Ozone Group Research Articles

QBO and QTO of atmospheric methane

The 12-month running means of methane (CH 4) concentrations at the surface/lower troposphere averaged for latitude groups 1–8 (1, 82–63°N; 2, 56–53°N; 3, 47–36°N; 4, 32–26°N; 5, 20–13°N; 6, 5–14°S, 7, 41°S only; 8, 65–90°S) showed oscillations but the peak spacings were similar to that of 30 mb wind (∼30 months) only for groups 3, 4 and 7. A cross-correlation with 30 mb wind showed maximum good correlations (+0.7) with a phase lag of about 6 months for CH 4 in group 7 (in agreement with Camp et al. [2001. The sensitivity of tropospheric CH 4 to the interannual variability in stratospheric ozone. Chemosphere-Global Change Science 3, 147–156]) and about 12 months for CH 4 in groups 6 (+0.7). A spectral analysis indicated for 30 mb wind, a prominent Quasi-biennial oscillation (QBO) at 2.34 years and a minor peak at 2.06 years. For Southern Oscillation Index (SOI) (T−D), there was a prominent Quasi-triennial oscillation (QTO) peak at 3.6 years, but there was also a less prominent but significant QBO at 2.54 years. All CH 4 groups showed significant QBOs in the range 2.22–2.58 years but also showed more prominent QTOs in the range 3.2–4.1 years, and barely significant peaks in the range 1.6–1.9 years (19–22 months). To test the ozone mechanism proposed by Hamilton and Fan [2000. Effects of the stratospheric QBO on long-lived greenhouse gases in the troposphere. Journal of Geophysical Research 105, 20581–20587] (stratospheric wind QBO affecting stratospheric ozone, in turn affecting the filtered UV, the tropospheric OH radical, and finally tropospheric CH 4), TOMS-SBUV data were analyzed. Many CH 4 and ozone groups showed QBOs in the range 2.22–2.77 years, and lower periodicities in the range 1.60–1.91 years (19–22 months [Tung, K.K., Yang, H., 1994. Global QBO in circulation and ozone. Part I. Reexamination of observational evidence. Journal of Atmospheric Science 51, 2699–2707]), confirming that the ozone mechanism was operative. A disconcerting feature is the QTO of ∼3.5 years, which was present in CH 4 in all latitude groups, but in ozone, only in groups 3, 6, 7.

Diurnal discrepancies in spectral solar UV radiation measurements

Unexpected diurnal discrepancies between high-quality spectroradiometers were observed during the 2000 Nordic Ozone Group Intercomparison campaign. The spectral ratios of the irradiances showed a diurnal variation of approximately 2-9%. This cannot be explained by the nonideal angular response of the instruments' input optics in one plane (cosine effect). Instead, by using a radiative transfer model, we show that differences in the angular response in four azimuth planes have the potential to bias the measured data by up to 4.4% (azimuth effect). Other relevant factors are also discussed and quantified and are shown to be significant when diurnal changes in radiation are explained by environmental factors, or when measured data are compared with model or satellite data. Again, intercomparison campaigns have the potential to reveal errors that would otherwise remain undetected.

Efficiency of activated carbon to transform ozone into OH radicals: Influence of operational parameters

Based on previous findings (Jans, U., Hoigné, J., 1998. Ozone Sci. Eng. 20, 67-87), the activity of activated carbon for the transformation of ozone into *OH radicals including the influence of operational parameters (carbon dose, ozone dose, carbon-type and carbon treatment time) was quantified. The ozone decomposition constant (k(D)) was increased by the presence of activated carbon in the system and depending on the type of activated carbon added, the ratio of the concentrations of *OH radicals and ozone, the R(ct) value ([*OH]/[O3]), was increased by a factor 3-5. The results obtained show that the surface chemical and textural characteristics of the activated carbon determines its activity for the transformation of ozone into *OH radicals. The most efficient carbons in this process are those with high basicity and large surface area. The obtained results show that the interaction between ozone and pyrrol groups present on the surface of activated carbon increase the concentration of O2*- radicals in the system, enhancing ozone transformation into *OH radicals. The activity of activated carbon decreases for extended ozone exposures. This may indicate that activated carbon does not really act as a catalyst but rather as a conventional initiator or promoter for the ozone transformation into *OH radicals. Ozonation of Lake Zurich water ([O3] = 1 mg/L) in presence of activated carbon (0.5 g/L) lead to an increase in the k(D) and R(ct) value by a factor of 10 and 39, respectively, thereby favouring the removal of ozone-resistant contaminants. Moreover, the presence of activated carbon during ozonation of Lake Zurich water led to a 40% reduction in the content of dissolved organic carbon during the first 60 min of treatment. The adsorption of low concentrations of dissolved organic matter (DOM) on activated carbon surfaces did not modify its capacity to initiate/promote ozone transformation into *OH radicals.

Ozone therapy on rats submitted to subtotal nephrectomy: role of antioxidant system.

Chronic renal failure (CRF) represents a world health problem. Ozone increases the endogenous antioxidant defense system, preserving the cell redox state. The aim of this study is to evaluate the effect of ozone/oxygen mixture in the renal function, morphology, and biochemical parameters, in an experimental model of CRF (subtotal nephrectomy). Ozone/oxygen mixture was applied daily, by rectal insufflation (0.5 mg/kg) for 15 sessions after the nephrectomy. Renal function was evaluated, as well as different biochemical parameters, at the beginning and at the end of the study (10 weeks). Renal plasmatic flow (RPF), glomerular filtration rate (GFR), the urine excretion index, and the sodium and potassium excretions (as a measurement of tubular function) in the ozone group were similar to those in Sham group. Nevertheless, nephrectomized rats without ozone (positive control group) showed the lowest RPF, GFR, and urine excretion figures, as well as tubular function. Animals treated with ozone showed systolic arterial pressure (SAP) figures lower than those in the positive control group, but higher values compared to Sham group. Serum creatinine values and protein excretion in 24 hours in the ozone group were decreased compared with nephrectomized rats, but were still higher than normal values. Histological study demonstrated that animals treated with ozone showed less number of lesions in comparison with nephrectomized rats. Thiobarbituric acid reactive substances were significantly increased in nephrectomized and ozone-treated nephrectomized rats in comparison with Sham group. In the positive control group, superoxide dismutase (SOD) and catalase (CAT) showed the lowest figures in comparison with the other groups. However, ozone/oxygen mixture induced a significant stimulation in the enzymatic activity of CAT, SOD, and glutathione peroxidase, as well as reduced glutathione in relation with Sham and positive control groups. In this animal model of CRF, ozone rectal administrations produced a delay in the advance of the disease, protecting the kidneys against vascular, hemorheological, and oxidative mechanisms. This behavior suggests ozone therapy has a protective effect on renal tissue by downregulation of the oxidative stress shown in CRF.

Efeito terapêutico da aplicação intra-ocular de ozônio em modelo experimental de endoftalmite por Staphylococcus epidermidis em coelhos

PURPOSE: To evaluate the anti-inflammatory and antimicrobial effect of intraocular ozone diluted in BSS on experimental Staphylococcus epidermidis endophthalmitis. METHODS: We injected 0.1ml of S. epidermidis colonies (105 colonies/ml) to produce experimental endophthalmitis in the right eyes of 17 New Zealand rabbits. Seven rabbits were assigned to a control group and received an intravitreal injection of 0.1ml BSS. Ten rabbits were treated with intravitreal injection of 0.1ml BSS-diluted ozone (2 ppm). Data were distributed according to clinical and histological findings after 24 hours, each rabbit receiving a score. Mean scores and standard deviations were compared using the two-sample t test. RESULTS: Mean clinical score for the control group was 11.14 ± 1.04. Mean clinical score for the treated group was 4.90 ± 1.29, which was significantly lower (p<0.01). Mean histological scores were, respectively, 17.00+ 0.57 and 10.20 ±1.30 for the control group and the treated group. The histological scores were significantly lower for the treated group (p<0.01). All cultures in both control and ozone groups were positive after 24 hours of experiment. CONCLUSION: Treatment with diluted ozone significantly reduced the inflammatory reaction in our model of experimental endophthalmitis. This probably occurred due to a decrease in bacterial content after ozone injection. It is necessary to study other ozone concentrations in different experimental models in order to determine ozone efficacy with a higher precision.

Catalytic ozonation of refractory organic model compounds in aqueous solution by aluminum oxide

Batch experiments on catalytic ozonation in buffered and non-buffered solution of refractory organic compounds like oxalic, acetic, salicylic and succinic acids are presented. The concentration of dissolved organic carbon (DOC) in each test was 60mg/l and the applied batch procedure allowed a clear distinction between adsorptive and reaction processes. Results have confirmed that Al2O3 can be an effective catalyst for the conversion of dissolved organic compounds into CO2, but strength and performance of the catalysis are directly depending on the applied model compound and the matrix of solution. Catalytic effects were mostly pronounced in non-buffered solution and succinic acid exhibited the highest affinity for the reaction with an applied γ-Al2O3. Semi-continuous trails in buffered and non-buffered solution of succinic acid confirmed the catalytic activity of Al2O3 for oxidation and, moreover, showed increasing catalytic effectiveness of the alumina with rising ozone dosage. The performance was comparable or superior to classical perozone treatment depending on the applied dosage of ozone. Different reaction mechanisms of the heterogeneous system are discussed and a suggestion of possibly involved reaction paths is presented. Higher oxidation performance might be explained by an interaction between ozone and OH surface groups of the alumina.

Atypical development of the tracheal basement membrane zone of infant rhesus monkeys exposed to ozone and allergen

Development of the basement membrane zone (BMZ) occurs postnatally in the rhesus monkey. The purpose of this study was to determine whether house dust mite allergen (HDMA) plus ozone altered this process. Rhesus monkeys were exposed to a regimen of HDMA and/or ozone or filtered air for 6 mo. To detect structural changes in the BMZ, we measured immunoreactivity of collagen I. To detect functional changes in the BMZ, we measured perlecan and fibroblast growth factor-2 (FGF-2). We also measured components of the FGF-2 ternary signaling complex [fibroblast growth factor receptor-1 (FGFR-1) and syndecan-4]. The width of the BMZ was irregular in the ozone groups, suggesting atypical development of the BMZ. Perlecan was also absent from the BMZ. In the absence of perlecan, FGF-2 was not bound to the BMZ. However, FGF-2 immunoreactivity was present in basal cells, the lateral intercellular space (LIS), and attenuated fibroblasts. FGFR-1 immunoreactivity was downregulated, and syndecan-4 immunoreactivity was upregulated in the basal cells. This suggests that FGF-2 in basal cells and LIS may be bound to the syndecan-4. We conclude that ozone and HDMA plus ozone effected incorporation of perlecan into the BMZ, resulting in atypical development of the BMZ. These changes are associated with specific alterations in the regulation of FGF-2, FGFR-1, and syndecan-4 in the airway epithelial-mesenchymal trophic unit, which may be associated with the developmental problems of lungs associated with exposure to ozone.

Ozone Therapy in Patients with Retinitis Pigmentosa

The aim of this study is to determine the efficacy of ozone therapy in patients with Retinitis Pigmentosa (RP). A controlled, randomized, double blind clinical trial involving 68 patients was performed. Patients were divided into 2 groups: ozone, patients treated with ozone by rectal administration (dose=10 mg), during 15 sessions; control, as ozone group, but using oxygen. The main outcome variable was the visual field area (VFA). Results demonstrated a significant improvement (SI) in 88.2% of patients treated with ozone in comparison with 23.5% achieved in the control group. In the ozone group, VFA tend to stabilize beyond a mean time of 6.83 months with a loose in SI afterward. A temporal positive effect of ozone therapy. Over the natural course of RP, was found.

Ozone Biological Response in Kidneys of Rats Submitted to Warm Ischemia

A biochemical and morphofunctional renal study, applying different sessions of rectal ozone (O3) before a warm ischemia, was performed. Rats were divided in: 1-control, a medial abdominal incision was performed for the exposure of the kidneys; 2-ischemia, animals with a bilateral renal ischemia (30 min), with subsequent reperfusion (3 h); groups 3, 4 and 5 – (O3+ischemia), as group 2, but with previously treatment of 5, 10 and 15 sessions of rectal ozone, respectively; groups 6, 7 and 8 – (O2+ischemia), as groups 3, 4 and 5, respectively, but using rectal oxygen. A significant decrease of the flow and renal filtration, with high values of fructosamine and phospholipase A2, in the ischemia and oxygen groups, with respect to control and ozone groups was obtained without any statistical difference among them. Morphological alterations were significantly less in the groups pretreated with ozone, with better results for 10 and 15 sessions.

The relationship between alveolar epithelial proliferation and airway obstruction after ozone exposure.

Proliferating cell nuclear antigen (PCNA) is a component of multiprotein complexes that are expressed during cell proliferation. Ozone induces cell necrosis and a consequent increase in cell proliferation. To investigate the effects of acute ozone inhalation on cell proliferation and airway obstruction in BALB/C mice, we examined enhanced pause (Penh) as an index of airway obstruction and PCNA expression by immunohistochemical staining. Compared with controls that received filtered air, the ozone-exposed groups had increased PCNA expression in the alveolar epithelial cells. In rank order, the highest PCNA index was found following 2.0 p.p.m. ozone exposure. In the 2.0 p.p.m. ozone group, there was a PCNA index of 16.83 +/- 0.57% (mean +/- SEM; P< 0.01), compared with 4.25 +/- 0.5% at 0.12 p.p.m., 6.83 +/- 0.60 at 0.5 p.p.m and 12.16 +/- 0.48% at 1 p.p.m. Following ozone exposure, Penh was increased in a dose-dependent manner. There was a significant correlation between the PCNA index in alveoli and Penh (r = 0.63, P< 0.01). These data suggest that ozone can induce alveolar epithelial cell proliferation in a dose-dependent manner, and that alveolar epithelial cell proliferation is correlated with airway obstruction.

Effect of inhaled indomethacin on distilled water-induced airway epithelial cell swelling.

We evaluated the mechanism of the anti-asthmatic effect of inhaled indomethacin (Indo) by using an animal model (guinea pigs) of airway inflammation. After being exposed to either ozone or room air at identical flow rates (5 l/min) for 2 h, guinea pigs were anesthetized, tracheostomized, and lung resistance (RL) was subsequently measured. Guinea pigs inhaled either saline or Indo (1.5 mg/ml) for 1 min before undergoing an ultrasonically nebulized distilled water (UNDW) inhalation test. RL increased significantly after 10 min of UNDW inhalation in the room air and ozone groups but more so in the ozone group. This increase in RL was significantly suppressed by pretreatment with Indo. In the morphometric assessment of airway mucosa, a significant swelling of the epithelial cells after UNDW inhalation was observed in both the room air and ozone groups but especially so in the ozone group. This increase was also suppressed with Indo pretreatment. These results suggest that the increase in RL and the swelling of airway epithelial cells induced by inhaled UNDW in ozone-exposed guinea pigs was suppressed by pretreatment of inhaled Indo and that this suppression may be one of the reasons for the anti-asthmatic effect of inhaled Indo.

Ozone treatment reduces markers of oxidative and endothelial damage in an experimental diabetes model in rats

Ozone has been used as a therapeutical agent and beneficial effects have been observed. However so far only a few biochemical and pharmacodynamic mechanisms have been elucidated. We demonstrate that controlled ozone administration may promote an oxidative preconditioning or adaptation to oxidative stress, preventing the damage induced by reactive oxygen species (ROS). Taking into account that diabetes is a disorder associated with oxidative stress, we postulate that ozone treatment in our experimental conditions might protect antioxidant systems and maintain, at a physiological level, other markers of endothelial cell damage associated with diabetic complications. Five groups of rats were classified as follows: (1) control group treated only with physiological saline solution; (2) positive control group using streptozotocin (STZ) as a diabetes inductor; (3) ozone group, receiving 10 treatments (1.1 mg kg−1), one per day after STZ-induced diabetes; (4) oxygen group (26 mg kg−1), one per day, as in group 3 but using oxygen only; (5) control ozone group, as group 3, but without STZ. The ozone treatment improved glycemic control and prevented oxidative stress, the increase of aldose reductase, fructolysine content and advanced oxidation protein products. Nitrite and nitrate levels were maintained without changes with regard to non-diabetic control. The results of this study show that repeated administration of ozone in non-toxic doses might play a role in the control of diabetes and its complications.

Effect of ultrasonically nebulized distilled water on airway epithelial cell swelling in guinea pigs.

To investigate the pathogenesis of ultrasonically nebulized distilled water-induced airway narrowing, we studied the role of airway epithelial cells during a distilled water-inhalation challenge in an animal model of airway inflammation. Guinea pigs were divided into four groups: 1) a sham/saline (S/S) group: sham ozone followed by saline inhalation; 2) a sham/water (S/W) group: sham ozone followed by water inhalation; 3) an ozone/saline (O/S) group: ozone followed by saline inhalation; and 4) an ozone/water (O/W) group: ozone followed by water inhalation. After exposure to either 3.0 parts/million ozone or air at the same flow rate for 2 h, guinea pigs were anesthetized and tracheostomized, and then lung resistance (RL) was measured. For morphometric assessment, tissues were fixed with formaldehyde, stained with hematoxylin and eosin, and cut into transverse sections. Airway dimensions were either measured directly or calculated from the internal perimeter, the external perimeter, and airway wall area. There were no statistical differences in the values of RL before distilled water inhalation between the sham groups and the ozone groups. RL increased significantly after 10 min of distilled water inhalation in both the S/W group and the O/W group. In the S/W group, epithelial cells were swollen, and intercellular spaces were wider, resulting in significant increase in epithelial wall thickness, but there was no significant infiltration by inflammatory cells. In the O/S group, the epithelium showed infiltration by inflammatory cells without change in cell volume. In the O/W group, the epithelium showed both infiltration and a greater increase in epithelial wall thickness compared with the S/W group. These results suggest that airway epithelial cell swelling, induced by inhaled distilled water, increases with RL in guinea pigs and that this reaction may be accelerated by airway inflammation.

Cell injury and interstitial inflammation in rat lung after inhalation of ozone and urban particulates.

Coexposure of the lung to urban dust along with ozone appears to potentiate ozone-induced injury. This conclusion was derived from whole-lung studies involving tissue and lavaged cells, but we now speculate that the injury and inflammatory response at the main site of reactivity, the bronchoalveolar duct region, is underestimated by such whole-lung studies. We exposed rats to ozone at 0.8 ppm and urban particulates (EHC93) at 50 mg/m3 for 4 h. Animals were killed 33 h later with tritiated thymidine (3HT) injected 1.5 h before death. Lungs were fixed by vascular perfusion to avoid disturbing any epithelial cell changes or local inflammation and edema in the air spaces. Tissue was embedded from central and peripheral areas of the lung, then counts of labeled cells, polymorphonuclear leukocytes (PMN), and macrophages (MAC) were made separately on methacrylate sections. The results showed that epithelial cell injury and regeneration (% of 3HT-labeled cells) was greatest in the ozone plus dust group, and was three times higher in periductal areas than in whole-lung counts. Although some increase in inflammatory cells in the air spaces was found in the coexposure group, much higher numbers of PMN and MAC were counted in the lung tissue compartment, and counts were significantly higher than those found after ozone or dust alone. Values from the latter groups were also higher than those from air controls or samples of distal lung taken from any inhalation group. The results demonstrate that inhalation of an urban dust at a level that causes few lung effects when inhaled alone can potentiate ozone toxicity, particularly in the vicinity of the alveolar duct, where the accumulation of interstitial inflammatory cells may be an important factor in the development of any subsequent pathologic changes.

Regional ozone group ends study; States, EPA near plan to cut Nox

Regional ozone group ends study; States, EPA near plan to cut Nox

Interaction of ozone and allergen challenges on bronchial responsiveness and inflammation in sensitised guinea pigs.

Environmental pollutants such as ozone may interact with airway responses to allergen in sensitised individuals. We examined the effects of a single exposure to ozone (1 ppm for 1 h) on bronchial responsiveness to acetylcholine (ACh) aerosol 3 and 24 h after single ovalbumin (OA) challenge in OA-sensitised anaesthetised guinea pigs. Broncho-alveolar lavage (BAL) was performed and protein content and differential cell counts were determined. Ozone increased bronchial responsiveness at 3 h but not at 24 h, while OA alone had no effect. At 3 h after ozone, OA induced further, but non-significant increases in bronchial responsiveness to ACh, but at 24 h after ozone, there was enhanced responsiveness. Neutrophil counts in BAL fluid increased at 3 and 24 h after exposure to ozone alone, but there were no further increases with ozone followed by OA exposure. Protein concentration was significantly increased in the ozone and OA groups at 3 and 24 h (163.4 +/- 25.6 and 128.7 +/- 7.4 mg/ml, respectively) compared to 54.0 +/- 18.1 mg/ml in the control group (p < 0.02 and p < 0.01, respectively). Our data demonstrate an interaction of OA with ozone exposure on bronchial responsiveness; one underlying mechanism could be through damage at the endothelial-epithelial barrier.

Serum Clara cell protein (CC16): a new valid marker of the distal airway damages caused by air pollutants in rats.

Cell count, LDH, total protein, Clara cell protein (CC16) and lysozyme in bronchoalveolar lavage fluid (BAL) and serum were determined in rats. 30-50 ppm sulfur dioxide for 4 h. 12 h and 2 week exposure didn't produce any change of above parameters. 1.0 ppm, 0.5 ppm, 0.38 ppm, 0.25 ppm and 0.20 ppm ozone for 7 h exposure tests were performed. CC16, total protein and LDH in BAL had significantly changes in BAL in ozone groups. Only serum CC16 showed significant increase among ozone groups. Both BAL and serum CC16 were of the best exposure-response relationship with ozone concentration. The change of BAL fluid reached high peak 18-24 h after ozone exposure. Serum CC16 seemed to be a valid marker of the distal airway damages caused by air pollutants.

Phagocytosis and chemotaxis of rat alveolar macrophages after a combined or separate exposure to ozone and carbon black.

Male Wistar rats were treated by ozone or carbon black (CB) alone as well as in combination. Intratracheal instillation with various amounts of CB was followed either by an acute 7-day or subchronic 2-month ozone exposure (0.5 ppm). Two functional parameters were investigated in alveolar macrophages from bronchoalveolar lavagates, the phagocytotic capacity and the chemotactic migration capability. In the phagocytosis assay, the percentage of phagocytizing macrophages decreased significantly in the CB-exposed groups whereas the ozone groups remained close to or at the control level after 7 days and 2 months of exposure, respectively. The number of ingested particles per macrophage and the formation of superoxide anion radicals were not changed after a 7-day exposure to ozone compared to the control group but were increased after a 2-month ozone exposure. However, a reduction was found in the CB groups. A stimulating effect of ozone was observed in the combined groups. Chemotactic migration was generally retarded in the CB-treated groups. From the results it can be concluded that ozone is able to stimulate the phagocytotic and chemotactic activity of alveolar macrophages whereas CB impairs these functions.

Ozone inhibition of tissue cholinesterase in guinea pigs.

This study sought to determine if ozone at levels known to induce bronchial hyperreactivity in guinea pigs would inhibit tissue cholinesterase activity. Male, Hartley guinea pigs were exposed to filtered air, 0.1 ppm ozone, or 0.8 ppm ozone for 1 hr. Two hours after exposure, brain, lung, and diaphragm tissue samples were frozen for assay of cholinesterase activity. Brain cholinesterase activity was only minimally inhibited in either ozone exposure group. Both levels of ozone significantly inhibited lung cholinesterase activity compared to control animals' activity: a 17% decrease in activity in the 0.1 ppm ozone group (P less than .05) and a 16% decrease in the 0.8 ppm ozone group (P less than .05). Ozone at 0.8 ppm also inhibited activity in the diaphragm by 14% (P less than .02). To determine the degree of involvement of cholinesterase inhibition in bronchial hyperreactivity, parathion pretreated animals were challenged with histamine and the pulmonary function changes monitored. Parathion-treated animals had a peak resistance increase of 330 +/- 104% (mean +/- SE), while the control vehicle animals' increase was 165 +/- 48%. The differences were not statistically significant, but show that cholinesterase inhibition may contribute to ozone-induced bronchial hyperreactivity.

Ozone exposure and intelligence tests.

The effect of ozone on mental functioning was studied by administering intelligence tests to 99 university students. The subjects were divided into treatment (exposed to 0.2 to 0.3 ppm ozone during the writing of the test), placebo, and control (not exposed to ozone) groups. After statistical adjustment had been made for the effects of the covariants (age, sex, anxiety, and initial intelligence test score) no significant difference was found between the groups. This study indicated that exposure to concentrations of 0.2 to 0.3 ppm ozone over a period of 70 minutes had no noticeable effect on mental functioning during the exposure period.