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PubMed1993

Alveolar and airway cell kinetics in the lungs of rats exposed to nitrogen dioxide, ozone, and a combination of the two gases.

Rats carrying minipumps filled with 5-bromo-2'deoxyuridine were exposed to ozone, NO2, or a mixture of the two gases using four different protocols: (A) ozone 0.2 ppm, NO2 3.6 ppm, or their mixture for 24 hr a day; (B) ozone 0.2 ppm, NO2 7.2 ppm, or their mixture for 12 hr per night; (C) ozone 0.6 ppm, NO2 10.8 ppm, or their mixture for 8 hr per night; and (D) ozone 0.8 ppm, NO2 14.4 ppm, or their mixture for 6 hr per night. After three consecutive daily exposures, the animals were returned to filtered air and killed 7 days after implantation of the minipump. Alveolar labeling indices were comparable to control values except in the group of animals exposed for 6 hr nightly to a combination of 0.8 ppm of ozone and 14.4 ppm of NO2. Labeling indices in the peripheral airways were the most sensitive exposure index since they were significantly increased over control values in all animals exposed to ozone, NO2, or a mixture of the two gases, regardless of concentration or exposure duration. Labeling indices increased with elevated dose rate, i.e., concentration of the gases in the inspired air. The response to the combined gases was greater than the calculated sum of the responses to the two individual gases for the three higher dose rates in the large airways and for the highest dose rate in the peripheral airways. The results led to the following conclusions: (1) By the criterion of analysis of cell kinetics in rat large and peripheral airways, neither ozone, NO2, nor their mixture follows Haber's law (c x t = k) over the concentration ranges studied; and (2) at the higher dose rates studied, there is a more than additive (synergistic) airway response to the combination of ozone and NO2.

Animals↗
PubMed1996

The local C-fiber contribution to ozone-induced effects on the isolated guinea pig lung.

We studied the local role of C-fibers, in the absence of systemic effects and blood components of inflammation, on lung responses to ozone. Guinea pigs were pretreated with capsaicin to deplete C-fibers or with vehicle. One week later their isolated, buffer-perfused lungs were exposed to 0.8 ppm ozone or air for 2 hr. In some lungs (9 or 10 each group), increasing doses of methacholine followed by capsaicin were injected into the pulmonary artery. In separate lungs (n = 5, each group), lung Substance P content by EIA and NK1 receptor characteristics by radioligand binding were measured. Analyses were performed by two-way ANOVA with a significant interaction indicative of C-fibers playing a role in ozone responses. Ozone increased R(L) and decreased C(dyn), effects which were apparently not dependent on C-fibers. Ozone increased responsiveness to methacholine, an effect which was reduced by depletion of C-fibers. Ozone increased and C-fiber depletion decreased lung responses to capsaicin. C-fiber depletion but not ozone decreased lung substance P content. C-fiber depletion increased the affinity but did not change the number of NK1 receptors, while ozone had no effect. We conclude that the ozone, in the absence of systemic effects and the blood components of inflammation, increased muscarinic reactivity in part via the local effects of C-fibers.

Animals↗
PubMed1997

Influence of acid aerosol droplet size on structural changes in the rat lung caused by acute exposure to sulfuric acid and ozone.

To investigate whether aerosol droplet size influences structural changes in the lung produced by short-term, concomitant exposure to ozone and sulfuric acid, groups of 10 rats were exposed 4 hr/day for 2 days to filtered air, 0.6 ppm ozone, 0.5 mg/m3 fine (aerosol mass median diameter (MMD) = 0.3 microm) or ultrafine (MMD = 0.06 microm) sulfuric acid, or a mixture of ozone and 0.5 mg/m3 fine or ultrafine sulfuric acid. The volume percentage of total parenchyma containing markedly to severely injured alveolar septae was measured morphometrically. There were no differences between the ultrafine or fine acid exposure groups and the sham group for any of the morphologic endpoints. Volume percentage of markedly to severely injured tissue was increased in the ultrafine, but not fine, mixture animals when compared with the ozone-only group. In addition, a synergistic interaction between ozone and ultrafine, but not fine, sulfuric acid was found for this endpoint. The bromodeoxyuridine cell labeling index in the periacinar region was greater in the rats exposed to the fine sulfuric acid and ozone mixture than that in rats exposed to ozone alone, and a synergistic interaction between ozone and fine sulfuric acid was found for this end point. None of the exposures produced any changes in ventilatory parameters. Thus, acid aerosol droplet size was found to influence the effect of sulfuric acid in modifying ozone-induced structural changes in the rat lung.

Administration, Inhalation↗
PubMed1998

Lipid ozonation products activate phospholipases A2, C, and D.

Ozone exposure, in vitro, has been shown to activate phospholipases A2 (PLA2), C (PLC), and D (PLD) in airway epithelial cells. However, because of its high reactivity, ozone cannot penetrate far into the air/lung tissue interface. It has been proposed that ozone reacts with unsaturated fatty acids (UFA) in the epithelial lining fluid (ELF) and cell membranes to generate a cascade of lipid ozonation products (LOP) that mediate ozone-induced toxicity. To test this hypothesis, we exposed cultured human bronchial epithelial cells (BEAS-2B) to LOP (1-100 microM) produced from the ozonation of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylcholine (POPC) and measured the activity of PLA2, PLC, and PLD. The PLA2 isoform responsible for arachidonic acid release (AA) in stimulated cultures was also characterized. Activation of PLA2, PLC, and PLD by three oxidants, hydrogen peroxide (H2O2), tert-butyl hydroperoxide (t-BOOH) and 2,2'-azobis(2-amidinopropane)dihydrochloride (AAPH) also was measured and compared to that of LOP. The derivatives of ozonized POPC at the sn-2 residue, 9-oxononanoyl (PC-ALD), 9-hydroxy-9-hydroperoxynonanoyl (PC-HHP), and 8-(-5-octyl-1,2,4-trioxolan-3-yl-) octanoyl (POPC-OZ) selectively activated PLA2 in a dose-dependent fashion. Cytosolic PLA2 (cPLA2) measured in the cytosolic fraction of stimulated cell lysates was found to be the predominant isoform responsible for AA release. PLC activation was exclusively induced by the hydroxyhydroperoxide derivatives. PC-HHP and the 9-carbon hydroxyhydroperoxide (HHP-C9) increased PLC activity. PLD activity also was induced by LOP generated from POPC. Incubation of cultures with H2O2 alone did not stimulate PLC; however, in the presence of the aldehyde, nonanal, a 62 +/- 2% increase in PLC activity was found, suggesting that the increase in activity was due to the formation of the intermediate HHP-C9. t-BOOH, and AAPH also failed to induce PLA2 activation, but did activate PLC, under conditions of exposure identical to that of LOP. Only t-BOOH activated PLD. These results suggest that biologically relevant concentrations of LOP activate PLA2, PLC, and PLD in the airway epithelial cell, a primary target to ozone exposure. The activation of these phospholipases may play a role in the development of lung inflammation during ozone exposure.

Arachidonic Acid↗
PubMed2001

Hyperthyroidism increases the risk of ozone-induced lung toxicity in rats.

The risk of lung injury from ozone exposure has been well documented. It is also known that various factors may significantly influence the susceptibility of animals to the toxic effects of ozone. In the present study, we investigated the possibility that hyperthyroidism might be associated with increases in ozone-induced pulmonary toxicity. To create a hyperthyroid condition, mature male Sprague--Dawley rats were given injections of thyroxine (dose range: 0.1 to 1 mg/kg body wt daily for 7 days). Control rats received vehicle injections. The animals were then exposed to air or ozone (dose range: 0.5 to 3 ppm for 3 h). At 18 h postexposure, bronchoalveolar lavage fluid and cells were harvested. In hyperthyroid animals, ozone exposure was associated with three- to sixfold increases in bronchoalveolar lavage fluid lactate dehydrogenase activities and albumin levels as well as the number of polymorphonuclear leukocytes harvested by bronchoalveolar lavage above levels observed in ozone-exposed control rats. Additional results from the present study suggest that these thyroid hormone-linked effects cannot be fully explained by differences in whole-body metabolic rate or changes in the inhaled dose of ozone. These findings indicate that the risk of ozone-induced lung toxicity is substantially increased in a hyperthyroid state and suggest that the susceptibility of the lung to damage from ozone exposure may be significantly influenced by individual thyroid hormone status.

Albumins↗
PubMed1995

Seed characteristics and nutrient composition of selected beans (Phaseolus vulgaris L.) with different ozone tolerance.

Ozone sensitivity, nutritional quality, seed characteristics, and growth habit of beans (Phaseolus vulgaris L.) were evaluated in two separate experiments. In the first experiment the data showed a significant variation among 34 bean accessions for ozone sensitivity following acute exposure of 18-day-old plants to 0.6 microliters/l O3 for 2 hours under environmentally controlled greenhouse conditions. PI-163579, PI-169735, PI-171790, PI-176684, PI-201374, PI-310711, PI-345576, PI-370569, PI-379435, and PI-414831 were identified as tolerant to acute ozone exposures. Protein, oil, starch, sugar, and ash contents in the seed of selected germplasm were determined and no correlation was found between these components and ozone sensitivity. Seed size and growth habit varied considerably among the 34 accessions but were not correlated to ozone sensitivity. In a second experiment, ten accessions, selected from the tolerant ones identified in the first experiment, were subjected to chronic ozone exposure in open-top chambers at 0.04 and 0.08 microliters/l concentrations for 7 hours/day 44 days after transplanting. Based on foliar injury and yield reductions, only PI-370569 and PI-414831 were tolerant to prolonged ozone exposure (0.08 microliters/l). A significant positive correlation (r = 0.83) existed between foliar injury rating from chronic treatments involving 0.04 and 0.08 microliters O3/l and acute exposure (0.6 microliter O3/l/2 hours). The data indicated that acute ozone exposure can be used to initially screen a large number of bean accessions, however, this is an imperfect indicator of ozone sensitivity with chronic exposure.

Carbohydrates↗
PubMed2004

The extraordinary events of the major, sudden stratospheric warming, the diminutive antarctic ozone hole, and its split in 2002.

GOAL, SCOPE AND BACKGROUND: Great interest in the unprecedented events of the major, sudden stratospheric warming and the ozone hole split over Antarctica in September 25, 2002 motivates a necessity to analyze the current understanding on the dynamics, chemistry and climate impacts that are associated with both events. METHODS: Significant progress in the analysis of the observational data obtained, as well as successful development and application of dynamical modeling, which have been achieved very recently, create a basis for the first survey on the role of the major, sudden stratospheric warming observed in the southern hemisphere and its relationship to the diminutive Antarctic ozone hole and its break up into two parts. RESULTS AND DISCUSSION: Special attention has been paid to assessments of the causes of the major warming event and the future expectations concerning the stratospheric ozone depletion effect. Among the principal results is the fact that, as the polar vortex elongated, it became hydrodynamically unstable, and this insta-, bility affected the upper troposphere and stratosphere. During the major, sudden stratospheric warming, the middle stratospheric vortex split into two pieces; one piece rapidly mixed with extra vortex air, while the other returned to the pole as a much weaker and smaller vortex. The polar night jet was considerably weaker than normal, and was displaced more poleward than has been observed in previous winters, resulting from a series of wave events (propagated from the troposphere) that took place over the course of the winter. Finally, the relative ozone decrease (increase) in the eastern Antarctic is tightly associated with westerly (easterly) zonal wind anomalies near the southern tip of South America, and the unusual behavior of the ozone hole in 2002 therefore appears to be caused by great easterlies in this region. CONCLUSIONS: The main conclusion is that the southern polar vortex and the diminutive ozone hole split into two parts in September 2002, due to the prevalence of very strong planetary waves, led to the appearance of a major, sudden stratospheric warming. Although there is evidence that sea surface temperature anomalies contributed to the excitation of the quite strong planetary waves over Antarctica in 2002, there is not yet a widely approved mechanism supporting that. RECOMMENDATIONS AND OUTLOOK: The appearance of the near-record size of the 2003 ozone hole confirmed that the 'no-ozone-hole' episode observed in the year 2002 does not denote a recovery of the ozone layer. Despite the current successful attempts to get a sufficient understanding for the genesis of both extraordinary events, more observations and further modeling efforts are necessary to more reliably assess the contribution of various dynamic mechanisms to the recently observed tropo-stratospheric surprises.

Air Movements↗
PubMed1983

Interaction of ozone and cigarette smoke exposure.

Possible interactions of ozone and cigarette smoke exposure have been tested in 2-hr chamber exposures of 26 male and 6 female subjects, all of whom were habitual smokers. Treatment conditions were air alone, air + cigarette smoking, ozone alone, and ozone + cigarette smoking. Ozone levels were increased progressively over four trials (0.37 ppm, 0.75 ppm, 0.50 ppm + intermittent exercise, and 0.75 ppm + intermittent exercise); exercise (50 W for 15 min alternating with 15-min rest) was intended to increase ventilation by a factor of 2.5. Ozone exposure reduced the carbon monoxide intake normally seen with smoking, as judged from smaller increments of blood carboxyhemoglobin readings. Ozone exposure alone gave rise to a decrease of lung function (forced vital capacity (VC), 1-sec forced expiratory volume, and maximum flow rates at 25 and 50% of VC), but the onset was slower and the response less dramatic than previously seen in nonsmokers, suggesting that the chronic effect of smoking may be to delay bronchial irritation by ozone. Smoking increased heart rate both at rest and during exercise, but this response was not materially influenced by simultaneous ozone exposure. It is concluded that over an acute 2-hr exposure, there is no appreciable interaction between cigarette smoking and responses to ozone.

Adult↗
PubMed1988

Effects of ozone on the defense to a respiratory Listeria monocytogenes infection in the rat. Suppression of macrophage function and cellular immunity and aggravation of histopathology in lung and liver during infection.

We have investigated the effect of exposure to ozone on defense mechanisms to a respiratory infection with Listeria monocytogenes in the rat. For this purpose rats were continuously exposed to O3 concentrations ranging from 0.25 to 2.0 mg/m3 for a period of 1 week. In this model defense to a respiratory infection with Listeria depends on acquired specific cellular immune responses, as well as on natural nonspecific defense mechanisms. The results confirm earlier findings that show that ozone exposure can suppress the capacity of macrophages to ingest and kill Listeria. Moreover, the results show that ozone can also have a suppressive effect on the development of cellular immune responses to a respiratory Listeria infection, i.e., on T/B ratios in lung draining lymph nodes, delayed-type hypersensitivity responses to Listeria antigen, and lymphoproliferative responses in spleen and lung draining lymph nodes to Listeria antigen. The effects on the specific immune responses are especially overt if exposure to the oxidant gas occurs during an ongoing primary infection. The pathological lesions induced by a pulmonary Listeria monocytogenes infection were characterized by multifocal infiltrates of histiocytic and lymphoid cells. The foci sometimes had a granulomatous appearance. Moreover, the cellularity of the interstitial tissues was increased. In the lung many diffuse alveolar macrophages could be seen in the alveoli. Ozone exposure greatly increased the severity of the lung lesions and also of liver lesions resulting from the pulmonary infection. A prominent finding was the formation of granulomas in ozone-exposed and Listeria-infected rats. This increased severity of the lesions after ozone exposure and subsequent infection with Listeria was presumably not a result of additive ozone and Listeria-induced lesions, but rather an effect of ozone-induced impaired clearance of the bacteria, caused by depressed macrophage activity and cellular immunity. T-cell-dependent immune responses form an important component of defense to respiratory infections with bacteria and viruses, and possibly also to neoplasms. Since our study unequivocally shows an effect on T-cell-dependent immunity, ozone exposure has to be judged potentially hazardous with respect to such challenges of the lung.

Animals↗
PubMed1985

An anti-inflammatory drug (BW755C) inhibits airway hyperresponsiveness induced by ozone in dogs.

To follow up our previous observation that airway hyperresponsiveness induced by ozone is linked to airway inflammation, we investigated the effect of BW755C, an anti-inflammatory drug, on ozone-induced hyperresponsiveness in dogs. Airway responsiveness was assessed with dose-response curves of acetylcholine aerosol versus pulmonary resistance in two sets of experiments. In one set (placebo treatment), five dogs were given only saline solution treatment and were studied before treatment or ozone exposure and then after treatment both before and after ozone (3.0 ppm, 2 hours); in another set (BW755C treatment), the same dogs were studied before BW755C treatment or ozone and then after treatment (10 mg/kg intravenously) both before and after ozone. When the dogs were given no BW755C treatment, ozone induced a marked increase in airway responsiveness to acetylcholine. When the dogs were given BW755C, responsiveness was no different during treatment than before treatment but, more importantly, responsiveness did not increase significantly after ozone. We conclude that BW755C markedly inhibits ozone-induced airway hyperresponsiveness in dogs, probably by inhibiting the formation of oxygenation products of arachidonic acid.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1991

Effect of low concentrations of ozone on inhaled allergen responses in asthmatic subjects.

The relation between inhalation of ambient concentrations of ozone and airway reactivity to inhaled allergens may be important in asthma, since both agents can produce inflammatory changes in the airways. Seven asthmatic patients (mean age 40 [SD 13] years), with seasonal symptoms of asthma and positive skin tests for ragweed or grass, took part in a study to investigate whether exposure to low concentrations of ozone potentiates the airway allergic response. The patients were studied during 4 separate weeks in the winter. In each week there were 3 study days: on days 1 and 3 methacholine challenges were carried out; and on day 2 the subject received one of four combined challenges in a single-blind design--air breathing followed by inhalation of allergen diluent (placebo); ozone followed by inhalation of allergen diluent; air followed by allergen; or ozone followed by allergen. The ozone concentration was 0.12 ppm during 1 h of tidal breathing at rest, and allergens were inhaled until the forced expiratory volume in 1 s (FEV1) had fallen by 15% (PC15). There were no significant differences in baseline FEV1 after exposure to ozone but PC15 was significantly reduced when allergen was preceded by ozone inhalation: the mean PC15 after air was 0.013 (SD 0.017) mg/ml compared with 0.0056 (0.0062) mg/ml after ozone (p = 0.042). Thus, low ozone concentrations, similar to those commonly occurring in urban areas, can increase the bronchial responsiveness to allergen in atopic asthmatic subjects. This effect does not seem to be the result of changes in baseline airway function.

Adult↗
PubMed1994

In vitro exposure of tracheobronchial epithelial cells and of tracheal explants to ozone.

An in vitro system for exposing respiratory epithelial cells or explant tissues to ozone has been developed and characterized. This system is designed to generate and monitor consistent, reproducible levels of ozone, over a range of concentrations, in a humidified atmosphere, and to allow an exposure time of 24 h or longer. Based on chemical analysis, highly reproducible concentrations of ozone are delivered throughout the chamber, with a coefficient of variation of < 5% between five replicate vials exposed to 0.5 ppm of ozone for 50 min. The viability of cultured human tracheobronchial epithelial cells, as measured by the ability to oxidize a vital dye, and of rat tracheal epithelium, as measured by total numbers of necrotic cells in tracheal explants, after ozone exposure was examined in this system. Responses of cultured cells to ozone exposure as measured by bioassay were consistent with the observed low level of variability of ozone concentration between replicate incubation dishes or vials. Responses of cultured cells to ozone were proportional to duration of exposure and inversely proportional to the volume of medium covering the cells. We conclude that this newly developed in vitro exposure system will allow relatively simple and convenient exposure of cultured cells or organs to ozone or other gaseous agents under highly controlled and reproducible conditions.

Air Pollution↗
PubMed1991

Aldehydes, hydrogen peroxide, and organic radicals as mediators of ozone toxicity.

It is generally agreed that unsaturated fatty acids (UFA) are an important class of target molecule for reaction with ozone when polluted air is inhaled. Most discussions have implicated the UFA in cell membranes, but lung lining fluids also contain fatty acids that are from 20 to 40% unsaturated. Since UFA in lung lining fluids exist in a highly aquated environment, ozonation would be expected to produce aldehydes and hydrogen peroxide, rather than the Criegee ozonide. In agreement with this expectation, we find that ozonations of emulsions of fatty acids containing from one to four double bonds give one mole of H2O2 for each mole of ozone reacted. Ozonation of oleic acid emulsions and dioleoyl phosphatidyl choline gives similar results. with two moles of aldehydes and one mole of H2O2 formed per mole of ozone reacted. The net reaction that occurs when ozone reacts with pulmonary lipids is suggested to be given by equation 1. [formula: see text]. From 5 to 10% yields of Criegee ozonides also appear to be formed. In addition, a direct reaction of unknown mechanism occurs between ozone and UFA in homogeneous organic solution, in homogeneous solutions in water, in aqueous emulsions, and in lipid bilayers to give organic radicals that can be spin trapped. These radicals are suggested to be responsible for initiating lipid peroxidation of polyunsaturated fatty acids. Thus, aldehydes, hydrogen peroxide, and directly produced organic radicals are suggested to be mediators of ozone-induced pathology.

Aldehydes↗
PubMed2005

Natural ozone scavenger prevents asthma in sensitized rats.

The assumption that ozone is not only a strong oxidant, but also an important inflammatory mediator, is heavily supported by the ample literature on the pulmonary toxicity and biological effects of environmental ozone and by the recent discovery that antibodies, human neutrophils, and inflammatory lesions catalyze the formation of ozone in vivo. We hypothesized that the pulmonary inflammation in asthma involves a vicious circle of ozone production and recruitment of white blood cells, which produce more ozone. Accordingly, we predicted that electron-rich olefins, which are known ozone scavengers, could be used for prophylactic treatment of asthma. In particular, volatile, unsaturated monoterpenes, could saturate the pulmonary membranes and thereby equip the airways with local chemical protection against either exogenous or endogenous ozone. Here we present experimental evidence using a sensitized rat model to support this hypothesis. Examination of the pulmonary function of sensitized rats that inhaled either limonene (unsaturated, ozone scavenger) or eucalyptol (saturated, inert to ozone) showed that limonene inhalation significantly prevents bronchial obstruction while eucalyptol inhalation does not cause any effect. The anti-inflammatory effect of limonene was also evident from pathological parameters, such as diminished peribronchiolar and perivascular inflammatory infiltrates.

Administration, Inhalation↗
PubMed2004

Decomposition of 2-mercaptothiazoline in aqueous solution by ozonation.

This study investigates the ozonation of 2-mercaptothiazoline (2-MT). The 2-MT is one of the important organic additives for the electroplating solution of the printed wiring board industry and has been widely used as a corrosion inhibitor in many industrial processes. It is of concern for the aquatic pollution control especially in the wastewaters. Semibatch ozonation experiments in the completely stirred tank reactor are performed under various concentrations of input ozone. The concentrations of 2-MT, sulfate, and ammonium are analyzed at specified time intervals to elucidate the decomposition of 2-MT during the ozonation. In addition, the time variation of the dissolved ozone concentration (C(ALb)) is continuously monitored in the course of experiments. Total organic carbon (TOC) is chosen and measured as a mineralization index of the ozonation of 2-MT. The results indicate that the decomposition of 2-MT is efficient, while the mineralization of TOC is limited via the ozonation only. Simultaneously, the yield of sulfate with the maximum value of about 47% is characterized by the increases of TOC removal and ozone consumption. These results can provide some useful information for assessing the feasibility of the treatment of 2-MT in the aqueous solution by the ozonation.

Carbon↗
PubMed2005

Appropriate combination of physico-chemical methods (coagulation/flocculation and ozonation) for the efficient treatment of landfill leachates.

An integrated technique consisted of ozonation and coagulation/flocculation processes was studied, aiming to provide an efficient method for the treatment of stabilized/biologically pre-treated leachates, in order to reduce the organic pollutants' content to concentration values lower than the corresponding limits, imposed by the legislation. Leachates were collected from a municipal landfill site; samples containing around 1000 mg l(-1) COD and BOD(5)/COD ratio about 0.17 were treated by using two different processes or combinations between them, i.e. ozonation, coagulation-flocculation, ozonation followed by coagulation/flocculation and coagulation/flocculation followed by ozonation. The application of single ozonation resulted to the efficient removal of color and organic loading, due to the respective oxidation, induced by ozonation; however, COD values lower than 200 mg l(-1) could be only achieved after prolonged reaction times and for high ozone production rates. The coagulation of leachate samples was studied by the addition of ferric chloride or poly-aluminum chloride agents at various dosages. Maximum COD removal rates (up to 72%) were achieved by the addition of 7 mM Fe, or of 11 mM Al respectively. However, final COD values higher than 200 mg l(-1) were obtained indicating the requirement of an additional treatment step. Pre-ozonation followed by coagulation/flocculation was not found to be an efficient treatment approach for this aim, but coagulation/flocculation followed by ozonation, was proved to be an efficient process for the reduction of COD to lower than 180 mg l(-1).

Chemistry, Physical↗
PubMed2005

The use of ozone in the remediation of polycyclic aromatic hydrocarbon contaminated soil.

The potential of using ozone for the removal of phenanthrene from several different soils, both alone and in combination with biodegradation using a microbial inoculant (Pseudomonas alcaligenes PA-10), was examined. The greater the water content of the soil the less effective the ozone treatment, with air-dried soils showing the greatest removal of phenanthrene; while soils with higher levels of clay also reduced the effectiveness of the ozone treatments. However, at least a 50% reduction in phenanthrene levels was achieved in air-dried soil after an ozone treatment of 6 h at 20 ppm, with up to 85% removal of phenanthrene achieved in sandy soils. The biodegradation results indicate that P. alcaligenes PA-10 may be useful as an inoculant for the removal of PAHs from contaminated soils. Under the conditions used in our experiments, however, pre-ozonation did not enhance subsequent biodegradation of phenanthrene in the soils. Similar levels of phenanthrene removal occurred in both non-ozonated and ozonated Cruden Bay soil inoculated with P. alcaligenes PA-10. However, the biodegradation of phenanthrene in ozonated Boyndie soil was much slower. This may be due to the release of toxic products in this soil during ozonation.

Biodegradation, Environmental↗
PubMed2003

Functional group analysis during ozonation of sunflower oil methyl esters by FT-IR and NMR.

Ozonation of neat sunflower oil (SFO) methyl esters was monitored by FT-IR and 1H and 13C NMR spectroscopy. During the early stage of ozonation, ozone absorption was essentially quantitative. This was accompanied by the formation of 1,2,4-trioxolane. IR and NMR spectra of ozonated samples showed that scission of ozonide to give aldehyde were minimal. 1H NMR analysis revealed that the amount of ozonide relative to aldehyde was more than 90% regardless of the extent of ozonation. Complete ozonation was attained after supplying around 0.20 g O3/ml methyl ester after which ozone absorption suddenly dropped to around 25%. At the latter part of ozonation, ozonide and aldehyde reacted with excess ozone to give carboxylic acid. Reaction products were identified according to Criegee mechanism.

Aldehydes↗