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PubMed1995

Tropospheric ozone: respiratory effects and Australian air quality goals.

OBJECTIVE: To review the health effects of tropospheric ozone and discuss the implications for public health policy. DESIGN: Literature review and consultation with scientists in Australia and overseas. Papers in English or with English language abstracts were identified by Medline search from the international peer reviewed published reports. Those from the period 1980-93 were read systematically but selected earlier papers were also considered. Reports on ozone exposures were obtained from environmental agencies in the region. RESULTS: Exposure to ozone at concentrations below the current Australian air quality goal (0.12 ppm averaged over one hour) may cause impaired respiratory function. Inflammatory changes in the small airways and respiratory symptoms result from moderate to heavy exercise in the presence of ozone at levels of 0.08-0.12 ppm. The changes in respiratory function due to ozone are short lived, vary with the duration of exposure, may be modified by levels of other pollutants (such as sulphur dioxide and particulates), and differ appreciably between individuals. Bronchial lavage studies indicate that inflammation and other pathological changes may occur in the airways before reductions in air flow are detectable, and persist after respiratory function has returned to normal. It is not known whether exposures to ozone at low levels (0.08-0.12 ppm) cause lasting damage to the lung or, if such damage does occur, whether it is functionally significant. At present, it is not possible to identify confidently population subgroups with heightened susceptibility to ozone. People with asthma may be more susceptible to the effects of ozone than the general population but the evidence is not consistent. Recent reports suggest that ozone increases airway reactivity on subsequent challenge with allergens and other irritants. Animal studies are consistent with the findings in human populations. CONCLUSION: A new one hour air quality ozone goal of 0.08 ppm for Australia, and the introduction of a four hour goal of 0.06 ppm are recommended on health grounds.

Adaptation, Physiological↗
PubMed1992

Effect of an anti-Mo1 MAb on ozone-induced airway inflammation and airway hyperresponsiveness in dogs.

Ozone inhalation causes neutrophil migration into the airway and airway hyperresponsiveness in dogs. The leukocyte adhesion molecule Mo1 (CD11b/CD18) is a heterodimeric glycoprotein the expression of which is necessary for neutrophil adhesion to endothelium. To evaluate the contribution of Mo1 to ozone-induced neutrophil influx and airway hyperresponsiveness, six dogs were treated intravenously with an Anti-Mo1 monoclonal antibody (3.75 mg/kg in normal saline) that binds to both human and canine Mo1, or the diluent alone, 1.5 h before inhaling ozone (3 ppm for 30 min), or dry air. Airway responses to doubling doses of inhaled acetylcholine (ACh) were measured before and after inhalation of ozone. Neutrophil influx was assessed by bronchoalveolar lavage (BAL) performed after the second ACh inhalation. Treatment with anti-Mo1 prevented the ozone-induced influx of neutrophils into BAL. After diluent and inhaled dry air, the neutrophil count in BAL was 1.49 +/- 1.26 (SE) x 10(4) (5.0% of total cells). After diluent and inhaled ozone, the neutrophil count increased to 7.27 +/- 3.22 (SE) x 10(4) (22.6% of total cells) (P < 0.05). After anti-Mo1 and inhaled ozone, the neutrophil count was 1.48 +/- 0.62 (SE) x 10(4) (8.5% of total cells). Treatment with anti-Mo1 also significantly reduced the number of eosinophils in BAL after ozone. Ozone-induced ACh airway hyperresponsiveness was not prevented by treatment with anti-Mo1. These results indicate that expression of Mo1 is necessary for ozone-induced neutrophil migration into the airway lumen.

Acetylcholine↗
PubMed1995

Ozone exposure of human tracheal epithelial cells inactivates cyclooxygenase and increases 15-HETE production.

We assessed the immediate and prolonged effects of ozone on arachidonic acid (AA) metabolism by primary cultured human tracheal epithelial (TE) cells. TE monolayers were exposed at a gas-fluid interface to air or 0.1, 0.25, or 0.5 ppm ozone (15 min air, then 45 min air/ozone), and serially collected effluents were analyzed by thin-layer chromatography (TLC) and/or high-performance liquid chromatography. Release of prostaglandin E2 (PGE2) and AA, but not 15-hydroxyeicosatetraenoic acid (15-HETE) or its metabolites, was detected from cultures prelabeled with [14C]AA. PGE2 production, measured by immunoassay, was nearly constant during air exposure. In contrast, PGE2 increased two- to threefold during the first 15-min exposure to all concentrations of ozone, but then progressively declined to 78 +/- 17, 57 +/- 12 (P < or = 0.05), and 45 +/- 15% (P < or = 0.05) of air controls after exposure to 0.1, 0.25, and 0.5 ppm ozone. Ozone did not induce a new spectrum of AA metabolites; only PGE2, lesser amounts of PGF2 alpha, and 15-HETE were present in media and cell extracts of air- or ozone-exposed cultures provided with 30 microM exogenous AA. However, cyclooxygenase (CO) activity (PGE2 produced from 30 microM AA) decreased to 82 +/- 9, 53 +/- 8 (P < or = 0.05), and 28 +/- 6% (P < or = 0.05) vs. controls after 0.1, 0.25, and 0.5 ppm ozone, whereas 15-HETE production was unimpaired. When cells exposed to 0.5 ppm ozone were maintained for up to 6 h in 5% CO2-air, spontaneous PGE2 production remained decreased and recovery of CO activity was extremely slow. TLC analysis of lipid extracts from [14C]AA-labeled cells revealed a nearly twofold increase in free intracellular 15-HETE, and hydrolysis of phospholipids demonstrated increased esterified 15-HETE. Exposure of human TE cells to ozone leads to a transient increase followed by prolonged decrease in PGE2 production and increased intracellular retention of 15-HETE. Loss of the bronchodilator and anti-inflammatory properties of epithelial PGE2, with or without increased 15-HETE, might contribute to ozone-induced airway dysfunction.

Air↗
PubMed1998

Chemokine regulation of ozone-induced neutrophil and monocyte inflammation.

Pulmonary inflammation has been observed in humans and in many animal species after ozone exposure. Inflammatory cell accumulation involves local synthesis of chemokines, including neutrophil chemoattractants such as macrophage inflammatory protein-2 (MIP-2), and monocyte chemoattractants, such as monocyte chemoattractant protein-1 (MCP-1). To better understand the mechanism of ozone-induced inflammation, we exposed mice and rats to ozone for 3 h and measured MIP-2 and MCP-1 gene expression. In C57BL/6 mice, steady-state mRNA levels for MCP-1 in the lung increased at 0.6 parts/million (ppm) ozone and were maximal at 2.0 ppm ozone. After exposure to 2 ppm ozone, MIP-2 mRNA levels peaked at 4 h postexposure, whereas MCP-1 mRNA levels peaked at 24 h postexposure. Neutrophils and monocytes recovered in bronchoalveolar lavage fluid peaked at 24 and 72 h, respectively. The accumulation of monocytes was thus delayed relative to that of neutrophils, consistent with the sequential expression of the corresponding chemokines. The role of MCP-1 in monocyte accumulation was evaluated in greater detail in rats. Ozone caused an increase in monocyte chemotactic activity in bronchoalveolar fluid that was inhibited by an antibody directed against MCP-1. Ozone-induced MCP-1 mRNA levels were higher in lavage cells than in whole lung tissue, indicating that lavage cells are an important source of MCP-1. In these cells, nuclear factor-kappa B, a nuclear transcription factor implicated in MCP-1 gene regulation, was also activated 20-24 h after ozone exposure. These findings indicate that monocyte accumulation subsequent to acute lung injury can be mediated through MCP-1 and that nuclear factor-kappa B may play a role in ozone-induced MCP-1 gene expression.

Animals↗
PubMed1998

Potential involvement of 4-hydroxynonenal in the response of human lung cells to ozone.

Ozone is a photochemically generated pollutant that can cause acute pulmonary inflammation and induce cellular injury and may contribute to the development or exacerbation of chronic lung diseases. Despite much research, the mechanisms of ozone- and oxidant-induced cellular injury are still uncertain. Ozone and secondary free radicals have been reported to cause the formation of aldehydes in biological fluids. One of the most toxic aldehydes formed during oxidant-induced lipid peroxidation is 4-hydroxynonenal (HNE). HNE reacts primarily with Cys, Lys, and His amino acids, altering protein function and forming protein adducts. The purpose of this study was to determine whether HNE could account for the acute effects of ozone on lung cells. Human subjects were exposed to 0.4 parts/million ozone or air for 1 h with exercise (each subject served as his/her own control). Six hours after ozone exposure, cells obtained by airway lavage were examined for apoptotic cell injury, and cells from bronchoalveolar lavage were examined for apoptosis, presence of HNE adducts, and expression of stress proteins. Significant apoptosis was evident in airway lung cells after ozone exposure. Western analysis demonstrated an increase in a 32-kDa HNE protein adduct and a number of stress proteins, viz., 72-kDa heat shock protein and ferritin, in alveolar macrophages (AM) after ozone exposure. All of these effects could be replicated by in vitro exposure of AM to HNE. Consequently, the in vitro results and demonstration of HNE protein adducts after ozone exposure are consistent with a potential role for HNE in the cellular toxic effects of ozone.

Air Pollutants↗
PubMedDate not supplied

Antimicrobial effect of a novel ozone- generating device on micro-organisms associated with primary root carious lesions in vitro.

The aims of this present study were (1) to assess the antimicrobial effect of ozone from a novel ozone-generating device (Heolozone, USA) [0.052% (v/v) in air delivered at a rate of 13.33 ml.s(-1)] on primary root carious lesions (PRCLs) and (2) to evaluate the efficacy of ozone specifically on Streptococcus mutans and Streptococcus sobrinus. In study 1, 40 soft PRCLs from freshly extracted teeth were randomly divided into two groups to test the antimicrobial effect on PRCLs from exposure to ozonated water for either 10 or 20 s. Half of a lesion was removed using a sterile excavator. Subsequently, the remaining lesion was exposed to the ozonised water for a period of either 10 or 20 s (corresponding to 0. 069 or 0.138 ml of ozone, respectively). Using paired Student t tests, a significant (p<0.001) reduction (mean +/- SE) was observed in the ozone-treated groups with either a 10-second (log(10) 3.57+/-0.37) or 20-second (log(10) 3.77+/-0.42) ozone application compared with the control groups (log(10) 5.91+/-0.15 and log(10) 6.18+/-0.21, respectively). In study 2, 40 sterile saliva-coated glass beads were randomly divided into two groups for each micro-organism. One glass bead was put into each bijou bottle with 3 ml of Todd-Hewitt broth. S. mutans and S. sobrinus were inoculated anaerobically overnight. Each glass bead was then washed with 2 ml of phosphate-buffered saline. Immediately, 10 s of ozone gas was applied to each glass bead in the test groups. There was a significant (p<0.0001) reduction (mean +/- SE) in ozone-treated samples for S. mutans (log(10) 1.01+/-0.27) and S. sobrinus (log(10) 1.09+/-0.36) compared with the control samples (log(10) 3.93+/-0.07 and log(10) 4.61+/-0.13, respectively). This treatment regime is an effective, quick, conservative and simple method to kill micro-organisms in PRCLs. Ozone gas application for a period of 10 s was also capable of reducing the numbers of S. mutans and S. sobrinus on saliva-coated glass beads in vitro.

Anaerobiosis↗
PubMed1995

An important role of tachykinins in ozone-induced airway hyperresponsiveness.

We investigated the role of tachykinins in ozone-induced airway hyperresponsiveness (AHR) in guinea pigs. Airway responsiveness was assessed by determining the provocative concentration (PC200) of a histamine aerosol. Ozone exposure (3.0 ppm for 2 h) caused significant AHR. For vehicle-pretreated animals, the geometric mean pre- and post-ozone PC200 values were 0.87 mg/ml (GSEM 1.33) and 0.11 mg/ml (GSEM 1.17), respectively. Tachykinin depletion by capsaicin (50 mg/kg) prevented this AHR, whereas it did not alter pre-ozone airway responsiveness. The PC200 was 0.36 mg/kg (GSEM 1.64) before ozone and 0.24 mg/kg (GSEM 1.72) after ozone for this group. Ozone also caused a significant increase in neutrophils in bronchoalveolar lavage fluid (BALF) compared with BALF from a normal control group (1.71 +/- 0.69 versus 0.07 +/- 0.02 x 10(5)/ml, respectively). Capsaicin pretreatment attenuated this neutrophil influx (0.23 +/- 0.16 x 10(5)/ml). Morphometric assessment revealed edema of the bronchiolar wall after ozone exposure, which was not observed in the capsaicin group. BAL and morphometry revealed that the degree of ozone-induced epithelial desquamation was similar in both groups. These results suggest that tachykinins may be responsible for ozone-induced AHR, possibly via neurogenic inflammation.

Animals↗
PubMed2000

Neutrophil-dependent and neutrophil-independent alterations in the nasal epithelium of ozone-exposed rats.

Ozone induces epithelial hyperplasia and mucous cell metaplasia (MCM) in nasal transitional epithelium (NTE) of rats. A transient neutrophil influx accompanies upregulation of mucin messenger RNA (mRNA) before the onset of MCM. The present study was designed to examine the role of neutrophils in ozone-induced epithelial changes in the NTE of rats. Fourteen hours before inhalation exposure, male F344/N rats were injected intraperitoneally with antirat neutrophil antiserum to deplete circulating neutrophils, or were injected with normal (control) serum. Rats were then exposed to 0 ppm (filtered air) or 0.5 ppm ozone (8 h/d) for 1 or 3 d. Maxilloturbinates lined with NTE were analyzed to determine the epithelial labeling index; numeric densities of neutrophils, total epithelial cells, and mucous secretory cells; amount of stored intraepithelial mucosubstances; and steady-state ratMUC-5AC (mucin) mRNA levels. At 2 h after 3 d of exposure, rats treated with antiserum had 90% fewer circulating neutrophils than did rats treated with control serum. Antiserum-treated, ozone-exposed rats had 87% fewer infiltrating neutrophils than did control serum-treated, ozone-exposed rats. At 4 d after 3 d of exposure, antiserum-treated, ozone-exposed rats had 66% less stored intraepithelial mucosubstances and 58% fewer mucous cells in their NTE than did control serum-treated, ozone-exposed rats. Antiserum treatment had no effects on ozone-induced epithelial cell proliferation or mucin mRNA upregulation. The results of this study indicated that ozone-induced MCM was neutrophil-dependent, whereas ozone-induced epithelial cell proliferation and mucin gene upregulation were neutrophil-independent.

Animals↗
PubMed1990

Effect of exposures to ambient ozone on ventilatory lung function in children.

This study was undertaken to determine if the ventilatory capacity of children is affected by hourly concentrations of ozone inhaled during their daily activity. Over a 3-wk period (June-July 1987) children who were attending a summer camp in the San Bernardino mountains of California performed spirometry up to three times per day during their stay at the camp. A total of 43 children were tested a total of 461 times. Ozone, oxides of nitrogen, sulfur dioxide, temperature, and relative humidity were measured continuously. Daily average measurements of total suspended particulate and the PM10 particulate fraction (less than or equal to 10 microns) were also made. Hourly ozone concentrations at the time of testing varied between 20 and 245 ppb. Regressions of each individual's FEV1 and FVC supported the view that high ozone levels reduced these lung function parameters. The average regression coefficient for FEV1 on ozone was -0.39 ml/ppb (SEM = 0.12) and for FVC -0.44 ml/ppb (SEM = 0.15), both of which were significantly different from zero. Statistical allowance for temperature and humidity increased the magnitude of these slopes. Nitrogen dioxide never exceeded 40 ppb during the time of testing and averaged 13 ppb. Sulfur dioxide's highest measurement was 8 ppb and often was at the limit of detection. Neither NO2 nor SO2 was considered in the statistical modeling. Data were divided based on whether each subject had been exposed to levels of ozone in excess of the National Ambient Air Quality Standard (NAAQS) during the several hours previous to being tested. Exposures exceeding the NAAQS indicated a significant negative relationship between ozone and FEV1, FVC, and PEFR. Data for nonexceedance periods did not indicate this negative relationship for any of the three lung function parameters, but it could not be determined if this was due to an absence of an ozone effect or to a combination of the increased variability and decreased size of this data subset. These data indicate that lung function changes on a daily basis relate in a negative fashion to ambient ozone levels. The magnitude of the changes are small and are reversed as ambient ozone decreases.

Air Pollutants↗
PubMed1984

Neutrophil depletion inhibits airway hyperresponsiveness induced by ozone exposure.

We studied whether ozone-induced hyperresponsiveness could be inhibited by neutrophil depletion in dogs. Responsiveness was assessed with dose-response curves of acetylcholine aerosol versus pulmonary resistance; depletion was assessed by counting neutrophils in venous blood and in biopsies of the airway epithelium. Responsiveness and neutrophil numbers were determined 5 days and 1 day before ozone and 1 h after ozone (3.0 ppm, 2 h) in 6 untreated dogs and in 6 dogs treated with hydroxyurea (200 mg/kg daily for 5 days starting 5 days before ozone). In untreated dogs, responsiveness and neutrophil numbers 5 days and 1 day before ozone did not change, but responsiveness and epithelial neutrophils increased markedly after ozone. In treated dogs, circulating neutrophils decreased from 8.9 +/- 2.2 to 0.6 +/- 0.01 X 10(3) per mm3 (mean +/- SEM), and responsiveness before ozone did not change. Furthermore, increases in responsiveness and epithelial neutrophils did not occur after ozone. Six wk after stopping hydroxyurea, responsiveness and epithelial neutrophils increased markedly after ozone. The results suggest that ozone-induced hyperresponsiveness may depend on the mobilization of neutrophils into the airways.

Animals↗
PubMed2006

Low-level ozone exposure and respiratory symptoms in infants.

OBJECTIVE: Recent studies indicate that the U.S. Environmental Protection Agency (EPA) ozone standards may not protect sensitive individuals. In this study we examined respiratory effects of ozone in infants who may be vulnerable, particularly if they are children of asthmatic mothers. DESIGN: Women delivering babies at one of five hospitals in southwestern Virginia between 1994 and 1996 were invited to participate in a cohort study; 780 women enrolled. Ambient air quality data (ozone and particulate matter) were collected at a central monitoring site. PARTICIPANTS: This analysis is of 691 infants followed for approximately 83 days between 10 June and 31 August 1995 and/or 1996 ; they contributed a total of 52,421 infant-days of follow-up. Mothers were interviewed at enrollment and approximately biweekly to report infants' daily symptoms. Repeated measures logistic regression models were run separately for wheeze, difficulty breathing, and cough. Ozone metrics included 24-hr average, peak 1-hr, and maximum 8-hr average. Analyses were repeated for the 61 infants whose mothers had asthma. RESULTS: For every interquartile-range increase in same-day 24-hr average ozone, likelihood of wheeze increased 37% [95% confidence interval (CI), 2-84%]. Among infants of asthmatic mothers, same-day 24-hr average ozone increased likelihood of wheeze 59% (95% CI, 1-154%) and of difficulty breathing 83% (95% CI, 42-136%). Maximum 8-hr ozone and peak 1-hr ozone were associated with difficulty breathing, but not wheeze, in infants of asthmatic mothers. Ozone was not associated with cough. CONCLUSIONS: At levels of ozone exposure near or below current U.S. EPA standards, infants are at increased risk of respiratory symptoms, particularly infants whose mothers have physician-diagnosed asthma.

Cohort Studies↗
PubMed1993

Identification of subpopulations that are sensitive to ozone exposure: use of end points currently available and potential use of laboratory-based end points under development.

A number of epidemiological studies have attempted to assess the effect of recurrent ozone exposure in humans. For the most part, they have failed to document convincingly an association between chronic ozone exposure and differences in lung function performance or respiratory symptoms. This is not surprising given the small respiratory effects observed in animals chronically exposed to ozone and assuming that people with abnormal respiratory function resulting from other occupational or environmental exposures, such as tobacco smoke, would make up a much larger percentage of the population than people with respiratory effects attributable to ozone. Therefore, either more sensitive end points must be developed to detect subtle changes due to chronic ozone exposure, or ways of selecting subpopulations that are especially sensitive to ozone must be devised. It has been well documented that there are large and reproducible differences in the acute response of individuals to ozone as measured by pulmonary function tests. Recently, it has also been shown that there are large differences in the acute response of individuals to ozone as measured by inflammatory and other biochemical parameters. This paper discusses the problems of selecting individuals who are sensitive to ozone depending on the end point chosen. It also describes potential new sensitive end points that might be available for ozone epidemiology studies in the near future.

Biomarkers↗
PubMed2004

Effect of ozone exposure on airway responses to inhaled allergen in asthmatic subjects.

BACKGROUND: Controlled human exposure studies have produced conflicting results regarding the effect of ozone on the early bronchoconstrictor response to inhaled allergen in specifically sensitized asthmatic subjects. Spirometric parameters do not necessarily reflect the airway inflammatory effects of inhaled ozone or allergen. OBJECTIVE: This study was designed to investigate whether exposure to ozone enhances the late airway inflammatory response, as well as the early bronchoconstrictor response, to inhaled house dust mite allergen in sensitized asthmatic subjects. DESIGN: Randomized, counter-balanced, cross-over study. SETTING: Human exposure laboratory. METHODS: Fourteen subjects were exposed to 0.2 ppm O(3) or filtered air, on separate days, for 1 h during exercise. After each exposure, the subjects were challenged with doubling doses of Dermatophagoides farinae (DF) allergen (provocative concentration of DF causing a 15% decrease in FEV(1) [PC(15)]). At 6 h after allergen challenge, bronchoscopy with BAL, proximal airway lavage (PAL), and endobronchial biopsy were performed. The second exposure/allergen challenge/bronchoscopy sequence was performed at least 4 weeks after the first sequence. RESULTS: No significant difference in cellular or biochemical markers of the late inflammatory response after allergen was found between the ozone and air exposures (although a trend toward increased neutrophils was noted after ozone exposure in the PAL fluid, p = 0.06). For the group as a whole, no significant difference in PC(15) was demonstrated after ozone exposure compared to air exposure. However, subjects with the greatest ozone-induced decrements in FEV(1) tended to have lower PC(15) values after ozone exposure. CONCLUSION: Exposure to a relatively low-level concentration of ozone does not enhance the late inflammatory or early bronchoconstrictor response to inhaled antigen in most allergic asthmatic subjects. Our results do suggest, however, that a subgroup of asthmatics may acquire increased sensitivity to aeroallergens after exposure to ozone.

Administration, Inhalation↗
PubMed1980

Effects of long-term ozone exposure and dietary vitamin E in rats.

Rats fed on a vitamin E-deficient diet (E-depleted group) and a vitamin E-supplemented diet (E-supplemented group) were exposed to 0.3 ppm ozone for three hours daily, five days a week for seven months. Then animals from each group were sacrificed, and electron microscopic studies on the lung and biochemical examinations on the lung and liver were performed. 1) Vitamin E concentration in serum decreased following ozone exposure in the E-supplemented group, whereas it remained unaffected the E-depleted group. 2) Both TAB value and % release of lysosomal enzyme (acid phosphatase) of the liver were increased in vitamin E-depleted air-exposed rats, and showed even higher values following ozone exposure. Levels of both components were highest in the vitamin E-depleted ozone-exposed rats, thus demonstrating that there are a marked increase in lipid peroxide and the increased labilization of lysosomes in this instance. 3) Arachidonic acid (20:4) of total lipid, phospholipid and lecithin in the lung tissue showed a tendency to decrease in vitamin E-depleted air-exposed rats. Those in the ozone-exposed animals showed in both groups a tendency to increase in total lipid and lecithin, and to decrease in phospholipid. However, a change in the fatty acid composition following ozone exposure was generally mild. 4) The fatty acid composition of phospholipid in lung washings did not show a remarkable change following ozone exposure in either group, thus suggesting that it has the resistivity to oxidation. 5) Morphological observations on the lung with the scanning and transmission electron microscopes did not reveal any clear differences between the two groups. The defensive effect of vitamin E on ozone toxicity induced by long-term exposure to ozone was not made clear by the morphological or biochemical examination of the lung. However, biochemical findings in liver of rats exposed to ozone suggested the possibility that vitamin E deficiency permits the damaging effects of lipid peroxidation on biological membranes.

Animals↗
PubMedDate not supplied

[Total atmospheric ozone column above the territory of Serbia and Montenegro].

INTRODUCTION: Atmospheric ozone attenuates ultraviolet radiation reaching the Earth's surface. Since UV-B radiation is considered the principal factor of causing the skin cancers, cataracts and some immunological disorders, determination of total ozone column has become everyday practice. In Serbia and Montenegro, such determinations are not being done. Satellite data for the entire globe are accessible. OBJECTIVE: The objective of our work was to collect and analyze data for the territory of Serbia and Montenegro, because ozone is an important parameter for the study of effects and protection from UV radiation. METHODS: Data collected during TOMS (Total Ozone Measuring Spectrometer) experiment are presented for grid whose elements are 1 degrees latitude by 1.25 degrees longitude. Grid elements in which the territory of Serbia and Montenegro comprises more than 50% of the element area were taken to represent the territory of Serbia and Montenegro. Eleven grid elements were selected and average monthly values for 272 months in the period from 1978 until 2004 were collected. Data for the period between 1993 and 1996 were unavailable. RESULTS: Mean values of total ozone column and mean monthly values of eleven grid elements differed very little. Differences were smaller than magnitudes of random error. Average annual values of total ozone column above the territory of Serbia and Montenegro were in the range from 316 Dobson units (DU) in 2002 to 347 DU in 1981. Annual cyclic changes of total ozone column showed spring maxima and autumn minima. Maximal recorded monthly value was 421 DU in March 1987 and minimal monthly value was 271 DU in October 2001. There was a trend of decreasing total ozone column values in the period between 1979 and 1992 at the rate of approximately 4.5% per decade. CONCLUSION: Mean total ozone column value above the territory of Serbia and Montenegro can represent total ozone column for the whole territory. Annual cycles with spring maxima and autumn minima are in accordance with oscillations observed for middle northern latitudes. The trend showing 4.5% decrease per decade in the period between 1979 and 1992 corresponds well to trends calculated for comparable locations.

Atmosphere↗
PubMedDate not supplied

Taurine protects rat bronchioles from acute ozone-induced lung inflammation and hyperplasia.

Ozone is a potent respiratory irritant known to induce lung injury in humans and experimental animals. The present studies determined if ozone-induced lung inflammation was modified by pretreatment of animals with taurine, a detoxifying antioxidant. Rats were pretreated for 10 days with 5% taurine in their drinking water (controls received water only) prior to exposure to 2 ppm ozone for 3 h. At 2, 6, 12, 24, 48, and 72 h after ozone exposure, rats were anesthetized and the lungs were perfusion-fixed for histopathologic evaluation. An additional group of rats was used to examine bronchoalveolar lavage cell counts and hydroxyproline levels. A count of bronchoalveolar lavage cells 48 h after ozone exposure showed significantly fewer total inflammatory cells and fewer polymorphonuclear leukocytes accompanied by a reduction in hydroxyproline in the lavage fluid of ozone-exposed rats pretreated with taurine compared to rats that did not receive taurine. Light microscopy revealed an inflammatory cell infiltrate in the lungs of rats exposed to ozone. This was followed by focal hyperplasia in the terminal and respiratory bronchioles. Rats pretreated with taurine and then exposed to ozone showed none of these alterations. In addition, although there was a significant reduction in cell proliferation as measured by DNA precursor incorporation in the lungs of rats pretreated with taurine prior to ozone exposure compared to unsupplemented rats, the distribution of labeled cells was the same in taurine supplemented and unsupplemented groups. Also, significantly higher levels of taurine were found in the plasma, whole blood, and lavage fluid of rats pretreated with dietary taurine compared to rats that received water only. The results suggest that supplemental taurine protects rat lung epithelium from acute ozone-induced lung inflammation and hyperplasia.

Acute Disease↗
PubMed1988

Enhancement of allergic lung sensitization in mice by ozone inhalation.

Inhaled ozone was found to exert an enhancing effect for allergic lung sensitization when mice contracted an aerosolized allergen. The animals were exposed to ozone concentrations of 0.24, 0.16, 0.13, and 0.10 ppm. After 4 days of continuous ozone exposure, the mice had allergen contact from an aerosolized solution of ovalbumin. The animals were then maintained in ambient air for several days before the cycle of ozone and aerosolized allergen was repeated over four allergen contact cycles. Mice were rested in ambient air for a week after the last allergen contact, and they were then tested for allergic sensitization by the intravenous injection of 2 mg of ovalbumin to induce anaphylactic shock in allergic individuals. The control groups of mice were maintained in ambient air throughout the experiment, but they experienced identical allergen contact with the ozone-exposed mice. The phenomenon of allergic enhancement from ozone inhalation was detected at 0.24, 0.16, and 0.13 ppm of ozone. The enhancing effect disappeared at 0.10 ppm of ozone. The study indicated a potential for increasing the number of allergically sensitized individuals when various allergens are inhaled during periods of high ozone exposure with the consequent adverse changes on respiratory membranes. The significance to human health of the allergic enhancement phenomenon by ozone needs investigation.

Aerosols↗
PubMed2002

Inactivation of Escherichia coli O157:H7 on inoculated alfalfa seeds with ozonated water and heat treatment.

Alfalfa seeds inoculated with a five-strain mixture of Escherichia coli O157:H7 were immersed in water containing 4, 8, 10, and 21 ppm of ozone for 2, 4, 8, 16, 32, and 64 min at 4 degrees C. Direct ozone sparging of seeds in water was used as an alternative mode of ozone treatment. Ozone-sparged seeds were also subsequently exposed to heat treatment at 40, 50, and 60 degrees C for 3 h. Populations of E. coli O157:H7 on untreated and treated seeds were determined by spread plating diluted samples on tryptic soy agar supplemented with 50 microg/ml of nalidixic acid. Since E. coli O157:H7 was released from inoculated seeds during treatment with ozone, the rate of release of cells from inoculated seeds soaked in 0.1% peptone water for up to 64 min was also determined. The overall reduction of E. coli O157:H7 on seeds treated with ozonated water without continuous sparging ranged from 0.40 to 1.75 log10 CFU/g (59.6 to 98.2%), whereas reductions for control seeds were 0.32 to 1.03 log10 CFU/g (51.7 to 90.5%). Treatment with higher ozone concentrations enhanced inactivation, but contact time longer than 8 min did not result in significantly higher reductions (P > 0.05). For seeds treated by ozone sparging, a 1.12-log10 CFU/g (92.1%) reduction was achieved using a 2-min contact time, and a 2.21-log10 CFU/g (99.4%) reduction was achieved with a 64-min contact time. The corresponding reductions for control seeds were 0.71 log10 CFU/g (79.5%) and 2.21 log10 CFU/g (99.4%), respectively. Treatment of ozone-sparged seeds at 60 degrees C for 3 h reduced the population to an undetectable level by direct plating (4 to 4.8 log10 CFU/g), although survivors were detected by enrichment. Ozone did not have a detrimental effect on seed germination percentage.

Colony Count, Microbial↗