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PubMed2000

Lung tissue neutrophil content as a determinant of ozone-induced injury.

Short-term exposure of rats to ozone results in lung inflammation characterized by increased permeability damage and the infiltration of neutrophils into the airways. The present study compared these ozone-induced inflammatory responses in different strains of male rat, Brown Norway rats from Charles River Laboratories, Inc. (BN-CRL), and Harlan Sprague Dawley, Inc. (BN-HSD), and Fischer 344 (F344), Sprague-Dawley (SPD), and Wistar (WSTR) male rats from Hilltop Lab Animals, Inc. Ozone-induced permeability damage was indicated by recoveries of bronchoalveolar lavage fluid (BALF) albumin 20 h following single exposures of 6 h to either air or 1 ppm or 2 ppm O3. Although BALF albumin recoveries from air-exposed rats were not significantly different between strains, ozone exposures resulted in a range of enhancements of BALF albumin of 2-, 9-, 17-, 7-, and 20-fold following exposures of BN-CRL, BN-HSD, F344, SPD, and WSTR rats to 2 ppm ozone, respectively. Concomitant strain differences in the number of ozone-induced BAL-recoverable neutrophils were not observed, except for BN-CRL rats, which demonstrated significantly lower numbers. However, the degree of ozone-induced permeability damage did directly correspond to differences observed in the numbers of neutrophils and eosinophils in the peripheral blood and collagenase tissue digest of lavaged and perfused lungs prior to ozone exposure. Ozone-resistant BN-CRL rats exhibited the highest numbers of blood and lung tissue neutrophils and eosinophils when compared with ozone-susceptible WSTR rats exhibiting the lowest number of these granulocytes. These data suggested that the presence of high numbers of blood and tissue granulocytes at the onset of short-term ozone exposures might provide a certain degree of protection against subsequent pathological events.

Albumins↗
PubMed2000

Protection against ozone-induced pulmonary inflammation and cell death by endotoxin pretreatment in mice: role of HO-1.

Ozone is a ubiquitous air pollutant that can cause acute pulmonary inflammation and cell injury and may contribute to the exacerbation of chronic pulmonary diseases. The molecular mechanisms of ozone-induced cell injury, as well as protective mechanisms against ozone-injury, are not well understood. Since ozone is a reactive oxidant, and heme oxygenase-1 (HO-1) is an antioxidant enzyme induced by many oxidative stimuli, we hypothesized that HO-1 is one of the protective mechanisms against ozone-induced cell injury, as well as pulmonary inflammation. In the current study, C57Bl/6 mice were pretreated with a low level of endotoxin (lipopolysaccharide, LPS) (0.5 mg/kg) to induce HO-1, and 16 h later were exposed to 1 ppm ozone for 3 h. Endotoxin pretreatment caused a significant protection against ozone-induced pulmonary inflammation and cell injury in bronchoalveolar lavage (BAL) cells. The protection by endotoxin pretreatment against ozone-induced inflammation and necrosis in BAL cells was abolished by the cotreatment with a heme oxygenase inhibitor, tin protoporphyrin IX dichloride (SnPP), suggesting that HO-1 is responsible for the protection against ozone-induced pulmonary inflammation and BAL cell necrosis. Therefore, since HO-1 is induced following ozone exposure, HO-1 may contribute to the development of cellular adaptation to chronic ozone exposure.

Animals↗
PubMed2001

Ozone exposure and the production of reactive oxygen species by bronchoalveolar cells in humans.

Exposure to ozone injures respiratory epithelium, and the mechanisms may involve the generation of reactive oxygen species (ROS). This study tested the hypothesis that ozone exposure increases the airway burden of ROS to a greater degree in smokers than nonsmokers, and that this effect is independent of ozone-induced changes in spirometry. Healthy subjects were selected as either responders (decrement in FEV1 > 15%) or nonresponders (decrement in FEV1 < 5%) to ozone; each underwent 2 exposures to ozone and 1 to air, with bronchoalveolar lavage (BAL) performed 30 min (early) and 18 h (late) after exposure. Release of superoxide anion (O2(-)) was used as a measure of ROS release by all BAL cells, and flow cytometry was used to detect ROS production in alveolar macrophages (AM) only. Recovery of AM was approximately threefold greater in smokers than nonsmokers. Unstimulated, but not stimulated, cells obtained by BAL from smokers released approximately twofold greater amounts of O2(-) than cells from nonsmokers, both early and late after ozone exposure (p =.012 and p =.046, respectively). Stimulated, but not unstimulated, ROS generation by AM from smokers increased following ozone exposure, but the ozone effect was not significant. ROS production by AM decreased in nonsmokers (air vs. ozone late, p =.014). Total protein, albumin, and immunoglobulin M (IgM) increased in BAL fluid, consistent with an increase in epithelial permeability. In addition, the concentration of alpha2-macroglobulin increased approximately threefold 18 h after exposure in nonsmokers (p <.001). No relationship was found between measures of ROS production and lung function responsiveness to ozone. These studies suggest the airways of smokers experience a greater burden of ROS than those of nonsmokers following ozone exposure.

Administration, Inhalation↗
PubMed2005

Ozonation of membrane bioreactor effluent for landfill leachate treatment.

Ozonation of leachate effluent obtained from a Membrane Bioreactor (MBR) process treating a medium-aged landfill leachate was investigated. The sequence of ammonia stripping, membrane bioreactor, and ozonation was used in the experiment. Ozonation of the MBR effluent showed reduction in Chemical Oxygen Demand (COD) and Total Organic Carbon (TOC) with an increase in five days Biochemical Oxygen Demand (BOD5) concentration. About 73% of COD could be removed at an ozone (O3) dosage of 4.2 mg O3 mg COD(-1). The biodegradability indicated by BOD5/COD ratio increased from 0.03 to 0.08 after ozonation at optimum ozone condition. While analyzing the molecular weight distribution, the fraction of molecular weight (MW) greater than 50 kDa of MBR effluent was transferred to MW 10-50 kDa (38%) at an ozone dosage of 810 mg O3. When O3 dosage was increased to 2,025 mg O3, a rapid change occurred in MW > 50 kDa fraction. This fraction was completely broken down into lower molecular weight fractions. This indicates partial degradation of landfill leachate by ozonation. The colour removal from the leachate was found to be greater than 95%. When the ozonated leachate was recirculated into the MBR system, along with an improvement in the performance of MBR, overall COD removal increased from 78% to 83%. Further, the ozone consumption decreased from 6.1 to 3.4 mg O3 mg COD(-1) removed, thus reducing the ozone requirement.

Bioreactors↗
PubMed1995

Personal and fixed-site ozone measurements with a passive sampler.

Personal exposures to ozone were measured in the summers of 1992 and 1993 in the Fraser Valley, a suburban and rural river valley bordering the metropolitan region of Vancouver, British Columbia (population approximately 1.8 million). In 1992, two groups of 25 healthy individuals were selected for 14 consecutive days of 24-hour personal monitoring, based on prior expectations of their activity patterns. The first group, composed of adult healthcare workers, was expected to spend most of the work day indoors or commuting. The second group, teenage camp counselors, was expected to spend more time outdoors. Time-activity data were collected to investigate the association between activity patterns and ozone exposures. In 1993, 15 adult farmworkers wore personal ozone samplers during their workday, which was spent entirely outdoors. Personal monitoring was conducted with a nitrite-coated filter passive ozone sampler described by Koutrakis and colleagues. Ozone collection rates were determined empirically by collocation of the passive samplers with continuous ozone analyzers at fixed sampling sites. Sampler performance was assessed by collecting several duplicate personal samples. Although ozone levels were low (< 35 ppb 24-hour average) during both summer sampling periods, the passive ozone samplers agreed well with collocated UV absorption ozone measurements. Based on replicate personal samples, we estimated that personal measurements differing by more than 35% were associated with true differences in exposure. Within the two groups with varying time activities, differences in ozone exposures were associated with the fraction of time spent outdoors. Similarly, differences in ozone exposures were observed between the three sampling populations, with higher exposures recorded in the group that spent more time outdoors.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants↗
PubMed1986

Toxicity of ozone and nitrogen dioxide to alveolar macrophages: comparative study revealing differences in their mechanism of toxic action.

The toxicity of ozone and nitrogen dioxide is generally ascribed to their oxidative potential. In this study their toxic mechanism of action was compared using an intact cell model. Rat alveolar macrophages were exposed by means of gas diffusion through a Teflon film. In this in vitro system, ozone appeared to be 10 times more toxic than nitrogen dioxide. alpha-Tocopherol protected equally well against ozone and nitrogen dioxide. It was demonstrated that alpha-tocopherol provided its protection by its action as a radical scavenger and not by its stabilizing structural membrane effect, as (1) concentrations of alpha-tocopherol that already provided optimal protection against ozone and nitrogen dioxide did not influence the membrane fluidity of alveolar macrophages and (2) neither one of the structural alpha-tocopherol analogs tested (phytol and the methyl ether of alpha-tocopherol) could provide a protection against ozone or nitrogen dioxide comparable to the one provided by alpha-tocopherol. It was concluded that reactive intermediates scavenged by alpha-tocopherol are important in the toxic mechanism of both ozone and nitrogen dioxide induced cell damage. However, further results presented strongly confirmed that the kind of radicals and/or reactive intermediates, and thus the toxic reaction mechanism involved, must be different in ozone- and nitrogen dioxide-induced cell damage. This was concluded from the observations that showed that (1) vitamin C provided significantly better protection against nitrogen dioxide than against an equally toxic dose of ozone, (2) glutathione depletion affected the cellular sensitivity toward ozone to a significantly greater extent than the sensitivity towards nitrogen dioxide, and (3) the scavenging action of alpha-tocopherol was accompanied by a significantly greater reduction in its cellular level during nitrogen dioxide exposure than during exposure to ozone. One of the possibilities compatible with the results presented in this study might be that lipid (peroxyl) free radicals formed in a radical-mediated peroxidative pathway, resulting in a substantial breakdown of cellular alpha-tocopherol, are involved in nitrogen dioxide-induced cell damage, and that lipid ozonides, scavenged by alpha-tocopherol as well, are involved in ozone-induced cell damage.

Animals↗
PubMed1990

Morphologic injury and lipid peroxidation in monolayer cultures of rabbit tracheal epithelium exposed in vitro to ozone.

Numerous reports have documented airway epithelial damage and lipid peroxidation in the lungs of animals exposed to ozone. However, the response of isolated tracheal epithelial (TE) cells to ozone has not been extensively studied. To assess ozone-induced injury in cultured TE cells, an in vitro exposure system was developed in which cells were maintained at gas-fluid interface analogous to in vivo conditions. Confluent monolayer cultures of rabbit TE cells were exposed for 30 min to atmospheres of 5% CO2/air containing 0.05, 0.1, 0.5, 1, 2, 4, 6, or 8 ppm ozone. Morphologic injury was assessed by phase-contrast microscopy and by determination of TE cell number and viability (trypan blue dye exclusion) pre- and postexposure, and the lipid peroxide content of TE cells was measured as thiobarbituric acid (TBA) reactive substances. Exposure to 5% CO2/air alone did not affect monolayer morphology, cell number of viability. Cultures exposed to 0.05 or 0.1 ppm ozone demonstrated no consistent light microscopic changes, whereas exposure to 0.5 ppm and higher ozone concentrations caused distortion of monolayer morphology, cytoplasmic vacuolization, and decreased viability. Exposure to 0.5 or 1 ppm resulted primarily in cytoplasmic vacuolization while exposure to 2, 4, 6, or 8 ppm induced more pronounced cellular injury associated with cell necrosis (viability post 8 ppm ozone 75.0 +/- 7.0%, vs. 95.9 +/- 2.6% for 5% CO2/air controls). Ozone exposure also caused changes in cell shape, which on occasion resulted in loss of cell-to-cell contact. Increased production of TBA-reactive substances was detected in TE cells following ozone exposure, including exposure to 0.05 and 0.1 ppm. The morphologic changes induced by in vitro ozone exposure in the cultured TE cells were similar to those described in the tracheal epithelium of ozone-exposed animals and occurred independent of recruited inflammatory cells or extravasated circulating mediators.

Animals↗
PubMed2004

Ozone effects on the ultrastructure of peatland plants: Sphagnum mosses, Vaccinium oxycoccus, Andromeda polifolia and Eriophorum vaginatum.

BACKGROUND AND AIMS: Ozone effects on peatland vegetation are poorly understood. Since stress responses are often first visible in cell ultrastructure, electron microscopy was used to assess the sensitivity of common peatland plants to elevated ozone concentrations. METHODS: Three moss species (Sphagnum angustifolium, S. magellanicum and S. papillosum), a graminoid (Eriophorum vaginatum) and two dwarf shrubs (Vaccinium oxycoccus and Andromeda polifolia), all growing within an intact canopy on peat monoliths, were exposed to a concentration of 0, 50, 100 or 150 ppb ozone in two separate growth chamber experiments simulating either summer or autumn conditions in central Finland. After a 4- or 5-week-long exposure, samples were photographed in a transmission electron microscope and analysed quantitatively using image processing software. KEY RESULTS: In the chlorophyllose cells of the Sphagnum moss leaves from the capitulum, ozone exposure led to a decrease in chloroplast area and in granum stack thickness and various changes in plastoglobuli and cell wall thickness, depending on the species and the experiment. In E. vaginatum, ozone exposure significantly reduced chloroplast cross-sectional areas and the amount of starch, whereas there were no clear changes in the plastoglobuli. In the dwarf shrubs, ozone induced thickening of the cell wall and an increase in the size of plastoglobuli under summer conditions. In contrast, under autumn conditions the cell wall thickness remained unchanged but ozone exposure led to a transient increase in the chloroplast and starch areas, and in the number and size of plastoglobuli. CONCLUSIONS: Ozone responses in the Sphagnum mosses were comparable to typical ozone stress symptoms of higher plants, and indicated sensitivity especially in S. angustifolium. The responses in the dwarf shrubs suggest stimulation of photosynthesis by low ozone concentrations and ozone sensitivity only under cool autumn conditions.

Cyperaceae↗
PubMed2003

Ozone exposure enhances endotoxin-induced mucous cell metaplasia in rat pulmonary airways.

Coexposure to different airborne pollutants can be more toxic to airway epithelium than an inhalation exposure to a single pollutant. We have previously reported that coexposure to ozone, the primary oxidant gas in photochemical smog, and unique inflammatory biogenic substances such as allergens or bacterial endotoxin, results in augmented epithelial and inflammatory responses in rat nasal airways (M. V. Fanucchi et al., 1998, Toxicol. Appl. Pharmacol. 152, 1-9; J. G. Wagner et al., 2002a, Toxicol. Sci.67, 284-294). In the present study, we investigated the toxic interaction of ozone and endotoxin on the respiratory epithelium in the pulmonary airways of laboratory rodents. F344 rats were intranasally instilled with 0, 2, or 20 microg endotoxin dissolved in sterile saline (150 microl/nasal passage). Six h after instillation rats were exposed to air or 1 ppm ozone for 8 h. One day later, endotoxin and ozone exposures were repeated. Three days after the last exposure, rats were sacrificed, the lungs were lavaged with saline, and the collected bronchoalveolar lavage fluid (BALF) was analyzed for inflammatory cells and secreted mucosubstances (mucin 5AC). Lung tissues were processed for light microscopic examination and morphometric analysis of numeric density of epithelial cell populations and volume densities of intraepithelial mucosubstances (IM). Conducting airways were microdissected and analyzed by quantitative RT-PCR to determine steady-state mucin gene (rMuc5AC) mRNA levels in respiratory epithelium. Endotoxin instillation caused a dose-dependent increase in BALF neutrophils that was further increased twofold in ozone-exposed rats given 20 microg endotoxin. Mucin glycoprotein 5AC was elevated in BALF from rats exposed to 20 microg, but not 2 microg endotoxin. Exposure to ozone alone did not cause mucus hypersecretion, but ozone potentiated mucus secretion in rats given 2 or 20 microg endotoxin. Airways of rats exposed to air or ozone alone had scant amounts of IM. Endotoxin instillation induced a dose-dependent increase in IM in airway epithelium that was significantly increased (twofold) in rats that were also exposed to ozone. Expression of rMuc5AC was induced in axial pulmonary airways by 2 and 20 microg endotoxin, and was increased further by ozone-exposure in rats instilled with 20 microg endotoxin. These data demonstrate that ozone exposure potentiates neutrophilic inflammation and mucus production and secretion elicited by a biogenic substance in rat pulmonary airways.

Administration, Intranasal↗
PubMed2001

Blue wild-rye grass competition increases the effect of ozone on ponderosa pine seedlings.

Individual ponderosa pine (Pinus ponderosa Dougl. ex Laws.) seedlings were grown in mesocosms with three densities of blue wild-rye grass (Elymus glaucus Buckl.) (equivalent to 0, 32 or 88 plants m-2) to determine if the presence of a natural competitor alters the response of ponderosa pine seedlings to ozone. After 3 years of ozone exposure, grass presence reduced total ponderosa pine dry mass by nearly 50%, whereas ozone alone had no significant effect on ponderosa pine growth. The combination of ozone and grass further reduced needle, stem and branch dry mass significantly below that induced by grass competition alone. Root:shoot ratios increased in response to the combined grass and ozone treatments. Grass competition significantly reduced soluble sugar concentrations in all ponderosa pine tissue components examined. Starch concentrations were highly variable but did not differ significantly between treatments. Ozone significantly reduced soluble sugar concentrations in fine roots and stems. In the absence of grass, ozone-treated seedlings tended to have higher tissue N concentrations than controls. In the presence of grass, ozone-treated seedlings had lower N concentrations than controls, resulting in a significant interaction between these two stresses in 1- and 2-year-old needles. Needle C:N ratios decreased in response to grass competition, as a result of increased N concentration and no change in C concentration. The opposite response was observed in ozone-treated seedlings as a result of decreased N concentrations, indicating that ozone-treated seedlings were unable to take up or retain as much nitrogen when grown in the presence of grass. We conclude that ponderosa pine seedlings are more susceptible to ozone when grown in competition with blue wild-rye grass.

California↗
PubMed2004

Genetic susceptibility to ozone-induced lung inflammation in animal models of asthma.

PURPOSE OF REVIEW: Epidemiological associations between ozone exposure and allergic responsiveness are well-documented and have been corroborated in animal studies. The complex interaction between ozone and allergen has genetic and environmental components that affect atopic individuals and may increase the incidence of allergy in susceptible individuals. This review describes the advances that have been made in understanding mechanisms of genetic susceptibility to ozone-induced inflammation, and the interaction between ozone and allergen exposure in mice and a non-human primate model. RECENT FINDINGS: Antioxidant and innate immune defense genes contribute to ozone-induced inflammation and hyperpermeability in mice and humans. Ozone exposure during the allergic challenge phase induces greater enhancement of allergic responsiveness than the sensitization stage. Ovalbumin-pulsed dendritic cells injected into naïve mice successfully sensitize the mouse to ovalbumin in the absence of adjuvant. Debate continues over the role of T helper 1-T helper 2 immune profile development in mediating the ozone-allergen interaction, and the potential confounding influence of the predominant T helper 2 system most commonly used to study these responses. SUMMARY: The role of genetic background in susceptibility to ozone-induced lung inflammation has been confirmed, and promising candidate genes have been identified. Descriptive studies confirm that ozone exacerbates allergic responsiveness. Ozone administered during the challenge phase of ovalbumin allergen exposure induces greater responsiveness than during the sensitization phase. Allergen-induced responses enhanced by concurrent ozone exposure warrant further mechanistic research, particularly regarding the influence of susceptibility genes.

Allergens↗
PubMed2001

Ozone quenching properties of isoprene and its antioxidant role in leaves.

Isoprene is formed in and emitted by plants and the reason for this apparent carbon waste is still unclear. It has been proposed that isoprene stabilizes cell and particularly chloroplast thylakoid membranes. We tested if membrane stabilization or isoprene reactivity with ozone induces protection against acute ozone exposures. The reduction of visible, physiological, anatomical, and ultrastructural (chloroplast) damage shows that clones of plants sensitive to ozone and unable to emit isoprene become resistant to acute and short exposure to ozone if they are fumigated with exogenous isoprene, and that isoprene-emitting plants that are sensitive to ozone do not suffer damage when exposed to ozone. Isoprene-induced ozone resistance is associated with the maintenance of photochemical efficiency and with a low energy dissipation, as indicated by fluorescence quenching. This suggests that isoprene effectively stabilizes thylakoid membranes. However, when isoprene reacts with ozone within the leaves or in a humid atmosphere, it quenches the ozone concentration to levels that are less or non-toxic for plants. Thus, protection from ozone in plants fumigated with isoprene may be due to a direct ozone quenching rather than to an induced resistance at membrane level. Irrespective of the mechanism, isoprene is one of the most effective antioxidants in plants.

Antioxidants↗
PubMed2005

An in vitro evaluation of the ability of ozone to kill a strain of Enterococcus faecalis.

AIM: To evaluate the potential of ozone as an antibacterial agent using Enterococcus faecalis as the test species. METHODOLOGY: Ozone was produced by a custom-made bench top generator and its solubility in water determined by ultraviolet (258 nm) spectrophotometric analysis of solutions through which ozone was sparged for various time-periods. The antibacterial efficacy of ozone was tested against both broth and biofilm cultures. Ozone was sparged for 30, 60, 120 and 240 s, through overnight broth cultures of a strain of E. faecalis (E78.2) and compared with those that were centrifuged, washed and resuspended in water. Enterococcus faecalis (E78.2) biofilms were grown on cellulose nitrate membrane filters for 48 h and suspended in water through which ozone gas was sparged with stirring for 60, 120 and 240 s in a standard fashion. In a separate test, biofilms were also exposed to gaseous ozone. Sodium hypochlorite (NaOCl) was used as a positive control. All experiments were repeated four times. RESULTS: There were significant (P < 0.05) reductions of bacteria in the unwashed (2 log(10) reductions) and washed (5 log(10) reductions) broth cultures following 240 s applications. Biofilms incubated for 240 s with ozonated water showed no significant reduction in cell viability attributable to ozone alone, whereas with NaOCl no viable cells were detected over the same time. Gaseous ozone applied for 300 s had no effect on these biofilms. CONCLUSIONS: Ozone had an antibacterial effect on planktonic E. faecalis cells and those suspended in fluid, but little effect when embedded in biofilms. Its antibacterial efficacy was not comparable with that of NaOCl under the test conditions used.

Anti-Bacterial Agents↗
PubMed2005

ROS perception in Arabidopsis thaliana: the ozone-induced calcium response.

Ozone is responsible for more crop losses than any other air pollutant. The changes in gene expression, which occur in plants in response to ozone, have been well characterized, yet little is known about how ozone is perceived or the signal transduction steps that follow. The earliest characterized response to ozone is an elevation in cytosolic-free calcium, which takes place within seconds of exposure. In this study, the calcium response to ozone was investigated in Arabidopsis thaliana seedlings using a variety of fumigation protocols. Ozone elicited distinct calcium responses in the aerial tissue and roots of seedlings. The calcium response in the cotyledons and leaves was biphasic and sensitive to the rate at which the ozone concentration increased. The response in the root was monophasic and insensitive to the rate of increase in ozone concentration. Experiments utilizing inhibitors of antioxidant metabolism demonstrated that the magnitude of the first peak in calcium in the aerial tissues was dependent upon the redox status of the plant. Seedlings were shown to be able to distinguish between ozone and hydrogen peroxide, producing a calcium signal in response to one of these reactive oxygen species (ROS) when they had become refractory to the other. Pre-treatment with ozone altered the calcium response to hydrogen peroxide and vice versa, indicating that the calcium response to a given ROS may reflect the stress history of the plant. These data suggest ROS signalling is more sophisticated than previously realized and raise questions over current models of ozone perception.

Arabidopsis↗
PubMed2004

Ozone exposures during trans-continental and trans-Pacific flights.

UNLABELLED: Ozone concentrations were passively monitored in passenger cabins of commercial airliners flying domestic, Pacific, and south-east Asian routes. One-hundred and six flight segments were monitored for either the full duration and/or approximately 3 h during the middle portion of the flight for a total of 145 time-integrated measurements. Over all samples the mean (+/-SD) concentration was 80 p.p.b. (30.1). Twenty percent of the measurements exceeded 100 p.p.b., the FAA-recommended level. Eleven percent of the measurements exceeded 120 p.p.b., the US EPA's short-term National Ambient Air Quality Standard for ozone. Ozone concentrations measured on Pacific flights were substantially higher during mid-flight than over the full flight (95 p.p.b. vs. 56 p.p.b). Ozone concentrations on the northern Pacific routes were higher than concentrations for other Pacific flights. Season comparison showed that ozone levels were higher during the winter and spring than for the summer and fall. Our study shows that even in aircraft with catalytic ozone converters, passengers and flight crew may be exposed to elevated ozone levels on domestic and international flights. Given the frequency of ozone excess, it is recommended that (1) ozone converters should be required equipment on all commercial passenger aircraft for mid and high latitude routes (2) improved maintenance procedures should be required for catalytic converters (e.g., more frequent servicing/replacement), and (3) ozone should be routinely monitored on all mid and high latitude flights. PRACTICAL IMPLICATIONS: The authors have demonstrated elevated ozone concentrations in passenger cabins. They give several practical recommendations to help solve the problem.

Air Pollution, Indoor↗
PubMed2006

Influence of ozone-limonene reactions on perceived air quality.

UNLABELLED: This study conducted short-term assessments of perceived air quality (PAQ) for six different realistic concentrations of ozone and limonene, separately or together, in room air. The impact of filtration and the influence of the ozone generation method were also examined. The evaluations were made in four identical 40 m3 low-polluting test offices ventilated at 1.4 h(-1) or in two identical 30 m3 stainless-steel chambers ventilated at 1.9 h(-1). Concentrations of ozone, total volatile organic compounds and size-fractionated particles were continuously monitored in each experiment. The results indicate that, for each of the six conditions, the PAQ was poorer when ozone and limonene were present together compared with when only ozone or only limonene was present. In the test offices a correlation was observed between the number of secondary organic aerosols produced by a given ozone/limonene condition and the sensory pollution load for that condition. The particles themselves do not appear to be the primary causative agents, but instead are co-varying surrogates for sensory offending gas-phase species. PRACTICAL IMPLICATIONS: Although the health consequences of long-term exposures to the products of ozone-initiated indoor chemistry remain to be determined, we judge that the sensory offending nature of selected products provides an additional reason to limit indoor ozone levels. Devices that emit ozone at significant rates should not be used indoors. Ozone-filtration of make-up air should also be beneficial in mechanically ventilated buildings located in regions that repeatedly violate outdoor ozone standards. Additionally, the use of limonene containing products should be curtailed during periods when indoor ozone levels are elevated.

Aerosols↗
PubMed1995

Ozone-induced oxygen radical release from bronchoalveolar lavage cells and airway hyper-responsiveness in dogs.

1. Ozone inhalation causes airway hyper-responsiveness and airway inflammation in dogs. The purpose of this study was to determine whether these effects are associated with increases in oxygen radical production from bronchoalveolar lavage (BAL) cells. 2. Twelve randomly selected dogs were studied twice, 4 weeks apart. On each study day, acetylcholine (ACh) airway responsiveness was measured before and 1 h after ozone (3 p.p.m., 30 min) or dry air inhalation, followed by BAL. The response to ACh was expressed as the concentration causing an increase in lung resistance of 5 cmH2O l-1 s-1 above baseline. Spontaneous and phorbol myristate acetate (PMA) (2.4 mumol l-1)-stimulated oxygen radical release from washed BAL cells (4 x 10(6) cells ml-1) was measured by luminol-enhanced chemiluminescence in a luminometer at 37 degrees C. 3. Ozone inhalation caused airway hyper-responsiveness. The concentration of ACh causing an increase in lung resistance of 5 cmH2O l-1 s-1 (the 'provocative' concentration) fell from 4.68 mg ml-1 (% S.E.M., 1.43) before, to 0.48 mg ml-1 (% S.E.M., 1.60) after ozone (P < 0.0001). Spontaneous chemiluminescence area under the curve (AUC) significantly increased after ozone from 4.08 mV (10 min) (% S.E.M., 1.28) after dry air to 8.25 mV (10 min; % S.E.M., 1.29) after ozone (P = 0.007). Ozone inhalation also increased PMA-stimulated chemiluminescence AUC from 18.97 mV (10 min; % S.E.M., 1.18) after dry air to 144.03 mV (10 min; % S.E.M., 1.45) after ozone (P = 0.0001). The increase in PMA-stimulated chemiluminescence was significantly correlated with ozone-induced ACh airway hyper-responsiveness (r = 0.83, P < 0.001). 4. These results indicate that inhaled ozone increases oxygen radical release from BAL cells and suggest that oxygen radicals are important in causing ozone-induced airway hyper-responsiveness.

Acetylcholine↗
PubMed1997

Ozone inactivates cyclooxygenase in human tracheal epithelial cells without altering PGHS-2 mRNA or protein.

Exposure of human tracheal epithelial (TE) cells to ozone (0.1-0.5 ppm) leads to a transient increase followed by decreased production of prostaglandin (PG) E2 concomitant with dose-dependent loss and delayed recovery of cyclooxygenase (CO) activity [S.E. Alpert and R.W. Walenga. Am. J. Physiol. 269 (Lung Cell. Mol. Physiol. 13): L734-L743, 1995]. Formation of reactive oxygen species (ROS) in cultured tracheobronchial epithelial cells during ozone exposure was recently demonstrated (L.C. Chen and Q.Qu. Toxicol. Appl. Pharmacol. 143: 96-101, 1997). In the present study, we investigated if ROS generated by ozone-exposed human TE cells contribute to PGE2 production and/or CO inactivation and whether the delay in recovery of CO activity after ozone reflects impaired gene transcription and/or protein synthesis. Rapid, dose-dependent ROS generation, assessed by fluorescence of dihydrorhodamine 123, was detected in human TE monolayers exposed to 0.21-0.63 ppm ozone. In a different system, TE cells were exposed to air or 0.5 ppm ozone for 1 h by serial renewal/collection of an adherent film of media. Ozone-induced ROS formation, the transient increase and decline in PGE2, and CO inactivation were attenuated by an intracellular hydroxyl radical scavenger, 1,3-dimethyl-2-thiourea. Ibuprofen, a reversible CO inhibitor, prevented PGE2 release during ozone exposure (and hence autocatalytic CO inactivation) but not loss of CO activity. Although CO activity remained depressed for hours after ozone exposure, compared with air-exposed cultures, no differences were detected in mRNA and protein levels of prostaglandin endoperoxide G/H synthase 2 (PGHS-2), the only CO isoform present in human TE cells, or in the rate of de novo PGHS-2 synthesis. Our findings suggest that ozone-induced PGE2 production and CO inactivation are primarily the result of formation of intracellular oxidant molecules and that delayed recovery of CO activity in human TE cells after short-term ozone exposure is due to persistent inactivation of PGHS-2, rather than to interference with its synthesis.

Air↗