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PubMed1985

Toxicity of polycyclic aromatic hydrocarbons. I. Effect of phenanthrene, pyrene, and their ozonized products on blood chemistry in rats.

Male Sprague-Dawley rats were treated with a single ip injection of physiological saline (3.0 ml/kg), dimethyl sulfoxide (DMSO, 3.0 ml/kg), phenanthrene (150 mg/kg), ozonized products of phenanthrene (150 mg/kg), pyrene (150 mg/kg), or ozonized products of pyrene (150 mg/kg). Phenanthrene, pyrene, and their ozonized products were dissolved in DMSO (50 mg/ml). Serum aspartate aminotransferase (AST) activity was increased significantly 24 hr after ip administration of DMSO when compared with physiological saline. Phenanthrene produced a significant elevation of serum AST and gamma-glutamyl transpeptidase (GGTP) levels related to physiological saline and DMSO-injected rats 24 hr after injection. However, GGTP levels for groups treated with DMSO or phenanthrene were not significantly increased when compared with saline groups 72 hr after injection. Ozonized products of phenanthrene produced a significant elevation of serum AST, alanine aminotransferase (ALT), GGTP, and bilirubin levels when compared with groups treated with physiological saline, DMSO, and phenanthrene 24 or 72 hr after injections. The ozonized products of phenanthrene also produced significant elevation of serum creatinine levels compared with physiological saline, DMSO, and phenanthrene groups at 24 hr after treatment and of blood urea nitrogen (BUN) levels at 24 and 72 hr. Although pyrene caused a small but significant increase in the serum AST and bilirubin levels 24 hr after treatment, no significant change in the serum AST, ALT, GGTP, BUN, and creatine levels were observed with the ozonized products of pyrene at 24 or 72 hr. This study demonstrates significant alterations in serum chemistry induced by reaction products of ozone with phenanthrene. No such effect was observed when the products of pyrene ozonation were administered. Although the ozonation products of pyrene were not toxic under the conditions of this study, phenanthrene products were more hepatotoxic than was phenanthrene itself. Nephrotoxicity was also an apparent effect of ozonized phenanthrene. Since ozone-polycyclic aromatic hydrocarbon (PAH) reactions may occur in the atmosphere, these reactions might produce compounds that are more toxic than either ozone or the PAH alone.

Alanine Transaminase↗
PubMed1990

An immunofluorescence study of T and B lymphocytes in ozone-induced pulmonary lesions in the mouse.

Ozone is a photochemical oxidant which reacts with a variety of biological molecules. In experimental animals the toxicity of ozone results from damage to cells in the lung and is associated with the process of reactive repair and an influx of inflammatory cells. In this work we used an indirect immunofluorescence technique to study the effect of ozone on T and B lymphocytes with special reference to their presence in ozone-induced pulmonary lesions. BALB/c mice were exposed to ozone at a concentration of 0.7 ppm for 20 hr per day, 7 days per week, for 4 or 14 days. Control mice were housed in comparable chambers lacking ozone. Frozen sections of lung were prepared and stained for the surface markers Thy-1.2 (T lymphocyte) and sIgM (B lymphocyte). These experiments showed that T lymphocytes infiltrate the lung lesions during ozone inhalation, and increase their presence as ozone exposure continues. They were present in the centroacinar region and tended to occur in clusters within the ozone-induced lesions. In contrast, the infiltration of B lymphocytes was virtually nonexistent with few or no sIgM positive cells present in the lesions after either 4 or 14 days of exposure to ozone. These results show that T lymphocytes occur within the sites of ozone-induced damage and support that this cell type plays a role in the reactive host response to ozone inhalation.

Animals↗
PubMed1990

Response of rat tracheal epithelium to ozone and oxygen exposure in vitro.

Although ozone-induced epithelial injury in vivo has been morphologically characterized, effects of gaseous oxidants on respiratory epithelium in organ culture, where tissue organization is maintained but systemic influences are eliminated, have not been thoroughly investigated. In this study, we exposed tracheal organ cultures from rats to 95% oxygen and 1 ppm ozone, alone and in combination, to determine (1) whether epithelial responses to ozone similar to those observed in vivo occur in airways separated from systemic physiologic, secretory, and inflammatory reactions; (2) whether concentrations of oxygen sufficient to potentially cause oxidant injury result in morphologic epithelial alterations similar to those that occur in ozone toxicity; and (3) if the combined oxidant insult of oxygen and ozone results in more severe damage to the tracheal epithelium than occurs with ozone in air. Tracheal organ cultures were exposed to filtered air and 5% carbon dioxide; filtered air, 5% carbon dioxide, and 1 ppm ozone; 95% oxygen and 5% carbon dioxide; or 95% oxygen, 5% carbon dioxide, and 1 ppm ozone for 96 hr. Light- and quantitative electron-microscopic evaluation showed that epithelia exposed to 1 ppm ozone in air exhibited loss of ciliated cells and ciliated cell damage. The epithelia exposed to 95% oxygen and 5% carbon dioxide were pseudostratified, columnar, ciliated, and hyperplastic. Epithelia exposed to 95% oxygen plus 1 ppm ozone were stratified and nonciliated or very sparsely ciliated. The predominant cell types in epithelia exposed to oxygen plus ozone were serous cells and metaplastic cells, and focal aggregates of adherent necrotic cells were present. We conclude that there was a synergism between oxygen and ozone exposure leading to enhanced epithelial injury and metaplasia.

Animals↗
PubMed2003

Ozone-induced inactivation of antioxidant enzymes.

Ozone is an air pollutant that damages a variety of biomolecules. We investigated ozone-induced inactivation of three major antioxidant enzymes. Cu/Zn superoxide dismutase was inactivated by ozone in a concentration-dependent manner. The concentration of ozone for 50% inactivation was approximately 45 microM when 10 microM Cu/Zn superoxide dismutase was incubated for 30 min in the presence of ozone. SDS-polyacrylamide gel electrophoresis (PAGE) showed that the enzyme was randomly fragmented. Both ascorbate and glutathione were very effective in protecting Cu/Zn superoxide dismutase from ozone-induced inactivation. The other two enzymes, catalase and glutathione peroxidase, were much more resistant to ozone than Cu/Zn superoxide dismutase. The ozone concentrations for 50% inactivation of 10 microM catalase and glutathione peroxidase were 500 and 240 microM, respectively. SDS-PAGE demonstrated that ozone caused formation of high molecular weight aggregates in catalase and dimerization in glutathione peroxidase. Glutathione protected catalase and glutathione peroxidase from ozone but the effective concentrations were much higher than that for Cu/Zn superoxide dismutase. Ascorbate was almost ineffective. The result suggests that, among the three antioxidant enzymes, Cu/Zn superoxide dismutase is a major target for ozone-induced inactivation and both glutathione and ascorbate are very effective in protecting the enzyme from ozone.

Animals↗
PubMed2006

Assessment of the safety of two ozone delivery devices.

OBJECTIVES: To evaluate the safety of an ozone gas device designed for use in dentistry. METHODS: Two commercially available ozone applicators, Ozi-cure and HealOzone were used in a clinical simulation using a phantom head while recordings of ozone levels were made in pharyngeal and nasal regions of the patient and near the mouth of the operator. Clinical simulations included ozone application for caries management and endodontic treatment. Recordings were made five times with different levels of suction to assess the effect on ozone levels. RESULTS: The results with Ozi-cure on caries mode resulted in a peak ozone level in the pharynx of 1.33+/-0.52 ppm when no suction was used. The use of suction nearby reduced the ozone level to zero while suction on the opposite side of the mouth reduced the level to 0.22+/-0.04 ppm. Used on endodontic mode the peak ozone level in the pharynx was 5.51+/-1.63 ppm when no suction was used. The use of suction nearby reduced the ozone level to zero while suction on the opposite side of the mouth reduced the level to 0.84+/-0.54 ppm. Recordings in the patient's nasal region gave a peak of 0.22 ppm when using the Ozi-cure on endodontic mode with no suction. At the operator's mouth the ozone level did not exceed 0.01 ppm although the characteristic smell of ozone was detectable. All recordings with HealOzone were zero. Concentrations of 15 ppm were recorded in a simulated tooth cavity with Ozi-cure and >20 ppm with HealOzone. CONCLUSIONS: The Ozi-cure device when used without adequate suction allows ozone to be reach a concentration above permitted levels and therefore should not be used. The HealOzone was safe to use.

Air Pollutants↗
PubMed2003

Clover as a tool for bioindication of phytotoxic ozone--5 years of experience from southern Sweden--consequences for the short-term critical levels.

Critical levels (CLs) for ozone effects on plants in Europe have been defined within the UN-ECE Convention on Long-Range Transboundary Air Pollution, CLRTAP. The purpose of the short-term CLs is to ensure protection of all crops to acute ozone injury. The currently used CLs are based on the ozone exposure of the plants during daylight hours expressed as AOT40 (Accumulated exposure Over the Threshold 40 nmol mol(-1) ozone). The aims of this study were: to test the performance of the current short-term CLs, to test alternative ozone exposure indices and to test if changes in the ozone cut-off concentration, the inclusion of a lag-period (LP) between exposure and identification of visible ozone injury or the duration of the ozone integration period improved the performance of the exposure index. The analysis was based on 38 different datasets from experiments with subterranean clover, Trifolium subterraneum in southern Sweden. AOT indices generally performed better than averaged ozone concentrations or SUM (Sum of ozone concentrations when a threshold is exceeded) indices. Regression analysis showed that the current short-term CL, AOT40 with a VPD (water vapour pressure deficit) threshold of 1.5 kPa, explained 56% of the variation in visible injury. A longer exposure period and the introduction of a LP, admitting visible ozone injury time to develop after exposure, improved the performance of the exposure index. AOT30 accumulated over 10 days before harvest, excluding a LP of 3 days before injury observation, performed best and explained 88% of the variation in visible injury. AOT40 indices left a rather large amount of visible injury unexplained indicating that a lower cut-off concentration for ozone is preferable. The results of the investigation indicated that a visible injury threshold of 10% improved the distinction between harmful and less harmful exposure.

Environmental Exposure↗
PubMed2003

High-resolution spatial analysis of stomatal ozone uptake in arable crops and pastures.

Ozone effects on plants depend on atmospheric transport and stomatal uptake. Thus, ozone-risk assessments should use measured ozone concentrations and account for the influence of atmospheric conditions and soil moisture on stomatal and nonstomatal ozone deposition. This requires disaggregated data for the physical input parameters and species-specific data for specific stomatal conductance (g(s)). In this study, an approach was developed based on a resistance analogue transport model. This model requires interpolated routine-measuring data for ozone concentration at 3-5 m height, wind speed, precipitation, and soil moisture content as inputs to estimate the amount of ozone taken up by wheat (Triticum aestivum) and grass/clover pastures with a 1x1-km resolution. The model was applied to the area under agricultural production in Switzerland. Using data for June 1994, the calculations revealed that the median of the distribution of stomatal ozone uptake was 88% higher in wheat compared to grassland. This was mainly due to the higher maximum stomatal conductance in wheat. Because ozone flux to soil and to external plant surfaces was comparable in both vegetation types, the difference in the stomatal fluxes was mainly responsible for distinct differences in flux partitioning. In both cases, only about 11% of the total cumulative flux was absorbed by external plant surfaces, whereas the soil was a strong sink responsible for as much as 50% of the total flux into grasslands. The higher-ozone flux to wheat resulted in clearly lower-ozone concentrations at canopy height, but no significant correlation between cumulative canopy-level ozone exposure, expressed as accumulated exposure above 40 ppb (AOT40), and stomatal uptake was found. Thus, to estimate the ozone risk for crops using a flux-based approach may lead to results that differ substantially from those obtained with a concentration-based approach.

Ecosystem↗
PubMed2002

Modeling in situ ozonation for the remediation of nonvolatile PAH-contaminated unsaturated soils.

Mathematical models were developed to investigate the characteristics of gaseous ozone transport under various soil conditions and the feasibility of in situ ozone venting for the remediation of unsaturated soils contaminated with phenanthrene. On the basis of assumptions for the mass transfer and reactions of ozone, three approaches were considered: equilibrium, kinetic, and lump models. Water-saturation-dependent reactions of gaseous ozone with soil organic matter (SOM) and phenanthrene were employed. The models were solved numerically by using the finite-difference method, and the model parameters were determined by using the experimental data of Hsu [The use of gaseous ozone to remediate the organic contaminants in the unsaturated soils, PhD Thesis, Michigan State Univ., East Lansing, MI, 1995]. The transport of gas-phase ozone is significantly retarded by ozone consumption due to reactions with SOM and phenanthrene, in addition to dissolution. An operation time of 156 h was required to completely remove phenanthrene in a 5-m natural soil column. In actual situations, however, the operation time is likely to be longer than the ideal time because of unknown factors including heterogeneity of the porous medium and the distribution of SOM and contaminant. The ozone transport front length was found to be very limited (< 1 m). The sensitivity analysis indicated that SOM is the single most important factor affecting in situ ozonation for the remediation of unsaturated soil contaminated with phenanthrene. Models were found to be insensitive to the reaction mechanisms of phenathrene with either gas-phase ozone or dissolved ozone. More study is required to quantify the effect of OH* formation on the removal of contaminant and on ozone transport in the subsurface.

Gases↗
PubMed2005

Ozonation of carbamazepine in drinking water: identification and kinetic study of major oxidation products.

Kinetics and product formation of the anti-epileptic drug carbamazepine (CBZ) were investigated in lab-scale experiments during reactions with ozone and OH radicals. Ozone reacts rapidly with the double bond in CBZ, yielding several ozonation products containing quinazoline-based functional groups. The structures for three new oxidation products were elucidated using a combination of mass spectrometric and NMR techniques. The three products were determined to be 1-(2-benzaldehyde)-4-hydro-(1H,3H)-quinazoline-2-one (BQM), 1-(2-benzaldehyde)-(1H,3H)-quinazoline-2,4-dione (BQD), and 1-(2-benzoic acid)-(1H,3H)-quinazoline-2,4-dione (BaQD). Additional kinetic studies of the ozonation products showed very slow subsequent oxidation kinetics with ozone (second-order rate constants, kO3 = approximately 7 M(-1)s(-1) and approximately 1 M(-1)s(-1) at pH = 6 for BQM and BQD, respectively). Rate constants for reactions with OH radicals, kOH, were determined as approximately 7 x 10(9) M(-1)s(-1) for BQM and approximately 5 x 10(9)M(-1)s(-1) for BQD. Thus, mainly reactions with OH radicals lead to their further oxidation. A kinetic model including ozone and OH radical reactions allows a prediction of the time-dependent product distribution during ozonation of natural waters. In Rhine River water, CBZ spiked at 500 ng/L was completely oxidized by ozone with applied doses > or =0.3 mg/L. To confirm that the two major ozonation products BQM and BQD are produced as a result of the ozonation of a CBZ-containing natural water, Lake Zurich water samples were spiked with CBZ (1 microM, 236 microg/L). The oxidation products were identified via LC-UV. Concentrations of 0.48 and 0.15 microM for BQM and BQD, respectively, were measured for an ozone dose of 1.9 mg/L. BQM and BQD were also identified in ozonated water from a German waterworks containing CBZ in its raw water with 0.07-0.20 microg/L. Currently, there are no data available on the biological effects of the formed oxidation products.

Carbamazepine↗
PubMed2001

Ozone enema: a model of microscopic colitis in rats.

Ozone is one of the most powerful oxidants available, with many applications in industry and medicine. Medically relevant features of ozone include bacterial and virucidal properties, disinfection, sterilization, circulatory stimulation, and disruption of malignant cells. Ozone therapy is administered in various ways, including intravenously, intramuscularly, and intrarectally. The latter modality is used for the treatment of colitis and hepatitis. Our aim was to examine the effect of ozone water enema on normal and inflamed rat colonic mucosa. Ozone water (20 microg/ml) was prepared via ozone generator and administered intrarectally (0.5 ml) daily. Rats were killed one, three, and seven days after rectal ozone water administration, and their colons resected, rinsed, and weighed (grams per 10 cm). Damage was assessed macro- and microscopically and tissue processed for myeloperoxidase and nitric oxide synthase activity. Rats receiving saline served as controls. In an additional experiment colitis was induced by intrarectal iodoacetamide. Ozone therapy caused no macroscopic damage. Ozone therapy induced microscopic colitis, which lasted for at least a week and was accompanied by increase in segmental weight, myeloperoxidase and nitric oxide activity, and prostaglandin E2 generation. Ozone therapy had no protective effect on inflamed mucosa. In conclusion, ozone water therapy had a deleterious effect on normal colonic mucosa, suggesting intrarectal administration be reevaluated. Ozone water enema may serve as a model of microscopic colitis.

Administration, Rectal↗
PubMed1996

Decadal evolution of the Antarctic ozone hole.

Ozone column amounts obtained by the total ozone mapping spectrometer (TOMS) in the southern polar region are analyzed during late austral winter and spring (days 240-300) for 1980-1991 using area-mapping techniques and area-weighted vortex averages. The vortex here is defined using the -50 PVU (1 PVU = 1.0 x 10(-6) K kg-1 m2 s-1) contour on the 500 K isentropic surface. The principal results are: (1) there is a distinct change after 1985 in the vortex-averaged column ozone depletion rate during September and October, the period of maximum ozone loss, and (2) the vortex-averaged column ozone in late August (day 240) has dropped by 70 Dobson units (DU) in a decade due to the loss in the dark and the dilution effect. The mean ozone depletion rate in the vortex between day 240 and the day of minimum vortex-averaged ozone is about 1 DU d-1 at the beginning of the decade, increasing to about 1.8 DU d-1 by 1985, and then apparently saturating thereafter. The vortex-average column ozone during September and October has declined at the rate of 11.3 DU yr-1 (3.8%) from 1980 to 1987 (90 DU over 8 years) and at a smaller rate of 2 DU yr-1 (0.9%) from 1987 to 1991 (10 DU over 5 years, excluding the anomalous year 1988). We interpret the year-to-year trend in the ozone depletion rate during the earlier part of the decade as due to the rise of anthropogenic chlorine in the atmosphere. The slower trend at the end of the decade indicates saturation of ozone depletion in the vortex interior, in that chlorine amounts in the mid-1980s were already sufficiently high to deplete most of the ozone in air within the isolated regions of the lower-stratospheric polar vortex. In subsequent years, increases in stratospheric chlorine may have enhanced wintertime chemical loss of ozone in the south polar vortex even before major losses during the Antarctic spring.

Antarctic Regions↗
PubMed2003

Ozonation characteristics of bisphenol A in water.

Ozonation characteristics of bisphenol A were investigated as a function of gaseous ozone dose, initial concentration of bisphenol A, pH, radical scavenger (tert-butanol), and radical initiator (hydrogen peroxide). The ozonation led to a complete removal of bisphenol A in water within a certain period of time. The overall rate of the ozonation linearly increased with the ozone dose. The stoichiometry in the ozonation of bisphenol A was found to be 1.5 - 1.8 mole of ozone per mole of bisphenol A. The direct reaction rate constants were 1.3 x 10(4) M(-1)s(-1) for bisphenol A (at pH = 2) and 1.6 x 10(9) M(-1)s(-1) for dissociated bisphenol A (at pH = 12). Bisphenol A degraded via the direct reaction with molecular ozone in the pH range from 2 to 12. Degradation by OH radical was minor even at pH = 12. The overall degradation rate in heterogeneous conditions was independent of pH as it was limited by ozone mass transfer rate. Use of hydrogen peroxide did not alter the main degradation route and the molecular ozone remained a principal oxidant as a substantial portion of the OH radical is scavenged by hydrogen peroxide. Effective ozone mass transfer may appear essential to enhance the ozonation kinetics of bisphenol A.

Benzhydryl Compounds↗
PubMed2000

Associations between ambient ozone, hydrocarbons, and childhood wheezy episodes: a prospective observational study in south east London.

OBJECTIVES: To explore the hypothesis that hydrocarbon species and other air pollutants which accumulate at low and high concentrations of ozone are more directly associated with childhood wheezy episodes than ozone. METHODS: Prospective observational study over 1 year set in the Lewisham district of south east London. The daily attendance rate of children with acute wheeze at the accident and emergency department of Lewisham Hospital was related to local measurements of ozone, hydrocarbon species, nitrogen dioxide (NO2), sulphur dioxide (SO2) and small particulate matter with diameter < 10 microns (PM10). RESULTS: An inverse relation was found between the air pollutants and ozone. After seasonal and meteorological adjustment a non-linear U shaped trend was found between incidence of wheeze and ozone. The trend was significant in children < 2 years of age but not in older children. In the younger age group, after adjustment for season, temperature, wind speed, and respiratory infection, the incidence relative to that at the mean daily ozone concentration of 32.7 micrograms/m3, was estimated to increase by 65% (95% confidence interval (95% CI) 22% to 122%) at an ozone concentration of 5 micrograms/m3 (1.5 SDs below the mean) and by 63% (95% CI -6% to 184%) at 80 micrograms/m3 (2.5 SDs above the mean). For several hydrocarbons there were significant positive linear relations found, again in children < 2 years of age but not older children. For benzene, the incidence increased by 8% (95% CI 2 to 13%) per SD (SD 2.8 micrograms/m3) increase in benzene concentration. A same day association between incidence and ozone was found to be the most significant but for other pollutants a lag of 2 days gave the most significant associations. No significant association was found for the non-hydrocarbon pollutants including SO2, NO2, and PM10. CONCLUSIONS: A U shaped relation was found between ozone and the incidence of wheezy episodes in young children. Certain hydrocarbon pollutants accumulate in the atmosphere when ozone concentrations are low, and are associated with childhood wheezy episodes. However, the U shaped association of ozone on incidence cannot be explained by these other pollutants. The finding supports an earlier finding that incidences of wheeze are at a minimum when ozone concentrations are 30-40 micrograms/m3.

Adolescent↗
PubMed1995

Modulation of mast cell functions by in vitro ozone exposure.

Exposure to ozone has been reported to cause increased immediate bronchial reactivity to inhaled allergen in asthmatics. The purpose of these studies was to determine whether ozone induces either spontaneous physiological degranulation or enhanced immunoglobulin E (IgE)-mediated degranulation of mast cells, thus accounting for the in vivo effects noted in asthmatics. A rat mast cell line (RBL-2H3) was exposed to different levels of ozone (0.1, 0.3, 0.5, and 1.0 ppm), covered by different amounts of buffer, and both cytotoxic and nontoxic exposure conditions were determined. In addition to cytotoxicity, spontaneous release of granule products and prostaglandin D2 (PGD2) associated with ozone exposure were assessed. RBL-2H3 cells were also exposed to ozone under noncytotoxic conditions followed by stimulation with alpha-IgE to cross-link membrane-bound IgE and A23187 so that the effect of ozone on stimulated degranulation could be examined. Only exposure conditions associated with cytotoxicity were associated with spontaneous release of mast cell serotonin, indicating no physiologic degranulation due to ozone exposure. Data presented herein also demonstrate that ozone substantially inhibited both IgE- and A23187-induced degranulation. Neither catalase nor superoxide dismutase protected cells from the inhibitory effect of ozone, indicating that ozone does not act through generation of H2O2 or superoxide. Additionally, ozone caused a modest increase in spontaneous PGD2 generation only under cytotoxic conditions. Thus ozone appears to inhibit mast cell degranulation after IgE- or A23187-mediated stimulation and causes direct release of mast cell granule products and PGD2 only under conditions associated with membrane cytotoxicity.

Animals↗
PubMed1995

Neutrophils enhance removal of ozone-injured alveolar epithelial cells in vitro.

After acute exposure to oxidant gases in vivo, migration and accumulation of inflammatory cells in pulmonary epithelium coincides with epithelial cell necrosis. The present study was designed to test quantitatively the hypothesis that quiescent neutrophils enhance the removal of oxidant-injured pulmonary epithelial cells after exposure to ozone in vitro. Primary isolated rat alveolar type II cells were cultured as monolayers, using serum-free medium. After exposure to 0.1-0.5 ppm ozone for 0.5 h, apical sides of monolayers were administered either fresh nutrient medium only or medium containing quiescent human neutrophils. Monolayer bioelectric properties and cellular uptake of vital dye were recorded from 5 to 48 h after ozone exposure. Ozone dose-dependent increases in monolayer permeability were associated with proportionally higher numbers of injured epithelial cells. However, the direction and magnitude of neutrophil effects on monolayer permeability after ozone exposure were dependent on ozone concentration. Furthermore, neutrophil-treated monolayers exposed to 0.1 ppm ozone had significantly fewer attached cells positive for uptake of vital dye relative to monolayers exposed to the low level of ozone only; this effect was ablated with increasing ozone concentration. These data suggest that at high levels of ozone neutrophils may exacerbate injury to oxidant-impaired epithelial cells, whereas the presence of neutrophils after exposure to ambient concentrations of ozone may expedite the restoration of epithelial barrier function. We conclude that, by enhancing the removal of injured cells, neutrophils may facilitate the repair of centriacinar epithelium after ozone exposure in vivo.

Animals↗
PubMed1997

In vivo salicylate hydroxylation: a potential biomarker for assessing acute ozone exposure and effects in humans.

Ozone is known to yield hydroxyl radical, which may contribute to ozone-mediated lung injury. In the presence of hydroxyl radical, salicylate is hydroxylated to form 2,3-dihydroxybenzoic acid (2,3-DHBA). There is no evidence of enzymatic formation of 2,3-DHBA. We hypothesized that salicylate hydroxylation might be used as a biomarker indicating human exposure to ozone. Healthy, nonsmoking volunteers, 18 to 34 yr of age, were given acetylsalicylic acid (975 mg) or placebo orally 0.5 h before an exposure. Subjects were exposed to ozone (0.12 or 0.4 ppm) or filtered air in an environmental chamber for 2 h, while performing intermittent exercise. Results indicate significant decrements in FVC, FEV1.0, forced expiratory flows at 50% and 75% of FVC, and peak expiratory flow rate, and an increase in airway resistance, after exposure to 0.4 ppm ozone in comparison with air control (p < 0.05). Exposure to 0.4 ppm ozone also resulted in increased symptom numbers and severity (p < 0.05). When subjects were exposed to 0.12 ppm ozone, changes of pulmonary function and symptoms reported were minimal. Plasma concentration of 2,3-DHBA was significantly increased after exposure to 0.12 and 0.4 ppm ozone in comparison with air control (p < 0.05). There was a significant correlation between ozone-induced changes of pulmonary function and normalized salicylate hydroxylation (p < 0.05). The results indicate that exposure to ozone can initiate in vivo production of hydroxyl radical, a potent reactive agent. Salicylate hydroxylation may then serve as a sensitive dosimetric biomarker for ozone exposure, even at subclinical ozone exposure levels.

Adolescent↗
PubMed1993

Ambient ozone causes upper airways inflammation in children.

Ozone constitutes a major air pollutant in Western Europe. During the summer national air quality standards are frequently exceeded, which justifies concern about the health effects of ozone at ambient concentrations. We studied upper airways inflammation after ozone exposure in 44 children by repeated nasal lavages from May to October 1991. During this time period five to eight lavages were performed for each child. On 14 days following high ozone exposure (daily maximum > or = 180 micrograms/m3) 148 nasal lavages were performed, and on 10 days following low ozone exposure (daily maximum < or = 140 micrograms/m3) 106 nasal lavages were performed. A significant increase of intra-individual mean polymorphonuclear leukocytes (PMN) counts from low ozone days (median, 20.27 x 10(3)) to high ozone days (median, 27.38 x 10(3); p < 0.01) was observed. Concomitant with a decrease of ozone concentrations in the fall mean PMN counts showed a downward trend. Linear regression analysis of log-PMN counts yielded a significant effect for ozone (p = 0.017). In a subsample humoral markers of inflammation were measured for each child's highest and lowest exposure. A significant increase was observed for eosinophilic cationic protein (median, 77.39 micrograms/L on low ozone days versus 138.6 micrograms/L on high ozone days; p < 0.05). Thus we conclude that ozone at ambient concentrations initiates a reversible inflammatory response of the upper airways in normal children.

Air Pollutants↗
PubMed2003

Anaerobic digestion of excess activated sludge with ozone pretreatment.

Source minimization of excess sludge production by economical means can be considered an attractive option to deal with the problem of sludge disposal under strict disposal standards. In this paper long-term operational results for a process that combines the oxidative ozone pretreatment with anaerobic sludge digestion are described. The ozone pretreatment solubilized around 19% and 37% of the solids at 0.015 and 0.05 gO3/gTS ozone dose. The solubilization ratios during ozonation did not show any significant difference for the sludge concentrations ranging from 1.8-2.6%. The TVS concentrations after ozone treatment were observed to be about 3% lower than the feed sludge concentrations suggesting only partial mineralization during ozonation. The ozone pretreatment resulted in improved solid reduction efficiencies during anaerobic digestion leading to higher methane recovery. The TVS removal efficiencies during anaerobic digestion were observed to increase by a maximum of 35-90% depending on the applied ozone dose during ozone pretreatment. The improvement in TVS degradation efficiency at different applied ozone doses correlated well with the extent of solubilization during ozonation. Long-term data also suggested that biomass acclimation to ozonated sludge was necessary before higher degradation efficiencies could be achieved.

Bacteria, Anaerobic↗