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PubMed1998

Determining toxicity trends in the ozonation of synthetic dye wastewaters using the nematode Caenorhabditis elegans.

The nematode Caenorhabditis elegans was used in 72-h toxicity tests to evaluate the influence of ozonation on the toxicity of three synthetic azo dye wastewaters (two reactive dyes and one acid-based dye). The two reactive dye wastewaters contained high concentrations of NaCl (89-112 g/L) in addition to potentially toxic dye components. To determine the contribution of NaCl to toxicity, simulated dye wastewater samples with and without NaCl were tested. Samples were collected at various times during ozonation (t = 0, 8, 32, 64 min); nematodes were exposed to the samples for 72 h. The influence of ozonation on toxicity varied between dye wastewater types. For the acid-based dye wastewater, toxicity increased as duration of ozonation increased. For the reactive dyes without NaCl, toxicity did not appear to be influenced by ozonation. For the reactive dyes with NaCl, mortality was 100% with or without ozonation. Range-finding experiments with NaCl in water and NaCl in dye wastewaters suggested an additive toxic interaction between NaCl and the dyes in wastewater to the nematodes. The duration of ozonation for acid-based dyes and the relatively high NaCl concentrations for the reactive dyes appear to influence effluent toxicity in the ozonated dye wastewaters.

Animals↗
PubMed2001

Flow cytometric analysis of lymphocyte subpopulations in bronchoalveolar lavage fluid after repeated ozone exposure.

As known from studies in animal and human subjects, ozone can exert effects on the immune response including allergic sensitisation and allergen responsiveness. The objective of the present study was to assess the changes in lymphocyte subsets in bronchoalveolar lavage fluid (BALF) after single and repeated ozone exposures. Twenty-three healthy subjects underwent single exposures to 200 ppb ozone or filtered air (FA), as well as repeated exposures to 200 ppb ozone on four consecutive days, each during 4 h of intermittent exercise. Bronchoalveolar lavage was performed 20 h after the single exposure or the last of the repeated exposures. Lymphocytes were identified by sideward scatter and CD45 expression, and their subsets by eight different panels of antibodies. Checksums were calculated to assess the validity of the results. The percentage and the absolute number of lymphocytes, mostly comprising T-lymphocytes (CD2+; overall mean 98.8%), increased after single (P < 0.05; each), but not after repeated ozone exposure, compared with FA (7.4 vs 5.8 vs 6.5%; 680 vs 419 vs 301 x 10(3)). In addition, we observed small but statistically significant changes in the proportions of lymphocyte subpopulations. The percentage of CD4+ lymphocytes increased after single (P < 0.05) and repeated ozone exposure (P < 0.01), whereas the percentage of CD8+ cells decreased after repeated exposure (P < 0.05). The proportion of activated lymphocytes (CD25+) was elevated after repeated, compared with single, ozone exposure (P < 0.01), and the percentages of natural killer (NK) cells were decreased after both single (P < 0.05) and repeated (P < 0.01) exposures. Our data suggest that single but not repeated ozone exposures cause a change in absolute numbers of lymphocytes in BALF, whereas the proportions of lymphocyte subsets are affected by single as well as repeated exposures.

Adult↗
PubMed2005

Ozone has dramatic effects on the regulation of the prechorismate pathway in tobacco (Nicotiana tabacum L. cv. Bel W3).

The accumulation of aromatic secondary metabolites is a well-known element of the plant response to ozone. Most of these metabolites are synthesized via the three aromatic amino acids phenylalanine, tyrosine and tryptophan. Before branching, the biosynthetic pathway to the three amino acids shares seven enzymatic steps, called the prechorismate pathway, catalysed by 3-deoxy-D: -arabino-heptulosonate-7-phosphate (DAHP) synthase [EC 2.5.1.54], 3-dehydroquinate synthase [EC 4.2.3.4], 3-dehydroquinate dehydratase [EC 4.2.1.10]-shikimate 5-dehydrogenase [EC 1.1.1.25], shikimate kinase [EC 2.7.1.71], 5-enolpyruvylshikimate 3-phosphate synthase [EC 2.5.1.19] and chorismate synthase [EC 4.2.3.5]). We have studied the transcript level of these enzymes and the aromatic metabolite profile in the ozone sensitive tobacco cultivar BelW3 (Nicotiana tabacum L. cv Bel W3), when exposed to an acute ozone pulse (160 nl l(-1), 5 h). Specific cDNA-fragments of the corresponding six genes were isolated from tobacco Bel W3 and used as probes for determining the expression of the prechorismate pathway genes. The fully expanded leaves of ozone treated plants, which developed symptoms like necrotic leaf spots and accumulation of aromatic metabolites, showed a clear induction of the shikimate pathway genes; indicating, that this induction is linked to the development of the symptoms. Distinct kinetics and magnitudes were observed in tobacco leaves for the ozone dependent enhanced mRNA accumulation of the aforementioned genes in BelW3. The strongest and earliest induction due to ozone treatment could be observed for DAHP synthase. An isoform-specific analysis of the transcripts showed a strong induction on transcript level only for one of three isoforms, which was followed by the induction of the DAHP synthase also on protein level. The different induction kinetics of the prechorismate pathway genes indicate that their regulation in response to ozone might be regulated by different signals, for example, ethylene, reactive oxygen species or salicylic acid, which also occur with different kinetics and thus may play different roles in the plant response to ozone.

3-Deoxy-7-Phosphoheptulonate Synthase↗
PubMed1997

Indoor/outdoor concentrations of ozone and peroxyacetyl nitrate (PAN).

Photochemical pollutants such as ozone and peroxyacetyl nitrate (PAN) could adversely affect human health, especially with relation to effects on lung function. For a realistic assessment of ambient concentrations, both outdoor and indoor measurements of ozone and PAN are required, because people stay indoors for most of the time. Indoor/outdoor concentration ratios, indoor half-life times and indoor chemistry including physicochemical reactions on surfaces are quite well known for ozone, but not for PAN. While ozone is removed very rapidly mainly by heterogeneous reactions on surfaces or by gasphase reactions with e.g. carpet emissions, no such processes are known for PAN at present. The main removal process for PAN is thermal decay. Indoor concentrations of ozone and PAN can be a significant fraction of those outdoors highly depending on the ventilation pattern. Our measurements in various kinds of non-air-conditioned rooms show maximal indoor concentrations between 80 and 100% of those outdoors for ozone and PAN, respectively. Average indoor/outdoor ratios were calculated of 0.5 for ozone and between 0.7 and 0.9 for PAN. The half-life times ranged between only a few minutes for ozone and 0.5 to 1 h for PAN.

Air Pollution, Indoor↗
PubMed1984

Effect of short-term ozone exposure on exogenous thyroxine levels in thyroidectomized and hypophysectomized rats.

Short-term ozone exposure (1 ppm X 24 hr) of male rats results in a significant reduction of circulating thyroid hormones and thyroid stimulating hormone (TSH). The reduction of thyroid hormone levels after ozone exposure has been hypothesized as a possible adaptive mechanism to enhance survival of rats during ozone exposure. In this study, we investigated the effect of ozone on thyroid hormone (T4) levels in thyroidectomized and hypophysectomized rats which received exogenous T4 in the drinking water. Groups of normal, intact rats, thyroidectomized rats maintained on T4 at doses ranging from 75 to 1000 micrograms/liter, and hypophysectomized rats maintained on 300 micrograms T4/liter were exposed to ozone (1 ppm X 24 hr), Plasma T4 concentrations were significantly reduced after ozone exposure, and the results indicated that the higher the circulating T4 levels before exposure the more they were reduced after ozone exposure. This reduction in T4 levels cannot be accounted for in these animals by reduced pituitary TSH levels or the effects of fasting, but is likely to be due to peripheral changes in plasma thyroid binding proteins initiated by ozone exposure.

Animals↗
PubMed1992

Assessment of toxicologic interactions resulting from acute inhalation exposure to sulfuric acid and ozone mixtures.

Studies examining effects of air pollutants often use single compounds, while "real world" exposures are to more than one chemical. Thus, it is necessary to assess responses following inhalation of chemical mixtures. Rabbits were exposed for 3 hr to sulfuric acid aerosol at 0, 50, 75, or 125 micrograms/m3 in conjunction with ozone at 0, 0.1, 0.3, or 0.6 ppm, following which broncho-pulmonary lavage was performed. Various pulmonary response endpoints related to general cytotoxicity and macrophage function were examined. In addition, a goal of the study was to define an improved approach to the analysis of data sets involving binary pollutant mixtures. Results were evaluated using analysis of variance with multiple linear contrasts to determine the significance of any effect in the pollutant-exposed groups compared to sham control animals and to assess the type, and extent, of any toxicological interaction between acid and ozone. Interaction was considered to occur when the effects of combined exposure were either significantly greater or less than additive. Pollutant exposures had no effect on lavage fluid levels of lactate dehydrogenase, prostaglandins E2 and F2 alpha, nor on the numbers, viability, or types of immune cells recovered by lavage. Phagocytic activity of macrophages was depressed at the two highest acid levels and at all levels of ozone. Exposure to all mixtures showed significant antagonism. Superoxide production by stimulated macrophages was depressed by acid exposure at the two highest concentrations, while ozone alone had no effect. Significant antagonistic interaction was observed following exposure to mixtures of 75 or 125 micrograms/m3 acid with 0.1 or 0.3 ppm ozone. The activity of tumor necrosis factor elicited from stimulated macrophages was depressed by acid at 75 and 125 micrograms/m3 while ozone had no effect. Exposure to mixtures of 125 micrograms/m3 acid with 0.3 or 0.6 ppm ozone resulted in synergistic interaction. This study provided additional evidence for antagonism between two common air pollutants and demonstrated that the type of interaction between sulfuric acid and ozone depended upon the endpoint but that the magnitude of any interaction was not always related to the exposure concentrations of the constituent pollutants.

Administration, Inhalation↗
PubMed1987

Ozone inhibits endothelial cell cyclooxygenase activity through formation of hydrogen peroxide.

We have previously demonstrated that a 2H exposure of cultured pulmonary endothelial cells to ozone (0.0-1.0 ppm) in-vitro resulted in a concentration-dependent reduction of endothelial prostacyclin production (90% decrease at the 1.0 ppm level). Ozone-exposed endothelial cells, incubated with 20 uM arachidonate, also demonstrated a significant inhibition of prostacyclin synthesis. To further examine the mechanisms of the inhibition of prostacyclin synthesis, bovine pulmonary endothelial cells were exposed to 1.0 ppm ozone for 2H. A significant decrease in prostacyclin synthesis was found within 5 min of exposure (77 +/- 36% of air-exposed control values, p less than 0.05). Endothelial prostacyclin synthesis returned to baseline levels by 12H after ozone exposure, a time point which was similar to the recovery time of unexposed endothelium treated with 0.5 uM acetylsalicylic acid. Incubation of endothelial cells, previously exposed to 1.0 ppm ozone for 2 hours, with 4 uM PGH2 resulted in restoration of essentially normal prostacyclin synthesis. When endothelial cells were co-incubated with catalase (5 U/ml) during ozone exposure, no inhibition of prostacyclin synthesis was observed. Co-incubation with either heat-inactivated catalase or superoxide dismutase (10 U/ml) did not affect the ozone-induced inhibition of prostacyclin synthesis. These data suggest that H2O2 is a major toxic species produced in endothelial cells during ozone exposure and responsible for the inhibition of endothelial cyclooxygenase activity.

Animals↗
PubMed1988

Synergistic interaction of ozone and respirable aerosols on rat lungs. IV. Protection by quenchers of reactive oxygen species.

In previous studies we have shown interactions between ozone and acidic respirable aerosols as evaluated by sensitive biochemical and quantitative morphological endpoints. In the present paper we have attempted to test the hypothesis that active oxygen species might play a role in lung damage caused by ozone +/- sulfuric acid aerosol. Rats were administered various scavengers of active oxygen species via the intraperitoneal (i.p.) route before and during exposure to 0.12, 0.20, or 0.64 ppm of ozone +/- 0.04, 0.1, 0.2, 0.5, or 1.0 mg/m3 of sulfuric acid aerosol. Vitamin E, a lipid-soluble free radical scavenger, beta-carotene (the precursor of vitamin A), a singlet oxygen scavenger, and dimethylthiourea, a hydrogen peroxide scavenger, were tested. Dimethylthiourea at doses of 50-500 mg/kg per day was able to protect rats from the effects of ozone, suggesting a role for hydrogen peroxide in ozone-induced lung damage in vivo. Neither vitamin E nor beta-carotene at 100 mg/kg doses had any protective activity in our experiments, despite documentation of increased lung content of the scavengers in animals receiving these agents. These results suggest that water solubility may play a role in the efficacy of the scavenging agents under our exposure protocols. We conclude that: (1) hydrogen peroxide may be involved in ozone-induced lung damage; and (2) that lung injury by ozone and by ozone + sulfuric acid aerosol may share common pathways.

Aerosols↗
PubMed1993

Effects of 20 months of ozone exposure on lung collagen in Fischer 344 rats.

Fischer 344 rats were exposed to filtered air (controls) or to 0.12, 0.5, or 1.0 ppm of ozone for 6 h/day, 5 days/week, for 20 months. We examined lung collagen deposition and metabolism in tissue from these animals to determine whether chronic exposure of rats to ozone causes pulmonary fibrosis. We observed excess stainable collagen in the centriacinar region of lungs from the rats exposed to 0.5 or 1.0 ppm of ozone. Biochemical analysis indicated a slight, yet significant, excess collagen deposition in the female rats exposed to 0.5 or 1.0 ppm of ozone. Collagen in the lungs of the females also contained relatively more hydroxylysine-derived crosslinks than did lung collagen from age-matched control animals. No excess of type I procollagen mRNA could be appreciated by in situ hybridization in lungs of the rats exposed to 1.0 ppm of ozone for 20 months, although this mRNA was detected in occasional alveolar interstitial cells at 2 months of exposure to ozone under the same protocol. These findings indicate that chronic exposure of rats to ozone causes mild, persistent fibrosis. The significance of these observations with regard to human health risks of chronically inhaling ozone at ambient levels in polluted air remains to be determined.

Animals↗
PubMed1994

Biochemical and histopathological changes in nasal epithelium of rats after 3-day intermittent exposure to formaldehyde and ozone alone or in combination.

To get a better insight into the pathophysiology of the nasal changes induced by formaldehyde-ozone mixtures, a 3-day inhalation study was carried out in rats, using intermittent exposure to formaldehyde (3.6 ppm) and ozone (0.4 ppm) alone or in combination and focusing on biochemical and histopathological changes in rat nasal respiratory epithelium. Formaldehyde dehydrogenase, glutathione S-transferase, glutathione reductase, and glucose-6-phosphate dehydrogenase activities in this epithelium were not affected by the individual compounds. However, combined exposure to formaldehyde and ozone resulted in slightly decreased activities of these enzymes. Formaldehyde was found to induce rhinitis, degeneration, frank necrosis, hyperplasia and squamous metaplasia of the ciliated and non-ciliated nasal respiratory epithelium, while ozone induced disarrangement, flattening and slight basal cell hyperplasia of the non-ciliated cuboidal epithelium accompanied by influx of neutrophils. Proliferating cell nuclear antigen (PCNA) expression was elevated not only in nasal areas showing ozone-induced histopathological changes but also in the otherwise normal-appearing epithelium of the nasal septum. No interactive effects were found with respect to proliferative response of the nasal respiratory epithelium after exposure to the formaldehyde-ozone mixture. The present study did not provide evidence of a major role of glutathione and glutathione-dependent enzymes in the pathogenesis of nasal lesions induced by formaldehyde and/or ozone, demonstrated the potential of ozone to affect the mucociliary epithelium lining the nasal septum, and suggested that PCNA expression is a sensitive tool for detection of early effects of respiratory irritants.

Administration, Inhalation↗
PubMed1995

Long-term toxicity studies of ozone in F344/N rats and B6C3F1 mice.

The toxicity and carcinogenicity of ozone was evaluated in Fischer 344/N rats and B6C3F1 mice exposed to 0, 0.12 (2 years only), 0.5 or 1.0 ppm ozone by inhalation for 2-year and lifetime exposures. A 2-year cocarcinogenicity study (male rats only) included the subcutaneous administration of 0, 0.1 or 1.0 mg/kg/body wt. of 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) for the first 20 weeks along with inhalation exposure to 0 or 0.5 ppm ozone followed by additional 84 weeks of ozone exposure alone. Ozone exposure in rats did not cause an increased incidence of lung neoplasms. In the cocarcinogenicity study, ozone exposure did not have an additive carcinogenic effect. Lifetime and 2-year ozone exposure was associated with a marginal increase in lung tumors in male B6C3F1 mice and a more pronounced increase in females. Unique mutations in the K-ras gene were found in the mouse lung neoplasms from the ozone-exposed mice.

Animals↗
PubMed1995

A new mechanism for the toxicity of ozone.

Ozone, with its high reactivity, is entirely consumed as it passes through the first layer of tissue it contacts at the lung/air interface. This layer includes the epithelial cell lining fluid (ELF) and, where the ELF is thin or absent, the membranes of the epithelial cells that line the airways. Thus the biochemical changes that follow the inhalation of ozone must be relayed into deeper tissue strata by a cascade of ozonation products. Lipid ozonation products (LOP) are suggested to be the most likely relay molecules of ozone's signal. This is because unsaturated fatty acids are present in relatively high concentrations in both the ELF and in pulmonary cell bilayers, and ozone reacts with unsaturated fatty acids to produce ozone-specific products. Further, LOP are finite in number, have structures that are predictable from the Criegee ozonation mechanism, and are small, diffusible, stable (or meta-stable) molecules, similar to other lipid-derived signal transduction species. Preliminary data show that individual LOP cause the activation of specific lipases, which trigger the release of endogenous mediators of inflammation.

Animals↗
PubMed1995

Depletion of urate in human nasal lavage following in vitro ozone exposure.

Ozone, a strong oxidant present in summer smog, is thought to primarily react with antioxidant molecules found in the epithelial lining fluid of the respiratory tract. In humans, as much as 40% of inhaled ozone can be removed in the nasal cavity where the major extracellular antioxidant has been identified as uric acid. The present study was undertaken to examine urate/oxidant interactions in human nasal lavage fluid following in vitro exposure to ozone at concentrations relevant to the U.K. Lavage fluid was collected from 8 volunteers using a modified Foley catheter which permits prolonged contact of isotonic saline with the anterior nasal cavity. Nasal lavage samples in multiwell plates were exposed to ozone at concentrations of 50, 100 and 250 ppb. Samples were removed at intervals from 15 to 240 min following exposure and assayed for uric acid depletion. Uric acid concentrations in the nasal lavage were found to fall from 8.52 (time zero) to 3.99 microM, 0.05 and 0.07 microM after 240 min at 50, 100 and 250 ppb ozone respectively. At a non-environmentally relevant ozone concentration of 1000 ppb, uric acid was completely depleted after 60 min. Regression analysis showed a linear correlation between rate of loss of urate and ozone concentration (R2 = 0.97). A novel, non-invasive technique is described to investigate antioxidant compromise and its importance in individual subjects. We conclude that uric acid in nasal lavage samples is scavenged by ozone in a dose and time dependent manner.

Ascorbic Acid↗
PubMed2006

Effects of ozone exposure on inactivation of intra- and extracellular enterovirus 71.

In this study, the potential of ozone in inactivating enterovirus 71 (EV71) free particles was investigated using either various ozone flow rates of 100, 80 or 60 mg/h or a constant flow rate of 80 mg/h, given to culture medium or various pH culture media containing EV71, respectively. Results demonstrated that EV71 inactivation by ozone was related to the kinetics of ozone solubility, approximately 99% inactivation being obtained in the exponential phase of ozone solubility. However, the inactivation rate was dependent on the ozone input flow rate and positively enhanced at acidic pH. Inactivation of intracellular EV71 was also studied. At a constant ozone supply of 60 mg/h, a significant reduction of intracellular virus titer (> or =99%, p < 0.01) was obtained after 45 or 60 min exposure but with low cell viability. Upon 30 min exposure, however, 45% cell viability was retained. The results indicate that the inactivating effect of ozone on intracellular EV71 virus is dependent on exposure duration.

Animals↗
PubMed2005

Effects of in-situ ozonation on indigenous microorganisms in diesel contaminated soil: survival and regrowth.

Soil column experiments were conducted to investigate the effects of chemical oxidation on the survival of indigenous microbes (i.e., heterotrophic microbes, phenanthrene-degrading microbes, and alkane-degrading microbes) for field soil contaminated with diesel fuel. Rapid decreases of total petroleum hydrocarbons (TPH) and aromatics of diesel fuel were observed within the first 60 min of ozone injection; after 60 min, TPH and aromatics decreased asymptotically with ozonation time. The three types of indigenous microbes treated were very sensitive to ozone in the soil column experiment, hence the microbial population decreased exponentially with ozonation time. The numbers of heterotrophic, alkane-degrading, and phenanthrene-degrading bacteria were reduced from 10(8) to 10(4), 10(7) to 10(3), and 10(6) CFU g soil(-1) to below detection limit after 900 min of ozonation, respectively. Except for the soil sample ozonated for 900 min, incubation of ozone-treated soil samples that were not limited by oxygen diffusion showed further removal of TPH. The soil samples that were ozonated for 180 min exhibited the lowest concentration of TPH and the highest regrowth rate of the heterotrophic and alkane-degrading populations after the 9 weeks of incubation.

Bacteria↗
PubMed2006

Enhancement of ozone oxidation and its associated processes in the presence of surfactant: degradation of atrazine.

In this study, the degradation of atrazine (ATZ) by ozone (O3) oxidation and its associated processes (i.e. UV, UV/O3) in the presence and absence of surfactant was investigated and compared. A non-ionic surfactant, Brij 35, was selected. It was found that the presence of a low concentration of surfactant could improve the removal of ATZ by increasing the dissolution of ozone and the indirect generation of hydroxyl radicals. The saturated ozone level and the reaction rate constants were increased with increasing the concentration of surfactant and then decreased at higher surfactant doses at pH level of 2.5. A similar trend was observed at pH level of 7.0 in the presence of bicarbonate ion, because it is capable of deactivating the hydroxyl radicals generating at higher pH level. However, when the radical reactions become dominant in the ozonation (at pH 7.0 without bicarbonate), the saturated ozone level was higher than that with bicarbonate and the kinetic rate constants were increased first and levelled off with increasing of the dose of surfactant. Through the examining of a proposed unit performance index, the low concentration of surfactant is surely beneficial to the ozonation process. Besides, the direct photolysis and photo-assisted ozonation were compared to the ozonation. A significant enhancement on the decay rate of ATZ was resulted exclusively by adding the surfactant. An enhancement index for quantifying the improvement of the various processes was developed.

Atrazine↗
PubMed2006

Heterogeneous and homogeneous catalytic ozonation of benzothiazole promoted by activated carbon: kinetic approach.

Ozone oxidation combined with activated carbon adsorption (O(3)/AC) has recently started to be developed as a single process for water and wastewater treatment. While a number of aspects of aqueous ozone decomposition are well understood, the importance and relationship between aqueous ozone decomposition and organic contaminant degradation in the presence of activated carbon is still not clear. This study focuses on determining the contribution of homogeneous and heterogeneous reactions to organic contaminants removal in O(3)/AC system. Benzothiazole (BT) was selected as a target organic pollutant due to its environmental concern. A reactor system based on a differential circular flow reactor composed by a 19 cm(3) activated carbon fixed bed column and 1 dm(3) storage tank was used. Ozone was produced from pure and dry oxygen using an Ozocav ozone generator rated at 5 g O(3)h(-1). Experimental results show that BT removal rate was proportional to activated carbon dosage. Activated carbon surface contribution to BT oxidation reactions with ozone, increased with pH in absence of radical scavengers. The radical reaction contribution within the pH range 2-11 accounted for 67-83% for BT removal in O(3)/AC simultaneous treatment. Results suggest that at pH higher than the pH of the point of zero charge of the activated carbon dissociated acid groups such as carboxylic acid anhydrides and carboxylic acids present on activated carbon surface could be responsible for the observed increase in the ozone decomposition reaction rate. A simplified mechanism and a kinetic scheme representing the contribution of homogeneous and heterogeneous reactions on BT ozonation in the presence of activated carbon is proposed.

Benzothiazoles↗
PubMed2006

Ozonation of aniline promoted by activated carbon.

The removal of aniline from aqueous solutions by simultaneous use of ozone and activated carbon was investigated at different solution pH. For comparative purposes, single ozonation and adsorption on activated carbon were carried out in the same experimental set-up. In order to evaluate the role of the activated carbon surface chemistry during ozonation, a commercial activated carbon, Norit GAC 1240 PLUS, was submitted to oxidation in the liquid phase with HNO(3). The texture and surface chemistry of the activated carbon samples were characterized. During ozonation, complete conversion of aniline was achieved after approximately 20 min, regardless of the presence of activated carbon. In all cases, several by-products were formed during ozonation. Nitrobenzene, o- and p-aminophenol were the primary aromatic oxidation by-products identified. In terms of TOC removal, best results were achieved by the simultaneous use of ozone and activated carbon. Though there is a strong contribution of adsorption, a considerable synergetic effect between ozone and activated carbon is observed. In general, activated carbon promotes the reaction of ozonation enhancing the efficiency of this treatment process. The basic activated carbon presented greater activity in this process leading to higher mineralization rates.

Aminophenols↗