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PubMed2002

Slurry-phase ozonation for remediation of sediments contaminated by polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are a group of toxic, persistent, bioaccumulating organic compounds containing two or more fused aromatic rings. They are listed by the U.S. Environmental Protection Agency as priority pollutants because of their carcinogenicity and toxicity. Employing ozonation as a remediation technique, this work investigated the treatability of a sediment sample from a freshwater boat slip subjected to coal tar contamination over a long period. The contaminated sediment sample contained high levels of PAHs in the forms of naphthalene, phenanthrene, pyrene, and benzo[a]pyrene, among other byproducts present in the humic and solid phases of the sediment. The objectives of this work were to examine (1) the degradation of PAHs in the contaminated sediment as treated by ozonation in the slurry form, (2) the effects of ozonation upon the soil matrix and the biodegradability of the resultant PAH intermediates, and (3) the feasibility of a combined technique using O3 as a pretreatment followed by biological degradation. The sediment was made into 3% w/w soil slurries and ozonated in a 1.7-L semi-batch, well-stirred reactor equipped with pH control and a cold trap for the gaseous effluent. Samples were collected after different ozonation durations and tested for biochemical oxygen demand (BOD), chemical oxygen demand (COD), UV absorbance, and toxicity, along with quantitative and qualitative determinations of the parent and daughter intermediates using gas chromatography/flame ionization detection (GC/FID), GC/mass spectrometry (MS), and ion chromatography (IC) techniques. The GC/MS technique identified 16 compounds associated with the humic and solid phases of the sediment. Intermediates identified at different ozonation times suggested that the degradation of PAHs was initiated by an O3 attack resulting in ring cleavage, followed by the intermediates' oxidation reactions with O3 and the concomitant OH radical toward their mineralization. Results suggested that ozonation for 2 hr removed 50-100% of various PAHs in the solid and liquid phases (as well as the aqueous and gaseous media resulting from the treatment process) of the sediment sample and that organic and inorganic constituents of the sediment were also altered by ozonation. Measurements and comparisons of BOD, COD, UV absorbance, and toxicity of the samples further suggested that ozonation improved the bioavailability and biodegradability of the contaminants, despite the increased toxicity of the treatment effluent. An integrated chemical-biological system appeared to be feasible for treating recalcitrant compounds.

Environmental Pollution↗
PubMed2004

Ozone measurements in South Carolina using passive samplers.

Passive samplers with two different collection substrates were used to obtain an average ozone concentration for 1 month during the summer of 2002 for each South Carolina county. One sampler contained a filter coated with indigo carmine, whose color fades when exposed to ozone. The fading was measured by reflectance spectroscopy. The other sampler contained filters that were coated with nitrite, which is oxidized to nitrate when exposed to ozone. The nitrate was measured by ion chromatography. Calibration curves were developed for the two methods by comparing color fading from indigo carmine and nitrate ion concentration from the nitrite filter with ambient ozone concentration measured by a co-located reference continuous UV ozone analyzer. These curves were used to calculate integrated ozone concentrations for samplers distributed across South Carolina. Using the indigo carmine method, the average ozone concentrations ranged from 21 to 64 ppb (average = 46 +/- 7.9 ppb, n = 58) across the 46 counties in the state during one summer month of 2002. Concentrations for the same time period from the nitrite-coated filters ranged from 23 to 62 ppb (average = 41 +/- 8.1 ppb, n = 58). Also for the same time period, the 23 continuous UV photometric ozone monitors operated by the South Carolina Department of Health and Environmental Control at sites within 10 miles of some of the passive monitors showed ozone concentrations ranging from 28 to 50 ppb (average = 39 +/- 6.3 ppb, n = 22).

Air Pollutants↗
PubMed1999

Does ozone exposure protect from photoinhibition?

Tropospheric ozone and high light intensities are two stress factors that often occur simultaneously under natural conditions. Ozone is well known to form oxygen radicals in the apoplastic water and long lasting photoinhibition can cause photooxidative damage also by formation of several species of oxygen radicals. We were interested whether moderate levels of ozone would be able to modulate the response of leaves to photoinhibitory conditions naturally occurring around noon on a bright day. Cuttings of Populus sp. were cultivated in two separate greenhouse-compartments adapted as fumigation chambers. In the two compartments plants were grown in ambient air containing about 20 nmol mol(-1) ozone and in elevated ozone concentrations supplied for 8 h per day. During the midday of bright days Fv/Fm decreased by the same amount in all leaves, indicating photoinhibition. At the same time Fo increased in control leaves more than in ozone-exposed leaves indicating a higher amount of heat-deactivating PSII centres in the latter. This was confirmed by a higher epoxidation state in ozone-exposed leaves during midday of a bright day. The contents of chlorophyll a and chlorophyll b were significantly decreased in ozone-exposed leaves. In older leaves the ratios chlorophyll a : b, and xanthophylls: chlorophyll b were increased indicating an adaptation to higher light stress. From this we conclude that by increasing the amount of heat-deactivating centres ozone seems to protect PSII from photoinhibition.

Chlorophyll↗
PubMed2001

Inflammatory cell availability affects ozone-induced lung damage.

Identifying whether or not neutrophils have a role to play in the early stages of acute lung epithelial injury brought about by inhalation of reactive substances continues to be a major area of investigation. In this study, the availability of circulating neutrophils was manipulated by treatment with either cyclophosphamide or rabbit antiserum against rat neutrophils, prior to exposures to air, a single high ozone exposure of 1 or 2 ppm for 3 h, or a continuous exposure to 0.8-1.0 ppm for up to 48 h. Although cyclophosphamide treatment resulted in undetectable levels of neutrophils in the blood, the recovery of tissue marginated-interstitial neutrophils of 1 x 10(6) cells by collagenase tissue digestion was not significantly diminished at the onset of air and ozone exposures. Cyclophosphamide treatment alone did not cause any permeability damage to air-exposed rat lungs, but did ameliorate ozone-induced increases in bronchoalveolar lavage (BAL) neutrophil and albumin recoveries after both short-term and 1 d of continuous ozone exposure. In contrast to cyclophosphamide, antiserum treatment resulted in greater than a 90% decrease in neutrophil recoveries from both blood and lung tissue at the onset of air and ozone exposures. Antiserum treatment also abrogated ozone-induced neutrophil accumulations in lung lavageable spaces following both single and continuous ozone exposures, but did not significantly affect ozone-associated lung permeability damage indicated by unaltered BAL fluid albumin recoveries. These data demonstrated that under experimental conditions when neutrophils remain within lung tissue marginated and interstitial pools, reduction in circulating blood neutrophil availability is associated with a concomitant decrease in ozone-induced lung damage.

Animals↗
PubMed1980

Effect of ozone on respiratory response of guinea pigs to histamine.

The effect of preexposure to ozone on the respiratory response to histamine was studied. The Amdur-Mead technique was used to measure respiratory mechanics in Charles River Hartley guinea pigs. Groups of animals were exposed for 1 h to filtered control air or ozone. Control measurements were made 1 1/2 h after exposure, followed by sc injection of 0.125 mg/kg histamine dihydrochloride. Respiratory measurements were continued at 2-min intervals for 16 min, at which time resistance and compliance had returned to control values. The 2-h interval between exposure and injection and the 0.125 mg/kg histamine were the optimum time interval and dose, respectively, as determined by appropriate time-response and dose-response studies. Although control values did not differ between air-exposed and ozone-exposed animals, animals preexposed to 0.1, 0.2, 0.4, and 0.8 ppm ozone had increases in resistance of 111, 110, 93, and 97% after histamine administration, compared to the air-exposed animals, which had increases of 86, 86, 67, and 46%, respectively. Whereas the only significant difference in resistance between air and ozone animals was at the 0.8-ppm level (p less than 0.05), significant differences in compliance changes were found at all levels of ozone exposure. Ozone animals had compliance decreases of 40, 45, 46, and 46% after histamine injection, while their respective air controls decreased 24, 24, 27, and 31%. Exposures to ozone of 0.2 ppm for 4 h and 0.4 ppm for 2 h provided doses equal to that of 0.8 ppm for 1 h, yet no significant dose-time relationship was found. Lingering sensitivity to pharmacologically active agents is a subtle but important manifestation of ozone toxicity.

Airway Resistance↗
PubMed1987

Enhancement of pulmonary metastasis of murine fibrosarcoma NR-FS by ozone exposure.

The effects of ozone exposure on the metastasis of a fibrosarcoma (NR-FS) that arose spontaneously in a C3H/He mouse was studied. Male C3H/He mice were exposed to 0.8, 0.4, 0.2, and 0.1 ppm ozone for 1, 3, 5, 7, and 14 d. After the exposure periods, the mice were infused intravenously with NR-FS cells. At 2 wk postinfusion, the lungs were examined for colony development of metastasis. A significantly higher rate of pulmonary metastasis than that of normal mice was observed in the ozone-exposed mice. The enhancement of metastasis due to ozone exposure varied with length of exposure and concentration of ozone. When 1 X 10(5) cells of NR-FS were injected into the tail veins of mice, the maximal enhancement (459%) of pulmonary metastasis was observed in the mice exposed to 0.8 ppm ozone for 1 d. A longer period of exposure to 0.8 ppm ozone also enhanced pulmonary metastasis, although the prolonged exposure (14 d) gradually suppressed the enhancement (268%). In the mice exposed to the lower concentration of ozone, a lower rate of the lung matastasis was observed; even in the mice exposed to 0.1 ppm ozone for the period of from 1 to 14 d, a significantly higher rate of metastasis than that of nonexposed mice was observed.

Administration, Inhalation↗
PubMed1989

Exposure to 1 ppm ozone attenuates the immediate antigenic response of canine peripheral airways.

The effect of oxidant exposure on the immediate airway response to immunologic challenge is controversial. We investigated the response of canine peripheral airways to antigen aerosol, 1-3 h and 24 h after a 5-min exposure to 1 ppm ozone. In dogs that were natively sensitive to Ascaris suum antigen, resistance to flow through the collateral system (Rcs) was measured using the wedged bronchoscope technique. In eight dogs, four sublobar segments of each lung were wedged: two were exposed to ozone for 5 min and two (control) received air with 5% CO2. Ozone caused a mean ( +/- SE) increase in Rcs of 75 +/- 15%, which returned to baseline after 1-3 h. The increase in Rcs elicited by subsequent administration of antigen aerosol (25 microliters, 0.27 mg protein/ml) to the ozone-exposed segments (312.0 +/- 70.6%) was attenuated by 22% compared to controls (398.9 +/- 83.0%; p less than .05). In another series of experiments (n = 5), segments were exposed to ozone or air and challenged with antigen 24 h later and a significant attenuation (38%) of the antigen-induced increase in Rcs was detected compared to controls (178.5 +/- 57.9 vs 289.0 +/- 62.2; p less than .05). Cellular influx of polymorphonuclear leukocytes (PMNs) was not detected by bronchoalveolar lavage (BAL) 1-3 h after ozone, but was found after 24 h (19.8 vs. 4.7%; p less than .01). A significant increase in PMNs was detected in exposed subepithelial tissues 1-3 h after ozone compared to unexposed tissues. Tissue PMNs were not significantly different from unexposed tissues after 24 h, but a shift toward degranulation of mast cells was detected in ozone-exposed tissues at this time. These data suggest that the Rcs response to antigen is attenuated 1-3 h and 24 h after acute (5 min) exposure to 1 ppm ozone, and this effect occurs independently of PMNs in the airways.

Administration, Inhalation↗
PubMed1999

Mechanism of oxidative damage to fish red blood cells by ozone.

The present study was conducted to elucidate the adverse effects of ozone exposure on rainbow trout (Oncorhynchus mykiss) red blood cells (RBCs). We evaluated whether hemoglobin (Hb) or Hb-derived free iron could participate in the RBC damage using an in vitro ozone exposure system. Ozone exposure induced hemolysis, formation of methemoglobin, and RBC membrane lipid peroxidation. This RBC damage was not suppressed by the addition of a specific iron chelator (deferoxamine mesilate) to the medium but was suppressed by carbon monoxide (CO) treatment before ozone exposure. Generation of hydrogen peroxide (H2O2) in RBC was observed upon ozone exposure but was significantly suppressed by CO treatment before ozone exposure. Thus the Hb status (i.e., Hb redox condition) and H2O2 generation in RBC should play important roles in mediating RBC damage by ozone exposure. In other words, neither ozone nor its derivative directly attacked from the outside of the cell, but ozone that penetrated through the membrane derived the reactive oxygen species from Hb inside of the cell.

Animals↗
PubMed2002

Variation of toxicity during the ozonation of monochlorophenolic solutions.

This study investigates the variation of toxicity during ozonation of 2-chlorophenol (2-CP), 3-chlorophenol (3-CP) and 4-chlorophenol (4-CP) in neutral condition. Acute toxicity of pure chlorophenols (CPs) and their ozonated intermediates was evaluated by Microtox assay. The results revealed that the intermediates of oxidized CPs induced new toxicity during the early stage of ozonation, and the ozonated 2-CP showed higher degree of toxicity increase than 3-CP and 4-CP. The maximum toxicity normally occurred before the maximum color intensity was monitored, while ozone dosage applied was within 1 mg of ozone per mg of initial CPs. This increasing toxicity was mainly contributed from ozonated intermediates. Formation of chlorocatechols, chloromuconic acids and hydroxylated/chlorinated dimeric compounds were detected in ozonation of CPs. These chlorinated by-products may cause greater toxicity than the parent chlorophenols. The required ozone dosage to detoxify the CPs solution into a complete non-toxic condition follows the order: 4-CP > 3-CP > 2-CP.

Chlorophenols↗
PubMed2003

The effectiveness of a new gas-induced reactor in treating phenolic wastewater by ozonation and hydrogen peroxide.

A new Gas-Induced Reactor (GIR) has been developed to improve the efficiency of ozone utilization in water treatment. In this study, the GIR was used to investigate the behavior of ozonation of aqueous phenol solution by means of O3 and O3/H2O2 processes in order to explore the feasibility and efficiency of treating such wastewater using the new GIR. The study observed the decomposition of phenol, utilization of ozone, and variation of TOC during ozonation, varying pH values, phenol initial concentrations, ozone input concentrations, and hydrogen peroxide dosages. The study concluded that the new GIR was capable of performing effective and efficient ozonation of phenolic wastewater, maintaining high ozone utilization ratios at all experimental pH values and initial phenol and ozone concentrations. The optimal pH condition for phenol removal was around 11. The best molar ratios of initial hydrogen peroxide over input ozone among the performed experiments were about 20 at pH 7 and 10 at pH 9 and 11. The primary operational energy used for treating a tonne of wastewater was 66 MJ, giving treatment costs of about USS1.0 per tonne.

Gases↗
PubMed2004

Decolorization of dye RB-19 solution in a continuous ozone process.

This work studied the decolorization of dye C.I. Reactive Blue 19 (RB-19) solution in a new gas-inducing reactor under continuous process. The decolorization behavior, decolorization kinetic, ozone utilization rate (UO3), and Chemical Oxygen Demand (COD) are examined under various operation conditions, such as input ADMI color values (ADMIo), input liquid flow rates (QL), input ozone gas concentrations (CO3,i), input gas flow rates (Qg), and agitation speeds (N). Experimental results of decolorization behavior indicate that the American Dye Manufactures Institute (ADMI) removal percentage (RADMI) decreases with increasing ADMI color value input rate or decreasing ozone input rate. For the study of ozone utilization rate, UO3 increases with increasing ADMI color value input rate or decreasing ozone input rate. The 70% ADMI removal percentage can be regarded as the index of the competition of dye and its unknown intermediates for ozone. In addition, the increase of the agitation speed can improve the ADMI removal percentage as well as the ozone utilization rate. A pseudo-first order kinetic model is adopted to describe the decolorization behavior. At steady state, the overall decolorization rate constant, kADMIs.s., can be expressed as a function of liquid flow rate, input ADMI color value, input ozone gas concentration, gas flow rate, and agitation speed. This correlation can be used to predict the ADMI color value at steady state (ADMIs.s.) and the reactor size in the continuous process. The deltaO3/deltaCOD is dependent on the liquid composition. The higher the dye concentration in the liquid, the higher the deltaO3/deltaCOD. The COD removal percentage (RCOD) and the ozone utilization rate can be further improved by using the continuous operation with two reactors in series.

Anthraquinones↗
PubMed1999

Ozone carcinogenesis revisited.

The question was asked whether ozone would act as a lung carcinogen in mice. To test the hypothesis, female strain A/J mice were exposed for 6 h/day, 5 days/week to 0.12 ppm, 0.5 ppm, or 1.0 ppm of ozone; control animals were kept in filtered air. No ozone-related deaths were observed at any time during the experiment. After 5 months, one-third of the animals were killed. The remaining animals were split into two groups: exposure to ozone continued for one group, whereas the other group was transferred into filtered air. Four months later, these animals were killed. No significant increase in lung tumor multiplicity (average number of tumors per lung) or lung tumor incidence (percentage of tumor-bearing animals) was found in the animals exposed to ozone when compared to animals kept in filtered air, regardless of ozone concentration. Morphometric analysis of lungs of animals exposed to the highest ozone concentration (1.0 ppm) showed a small, statistically not significant increase in centriacinar lesions. It was concluded that ozone is not a lung carcinogen in strain A/J mice at those exposure levels. Moreover, this mouse strain appears to be particularly resistant towards chronic ozone toxicity.

Administration, Inhalation↗
PubMed2001

Endotoxin enhancement of ozone-induced mucous cell metaplasia is neutrophil-dependent in rat nasal epithelium.

Ozone, the primary oxidant gas in photochemical smog, causes neutrophilic inflammation and mucous cell metaplasia (MCM) in the nasal transitional epithelium (NTE) of rats and monkeys. Bacterial endotoxin is another common airborne agent that induces acute neutrophilic inflammation, but not MCM, in NTE. It does, however, enhance ozone-induced MCM in rat nasal airways (Fanucchi et al., 1998, Toxicol. Appl. Pharmacol. 152, 1-9). In the present study, F344 rats exposed to filtered air or 0.5 ppm ozone (8 h/day for 3 days) were intranasally instilled with sterile saline or 100 microg endotoxin 24 h and 48 h after the third ozone exposure. To determine the role of neutrophilic inflammation in endotoxin-induced potentiation of the MCM caused by ozone, half of the rats were depleted of circulating neutrophils prior to saline or endotoxin instillations. Rats were killed 6 h or 3 days after the last intranasal instillation, and nasal tissues were processed for (1) light microscopy and morphometric analysis to determine the number of infiltrating neutrophils and the volume amount (density) of stored mucosubstances in the NTE, and (2) quantitative RT-PCR analysis of steady-state mucin gene (rMuc-5AC) mRNA levels in the NTE. Endotoxin induced a transient influx of neutrophils in both air- and ozone-exposed rats that was completely blocked by neutrophil depletion. Endotoxin increased rMuc-5AC mRNA levels in the NTE of ozone-exposed rats. Neutrophil depletion, however, had no effect on endotoxin-induced upregulation of mucin gene mRNA levels. Endotoxin enhanced the ozone-induced increase in stored mucosubstances (4-fold increase), but only in neutrophil-sufficient rats. These data indicate that endotoxin enhancement of ozone-induced upregulation of rMuc-5AC mRNA levels is neutrophil-independent, while its effects on intraepithelial production and storage of mucus glycoproteins is dependent on the presence of neutrophils.

Air Pollutants↗
PubMed2006

Stratospheric ozone depletion.

Solar ultraviolet radiation creates an ozone layer in the atmosphere which in turn completely absorbs the most energetic fraction of this radiation. This process both warms the air, creating the stratosphere between 15 and 50 km altitude, and protects the biological activities at the Earth's surface from this damaging radiation. In the last half-century, the chemical mechanisms operating within the ozone layer have been shown to include very efficient catalytic chain reactions involving the chemical species HO, HO2, NO, NO2, Cl and ClO. The NOX and ClOX chains involve the emission at Earth's surface of stable molecules in very low concentration (N2O, CCl2F2, CCl3F, etc.) which wander in the atmosphere for as long as a century before absorbing ultraviolet radiation and decomposing to create NO and Cl in the middle of the stratospheric ozone layer. The growing emissions of synthetic chlorofluorocarbon molecules cause a significant diminution in the ozone content of the stratosphere, with the result that more solar ultraviolet-B radiation (290-320 nm wavelength) reaches the surface. This ozone loss occurs in the temperate zone latitudes in all seasons, and especially drastically since the early 1980s in the south polar springtime-the 'Antarctic ozone hole'. The chemical reactions causing this ozone depletion are primarily based on atomic Cl and ClO, the product of its reaction with ozone. The further manufacture of chlorofluorocarbons has been banned by the 1992 revisions of the 1987 Montreal Protocol of the United Nations. Atmospheric measurements have confirmed that the Protocol has been very successful in reducing further emissions of these molecules. Recovery of the stratosphere to the ozone conditions of the 1950s will occur slowly over the rest of the twenty-first century because of the long lifetime of the precursor molecules.

Air Pollutants↗
PubMed2001

Spatial distribution of tropospheric ozone in national parks of California: interpretation of passive-sampler data.

The National Park Service (NPS) has tested and used passive ozone samplers for several years to get baseline values for parks and to determine the spatial variability within parks. Experience has shown that the Ogawa passive samplers can provide +/-10% accuracy when used with a quality assurance program consisting of blanks, duplicates, collocated instrumentation, and a standard operating procedure that carefully guides site operators. Although the passive device does not meet EPA criteria as a certified method (mainly, that hourly values be measured), it does provide seasonal summed values of ozone. The seasonal ozone concentrations from the passive devices can be compared to other monitoring to determine baseline values, trends, and spatial variations. This point is illustrated with some kriged interpolation maps of ozone statistics. Passive ozone samplers were used to get elevational gradients and spatial distributions of ozone within a park. This was done in varying degrees at Mount Rainier, Olympic, Sequoia-Kings Canyon, Yosemite, Joshua Tree, Rocky Mountain, and Great Smoky Mountains national parks. The ozone has been found to vary by factors of 2 and 3 within a park when average ozone is compared between locations. Specific examples of the spatial distributions of ozone in three parks within California are given using interpolation maps. Positive aspects and limitations of the passive sampling approach are presented.

Air Pollution↗
PubMed2006

Analysis of oxidative signalling induced by ozone in Arabidopsis thaliana.

We are using acute ozone as an elicitor of endogenous reactive oxygen species (ROS) to understand oxidative signalling in Arabidopsis. Temporal patterns of ROS following a 6 h exposure to 300 nL L(-1) of ozone in ozone-sensitive Wassilewskija (Ws-0) ecotype showed a biphasic ROS burst with a smaller peak at 4 h and a larger peak at 16 h. This was accompanied by a nitric oxide (NO) burst that peaked at 9 h. An analysis of antioxidant levels showed that both ascorbate (AsA) and glutathione (GSH) were at their lowest levels, when ROS levels were high in ozone-stressed plants. Whole genome expression profiling analysis at 1, 4, 8, 12 and 24 h after initiation of ozone treatment identified 371 differentially expressed genes. Early induction of proteolysis and hormone-responsive genes indicated that an oxidative cell death pathway was triggered rapidly. Down-regulation of genes involved in carbon utilization, energy pathways and signalling suggested an inefficient defense response. Comparisons with other large-scale expression profiling studies indicated some overlap between genes induced by ethylene and ozone, and a significant overlap between genes repressed by ozone and methyl jasmonate treatment. Further, analysis of cis elements in the promoters of ozone-responsive genes also supports the view that phytohormones play a significant role in ozone-induced cell death.

Arabidopsis↗
PubMed2004

Efficacy of ozone on survival and permeability of oral microorganisms.

In the present study, we examined the effect of ozonated water on oral microorganisms and dental plaque. Almost no microorganisms were detected after being treated with ozonated water (4 mg/l) for 10 s. To estimate the ozonated water-treated Streptococcus mutans, bacterial cells were stained with LIVE/DEAD BacLight Bacterial Viability Kit. Fluorescence microscopic analysis revealed that S. mutans cells were killed instantaneously in ozonated water. Some breakage of ozonated water-treated S. mutans was found by electron microscopy. When the experimental dental plaque was exposed to ozonated water, the number of viable S. mutans remarkably decreased. Ozonated water strongly inhibited the accumulation of experimental dental plaque in vitro. After the dental plaque samples from human subjects were exposed to ozonated water in vitro, almost no viable bacterial cells were detected. These results suggest that ozonated water should be useful in reducing the infections caused by oral microorganisms in dental plaque.

Aggregatibacter actinomycetemcomitans↗
PubMed2004

Ozone exposure in vivo and formation of biologically active oxysterols in the lung.

Ozone toxicity in the lung is thought to be mediated by products derived from the reaction of ozone with components of the lung epithelial lining fluid. Cholesterol is an abundant component of this epithelial lining fluid, and it is susceptible to ozonolysis, yielding several stable products including 3beta-hydroxy-5-oxo-5,6-secocholestan-6-al and 5beta,6beta-epoxycholesterol. Both 5beta,6beta-epoxycholesterol and its metabolite, cholestan-6-oxo-3,5-diol, have been shown to cause cytotoxicity in vitro, suggesting that they may be potential mediators of ozone toxicity in vivo. An ozone-sensitive mouse strain, C57BL/6J, was exposed to varying concentrations of ozone (0.5-3.0 ppm), and subsequently the levels of these cholesterol ozonolysis products were quantitated by electrospray ionization mass spectrometry in bronchoalveolar lavage fluid, lavaged cells, and lung homogenate. An ozone dose-dependent formation of these biologically active oxysterols was observed in vivo, supporting a role for these compounds in ozone toxicity. Since the 5beta,6beta-epoxycholesterol metabolite, cholestan-6-oxo-3,5-diol, was isobaric with other cholesterol ozonolysis products, 3beta-hydroxy-5-oxo-5,6-secocholestan-6-al and its aldol condensation product, 3beta-hydroxy-5beta-hydroxy-B-norcholestan-6beta-carboxaldehyde, detailed mass spectral analysis using electron impact ionization was utilized to differentiate these isobaric cholesterol ozonolysis products. The specific detection of cholestan-6-oxo-3,5-diol in lung homogenate after ozone exposure established formation of 5beta,6beta-epoxycholesterol within the lung after exposure to 0.5 ppm ozone.

Animals↗