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PubMed2004

Advanced treatment of biotreated textile industry wastewater with ozone, virgin/ozonated granular activated carbon and their combination.

Biotreated textile wastewater (CODo = 248 mg L(-1); TOCo = 58 mg L(-1); A620 = 0.007 cm(-1); A525 = 0.181 cm(-1); A436 = 0.198 cm(-1)) was subjected to advanced treatment with ozonation, granular activated carbon (GAC) adsorption in serial and simultaneous applications. Experiments were conducted to investigate the effects of applied ozone dose, ozone absorption rate, specific ozone absorption efficiency, GAC dose, and reaction pH on the treatment performance of the selected tertiary treatment scheme. In separate experiments, the impact of virgin GAC ozonation on its adsorptive capacity for biotreated and biotreated + ozonated textile effluent was also investigated. Ozonation appeared to be more effective for decolorization (kd = 0.15 min(-1) at pH = 3), whereas GAC adsorption yielded higher COD removal rates (54% at pH = 3). It was also found that GAC addition (4 g/L) at pH = 7 and 9 enhanced the COD abatement rate of the ozonation process significantly and that the sequential application of ozonation (at pH = 3-11, 675 mg L(-1) O3) followed by GAC adsorption (at pH = 3-7, 10 g L(-1) GAC) resulted in the highest treatment performances both in terms of color and COD reduction. Simultaneous application of GAC and ozone at acidic and alkaline pH seriously inhibited COD abatement rates as a consequence of competitive adsorption and partial oxidation of textile components and GAC. It could also be established that ozone absorption efficiency decreased after color removal was complete. Ozonation of biotreated textile wastewater with 113 mg L(-1) ozone resulted in an appreciable enhancement of GAC adsorptive capacity in terms of residual color removal. Ozonation of GAC at relatively low doses (= 10.8 mg/g GAC) did not improve its overall adsorption capacity.

Adsorption↗
PubMed1996

4-Hydroxynonenal mimics ozone-induced modulation of macrophage function ex vivo.

Ozone is a ubiquitous pollutant that can cause acute pulmonary inflammation, cellular injury and may contribute to the development or exacerbation of chronic lung diseases. Despite much research, the effects of ozone on humans and potential cellular mechanisms of injury are still uncertain. However, ozone has been reported to increase the formation of aldehydes that could react with cellular proteins. Therefore, the purpose of these studies was to determine whether 4-hydroxynonenal (HNE), a previously unidentified aldehyde product of ozone exposure, is formed in human subjects exposed to ozone, and whether the response of human alveolar macrophages (AM) following a 1-h exposure to 0.25 ppm ozone with moderate exercise could be mimicked by in vitro incubation of AM with HNE. Western analysis demonstrated increased HNE protein adducts in airway fluid and alveolar macrophages after ozone exposure. AM were examined for endotoxin (lipopolysaccharide [LPS])-stimulated interleukin-1 beta (IL-1 beta) release and expression of heat shock protein 72 (HSP72). Immediately after ozone exposure there was no change in HSP72, but a 5-fold increase occurred 4 h after exposure. By 18 h after exposure, HSP72 levels decreased to below comparable air-exposed levels. Immediately after ozone exposure there was no effect on IL-1 beta release stimulated by LPS. However, IL-1 beta release stimulated by LPS was significantly inhibited 4 h after ozone exposure. By 18 h after ozone exposure, IL-1 beta release stimulated by LPS returned to normal. Incubation of human AM in vitro with HNE induced HSP72 and blocked LPS-stimulated IL-1 beta release possibly by inhibiting interleukin converting enzyme. Consequently, the in vitro results and demonstration of HNE protein adducts following ozone exposure are consistent with HNE being involved in this process in vivo and suggest that the cellular toxic effects of ozone could be a result of thiol reactive aldehydes produced by ozone.

Aldehydes↗
PubMedDate not supplied

Effects of ozone exposure at ambient air pollution episode levels on exercise performance.

Ozone is a principal component of photochemical air pollution endogenous to numerous metropolitan areas, which may induce irritant effects on the respiratory tract which impair pulmonary function, result in subjective symptoms of respiratory discomfort, including cough and shortness of breath, and can limit exercise performance. The effects of moderate ambient photochemical air pollution observed in a mobile laboratory have also been shown to be similar to those induced in laboratory chamber exposures to the same level of ozone alone. The metabolic demand of exercise increases minute ventilation (VE) and thus, the rate of ozone inhalation over that at rest. Potentially, exercise can also enhance the effects of ozone by: (a) reducing nasal passage absorption; (b) increasing the uniformity of ventilation throughout the lungs; and (c) replacing reacted ozone at a faster rate. However, results from 2-hour intermittent exercise and 1-hour continuous exercise exposures at the same total ventilation and ozone concentration have been shown to yield similar pulmonary function effects. It has been shown via significant variation in exercise intensity, and thus VE, that the simple product of ozone concentration, VE and exposure time (termed the ozone effective dose) predicts pulmonary function and exercise ventilatory pattern (induced rapid, shallow breathing) effects more precisely than ozone concentration alone. Better prediction of pulmonary function effects has been achieved via multiple regression analysis in which ozone concentration is given a greater weighting than VE and exposure time. Light intermittent exercise was first studied in 2-hour laboratory exposures to ozone at concentrations rarely seen in the ambient environment. In recent studies, heavy continuous exercise has been used in 1-hour exposures to ozone at levels routinely observed in photochemical episodes (less than or equal to 0.35 ppm). Statistically significant impairment of exercise performance has been observed at 0.18 ppm, a level reached for 1 hour, or more, on about 180 days per year in the Los Angeles basin. Responses of subpopulation groups, such as children, young adult females, older adults, and those with pre-existing pulmonary disease are not notably different from those of young adult males provided that the ozone effective dose is proportional to body size. Conversely, highly trained endurance athletes demonstrate significant responses at rather low ozone concentrations due to their ability to sustain very high VE over prolonged periods.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1998

In vitro testing of a denture cleaning method using ozone.

The purpose of this study was to compare the microbicidal effect of gaseous ozone with that of ozonated water in order to determine its usefulness as a method for disinfecting dentures. Although a large number of research studies have been done on the bactericidal effect of ozone, little is known about its microbicidal effects on oral microorganisms. Therefore, we tested the effect of ozone on three standard strains of oral microorganisms: Streptococcus mutans (strain IID 973), Staphylococcus aureus (strain 209-P), and Candida albicans (strain LAM 14322). When the gaseous ozone injection method was used, the numbers of cells of all three strains decreased to 1/10(5) at 1 min, and by 3 min they were below the detection limit. Thus, the microbicidal effect of gaseous ozone was ascertained in a short time. In contrast, when ozonated water at 1 ppm and 3 ppm was used, C. albicans decreased to 1/10. A 700 mg/h ozone production level was needed to prepare 1 ppm ozonated water, whereas 20 mg/h of ozone was required by the gaseous ozone generator. These findings indicate that direct exposure to gaseous ozone seems to be a more effective microbicide compared with ozonated water, and that gaseous ozone can be clinically useful for disinfection of dentures.

Candida albicans↗
PubMed2006

[Impact of catalytic ozonation with ferric hydroxide on HAAs formation potential of a filtered surface water].

Formation potential of five haloacetic acids (HAA5FP) of a filtered surface water was studied after ozonation alone and catalytic ozonation with a ferric hydroxide (FeOOH). Factors studied were oxidation time, bromide, pH, bicarbonate alkalinity, and ozone dosages. The haloacetic acids detected were dichloroacetic acid (DCAA), trichloroacetic acid (TCAA), and dibromoacetic acid (DBAA) when bromide existed. The catalytic ozonation caused a reduction of HAA5FP of the non-bromide containing water for 9.5% - 18.3% compared to that of ozonation in 5-20 minutes. Incremental addition of bromide led to a much lower HAA5FP after catalytic ozonation than that after ozonation. HAA5FP of the water at neutral pH was higher than that at acidic and basic conditions. Catalytic ozonation showed a most advantageous potential in controlling HAA5FP over ozonation at neutral pH. The HAA5FP decreased as bicarbonate concentration increased, and the disparity between ozonation and catalytic ozonation was also reduced. The HAA5FP after catalytic ozonation was 11.2% to 28.0% lower than that after ozonation while the ratio of O3/TOC ranging from 0.45 to 1.43. The effect of catalytic ozonation on HAA5FP of the water is closely related to its enhanced generation of hydroxyl radicals in catalytic process.

Acetates↗
PubMed1994

Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies. Part VII: Effects on the nasal mucociliary apparatus.

Besides the centriacinar region of the lung, the nose is a principal target for ozone toxicity. Acute exposures to concentrations of ozone in ambient air induce secretory cell metaplasia in the nasal transitional epithelium of rats. This study examined the effects of chronic ozone exposure on the structure and function of the nasal mucociliary apparatus of the rat. Male and female F344/N rats were exposed to ozone concentrations of 0.0 (controls), 0.12, 0.5, or 1.0 parts per million (ppm), six hours per day, five days per week, for 20 months. All rats were killed seven or eight days after the end of the exposure. Immediately after death, mucous flow rates throughout the nasal passages were determined using in vitro video motion analysis. Following assessment of mucociliary function, the nasal tissues were processed for light microscopy and stained with Alcian blue (pH 2.5)/periodic acid-Schiff to detect intraepithelial mucus. Image analysis was used to quantitate the amount of mucus within the nasal transitional epithelium. In rats exposed to 0.5 or 1.0 ppm ozone, mucous flow rates were markedly slower over the lateral wall and turbinates of the proximal third of the nasal airways than they were in rats exposed to 0.0 or 0.12 ppm ozone. These intranasal regions in the rats exposed to 0.5 or 1.0 ppm ozone contained marked mucous cell metaplasia and 25 to 300 times more mucus in nasal transitional epithelium than was found in control rats. In addition, male and female rats exposed to 0.5 or 1.0 ppm ozone had marked epithelial hyperplasia in nasal transitional epithelium, increases in eosinophilic globules in the surface epithelium lining the distal nasal airways, and a mild to moderate inflammatory cell influx in the nasal mucosa in the proximal and middle nasal passages. Male rats also had conspicuous bony atrophy in maxilloturbinates and nasoturbinates. There were no significant decreases between the mucous flow rates of rats exposed to 0.12 ppm ozone and those of control rats. There were, however, mild increases in various flow rates in some areas of the nasal airways in rats exposed to 0.12 ppm ozone compared with control rats. No significant morphologic alterations were evident in the rats exposed to 0.0 or 0.12 ppm ozone. The results of this study indicate that rats chronically exposed to 0.5 or 1.0 ppm ozone have significant alterations in the function and structure of the nasal mucociliary apparatus. Though there was a mild increase in mucous flow rates in a few nasal regions of some rats exposed to 0.12 ppm ozone, this functional change was interpreted as a physiologic, rather than a pathologic, response to ozone at this relatively low concentration.

Administration, Inhalation↗
PubMed1994

Active and passive ozone samplers based on a reaction with a binary reagent.

Ozone is one of the most toxic common air pollutants (judging from short-term animal and human exposure studies at realistic concentrations) and one of the most difficult and expensive pollutants to control. Because of ozone's high chemical reactivity, its concentrations may vary greatly over short distances, and fixed-site air quality monitors may not accurately estimate exposures of human populations. Epidemiologic research on ozone's long-term health effects has been inconclusive, partly because of the lack of reliable personal exposure information. The objective of this project was to develop a practical personal ozone exposure monitoring technique, and to document its precision and accuracy in actual use by representatives of freely ranging, ozone-exposed populations. The project site, Los Angeles, is the nation's metropolitan area with the highest level of ozone pollution and, thus, probably the most important locale for personal exposure assessment. Our overall strategy was (1) to select the most promising laboratory technique for ozone detection from published literature and private communications; (2) to design and test personal monitors using this technique; and (3) when feasible, to evaluate concurrently alternative methodologies developed by others. As indicated below, parts 1 and 2 of our strategy yielded a limited success with respect to short-term active sampling, i.e., measuring personal ozone exposure levels during one to two hours with a monitor incorporating a battery-powered air pump of the type used in industrial hygiene investigations. The same approach was not successful in passive sampling, i.e., measuring exposure levels during multihour or multiday periods with a light-weight, diffusion-controlled "badge" sampler having no moving parts. Passive badge samplers could be calibrated reasonably well in laboratory exposures to ozone in otherwise pure air, but they greatly overestimated ozone levels in outdoor ambient air. Part 3 of our strategy yielded more promising information on an alternative passive badge design. After testing and rejecting two other possibilities, we chose a binary organic reagents, 3-methyl-2-benzothiazolinone acetone azine with 2-phenylphenol, as the most promising chemical detector of ozone. Filter papers impregnated with the binary reagent develop a characteristic intense pink color when exposed to ozone. The inventors, J.E. Lambert and associates of Kansas State University, had intended only to develop a rough qualitative ozone monitor (Lambert et al. 1989). However, our initial laboratory testing (in exposure chambers containing ozone in otherwise very clean air, away from humans), revealed fairly accurate quantitative response.(ABSTRACT TRUNCATED AT 400 WORDS)

Benzothiazoles↗
PubMed1990

Surface ozone exposures measured at clean locations around the world.

For assessing the effects of air pollution on vegetation, some researchers have used control chambers as the basis of comparison between crops and trees grown in contemporary polluted rural locations and those grown in a clean environment. There has been some concern whether the arbitrary ozone level of 0.025 ppm and below, often used in charcoal-filtration chambers to simulate the natural background concentration of ozone, is appropriate. Because of the many complex and man-made factors that influence ozone levels, it is difficult to determine natural background. To identify a range of ozone exposures that occur at 'clean' sites, we have calculated ozone exposures observed at a number of 'clean' monitoring sites located in the United States and Canada. We do not claim that these sites are totally free from human influence, but rather than the ozone concentrations observed at these 'clean' sites may be appropriate for use by vegetation researchers in control chambers as pragmatic and defensible surrogates for natural background. For comparison, we have also calculated ozone exposures observed at four 'clean' remote sites in the Northern and Southern Hemispheres and at two remote sites (Whiteface Mountain, NY and Hohenpeissenberg, FRG) that are considered to be more polluted. Exposure indices relevant for describing the relationship between ozone and vegetation effects were applied. For studying the effects of ozone on vegetation, the higher concentrations are of interest. The sigmoidally-weighted index appeared to best separate those sites that experienced frequent high concentration exposures from those that experienced few high concentrations. Although there was a consistent seasonal pattern for the National Oceanic and Atmospheric Administration (NOAA) Geophysical Monitoring for Climate Change (GMCC) sites indicating a winter/spring maximum, this was not the case for the other remote sites. Some sites in the continental United States and southern Canada experienced ozone exposures in the range between those values experienced at the South Pole and Mauna Loa NOAA GMCC sites. The 7-month average of the daily 7 h average ozone concentration at 'clean' sites located in the continental United States and southern Canada ranged from 0.028 to 0.050 ppm. Our analysis indicates that seasonal 7 h average values of 0.025 ppm and below, used by some vegetation researchers as a reference point, may be too low and that estimates of crop losses and tree damage in many locations may have been too high. Our analysis indicates that a more appropriate reference point in North America might be between 0.030 and 0.045 ppm. We have observed that the subtle effects of changing distribution patterns of hourly average ozone concentrations may be obscured with the use of exposure indices such as the monthly average. Future assessments of the effects associated with ground-level ozone should involve the use of exposure indices sensitive to changes in the distribution patterns of hourly average ozone concentrations.

Journal Article↗
PubMed1994

Effects of various ozone exposures on the susceptibility of bean leaves (Phaseolus vulgaris L.) to Botrytis cinerea.

The effects of various ozone exposures in predisposing bean leaves (Phaseolus vulgaris L.) to Botrytis cinerea have been investigated under laboratory conditions. Seedlings of two bean cultivars were exposed to incremental ozone concentrations (120, 180 and 270 microg m(-3) for 8-h day(-1)) for five days and primary leaves were subsequently inoculated with conidia suspended in water or in an inorganic phosphate solution (Pi), and with mycelium. Ozone injury increased with increasing ozone concentration and was much higher in the ozone-sensitive cultivar 'Pros' than in the ozone-insensitive 'Groffy'. Ozone only increased the number of lesions on leaves of Pros after inoculation with either of the conidial suspensions. The Pi-stimulated infection in Groffy was reduced by the lower ozone concentrations. Ozone decreased lesion expansion after inoculation with mycelium. In a chronic fumigation experiment, plants of the two cultivars were exposed to 90 microg m(-3) (7-h day(-1)) and the primary and the oldest tree trifoliate leaves were inoculated after five and seven weeks of exposure. Ozone enhanced the senescence-related injury only in Pros. The number of lesions was not influenced by ozone for either cultivar, conidial suspension or inoculation date. Lesion expansion after inoculation with mycelium was generally reduced in exposed plants. Thus, contrasting effects of ozone on the susceptibility of bean leaves to B. cinerea were observed depending on the cultivar, the conidial suspension, the disease parameter and the ozone exposure pattern. In extrapolating the laboratory results to the field, it is suggested that episodic and chronic exposures to ambient ozone are of minor importance in increasing the susceptibility of bean leaves to B. cinerea.

Journal Article↗
PubMed2000

The effect of ozone on below-ground carbon allocation in wheat.

Short-term (14)CO(2) pulse and chase experiments were conducted in order to investigate the effect of ozone on below-ground carbon allocation in spring wheat seedlings (Triticum aestivum L. 'ANZA'). Wheat seedlings were grown in a sand-hydroponic system and exposed to either high ozone (38-40 ppm-h) or low ozone (23-31 ppm-h) for 21 days in a series of replicated experiments. Following the ozone exposures, the plants were pulsed with (14)CO(2) and allocation of (14)C-labeled photosynthate was measured in the plant and growth media. Soluble root exudates were measured, without disturbing the plant roots, 24 h after the (14)CO(2) pulse. Shoot biomass was reduced by 17% for the high ozone and 9% for the low ozone exposures, relative to control treatments. Root biomass was reduced by 9% for the high ozone exposures, but was not significantly different than the controls for the low ozone. The amount of (14)C activity in the shoot and root tissue 24 h after the (14)CO(2) pulse, normalized to tissue weight, total (14)CO(2) uptake, or the total (14)C retention in each plant, was not affected by either high or low ozone exposures. The amount of (14)C activity measured in the growth media solution surrounding the roots increased 9% for the high ozone exposures, and after normalizing to root size or root (14)C activity, the growth media solution (14)C activity increased 29 and 40%, respectively. Total respiration of (14)CO(2) from the ozone-treated plants decreased, but the decrease was not statistically significant. Our results suggest that soluble root exudation of (14)C activity to the surrounding rhizosphere increases in response to ozone. Increased root exudation to the rhizosphere in response to ozone is contrary to reports of decreased carbon allocation below ground and suggests that rhizosphere microbial activity may be initially stimulated by plant exposure to ozone.

Journal Article↗
PubMed2006

Mass-dependent and non-mass-dependent isotope effects in ozone photolysis: resolving theory and experiments.

In addition to the anomalous (17)O and (18)O isotope effects in the three-body ozone formation reaction O+O(2)+M, isotope effects in the destruction of ozone by photolysis may also play a role in determining the isotopic composition of ozone and other trace gases in the atmosphere. While previous experiments on ozone photolysis at 254 nm were interpreted as evidence for preferential loss of light ozone that is anomalous (or "non-mass-dependent"), recent semiempirical theoretical calculations predicted a preferential loss of heavy ozone at that wavelength that is mass dependent. Through photochemical modeling results presented here, we resolve this apparent contradiction between experiment and theory. Specifically, we show that the formation of ozone during the UV photolysis experiments is not negligible, as had been assumed, and that the well-known non-mass-dependent isotope effects in ozone formation can account for the non-mass-dependent enrichment of the heavy isotopologs of ozone observed in the experiment. Thus, no unusual non-mass-dependent fractionation in ozone photolysis must be invoked to explain the experimental results. Furthermore, we show that theoretical predictions of a mass-dependent preferential loss of the heavy isotopologs of ozone during UV photolysis are not inconsistent with the experimental data, particularly if mass-dependent isotope effects in the chemical loss reactions of ozone during the photolysis experiments or experimental artifacts enrich the remaining ozone in (17)O and (18)O. Before the calculated fractionation factors can be quantitatively evaluated, however, further investigation of possible mass-dependent isotope effects in the reactions of ozone with O((1)D), O((3)P), O(2)((1)Delta), and O(2)((1)Sigma) is needed through experiments we suggest here.

Journal Article↗
PubMed1996

4-hydroxy-2-nonenal-protein adducts and apoptosis in murine lung cells after acute ozone exposure.

Ozone is a photochemically generated pollutant that can cause acute pulmonary inflammation and induce cellular injury and may contribute to the development or exacerbation of chronic lung diseases. Despite extensive investigation, the mechanisms of ozone and oxidant-induced cellular injury are still uncertain. Ozone has been reported to cause the formation of aldehydes in biological fluids that could explain many of the cellular effects caused by ozone. One of the most toxic aldehydes formed during oxidant-induced lipid peroxidation is 4-hydroxy-2-nonenal (HNE). HNE reacts primarily with Cys and secondarily with Lys and His amino acids, altering protein function and forming protein adducts that can be detected using specific adducts. In this study, we investigated whether ozone could cause the formation of HNE by assaying for HNE-protein adducts in cells isolated by lung lavage from C3H/HeJ mice exposed to 2.0 and 0.25 ppm ozone for 3 hr. Since oxidative stress and HNE have been shown to cause apoptosis we also examined the lung lavage cells for evidence of apoptosis following ozone exposure. Using a specific polyclonal antibody against HNE-amino acid adducts, two principle HNE-protein adducts were detected by Western analysis in cells obtained after ozone exposure at approximately 86-90 and 32 kDa. In addition to cell necrosis, apoptosis of lung cells was significant 3 hr after ozone exposure as detected using a Cell Death ELISA procedure and confirmed with DNA ladder and morphological analysis. The apoptotic cell injury peaked at 6 hr postexposure and decreased by 24 hr. Taken together, these results demonstrate that HNE is formed in vivo following ozone exposure and HNE appears to form specific protein adducts in lung cells. Furthermore, ozone can cause lung cell injury by an apoptotic mechanism in addition to a necrotic mechanism. Since HNE is toxic to cells and is formed as a result of ozone exposure, it may contribute to the lung cell injury following ozone exposure.

Aldehydes↗
PubMed1991

Preneoplastic transformation of rat tracheal epithelial cells by ozone.

The transforming potency of ozone for rat tracheal epithelial (RTE) cells exposed in vivo or in vitro was determined. RTE cells isolated from rats exposed to ozone (0, 0.14, 0.6, or 1.2 ppm, 6 hr/day, 5 days/week for 1, 2, or 4 weeks) showed no increase in the frequency of preneoplastic transformation compared to cells isolated from unexposed rats, although ozone-induced morphologic changes were observed in exposed tracheas. In contrast, preneoplastic variants of RTE cells were induced by multiple, but not single, exposures of RTE cells to ozone in culture. RTE cells exposed biweekly to ozone (approximately 0.7 ppm for 40 min, nine total exposures) had approximately twofold increases in the frequency of preneoplastic transformation compared to that of concurrent controls exposed to air. Single, 40-min exposures to ozone (approximately 1 or approximately 10 ppm) did not induce preneoplastic variants. However, single, 40-min exposures of RTE cells to approximately 10 ppm ozone did result in approximately 40% decreases in colony-forming efficiency. In addition, single, 40-min exposures of RTE cells to approximately 1 ppm ozone reduced the transforming potency of a subsequent exposure to the direct-acting chemical carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). When multiple ozone exposures followed exposure to MNNG (approximately 0.7 ppm ozone for 40 min, nine biweekly exposures), an additive (or possibly a multiplicative) effect of ozone on MNNG-induced preneoplastic transformation was seen. These results demonstrate that ozone can, under some conditions, induce preneoplastic variants of RTE cells. In addition, depending on the sequence or combinations of exposures, ozone can reduce or, possibly, increase, the transforming potency of the carcinogen MNNG for rat tracheal cells in culture.

Animals↗
PubMed2005

Ozonation of Procaine Penicillin G formulation effluent Part I: Process optimization and kinetics.

Ozonation characteristics of synthetic Procaine Penicillin G (PPG) formulation effluent were investigated in a semi-batch ozone reactor at different pH (3, 7 and 12), ozone feed rates (600-2600 mg h-1) and COD values (200-600 mg l-1). Ozonation of aqueous PPG effluent resulted in 37 (82)% COD removal after 60 (120) min ozonation when the reaction pH was kept constant at pH=7.900 mg l-1 (corresponding to 50% of the total introduced) ozone was absorbed during a reaction period of 1 h. The effects of increasing the applied ozone dose and the initial COD on the COD abatement rates of PPG effluent were also studied. Results have indicated that increasing the ozone dose and decreasing the COD content both have positive effects on COD removal rates. The significant contribution of the free radical (.OH) reaction pathway to PPG ozonation could be traced using tert-butyl alcohol as the .OH probe compound at varying concentrations. The bimolecular reaction rate constants for the direct reaction of PPG with ozone were found as 152 and 2404 M-1 h-1 at pH=3 and 7, respectively, using the gas phase ozone partial pressures determined from of the outlet gas stream analysis. It could be demonstrated that ozone decomposition to free radicals being triggered by increasing the pH from 3 to 7 is essential for the rate enhancement of PPG effluent ozonation.

Free Radical Scavengers↗
PubMed2003

Ozonation of drinking water: part I. Oxidation kinetics and product formation.

The oxidation of organic and inorganic compounds during ozonation can occur via ozone or OH radicals or a combination thereof. The oxidation pathway is determined by the ratio of ozone and OH radical concentrations and the corresponding kinetics. A huge database with several hundred rate constants for ozone and a few thousand rate constants for OH radicals is available. Ozone is an electrophile with a high selectivity. The second-order rate constants for oxidation by ozone vary over 10 orders of magnitude, between < 0.1 M(-1)s(-1) and about 7 x 10(9) M(-1)s(-1). The reactions of ozone with drinking-water relevant inorganic compounds are typically fast and occur by an oxygen atom transfer reaction. Organic micropollutants are oxidized with ozone selectively. Ozone reacts mainly with double bonds, activated aromatic systems and non-protonated amines. In general, electron-donating groups enhance the oxidation by ozone whereas electron-withdrawing groups reduce the reaction rates. Furthermore, the kinetics of direct ozone reactions depend strongly on the speciation (acid-base, metal complexation). The reaction of OH radicals with the majority of inorganic and organic compounds is nearly diffusion-controlled. The degree of oxidation by ozone and OH radicals is given by the corresponding kinetics. Product formation from the ozonation of organic micropollutants in aqueous systems has only been established for a few compounds. It is discussed for olefines, amines and aromatic compounds.

Hydroxyl Radical↗
PubMed2002

Transport characteristics of gas phase ozone in unsaturated porous media for in-situ chemical oxidation.

Laboratory column experiments were conducted by employing various porous media to delineate the characteristics of gaseous ozone transport in the unsaturated zone under various conditions. Water content, soil organic matter (SOM), and metal oxides (MOs) were found to be the factors most influential in the fate and transport of gaseous ozone in unsaturated porous media. The migration velocity of the gaseous ozone front was inversely proportional to the MO content of the porous media. Increased water content at fixed gas flux decreased the ozone breakthrough time proportionally as a result of reduced gas pore volume (PV) in the column, and increased pore water interfered with reactions of gaseous ozone with SOM and MOs on the surface of porous media. The feasibility of in-situ ozone injection for the remediation of unsaturated soils contaminated with either phenanthrene or diesel-range organics (DROs) was investigated under various conditions. The maximum removal after 1 h of ozone injection was achieved in columns packed with baked sand, followed, in descending order, by glass beads and by sand, indicating that catalytic ozone dccomposition with MOs in columns packed with baked sand enhanced hydroxyl radical formation and resulted in increased contaminant removal. Overall removal efficiency of multicomponent C10-C24 DROs after 14 h of ozonation was 78.7%. Ozone transport was retarded considerably because of the high ozone demand of DROs, requiring more than 6 h for the gaseous ozone to initially break through the soil column under the experimental conditions tested in this study. Overall, gaseous ozone was readily delivered and transported to remediate unsaturated soils contaminated with phenanthrene and DROs.

Carcinogens, Environmental↗
PubMed2003

Ozone-induced gene expression occurs via ethylene-dependent and -independent signalling.

Recent studies suggest that ethylene is involved in signalling ozone-induced gene expression. We show here that application of ozone increased glucuronidase (GUS) expression of chimeric reporter genes regulated by the promoters of the tobacco class I beta-1,3-glucanases (GLB and Gln2) and the grapevine resveratrol synthase (Vst1) genes in transgenic tobacco leaves. 5'-deletion analysis of the class I beta-1,3-glucanase promoter revealed that ozone-induced gene regulation is mainly mediated by the distal enhancer region containing the positively acting ethylene-responsive element (ERE). In addition, application of 1-methylcyclopropene (1-MCP), an inhibitor of ethylene action, blocked ozone-induced class I beta-1,3-glucanase promoter activity. Enhancer activity and ethylene-responsiveness depended on the integrity of the GCC boxes, cis-acting elements present in the ERE of the class I beta-1,3-glucanase and the basic-type pathogenesis-related PR-1 protein (PRB-1b) gene promoters. The minimal PRB-1b promoter containing only the ERE with intact GCC boxes, was sufficient to confer 10-fold ozone inducibility to a GUS-reporter gene, while a substitution mutation in the GCC box abolished ozone responsiveness. The ERE region of the class I beta-1,3-glucanase promoter containing two intact GCC boxes confered strong ozone inducibility to a minimal cauliflower mosaic virus (CaMV) 35S RNA promoter, whereas two single-base substitution in the GCC boxes resulted in a complete loss of ozone inducibility. Taken together, these datastrongly suggest that ethylene is signalling ozone-induced expression of class I beta-l,3-glucanase and PRB-1b genes. Promoter analysis of the stilbene synthase Vst1 gene unravelled different regions for ozone and ethylene-responsiveness. Application of 1-MCP blocked ethylene-induced Vst1 induction, but ozone induction was not affected. This shows that ozone-induced gene expression occurs via at least two different signalling mechanisms and suggests an additional ethylene independent signalling pathway for ozone-induced expression of genes involved in phytoalexin biosynthesis.

Acyltransferases↗
PubMed2000

Ozone in indoor environments: concentration and chemistry.

The concentration of indoor ozone depends on a number of factors, including the outdoor ozone concentration, air exchange rates, indoor emission rates, surface removal rates, and reactions between ozone and other chemicals in the air. Outdoor ozone concentrations often display strong diurnal variations, and this adds a dynamic excitation to the transport and chemical mechanisms at play. Hence, indoor ozone concentrations can vary significantly from hour-to-hour, day-to-day, and season-to-season, as well as from room-to-room and structure-to-structure. Under normal conditions, the half-life of ozone indoors is between 7 and 10 min and is determined primarily by surface removal and air exchange. Although reactions between ozone and most other indoor pollutants are thermodynamically favorable, in the majority of cases they are quite slow. Rate constants for reactions of ozone with the more commonly identified indoor pollutants are summarized in this article. They show that only a small fraction of the reactions occur at a rate fast enough to compete with air exchange, assuming typical indoor ozone concentrations. In the case of organic compounds, the "fast" reactions involve compounds with unsaturated carbon-carbon bonds. Although such compounds typically comprise less than 10% of indoor pollutants, their reactions with ozone have the potential to be quite significant as sources of indoor free radicals and multifunctional (-C=O, -COOH, -OH) stable compounds that are often quite odorous. The stable compounds are present as both gas phase and condensed phase species, with the latter contributing to the overall concentration of indoor submicron particles. Indeed, ozone/alkene reactions provide a link between outdoor ozone, outdoor particles and indoor particles. Indoor ozone and the products derived from reactions initiated by indoor ozone are potentially damaging to both human health and materials; more detailed explication of these impacts is an area of active investigation.

Air Pollution, Indoor↗