sites in the suburbs of Zagreb. Methods of active and passive sampling with nitrite ion as a reagent were used. In the northern part of the town ozone was analyzed by an automatic device. Automatic device measurements in the years 1999 and 2000 showed that hourly averages of ozone concentrations did not exceed the Croatian recommended value of the 98th percentile (180 micro/g m(-3)). Over the two-year period, 24-h averages occasionally exceed 110 microg m(-3) in city center and in the northern part of the town. Regardless of these isolated examples, ozone was well within acceptable concentrations. Ozone concentrations measured in summer 2000 were higher in the suburbs of Zagreb than in the city. The 98th percentile values higher than 110 microg m(-3) were recorded at three sites.

Cities↗
PubMed2006

Variations and trends of ground-level ozone and AOT40 in the rural areas of Lithuania.

The analysis of data of the ground-level ozone concentration and accumulated ozone exposure over a threshold of 40 ppb (AOT40) in the rural areas of Lithuania is presented. Trends in the annual ozone mean, 95th and 25th percentiles were determined as statistically not significant at Preila and Rugsteliskes sites during the 1994-2004 period. Trends in the ozone concentration and its percentiles in the air masses arriving to Preila station in "polluted" and "unpolluted" sectors have been examined. Statistically significant changes in the ozone annual mean and 25th percentile were found in air masses in both "polluted" and "unpolluted" sectors in the 1988-2002 period. The trend analysis in the ozone monthly mean and percentiles for each month of the year revealed the main changes in the ozone level in both sectors during January-May. Insignificant downward trends in monthly 95th percentile in "unpolluted" sector and upward trends in "polluted" sector were found during summer months. Values of AOT40 for the protection of forests as well as crops and semi-natural vegetation were determined during the 1994-2004 period. The estimated AOT40 values for the protection of forests were lower than the critical level at Lithuanian rural sites but AOT40 values for the protection of crops and semi-natural vegetation were found to be higher than the critical level at both sites.

Air Pollutants↗
PubMed1984

The reaction of ozone with glyceraldehyde-3-phosphate dehydrogenase.

Inactivation of glyceraldehyde-3-phosphate dehydrogenase (GPDH) by ozone can be correlated with oxidation of the active-site -SH residue. Oxidation of peripheral -SH groups, and tryptophan, methionine, and histidine residues occurs concomitantly, but loss of activity depends solely on active-site oxidation. Inactivation is only slightly reversible by dithiothreitol. Kinetic studies show that inhibition of GPDH by ozone mimics noncompetitive inhibition and is characterized as irreversible enzyme inactivation. Analysis of products resulting from ozone oxidation of glutathione suggests that cysteic acid is the product of protein-SH oxidation. Despite oxidation of the active-site -SH , no significant decrease in the Racker band absorbance occurs. This is explained by the appearance of a new chromophore in this region of the absorbance spectrum. Increased absorbance at 322 nm following ozone treatment indicates that tryptophan is converted quantitatively to N-formylkynurenine. When the active-site -SH is reversibly blocked by tetrathionate, enzyme activity is completely recoverable following reaction of the derivatized enzyme with a 1.3X excess of ozone over enzyme monomer. Activity is fully recovered despite the oxidation of peripheral -SH, tryptophan, and histidine residues. Circular dichroism spectra of ozone-treated enzyme show that reaction of GPDH with up to a threefold excess of ozone over enzyme monomer results in no significant disruption of protein secondary structure. Spectra in the near-uv show distinct changes that reflect tryptophan oxidation.

Amino Acids↗
PubMed1987

Induction and inactivation of catalase and superoxide dismutase of Escherichia coli by ozone.

Oxyradicals have been implicated in ozone (O3) toxicity and in other oxidant stress. In this study, we investigated the effects of O3 on the biosynthesis of the antioxidant enzymes catalase and superoxide dismutase in Escherichia coli to determine their role in the defense against ozone toxicity. Inhibition of growth and loss of viability were observed in cultures exposed to ozone. Results also showed an increase in the activities of catalase and superoxide dismutase in cultures exposed to ozone, which was shown to be due to true induction rather than activation of preexisting apoproteins. Cessation of O3 exposure resulted in 30 min of continual high rate of catalase biosynthesis followed by a gradual decrease in the level of the enzyme approaching that of control cultures. This decrease was attributed to a concomitant cessation of de novo enzyme synthesis and dilution of preexisting enzyme by cellular growth. Ozonation of cell-free extracts showed that superoxide dismutase and catalase are subject to oxidative inactivation by ozone. In vivo induction of these enzymes may represent an adaptive response evolved to protect cells against ozone toxicity.

Catalase↗
PubMed1992

Reaction of ozone with glycophorin in solution and in lipid vesicles.

Glycophorin from human red blood cells was exposed to ozone in aqueous solution. Amino acid analysis of glycophorin exposed to a 10-fold molar excess of ozone showed that the only residue affected was methionine. Both methionine residues of the protein were oxidized to methionine sulfoxide. Exposure of the oxidized protein to cyanogen bromide caused no cleavage of the polypeptide chain. Glycophorin was incorporated into unilamellar lipid vesicles made from phosphatidylcholine. The protein containing vesicles were exposed to ozone in a 10-fold molar excess to the glycophorin. Gas chromatography of the methyl esters showed negligible change in the fatty acid composition. Amino acid analysis of the ozone-treated protein showed the oxidation of only one methionine residue per polypeptide chain to methionine sulfoxide. Ghosts of human erythrocytes were exposed to ozone. Cyanogen bromide treatment of the oxidized glycophorin yielded fragments showing that the only methionine residue oxidized by ozone was residue 8. These results indicate that in this membrane model (a) amino acid is more susceptible to ozone than is the lipid, and (b) amino acids external to the membrane are more susceptible than those in the polypeptide chain spanning the membrane.

Amino Acids↗
PubMed1993

Proteolytic activity is altered in brain tissue of rats upon chronic exposure to ozone.

Tissue from pons medulla of rats exposed in vivo to various levels of ozone was assayed for calpain and cathepsin D activity. Chronic exposure to ozone increased calpain activity, which was 35% to 46% higher in the homogenates of animals exposed to 1.0 ppm ozone than in those of animals exposed to 0.5 ppm ozone or of controls. An increase in activity of 26% was also observed in the soluble supernatant. The increase in activity did not seem to be caused by ozone effects on calpastatin. Addition of 32 mM carnitine to the incubation mixture increased total activity 3-4 fold, making the differences in activity proportionately smaller. Cathepsin D activity was little altered. Changes in calpain activity and in the generation of free oxygen radicals have been implicated in the aging process, long-term exposure to ozone may magnify changes. Ozone exposure may cause changes in brain protein metabolism.

Animals↗
PubMed1982

pH-sensitive mutagenic activity in ozone-treated 1,2-dimethylhydrazine in the Salmonella/microsome assay.

Treatment with ozone inactivates the mutagenicity of many carcinogens in aqueous solution. The colon carcinogen, 1,2-dimethylhydrazine (DMH) has been reported an exception; ozone treatment converts dimethylhydrazine from a non-mutagen into a mutagen. In the Salmonella/microsome assay, the mutagenicity of ozone-treated dimethylhydrazine was dependent on pH. The ozonation product was a strong mutagen in acidic solution but was not mutagenic in basic solution. The mutagenicity of the acidic ozonation product was inactivated by raising the pH of the solution. Unlike untreated dimethylhydrazine, its ozonation product in basic solution was not converted to a mutagen in this ozone-low pH system.

1,2-Dimethylhydrazine↗
PubMed1990

Effects of in vitro ozone exposure on peroxidative damage, membrane leakage, and taurine content of rat alveolar macrophages.

Rat alveolar macrophages (AM) were isolated by pulmonary lavage, allowed to adhere to a tissue culture flask, and then exposed to 0.45 +/- 0.05 ppm ozone. After exposures ranging from 0 to 60 min, the medium was decanted and cells were harvested. Cells were assayed for oxidant damage and media analyzed for leakage of intracellular components. Increasing length of exposure to ozone resulted in a decreased number of adherent AM and decreased cell viability. Resting and zymosan-stimulated chemiluminescence increased immediately after ozone exposure and reached a maximum at 15-30 min, then declined to initial levels after 60 min of ozone exposure. Lipid peroxidation and leakage of protein and K+ ions increased with increasing length of exposure to ozone, while leakage of reduced and oxidized glutathione increased through 30 min, then declined (reduced) or leveled off (oxidized). Activity of the Na+/K+ ATPase decreased with time while intracellular taurine concentration exhibited an initial rise, peaked at 30 min, and then returned to the untreated level. Leakage of taurine into the medium increased with time of exposure, suggesting that exposure of AM to ozone results in a shift from bound to free intracellular taurine. These data indicate that in vitro exposure of AM to ozone results in a time-dependent alteration of cell function, membrane integrity, and viability.

Adenosine Triphosphatases↗
PubMed1976

Characterization of an episode with elevated ozone concentrations.

A detailed analysis has been made of a seven day period in 1973, during which elevated ozone levels were observed at Ottawa. In addition to the ozone data, results are also presented for oxides of nitrogen, carbon monoxide, methane, total hydrocarbons and particulate matter. The particulates were analyzed for seven constituents, including the cations ammonium, calcium, sodium, potassium and lead and the anions sulfate and nitrate. Also measured were several other properties of the particulates, including the size distribution. It was found that none of the other gaseous pollutants showed any increase in concentration when high ozone levels were present. In contrast, the particulate matter did increase and several constituents, notably ammonium and sulfate, showed a dramatic rise. A comparison with ozone data from Toronto and upper New York state showed that the high ozone concentrations were widespread. A meteorological analysis showed that elevated ozone levels were associated with a Tropical air mass with a moderate southwesterly flow of air. Trajectory calculations were carried out to show the origin of the air over Ottawa before, during and after the period of increased ozone.

Air Movements↗
PubMed1982

Background continental ozone levels in the rural U.S. southwest desert.

From 1969 through 1978 an extensive ambient air quality monitoring program, including the measurement of atmospheric concentrations of ozone, has been conducted in a remote section of the desert in the southwestern U.S. Using a Monitor Labs chemiluminescent ozone instrument, these levels were measured atop a small mountain 500 feet above the valley floor of the Colorado River. During the winter months, when the prevailing low level winds are northerly in this river valley, rural continental background levels of ozone are attainable. From this continuous ozone data base, 13 of these representative high pressure periods have been selected for analysis. Results indicate a very distinct diurnal trend with an ozone minimum occurring from 0800-1000 hours Mountain Standard Time (MST) and an ozone maximum from 1600-1900 hours MST. Ozone concentrations range from a low of 19 ppb to a high of 44 ppb with the diurnal pattern exhibiting marked repeatability with respect to time of minima and maxima, seasonal changes and concentration levels.

Air Pollution↗
PubMed1992

Mutagenicity from ozonation of humic substances.

Eight structural components of humic substances were ozonated. Mutagenic activity was found using TA100 with and without S9 mix for all ozonated components. p-Hydroxybenzaldehyde was chosen as an important component and ozonation products were determined by gas chromatography-mass spectrometry (GC-MS). Aldehydes, ketones and carboxylic acids were identified as the ozonation products. Among these products, acetaldehyde, formaldehyde, glyoxal, methylglyoxal and glyoxylic acid were recognized to be mutagenic. Furthermore, p-hydroxybenzaldehyde was first ozonated and then chlorinated. A great variety of chlorinated organic compounds, many of which are known mutagens, have been identified by GC-MS in the ether extract. The same compounds have previously been reported as chlorination products of humic substances. Aldehydic products by ozonation were identified from ozonation followed by chlorination of humic substances and p-hydroxybenzaldehyde.

Animals↗
PubMed1985

Ozone inhibits prostacyclin synthesis in pulmonary endothelium.

The effects of ozone on lung arachidonate metabolism in-vitro were studied in cultured bovine pulmonary endothelial cells exposed for 2 hours to ozone in concentrations up to 1.0 ppm. A concentration-dependent decrease in prostacyclin synthesis was found (90% decrease at the highest ozone level of 1.0 ppm). The inhibition of prostacyclin synthesis was not due to a decreased release of arachidonic acid from membrane lipids. We also examined the hypoxic pulmonary vasoconstrictive response to 10% oxygen inhalation in anesthetized dogs in-vivo after exposure to 1.0 ppm ozone for 1 hour. Pulmonary vascular resistance was significantly increased after ozone exposure, similar to the findings in dogs given indomethacin (15 mg/kg). The percentage change in the hypoxic pulmonary pressor response was similar between the ozone exposure and indomethacin-treated groups, although due to the variance of the pulmonary vascular resistance values during hypoxia the results did not reach statistical significance. These results suggest that ozone inhalation affects pulmonary endothelial arachidonate metabolism in-vivo as well as in-vitro.

Animals↗