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PubMed2000

Measurements of (18)O-Enriched Ozone Isotopomer Abundances Using High-Resolution Fourier Transform Far-IR Spectroscopy.

The distribution of ozone isotopomers in ozone mixtures produced by electric discharge in mixtures of (16)O(2) and (18)O(2) at 77 K was measured by high-resolution FTIR spectroscopy. It was of key importance to assess not only the total amount of isotopomers of a certain mass but also the relative amounts of corresponding asymmetric and symmetric ozone species of the same mass given as the ratios [(16)O(16)O(18)O]/[(16)O(18)O(16)O] and [(16)O(18)O(18)O]/[(18)O(16)O(18)O]. For many purposes both ratios have been assumed to have the statistical value 2.00. Pure rotational spectra in the far-IR region (30-100 cm(-1)) were recorded for three different (18)O-enriched ozone mixtures, all at 0.00185 cm(-1) resolution. All the spectra were corrected for thermal emission. Linestrengths for individual lines in a particular spectrum were measured by means of a fitting technique taking into account contributions from all other lines in the spectrum. For this purpose theoretical linestrengths for all six ozone species containing (16)O and (18)O obtained from a quantum-number-dependent dipole operator were used. The ratios between observed and theoretical linestrengths were used to determine the abundances of individual isotopomers in a particular ozone mixture. For one of the ozone samples the abundances of all six ozone species were determined within 1% relative uncertainty. For the three ozone mixtures studied, the ratio between asymmetric and symmetric species of mono-(18)O ozone were determined to 1.99(2), 2.01(2), and 2.10(6). The ratio between asymmetric and symmetric species of di-(18)O ozone were determined to 2.51(4), 2.42(10), and 2.46(3). Copyright 2000 Academic Press.

Journal Article↗
PubMed1993

Physiological effects of ozone on cultivars of watermelon (Citrullus lanatus) and muskmelon (Cucumis melo) widely grown in Spain.

Two cultivars of watermelon (Citrullus lanatus) and muskmelon (Cucumis melo), which are widely grown in Spain, were exposed to ozone (70 nl litre(-1), 6 h d(-1)) for 21 days. Ozone sensitivity was assessed by recording the extent of visible injury, changes in fast-fluorescence kinetics, the relative-growth rate (R) of root (RR) and shoot (RS), and effects on the number of flowers produced per plant. Leaf gas exchange was measured in order to provide some indication of the factors underlying differential response to ozone. After 9-10 days of fumigation, all the cultivars developed typical visible symptoms of zone injury on the older leaves. However, significant (P < 0.05) changes in fast-fluorescence kinetics were detected prior to the development of visible foliar injury, indicating that detectable effects of ozone on primary photochemical processes supersede the appearance of visible symptoms. In both muskmelon and watermelon, there was a marked reduction in the rate of CO(2) assimilation as a result of exposure to ozone, and this was accompanied by a parallel decrease in stomatal conductance. Mean plant-relative-growth rate (R) was markedly (P < 0.01) suppressed by ozone in the two cultivars of watermelon, but there were no significant effects on R in muskmelon. Ozone reduced root growth relative to the shoot in three out of four cultivars-an effect that may be of considerable ecological significance. Moreover, exposure to ozone reduced flower production in both muskmelon and watermelon, which indicated effects on yield. There was no correlation between a variety of methods used to assess ozone sensitivity and visible injury, and reasons for this are discussed. This observation draws clear attention to the dangers in ranking plants for ozone sensitivity purely on the basis of visible symptoms. It is concluded from this study that ozone-insensitive genotypes should be identified and considered for planting in the major areas of melon production concentrated on the Mediterranean coast of Spain.

Journal Article↗
PubMed2000

Modelling of stomatal conductance and ozone flux of Norway spruce: comparison with field data.

It has been proposed that stomatal flux of ozone would provide a more reliable basis than ozone exposure indices for the assessment of the risk of ozone damage to vegetation across Europe. However, implementation of this approach requires the development of appropriate models which need to be rigorously tested against actual data collected under field conditions. This paper describes such an assessment of the stomatal component of the model described by Emberson et al. (2000. Modelling stomatal ozone flux across Europe. Environmental Pollution 110). Model predictions are compared with field measurements of both stomatal conductance (g(s)) and calculated ozone flux for shoots of mature Norway spruce (Picea abies) growing in the Tyrol Mountains in Austria. The model has been developed to calculate g(s) as a function of leaf phenology and four environmental variables: photosynthetic flux density (PFD), temperature, vapour pressure deficit (VPD) and soil moisture deficit (SMD). The model was run using climate data measured on site, although the SMD component was omitted since the necessary data were not available. The model parameterisation for Norway spruce had previously been collected from the scientific literature and therefore established independently from the measurement study. Overall, strong associations were found between model predictions and measured values of stomatal conductance to ozone (GO(3)) and calculated stomatal ozone flux (FO(3)). Average diurnal profiles of GO(3) and FO(3) showed good agreement between the field data and modelled values except during the morning period of 1990. The diurnal pattern of ozone flux was determined primarily by PFD and VPD, as there was little diurnal variation in ozone concentration. In general, the model predicted instances of high ozone flux satisfactorily, indicating its potential applicability in identifying areas of high ozone risk for this species.

Journal Article↗
PubMed2001

Effect of a chronic and moderate ozone pollution on the phenolic pattern of bean leaves (Phaseolus vulgaris L. cv Nerina): relations with visible injury and biomass production.

From sowing, bean (Phaseolus vulgaris L. cv Nerina) plants were exposed to three chronic doses of ozone for 7h.day(-1): non-filtered air (NF), non-filtered air supplied with 40nl.l(-1) ozone (NF+40) and non-filtered air supplied with 60nll(-1) ozone (NF+60). Four harvests were carried out 6, 13, 20 and 27 days after emergence. Either primary leaves, or first trifoliate leaves, or both were sampled as far as possible. For each sampled leaf, visible ozone injuries were registered, the free polyphenolic pool was analysed using HPLC and the dry matter was weighed. Visible damage on leaves was related to both exposure time and ozone concentration added. There were no adverse effects of added ozone on the biomass of primary leaves while a significant reduction of first trifoliates dry matter could be observed (NF+60 atmosphere, third and fourth harvest). Among the normally occurring phenolics, we detected a significant decrease in the accumulation of a hydroxycinnamic acid derivative as the ozone concentration increased. Nevertheless, we demonstrated that this ozone-induced modification could be sometimes distinguishable with difficulties from changes expected to be of development relevance. Beside this phenolic disbalance, we detected a de novo biosynthesis of compounds that closely depended on the level of visible ozone injury. Since their accumulation increased with leaf damage, these ozone-induced phenolics could be used to detect phytotoxic ambient levels of tropospheric ozone.

Journal Article↗
PubMed2002

Effect of ozone on bronchial mucosal inflammation in asthmatic and healthy subjects.

Epidemiological studies suggestthat asthmatics are more affected by ozone than healthy people. This study tested three hypotheses (1) that short-term exposure to ozone induces inflammatory cell increases and up-regulation of vascular adhesion molecules in airway lavages and bronchial tissue 6 h after ozone exposure in healthy subjects; (2) these responses are exaggerated in subjects with mild allergic asthma; (3) ozone exacerbates pre-existent allergic airways inflammation. We exposed 15 mild asthmatic and 15 healthy subjects to 0.2 ppm of ozone or filtered air for 2 h on two separate occasions. Airway lavages and bronchial biopsies were obtained 6 h post-challenge. We found that ozone induced similar increases in bronchial wash neutrophils in both groups, although the neutrophil increase in the asthmatic group was on top of an elevated baseline. In healthy subjects, ozone exposure increased the expression of the vascular endothelial adhesion molecules P-selectin and ICAM- 1, as well as increasing tissue neutrophil and mast cell numbers. The asthmatics showed allergic airways inflammation at baseline but ozone did not aggravate this at the investigated time point. At 6 h post-ozone-exposure, we found no evidence that mild asthmatics were more responsive than healthy to ozone in terms of exaggerated neutrophil recruitment or exacerbation of pre-existing allergic inflammation. Further work is needed to assess the possibility of a difference in time kinetics between healthy and asthmatic subjects in their response to ozone.

Adult↗
PubMed1994

Ozone-Induced Expression of Stress-Related Genes in Arabidopsis thaliana.

Ozone is a major gaseous pollutant that is known to have detrimental effects on plant growth and metabolism. We have investigated the effects of ozone on Arabidopsis thaliana growth and the pattern of expression of several stress-related genes. A. thaliana plants treated with either 150 or 300 parts per billion (ppb) ozone daily for 6 h exhibited reduced growth and leaf curling. Fresh and dry weights of ozone-treated plants were reduced 30 to 48% compared to ambient air controls. RNA blot analyses demonstrated that mRNA levels for glutathione S-transferase (GST), phenylalanine ammonia-lyase (PAL), a neutral peroxidase, and a cytosolic Cu/Zn superoxide dismutase (SOD) were higher in plants treated with 300 ppb ozone than in ambient air-treated controls. The mRNA levels of lipoxygenase and a catalase were not affected by ozone treatment. Of the transcripts examined, GST mRNA levels increased the most, showing a 26-fold induction 3 h after the initiation of ozone treatment. PAL mRNA was also rapidly induced, reaching 3-fold higher levels than controls within 3 h of ozone treatment. The neutral peroxidase and SOD mRNA levels rose more slowly, with both reaching maximum levels corresponding to 5-fold and 3-fold induction, respectively, approximately 12 h after ozone treatment. These studies indicate that ozone-induced expression of stress-related genes in A. thaliana provides an excellent model system for investigating the molecular and genetic basis of ozone-induced responses in plants.

Journal Article↗
PubMed1989

Increased 8-hydroxyguanine content of chloroplast DNA from ozone-treated plants.

The mechanism of ozone-mediated plant injury is not known but has been postulated to involve oxygen free radicals. Hydroxyl free radicals react with DNA causing formation of many products, one of which is 8-hydroxyguanine. By using high performance liquid chromatography with electrochemical detection, the 8-hydroxy-2'-deoxyguanosine (8-OHdG) content of a DNA enzymatic digest can be sensitively quantitated. Beans (Phaseolus vulgaris L.) and peas (Pisum sativum L.) were treated with an ozone regime that caused acute injury. Chloroplast DNA was obtained from plants harvested either immediately after ozone treatment or 24 hours later. Ozone-exposed plants in general had nearly two-fold higher levels of 8-OHdG as compared to control plants. In vitro treatment of DNA in buffer solution with ozone did not cause formation of 8-OHdG in DNA, even though ozone did react directly with the macromolecule per se. Exposure of isolated, illuminated chloroplasts to ozone caused nearly a seven-fold increase in the amount of 8-OHdG in the chloroplast DNA as compared to none-ozone-exposed chloroplasts. These results suggest that ozone exposure to plants causes formation of enhanced levels of oxygen free radicals, thus mediating formation of 8-OHdG in chloroplast DNA. The reaction of ozone with DNA per se did not cause formation of 8-OHdG. Therefore, it is the interaction of ozone with plant cells and isolated chloroplasts which mediates oxygen free radical formation.

Journal Article↗
PubMed1982

Adult toxicity and dominant lethals induced by ozone at specific stages in spermatogenesis in Drosophila virilis.

Ozone, a highly reactive three-atom allotrope of oxygen, is formed in high concentrations in various kinds of microenvironments, including electron microscopes, office copy machines, and X-ray devices. Mutagenicity and action modus operandi of ozone suggest its radiomimetic property. In order to test for ozone-induced dominant lethals in Drosophila virilis, we determined that four-hr and longer exposures to 30 +/- 2 ppm ozone were lethal on or before day 25 postexposure. Accordingly, we used a three-hr ozone exposure to investigate dominant lethals induced at specific spermatogenic stages. Ozone increased the percentage of dominant lethals in the stages of spermatogenesis which were investigated. Under the conditions of this experiment, the sperm-sperm bundle stage showed the greatest percentage of dominant lethals induced by ozone. Meiotic cells were the least sensitive to ozone mutagenicity. The induction of dominant lethals is discussed on the basis of chemical reactions from the molecular decomposition of water by radiations and/or ozone. Alternative explanations are presented due to the definition of induced dominant lethals and to associated modifications from ozone exposure.

Animals↗
PubMed1985

Alveolar permeability to protein in rats differentially susceptible to ozone.

Sprague-Dawley rats susceptible (DS) to NaCl-induced hypertension suffer higher mortality when exposed daily to 2.0 ppm ozone than do hypertension-resistant (DR) rats, independent of salt in the diet or systemic blood pressure. To investigate one possible contribution to this differential sensitivity to ozone, alveolar permeabilities to serum albumin were measured both in ozone-exposed and in control DS and DR rats. Female rats aged 5-7 weeks maintained on a low-salt (0.4% NaCl) diet were injected intravenously with 125I-bovine serum albumin and were then exposed to either 2.0 ppm ozone or air for 5 h. After pentobarbital anesthesia, the rats were exsanguinated and their lungs were lavaged in situ with saline. Lavage fluids and blood samples were measured for radioactivity using a NaI-well gamma counter. The results indicated that while DS and DR control rats have similar pulmonary permeabilities to 125I-albumin, the lungs of the ozone-exposed DS animals were 63% (p less than 0.02) more permeable than those of DR rats exposed to ozone. Sloughing of epithelial tissue, mucous formation and an accumulation of macrophages in the end-airways were more pronounced among ozone-exposed DS animals than in DR-ozone-exposed rats. This increased damage among DS rats correlated well with the increased protein permeability levels. In similar studies, Sprague-Dawley (D) rats were more variable in their response to ozone than either inbred strain. However, the results appeared generally more like those of the DS animals, suggesting that the trait selected by inbreeding may have been resistance rather than sensitivity to ozone-induced lung injury.

Albumins↗
PubMed1995

Sulfuric acid aerosol followed by ozone exposure in healthy and asthmatic subjects.

These studies evaluated symptom and pulmonary function responses of humans sequentially exposed to sulfuric acid aerosol and ozone. Thirty healthy subjects and 30 allergic asthmatic subjects underwent 3-hr exposures in an environmental chamber to 100 micrograms/m3 sulfuric acid and sodium chloride (control) aerosols (in random order), followed 24 hr later by 3-hr exposures to ozone (0.08, 0.12, or 0.18 ppm). Each subject was studied four times, receiving each aerosol preexposure followed by two of the three ozone concentrations. For the healthy group, no convincing symptomatic or physiologic effects of exposure to either the aerosol or ozone on lung function were found. For the asthmatic group, preexposure to sulfuric acid altered the pattern of response to ozone in comparison with sodium chloride preexposure and appeared to enhance the small mean decrements in FVC that occurred in response to 0.18 ppm ozone (means +/- SE: -3.6 +/- 1.5% with sodium chloride preexposure, -6.8 +/- 1.7% with sulfuric acid preexposure). Individual responses among asthmatic subjects were quite variable, some demonstrating reductions in FEV1 of more than 35% following ozone exposure. Analysis of variance of changes in FVC revealed evidence for interactions between aerosol and ozone exposure both immediately after (P = 0.005) and 4 hr after (P = 0.030) exposure. Similar effects were seen for FEV1. When normal and asthmatic subjects were combined, four-way analysis of variance revealed an interaction between ozone and aerosol for the entire group (P = 0.0022) and a difference between normal and asthmatic subjects (P = 0.0048). There was no significant effect of exposures on symptoms for either normal or asthmatic subjects. Asthmatic subjects differ from healthy volunteers in their functional responses following sequential exposures to aerosols and ozone and appear to represent a susceptible population.

Adult↗
PubMed1993

Ozone inhalation stimulates expression of a neutrophil chemotactic protein, macrophage inflammatory protein 2.

Short-term exposure of humans and animals to ozone results in increased lung neutrophils; however, the mechanisms underlying this response are not completely understood. We examined the potential involvement of the neutrophil chemotactic factor, macrophage inflammatory protein 2 (MIP-2), in ozone-induced inflammation. Exposure-response relationships for ozone and MIP-2 expression were characterized by exposing C57B1/6 mice to 0.1-2 ppm ozone for 3 hr and determining lung levels of MIP-2 mRNA 6 hr after exposure. Temporal relationships between ozone and MIP-2 were determined by exposing mice (2 ppm ozone x 3 hr) and characterizing MIP-2 mRNA expression 0, 2, 6, and 24 hr after exposure. Neutrophils in lung lavage fluid were determined in both exposure-response and time course studies. Ozone concentrations > or = 1.0 ppm increased MIP-2 mRNA and this increase corresponded with recruitment of neutrophils. MIP-2 mRNA was increased immediately after ozone exposure and decreased to control levels by 24 hr. To examine the role of direct oxidant effects in ozone-induced MIP-2 expression, alveolar macrophages were exposed in vitro for 4 hr to 10(-10)-10(-5) M hydrogen peroxide and MIP-2 expression was characterized. MIP-2 mRNA levels in lung macrophages were increased by > or = 10(-9) M hydrogen peroxide. In summary, our findings suggest the chemotactic protein MIP-2 may be responsible, at least in part, for ozone-induced increases in lung neutrophils and indicate that direct exposure of alveolar macrophages to an oxidant is sufficient to induce MIP-2 expression.

Administration, Inhalation↗
PubMed1995

Expression of Arabidopsis cytosolic ascorbate peroxidase gene in response to ozone or sulfur dioxide.

The effects of ozone or sulfur dioxide on antioxidant enzymes were investigated in Arabidopsis thaliana. Plants were fumigated with 0.1-0.15 ppm ozone or sulfur dioxide up to about 1 week in an environment-controlled chamber. Both pollutants increased the activities of ascorbate peroxidase and guaiacol peroxidase in leaves, but had little effect on the activities of superoxide dismutase, catalase, monodehydroascorbate reductase, dehydroascorbate reductase or glutathione reductase. Ozone was more effective than sulfur dioxide in increasing the activities of the peroxidases. Ascorbate peroxidase activity increased 1.8-fold without a lag period during fumigation with 0.1 ppm ozone, while guaiacol peroxidase activity increased 4.4-fold with a 1-day lag. Expression of the APX1 gene encoding cytosolic ascorbate peroxidase was further investigated. Its protein levels in leaves exposed to 0.1 ppm ozone for 4 or 8 days were 1.5-fold higher than in controls. Both ozone and sulfur dioxide elevated APX1 mRNA levels in leaves at 4 and 7 days, whereas at 1 day only ozone was effective. The induction of APX1 mRNA levels by ozone (3.4- to 4.1-fold) was more prominent than that by sulfur dioxide (1.6- to 2.6-fold). The APX1 mRNA level increased by day and decreased by night. Exposure of plants to 0.1 ppm ozone enhanced the APX1 mRNA level within 3 h, which showed a diurnal rhythm similar to that of the control. These results demonstrate that near-ambient concentrations of ozone as well as similar concentrations of sulfur dioxide can induce APX1 gene expression in A. thaliana.

Air Pollutants↗
PubMed2006

Vertical ozone distributions observed using tethered ozonesondes in a coastal industrial city, Kaohsiung, in southern Taiwan.

This work presents the vertical distributions of ozone and meteorological parameters observed with tethered ozonesondes and meteorological radiosondes in the lower atmosphere during an ozone episode on March 25-27, 2003, in Kaohsiung City in southern Taiwan. Kaohsiung is a coastal industrial city with inland mountain ranges to the east. Extremely complicated ozone structures were identified that spanned day and night during the experimental period. During afternoons, the lower atmosphere was divided into two stratified air layers with substantially different ozone concentrations. On the episode day (March 26), average ozone concentration in the near-ground layer was 85 ppb and the aloft layer was 140 ppb. A very high ozone peak of 199 ppb measured aloft likely resulted from an elevated large point source. Several no-ozone air layers, distributed throughout 400-750 m, were observed to transport on shore during the night. As well, elevated ozone layers peaking at 60-90 ppb and 90-160 ppb were detected below and above the no-ozone air layers, respectively. These complicated ozone structures were likely formed through titration of plumes from large point sources and the circulations of sea breezes or combined sea-breeze/mountain flows in the study area.

Environmental Monitoring↗
PubMed1985

Behavioral evaluation of the irritating properties of ozone.

The sensory irritant properties of ozone have been considered to be responsible for symptoms that occur in humans after exposure. This assumption has not been studied explicitly. One way to assess the aversive properties of airborne irritants is to give the exposed individual an opportunity to control the duration of exposure, i.e., escape from the irritant. Mice were trained to turn off 1000-ppm ammonia, a concentration that, in humans, is irritating to the upper airways. Each mouse could terminate irritant delivery for 1 min by inserting its nose five times into one of two conical response sensors. Daily exposure was limited to a maximum of twenty-five 1-min exposures, every other minute. After the determination of ammonia concentration-effect curves, ozone was substituted for ammonia. Ozone exposures were alternated every other day with ammonia as a control for any changes that might occur as a result of repeated ozone exposure. Ozone reliably maintained escape behavior. Additional mice with no history of ammonia termination were trained to terminate ozone exposure, indicating that the aversive properties of ozone were not dependent on previous experience with other airborne irritants. As the concentration of ozone increased from 0.25 to 24 ppm, the number of escape responses increased, and the duration of ozone tolerated decreased. Ozone concentrations of 0.5 ppm or greater were significantly more aversive than control.

Ammonia↗
PubMed1989

Pretreatment with EDU decreases rat lung cellular responses to ozone.

The phenylurea compound EDU (N-[2-(2-oxo-1-imidazolindinyl)ethyl]-N'-phenylurea) has been shown to protect plants from the damaging effects of ozone exposure. Models of rat lung injury, based on acute exposure to 2 ppm ozone for 3 hr and on exposure to 0.85 ppm ozone for 2 days, were used to determine whether EDU pretreatment of rats protected lungs from oxidant injury. Rats were pretreated with 100 mg/kg body wt EDU by ip administration for 2 days prior to and on the days of ozone exposure. No adverse toxicological effects of EDU pretreatment were observed. Lung superoxide dismutase (SOD) and catalase (CAT) activities were significantly enhanced from 636 to 882 U/lung and from 599 to 856 U/lung, respectively. One day following acute exposure (2 ppm for 3 hr), an ozone-induced increase of polymorphonuclear leukocytes (PMNs) from 0.01 to 1.18 million cells/lung was decreased to 0.68 million by EDU pretreatment. No alteration occurred in the degree of lung permeability indicated by increased lavage fluid albumin. EDU pretreatment also significantly decreased ozone-induced increases in PMN recovery after 2 days exposure to 0.85 ppm ozone from 5.54 to 2.12 million cells/lung. However, in this second case, EDU pretreatment reduced the observed ozone damage, indicated by a decrease in lavage fluid albumin and by a decrease in the macrophage and lymphocyte infiltration associated with this length of ozone exposure. The observation that EDU-treated cultured pulmonary arterial endothelial cells increased SOD and CAT activities identified a potential lung site of EDU interaction. These data demonstrated that although EDU pretreatment appears not to prevent initial ozone damage, it does reduce the infiltration of PMNs and might therefore prevent amplification of the injury associated with this cell type.

Animals↗
PubMed1991

The effect of ozone inhalation on metabolic functioning of vascular endothelium and on ventilatory function.

The primary purpose of this research was to determine the effect of ozone inhalation on pulmonary vascular endothelium. Male Fischer-344 rats were exposed to 0.5 or 0.7 ppm ozone, 20 hr/day for 7 days. Lungs were excised and perfused with Krebs medium containing [14C]serotonin or [14C]hippurylhistidylleucine (HHL). When compared to controls, the animals exposed to the lower ozone concentration showed no statistically significant changes in serotonin removal. In contrast, the higher ozone concentration resulted in a 32% decrease (p less than 0.0001) in serotonin removal, but had no effect on HHL. Rats similarly exposed to 0.7 ppm ozone but allowed to recover for 14 days in clean air showed no decrease in serotonin removal compared to their controls. Animals exposed sequentially to 0.5 ppm ozone for 7 days and then to 0.7 ppm for 7 days showed no alteration in serotonin metabolism, suggesting the development of tolerance initiated by the lower dose. After 7 days exposure to 0.7 ppm ozone, lung ventilatory function measurements revealed small though significant decreases in several parameters. Electron microscopic evaluation of lung capillary endothelium from animals exposed to the 0.7 ppm ozone showed no changes. Positive control animals exposed to greater than 95% oxygen, 20 hr/day for 2 days showed a 23% decrease in serotonin removal (p less than 0.03) and a 12% decrease in HHL removal (p less than 0.017). These studies indicate that inhalation of ozone can induce functional alterations in the lung endothelium, and that this effect occurs at a dosage of ozone that produces minimal ventilatory changes and no observable endothelial ultrastructural changes.

Administration, Inhalation↗
PubMed1992

Synergistic interaction of nitrogen dioxide and ozone on rat lungs: acute responses.

Rats were exposed for 6 hr per day to either ozone alone (0.2-0.8 ppm), nitrogen dioxide (NO2) alone (3.6-14.4 ppm), or to combinations of these two oxidant air pollutants. Their response was quantified by changes in the total protein content of lung lavage supernatants or by changes in the content of specific cell types in the lung lavage pellets. A concentration-dependent synergistic response was observed when rats were exposed to the combination of ozone and NO2. Apparent threshold concentrations for the observation of synergistic interaction between ozone and NO2 were assay specific, with epithelial cell content of lung lavage fluid being the most sensitive parameter evaluated, showing positive interaction (greater than additive response) at the lowest concentrations tested. Concurrent exposure to ozone and NO2 was necessary to elicit greater than additive responses; no such interactions were seen upon sequential exposure to ozone or NO2 in either order of presentation. Based upon apparent disappearance rates of ozone in the chambers during exposure of rats to ozone and NO2, we modelled the predicted outcomes based upon the assumption that the two oxidant gases were reacting to form nitrogen pentoxide (N2O5) in the chambers. Agreement between predicted concentrations of ozone and NO2 and those actually observed was excellent. Based upon such modelling estimates and our acute toxicological data, we conclude that synergistic toxicologic interactions between ozone and NO2 are found only at concentrations very much higher than would be encountered in environmental or occupational settings. It remains to be determined whether there are any chronic toxicological responses to exposure to combinations of ozone and NO2 at concentrations below the thresholds for observing acute responses.

Administration, Inhalation↗
PubMed1995

Release of prostaglandin E2 and leukotriene C4/D4 from airway segments isolated from rats after exposure to ozone for 20 months.

Metabolites of arachidonic acid have been implicated as mediators of some of the pulmonary effects observed after acute exposure to ozone. Accordingly, recent studies have focused on the effects of acute ozone exposure on the arachidonic acid cascade, however, whether eicosanoid metabolism is altered after chronic exposure to ozone is unknown. To begin to address this issue, we examined the effects of near-lifetime exposure to ozone on release of prostaglandin E2 (PGE2) and leukotriene C4/D4 from airway segments isolated from exposed Fischer-344 rats. Airway segments representing approximately eighth to tenth generation airways were isolated from rats of both genders that had been exposed for 6 h per day, 5 days per week for 20 months to filtered air or 0.12, 0.5 or 1.0 parts per million (ppm) ozone. Basal and stimulated release of eicosanoids were measured in the medium surrounding airway segments using enzymoimmunoassay. Basal release of PGE2 was detected in the medium surrounding airway segments and this release was unaffected by ozone exposure. Incubation of the segments with the calcium ionophore, A23187, increased the release of the prostaglandin; the A23187-induced release of PGE2 was significantly enhanced in airway segments isolated from rats in the 1.0 ppm exposure group. Basal release of leukotriene C4/D4 was not detected in the medium surrounding airway segments regardless of ozone exposure. Measurable amounts of the leukotriene were released during incubation with A23187, however, ozone was without affect on these levels. The results suggest that the cyclooxygenase pathway of the arachidonic acid cascade appears to be affected by ozone exposure. Which of the processes of prostaglandin production and release are affected by chronic ozone exposure remains to be determined.

Administration, Inhalation↗