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PubMed1986

Effect of ozone and histamine on airway permeability to horseradish peroxidase in guinea pigs.

Airway permeability was studied in groups of male guinea pigs at 2, 8, and 24 h after a 1-h exposure to 1 ppm ozone or at 2 h after a 1-h exposure to filtered air (control). Intratracheal administration of 2 mg horseradish peroxidase (HRP) was followed by blood sampling at 5-min intervals up to 30 min. The rate of appearance of HRP in plasma was significantly higher at 2 and 8 h after ozone exposure than that found in animals examined 2 h after air exposure or 24 h after ozone exposure. A dose of 0.12 mg/kg of subcutaneous histamine given after the 15 min blood sample significantly increased the already elevated permeability seen at 2 h post ozone, but had no effect on animals exposed to filtered air 2 h earlier or to ozone 24 h earlier. No difference was seen in the amount of subcutaneous radiolabeled histamine in the lungs of animals exposed 2 h earlier either to air or to ozone. These data indicate that a short-term exposure to ozone produced a reversible increase in respiratory epithelial permeability to HRP in guinea pigs. The potentiation of this increased permeability by histamine may be another manifestation of ozone-induced hyperreactivity.

Animals↗
PubMed1987

DNA synthesis in pulmonary alveolar macrophages and type II cells: effects of ozone exposure and treatment with alpha-difluoromethylornithine.

An increase in the number of pulmonary alveolar macrophages (AM) can be induced by a number of toxic insults to the lung, including ozone, an important photochemical oxidant air pollutant. This increase could arise from an influx of monocytes from the vascular or interstitial compartments, or from proliferation of AM in situ. While proliferation of alveolar type II cells after oxidant exposure has been well documented, it is not clear whether AM are also capable of this response. Rats were exposed to air or to 0.12, 0.25, or 0.50 ppm ozone for 1, 2, 3, 7, or 14 d, 20 h/d. The labeling index in both AM and type II cells increased about 10-fold after 2 d of exposure to 0.25 and 0.50 ppm of ozone, but returned to control levels by the end of 1 wk of exposure. These changes closely paralleled the temporal and dose-response characteristics of changes in total lung DNA synthesis. alpha-Difluoromethylornithine (DFMO) administered to rats during a 2-d exposure to 0.50 ppm ozone did not inhibit the ozone-induced increase in labeling index in AM or type II cells, although evidence of inhibition of lung ornithine decarboxylase activity was obtained, and the ozone-induced increase in total lung DNA synthesis was inhibited by 23%. These results suggest that, like type II cells, AM are capable of entering the cell cycle and synthesizing new DNA in situ in response to short-term exposure to environmentally relevant doses of ozone, and that the ozone-induced stimulation of DNA synthesis in these cell types was refractory to inhibition by DFMO.

Animals↗
PubMed1989

In vitro ozone exposure inhibits mitogen-induced lymphocyte proliferation and IL-2 production.

Human blood mononuclear cells were exposed to ozone in vitro and thereafter analyzed for competence in mitogen-induced proliferation as well as IL-1 and IL-2 production. Proliferative responses induced by phytohemagglutinin (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM) were all depressed in lymphocytes exposed to an ozone concentration of 1 ppm for 4-6 h. The response to PWM was most sensitive to the ozone effect (38% suppression); responses to Con A and PHA were suppressed to a lesser extent, 23% and 18%, respectively, and were not significantly different from each other. PWM responses were affected at an ozone concentration as low as 0.1 ppm; however, no suppression of Con A-induced proliferation was seen below 0.18 ppm or of PHA-induced proliferation below 0.5 ppm. When lymphocytes and monocytes were exposed separately to ozone and then mixed back with control air-exposed monocytes or lymphocytes, both cell types appeared to be affected and the functional defects caused by the pollutant were additive. Monocyte IL-1 production induced by endotoxin was not affected by ozone exposure, while surface expression of HLA-DR on exposed monocytes was reduced by 40% 24 h after exposure. Moreover, lymphocytes exposed to ozone produced 46% less IL-2 while expressing similar surface density of IL-2 receptors. Taken together, these results show that exposure to ozone has distinct adverse effects on lymphocytes and monocytes, both of which are important in local immune defenses in the lung.

Adolescent↗
PubMed1990

Surface morphology and morphometry of rat alveolar macrophages after ozone exposure.

As the ultrastructural data on the effects of ozone on pulmonary alveolar macrophages (PAM) are lacking, transmission (TEM) and scanning (SEM) electron microscopy were performed on rat PAM present in alveolar lavages following exposure to ozone. Rats were continuously exposed for 7 d to ozone concentrations ranging from 0.25 to 1.50 mg/m3 for 7 d followed by a 5-d recovery period. Additionally, morphometry on lung sections was performed to quantitate PAM. In a second experiment rats were continuously exposed to 1.50 mg O3/m3 for 1, 3, 5, or 7 d. To study the influence of concurrent ozone exposure and lung infection, due to Listeria monocytogenes, rats were exposed for 7 d to 1.50 mg O3/m3 after a Listeria infection. The surface area of lavaged control PAM was uniformly covered with ruffles as shown by SEM and TEM. Exposure to 0.5 mg ozone/m3 for 7 d resulted in cells partly covered with microvilli and blebs in addition to normal ruffles. The number of large size PAM increased with an increase in ozone concentration. After 1 d of exposure, normal-appearing as well as many small macrophages with ruffles and scattered lymphocytes were seen. Lavage samples taken after 5 or 7 d of exposure showed an identical cell composition to that taken after 3 d of exposure. After Listeria infection alone, lavage samples consisted of mainly lymphocytes and some macrophages. Small quantitative changes, such as an increase in the number of polymorphonuclear neutrophils and large-size PAM, occurred in lavages after ozone exposure and infection with L. monocytogenes. Morphometric examination of lung sections revealed a concentration-related increase in the number of PAM, even in animals exposed to 0.25 mg ozone/m3 for 7 d. Centriacinar regions were more severely affected than other regions of lung tissue. By 5 d after termination of exposure to ozone, the number of lysozyme-positive alveolar cells was still significantly increased in centriacinar areas of the lung. The results indicate that ozone exposure causes major changes in the number, size, and surface morphology of PAM in rat lung. Furthermore, the results presented here suggest that changes in alveolar macrophage function are reflected by morphological changes.

Animals↗
PubMedDate not supplied

Demonstration of a hermetic airborne ozone disinfection system: studies on E. coli.

An enclosed flow-through system using airborne ozone for disinfection and which removes the ozone with a catalytic converter was tested with a strain of Escherichia coli. Petri dishes containing the microorganisms were inserted in a chamber and exposed for 10-480 min to ozone concentrations between 4 and 20 ppm. Death rates in excess of 99.99% were achieved. Survival data is fitted to a two-stage curve with a shoulder based on the multihit target model. Ozone was removed from the exhaust air to nondetectable levels using a metal oxide based catalyst. The possibility of using ozone as an airborne disinfectant for internal building surfaces and catalytically removing the ozone on exhaust is demonstrated to be feasible. A model for the decay of Bacillus cereus under ozone exposure is proposed as an example for predicting the sterilization of buildings contaminated with anthrax. The potential for disinfecting airstreams and removing ozone to create breathable air is also implied by the results of this experiment.

Air Movements↗
PubMed2001

The biotoxicity and color formation results from ozonation of wastewaters containing phenol and aniline.

This study was undertaken to investigate the color forming phenomena and biotoxicity related problems during the initial stage of ozonation in the wastewater containing phenol or aniline. Experimental results indicate that the phenol under alkaline condition and aniline in all pH conditions cause a serious color problem during the period of early initial ozonation. In addition, the ozonated aniline exhibited more severe color formation than the ozonated phenol did. Both of these compounds revealed that either a high compound concentration or low ozone dosage applied incurred a strong color forming phenomena. Moreover, according to the Microtox test, both ozonated byproducts increased the toxicity during early ozonation when the color formation occurred. The EC50-value as COD decreased from 0.72 (for phenol, pH = 7) to 1.38 (for aniline, pH = 4) orders-of-magnitude. This observation implies that the ozonated color formation would generate new toxicity problems if these colored matters were not further oxidized.

Aniline Compounds↗
PubMed2001

Effects of some water-quality and operating parameters on the decolorization of reactive dye solutions by ozone.

The ozonation of reactive dye solutions has been investigated. Results of studies on ozone mass transfer indicated that the volumetric mass transfer coefficient of ozone increased with the following water-quality and operating parameters: pH, initial dye concentration, applied ozone dose, and temperature. A model was developed to predict the volumetric mass transfer coefficient of ozone from the above parameters. The results of kinetic studies showed that ozonation of the aqueous reactive dye was a pseudo-first-order reaction with respect to the dye. The apparent rate constant increased with the pH, applied ozone dose and temperature, however, it declined logarithmically with the initial dye concentration. Meanwhile, Ozonation enhanced the biodegradability and reduced the COD of the reactive dye wastewater effectively.

Biodegradation, Environmental↗
PubMed2003

Effect of ozone therapy on muscle oxygenation.

BACKGROUND AND OBJECTIVE: Ozone therapy is being used to treat ischemic disorders. However, the underlying mechanisms for the success are unknown and the therapy has not been accepted fully within conventional medicine. This study sought to assess the effect of ozone therapy on resting muscle oxygenation. PATIENTS AND DESIGN: Twenty-three (23) patients and 3 volunteers were recruited for this prospective study. Systemic ozone therapy was administered by autohemotransfusion on three alternate days over 1 week. Tissue oxygenation (mmHg) was directly measured in the tibialis anterior muscle using polarographic needle electrodes before and after the first and the third ozone therapy session. RESULTS: Globally, the differences in oxygenation were not statistically significant but there was a significant decrease in the percentage of low-oxygenated values (pO(2) < 5 mmHg) following ozone sessions (p < 0.02). The change in muscle oxygenation following ozone therapy was inversely correlated with age (r = -0.398; p = 0.044) and with the initial (baseline pretherapy) muscle oxygenation values (r = -0.644; p < 0.001), indicating that the more poorly oxygenated muscles benefited most from the therapy. A significant (p = 0.031) higher oxygenation in these tissues was observed 48 hours after the second session. CONCLUSIONS: Ozone therapy can modify oxygenation in resting muscles, particularly of those that are most hypoxic. Our results suggest that ozone therapy could be used effectively as a complementary treatment of hypoxic and ischemic syndromes and that the therapy warrants further investigation for possible application in other clinical conditions.

Adult↗
PubMed2003

Cell structural changes in the needles of Norway spruce exposed to long-term ozone and drought.

Effects of ozone and/or drought on Norway spruce needles were studied using light microscopy and electron microscopy. Saplings were exposed to ozone in open-top chambers during 1992-1995 and also to drought in the late summers of 1993-1995. Samples from current and previous year needles were collected five times during 1995. Ozone increased the numbers of peroxisomes and mitochondria, which suggests that defence mechanisms against oxidative stress were active. The results from peroxisomes suggest that the oxidative stress was more pronounced in the upper side of the needles, and those from mitochondria that defence was more active in the younger needle generation. Possibly due to the good nitrogen status and the active defence, no ozone-specific chloroplast alterations were seen. At the end of the season, older needles from ozone treatments had smaller central vacuoles compared with other needles. Cytoplasmic vacuoles around the nucleus were increased by ozone in the beginning of the experiment, and did not increase towards the end of the season as in the controls. These results from vacuoles may indicate that ozone affected the osmotic properties of the cells. Decreased number and underdevelopment of sclerenchyma cells and proliferation of tonoplast were related to nutrient imbalance, which was enhanced by drought. Larger vascular cylinders and more effective starch accumulation before and after the drought periods compensated for the reduced water status. Numbers of peroxisomes and mitochondria were increased in the drought-exposed needles before the onset of drought treatments of the study year, i.e. these changes were memory effects. Interactions between ozone and drought were few.

Chloroplasts↗
PubMed1989

Ozone activates transforming genes in vitro and acts as a synergistic co-carcinogen with gamma-rays only if delivered after radiation.

An earlier study indicated that ozone (O3), a major pollutant in our atmosphere, acts as a carcinogen as well as a synergistic co-carcinogen with radiation in cultured hamster embryo cells and in mouse C3H10T1/2 cells. In this investigation we further characterize the oncogenic action of ozone, alone or in combination with radiation, on C3H10T1/2 cells with particular emphasis on transformation produced by different temporal patterns of dose delivery of these two agents and low dose effects. We report that ozone-induced transformation involves the activation of dominant transforming genes, thereby indicating that DNA is a target in ozone induced carcinogenesis. We also report that ozone (5 p.p.m. for 5 min) acts as a synergistic co-carcinogen only if delivered after radiation (4 Gy or gamma-rays); when cells are exposed to ozone prior to radiation no enhanced rates of transformation are observed. Our findings also show that ozone at a low dose of 1 p.p.m. (for 5 min) does not act as a carcinogen but does interact as a co-carcinogen with ionizing radiation. The data indicate that the dose and sequence in which ozone and radiation are delivered have important implications for the putative carcinogenic effects of these two agents, a factor that heretofore has not been recognized.

Animals↗
PubMed2003

Isolation of an ozone-sensitive and jasmonate-semi-insensitive Arabidopsis mutant (oji1).

A novel ozone-sensitive mutant was isolated from Arabidopsis T-DNA tagging lines. This mutant revealed severe foliar injury and higher ethylene emission than the wild type under ozone exposure. The ozone-induced injury and ethylene emission were suppressed by pretreatment with aminoethoxyvinyl glycine, an inhibitor of ethylene biosynthesis, both in this mutant and wild-type plants. Pretreatment with methyl-jasmonate (MeJA) at 10 micro M, however, suppressed the ozone-induced ethylene emission and foliar injury only in the wild-type plants. This mutant was less sensitive to jasmonate than the wild type, estimated by the MeJA-induced inhibition of root elongation and ozone-induced expression of AtVSP1, a jasmonate-inducible gene. Thus, this mutant was named oji1 (ozone-sensitive and jasmonate-insensitive 1). These results suggest that the ozone sensitivity of oji1 is caused by the increase in ozone-induced emission of ethylene as a result of low sensitivity to jasmonate, which plays defensive roles under stress conditions.

Acetates↗
PubMed1999

Inflammatory and epithelial responses during the development of ozone-induced mucous cell metaplasia in the nasal epithelium of rats.

Rats repeatedly exposed to high ambient concentrations of ozone develop mucous cell metaplasia (MCM) in the nasal transitional epithelium (NTE). The present study was designed to determine the temporal relationships of ozone-induced inflammatory and epithelial responses and their correlation with subsequent MCM in the NTE of rats. Male F344/N rats were exposed to 0.5 ppm ozone, 8 h/day for 1, 2, or 3 days. Two h prior to sacrifice, all the rats were injected intraperitoneally with 5'-bromo-2-deoxyuridine (BrdU) to label epithelial cells undergoing DNA synthesis. Rats exposed to ozone for 1 or 2 days were killed 2 h after the exposure. Rats exposed to ozone for 3 days were killed 2 h or 1, 2, or 4 days after the exposure. Control rats were killed after a 7-day exposure to filtered air. One nasal passage from the anterior nasal cavity of each rat was fixed and processed for light microscopy to morphometrically determine the numeric densities of epithelial cells, neutrophils, and mucous cells, and the amount of intraepithelial mucosubstances in the NTE. The maxilloturbinate from the other nasal passage was processed for analysis of an airway mucin-specific gene (i.e., rMuc-5AC mRNA). Acute ozone exposure induced a rapid increase in rMuc-5AC mRNA levels prior to the onset of MCM, and the increased levels of rMuc-5AC mRNA persisted with MCM. Neutrophilic inflammation coincided with epithelial DNA synthesis and upregulation of rMuc-5AC, but was resolved when MCM first appeared in the NTE. The results of the present study suggest that upregulation of mucin mRNA by acute ozone exposure may be associated with the concurrent neutrophilic inflammation and epithelial hyperplasia in the NTE. Ozone-induced MCM may be dependent on these important pre-metaplastic responses (i.e., mucin mRNA upregulation, neutrophilic inflammation, and epithelial proliferation).

Administration, Inhalation↗
PubMed2002

Short-term exposure to aged and diluted sidestream cigarette smoke enhances ozone-induced lung injury in B6C3F1 mice.

To determine the effects of aged and diluted sidestream cigarette smoke (ADSS) as a surrogate of environmental tobacco smoke (ETS) on ozone-induced lung injury, male B6C3F1 mice were exposed to (1) filtered air (FA), (2) ADSS, (3) ozone, or (4) ADSS followed by ozone (ADSS/ozone). Exposure to ADSS at 30 mg/m3 of total suspended particulates (TSP) for 6 h/day for 3 days, followed by exposure to ozone at 0.5 ppm for 24 h was associated with a significant increase in the number of cells recovered by bronchoalveolar lavage (BAL) compared with exposure to ADSS alone or ozone alone. The proportion of neutrophils and lymphocytes, as well as total protein level in BAL, was also significantly elevated following ADSS/ozone exposure, when compared with all other groups. Within the centriacinar regions of the lungs, the percentage of proliferating cells identified by bromodeoxyuridine (BrdU) labeling was unchanged from control, following exposure to ADSS alone, but was significantly elevated following exposure to ozone (280% of control) and further augmented in a statistically significant manner in mice exposed to ADSS/ozone (402% of control). Following exposure to ozone or ADSS/ozone, the ability of alveolar macrophages (AM) to release interleukin (IL)-6 under lipopolysaccharide (LPS) stimulation was significantly decreased, while exposure to ADSS or ADSS/ozone caused a significantly increased release of tumor necrosis factor alpha from AM under LPS stimulation. We conclude that ADSS exposure enhances the sensitivity of animals to ozone-induced lung injury.

Air Pollutants↗
PubMed2004

Ozone uptake, water loss and carbon exchange dynamics in annually drought-stressed Pinus ponderosa forests: measured trends and parameters for uptake modeling.

This paper describes 3 years of physiological measurements on ponderosa pine (Pinus ponderosa Dougl. ex Laws.) growing along an ozone concentration gradient in the Sierra Nevada, California, including variables necessary to parameterize, validate and modify photosynthesis and stomatal conductance algorithms used to estimate ozone uptake. At all sites, gas exchange was under tight stomatal control during the growing season. Stomatal conductance was strongly correlated with leaf water potential (R2=0.82), which decreased over the growing season with decreasing soil water content (R2=0.60). Ozone uptake, carbon uptake, and transpirational water loss closely followed the dynamics of stomatal conductance. Peak ozone and CO2 uptake occurred in early summer and declined progressively thereafter. As a result, periods of maximum ozone uptake did not correspond to periods of peak ozone concentration, underscoring the inappropriateness of using current metrics based on concentration (e.g., SUM0, W126 and AOT40) for assessing ozone exposure risk to plants in this climate region. Both Jmax (maximum CO2-saturated photosynthetic rate, limited by electron transport) and Vcmax (maximum rate of Rubisco-limited carboxylation) increased toward the middle of the growing season, then decreased in September. Intrinsic water-use efficiency rose with increasing drought stress, as expected. The ratio of Jmax to Vcmax was similar to literature values of 2.0. Nighttime respiration followed a Q10 of 2.0, but was significantly higher at the high-ozone site. Respiration rates decreased by the end of the summer as a result of decreased metabolic activity and carbon stores.

California↗
PubMed2000

Effects of short-term exposure to 0.2 ppm ozone on biomarkers of inflammation in sputum, exhaled nitric oxide, and lung function in subjects with mild atopic asthma.

To gain further insight into the kinetics of airway inflammatory response and explore the possibility of nitric oxide as a surrogate marker of the lower airway inflammatory response to ozone, nine subjects with mild atopic asthma were exposed to filtered air or 0.2 ppm ozone for 2 hours with intermittent exercise. Lung function was measured at baseline and immediately after exposures. Sputum induction was performed at 6 hours and at 24 hours after exposures, and exhaled nitric oxide levels were measured at baseline, immediately, 6, and 24 hours after both exposures. A significant decline in forced expiratory volume in one second and inspiratory capacity was detectable following exposure to ozone. In addition, a 2-fold increase was observed in the percentage of polymorphonuclear leukocytes 6 hours after exposure to ozone, with no changes in other biomarkers at this time point. By 24 hours after ozone exposure, the neutrophilia had subsided but there was an increase in albumin, total protein, myeloperoxidase, and eosinophil cationic protein. Exhaled nitric oxide levels, histamine, interleukin-8, and growth-related oncogene-alpha in sputum did not change significantly following ozone exposure. It was concluded that short-term ozone exposure induces an acute inflammatory response in asthmatic airways, characterized by early polymorphonuclear leukocyte influx followed by plasma extravasation and activation of eosinophils and neutrophils. Exhaled nitric oxide is not a useful marker for detecting inflammatory response to ozone in persons with mild asthma.

Administration, Inhalation↗
PubMed2005

Ozone exposure and mortality: an empiric bayes metaregression analysis.

BACKGROUND: Results from time-series epidemiologic studies evaluating the relationship between ambient ozone concentrations and premature mortality vary in their conclusions about the magnitude of this relationship, if any, making it difficult to estimate public health benefits of air pollution control measures. We conducted an empiric Bayes metaregression to estimate the ozone effect on mortality, and to assess whether this effect varies as a function of hypothesized confounders or effect modifiers. METHODS: We gathered 71 time-series studies relating ozone to all-cause mortality, and we selected 48 estimates from 28 studies for the metaregression. Metaregression covariates included the relationship between ozone concentrations and concentrations of other air pollutants, proxies for personal exposure-ambient concentration relationships, and the statistical methods used in the studies. For our metaregression, we applied a hierarchical linear model with known level-1 variances. RESULTS: We estimated a grand mean of a 0.21% increase (95% confidence interval = 0.16-0.26%) in mortality per 10-microg/m increase of 1-hour maximum ozone (0.41% increase per 10 ppb) without controlling for other air pollutants. In the metaregression, air-conditioning prevalence and lag time were the strongest predictors of between-study variability. Air pollution covariates yielded inconsistent findings in regression models, although correlation analyses indicated a potential influence of summertime PM2.5. CONCLUSIONS: These findings, coupled with a greater relative risk of ozone in the summer versus the winter, demonstrate that geographic and seasonal heterogeneity in ozone relative risk should be anticipated, but that the observed relationship between ozone and mortality should be considered for future regulatory impact analyses.

Air Pollutants↗
PubMed2001

Spatial and annual temporal distribution of ozone concentrations in the madrid basin using passive samplers.

Passive samplers are useful tools for helping to describe the ozone distribution in complex terrain situations. They are also a good complement to continuous monitoring stations. This paper discusses the results of a pilot study that used ozone passive samplers to describe the spatial and annual temporal distribution of ozone in several forested areas around the city of Madrid. The ozone concentrations around Madrid were found to be higher on the elevated sites located at a certain distance from the city"s urban zone. A seasonal ozone cycle was observed, with maximum concentrations found in the basin in late spring or summer depending on the location. The information obtained allowed us to group the locations into four classes. Altitude and distance to the city during the summer and winter explained the observed ozone concentrations. However, during the transition periods, especially in early spring and to a lesser extent in autumn, there was not a good correlation between ozone levels and elevation or distance from precursor sources. These data strongly suggest that altitudinal gradients for ozone are not always the case in the Madrid Basin.

Air Pollutants↗
PubMed2002

Artichoke cultivars (var. "Blanca de Tudela") under elevated ozone concentrations.

Ozone concentrations rise to phytotoxic levels from spring to autumn at western Mediterranean basin coastal sites, where artichoke is one of the most important crops. Simultaneously, from year to year and especially since the early 1980s, resprouting of the stumps has been decreasing in Valencian Community artichoke plantations. To see if ozone might be playing a role in this decrease, a number of plants were exposed to different levels of ozone. Results of the ozone treatments showed reduced biomass in the offshoots of plants exposed to the highest ozone treatment. The exposure to ambient ozone during the stump-establishment period, when compared to filtered-air conditions, resulted in a reduction in yield when plants were transplanted in the field under ambient ozone concentrations. And when plants were exposed to acute short picks, typical ozone visual injury appeared in the older leaves.

Agriculture↗