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PubMed2003

The ozone tolerance: I) Enhancement of antioxidant enzymes is ozone dose-dependent in Jurkat cells.

We have begun to examine the biological and toxic effects of ozone on Jurkat T cells incubated thereafter for 24, 48 and 72 h. Tissue culture medium was strengthened by adding 20% fetal calf serum with an albumin content of about 6 mg/ml. Ozonization was performed by exposing for 10 min a volume of cell suspension (4 x 10(5)/ml) to an equal volume of a gas mixture composed of oxygen-ozone with precise ozone concentrations ranging from 1.5 up to 72 microg/ml (31.5-1512 microM). The proliferation index declined progressively and was ozone dose-dependent. The response of enzymatic activities varied depending upon the enzyme and ozone concentrations: glucose-6-phosphate dehydrogenase begins to increase at an ozone dose of 6 microg/ml (126 microM), reached a peak at 12 microg/ml (252 microM) and rapidly declined thereafter. On the other hand activities of superoxide dismutase, glutathione peroxidase and glutathione reductase increased progressively from the ozone concentration of 12 microg/ml. Thus, as we have observed in blood, the biological response is linked to the ozone dose that must reach a threshold to be effective.

Antioxidants↗

PubMed2005

Overexpression of SIPK in tobacco enhances ozone-induced ethylene formation and blocks ozone-induced SA accumulation.

Ozone induces rapid activation of SIPK, a mitogen-activated protein kinase (MAPK) in tobacco. Through transgenic manipulation it has previously been shown that overexpression of SIPK leads to enhanced ozone-induced lesion formation with concomitant accumulation of ROS. In spite of this hypersensitive phenotype, the effect of this altered SIPK expression on the levels of various hormones that regulate ozone-induced cell death has remained unexplored. The response of both salicylate and ethylene, the major phytohormones that modulate ozone-induced cell death, have now been analysed in SIPK-OX tobacco plants. Ozone treatment strongly induced ethylene formation in the sensitive SIPK-OX plants at ozone concentrations that failed to elicit stress ethylene release in WT plants. By contrast, SIPK-overexpressing plants displayed no ozone-induced SA accumulation, whereas WT plants accumulated SA upon ozone exposure. Epistatic analysis of SIPK-OX function suggests that the ozone-induced cell death observed in SIPK-OX plants is either independent, or upstream, of SA accumulation.

Apoptosis↗

PubMed1983

Preexposure to low ozone concentrations does not diminish the pulmonary function response on exposure to higher ozone concentrations.

To determine whether persons repeatedly exposed to low ozone concentrations would demonstrate a diminished responsivity, as a result of adaptation or desensitization, when subsequently exposed to a higher ozone concentration, we performed the following study. Respiratory sensitivity (pulmonary function response) to 2 h of exposure to 0.42 or 0.50 ppm ozone (acute exposure) was determined 3 months before or 6 to 8 wk after the study. Twenty-one subjects (8 men, 13 women) were exposed for 2 h or 5 consecutive days to filtered air, 0.20, 0.20, 0.20, and 0.42 to 0.50 ppm ozone, respectively. There were no significant differences between the responses of men and women to ozone. Subjects were divided into a sensitive group (greater than 20% drop in FEV1) and a nonsensitive group (less than 10% drop in FEV1) on the basis of their responses to the acute exposure. Neither the overall group nor the nonsensitive group showed a significant response to 0.20 ppm. Sensitive subjects (n = 9) showed small but significant decreases in FEV1 on exposure to 0.20 ppm. The predominant finding was that the 3 days of preexposure to 0.20 ppm ozone had no effect on the response to 0.42 or 0.50 ppm ozone on the fourth day (when compared with the previous acute exposure to 0.42 or 0.50 ppm). We conclude that subjects repeatedly (3 times) exposed to a low (0.20 ppm) concentration of ozone do not demonstrate a pulmonary function adaptation or desensitization on a subsequent exposure to a higher (0.42 or 0.50 ppm) ozone concentration.

Adaptation, Physiological↗

PubMed2005

Extracorporeal blood oxygenation and ozonation: clinical and biological implications of ozone therapy.

Some lines of evidence have suggested that the challenge to antioxidants and biomolecules provoked by pro-oxidants such as ozone may be used to generate a controlled stress response of possible therapeutic relevance in some immune dysfunctions and chronic, degenerative conditions. Immune and endothelial cells have been proposed to be elective targets of the positive molecular effects of ozone and its derived species formed during blood ozonation. On the bases of these underlying principles and against often prejudicial scepticism and concerns about its toxicity, ozone has been used in autohemotherapy (AHT) for four decades with encouraging results. However, clinical application and validation of AHT have been so far largely insufficient. Latterly, a new and more effective therapeutic approach to ozone therapy has been established, namely extracorporeal blood oxygenation and ozonation (EBOO). This technique, first tested in vitro and then in vivo in sheep and humans (more than 1200 treatments performed in 82 patients), is performed with a high-efficiency apparatus that makes it possible to treat with a mixture of oxygen-ozone (0.5-1 microg/ml oxygen) in 1 h of extracorporeal circulation up to 4800 ml of heparinized blood without technical or clinical problems, whereas only 250 ml of blood can be treated with ozone by AHT. The EBOO technique can be easily adapted for use in hemodialysis also. The standard therapeutic cycle lasts for 7 weeks in which 14 treatment sessions of 1 h are performed. After a session of EBOO, the interaction of ozone with blood components results in 4-5-fold increased levels of thiobarbituric acid reactants and a proportional decrease in plasma protein thiols without any appreciable erythrocyte haemolysis. On the basis of preliminary in vitro evidence, these simple laboratory parameters may represent a useful complement in the routine monitoring of biological compliance to the treatment. The clinical experience gained so far confirms the great therapeutic potential of EBOO in patients with severe peripheral arterial disease, coronary disease, cholesterol embolism, severe dyslipidemia, Madelung disease, and sudden deafness of vascular origin. Extensive investigation on oxidative stress biomarkers and clinical trials are under way to validate this new technique further.

Animals↗

PubMed1995

The cascade mechanism to explain ozone toxicity: the role of lipid ozonation products.

Ozone is so reactive that it can be predicted to be entirely consumed as it passes through the first layer of tissue it contacts at the lung/air interface. This layer includes the lung lining fluid (tracheobronchial surface fluid and alveolar and small airway lining fluid) and, where the lung lining fluid is thin or absent, the membranes of the epithelial cells that line the airways. Therefore, the biochemical changes that follow the inhalation of ozone must be relayed into deeper tissue strat by a cascade of ozonation products. Lipid ozonation products (LOP) are suggested to be the most likely species to act as signal transduction molecules. This is because unsaturated fatty acids are present in the lipids in both the lung lining fluid and in pulmonary cell bilayers, and ozone reacts with unsaturated fatty acids to produce ozone-specific products. Further, lipid ozonation products are finite in number, have structures that are predictable from the Criegee ozonation mechanism, and are small, diffusible, stable (or metastable) molecules. Preliminary data show that individual LOP cause the activation of specific lipases, which trigger the release of endogenous mediators of inflammation.

Animals↗

PubMed2001

Ozone predictions in Atlanta, Georgia: analysis of the 1999 ozone season.

Ozone prediction has become an important activity in many U.S. ozone nonattainment areas. In this study, we describe the ozone prediction program in the Atlanta metropolitan area and analyze the performance of this program during the 1999 ozone-forecasting season. From May to September, a team of 10 air quality regulators, meteorologists, and atmospheric scientists made a daily prediction of the next-day maximum 8-hr average ozone concentration. The daily forecast was made aided by two linear regression models, a 3-dimensional air quality model, and the no-skill ozone persistence model. The team's performance is compared with the numerical models using several numerical indicators. Our analysis indicated that (1) the team correctly predicted next-day peak ozone concentrations 84% of the time, (2) the two linear regression models had a better performance than a 3-dimensional air quality model, (3) persistence was a strong predictor of ozone concentrations with a performance of 78%, and (4) about half of the team's wrong predictions could be prevented with improved meteorological predictions.

Air Pollution↗

PubMed1998

Relationship of inhaled ozone concentration to acute tracheobronchial epithelial injury, site-specific ozone dose, and glutathione depletion in rhesus monkeys.

Acute pulmonary epithelial injury produced by short-term exposure to ozone varies by site within the tracheobronchial tree. To test whether this variability is related to the local dose of ozone at the tissue site or to local concentrations of glutathione, we exposed adult male rhesus monkeys for 2 h to filtered air or to 0.4 or 1.0 ppm ozone generated from 18O2. Following exposure, lungs were split into lobes and specimens were selected by microdissection so that measurements could be made on airway tissue of similar branching history, including trachea, proximal (generation one or two) and distal (generation six or seven) intrapulmonary bronchi, and proximal respiratory bronchioles. One half of the lung was lavaged for analysis of extracellular components. In monkeys exposed to filtered air, the concentration of reduced glutathione (GSH) varied throughout the airway tree, with the proximal intrapulmonary bronchus having the lowest concentration and the parenchyma having the highest concentration. Exposure to 1.0 ppm ozone significantly reduced GSH only in the respiratory bronchiole, whereas exposure to 0.4 ppm increased GSH only in the proximal intrapulmonary bronchus. Local ozone dose (measured as excess 18O) varied by as much as a factor of three in different airways of monkeys exposed to 1.0 ppm, with respiratory bronchioles having the highest concentration and the parenchyma the lowest concentration. In monkeys exposed to 0.4 ppm, the ozone dose was 60% to 70% less than in the same site in monkeys exposed to 1.0 ppm. Epithelial disruption was present to some degree in all airway sites, but not in the parenchyma, in animals exposed to 1.0 ppm ozone. The mass of mucous and ciliated cells decreased in all airways, and necrotic and inflammatory cells increased. At 0.4 ppm, epithelial injury was minimal, except in the respiratory bronchiole, where cell loss and necrosis occurred, and was 50% that found in monkeys exposed to 1.0 ppm ozone. We conclude that there is a close association between site-specific O3 dose, the degree of epithelial injury, and glutathione depletion at local sites in the tracheobronchial tree.

Animals↗

PubMed2000

The Harvard Southern California Chronic Ozone Exposure Study: assessing ozone exposure of grade-school-age children in two Southern California communities.

The Harvard Southern California Chronic Ozone Exposure Study measured personal exposure to, and indoor and outdoor ozone concentrations of, approximately 200 elementary school children 6-12 years of age for 12 months (June 1995-May 1996). We selected two Southern California communities, Upland and several towns located in the San Bernardino mountains, because certain characteristics of those communities were believed to affect personal exposures. On 6 consecutive days during each study month, participant homes were monitored for indoor and outdoor ozone concentrations, and participating children wore a small passive ozone sampler to measure personal exposure. During each sampling period, the children recorded time-location-activity information in a diary. Ambient ozone concentration data were obtained from air quality monitoring stations in the study areas. We present ozone concentration data for the ozone season (June-September 1995 and May 1996) and the nonozone season (October 1995-April 1996). During the ozone season, outdoor and indoor concentrations and personal exposure averaged 48.2, 11.8, and 18.8 ppb in Upland and 60.1, 21.4, and 25.4 ppb in the mountain towns, respectively. During the nonozone season, outdoor and indoor concentrations and personal exposure averaged 21.1, 3.2, and 6.2 ppb in Upland, and 35.7, 2.8, and 5.7 ppb in the mountain towns, respectively. Personal exposure differed by community and sex, but not by age group.

Age Distribution↗

PubMedDate not supplied

Decolorization of the dye, Reactive Blue 19, using ozonation, ultrasound, and ultrasound-enhanced ozonation.

Reactive dyes constitute a significant portion of colorants used in industries ranging from the textile industry to the paper industry. In most cases, the effluent streams from textile plants are highly colored, and treatment methods for dye decolorization such as chemical oxidation need to be explored. The oxidation processes investigated in this study are those of ozonation, ultrasound, and ultrasound-enhanced ozonation. The oxidation of an anthraquinone dye was studied under conditions of varying ultrasonic power, dye concentration, ozone concentration, pH, and temperature. Laboratory experiments were performed using a semibatch reactor by ozonating dye samples with and without ultrasound. Under conditions of constant ultrasonic radiation and continuous gas application, decolorization rates have been enhanced by ultrasound. The apparent first-order rate constants increased between 35 and 204% for the ultrasonic power inputs between 40 W/L and 120 W/L compared with ozonation alone. The effects of ultrasonic power input on the gas-liquid mass-transfer coefficient were also investigated and the results indicate that an increase in ultrasonic power input increases the mass-transfer coefficient. The mass-transfer coefficient increased between 89 and 93% for ozone inlet concentrations between 5.4 and 9.4 mg/L at an ultrasonic power of 120 W/L compared with ozonation alone. The reactions of the dye with ultrasound-enhanced ozone occurred through the hydroxyl radical pathway.

Coloring Agents↗

PubMed1988

Effects of ozone on foliar leaching in Norway spruce (Picea abies L. Karst): confounding factors due to NOx production during ozone generation.

Previous experiments with conifers fumigated with O(3), produced by air-operated electric discharge ozonators, have provided evidence that O(3) increases the leaching of NO(3)(-), NH(4)(+), K(+), Ca(2+), Mg(2+) and some other cations from needles, when the trees are treated with acid mist. This evidence has provided the foundation of the ozone-acid mist hypothesis of spruce decline. We report experiments with Norway spruce saplings fumigated with purified and unpurified O(3). The results show that the accumulation of NO(3)(-) in the needles arises from the rapid deposition of N(2)O(5) and HNO(3) formed from N(2) in the ozonator. An increase in removal of NH(4)(+), Na(+), Ca(2+), Mg(2+), Zn(2+) and Mn(2+) from the needles during soaking in H(2)SO(4), pH3, was also observed, which was related to the increase in NO(3)(-) but was independent of O(3) concentration. It is concluded that results of previous experiments cited in support of the ozone-acid mist hypothesis arose from effects which were at least partly caused by N(2)O(5) produced as a contaminant, and were incorrectly attributed to ozone. Other effects, such as growth stimulations, visible symptons, enhanced frost sensitivity, and infestation by pests or pathogens, which have been attributed to O(3) generated by electric discharge in air, should be interpreted with caution. Future experiments with ozone must eliminate this problem by either using O(2)-driven ozonators, or by purifying the output from air-driven ozonators using cold and/or water traps.

Journal Article↗

PubMed2004

MTBE oxidation byproducts from the treatment of surface waters by ozonation and UV-ozonation.

In recent years, there has been considerable concern over the release of methyl tert-butyl ether (MTBE), a gasoline additive, into the aquifers used as potable water sources. MTBE readily dissolves in water and has entered the environment via gasoline spills and leaking storage tanks. In this paper, we investigate ozonation and UV-ozonation for treatment of MTBE in contaminated drinking water sources. We report the test protocol and results of using solid-phase microextraction (SPME) to determine the level of MTBE and its oxidation byproducts in samples drawn from laboratory-scale ozone and UV-ozone reactors being evaluated at a US EPA research facility. Analysis of a prepared MTBE standard indicated a detection limit on the order of 0.1 microgl(-1) with a repeatability of +/-0.4%. Results show that the overall rate of removal of MTBE via UV-ozonation in a relatively turbid surface water (15 ntu) is twice that of ozonation alone. In addition, GC-MS analysis of decomposition products showed that tert-butyl formate (TBF), methyl acetate, butene, acetone, and acetaldehyde were produced by both processes. TBF and butene reach similar maximum yields from the two processes, but are more efficiently degraded by UV-ozonation treatment. This indicates that these treatment processes also degrade these byproducts. In contrast, the remaining byproducts (methyl acetate, acetone, and acetaldehyde) are formed at similar levels during treatment, but are not degraded once formed. These byproducts may be resistant to hydrogen abstraction by hydroxyl radical.

Chromatography, High Pressure Liquid↗

PubMed2001

Simulating the growth response of aspen to elevated ozone: a mechanistic approach to scaling a leaf-level model of ozone effects on photosynthesis to a complex canopy architecture.

Predicting ozone-induced reduction of carbon sequestration of forests under elevated tropospheric ozone concentrations requires robust mechanistic leaf-level models, scaled up to whole tree and stand level. As ozone effects depend on genotype, the ability to predict these effects on forest carbon cycling via competitive response between genotypes will also be required. This study tests a process-based model that predicts the relative effects of ozone on the photosynthetic rate and growth of an ozone-sensitive aspen clone, as a first step in simulating the competitive response of genotypes to atmospheric and climate change. The resulting composite model simulated the relative above ground growth response of ozone-sensitive aspen clone 259 exposed to square wave variation in ozone concentration. This included a greater effect on stem diameter than on stem height, earlier leaf abscission, and reduced stem and leaf dry matter production at the end of the growing season. Further development of the model to reduce predictive uncertainty is discussed.

Air Pollutants↗

PubMed2001

Treatability of a simulated disperse dye-bath by ferrous iron coagulation, ozonation, and ferrous iron-catalyzed ozonation.

Dyeing and finishing of textile yarns and fabrics are extremely important processes in terms of both quality and environmental concerns. Among the commercial textile dyes, particularly disperse dyestuffs are of environmental interest because of their widespread use, their potential for formation of toxic aromatic amines and their low removal rate during aerobic waste treatment as well as advanced chemical oxidation. Thus, in the present paper ferrous iron coagulation, ozonation and ferrous iron-catalyzed ozonation were employed at varying pH (3-13) and Fe(II)-ion doses (0.09-18mM) for the treatment of a simulated disperse dye-bath (average initial apparent color as absorbance at 566nm=815.4m(-1); COD(0)=3784mgl(-1); TOC(0)=670mgl(-1); BOD(5,0)=58mgl(-1)) that more closely resembled an actual dyehouse effluent than an aqueous disperse dye solution. Coagulation with 5000mgl(-1) FeSO4-7H2O (18mM Fe(2+)) at pH 11 removed up to 97% color and 54% COD, whereas oxidation via ozonation alone (applied ozone dose=2300mgl(-1)) was only effective at pH 3, resulting in 77% color and 11% COD removal. Fe(II)-ion-catalyzed ozonation (3.6mM Fe(2+) at pH 3; Fe(2+):O3 molar ratio 1:14) eliminated 95% color and 48% COD and appeared to be the most attractive option among the investigated chemical treatment methods as for its applicability at the natural acidic pH of the disperse dye-bath effluent and at relatively low Fe(2+)-ion doses as compared to ferrous sulfate coagulation. However, no TOC reduction was observable for ozonation and catalytic ozonation at the investigated reaction conditions (14gl(-1) O3 at pH 3). An average six-fold enhancement in the biodegradability parameter of the synthetic dye wastewater expressed in terms of the BOD(5)/COD ratio could be achieved by the investigated chemical treatment methods.

Biodegradation, Environmental↗

PubMed1977

Mechanisms of inactivation of bacteriophage phiX174 and its DNA in aerosols by ozone and ozonized cyclohexene.

The mechanisms of inactivation of aerosolized bacteriophage phiX174 in atmospheres containing ozone, cyclohexene, or ozonized cyclohexene were studied by using 32P-labelled phage. The inactivation of the aerosolized phage in clear air or in air containing cyclohexene is due to damage of the protein coat since the deoxyribonucleic acid (DNA) extracted from the inactivated phage retains its biological activity. Inactivation of the phage in air containing ozonized cyclohexene is due both to protein and DNA damage. Sucrose gradient analysis shows that aerosolized inactivated phiX174 releases unbroken DNA. In contrast, the DNA from phage phiX174 inactivated by ozonized cyclohexene is broken. The inactivation of aerosolized phage phiX174-DNA was studied in the same atmospheres using 32P-labelled DNA. phiX174-DNA aerosolized in clear air or air containing cyclohexene at 75% r.h. is inactivated by a factor of 2 in 30 min. The inactivated DNA is broken. Ozone as well as ozonized cyclohexene inactivates KNA very fast causing breaks in the molecule. This is in contrast with the intact bacteriophage in which ozone does not produce breaks in the DNA.

Aerosols↗

PubMedDate not supplied

The ozonation of unsaturated fatty acids: aldehydes and hydrogen peroxide as products and possible mediators of ozone toxicity.

The products of the reactions of ozone with aqueous emulsions of unsaturated fatty acids and with liposomes made from phosphatidylcholine esters were characterized. Ozonolysis of emulsions of methyl oleate yields approximately 1 mol of hydrogen peroxide and 2 mol of aldehydes per mole of ozone used and fatty acid reacted. That is, the net equation that occurs is RCH = CHR' + O3 + H2O----RCHO + R'CHO + H2O2 . Ozonolysis of emulsions of oleic, linoleic, linolenic, and arachidonic acids gives 1 mol of hydrogen peroxide per mole of ozone used. Only very low yields (less than 5%) of reducible materials other than hydrogen peroxide are observed, suggesting that the yields of organic peroxidic materials, including Criegee ozonides and lipid hydroperoxides, are small. Ozonolysis of rat erythrocyte ghost membranes and rat bronchoalveolar lavage also gives significant yields (about 50%) of hydrogen peroxide based on the moles of ozone consumed. Reactions of ozone with bovine serum albumin, glutathione, and glucose do not produce hydrogen peroxide, implying that the hydrogen peroxide formed during the ozonation of biological materials arises almost exclusively from ozone/olefin reactions. Hydrogen peroxide and aldehydes are suggested to be important mediators of the modifications observed in both the lung and extrapulmonary tissues when ozone is inhaled.

Air Pollutants↗

PubMedDate not supplied

Relationship between acute ozone responsiveness and chronic loss of lung function in residents of a high-ozone community.

We hypothesized that acute respiratory responsiveness to ozone predicts chronic lung injury from repeated exposure to ozone-containing air pollution. We tested this hypothesis in 164 middle-aged nonsmoking residents of an ozone-polluted community who underwent lung-function measurements during 1986 and 1987 (i.e., time 3). The time-3 study was a follow up of more comprehensive studies conducted in 1977-1978 (time 1) and in 1982-1983 (time 2). In contrast to the apparent rapid (i.e., approximately 60 ml/y) decline in lung-function measurements between times 1 and 2, our subjects showed little change in forced vital capacity (FVC) or forced expired volume in 1 s (FEV1.0) between times 2 and 3, and they experienced a normal decline between times 1 and 3. A subgroup (n = 45) underwent 2-h laboratory ozone exposures to 0.4 ppm ozone, accompanied by intermittent exercise, and they experienced mild acute reductions in FEV1.0 and FVC, but there was little change in bronchial responsiveness to methacholine. Individual acute responses to laboratory ozone were not correlated with individual long-term changes between times 1 and 3. In summary, the results did not support our initial hypothesis, and they did not confirm rapid function decline in nonsmokers chronically exposed to ozone-containing air pollution.

Adult↗

PubMed2004

Effect of residual ozone on membrane fouling reduction in ozone resisting microfiltration (MF) membrane system.

The effect of residual ozone on reducing the membrane fouling was investigated using ozone resisting microfiltration membrane. It was found out that the fouling was reduced effectively by maintaining residual ozone in the membrane module. To clarify the reason why the residual ozone reduces the membrane fouling, research was focused on the molecular degradation reaction and particle destabilization reaction induced by residual ozone. The major reason of membrane fouling reduction was attributed to the reduction of reversible resistance induced by the cake layer. The reversible resistance was reduced due to degradation of organic substances in the cake layer. In addition to degradation reaction, the increase of fouling particle size due to residual ozone in the cake layer is another important process for fouling reduction. This effect has been referred to as ozone-induced destabilization reaction. The calcium present in the raw water influenced this reaction. The increase of fouling particles size improves the filterability through the cake layer and backwashing efficiency.

Biodegradation, Environmental↗

PubMed2002

Neural network scheme for the retrieval of total ozone from Global Ozone Monitoring Experiment data.

A novel approach to retrieving total ozone columns from the ERS2 GOME (Global Ozone Monitoring Experiment) spectral data has been developed. With selected GOME wavelength regions, from clear and cloudy pixels alike plus orbital and instrument data as input, a feed-forward neural network was trained to determine total ozone in a one-step inverse retrieval procedure. To achieve this training, ground-based total ozone measurements from the World Ozone and Ultraviolet Data Center (WOUDC) for the years 1996-2000, supplemented with Dobson-corrected Total Ozone Mapping Spectrometer (TOMS) data to provide global coverage, were collocated with GOME ground pixels into a training data set. Validation of the neural-network-retrieved ozone values relative to independent ground stations yielded a rms error of better than 11 Dobson units. Comparisons performed on the basis of operationally available TOMS and GOME level-3 maps exhibit good agreement in general, with a latitude-dependent offset.

Journal Article↗