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PubMed2003

Optimal process configuration for anaerobic digestion with ozonation.

Economical source minimization of excess sludge production is an attractive option to deal with the problem of sludge disposal under strict disposal standards. In this paper long-term operational results for two different process configurations that combine oxidative ozone treatment with anaerobic sludge digestion are described. In the first configuration ozone pretreatment was combined with chemostat anaerobic digestion while in the second configuration ozone pre/post-treatments were combined with an anaerobic digester operated without solid removal. From the results of chemostat experiments, the ozone pretreatment solubilized around 19% and 37% of the solids at 0.015 and 0.05 gO3/gTS ozone dose respectively. The ozone pretreatment resulted in improved TVS reduction efficiencies and the degradation efficiencies were observed to depend on the applied ozone dose and system SRT. The TVS degradation efficiency for pre-ozonated sludge at an ozone dose of 0.05 gO3/gTS was 59% as compared to 31% for the control reactor fed with un-ozonated sludge. Test results with the second configuration indicated that overall TVS removal efficiencies for a process scheme with post-ozonation could be improved up to 85% with a minimum ozone dose of 0.045 gO3/gTVS-fed. However, since no solids (except that for sampling) were withdrawn in this configuration, the accumulated total solids in the reactors increased to 28 g/l to 30 g/l at pseudosteady state. The average specific methane recoveries were observed to be 0.36 lCH4/gTVS fed which were slightly lower than theoretically expected. Based on the experimental results, important points in the choice of process configuration are discussed.

Bacteria, Anaerobic↗
PubMed1992

[The two ozone problems: too much in the troposphere, too little in the stratosphere].

Trends analysis based on the long-term Swiss ozone measurements from Arosa and Payerne operationally performed by the Swiss Meteorological Institute are presented. These measurement include stratospheric ozone (approximately 90% of total ozone) and tropospheric ozone. The total ozone measurements from Arosa, the world longest series started at 1926, indicate, that total ozone has declined since about 1970 by approximately 5%. The ozone balloon soundings, operationally performed at Payerne since 1969 (2-3 ascents per week) show, that stratospheric ozone has decreased strongly in the last 20 years, whereas tropospheric ozone, remarkably has increased during this period. The relative change was strongest in the troposphere (more than 10% per decade, 3-4% increase per year during 1982-1988). However, on an absolute scale, changes in the stratosphere were strongest (relative decrease: 6 to 7% per decade at 20-22 km). The present scientific theories of the two ozone problems are reviewed: stratospheric ozone decrease was caused by the anthropogenic emissions of fluorochlorocarbons and other compounds mainly released from the earth surface. Tropospheric ozone has increased due to photochemical production of mainly anthropogenically emitted nitrogen oxides, volatile organic compounds and CO.

Atmosphere↗
PubMed2004

Uptake distribution of ozone in human lungs: intersubject variability in physiologic response.

The primary hypothesis of this study was that intersubject variation in uptake of inhaled ozone causes corresponding variation in the resulting physiologic response. The second hypothesis was that differences in breathing pattern and lung anatomy induce differences in ozone uptake. Sixty healthy nonsmokers participated in three exposure protocols during which their minute ventilation was 30 L/min, corresponding to moderate exercise. For the intermittent bolus exposure to ozone (BO3*), we measured the penetration volume at which 50% of the bolus was taken up (VP50%). Before and after continuous clean air exposure (Ca) and continuous ozone exposure (CO3: 0.25 ppm ozone), we measured forced expiratory volume in 1 second (FEV1), calculated as the percent change after exposure relative to start of exposure [%FEV1]). We also measured the cross-sectional area of the peripheral lung (Ap) for carbon dioxide (CO2) diffusion, calculated as the percent change after exposure relative to start of exposure (%Ap). After the CO3 session, we also measured ozone uptake (as ozone uptake rate) and fractional ozone uptake efficiency. Uptake efficiency ranged from 0.70 to 0.98 among all subjects. It was inversely correlated with breathing frequency (P = 0.000) but was not correlated with conducting airways volume (P = 0.333). VP50% ranged from 67 to 135 mL among all subjects and was directly correlated with conducting airways volume (P = 0.000). These results indicate that overall ozone uptake was related to breathing frequency but not to airway size, whereas internal distribution of ozone shifted distally as airway size increased. Values of %FEV1 (mean +/- SD: -13.71 +/- 12.99) and %Ap (-7.80 +/- 9.34) were both significantly more negative (P = 0.000) in the CO3 session than in the Ca (control) session (-0.055 +/- 4.57 and 0.40 +/- 11.03, respectively). Ozone uptake rate correlated with individual %Ap (P = 0.008) but not with individual %FEV1 (P = 0.575). Nor were individual %Ap or %FEV1 correlated with VP50%. Therefore, ozone uptake did not explain intersubject differences in forced expiratory responses in this study, but it did partially explain differences in the cross-sectional area available for gas diffusion in the peripheral lung.

Adult↗
PubMed1975

[Comparative studies on the action of chlorine and ozone on polioviruses in the reprocessing of drinking water in Essen (author's transl)].

The present study was performed in order to evaluate comparatively the inactivation of polio virus type I strains (wild type and attenuated) by means of chlorine and ozone. Polio virus type I was chosen with regard to its epidemiological behaviour and high stability in drinking-water and sewage lines. In view of the lack of propagation techniques, hepatitis viruses A and B, unfortunately, could not be used for these experiments. The experiments were done under laboratory conditions only, and not in the water recovery plant because of hygienic reasons. Defined quantities of disinfectants were examined for their virus-inactivating effect in water without redox-potential (double-distilled water), water with low defined redox-potential (double-distilled water + KOH), previously chlorinated water with a residual chlorine content of 0.03 mg chlorine per liter (tap water) and water with a high redox-potential (well water from the drinking-water plant). Time-course studies were performed, both with chlorine and ozone, in order to evaluate the characteristics of the inactivation procedure. The experimental conditions chosen varied from experiment to experiment to obtain relevant conclusions for the practice. On the basis of our results, and taking into account the quantitative differences in effect, chlorine and ozone principially can be considered equivalent in their action of virus-disinfection. Both, the initial rate and the kinetics of virus disinfection are really identical. Both disinfectants are dependant on the condition of the water (redox-potential, pH etc.) to a great extent in their efficacy. Therefore, a decision of whether or not ozone should substitute for chlorine for the drinking-water supply in Essen cannot be drawn on the basis of virological experiments. This decision, then, depends more or less on other questions - such as relative costs and practicability of the ozonization on a large technical scale. The safety risk and technical reliability of the ozonization process is of particular significance. In the present condition of the Essen reservoir water, a good virus disinfection can be expected already with 1.0 to 1.5 mg ozone/liter (dissolved!); such a concentration guarantees very little residual ozone and, thus, makes then this procedure technically feasible. Continuous checking of the redox-potential and the amount of the ozone added is necessary. With regard to a continuous supply of ozone, the dependence on current supply must be guaranteed. Ozonization of water, probably by the cleavage of humic acid, promotes bacterial recontamination of the drinking-water in the city taps(Stalder und Klosterkötter, 45). Therefore only a combined pre-ozonization with subsequent chlorination would guarantee, both, safety and improvement of the cosmetical conditions of the drinking-water. Such a combination would be feasible with highly reduced amounts of ozone and chlorine.

Chlorine↗
PubMed1990

[The role of neutrophils in airway hyperresponsiveness in dogs after ozone exposure].

To determine whether neutrophils are involved in airway hyperresponsiveness after ozone exposure, we studied the effect of neutrophil depletion by cyclophosphamide treatment on ozone-induced airway hyperresponsiveness in seven dogs. Airway responsiveness to inhaled methacholine was determined by modified Astograph (7 Hz oscillation method), and the numbers of neutrophils in the peripheral blood, total cell counts and differential cell counts in BALF were measured before and after ozone exposure, and after ozone exposure of dogs undergoing cyclophosphamide treatment. Ozone exposure was carried out for 2 hrs at an ozone level of 3.07 +/- 0.01 ppm (mean +/- SE), and cyclophosphamide (10 mg/kg) was given intravenously daily for five days starting six days before ozone exposure. There was a significant increase in airway responsiveness to inhaled methacholine after ozone exposure in the seven dogs (p less than 0.001), and the numbers of neutrophils in the peripheral blood and the neutrophil counts in BALF increased significantly after ozone exposure (p less than 0.01). After ozone exposure of dogs undergoing cyclophosphamide treatment, the numbers of neutrophils in the peripheral blood decreased significantly (p less than 0.001) and the neutrophil counts in BALF did not increase, but the airway responsiveness to inhaled methacholine increased significantly (p less than 0.01). There was no significant correlation between the degree of the increase in airway responsiveness and the degree of the increase in neutrophil counts in BALF after ozone exposure. These results suggest that neutrophil infiltration into the airway is not necessary for an increase in airway responsiveness after ozone exposure in dogs.

Airway Resistance↗
PubMed1994

ICAM-1-independent, CD18-dependent adhesion between neutrophils and human airway epithelial cells exposed in vitro to ozone.

Inhalant exposure to ozone can cause diffuse airway epithelial injury that is associated with an inflammatory response, including the influx of neutrophils into lung and airway tissue. We have previously documented enhanced adhesiveness by neutrophils for human airway epithelial cells in in vitro models of diseases associated with airway inflammation and have suggested that this enhanced adhesion may contribute to neutrophil-mediated airway injury. When primary human tracheal epithelial cell (TEC) monolayers were exposed to ozone at 2.0 ppm for 30 min or 0.5 ppm for 2 h, the percentage of PMN adhering to these cells increased from < 5% to a maximum of approximately 75% by 18 to 24 h after the ozone exposure. No change was observed within the first 2 h after ozone exposure, but there was a statistically significant increase in PMN adhesion by 8 h after exposure. In contrast to previous studies with cytokine exposure or respiratory virus infection of TEC, the increased adhesion after ozone exposure was not associated with an increase in epithelial expression of ICAM-1. Consistent with the lack of induction of ICAM-1 by ozone exposure was the observation that anti-ICAM-1 mAbs (mAb; R6.5) previously shown to block PMN adhesion to TEC with increased ICAM-1 expression had no effect on PMN adhesion to ozone-exposed TEC. However, mAbs against CD11b or CD18 on PMN blocked PMN adhesion to ozone-exposed TEC by approximately 55 and 80%, respectively. Chemoattractant preactivation of PMN (e.g., with 10 nM FMLP) was necessary to achieve the highest levels of adhesion to ozone-treated TEC, in marked contrast to our earlier studies with PMN adhesion to cytokine-treated or virus-infected TEC in which resting and prestimulated PMN exhibited the same high levels of adhesion. We conclude that exposure of human TEC in vitro to ozone results in markedly increased adhesiveness for neutrophils that is caused by the induction of as yet uncharacterized epithelial cell adhesion molecules other than ICAM-1 that function as counterreceptors for the CD11/CD18 integrins on PMN. Maximal PMN adhesiveness to ozone-exposed TEC in this system requires preactivation of the PMN, e.g., with FMLP, suggesting important differences in the way PMN interact with ozone-treated vs cytokine-treated or virus-infected TEC.

Adult↗
PubMed1997

Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies. Part XII: Atrophy of bone in nasal turbinates.

As part of the National Toxicology Program/Health Effects Institute collaborative study of the health effects of prolonged ozone exposure, it was observed that rats chronically exposed to ozone had marked histopathologic changes in the upper respiratory tract, including atrophy of the nasal turbinates. The principal objective of the present study was to morphometrically assess the severity of the ozone-induced changes in the bony tissue of the maxilloturbinates in these chronically exposed rats. Male and female F344/N rats were exposed to 0, 0.12, 0.5, or 1.0 part per million (ppm) ozone, 6 hours/day, 5 days/week for 20 or 24 months. Rats were killed one week after the end of the exposure, and nasal tissues were processed for light and electron microscopy. Using image analysis and standard morphometric techniques, the amounts of bone, surface epithelium, and lamina propria comprising the maxilloturbinates were estimated by measuring the cross-sectional area of each tissue compartment at a defined location in the proximal nasal passage. Both male and female rats had significant morphologic and morphometric changes in the maxilloturbinates after prolonged exposures to 0.5 or 1.0 ppm ozone, but not to 0.12 ppm ozone. Ozone-exposed rats had significant reductions in the cross-sectional area of turbinate bone, reflecting the loss of bone in the maxilloturbinate after prolonged exposure. This ozone-induced bony atrophy was more severe in male than in female rats. Using electron microscopy, numerous bone-resorption sites were identified on the outer, periosteal, surface of the turbinate bone in ozone-exposed animals. Rats with bony atrophy also had a conspicuous influx and mixed inflammatory cells into the lamina propria surrounding the turbinate bone. In addition, ozone exposures caused reductions in the area of lamina propria, due to blood vessel constriction, and increases the in the area of the surface epithelium, due to hyperplasia and metaplasia. The results of the present tudy demonstrated that prolonged exposure of rats to ozone can cause marked loss of turbinate bone. The severity of this ozone-induced bony atrophy in rats is dependent on both concentration and gender.

Administration, Inhalation↗
PubMed1997

ENVIRONMENTAL AUDITING: An Approach for Characterizing Tropospheric Ozone Risk to Forests

/ The risk tropospheric ozone poses to forests in the United States is dependent on the variation in ozone exposure across the distribution of the forests in question and the various environmental and climate factors predominant in the region. All these factors have a spatial nature, and consequently an approach to characterization of ozone risk is presented that places ozone exposure-response functions for species as seedlings and model-simulated tree and stand responses in a spatial context using a geographical information systems (GIS). The GIS is used to aggregate factors considered important in a risk characterization, including: (1) estimated ozone exposures over forested regions, (2) measures of ozone effects on species' and stand growth, and (3) spatially distributed environmental, genetic, and exposure influences on species' response to ozone. The GIS-based risk characterization provides an estimation of the extent and magnitude of the potential ozone impact on forests. A preliminary risk characterization demonstrating this approach considered only the eastern United States and only the limited empirical data quantifying the effect of ozone exposures on forest tree species as seedlings. The area-weighted response of the annual seedling biomass loss formed the basis for a sensitivity ranking: sensitive-aspen and black cherry (14%-33% biomass loss over 50% of their distribution); moderately sensitive-tulip popular, loblolly pine, eastern white pine, and sugar maple (5%-13% biomass loss); insensitive-Virginia pine and red maple (0%-1% loss). In the future, the GIS-based risk characterization will include process-based model simulations of the three- to 5-year growth response of individual species as large trees with relevant environmental interactions and model simulated response of mixed stands. The interactive nature of GIS provides a tool to explore consequences of the range of climate conditions across a species' distribution, forest management practices, changing ozone precursors, regulatory control strategies, and other factors influencing the spatial distribution of ozone over time as more information becomes available.KEY WORDS: Ecological risk assessment; GIS; Ozone; Risk characterization; Forests; Trees

Journal Article↗
PubMed1991

Effects of open-top chamber fumigations with ozone on three fungal leaf diseases of wheat and the mycoflora of the phyllosphere.

Spring wheat (Triticum aestivum L. cv. Turbo) was exposed in open-top chambers to six different ozone levels (8-h daily means from 12.4 to 122 microg m(-3)), to non-filtered air and to chamberless field conditions for 31 days from seedling stage through ear emergence. Powdery mildew (Erysiphe graminis DC. f.sp. tritici Marchal) which developed during the exposure period was significantly enhanced from 0.3/0.6% (two chamber replicates), 1.2/2.1%, 0.9/2.2% in charcoal-filtered air (CF) to 1.5/1.6%, 3.7/4.3%, 4.4/4.6% at the highest level of ozone, on the flag leaf, second and third leaf position, respectively. Post-exposure inoculation with Septoria nodorum Berk. led to increases of disease severity on the flag leaf from 40.9/43.6% in CF to 66.3/70.6% at the highest ozone concentration and on the ears from 15.7/16.5% to 26.3/26.6%. In the same comparison, severity of spot blotch following inoculation with Bipolaris sorokiniana (Sacc.) Shoem. (syn. Helminthosporium sativum Pamm., King et Bakke) was increased on the flag leaf from 3.6/8.9% to 12.3/23.4%. The three diseases examined correlated significantly with the ozone treatments in fumigated chambers. Disease severity was enhanced even on undamaged plant tissue (flag leaves). Infections of the two facultative pathogens on lower leaf positions started only in part from visible ozone lesions, mildew did not start from such lesions. No significant effects of ozone in the chambers on the saprobial colonization of the phyllosphere were detected, whereas there were marked differences in this respect between plants from the field and the chambers. At the highest ozone treatment, contents of chlorophyll a and carotenoids on the second leaf position declined significantly, which was associated with symptoms of premature senescence. Senescing effects of ozone are therefore assumed to be one major factor in predisposing wheat for necrotrophic leaf pathogens. Surprisingly, injurious and predisposing effects of ozone were completely absent in chambers supplied with non-filtered air containing ambient ozone at doses equivalent to those in CF + ozone chambers. Evidently, biological effects of ozone in pure air and in ambient air may differ markedly.

Journal Article↗
PubMed1996

Size-mediated foliar response to ozone in black cherry trees.

Local ozone concentration and visible foliar injury were measured over the 1994 growing season on open-grown black cherry (Prunus serotina Ehrh.) trees of varying size (age) within forest stands and adjacent openings at a site in north-central Pennsylvania. Relationships were determined between visible ozone injury and ozone exposure, as well as calculated between injury and ozone uptake expressed as the product of stomatal conductance and ozone concentration. In addition, simultaneous measurements of visible symptoms and leaf gas exchange were also conducted to determine the correlation between visible and physiological injury and ozone exposure. By September, the amount of leaf area affected by visible foliar ozone injury was greatest for seedlings (46%), followed by canopy trees (20%) and saplings (15%). A large amount of variability in foliar ozone symptom expression was observed among trees within a size class. Sum40 and Sum60 (ozone concentration > 40 and > 60 nl liter(-1)) cumulative exposure statistics were the most meaningful indices for interpretation of foliar injury response. Seedlings were apparently more sensitive to ozone injury than larger trees because their higher rates of stomatal conductance resulted in higher rates of ozone uptake. Seedlings also had higher rates of early leaf abscission than larger trees with an average of nearly 30% of the leaves on a shoot abscised by 1 September compared to approximately 5% for larger trees. However, per unit ozone uptake into the leaf, larger trees exhibited larger amounts of foliar injury. The amount of visible foliar injury was negatively correlated (r(2) = 0.82) with net photosynthetic rates, but was not related to stomatal conductance. Net photosynthesis and stomatal conductance thus became uncoupled at high levels of visible foliar injury.

Journal Article↗
PubMed1997

Evaluation of ozone injury on foliage of black cherry (Prunus serotina) and tall milkweed (Asclepias exaltata) in Great Smoky Mountains National Park.

The incidence and severity of visible foliar ozone injury on black cherry (Prunus serotina) seedlings and saplings and tall milkweed (Asclepias exaltata) plants in Great Smoky Mountains National Park (GRSM) were determined by surveys along selected trails conducted during late summer 1992. The incidence (% injured plants) of ozone injury on black cherry was 47% and the percent injured leaves/injured plant and average leaf area injured were 43 and 6%, respectively. Maximum severity (avg. leaf area of the most severely injured leaf) was 12%. Black cherry seedlings and saplings exhibiting ozone injury were taller than non-injured plants. When insect feeding was present, it occurred 96% of the time on plants with ozone injury. Significantly more injury (p=0.007) on black cherry (% injured leaves/injured black cherry) occurred in the NW section of GRSM compared with the other Park sections. Regression analyses showed no relationships in ozone injury with respect to aspect, slope or elevation. Tall milkweed was evaluated twice during August for ozone injury. The incidence (% injured plants) of ozone injury was 74 and 79% for the first and second survey, respectively. The percentage of injured leaves per plant from the first to second survey was 63 to 79%, respectively. Tall milkweeds showing ozone injury were taller than the non-injured plants. The percentage of insect-damaged plants was 50% among plants without ozone injury and 60% among ozone-injured plants. Non-injured tall milkweed had fewer flowers and/or pods than the injured plants. Mean leaf area injured increased over time, and mean maximum leaf area injured increased from 8 to 11% during the same period. Regression analyses showed no differences in ozone injury regarding aspect, slope or elevation. Our findings indicate that ozone injury is widespread throughout the Park on sensitive vegetation.

Journal Article↗
PubMed2000

Interactive effects of elevated ozone and carbon dioxide on growth and yield of leaf rust-infected versus non-infected wheat.

Spring wheat (Triticum aestivum L. cv. Turbo) was grown from seedling emergence to maturity (129 days) in chambers simulating the physical climate and ozone pollution of a field site in Northern Germany from 1 April to 31 July with a mean 1-h daily maximum of 61.5-62.4 nl l(-1) ozone compared to a constant low level of 21.5-22.8 nl l(-1) ozone. The two ozone levels were combined with either a current (374.1-380.2 microl l(-1)) or enriched (610.6-615.0 microl l(-1)) CO(2) atmosphere. Additionally, a leaf rust epidemic (Puccinia recondita f. sp. tritici) was induced at tillering stage by repeated re-inoculations with the inoculum formed on the plants. Leaf rust disease was strongly inhibited by ozone, but largely unaffected by elevated CO(2). Ozone damage on leaves was strongly affected by CO(2) and infection. On infected plants, ozone lesions appeared 2-4 weeks earlier and were up to fourfold more severe compared to non-infected plants. Elevated CO(2) did not delay the onset of ozone lesions but it significantly reduced the severity of leaf damage. It also enhanced the photosynthetic rate of flag leaves and increased the water use efficiency, biomass formation and grain yield. The relative increases in growth and yield induced by CO(2) were much larger on ozone-stressed than on non-stressed plants. Both ozone and fungal infection reduced biomass formation, number of grains per plant, thousand grain weight and grain yield; however, adverse effects of leaf rust infection were more severe. Elevated CO(2) largely equalized the negative effects of ozone on the photosynthetic rate, growth and yield parameters, but was not capable of compensating for the detrimental effects of fungal infection. The data imply that the impact of ozone in the field cannot be estimated without considering the predisposing effects deriving from fungal infections and the compensating effects deriving from elevated CO(2).

Journal Article↗
PubMed2002

Ozone tolerance in snap bean is associated with elevated ascorbic acid in the leaf apoplast.

Ascorbic acid (AA) in the leaf apoplast has the potential to limit ozone injury by participating in reactions that detoxify ozone and reactive oxygen intermediates and thus prevent plasma membrane damage. Genotypes of snap bean (Phaseolus vulgaris L) were compared in controlled environments and in open-top field chambers to assess the relationship between extracellular AA content and ozone tolerance. Vacuum infiltration methods were employed to separate leaf AA into extracellular and intracellular fractions. For plants grown in controlled environments at low ozone concentration (4 nmol mol-1 ozone), leaf apoplast AA was significantly higher in tolerant genotypes (300-400 nmol g-1 FW) compared with sensitive genotypes (approximately 50 nmol g-1 FW), evidence that ozone tolerance is associated with elevated extracellular AA. For the open top chamber study, plants were grown in pots under charcoal-filtered air (CF) conditions and then either maintained under CF conditions (29 nmol mol-1 ozone) or exposed to elevated ozone (67 nmol mol-1 ozone). Following an 8-day treatment period, leaf apoplast AA was in the range of 100-190 nmol g-1 FW for all genotypes, but no relationship was observed between apoplast AA content and ozone tolerance. The contrasting results in the two studies demonstrated a potential limitation in the interpretation of extracellular AA data. Apoplast AA levels presumably reflect the steady-state condition between supply from the cytoplasm and utilization within the cell wall. The capacity to detoxify ozone in the extracellular space may be underestimated under elevated ozone conditions where the dynamics of AA supply and utilization are not adequately represented by a steady-state measurement.

Journal Article↗
PubMed1995

Detection of hydroxyl radicals upon interaction of ozone with aqueous media or extracellular surfactant: the role of trace iron.

As part of a study on mechanisms modulating ozone-induced surfactant perturbations, we used the electron paramagnetic resonance (EPR) spin trapping technique to determine the type and origin of radicals generated following interaction of ozone with aqueous solutions and cell-free bronchoalveolar lavage fluid (BAL) fractions. All aqueous media were exposed to ozone at 25 degrees C with or without added chelator, 1 mM diethylenetriaminepentaacetic acid, and spintrap, 100 mM 5,5'-dimethyl-1-pyrroline-1-oxide (DMPO). Exposure of distilled water to 0.5, 1.0, 2.0, and 3.0 ppm ozone for 1 h yielded four-line spectra, 1:2:2:1, consistent with hydroxyl radical adduct formation (DMPO-OH), the amplitudes of which increased with the ozone concentration. No signals were obtained from air-exposed samples. Similar four-line spectra were also produced following interaction of 3 ppm ozone with Hank's balanced salt solution (HBSS) alone or containing BAL fractions. Addition of the hydroxyl radical scavenger dimethyl sulfoxide (DMSO) to the incubation medium strongly inhibited formation of DMPO-OH adduct during ozone exposure. As an alternate method of demonstrating the generation of hydroxyl radicals, aqueous solutions of 1 mM L-phenylalanine were exposed to high concentrations of ozone and shown, using ion-exchange chromatography, to contain small amounts of L-tyrosine. Production of hydroxyl radicals upon interaction of ozone and water was further substantiated using the spintrap PBN (phenyl-N-tert-butylnitrone) in the presence of DMSO which reacts with the hydroxyl radical resulting in the formation of methyl radical. The methyl radical subsequently reacts with spintrap PBN, yielding PBN-methyl adduct. In the absence of DMSO there was no detectable formation of methyl radical adduct. EPR double distilled water containing DMPO showed a small amount of DMPO-OH adduct upon exposure to ozone. Addition of 10 microM ferrous sulfate to this mixture produced a 10-fold increase of the signal, which was attenuated in the presence of 1500 U catalase, strongly attenuated with 50-500 microM deferoxamine or 8000 U catalase and abolished by higher concentration of deferoxamine (1 mM). The signal was not influenced by 1000 U superoxide dismutase. These results indicate that hydroxyl radicals are produced via iron-dependent reactions during the initial interaction of ozone with aqueous media, including bronchoalveolar fluid.

Animals↗
PubMed1995

Bronchiolarized metaplasia and interstitial fibrosis in rat lungs chronically exposed to high ambient levels of ozone.

The cellular and tissue changes in the lungs of rats were studied using electron microscopy following 20 months exposure to a range of ozone levels from 0.12 to 1.0 ppm. Male and female Fischer 344 rats were exposed and morphometric methods were used to determine the volume, surface area, and cellular changes observed in bronchiole-alveolar duct regions following chronic ozone exposure. No major gender-related effects were observed in response to chronic inhalation of ozone nor were significant effects of ozone exposure found in either terminal bronchioles or the proximal alveolar regions in animals chronically exposed to 0.12 ppm ozone. The proximal alveolar regions of animals exposed for 20 months to 0.5 and 1.0 ppm ozone were significantly altered with exposure. The high-dose, long-term exposure to ozone resulted in a pronounced increase in volume of both the interstitium and epithelium in the proximal alveolar regions. The thickening of the epithelium was due to a change in tissue type from the normal squamous epithelium to a cuboidal epithelium similar, but not identical, to that found in terminal bronchioles. This bronchiolar epithelial metaplasia of proximal alveolar ducts, which was dose related, was composed of differentiated ciliated and Clara cells similar to those found in terminal bronchioles. In addition, unique cells which contained morphologic features of many different cell types were observed. These cells, which may represent stem cells or differentiated but transformed cells, were found associated with the bronchiolar metaplasia of alveolar ducts. In conjunction with the epithelial changes, cellular and matrix components in the interstitium were increased with chronic exposure to 0.5 and 1.0 ppm ozone. All matrix components were increased including collagen, elastin, and basement membrane, as well as other acellular spaces which did not contain identifiable structures. The total volume of interstitial fibroblasts was also increased in the high-dose exposure group. Alveolar macrophages were increased only in the 1.0 ppm exposed animals. The cell and tissue changes in the terminal bronchioles were less pronounced indicating a relative resistance of this tissue to ozone and mainly consisted of a change in cell type from ciliated to Clara cells in the 1.0 ppm exposed animals. The relative resistance of bronchiolar tissue to high concentration ozone exposure and the extensive bronchiolar epithelial metaplasia may be an adaptive mechanism following chronic ozone exposure.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Effects of ozone inhalation during exercise in selected patients with heart disease.

Although epidemiologic evidence suggests that patients with heart and lung disease are more vulnerable to the acute toxic effects of photochemical air pollution, no laboratory studies have been reported in patients with coronary heart disease. In the present investigation, six male volunteers, ages 46 to 64 years, with clinically documented coronary heart disease and a well-defined symptomatic angina pectoris threshold, served as subjects. Each patient was exposed on three 40-minute occasions to either filtered air or ozone at concentrations of 0.20 or 0.30 parts per million (ppm), while walking on a treadmill at workloads simulating their regularly prescribed exercise training regimen. Results of standard pulmonary function tests and periodic observations of exercise ventilation, respiratory metabolism, electrocardiographic changes, hemodynamic response, and clinical signs and symptoms were recorded. Analysis of variance revealed that none of the patients' physiologic responses to ozone exposure were statistically significant. Furthermore, neither onset of angina pain or ischemic changes were related to ozone exposure in a dose-dependent fashion. Hence, the patients not only failed to exhibit any unexpected cardiovascular strain while exposed to ozone during exercise, but also evidenced no significant pulmonary function impairment or exercise ventilatory pattern alteration, as has been observed in clinically normal subjects exercising at similar ozone concentration levels. This apparent incongruity may be due to the fact that acute ozone toxicity is more closely related to the total amount of ozone inhaled, which is a function of pulmonary ventilation volume and exposure time, as well as ozone concentration. In the patients with angina, symptom-limited exercise tolerance resulted in a lower total amount of ozone inhaled than that observed to effect ozone toxicity in clinically normal subjects who exercised at greater intensities and for longer durations. Patients with angina appear to be no more susceptible to ozone toxicity than are clinically normal subjects at the effective doses imposed. However, had the patients exercised longer, they might well have evidenced pulmonary function impairment and/or cardiovascular strain. Hence, caution is advised in generalizing these observations to other conditions and patient groups.

Angina Pectoris↗
PubMed1989

Comparison of acute ozone-induced nasal and pulmonary inflammatory responses in rats.

The centriacinar pulmonary lesion induced by ozone has been extensively characterized, but little is known about the effects of this oxidant gas in the upper airways. The present study was designed to compare the effects of acute ozone exposure in the nose and lungs of rats. We examined the cellular inflammatory responses in the nasal cavity and lower respiratory tract by means of nasal and bronchoalveolar lavage and morphometric quantitation of neutrophils within the nasal mucosa and pulmonary terminal bronchioloalveolar duct regions (i.e., centriacinar). Rats were exposed to 0.0, 0.12, 0.8, or 1.5 ppm ozone for 6 hr and were sacrificed immediately or 3, 18, 42, or 66 hr following exposure. Eighteen hours after exposure, increased numbers of neutrophils, as compared to controls, were recovered from nasal lavage fluid (NLF) of rats exposed to 0.12 ppm ozone. There was no change in the number of neutrophils recovered from bronchoalveolar lavage fluid (BALF) at any time after exposure. Rats exposed to 0.8 ppm ozone had more neutrophils in NLF than controls immediately after exposure, but no concomitant increase in BALF neutrophils at that time. However, as the number of neutrophils in BALF increased (maximum at 42 hr), the number of neutrophils recovered from NLF decreased (minimum at 42 hr). Rats exposed to 1.5 ppm ozone had no significant increases in nasal neutrophils in NLF at any time after exposure but had greatly increased numbers of neutrophils in BALF 3, 18, and 42 hr after exposure. The number of neutrophils recovered by nasal and bronchoalveolar lavage accurately reflected the tissue neutrophil response at sites within the nasal cavity and lung that were injured by acute ozone exposure. Our results suggest that at high ozone concentrations (0.8 and 1.5 ppm), the acute nasal inflammatory response is attenuated by a simultaneous, competing, inflammatory response within the centriacinar region of the lung. Analysis of nasal lavage fluid for changes in cellular composition may be a useful indicator of acute exposure to ambient levels of ozone, but at higher ozone levels, the nasal cellular inflammatory response may underestimate the effects of ozone on nasal and pulmonary epithelia.

Animals↗
PubMed1992

Application of the EPR spin-trapping technique to the detection of radicals produced in vivo during inhalation exposure of rats to ozone.

Ozone is known to induce lipid peroxidation of lung tissue, although no direct evidence of free radical formation has been reported. We have used the electron paramagnetic resonance (EPR) spin-trapping technique to search for free radicals produced in vivo by ozone exposure. The spin trap alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) was administered ip to male Sprague-Dawley rats. The rats were then exposed for 2 hr to either 0, 0.5, 1.0, 1.5, or 2.0 ppm ozone with 8% CO2 to increase their respiratory rate. A six-line 4-POBN/radical spin adduct signal (aN = 15.02 G and a beta H = 3.27 G) was detected by EPR spectroscopy in lipid extracts from lungs of rats treated with 4-POBN and then exposed to ozone. Only a weak signal was observed in the corresponding solution from rats exposed to 0 ppm ozone (air with CO2 only). The concentration of the radical adduct increased as a function of ozone concentration. After administration of 4-POBN, rats were exposed for either 0.5, 1.0, 2.0, or 4.0 hr to either 0 or 2.0 ppm ozone (with CO2). The radical adduct concentration of the ozone-exposed groups at exposure times of 2.0 and 4.0 hr was significantly different from that of the corresponding air control groups. A correlation was observed between the radical adduct concentration and the lung weight/body weight ratio. These results demonstrate that ozone induces the production of free radicals in rat lungs during inhalation exposure and that radical production may be involved in the induction of pulmonary toxicity by ozone. This is the first direct evidence for ozone-induced free radical production in vivo.

Administration, Inhalation↗