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PubMed2003

Traffic congestion and ozone precursor emissions in Bilbao, Spain.

GOAL, SCOPE AND BACKGROUND: In urban environments, the measured levels of ozone are the result of the interaction between emissions of precursors (mainly VOCs and NOx) and meteorological effects. In this work, time series of daily values of ozone, measured at three locations in Bilbao (Spain), have been built. Then, after removing meteorological effects from them, ozone and traffic data have been analyzed jointly. The goal was to identify traffic situations and link them to ozone levels in the area of Bilbao. METHODS: To remove meteorological effects from the selected ozone time series, the technique developed by Rao and Zurbenko was used. This is a widely used technique and, after its application, the fraction obtained from a given ozone time series represents an ozone forming capability attributable to emissions of precursors. This fraction is devoid of any meteorological influence and includes only the apportion of periodicities above 1.7 years. In the case of Bilbao, the ozone fractions obtained at three locations have been compared on that time scale with traffic data from the area. RESULTS AND DISCUSSION: For the 1993-1996 period, a regression analysis of the ozone and traffic fractions due to periodicities above 1.7 years (long-term fractions), shows that traffic is the main explanatory factor for ozone with R2 ranging from 0.916 to 0.996 at the three locations studied. Analysis of these longterm fractions has made it possible to identify two traffic regimes for the whole area, associated to different profiles of ozone forming capability. The first one favors low ozone forming capability, and is associated with a situation of fluent traffic. The second one shows high ozone forming capability and represents congestion. Joint analysis of raw data of ozone and traffic do not show any clear pattern due to the strong masking effects that seasonal-meteorological effects (mainly radiation) have on the measured ozone signal. If only immission data of ozone are available, as in this case, a comparison between ozone and traffic can only be made on the long-term time scale, since that is the only fraction embedded in the ozone time series that can exclusively be attributed to emissions of precursors. This fact stresses the need to study the different fractions embedded in the time series of ozone measured levels separately. CONCLUSION: Though the coefficients obtained in the regression are only valid for the 1993-1996 period, these traffic regimes represent long-term targets (congestion or fluent traffic) that can inspire policies for a joint management of the traffic and pollution by ozone in the area of Bilbao beyond that period. RECOMMENDATIONS AND OUTLOOK: The results of this work show the need of a joint management of ozone and traffic in Bilbao. Since an accurate knowledge of traffic was not available, the use of emission factors to relate traffic and actual ozone levels has not been possible. For this reason, this study has focused on the long-term fractions of traffic and ozone. In the future, if a more accurate knowledge of traffic is available, it will be possible to find relationships between traffic and ozone on all time scales.

Cities↗

PubMed2004

Ovalbumin-induced airway inflammation and fibrosis in mice also exposed to ozone.

A murine model of allergen-induced airway inflammation was used to examine the effects of exposure to ozone on airway inflammation and remodeling. Sensitized BALB/c mice were exposed to ovalbumin aerosol for 4 wk before and after 2 wk of exposure to either 0.2 ppm or 0.5 ppm ozone. Other groups of mice were exposed to ovalbumin aerosol for 6 wk with continuous concurrent exposure to ozone during wk 1-6, or during intermittent concurrent exposure to ozone. Lung inflammation was measured by quantitative differential evaluation of lung lavage cells and by histological evaluation of stained lung sections. Alterations in lung structure (airway fibrosis) were evaluated by quantitative biochemical analysis of microdissected airways. The same total number of cells was observed in lavage fluid from animals exposed for 4 wk to ovalbumin alone or to ovalbumin for 4 wk immediately before or after exposure to 2 wk of 0.2 or 0.5 ppm ozone. Mice exposed to ovalbumin for 6 wk with concurrent exposure to either 0.2 ppm or 0.5 ppm ozone during wk 3-6 had a significant decrease in the total number of cells recovered by lavage. Values as low as 7% of the cell number found in mice exposed to ovalbumin aerosol alone were observed in the mice exposed to ovalbumin plus 0.2 ppm ozone during wk 3-6. There were significant differences in the cell differential counts in the lavage fluid from mice exposed to ovalbumin alone as compared with values from mice exposed to ovalbumin and ozone under all of the protocols studied. When ozone was given for 2 wk prior to ovalbumin exposure (Experiment 1), there were a high percentage of macrophages and low percentages of lymphocytes and eosinophils in the lung lavage. When ozone was given for 2 wk after ovalbumin exposure (Experiment 2), there were a moderate percentage of macrophages, a low percentage of eosinophils, and a high percentage of lymphocytes in the lung lavage. When ozone and ovalbumin were given simultaneously (Experiments 3 and 4), there were a high percentage of macrophages in the lavage with 0.2 ppm ozone and a high percentage of eosinophils. Ozone appears to antagonize the specific inflammatory effects of ovalbumin exposure, especially when given before or during exposure to ovalbumin. Airway remodeling was examined by two different quantitative methods. None of the groups exposed concurrently to ovalbumin and ozone had a significant increase in airway collagen content as compared to the matched groups of mice exposed to ovalbumin alone. The findings were consistent with an additive response of mice to simultaneous exposure to ovalbumin and ozone. Ozone exposure alone for 6 wk did not affect the number of goblet cells in the airways, while mice exposed to ovalbumin aerosol alone for 6 wk had about 25% goblet cells in their conducting airways. Concurrent exposure to ovalbumin and 0.2 ppm ozone caused significant increases in goblet cells (to 43% of total cells) in the conducting airways of the exposed mice. We conclude that when mice with allergen-induced airway inflammation induced by ovalbumin are also exposed to ozone, the lung inflammatory response may be modified, but that this altered response is dependent on the sequence of exposure and the concentration of ozone to which they are exposed. At the concentrations of ozone tested, we did not see changes in airway fibrosis. However, goblet-cell hyperplasia appeared to be increased in mice exposed concurrently to ovalbumin and 0.2 ppm ozone.

Aerosols↗

PubMed2003

Dynamic behavior of ozonation with pollutant in a countercurrent bubble column with oxygen mass transfer.

The dynamic behavior of ozonation with pollutants in a countercurrent bubble column is studied for the model establishment. Bubble columns have been widely used for an ozonation system in the plants and laboratories. In addition, a countercurrent bubble column has been commonly recommended than a cocurrent one because it has a higher ozone transfer efficiency. Therefore, the investigation of this paper focuses on the countercurrent bubble column. As an ozonation process starts, the gas mixture of ozone and oxygen is introduced into the bottom of a column, and then transferred into the liquid. The pollutants in the wastewater are eliminated subsequently via oxidation by the dissolved ozone. There certainly exists a temporary and unsteady period before the ozonation system reaches steady state. However, available ozonation models employed to describe ozone and pollutant profiles have commonly been developed for steady state. The treating qualities of wastewater in the early stage of ozonation are usually not predicted, and the time required for the steady-state establishment remains to be determined. Moreover, oxygen mass transfer is usually neglected in previous ozonation models so that the increase of dissolved oxygen is uncertain. These information is desirable for the proper design and operation of ozonation system in a bubble column. Thus, the aim of this study is to model and investigate the dynamic processes of ozonation with pollutants including oxygen mass transfer. The dynamic axial dispersion model proposed is employed to predict the variation of the ozone, pollutant, and oxygen concentrations profiles. The validity of the model was demonstrated by comparing the predicted results with the experimental data. The o-cresol was chosen as the model pollutant. The temporal concentration variations of the residual o-cresol and dissolved oxygen in the effluent liquid, and the off-gas ozone in the free volume were measured accordingly. Furthermore, the variation of the enhancement factor of ozone and the amount of off-gas were predicted. Note that it usually needs 2-5 hydraulic retention times to approach steady state under the conditions of this study. Further, the effects of dimensionless system parameters on the performance of the ozonation processes are examined. As a result, the proposed dynamic model of ozonation with pollutants is useful for proper prediction of the variables of an ozonation system in a countercurrent bubble column.

Gases↗

PubMed1997

Reaction of ozone with protein tryptophans: band III, serum albumin, and cytochrome C.

Treatment of red cell ghosts with ozone inhibited both AChE (marking the outside of the membrane) and G3PDH (marking the inside of the membrane). There was no change in tryptophan fluorescence of the ghosts after the ozone treatment. Band 3 protein was isolated from the ozone-treated ghosts. The protein was digested with trypsin to obtain water soluble peptides from the cytoplasmic N-terminal tail and the interhelical loops. Fluorescent peptides included GWVIHPLGLR from the outer loop between helices 7 and 8, and peptide WMEAAR from the N-terminal cytoplasmic tail. Neither one of these peptides was oxidized by ozone. This was true whether or not the ghosts were sealed. We conclude that the position of these tryptophans either in the membrane structure, or because of binding to other proteins in the cytoplasmic tail, protects them from oxidation by ozone. Treatment of horse heart cytochrome c with ozone did not change the absorbance spectrum in the heme region or the tryptophan absorbing region. HPLC of the ozone-treated cytochrome c showed that cytochrome c was being modified, indicated by a change in the elution time. Treatment of cytochrome c with ozone did not change the activity in the NADH-cytochrome c reductase assay. Digestion of the ozone-treated cytochrome c with trypsin gave peptides which demonstrated normal fluorescence. (Cytochrome c has abnormally low fluorescence, which is not changed by ozone exposure.) The peptides were separated by HPLC. The fluorescence of the tryptophan-containing peptide (GITWK) was not decreased by treatment of the cytochrome c by ozone. Amino acid analysis of the ozone-treated cytochrome c indicated that methionine was oxidized. We conclude that tryptophan in cytochrome c is protected from oxidation by ozone because of the interaction with the porphyrin ring. Bovine serum albumin and human serum albumin were treated with ozone. There was a monotonic decrease in tryptophan fluorescence in both cases. Digestion of BSA with trypsin produced two fluorescent peptides. The peptide FWGK was identified by coelution with the authentic peptide. The putative peptide AWSVAR was not the same as the chemically synthesized peptide. The peptide sequences FWGK and "AWSVAR" were both oxidized in ozone-treated bovine serum albumin, with no detectable discrimination. Tryptic digestion of the ozone-treated human serum albumin produced a single fluorescent peptide, which was oxidized by ozone. The putative peptide AWAVAR in the tryptic digest of HSA was distinct from chemically synthesized peptide. The oxidation of tryptophans in proteins by ozone is markedly influenced by position in tertiary structure, position in membrane structure, and by chemical interactions within the protein.

Animals↗

PubMed1999

A comparison of biomarkers of ozone exposure in human plasma, nasal lavage, and sputum.

We examined ozone-induced upper and lower airway inflammatory responses and the concentrations of hydroxylated salicylate metabolites using nasal lavage fluid and induced sputum, in order to identify noninvasive and sensitive biomarkers for ozone exposure and effects. A time course for plasma concentration of 2, 3-dihydroxybenzoic acid (2,3-DHBA, a salicylate metabolite and an indicator for hydroxyl radical) in response to 0.12 ppm ozone was also studied. Healthy, young, nonsmoking volunteers were given acetylsalicylic acid (ASA, 975 mg) or placebo orally. Subjects were exposed to ozone (0.12 or 0.4 ppm) or filtered air in an environmental chamber for 2 h, while performing intermittent exercise. Blood was collected hourly over a 4-h period. After exposure, nasal lavage fluid was collected, and sputum was induced using hypertonic saline. Results show that in sputum the percentage of neutrophils was significantly higher after the subjects were exposed to 0.4 ppm ozone (p<.05) than after they were exposed to filtered air or 0.12 ppm ozone. The absolute number and the percentage of macrophages were significantly lower at 0.4 ppm ozone than for filtered air control or 0.12 ppm ozone. The percentage of lymphocytes in sputum was also significantly lower at 0.4 ppm ozone than for filtered air control or 0.12 ppm ozone. The sputum cellular responses to ozone were not significantly altered by ASA treatment. In nasal lavage, cell counts and differentials did not change significantly after exposure to ozone in comparison to filtered air control. The cellular data indicate an acute inflammation developed during ozone exposure in the lower respiratory tract. The concentrations of total protein and interleukin-8 and the activity of N-acetyl-beta-D-glucosaminidase (a lysosomal enzyme) in nasal lavage and sputum did not change significantly following exposure to ozone in comparison to filtered air control. Plasma 2,3-DHBA concentration increased significantly following exposure to 0.12 ppm ozone in an exposure-dependent temporal pattern. Salicylate metabolites in nasal lavage fluid and sputum did not increase significantly following exposure to ozone. There was a marked variation of 2,3-DHBA concentrations in airway fluids. Data suggest that plasma 2,3-DHBA is a sensitive marker indicating acute ozone exposure, even at an ozone concentration that causes minimal observable airway effects in healthy subjects.

Adolescent↗

PubMed2004

Modelling critical levels of ozone for the forested area of Austria. Modifications of the AOT40 concept.

GOAL, SCOPE AND BACKGROUND: Ozone is the most important air pollutant in Europe for forest ecosystems and the increase in the last decades is significant. The ozone impact on forests can be calculated and mapped based on the provisional European Critical Level (AOT40 = accumulated exposure over a threshold of 40 ppb, 10,000 ppb x h for 6 months of one growing season calculated for 24 h day(-1)). For Norway spruce, the Austrian main tree species, the ozone risk was assessed in a basis approach and because the calculations do not reflect the health status of forests in Austria, the AOT40 concept was developed. METHODS: Three approaches were outlined and maps were generated for Norway spruce forests covering the entire area of Austria. The 1st approach modifies the AOT40 due to the assumption that forests have adapted to the pre-industrial levels of ozone, which increase with altitude (AOTalt). The 2nd approach modifies the AOT40 according to the ozone concentration in the sub-stomata cavity. This approach is based on such factors as light intensity and water vapour saturation deficit, which affect stomatal uptake (AOTsto). The 3rd approach combines both approaches and includes the hemeroby. The pre-industrial ozone level approach was applied for autochthonous ('natural') forest areas, the ozone-uptake approach for non-autochthonous ('altered') forest areas. RESULTS AND DISCUSSION: The provisional Critical Level (AOT40) was established to allow a uniform assessment of the ozone risk for forested areas in Europe. In Austria, where ozone risk is assessed with utmost accuracy due to the dense grid of monitoring plots of the Forest Inventory and because the continuously collected data from more than 100 air quality measuring stations, an exceedance up to the five fold of the Critical Level was found. The result could lead to a yield loss of up to 30-40% and to a severe deterioration in the forest health status. However, the data of the Austrian Forest Inventory and the Austrian Forest Damage Monitoring System do not reflect such an ozone impact. Therefore, various approaches were outlined including the tolerance and avoidance mechanisms of Norway spruce against ozone impact. Taking into consideration the adaptation of forests to the pre-industrial background level of ozone, the AOT40 exceedances are markedly reduced (1st approach). Taking into account the stomatal uptake of ozone, unrealistic high amounts of exceedances up to 10,000 ppb x h were found. The modelled risk does not correspond with the health status and the wood increment of the Austrian forests (2nd approach). Consolidating the forgoing two approaches, a final map including the hemeroby was generated. It became clear that the less natural ('altered') forested regions are highly polluted. This means, that more than half of the spruce forests are endangered by ozone impact and AOT40 values of up to 30,000 ppb x h occur (3rd approach). CONCLUSIONS: The approaches revealed that a plausible result concerning the ozone impact on spruce forests in Austria could only be reached by combining pre-industrial ozone levels, ozone flux into the spruce needles and the hemeroby of forests.

Adaptation, Physiological↗

PubMed2003

DOC removal by multi-stage ozonation-biological treatment.

Multi-stage ozonation-biological treatment process for dissolved organic carbon (DOC) removal was evaluated to apply for drinking water treatment. Waters with different types of DOC were used, i.e. a reservoir water for drinking water supply, a secondary effluent from a municipal wastewater treatment plant and a solution of humic substances extracted from leaf mold. The multi-stage ozonation-biological treatment process was compared with conventional single-stage ozonation-biological treatment process. Amount of DOC removed in biological treatment was defined as amount of biodegradable dissolved organic carbon (BDOC) in influent of biological treatment. DOC removal in the multi-stage ozonation-biological treatment was higher than that in the conventional single-stage ozonation-biological treatment with the same total ozonation time for the reservoir water and humic substances solution. Moreover, three- or four-stage ozonation for 5 min followed by biological treatment (total ozonation time 15 or 20 min) showed higher removal of DOC than the single-stage ozonation (60 min) and biological treatment. The higher DOC removal in the multi-stage treatment was due to the production of BDOC by ozonation. The long-term ozonation was not effective to produce BDOC because most of ozone was utilized to oxidize BDOC produced in the early stage of ozonation. In the multi-stage treatment, ozonation was effective to decompose refractory DOC and to produce BDOC because BDOC was removed by biological treatment. However, multi-stage ozonation-biological treatment was not effective for the secondary effluent. The reason seems to be high concentration of ozone scavengers in that water and low reactivity of DOC for ozone.

Bioreactors↗

PubMed2005

Effect of some operational parameters on the decolorization of textile effluents and dye solutions by ozonation.

Treatment of three wastewaters and two acid dye solutions by ozonation with varying ozone dose, initial pH, and initial dye concentration were examined. Ozonation of all the wastewaters were shown to be pseudo-first-order reaction with respect to color, chemical oxygen demand (COD) and dissolved organic carbon (DOC). Increasing ozone dose increased the removal of color, COD, and DOC, as well as decreased ozone consumption ratio, and increased apparent rate constants. Ozonation was more successful at decolorization than the removal of COD and DOC or augmentation of biodegradability. Increasing initial dye concentration increased the ozone consumption and decreased the rate constant. Color removal efficiencies for different ozone dose application were in the range of 60-91% for sample A (dye bath effluent), and 70-96% for sample B (plant effluent). For sample A, COD and DOC removal efficiencies at several ozone dose applications were between 13-22 % and 8-13%, respectively. For sample B, they were between 11-33% and 6-15% respectively. Increasing pH could expand the efficiency of ozone slightly. Ozone consumption per unit color, COD and DOC removal at any time was found to bealmost the same whereas the applied ozone dose was different at a constant pH. Ozonation increased the biochemical oxygen demand (BOD,) of sample A and B 1.22 and 1.37 times by consuming 300 and 225 mg ozone, respectively. Ozonation of acid dyes was a pseudo-first order reaction with respect to dye. Increases in dye concentration raised specific ozone consumption. Specific ozone consumption for Acid Red 183 (AR-183) dye solution with 50 mg l(-1) of concentration rose from 0.32 to 0.72 mg-O3 per mg dye decomposed as the dye concentration was increased to 500 mg l(-1).

Coloring Agents↗

PubMed1980

Respiratory responses in humans repeatedly exposed to low concentrations of ozone.

The effect of repeated daily exposure to a low concentration of ozone was studied in healthy adult males to answer 2 questions: (1) Is there a cumulative effect of exposure to ozone from day to day, causing an exacerbation of changes in pulmonary function? (2) Does the subject develop resistance or adaptatin to the respiratory effects of ozone? The subjects were exposed for 2 h in an environmental chamber at 35 degrees C and 45% relative humidity to filtered air on day 1, to ozone on days 2 through 4, and to filtered air on day 5. Three groups of subjects were used, each exposed to a different concentration of ozone: group 1 (n = 10), 0.20 ppm of ozone; group 2 (n = 10), 0.35 ppm of ozone; group 3 (n = 8), 0.50 ppm of ozone. There were no acute or cumulative effects of repeated exposure to 0.20 ppm of ozone. With exposure to 0.35 ppm of ozone, there were decrements in forced expiratory parameters on day 2. These changes were greater on day 3, but wre largely absent on days 4 and 5. In group 3, there were marked effects of ozone on pulmonary function on day 2, but these changes were greatest on day 3. Significant effects (although of lesser magnitude) were also observed on day 4. The forced expiratory volume in 1 s decreased 8.7% on day 2, 16.5% on day 3, and 3.6% on day 4. The subjects claimed the most discomfort on day 3; many noted marked improvements on day 4, the third consecutive day of exposure to ozone. Two additional subjects were exposed to 0.50 ppm of ozone for 4 consecutive days. Although effects of ozone on pulmonary function were observed on the first 2 days of exposure, few effects were seen on the third day, and no effect was observed on the fourth day. We conclude that there is some short-term cumulative effect of exposure to concentrations of ozone above the threshold for producing acute respiratory effects. This is followed by a period of resistance or adaptation in which there is a marked lessening of the effect of ozone on pulmonary function and on the subjective feelings of discomfort associated with exposure to ozone.

Adolescent↗

PubMed1992

How far does ozone penetrate into the pulmonary air/tissue boundary before it reacts?

A simple method is suggested for calculating the time it takes ozone to traverse a biological region, such as a bilayer or a cell, and comparing this time to the halflife of ozone within that region. For a bilayer the calculations suggest that most of the ozone reacts within a bilayer, but a fraction may exit unreacted. For the lung lining fluid layer (LLFL), the calculations show that ozone cannot cross this layer without reacting where the LLFL is thicker than about 0.1 microns. However, since the LLFL varies from 20 to 0.1 microns in thickness with patchy areas in the lower airways that are virtually uncovered, some ozone could reach underlying cells, particularly in the lower airways. For cells (such as alveolar type I epithelial cells), the calculations show that ozone reacts within the cell too rapidly to pass through and exit unreacted from the other side. These calculations have implications for ozone toxicity. In vivo, the toxicity of ozone is suggested to result from the effects of a cascade of products that are produced in the reactions of ozone with primary target molecules that lie close to the air/tissue boundary. These products, which have a lower reactivity and longer lifetime than ozone itself, can transmit the effects of ozone beyond the air/tissue interface. The variation in thickness of the LLFL may modulate the species causing damage to the cells below it. In the lower airways, where the LLFL is thin and patchy, more cellular damage may be caused by ozone itself; in the upper airways where the LLFL is thicker, secondary products (such as aldehydes and hydrogen peroxide) may cause most of the damage. In vitro studies must be designed in an attempt to model the lung physiology. For example, if cells in culture are studied, and if the cells are exposed to ozone while under a supporting medium solution that contains ozone-reactive substances, then the cells may be damaged by products that are formed in the reactions of ozone with the cell medium rather than by ozone itself.

Air Pollutants↗

PubMed2003

Inactivation of fungi associated with barley grain by gaseous ozone.

The use of gaseous ozone as a fungicide to preserve stored barley was studied. The effects of the following operating parameters on the fungicidal efficacy of ozone were examined: 1) the applied ozone dose, 2) ozonation time, 3) water activity of barley, and 4) temperature of barley. The effect of ozonation on germination of barley was also investigated. The experimental results showed that ozone was very effective in inactivation of fungi associated with the barley regardless of whether the fungi were in the forms of spores or mycelia. However, the mycelia were less resistant to ozone. With 5 minutes of ozonation, 96% of inactivation were achieved for spores as well as for mixtures of spores and small amount of mycelia by applying 0.16 and 0.10 mg of ozone/(g barley) x min, respectively. In addition, for sealed storage silos, inactivation of fungi continued when the ozone-containing gas was held inside the silos following a continuous ozone supply. The experimental results also revealed that increases in water activity and temperature of barley enhanced the fungicidal efficacy of ozone. Results of this study also indicated that the inactivation processes could be controlled by simply monitoring the exit ozone from the reactor instead of performing the time-consuming microbial examination. This finding would make the application of ozone in the preservation of cereal grains easier, simpler, and more practically applicable. The experimental results demonstrated that although ozonation above certain strength may reduce barley germination, inactivation of fungi was achieved with ozonation strengths far below the critical point.

Dose-Response Relationship, Drug↗

PubMed1999

Long-lasting effects of chronic ozone exposure on rat nasal epithelium.

Ozone, the principal oxidant pollutant in photochemical smog, causes airway epithelial injury in the upper and lower respiratory tract of laboratory animals. We have recently reported that long-term inhalation exposure to ozone causes mucous-cell metaplasia (MCM) in the surface epithelium lining the nasal airways of F344 rats. The principal objective of the present study was to determine the persistence of ozone-induced MCM in the nasal epithelium after the end of a chronic exposure. Male F344/N rats were exposed to 0, 0.25, or 0.5 ppm ozone, for 8 h/d, 7 d/wk for 13 wk. Animals were killed 8 h, 4 wk, or 13 wk after the end of the chronic exposure. Ozone-related alterations in the nasal epithelium were qualitatively and quantitatively characterized through histochemistry, image analysis, and morphometric techniques. Some rats were exposed for an additional 8 h to 0.5 ppm ozone at 13 wk after the end of the chronic exposure to determine whether previous ozone exposure results in persistent changes in the sensitivity of nasal epithelium to acute injury. At the end of the chronic exposure, hyperplasia was present in the nasal epithelium of rats exposed to 0.25 and 0.5 ppm ozone. By 13 wk postexposure, this proliferative alteration was still evident only in the rats exposed to 0.5 ppm ozone. Ozone-induced MCM with associated intraepithelial mucosubstances was evident only in the nasal tissues of rats exposed to 0.5 ppm ozone. Though attenuated, these alterations in the nasal mucous apparatus were still detectable at 13 wk after the end of the exposure. At this same time after the chronic exposure, an acute (8 h) exposure to 0.5 ppm ozone induced an additional increase of mucosubstances in the nasal epithelium of rats previously exposed to 0.5 ppm ozone, but not in rats chronically exposed to 0 or 2.5 ppm ozone. The persistent nature of the ozone-induced MCM in rats documented in this report suggests that ozone exposure may have the potential to induce similar long-lasting alterations in the airways of humans.

Animals↗

PubMed1998

Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies. Part XIII. A comparison of changes in the tracheobronchial epithelium and pulmonary acinus in male rats at 3 and 20 months.

A limitation of the NTP/HEI Collaborative Ozone Project conducted with F344/N rats at the Battelle Pacific North-west Laboratories in Richland, WA (1991-1993) was that the study used only one time point (20 months) to examine the chronic effects of exposure to ozone. Issues the design of that study could not address were (1) the status of cellular differentiation at earlier time points during the course of ozone exposure; (2) whether changes that appeared to be compensatory after 20 months of exposure were due to ozone, or were aspects of the natural aging process in rats; (3) the inability to define adequately which effects were related specifically to the prolonged duration of exposure; and (4) how and what changes brought about by the natural aging process may have overridden or confounded a clear definition of the effects of exposure to ozone at ambient concentrations (e.g., 0.12 parts per million [ppm]), which are of most concern with long-term exposure to this pollutant. The present study examined the effects of a 3-month exposure to ozone under conditions identical to those of the 20-month NTP/HEI Collaborative Ozone Project. In our facilities at the University of California, Davis, we exposed 42 male F344/N rats to either filtered air or 0.12 or 1.0 ppm ozone. After 3 months of exposure to 1.0 ppm ozone, changes in the distribution of superoxide dismutase (SOD) in the copper-zinc (Cu-Zn) form were shown by a pattern of reduced staining in terminal bronchioles and the centriacinar region; and the manganese (Mn) form of SOD was elevated within the centriacinar region. Further analysis by transmission electron microscopy and immunogold labeling confirmed that Mn SOD was elevated within epithelial type II cells immediately distal to the bronchiole-alveolar duct, junction (BADJ). The trachea, three major bronchi, and a short-length and long-length airway path relative to the trachea were examined by morphometric techniques. The pulmonary acini arising from each of these two paths were also examined morphometrically as a function of distance into the alveolar duct. Cellular changes occurring in each of these anatomical regions after 3 months of exposure were analyzed and compared to the changes noted after the 20-month ozone exposures. We found significant increases in the volume density of nonciliated epithelial cells lining the trachea and caudal bronchi as well as in the proximal and terminal bronchioles of the cranial region at a concentration of 1.0 ppm ozone after both 3 and 20 months of exposure. Remodeling of the centriacinar region, particularly within the cranial region of the lungs after exposure to 1.0 ppm ozone, was statistically significant at both 3 and 20 months. No statistically significant effects were noted following exposure to 0.12 ppm ozone for either 3 or 20 months. An important finding was that age did not influence the effect of ozone on the lungs of rats. We conclude that long-term exposure to ozone, rather than the effects of aging, lead to significant alterations of epithelial cell populations lining the airways and centriacinar region of the lung. Marked cellular changes were noted after exposure to 1.0 ppm ozone, but not to 0.12 ppm.

Aging↗

PubMed1993

Model analysis of interactive effects of ozone and water stress on the yield of soybean.

The interactive effects of ozone and water stress on the yield of soybean (Glycine max (L.) Merr. 'Davis') were addressed with a growth model of soybean. Two simulations were conducted, using the data from the exposures of soybean to ozone in open-top chambers under two soil moisture regimes, and the results of the simulations were compared. In the original simulation, soil moisture content was calculated based on a water budget using the actual precipitation and irrigation data. In the modified simulation, the soil water content was given as input data. In this case, soil moisture content was maintained at the same level across the ozone treatments regardless of different water use by the plants. Both simulations included the effect of reduced ozone flux to the leaves due to water stress, whereas only the original simulation included the effect of mitigated water stress due to reduced water use by the plants under higher ozone concentration. The water stress reduced ozone impact on soybean yield in the original simulation on the basis of the ozone dosecrop yield response relationship, but not in the modified simulation. The ozone uptake rate was reduced by water stress in the original simulation, but the relationship between seasonal mean ozone uptake rate and relative yield still showed reduced impact of ozone due to water stress. These results indicated that the alleviation of water stress by ozone due to reduced plant water use in ozone-treated plots can be a contributing factor in the reduction of ozone impact by water stress. The above conclusion was partly confirmed by the actual data for soil water content, which was significantly lower in the lowest ozone treatment than in the higher ozone treatments. Further experimental and modelling studies are needed to elucidate the mechanism of the ozone X water stress interaction.

Journal Article↗

PubMed1998

Ozone sensitivity in hybrid poplar is correlated with a lack of defense-gene activation

Ozone is a major gaseous pollutant thought to contribute to forest decline. Although the physiological and morphological responses of forest trees to ozone have been well characterized, little is known about the molecular basis for these responses. Our studies compared the response to ozone of ozone-sensitive and ozone-tolerant clones of hybrid poplar (Populus maximowizii x Populus trichocarpa) at the physiological and molecular levels. Gas-exchange analyses demonstrated clear differences between the ozone-sensitive clone 388 and the ozone-tolerant clone 245. Although ozone induced a decrease in photosynthetic rate and stomatal conductance in both clones, the magnitude of the decrease in stomatal conductance was significantly greater in the ozone-tolerant clone. RNA-blot analysis established that ozone-induced mRNA levels for phenylalanine ammonia-lyase, O-methyltransferase, a pathogenesis-related protein, and a wound-inducible gene were significantly higher in the ozone-tolerant than in the ozone-sensitive plants. Wound- and pathogen-induced levels of these mRNAs were also higher in the ozone-tolerant compared with the ozone-sensitive plants. The different physiological and molecular responses to ozone exposure exhibited by clones 245 and 388 suggest that ozone tolerance involves the activation of salicylic-acid- and jasmonic-acid-mediated signaling pathways, which may be important in triggering defense responses against oxidative stress.

Journal Article↗

PubMed2005

Monitoring of petroleum hydrocarbon degradative potential of indigenous microorganisms in ozonated soil.

This study was performed to investigate the petroleum hydrocarbon (PH) degradative potential of indigenous microorganisms in ozonated soil to better develop combined pre-ozonation/bioremediation technology. Diesel-contaminated soils were ozonated for 0-900 min. PH and microbial concentrations in the soils decreased with increased ozonation time. The greatest reduction of total PH (TPH, 47.6%) and aromatics (11.3%) was observed in 900-min ozonated soil. The number of total viable heterotrophic bacteria decreased by three orders of magnitude in the soil. Ozonated soils were incubated for 9 weeks for bioremediation. The number of microorganisms in the soils increased during the incubation period, as monitored by culture- and nonculture-based methods. The soils showed additional PH-removal during incubation, supporting the presence of PH-degraders in the soils. The highest removal (25.4%) of TPH was observed during the incubation of 180-min ozonated soil during the incubation while a negligible removal was shown in 900-min ozonated soil. This negligible removal could be explained by the existence of relatively few or undetected PH-degraders in 900-min ozonated soil. After a 9-week incubation of the ozonated soils, 180-min ozonated soil showed the lowest TPH concentration, suggesting that appropriate ozonation and indigenous microorganisms survived ozonation could enhance remediation of PH-contaminated soil. Microbial community composition in 9-week incubated soils revealed a slight difference between 900-min ozonated and unozonated soils, as analyzed by whole cell hybridization. Taken together, this study provided insight into indigenous microbial potential to degrade PH in ozonated soils.

Hydrocarbons↗

PubMed2004

Kinetics of soil ozonation: an experimental and numerical investigation.

This study investigates the use of ozone for soil remediation. Batch experiments, in which ozone-containing gas was continuously recycled through a soil bed, were conducted to quantify the rate of ozone self-decomposition and the rates of ozone interaction with soil organic and inorganic matter. Column experiments were conducted to measure ozone breakthrough from a soil column. Parameters such as ozone flow rate, soil mass, and ozonation time were varied in these experiments. After ozone concentration had reached steady state, the total organic carbon concentration was measured for all soil samples. The ozonation efficiency, represented by the ratio of soil organic matter consumed to the total ozone input, was quantified for each experiment. Numerical simulations were conducted to simulate experimentally obtained column breakthrough curves. Experimentally obtained kinetic rate constants were used in these simulations, and the results were in good agreement with experimental data. In contrast to previous studies in which soil inorganic matter was completely ignored, our experiments indicate that soil inorganic matter may also promote depletion of ozone, thus reducing the overall ozonation efficiency. Three-dimensional numerical simulations were conducted to predict the efficacy of ozonation for soil remediation in the field. These simulations indicate that such ozonation can be very effective, provided that effective circulation of ozone is achieved through appropriately placed wells.

Bioreactors↗

PubMed2001

Estimating long-term population exposure to ozone in urban areas of Europe.

Tropospheric ozone concentrations regarded as harmful for human health are frequently encountered in Central Europe in summertime. Although ozone formation generally results from precursors transported over long distances, in urban areas local effects, such as reactions due to nearby emission sources, play a major role in determining ozone concentrations. Europe-wide mapping and modeling of population exposure to high ozone concentrations is subject to many uncertainties, because small-scale phenomena in urban areas can significantly change ozone levels from those of the surroundings. Currently the integrated assessment modeling of European ozone control strategies is done utilizing the results of large-scale models intended for estimating the rural background ozone levels. This paper presents an initial study on how much local nitrogen oxide (NOx) concentrations can explain variations between large-scale ozone model results and urban ozone measurements, on one hand, and between urban and nearby rural measurements, on the other. The impact of urban NOx concentrations on ozone levels was derived from chemical equations describing the ozone balance. The study investigated the applicability of the method for improving the accuracy of modeled population exposure, which is needed for efficient control strategy development. The method was tested with NOx and ozone measurements from both urban and rural areas in Switzerland and with the ozone predictions of the large-scale photochemical model currently used in designing Europe-wide control strategies for ground-level ozone. The results suggest that urban NOx levels are a significant explanatory factor in differences between urban and nearby rural ozone concentrations and that the phenomenon could be satisfactorily represented with this kind of method. Further research efforts should comprise testing of the method in more locations and analyzing the performance of more widely applicable ways of deriving the initial parameters.

Air Pollutants↗