Ppm O3 Research Articles

Prenatal Exposure to Ozone Disrupts Cerebellar Monoamine Contents in Newborn Rats

Ozone (O3) is widely distributed in environments with high levels of air pollution. Since cerebellar morphologic disruptions have been reported with prenatal O3 exposure, O3 may have an effect on some neurotransmitter systems, such as monoamines. In order to test this hypothesis, we used 60 male rats taken from either, mothers exposed to 1 ppm of O3 during the entire pregnancy, or from mothers breathing filtered and clean air during pregnancy. The cerebellum was extracted at 0, 5, and 10 postnatal days. Tissues were processed in order to analyze by HPLC, dopamine (DA) levels, 3,4 dihydroxyphenilacetic acid (DOPAC) and homovanillic acid (HVA), norepinephrine (NA), serotonin, and 5-hydroxy-indole-acetic acid (5-HIAA) contents. Results showed a decrease of DA, NA, DOPAC and HVA mainly in 0 and 5 postnatal days. There were no changes in 5-HT levels, and 5-HIAA showed an increase after 10 postnatal days. DOPAC + HVA/DA ratio showed changes in 0 and 10 postnatal days, while 5-HIAA/5-HT ratio showed a slight decrease in 0 days. The data suggest that prenatal O3 exposure disrupts the cerebellar catecholamine system rather than the indole-amine system. Disruptions in cerebellar NA could lead to ataxic symptoms and also could limit recovery after cortical brain damage in adults. These finding are important given that recovery mechanisms observed in animals are also observed in humans.

BREATH CONDENSATE LEVELS OF 8-ISOPROSTANE AND LEUKOTRIENE B4 AFTER OZONE INHALATION ARE GREATER IN SENSITIVE VERSUS NONSENSITIVE SUBJECTS

Ozone (O3) inhalation induces pulmonary function decrements and inflammation. The present study was designed to determine if a relationship exists between O3 induced pulmonary function changes and the presence of inflammatory markers as measured in exhaled breath condensates (EBCs) obtained from O3-sensitive and nonsensitive human subjects. Eight healthy adult volunteers (4 males/4 females, age 18 to 30 years) were studied, characterized as to their ozone sensitivity and placed into 2 groups (sensitive and nonsensitive) with each group having 2 males and 2 females. Subjects completed a 20-minute EBC collection and pulmonary function test (PFT) prior to a single 60-minute bout of cycle ergometer exercise (VE = 50–55 L/min) while breathing filtered air (FA) or 0.35 ppm O3. Subjective symptom scores (SSSs) were collected at 6, 20, 40, and 60 minutes during exposure. An immediate postexposure PFT was performed followed by an EBC collection. Subjective symptom scores, EBCs, and PFTs were collected at 1, 4 and 8 hours post exposure. EBCs were analyzed for prostaglandin E2 (PGE2), leukotriene B4 (LTB4), 8-isoprostane, and total nitric oxide (NO) metabolites (nitrate + nitrite content). Sensitive subjects, breathing O3, had significantly greater functional decrements in PFTs, increased SSSs, and increased rapid shallow breathing as well as elevated levels of 8-isoprostane and LTB4 in EBCs compared to those breathing FA. In addition, there were significant increases in nitrate + nitrite content in both sensitive and nonsensitive subjects breathing O3compared to FA. These results indicate that sensitive subjects have elevated arachidonic acid metabolites in EBCs compared to nonsensitive subjects after O3 inhalation.

Acute Pulmonary Function Response to Ozone in Young Adults As a Function of Body Mass Index

Recent studies have shown enhanced responsiveness to ozone in obese mice. Adiposity has not been examined as a possible modulator of ozone response in humans. We therefore examined the relationship between body mass index and the acute spirometric response to ozone (O3) exposure among 197 nonasthmatic young adults (aged 18–35 yr) studied in our human exposure facility from 1992 to 1998. Each subject had been exposed to 0.42 ppm O3 for 1.5 h with intermittent exercise designed to produce a minute ventilation of 20 L/min/m2 body surface area (BSA). Spirometry (pulmonary function) was measured pre- and immediately postexposure to determine acute ozone-induced changes. The decrement in forced expiratory volume in 1s (ΔFEV1) as percent of baseline was significantly correlated with BMI, r = −0.16, p = .03, with a slightly stronger correlation in women (n = 75), r = −0.22, p = .05, and no significant correlation in men. BMI had a greater range in women than in men in our study. In women greater ozone-induced decrements were seen in overweight (BMI > 25 kg/m2) than in normal weight (BMI 18.5 to 25 kg/m2), and in normal weight than in underweight (BMI < 18.5 kg/m2) for all spirometric variables considered (p trend ≤ .022). Although our population studied was predominantly normal weight, we found that higher body mass index may be a modest risk factor for adverse pulmonary effects associated with ozone exposure, especially for women.

Human Pulmonary Responses with 30-Minute Time Intervals of Exercise and Rest When Exposed for 8 Hours to 0.12 PPM Ozone Via Square-Wave and Acute Triangular Profiles

compared pulmonary function responses during 8-h square-wave exposures to FA and to 0.12 ppm O3, as well as to an acute triangular exposure to a mean O3 concentration of 0.12 ppm. With 30 min of moderate exercise each hour during 8 h of continuous exposure, significantly greater pulmonary function responses were observed between 5 h and 7 h when O3 was varied in an acute triangular configuration from 0.00 ppm to 0.24 ppm over the first 4 h and back to 0.00 ppm during the last 4 h than when O3 concentration was maintained constant at 0.12 ppm throughout. These investigators employed equal periods of 30 min of exercise, in which mean VE was ∼40 L/min, and 30 min of rest, with pulmonary function measurements taken at the end of each hour. This procedure (i.e., taking measurements at the end of each hour) could attenuate the full effect that would be observed very soon after exercise cessation, and permit some recovery to occur. Accordingly, in the present study, the primary objective was to determine what effect observations of pulmonary responses assessed immediately following repeated 30 min exercise bouts, as well as those at the end of each hour (following ∼30 min rest) during 8-h square-wave exposures to FA and to 0.12 ppm O3, as well as to an acute triangular exposure to a mean O3 concentration of 0.12 ppm. During the last 4 h of the 8-h, 0.12-ppm square-wave exposure, the 30-min mean increases in FEV1.0 responses were consistently greater at the end of the first half hour immediately following exercise (−1.22%) than at the end of the second half-hour following 30 min of rest (+0.01%). Further, even though O3 concentration was steadily decreasing from 0.24 ppm to 0 ppm during the last 4 h of the triangular exposure, similar increases in FEV1.0 decrement (−1.38%) immediately after each 30 min exercise bout, and small recovery at the end of each 30 min rest (+0.56%) were observed. Symptom scores in both exposures during the last 4 h also showed this effect.

Comparison of Chamber 6.6-h Exposures to 0.04–0.08 PPM Ozone via Square-wave and Triangular Profiles on Pulmonary Responses

It has become increasingly well realized that laboratory simulations of air pollution risk assessment need to employ O3 concentration profiles that more accurately mimic those encountered during summer daylight ambient air pollution episodes. The present study was designed to compare the pulmonary function and symptoms of breathing discomfort responses to a 6.6-h square-wave 0.08-ppm O3 chamber exposure to those observed in a triangular O3 exposure profile (mean of 0.08 ppm), as well as to both a 0.06-ppm square-wave and triangular mean 0.06-ppm exposure, and to those observed during a triangular mean 0.04-ppm exposure and to a filtered air (FA) square-wave exposure. Thirty young adults (15 of each gender) served as subjects, each completing all exposures. While the 6.6-h postexposure responses to the acute triangular exposure to a mean O3 concentration of 0.08 ppm did not differ significantly from those observed in the square-wave exposure, forced expiratory volume in 1 s (FEV)1.0 and total symptoms severity (TSS) were significantly different from preexposure at 4.6 h (when O3 concentration was 0.15 ppm) in the triangular exposure, but not until 6.6 h in the square-wave exposure. Thus, significant pulmonary function and symptoms responses were observed over a longer period in the triangular exposure protocol at a mean O3 concentration of 0.08 ppm. These results support previous evidence that O3 concentration has a greater singular effect in the total inhaled O3 dose than do VE and exposure duration. Subtracting pulmonary function effects consequent to O3 exposure to existent 8-h average background levels (e.g., ∼0.04 ppm, rather than those observed in FA exposures) from those observed at higher concentrations (e.g., ∼0.08 ppm) represents a means of focusing the regulatory effort on effects that can be controlled. The greatest pulmonary function and symptoms responses observed for a 0.04-ppm triangular exposure were nearly the same as those for the FA square-wave exposure. Thus, results of the present study show that calculating the net pulmonary function effect of exposure to 0.08 ppm with “correction” for FA response, or for that incurred for 0.04 ppm O3, does not result in any statistically significant difference.

Changes in the carbon dioxide expirogram in response to ozone exposure

The objectives of this study were to quantify pulmonary responses to ozone (O3) exposure by parameters computed from the carbon dioxide expirogram and to compare these responses to decrements in forced expired spirometry. Anatomical dead space (VD) was determined from the pure dead space and transition regions of the expirogram. Four alternative parameters were computed from the alveolar plateau: slope (S), normalized slope (NS), peripheral cross-sectional area (AP) and well-mixed peripheral volume (VMP). Forty-seven healthy nonsmokers (25 men and 22 women) participated in two research sessions in which they exercised on a cycle ergometer for 1 h while orally inhaling either room air at a minute ventilation of 30.6 +/- 3.6 L or room air mixed with 0.252 +/- 0.029 ppm O3 at a minute ventilation of 29.9 +/- 3.7 L. Carbon dioxide expirograms were measured before exposure, 10 min after exposure and 70 min after exposure. Percent changes (mean +/- SD) in expirogram parameters were significant (P < or = 0.002) at both 10 and 70 min after O3 exposure: VD(-4.2 +/- 5.1, -3.3 +/- 6.9), S(16.4 +/- 17.9, +15.1 +/- 20.2), NS(17.5 +/- 15.4, +15.9 +/- 19.2), AP(-8.1 +/- 7.6, -7.7 +/- 9.8) and VMP(-15.4 +/- 13.0, -13.0 +/- 15.2). Percent decrements of forced expired volume in one second (FEV1) were also significant at both 10 min (-13.3 +/- 13.4) and 70 min (-11.1 +/- 9.2) following O3 exposure. Changes in the expirogram as well as decrements in FEV1 were not significant at either time point after air exposure. Thus, the CO2 expirogram is useful for characterizing the effect of O3 exposure on gas transport, and for supplementing forced expired spirometry that is frequently used to quantify lung mechanics.

Sputum Induction and Bronchoscopy for Assessment of Ozone-Induced Airway Inflammation in Asthma

Neutrophilic airway inflammation, as defined by cell counts in respiratory tract lining fluid (RTLF), is a key end point in many studies of respiratory toxicity in both healthy and asthmatic subjects. BAL and sputum induction (SI) are the most common methods of sampling RTLF in such studies. However, the comparability of these methods (BAL and SI) after experimental treatment has not been investigated in a head-to-head controlled trial. To determine whether BAL and SI are comparable and can be used in place of each other in the assessment of neutrophilic airway inflammation after ozone (O(3)) exposure, we exposed 13 asthmatic subjects to either 0.2 ppm of O(3) or filtered air (FA) followed by either BAL or SI. Subjects then underwent the alternate (O(3) or FA) exposure followed by the same method of RTLF sampling. Next, subjects repeated the same exposure protocol with the alternate method of RTLF sampling. Differences in inflammatory indexes including the percentage of polymorphonuclear neutrophils (%PMNs) between the exposures were then correlated by regression analysis. The %PMNs in sputum was poorly correlated with that in BAL fluid (R = 0.12). The correlation between the %PMNs in sputum and in the bronchial fraction of BAL (BFx) fluid, however, was somewhat higher (R = 0.50). Furthermore, the uncertainty of the estimate of %PMN values in BFx fluid and BAL fluid based on those of sputum values, using regression models, was almost as great as the magnitude of the O(3) effect itself (ie, 9.7% and 5.5% estimate errors for O(3) effects of 17.0% and 7.5%, respectively). We concluded that SI and BAL indexes are not directly interchangeable in the assessment of O(3)-induced airway inflammation in asthmatic subjects.

Repeated Exposure to Ozone Increases Alveolar Macrophage Recruitment into Asthmatic Airways

Repeated, short-term exposures to ozone (O3) lead to attenuation of the acute lung function and airway inflammatory responses seen after a single exposure in healthy subjects, but it is unclear whether these acute responses also attenuate in subjects with asthma. To address this question by exposing 14 subjects with asthma to 0.2 ppm O3 for either 4 hours on a single day or 4 hours on 4 consecutive days (multiday [MD]). At least 3 weeks later, subjects underwent the alternate exposure. Spirometry was performed immediately pre- and postexposure and bronchoalveolar lavage (BAL) was obtained 18 hours after each exposure. The decrease in FEV1 was greatest across Day 2 of the MD (MD2) exposure and then gradually declined on successive days of the MD exposure (mean +/- SD decrease in FEV1 of 25.4 +/- 18.0% across MD2 compared with 4.2 +/- 6.5% across MD4). Respiratory symptoms followed a similar pattern to that of FEV1. Although the concentration of neutrophils in BAL after the MD4 exposure was not significantly different from that after the single-day exposure (1.7 +/- 1.3 x 10(4) cells/ml vs. 1.2 +/- 0.8 x 10(4) cells/ml, p = 0.20), the concentration of alveolar macrophages did significantly increase in BAL after the MD exposure (19.9 +/- 9.7 x 10(4) cells/ml after MD4 vs. 12.1 +/- 6.4 x 10(4) cells/ml after the single day). Alveolar macrophages are recruited to the airways of subjects with asthma with repeated short-term exposures to O3, suggesting a possible role for these cells in the chronic response to oxidant-induced injury.

A multi-parent assignment method for analyzing atmospheric chemistry mechanisms

Abstract A new chemical mechanism analysis tool known as multi-parent assignment (MPA) is used to explore reactant contributions to ozone formation in the SAPRC-99 atmospheric chemistry mechanism. Mathematical details of MPA, which extends an earlier method by accounting for multiple reactants, are presented. MPA uses reaction rate information and mechanism stoichiometry to trace reaction pathways within a mechanism from products back to parent reactants. The net contribution of different reactants to products, such as O3 or OH, is then determined. Three formulas for assigning products among multiple reactants in a reaction are defined and compared. MPA analysis of an urban ozone formation scenario at three different NOx levels shows that all individual reactants contribute in some degree to ozone formation. NO and NO2 contributions vary greatly depending on VOC/NOx ratio and on how parent reactants are weighted in individual reactions. The most productive hydrocarbons on a ppm O3 per ppmC basis are generally aldehydes, followed by alkenes and higher aromatics, and then alkanes and lower aromatics. Reactant contributions to ozone are shown to vary with time, and shifts in limiting reactant behavior are also observed.

Elimination of Listeria monocytogenes Biofilms by Ozone, Chlorine, and Hydrogen Peroxide

This study evaluated the efficacy of ozone, chlorine, and hydrogen peroxide to destroy Listeria monocytogenes planktonic cells and biofilms of two test strains, Scott A and 10403S. L. monocytogenes was sensitive to ozone (O3), chlorine, and hydrogen peroxide (H2O2). Planktonic cells of strain Scott A were completely destroyed by exposure to 0.25 ppm O3 (8.29-log reduction, CFU per milliliter). Ozone's destruction of Scott A increased when the concentration was increased, with complete elimination at 4.00 ppm O3 (8.07-log reduction, CFU per chip). A 16-fold increase in sanitizer concentration was required to destroy biofilm cells of L. monocytogenes versus planktonic cells of strain Scott A. Strain 10403S required an ozone concentration of 1.00 ppm to eliminate planktonic cells (8.16-log reduction, CFU per milliliter). Attached cells of the same strain were eliminated at a concentration of 4.00 ppm O3 (7.47-log reduction, CFU per chip). At 100 ppm chlorine at 20°C, the number of planktonic cells of L. monocytogenes 10403S was reduced by 5.77 log CFU/ml after 5 min of exposure and by 6.49 log CFU/ml after 10 min of exposure. Biofilm cells were reduced by 5.79 log CFU per chip following exposure to 100 ppm chlorine at 20°C for 5 min, with complete elimination (6.27 log CFU per chip) after exposure to 150 ppm at 20°C for 1 min. A 3% H2O2 solution reduced the initial concentration of L. monocytogenes Scott A planktonic cells by 6.0 log CFU/ml after 10 min of exposure at 20°C, and a 3.5% H2O2 solution reduced the planktonic population by 5.4 and 8.7 log CFU/ml (complete elimination) after 5 and 10 min of exposure at 20°C, respectively. Exposure of cells grown as biofilms to 5% H2O2 resulted in a 4.14-log CFU per chip reduction after 10 min of exposure at 20°C and in a 5.58-log CFU per chip reduction (complete elimination) after 15 min of exposure.

The innate immune surfactant protein (SP)-D plays a protective role in ozone (O3)-induced airway inflammation in mice

RATIONALE: The pulmonary surfactant protein SP-D may be an an important modulator of immune and inflammatory responses in the lung. O3 is a common air pollutant associated with exacerbation of asthma and chronic obstructive pulmonary disease. We hypothesized that SP-D plays a protective role the inflammatory response to acute ozone exposure. METHODS: C57BL/6 wild type mice were exposed to 3.0 ppm O3 for 6h. 2, 6, 12, 24, 48 and 72h post-exposure, lung function was assessed by whole body plethysmography. Broncho-alveolar lavage (BAL) cellular influx was quantified using cytospin preparations and inflammatory cytokine/chemokine and SP-D levels were measured by ELISA. The role of SP-D was investigated in 6-8 weeks old SP-D-/- and wild-type mice exposed to 0.5 ppm ozone for 24 hours. RESULTS: O3 exposure elicited a time-dependent increase in airway responsiveness, neutrophil, lymphocyte and macrophage influx with a peak 12-24h post-O3. These were preceded by release of IL-6, IL-12 IL-17, GM-CSF and KC, 2-6h after O3 treatment. Significant elevation of SP-D levels in the BAL (p<0.001, n=6) occurred in parallel with resolution of airway inflammation 48h post O3. O3 exposure of SP-D deficient mice resulted in a significantly greater number of neutrophils in the BAL and a delayed resolution of inflammation in comparison with wild-type controls (p<0.05, n=6). CONCLUSIONS: Elevation of SP-D levels in the lung is associated with resolution of the inflammatory changes after O3-induced acute oxidative stress. Absence of SP-D in gene deficient mice enhances and prolongs neutrophilia in the lung following ozone exposure.

Effect of 0.25 ppm Ozone exposure on pulmonary damage induced by bleomycin

To study the effect of ozone in a chronically damaged lung, we used a bleomycin (BLM) induced pulmonary fibrosis model. Both endotracheal instillation of BLM and O3 exposure both produce lung inflammation and fibrosis. Oxidative stress would be a common mechanism of damage for both BLM and O3. Our aim was to assess lung injury induced by 5 and 60 days of intermittent exposure to 0.25 ppm O3 in rats with bleomycin-induced pulmonary fibrosis. Thirty-day-old Sprague Dawley rats were endotracheally instilled with BLM (1 U/100 g body weight) and, 30 days later, exposed to 0.25 ppm 03 (0.25 ppm 4 h per day, 5 days a week). Histopatology controls were instilled with saline and breathing room air. Histopathological evaluation of lungs was done 5 and 60 days after O3 exposure. BLM-induced lung damage did not change after 60 days of intermittent O3 exposure. Five days of O3 exposure increased the mean score of BLM-induced pulmonary inflammation and fibrosis (p=0.06). Frequency of bronchopneumonia increased from 1/7 to 6/6 (p <0.001), suggesting that a short-term exposure to O3 in a previously damaged lung might be a risk factor for developing further lung injury.

Uptake of Ozone in Human Lungs and Its Relationship to Local Physiological Response

To investigate whether intersubject variations in the dose of inhaled ozone (O3) cause corresponding variations in the physiological response, 28 female and 32 male nonsmokers participated in a 1-h continuous inhalation of clean air or 0.25 ppm O3 while exercising on a cycle ergometer at a constant ventilation rate of 30 L/min. The exposure protocols included continuous monitoring of respiratory flow rate and O3 concentration from which O3 uptake (OZU) and fractional uptake efficiency (UE) were computed. Pre-to-post changes in forced expired volume in 1 s (%ΔFEV1), peripheral cross section for carbon dioxide diffusion (%Δ AP), and Fowler dead space volume (VD) were also measured for each exposure. Individual values of UE ranged from.70 to.98 among all the subjects, with significant differences (p < .05) existing between men and women. These intersubject differences were inversely correlated with breathing frequency and directly correlated with tidal volume. The mean ± SD values of %Δ FEV1, %Δ AP, and %Δ VD were all significantly more negative in the O3 exposure session (−13.31 ± 13.40, −8.14 ± 7.62, and −4.20 ± 5.12, respectively) than in the air exposure session (−0.06 ± 4.56, 0.22 ± 10.82, and −0.70 ± 6.88, respectively). Finally, our results showed that neither %ΔFEV1 nor %Δ VD was correlated OZU, whereas there was a significant relationship (ρ = −0.325, p = .0257) between %Δ AP and OZU. We conclude that the overall uptake of O3 is a weak predictor of intersubject variations in distal airspace response, but is not a predictor of intersubject variations in conducting airway responses.

Role of interleukin-6 in murine airway responses to ozone

This study sought to examine the role of interleukin-6 (IL-6) in ozone (O(3))-induced airway injury, inflammation, and hyperresponsiveness (AHR). Subacute (72 h) exposure to 0.3 ppm O(3) significantly elevated bronchoalveolar lavage fluid (BALF) protein, neutrophils, and soluble TNF receptors (sTNFR1 and sTNFR2) in wild-type C57BL/6 (IL-6(+/+)) mice; however, all four outcome indicators were significantly reduced in IL-6-deficient (IL-6(-/-)) compared with IL-6(+/+) mice. Acute O(3) exposure (2 ppm for 3 h) increased BALF protein, KC, macrophage inflammatory protein(MIP)-2, eotaxin, sTNFR1, and sTNFR2 in IL-6(+/+) mice. However, MIP-2 and sTNFR2 were not significantly increased following O(3) exposure in IL-6(-/-) mice. Increases in BALF neutrophils induced by O(3) (2 ppm for 3 h) were also significantly reduced in IL-6(-/-) vs. IL-6(+/+) mice. Airway responsiveness to methacholine was measured by whole body plethysmography before and following acute (3 h) or subacute (72 h) exposure to 0.3 ppm O(3). Acute O(3) exposure caused AHR in both groups of mice, but there was no genotype-related difference in the magnitude of O(3)-induced AHR. AHR was absent in mice of either genotype exposed for 72 h. Our results indicate that IL-6 deficiency reduces airway neutrophilia, as well as the levels of BALF sTNFR1 and sTNFR2 following acute high dose and/or subacute low-dose O(3) exposure, but has no effect on O(3)-induced AHR.

AIR POLLUTION AND MARKERS OF CARDIOVASCULAR RISK

ISEE-19 Abstract: Air pollution has been associated with increased risk of death and hospital admissions all over the world. Many of those associations are from cardiovascular disease, however the mechanism by which airborne particles increases the risk of cardiovascular deaths is still being explored. We looked at the effects of medium term and long term (annual mean) of particulate air pollution (PM2.5), ozone (O3), carbon monoxide (CO), and nitrogen dioxide (NO2), and changes in blood markers of cardiovascular risk, including HDL cholesterol, triglycerides and C-reactive protein, in the PRINCE study, a large, national randomized trial of the use of statins to lower such risk factors. A total of 5778 participants were matched to exposure from monitors in their county of resident. We controlled for subject, trend, season, age, gender, race, body mass index, education, smoking history, hormone replacement therapy, exercise, and whether receiving a statin or a placebo. We found a medium term (mean of the two previous months) effect between C-reactive protein and PM2.5, CO, NO2, with an increase of 7.7% (95% CI: 0.96-14.96) for 10 mg/m3 of PM2.5, an increase of 3.8% (95% CI: 0.3-7.3) for 5 ppm of NO2, an increase of 2.1% (95% CI: 0.1-4.1) for 0.5 ppm of CO. When we examined interactions with statin use we found a higher increase in subjects on placebo. We found a significant association between triglycerides and the mean of the three previous months of ozone with an increase of 0.95% (95% CI: 0.1-1.8) for 5 ppm of O3. For the same time period for PM2.5, we found that the association was almost entirely in the subjects not receiving statins. In those subjects we found for the mean of the three previous months an increase of 8.3% (95% CI: 1.2-15.8). For HDL cholesterol we fund an association with a longer averaging period (annual mean) of pollution, with a –3% increase (95% CI:-5.7- -0.3) for 10 mg/m3 of PM2.5 and a –1% increase (95% CI:-1.7- -0.3) for 5 ppm of O3. These results present new the evidence of possible mechanism for the association between air pollution and cardiac events, and the cancellation of the effect by statins points to mechanistic pathways effected by statins.

Exposure to ozone enhances antigen-presenting activity concentration dependently in rats.

The effect of ozone (O(3)) on the symptoms of allergic asthma and the mechanisms underlying have not yet been fully elucidated. Antigen presentation is one of the factors contributing to the allergic reaction. Therefore, we investigated the effects of repeated exposure to O(3) on antigen-presenting (AP) activity, on the expression of cell-surface molecules associated with antigen presentation (Ia, B7.1, B7.2 and CD11b/c) in bronchoalveolar lavage cells (BAL cells), and on allergic asthma-like symptoms. Rats were exposed to 0.3, 0.56, 1ppm O(3) or filtered air for a 3-day period every 2 weeks, this was replicated three times. AP activity was assessed by measuring antigen-specific T-cell proliferation; and the expression of cell-surface molecules, by flow cytometry. Rats were also made to inhale aerosolized 1% ovalbumin (OVA) or saline for 10min post-exposure to O(3), and allergic asthma-like symptoms were measured by determining the increase in enhanced pause (Penh), which correlates well with lung resistance. O(3) increased both AP activity and expression of Ia and costimulatory molecules in BAL cells concentration dependently. It also increased lung resistance, and the increase in lung resistance after O(3) exposure was significantly higher in the OVA-inhaled group than in the saline-inhaled group. The present results show that O(3) increased AP activity concentration dependently and suggest that O(3) might aggravate allergy symptoms by enhancing AP activity.

Toxicity of Chemical Components of Fine Particles Inhaled by Aged Rats: Effects of Concentration

This study tested the hypothesis that exposure to mixtures containing fine particles and ozone (O3) would cause pulmonary injury and decrements in functions of immunological cells in exposed rats (22–24 months old) in a dose-dependent manner. Rats were exposed to high and low concentrations of ammonium bisulfate and elemental carbon and to 0.2 ppm O3. Control groups were exposed to purified air or O3 alone. The biological end points measured included histopathological markers of lung injury, bronchoalveolar lung fluid proteins, and measures of the function of the lung’s innate immuno-logical defenses (macrophage antigen-directed phagocytosis and respiratory burst activity). Exposure to O3 alone at 0.2 ppm did not result in significant changes in any of the measured end points. Exposures to the particle mixtures plus O3 produced statistically significant changes consistent with adverse effects. The low-concentration mixture produced effects that were statistically significant compared to purified air but, with the exception of macrophage Fc receptor binding, exposure to the high-concentration mixture did not. The effects of the low- and high-concentration mixtures were not significantly different. The study supports previous work that indicated that particle + O3 mixtures were more toxic than O3 alone.

The use of ozone in trout hatchery to reduce saprolegniasis incidence

At present, the prophylactic measures in trout hatchery are based on the use of formaldehyde. The purpose of this work is to set up an alternative system of prevention of saprolegniasis, using ozone. The experiment was carried out in two successive cycles. The first experiment lasted 46 days and five different treatments were applied on every second day on the same number of lots of 250 eggs each, of which three were treated with ozone (O3) in concentrations of 0.01, 0.03 and 0.2 ppm (10 min), one reference treatment with formaldehyde (1–2 ml/l, 15 min) and one as control, without any disinfectants. The second experiment, which lasted 60 days, consisted also of five levels of treatment on the same number of lots of 100 eggs each, to which 0.01 ppm O3 (10 min) was applied on every second day, while 0.01, 0.1 and 0.3 ppm O3 (10 min) were applied daily. The formaldehyde treatment was performed in the same way as the experiment 1 (exp. 1). From the results, it has emerged that the treatment with ozone is effective and the hatching eggs range from 42.6% to 49.1% dose of ozone from 0.01 to 0.2 ppm. As observed in experiment 2 (exp. 2), the dose of 0.3 ppm applied every second day seems to be over the threshold of toxicity.

Measurement of negative ion mobilities at atmospheric pressure in O2/O3 mixtures

AbstractIn a previous work, we measured the negative ion mobilities in O2 at atmospheric pressure. The obtained zero‐field mobility of $\hbox{O}^{-}_{2}$ in O2 agreed well with the results of Snuggs and co‐workers. However, we mentioned that the apparent zero‐field mobility tended to small values with increase of the drift length. This paper describes experimental results for the negative ion mobilities in O2/O3 mixtures. Ozone was generated in a silent discharge tube and the ozone concentration was varied from 10 ppm up to 1200 ppm. It was found that the negative ion mobilities become smaller with increases of the ozone concentration. When ozone was mixed above 10 ppm in O2, the mobility decreased rapidly. The apparent zero‐field mobility was 1.69 cm2/V·s at 300 ppm O3 and 1.52 cm2V·s at 1200 ppm O3. Within this range from 300 to 1200 ppm O3, the apparent zero‐field mobility decreased linearly with increases of the ozone concentration. This suggests that cluster ions are formed by some ion‐molecule reactions in the drift space. © 2001 Scripta Technica, Electr Eng Jpn, 138(3): 26–33, 2002

Impact of Ozonated Water on the Quality and Shelf-life of Fresh Citrus Fruit, Stone Fruit, and Table Grapes

Spores of fungi that cause postharvest decay of fresh fruit die rapidly in ozonated water. We determined the impact of sporocidal or higher O3 doses on fruit shelf-life and quality. Green mold and sour rot on citrus fruit, caused by Penicillium digitatum and Geotrichum citri-aurantii, respectively, were not reduced by 20 min immersion in 10 ppm O3. These fungi infect through wounds; their spores were placed in shallow wounds (l mm wide by 2 mm deep) 24 hr before treatment. On five peach varieties, the average natural incidence of brown rot, caused by Monilinia fructicola, was reduced from 10.9 to 5.4% by 1 min immersion in 1.5 ppm O3. A treatment of 15 min with 5 ppm O3 further reduced decay to 1.7%, but consistent control of brown rot was associated only with this severe treatment and it caused shallow pits on the fruit. Brown rot caused by spores placed in wounds before treatment was not controlled. Immersion for 1 or 5 min in 5 ppm O3 reduced natural aerobic bacteria populations by 1.1 and 1.6 log10 units, respectively, and yeast and filamentous fungal populations by 0.7 and 1.3 log10 units, respectively. Spores of Botrytis cinerea, cause of gray mold, were sprayed on table grape clusters, the clusters were dried, and then immersed for 1 to 6 min in 10 ppm O3. In two tests, immersion for 1 min in O3 reduced gray mold from 35% among untreated grapes to about 10%, while in two other tests the incidence was only reduced from 35 to 26%. Minor injury to the rachis of grape clusters occurred at high O3 rates. Immersion in ozonated water did not control postharvest decay of citrus fruit, injured peaches and nectarines at doses that reliably controlled decay, and on table grapes control was irregular and caused minor rachis injury at high rates.