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PubMed2003

Changes in tropospheric composition and air quality due to stratospheric ozone depletion.

Increased UV-B through stratospheric ozone depletion leads to an increased chemical activity in the lower atmosphere (the troposphere). The effect of stratospheric ozone depletion on tropospheric ozone is small (though significant) compared to the ozone generated anthropogenically in areas already experiencing air pollution. Modeling and experimental studies suggest that the impacts of stratospheric ozone depletion on tropospheric ozone are different at different altitudes and for different chemical regimes. As a result the increase in ozone due to stratospheric ozone depletion may be greater in polluted regions. Attributable effects on concentrations are expected only in regions where local emissions make minor contributions. The vertical distribution of NOx (NO + NO2), the emission of volatile organic compounds and the abundance of water vapor, are important influencing factors. The long-term nature of stratospheric ozone depletion means that even a small increase in tropospheric ozone concentration can have a significant impact on human health and the environment. Trifluoroacetic acid (TFA) and chlorodifluoroacetic acid (CDFA) are produced by the atmospheric degradation of hydrochlorofluorocarbons (HCFCs) and hydrofluorocarbons (HFCs). TFA has been measured in rain, rivers, lakes, and oceans, the ultimate sink for these and related compounds. Significant anthropogenic sources of TFA other than degradation HCFCs and HFCs have been identified. Toxicity tests under field conditions indicate that the concentrations of TFA and CDFA currently produced by the atmospheric degradation of HFCs and HCFCs do not present a risk to human health and the environment. The impact of the interaction between ozone depletion and future climate change is complex and a significant area of current research. For air quality and tropospheric composition, a range of physical parameters such as temperature, cloudiness and atmospheric transport will modify the impact of UV-B. Changes in the chemical composition of the atmosphere including aerosols will also have an impact. For example, tropospheric OH is the 'cleaning' agent of the troposphere. While increased UV-B increases the OH concentration, increases in concentration of gases like methane, carbon monoxide and volatile organic compounds will act as sinks for OH in troposphere and hence change air quality and chemical composition in the troposphere. Also, changes in the aerosol content of the atmosphere resulting from global climate change may affect ozone photolysis rate coefficients and hence reduce or increase tropospheric ozone concentrations.

Acetates↗
PubMed2003

Understanding the effectiveness of precursor reductions in lowering 8-hr ozone concentrations.

Analyses of ambient measured ozone data were used in conjunction with the application of photochemical modeling to determine the technical feasibility of attaining the federal 8-hr ozone standard in central California. Various combinations of volatile organic compound (VOC) and oxides of nitrogen (NOx) emission reductions were effective in lowering modeled peak 1-hr ozone concentrations. However, VOC emissions reductions were found to have only a modest impact on modeled peak 8-hr ozone concentrations. NOx emission reductions generally lowered 8-hr ozone concentrations, but their effectiveness was partially or, in some cases, wholly offset by the increase in the number of NO cycles and, hence, in the ozone produced per NO. As a result, substantial NOx emission reductions--70 to 90%--were required to reduce peak 8-hr ozone concentrations to the level of the standard throughout the modeling domain. These modeling results provide a possible physical explanation for recent analyses that have reported more prominent trends in peak 1-hr ozone levels than in peak 8-hr ozone concentrations or in occurrences of mid-level (60-90 parts per billion by volume) ozone concentrations. The findings also have serious implications for the feasibility of attaining the 8-hr ozone standard in central California. Further efforts are needed to clarify the applicability of the modeling results to the full set of days with ozone levels exceeding the 8-hr ozone standard, as well as their applicability to other geographical areas.

Air Pollution↗
PubMed2004

Mechanisms of Bacillus subtilis spore resistance to and killing by aqueous ozone.

AIMS: To determine the mechanisms of Bacillus subtilis spore killing by and resistance to aqueous ozone. METHODS AND RESULTS: Killing of B. subtilis spores by aqueous ozone was not due to damage to the spore's DNA, as wild-type spores were not mutagenized by ozone and wild-type and recA spores exhibited very similar ozone sensitivity. Spores (termed alpha-beta-) lacking the two major DNA protective alpha/beta-type small, acid-soluble spore proteins exhibited decreased ozone resistance but were also not mutagenized by ozone, and alpha-beta- and alpha-beta-recA spores exhibited identical ozone sensitivity. Killing of spores by ozone was greatly increased if spores were chemically decoated or carried a mutation in a gene encoding a protein essential for assembly of the spore coat. Ozone killing did not cause release of the spore core's large depot of dipicolinic acid (DPA), but these killed spores released all of their DPA after a subsequent normally sublethal heat treatment and also released DPA much more readily when germinated in dodecylamine than did untreated spores. However, ozone-killed spores did not germinate with either nutrients or Ca(2+)-DPA and could not be recovered by lysozyme treatment. CONCLUSIONS: Ozone does not kill spores by DNA damage, and the major factor in spore resistance to this agent appears to be the spore coat. Spore killing by ozone seems to render the spores defective in germination, perhaps because of damage to the spore's inner membrane. SIGNIFICANCE AND IMPACT OF THE STUDY: These results provide information on the mechanisms of spore killing by and resistance to ozone.

Amines↗
PubMed1982

Ozone inactivation of cell-associated viruses.

The inactivation of HEp-2 cell-associated poliovirus (Sabin 1) and coxsackievirus A9 was investigated in three experimental systems, using ozone as a disinfectant. The cell-associated viral samples were adjusted to a turbidity of 5 nephelometric turbidity units. The cell-associated poliovirus and coxsackievirus samples demonstrated survival in a continuous-flow ozonation system at applied ozone dosages of 4.06 and 4.68 mg/liter, respectively, for 30 s. Unassociated viral controls were inactivated by the application of 0.081 mg of ozone per liter for 10 s. Ultrasonic treatment of cell-associated enteric viruses did not increase inactivation of the cell-associated viruses. The batch reactor with a declining ozone residual did not effect total inactivation of either cell-associated enteric virus. These cell-associated viruses were completely inactivated after exposure to ozone in a batch reactor using continuous ozonation. Inactivation of cell-associated poliovirus required a 2-min contact period with an applied ozone dosage of 6.82 mg/liter and a residual ozone concentration of 4.70 mg/liter, whereas the coxsackievirus was completely inactivated after a 5-min exposure to an applied ozone dosage of 4.81 mg/liter with an ozone residual of 2.18 mg/liter. These data indicate that viruses associated with cells or cell fragments are protected from inactivation by ozone concentrations that readily inactivate purified virus. The cell-associated viral samples used in this research contained particles that were 10 to 15 microns in size. Use of a filtration system before ozonation would remove these particles, thereby facilitating inactivation of any remaining viruses associated with cellular fragments.

Cell Line↗
PubMed1981

Bioassaying for ozone with pollen systems.

Sensitivity to ozone of pollen germinating in vitro is closely correlated with ozone sensitivity of the pollen parent. Ozone-sensitive and tolerant pollen populations have been identified in tobacco, petunia, and tomato cultivars. The rate of tube elongation can be reversibly slowed or stopped by exposure to low concentrations of ozone. Tube growth rates in the presence of a range of ozone dosages, of pollen populations exhibiting differing ozone sensitivity can be measured and different growth rates can be correlated with ozone dosages. The performance of selected pollen populations can then be used to bioassay ozone in ambient air by introducing the air sample into a growth chamber where ozone-sensitive pollen in growing. Petunia and tobacco pollen are especially useful because they store well at ordinary freezer temperatures and do not require special preparation prior to storage. Modified Brewbacker's growth medium is suitable for growth of both these pollen types. Four useful cultivars are Bel W-3, ozone-sensitive and Bel B, ozone-tolerant tobacco, and White Bountiful, ozone-sensitive and Blue Lagoon, ozone-tolerant petunia. Observations can be made directly by using a TV scanner, or by time lapse or interval photography. Year-round pollen production can be achieved in the greenhouse. Harvested pollen can be tested, packaged, and transported to user facilities without loss of vigor. Pollen populations are inexpensive to produce, respond reliably, and are simple to use as a bioassay for air quality.

Biological Assay↗
PubMedDate not supplied

Antioxidants in bronchoalveolar lavage fluid cells isolated from ozone--exposed normal and ascorbate-deficient guinea pigs.

Previous studies have indicated that systemic deficiency in one of the critical antioxidants, ascorbate, does not significantly exacerbate ozone-induced lung injury and changes in lung antioxidants following longer-term exposure. Because alveolar cells encounter the highest ozone dose upon exposure and lack direct blood supply, systemic ascorbate deficiency may exacerbate ozone response on antioxidants within these cells. Female Hartley guinea pigs (30 days old) were fed either a regular guinea pig chow or chow that lacked ascorbate. The dietary regimen was started 1 week prior to exposure, continued through ozone exposure (0, 0.2, 0.4, or 0.8 ppm, 23 h/day, 1 week), and during 1 week recovery in clean air following exposure. Immediately after 1 week of exposure or recovery, lungs were lavaged and cells were counted in bronchoalveolar lavage fluid (BALF). Protein, ascorbate, uric acid, total glutathione (GSH), and alpha-tocopherol were analyzed in these cells. Ozone caused an increase in total BALF cells and total cellular protein after 0.4 and 0.8 ppm ozone. The increase was more pronounced in ascorbate-deficient guinea pigs. Protein per million cells, however, was not changed by ozone or diet. In ascorbate-sufficient guinea pigs, ascorbate levels were increased only after 0.2 ppm ozone. However, uric acid (at 0.4 and 0.8 ppm ozone) and GSH (at all concentrations of ozone) levels were increased in both dietary groups. Ascorbate deficiency did not affect basal uric acid or GSH levels in BALF cells. There was a small diet-related depletion in cellular alpha-tocopherol. Ozone exposure also decreased alpha-tocopherol regardless of diet. The above changes except for alpha-tocopherol appeared to be reversed after 1 week of recovery in both dietary groups. In summary, ozone is capable of inducing a mechanism that increases antioxidants such as ascorbate, GSH, and uric acid. GSH and uric acid are not affected by ascorbate deficiency, but alpha-tocopherol is depleted. GSH and uric acid may be critical in ozone-induced adaptation during ascorbate deficiency.

Adaptation, Physiological↗
PubMed1992

The role of ozone in tracheal cell transformation.

This project examined the potential role of ozone as a respiratory carcinogen by characterizing its ability to induce or modulate the preneoplastic transformation of rat tracheal epithelial cells. The chemical reactivity of ozone and the types of damage it can cause suggest that it may have a role in environmental carcinogenesis. Previous reports have described an increase in the incidence and number of lung tumors per animal in strain A mice exposed to ozone. However, the role of ozone in the development of the tumors has not been clear. Ozone also has been reported to act alone and synergistically with ionizing radiation to induce changes related to neoplasia in primary hamster embryo cells and in the mouse C3H/10T1/2 cell line in culture. Few other studies have examined the direct cytotoxic or transforming effects of ozone after in vivo or in vitro exposure of cells, and no studies have been reported on the comparative effects of ozone on respiratory cells exposed in vivo or in vitro. The induction of early preneoplastic changes in populations of rat tracheal epithelial cells by carcinogens can be detected and quantified in vitro after exposures in vivo or in vitro of tracheal epithelial cells. This cell culture and transformation system was used to characterize the transforming potency of ozone. Tracheal epithelial cells were isolated from Fischer-344/N rats that had been exposed for six hours per day, five days per week for one, two, or four weeks to 0, 0.12, 0.5, or 1.0 parts per million (ppm)* ozone (sea-level equivalents). Cell populations were examined in culture for increases in the frequency of preneoplastic variants. Rats exposed to ozone did not exhibit an increase in the frequency of preneoplastic tracheal cells, although exposed tracheas did exhibit dose-dependent morphological changes. Rat tracheal epithelial cells were given single, 40-minute in vitro exposures to concentrations of ozone that did not result in any detectable decrease in colony-forming efficiency (approximately 0.7 ppm) and to concentrations that resulted in approximately a 40% decrease (approximately 10 ppm). Exposed cultures were examined for increases in the frequency of preneoplastic variants. The results of these experiments, like those for the in vivo experiments described above, suggest that a single ozone exposure does not induce preneoplastic variants of rat tracheal epithelial cells. In contrast, cultures of rat tracheal cells exposed to 0.7 ppm ozone twice weekly for about five weeks exhibited approximately a twofold increase in the frequency of preneoplastic variants compared with control cultures.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

[Control of THMs formation potential of filtered surface water with catalytic ozonation by ferric hydroxide].

Catalytic ozonation of a filtered surface water with ferric hydroxide (FeOOH) was compared with ozonation alone for trihalomathane formation potential (THMFP). Factors studied included bromide, pH, alkalinity, ratio of O3/TOC, reaction time, and dosage of FeOOH. THMFP of the water after catalytic ozonation was 30.5% lower than that after ozonation. High bromide concentration resulted in the predominance of brominated THMFP, at which condition the brominated THMFP after catalytic ozonation was 45%-65.5% of that after ozonation. The catalytic ozonation showed a significant advantage over ozonation in controlling THMFP of the water at the conditions applied in this experiment, i.e., at pH of 6.33-9.43, O3/TOC of 0.65-2.05, and reaction time of 2-20 min. High concentration of alkalinity decreased THMFP of the water after ozonation and catalytic ozonation. It also weakened the advantage of catalytic ozonation. There existed an optimal dosage of FeOOH in respect of controlling THMFP. The lower THMFP of the water after catalytic ozonation is caused by its higher TOC removal than ozonation, and the possible enhanced oxidation of some of the THM precursors by hydroxyl radicals generated in this process.

Catalysis↗
PubMed1989

[The effect of a selective 5-lipoxygenase inhibitor, AA-861 on airway hyperresponsiveness induced by ozone exposure in dogs].

To determine whether 5-lipoxygenase products are involved in hyperresponsiveness induced by ozone exposure, we studied the effect of a selective 5-lipoxygenase inhibitor, AA-861 on ozone-induced airway hyperresponsiveness in six dogs. Airway responsiveness to methacholine was measured by modified Astograph (7 Hz oscillation method) before and after ozone exposure, and TxB2 in plasma and in BALF, 6-keto-PGF1 alpha in BALF, numbers of neutrophils in the peripheral blood and differential cell counts in BALF were measured before and after ozone exposure. Ozone exposure was carried out for 2 hr at an ozone level of 3.04 +/- 0.01 ppm (mean +/- SE). There was a significant increase in airway responsiveness to methacholine after ozone exposure in the six dogs (p less than 0.01), and the numbers of neutrophils in the peripheral blood and the neutrophil counts in BALF increased significantly after ozone exposure (P less than 0.01). A selective 5-lipoxygenase inhibitor, AA-861 significantly inhibited the increase of airway responsiveness to methacholine induced by ozone exposure (p less than 0.05), and furthermore, the increase in the numbers of neutrophils in the peripheral blood and the neutrophil counts in BALF after ozone exposure were significantly inhibited by pretreatment with AA-861 (p less than 0.05). There was no significant change in the levels of TxB2 in plasma or in BALF, and also no apparent change in the levels of histamine was observed in BALF after ozone exposure. The levels of 6-keto-PGF1 alpha in BALF decreased after ozone exposure, but the decrease was not significant. These results suggest that 5-lipoxygenase products play an important role in the development of airway hyperresponsiveness and in the infiltration of neutrophils into the airway after ozone exposure in dogs.

Animals↗
PubMed1987

[Effect of ozone and ionizing radiation on an in vitro model--a pilot study of 4 gynecologic tumors].

In order to investigate the sensibility of cultured tumor cells to ozone and irradiation primary tissue cultures from one undifferentiated non-classified ovarian carcinoma, two solid adenocarcinomas of the ovary and one endometrial carcinoma were established. Cultivation was performed according to standard techniques involving the stem cell assay in soft agar as well as the monolayer technique in liquid nutrient media. The type of culture system did not influence the sensitivity of the culture cells to ozone and/or irradiation. Ozone treatment was performed with three different Ozone concentrations (0.03 ppm, 0.1 ppm, 0.3 ppm). Irradiation was done with 100 rd Ra226, Ir192 or Co60. A control experiment showed that the proliferative tendency of benign cells (skin fibroblasts) was not inhibited by the three ozone concentrations used in this study. Ra226 and even the combination of ozone and Radium did not influence the proliferative activity of these benign cells. Ir192 and Co60 were cytotoxic to benign as well as to carcinoma cells. Cultivated cells from endometrial carcinoma resisted to ozone treatment as well as to Ra226 (but they were destroyed by Ir119 and Co60). After pretreatment with ozone (0.1 ppm), Ra226 treatment of endometrial carcinoma cells induced a cytostatic effect implying that no cell divisions were observed after irradiation and the cells lysed within two weeks after irradiation. For the three ovarian carcinoma cell lines analysed in this study ozone treatment had a cytostatic effect even at the lowest concentration (0.03 ppm), with the two higher ozone concentrations a cytotoxic effect could be induced in ovarian carcinoma cells. Exclusive treatment with Ra226 induced a cytostatic effect, but it was cytotoxic after combination with ozone treatment of the lowest concentration (Ir192 and Co60 were cytotoxic in all cases). Our investigation confirmed the radiosensitizing effect of ozone treatment. Furthermore it was shown that exclusive ozone treatment even without combined irradiation displayed a selective cytotoxic action at the ovarian carcinoma cells.

Cells, Cultured↗
PubMed1989

Ozone concentration in leaf intercellular air spaces is close to zero.

Transpiration and ozone uptake rates were measured simultaneously in sunflower leaves at different stomatal openings and various ozone concentrations. Ozone uptake rates were proportional to the ozone concentration up to 1500 nanoliters per liter. The leaf gas phase diffusion resistance (stomatal plus boundary layer) to water vapor was calculated and converted to the resistance to ozone multiplying it by the theoretical ratio of diffusion coefficients for water vapor and ozone in air (1.67). The ozone concentration in intercellular air spaces calculated from the ozone uptake rate and diffusion resistance to ozone scattered around zero. The ozone concentration in intercellular air spaces was measured directly by supplying ozone to the leaf from one side and measuring the equilibrium concentration above the other side, and it was found to be zero. The total leaf resistance to ozone was proportional to the gas phase resistance to water vapor with a coefficient of 1.68. It is concluded that ozone enters the leaf by diffusion through the stomata, and is rapidly decomposed in cell walls and plasmalemma.

Journal Article↗
PubMed2003

Airway obstruction after acute ozone exposure in BALB/c mice using barometric plethysmography.

BACKGROUND: Airway responsiveness after acute inhalation of ozone is related to the concentration and duration of ozone exposure. Using barometric whole-body plethysmography and increase in enhanced pause (Penh) as an index of airway obstruction, we measured the response of BALB/c mice to acute ozone inhalation to study the time course change of pulmonary function after ozone exposure. METHODS: Penh was measured before and after exposure to filtered air or 0.12, 0.5, 1, or 2 ppm ozone for 3 hr (n = 6/group). In addition, Penh was measured 24, 48 and 72 hr after ozone exposure. Bronchoalveolar lavage (BAL) and histopathologic examinations were performed. RESULTS: The increase in Penh after ozone exposure was significantly higher in the 0.12, 0.5, 1 and 2 ppm groups compared with the control group (all p < 0.01). Increases in Penh 24 hr after ozone exposure were significantly lower than those immediately after acute ozone exposure; however, increases in Penh 72 hr after ozone exposure were significantly higher than those in the control group (each p < 0.01). The proportion of neutrophils in BAL fluid was significantly higher in the group exposed to 2 ppm ozone than in the groups exposed to filtered air or 0.12 ppm ozone (both p < 0.01). CONCLUSION: These results indicate that airway obstruction is induced following ozone exposure in a concentration-dependent manner and persists for at least 72 hr.

Airway Obstruction↗
PubMed1997

Effects of ambient ozone exposures during the spring and summer of 1994 on pulmonary function of schoolchildren.

To investigate the effect of natural exposure to ambient ozone over time, a follow-up study of school-aged children was performed in two small towns in southwestern Germany (Freudenstadt and Villingen) between March and October of 1994. Ozone half-hour mean concentrations were measured continuously and pulmonary function was tested in each child on four occasions (April, June, August, and September). To obtain an average short-term ozone effect, we first analyzed the data from the four time points separately and then constructed a model that included all information. During the study period the median (5th to 95th percentile) of all half-hour values of the ozone concentration was 101 micrograms/m3 or 50.6 ppb (45-179 micrograms/m3 or 22.5-89.8 ppb) in Freudenstadt and 64 micrograms/m3 or 32.1 ppb (1 to 140 micrograms/m3 or 0.5-70.1 ppb) in Villingen. To assess the effects of an individual ozone exposure we related the highest ozone concentration in the respective 24 hours before lung function testing to the results of the subconcentration in the respective 24 hours before lung function testing to the results of the subsequent pulmonary function tests. In the lung function test following the highest ozone exposure, the results of our cross-sectional linear regression analysis showed a significant negative correlation (P = 0.0181) between ozone exposure and forced vital capacity (FVC). In the longitudinal linear regression model we observed a negative statistical correlation between ozone exposure and lung function for the subpopulation living in the town with the high ozone levels (Freudenstadt). The association was more pronounced in boys than girls. For the children in Freudenstadt the decrement of FVC was -12.31 ml/10 micrograms/m3 ozone and the decrease in the forced expiratory volume in 1 second (FEV1) was -11.29 ml/10 micrograms/m3 ozone.

Air Pollutants↗
PubMed1996

Reaction of ozone with enzymes of erythrocyte membranes.

Ozone is a widespread component of polluted air. It is the cause of many adverse effects on the lung such as decreased athletic performance and exacerbation of asthma. Ozone inactivated acetylcholine esterase (AChE) both in intact washed human erythrocytes and in ghosts prepared from the erythrocytes. This is consistent (a) with the location of AChE on the outer face of the membrane and (b) with the change in structure of AChE when amino acids were oxidized. The glyceraldehyde-3-phosphate dehydrogenase (G3PDH) of intact washed erythrocytes was unaffected by ozone. However, ozone severely inactivated G3PDH of ghosts, much more severely than AChE in ghosts. This result raised questions about the relative permeability of intact erythrocytes and ghosts and also about the inherent susceptibility of the two enzymes. Inhibition of the ozone-treated erythrocyte AChE with the competitive inhibitor trimethyl-(p-aminophenyl) ammonium chloride was measured. The inhibited enzyme had a higher K(M) and slightly lower Vmax than the control. Ozone did not affect the K(M) of the uninhibited enzyme but decreased the K(M) of the inhibited enzyme. Ozone decreased the Vmax of both the inhibited and the uninhibited enzyme. The K(I) was unchanged by the treatment with ozone. This suggested that the active site of the enzyme was not affected by ozone, but other features of the protein were changed by ozone. The effects of products of lipid ozonolysis [hydrogen peroxide, nonanal, and 1-palmitoyl-2-(9-oxononanyl)-sn-3-glycerophosphorylcholine (PN1PC)] were tested on the ghost preparations. The ozonolysis products were tested at concentrations equivalent to calculated amounts that could have been produced by ozone. Hydrogen peroxide had no effect on the G3PDH and AChE. Nonanal slightly increased the permeability of the ghost membrane, as judged by the increase in rate of G3PDH in the absence of Triton X-100, but did not inhibit enzyme activity. PN1PC increased the permeability of the ghosts, as judged by the increase in rate of G3PDH in the absence of Triton X-100. There was also an increase in the activity of G3PDH in the presence of Triton X-100. AChE was not inhibited by ozone in the presence or absence of Triton X-100.

Acetylcholinesterase↗
PubMed1995

Environmental ozone field study on pulmonary and subjective responses of assumed risk groups.

Lung function parameters (measured with a body plethysmograph) and subjective votes on irritations of eyes or airways were taken from subjects belonging to four assumed ozone risk groups and one control group (40 subjects each: senior citizens, juvenile asthmatics, forestry workers, athletes, and clerks). Every subject was examined on 8 days both in the morning and in the afternoon. The intention was to obtain an equal distribution of measuring days with elevated and low ozone concentrations, respectively, for each subject. On average the ozone concentrations reached 0.070 ppm on "ozone days" [maximum concentration 0.112 ppm for clerks (outdoors), 0.100 ppm for senior citizens, 0.091 for juvenile asthmatics, 0.086 ppm for athletes, and 0.077 ppm for forestry workers] and 0.028 ppm on "control days" (minimum 0.001 ppm). The results show no relevant ozone effect for the group with the lowest ventilation rate (senior citizens) and only marginal reductions of respiratory flows and volumes for athletes. Pulmonary decrements of juvenile asthmatics on ozone days were small but larger than those documented in the literature for healthy children. Forestry workers and clerks had significantly higher airway resistances on ozone days, although having been exposed to the lowest ozone concentrations of all groups. Thus, on days with moderately elevated levels of ozone in the environment it is assumed that ozone itself has a minor influence on pulmonary responses compared to that of other constituents of the air in certain locations like in forests or indoors on these days. These could be reaction products of ozone with motor tool exhausts in the case of forestry workers or substances originating from ozone deposition on the surfaces of the offices.

Adolescent↗
PubMed1997

Mortality in the elderly and ambient ozone concentration during the hot summer, 1994, in Belgium.

Extensive investigations were carried out to study the relationship between daily mortality in the elderly, outdoor air temperature, and ozone concentration observed in Belgium during the hot summer, 1994. The two environmental variables were assessed through mean daily temperature and 24-hr ozone concentration, both measured the day before and averaged over the country. Data were stratified by terciles of mean daily temperature in order to reduce the degree of collinearity between the investigated environmental variables. In the first stratum, which ranged from 9.9 to 15.4 degrees C (41 days), mean daily temperature and 24-hr ozone concentration were not correlated while the mean number of daily deaths was higher when 24-hr ozone concentration increased from 45 to 55 micrograms/m3 (P < 0.05). In the second stratum, which ranged from 15.6 to 20.3 degrees C (42 days), mean daily temperature and 24-hr ozone concentration were strongly correlated (r = 0.54, P < 0.0001). In this stratum, the number of daily deaths did not depend on the mean daily temperature but increased linearly with 24-hr ozone concentration within the range 25 to 85.5 micrograms/m3 (P < 0.001). After having examined the possible confounding effect of sulfur dioxide, nitrogen dioxide, fine particulates, and humidity, ozone was found to be the only investigated variable contributing to the increased daily mortality. In the third stratum, which ranged from 20.4 to 27.6 degrees C (40 days), mean daily temperature and 24-hr ozone concentration were also strongly correlated (r = 0.71, P < 0.0001). Daily mortality, in this stratum, was correlated more with mean daily temperature (r = 0.68, P < 0.001) than with 24-hr ozone concentration (r = 0.55, P < 0.001). Nonparametric regression analyses were performed to model the number of daily deaths in the whole range of temperatures. These analyses confirmed the effect of 24-hr ozone concentration on daily mortality already uncovered by the least-squares regression analysis in the second stratum of mean daily temperature. In addition, at levels exceeding 20 degrees C, the effect of ozone concentration on daily mortality was enhanced by temperature owing to a positive interaction between these two variables. The present study thus demonstrated a statistical association between daily mortality, observed in the elderly during the hot summer, 1994, in Belgium, and ambient ozone concentration. This relationship was dependent on the range of temperatures.

Aged↗
PubMed2000

Effects of taurine on ozone-induced memory deficits and lipid peroxidation levels in brains of young, mature, and old rats.

To determine the antioxidant effects of taurine on changes in memory and lipid peroxidation levels in brain caused by exposure to ozone, we carried out two experiments. In the first experiment, 150 rats were separated into three experimental blocks (young, mature, and old) with five groups each and received one of the following treatments: control, taurine, ozone, taurine before ozone, and taurine after ozone. Ozone exposure was 0.7-0.8 ppm for 4 h and taurine was administered ip at 43 mg/kg, after or before ozone exposure. Subsequently, rats were tested in passive avoidance conditioning. In the second experiment, samples from frontal cortex, hippocampus, striatum, and cerebellum were obtained from 60 rats (young and old), using the same treatments with 1 ppm ozone. Results show both an impairment in short-term and long-term memory with ozone and an improvement with taurine after ozone exposure, depending on age. In contrast to young rats, old rats showed peroxidation in all control groups and an improvement in memory with taurine. When taurine was applied before ozone, we found high peroxidation levels in the frontal cortex of old rats and the hippocampus of young rats; in the striatum, peroxidation caused by ozone was blocked when taurine was applied either before or after ozone exposure.

Aging↗
PubMed2006

The pharmacological effects of ozone on isolated guinea pig tracheal preparations.

Ozone is a potent oxidizing agent with a variety of potential uses, including its antimicrobial and deodorising properties. The recent increased use of ozone led to questions regarding its safety in humans. This study specifically focussed on the in vitro effect of ozone on isolated guinea pig tracheal tissue as well as its effect on the isolated trachea in the presence of various drugs with well-known effects, including methacholine and isoproterenol. The results found in this study identified two direct effects on the isolated trachea due to ozone exposure: (1) a definite contraction of the isolated trachea immediately after exposure to ozone, and (2) a clearly visible and significant hyper responsiveness of the isolated trachea to irritants, e.g. methacholine. Although ozone has a negative effect on the trachea, it was concluded that ozone has no adverse effect on muscarinic receptors. We found that ozone has a significant desensitizing effect on the pharmacological response of beta sympathomimetics (isoproterenol), while isoproterenol itself has a relaxing effect on the ozone-induced contraction of the isolated trachea. Observations in this in vitro study further emphasised that ozone does have a negative effect on respiratory health. It is underlined that the inhalation of ozone should be avoided by workers who are often in contact with the gas, and especially by those with existing airway diseases. An apparent EC(50) value of ozone on the trachea was established by two different methods as 5.71 and 9.78 x 10(-3 )M, respectively.

Animals↗