Ppm Ozone Research Articles

An acute exposure to ozone impairs human olfactory functioning

IntroductionOzone is a ubiquitous and irritant gas. We questioned whether an acute exposure to 0.2 ppm ozone impaired olfactory functioning. MethodsHealthy, normosmic subjects were exposed according to a parallel group design either to 0.2 ppm ozone (n = 15) or to sham (n = 13) in an exposure chamber for two hours. Possible irritating effects were assessed by questionnaire (range 0–5). The detection threshold of n-butanol was measured with the Sniffin’ Sticks test before and after exposure. Olfactory thresholds were logarithmized and a two-way analysis of variance (ANOVA) with repeated measurements was carried out to test the effects of exposure (ozone vs. sham) and time (before vs. after exposure). Additionally, nasal secretions were taken at a preliminary examination and after exposure to determine interleukins 1ß and 8. ResultsNo irritating effects to the upper airways were observed. In the ozone group, the median score for cough increased from 0 to 2 at the end of exposure (sham group 0 and 0, respectively, p < 0.001). The ANOVA showed a main effect for ozone exposure (F (1, 26) = 27.6, p = 0.0002), indicating higher olfactory thresholds in the ozone group. Concentrations of interleukins in nasal secretions did not increase following ozone exposure. ConclusionsThis study shows a clear impairment of olfactory functioning following an acute exposure to 0.2 ppm ozone.

Susceptibility of the life stages of cigarette beetle, Lasioderma serricorne (F.) (Coleoptera: Anobiidae) to ozone

The ban of methyl bromide and problems associated with the use of other stored-product pest control methods have demanded search for potential alternatives. Ozone, an oxidizing gas, is one of such potential alternatives. In this study, the susceptibility of life stages of the cigarette beetle, Lasioderma serricorne (F.) (Coleoptera: Anobiidae) to ozone, was investigated. The concentration-mortality relationships for all life stages exposed to 100–400 ppm at 50 ppm increments for 1 h were determined. The time-mortality relationships for adult L. serricorne exposed to 100 ppm ozone concentration for 1–6 h were also determined. Mortality was recorded as percentages of eggs that failed to hatch 10 days after treatment (DAT), larvae or pupae that failed to develop into adults 28 or 15 DAT, respectively, and adults that died 2 DAT. The concentration-mortality estimates suggested that, generally, higher concentrations were required to kill 99% of insects when treated without food compared to when treated with food made of whole wheat flour and brewer's yeast. In the absence of food, larvae were the most tolerant and adults were the least tolerant to ozone treatment and required 15, 974 ppm and 3769 ppm to kill 99% of the individuals respectively. In the presence of food, eggs and pupae were the most and least tolerant respectively. An exposure time of 7.1 × 1030 h was required to kill 99% of adults treated in the presence of food and 99 h in the absence of food. When adult insects were exposed to 100 ppm ozone for 1–6 h in the absence of food, a weak relationship between survival rate and exposure duration observed initially became stronger in subsequent days. The present study suggests that ozone treatment could be a potential alternative for the management of all life stages of L. serricorne.

Sex-specific microRNA expression networks in an acute mouse model of ozone-induced lung inflammation

BackgroundSex differences in the incidence and prognosis of respiratory diseases have been reported. Studies have shown that women are at increased risk of adverse health outcomes from air pollution than men, but sex-specific immune gene expression patterns and regulatory networks have not been well studied in the lung. MicroRNAs (miRNAs) are environmentally sensitive posttranscriptional regulators of gene expression that may mediate the damaging effects of inhaled pollutants in the lung, by altering the expression of innate immunity molecules.MethodsMale and female mice of the C57BL/6 background were exposed to 2 ppm of ozone or filtered air (control) for 3 h. Female mice were also exposed at different stages of the estrous cycle. Following exposure, lungs were harvested and total RNA was extracted. We used PCR arrays to study sex differences in the expression of 84 miRNAs predicted to target inflammatory and immune genes.ResultsWe identified differentially expressed miRNA signatures in the lungs of male vs. female exposed to ozone. In silico pathway analyses identified sex-specific biological networks affected by exposure to ozone that ranged from direct predicted gene targeting to complex interactions with multiple intermediates. We also identified differences in miRNA expression and predicted regulatory networks in females exposed to ozone at different estrous cycle stages.ConclusionOur results indicate that both sex and hormonal status can influence lung miRNA expression in response to ozone exposure, indicating that sex-specific miRNA regulation of inflammatory gene expression could mediate differential pollution-induced health outcomes in men and women.

Impact of ozone on claudins and tight junctions in the lungs.

Claudins (CLDNs) are a major transmembrane protein component of tight junctions (TJs) in endothelia and epithelia. CLDNs are not only essential for sustaining the role of TJs in cell permeability but are also vital for cell signaling through protein-protein interactions. Ozone induces oxidative stress and lung inflammation in humans and experimental models, but the impact of ozone on claudins remains poorly understood. This study was to determine the expression of TJ proteins, such as claudin 3, 4, 5, and 14 following ozone exposure. Mice were exposed to 0.1, 1, or 2 ppm of ozone or ambient air for 6 h for 3 days. The impact of ozone on CLDNs, Nrf2, Keap1, and reactive oxygen species (ROS) were estimated using immunoblotting, immunohistochemical staining, confocal imaging, and ELISA analysis in mice and bronchial epithelial cells. Mice exposed to ozone experienced increased airway inflammatory cell infiltration and bronchial hyper-responsiveness compared to control mice. Additionally, CLDN3, CLDN4, ROS, Nrf2, and Keap1 protein expression increased, and lung CLDN14 protein expression decreased, in mice exposed to ozone compared with control mice. These results indicate that CLDNs are involved in airway inflammation following ozone exposure, suggesting that ozone affects TJ proteins through oxidative mechanisms.

Acute inhalation of ozone induces DNA methylation of apelin in lungs of Long-Evans rats

Apelin has cardiopulmonary protective properties that promote vasodilation and maintenance of the endothelial barrier. While reductions in apelin have been identified as a contributor to various lung diseases, including pulmonary edema, its role in the effect of air pollutants has not been examined. Thus, in the current study, we sought to investigate if apelin is a downstream target of inhaled ozone and if such change in expression is related to altered DNA methylation in the lung. Male, Long-Evans rats were exposed to filtered air or 1.0 ppm ozone for 4 h. Ventilation changes were assessed using whole-body plethysmography immediately following exposure, and markers of pulmonary edema and inflammation were assessed in the bronchoaveolar lavage (BAL) fluid. The enzymatic regulators of DNA methylation were measured in the lung, along with methylation and hydroxymethylation of the apelin promoter. Data showed that ozone exposure was associated with increased enhanced pause and protein leakage in the BAL fluid. Ozone exposure reduced DNA cytosine-5-methyltransferase (DNMT) activity and Dnmt3a/b gene expression. Exposure-induced upregulation of proliferating cell nuclear antigen, indicative of DNA damage, repair, and maintenance methylation. Increased methylation and reduced hydroxymethylation were measured on the apelin promoter. These epigenetic modifications accompanied ozone-induced reduction of apelin expression and development of pulmonary edema. In conclusion, epigenetic regulation, specifically increased methylation of the apelin promoter downstream of DNA damage, may lead to reductions in protective signaling of the apelinergic system, contributing to the pulmonary edema observed following the exposure to oxidant air pollution.

Assessing Sex‐Specific Effects of Ozone Exposure on Pulmonary Function and Lung Mechanics

BackgroundExposure to ground‐level ozone, an oxidative pollutant, causes lung inflammation, which can lead to pulmonary injury and impair lung innate immunity. There is emerging evidence that pulmonary diseases such as asthma affect women disproportionally with a greater degree of severity than men. In addition, most hospitalizations for asthma in women occur during the luteal phase or around the peri‐menstrual stage. However, the combined effect of ozone and sex hormones in respiratory mechanics is unclear. Here, we hypothesized that circulating estrogen levels can regulate pulmonary function and lung mechanics following ozone exposure.MethodsWe performed gonadectomy and hormone replacement (17β‐estradiol, 2 weeks) in a group of adult male and female C57BL/6 mice. In control females, the stages of the estrous cycle were monitored by daily by vaginal smear, and confirmed by serum sex hormone levels. We exposed animals to 1 ppm of ozone or filtered air (FA) for 3 hours, and we compared lung function 24h after exposure with a methacholine challenge (MCh; 0 – 50 mg/ml) using the FlexiVent system.ResultsWe observed significant changes in respiratory parameters (Ers, H, Rrs, RN, G) in males and females, and in females exposed to ozone at different stages of the estrous cycle, at the two highest MCh concentrations. The pressure‐volume curves obtained demonstrated similar MCh concentration‐dependent changes. Gonadectomized males exposed to ozone had higher Rrs and Ers than females and males exposed to FA, and treatment with estradiol ameliorated these effects. Surprisingly, female mice in the metestrus and diestrus stages exposed to FA had higher Rrs and Ers values than when compared to the proestrus and estrus stages. Contrarily, exposure to ozone caused a decrease in parameters (Ers, Rrs) during metestrus and diestrus stages, but a slight increase of these in the proestrus and estrus stages.ConclusionsOur results indicate that pulmonary function following ozone exposure can be affected by circulating hormone levels. Future studies examining diseases associated with environmental pollutants should consider the women's menstrual cycle.Support or Funding InformationThe authors thank the Pennsylvania State University College of Medicine Genome Sciences Core Facility for Bioanalyzer analysis. The authors also thank Todd Umstead and Susan Di Angelo for assistance with training and experiments, and Dr. Joanna Floros for the ozone equipment. NIH Grant K01HL133520.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Influence of Maternal High Fat Diet and Ozone Exposure on Serum Metabolomic Profiles in Juvenile Offspring

There is growing interest in understanding how maternal diet can affect the sensitivity of offspring to environmental exposures. Previous studies have demonstrated that adult offspring from dams given a high fat diet (HFD) prior to, during, and after pregnancy had elevated pulmonary responses to an acute ozone exposure. In this study, we examined the influence of maternal HFD on metabolic responses to ozone in male and female juvenile offspring. F0 female Long Evans rats began HFD (60% kcal from fat) or control diet (CD; 10.5% kcal from fat) at post‐natal day (PND) 30. Rats were bred on PND 75 and allowed to give birth. F1 litters were culled at PND 6 and offspring were weaned on PND 21. Offspring were maintained on respective HFD or CD until PND 30 when all groups were switched to CD. On PND 40, male and female offspring (n=8/group) were exposed to air or 0.8 ppm ozone for 5h. Immediately following exposure, animals were necropsied, serum was collected, and samples were subsequently assessed for changes in metabolite abundance using a metabolomic approach. Overall, analysis revealed significant changes in circulating metabolites due to sex, diet, and exposure. Maternal HFD increased serum microbiome‐associated histidine metabolites in male and tyrosine metabolites in female offspring, whereas selected free fatty acids were increased and phospholipids were decreased in both sexes. Furthermore, lower levels of 1,5‐anhydroglucitol were observed in all HFD groups regardless of sex or exposure. During hyperglycemic episodes, this metabolite is competitively inhibited by glucose for renal tubular reabsorption, thus decreases here may point towards development of insulin resistance in the offspring of mothers fed the HFD. Ozone exposure also had significant effects on serum metabolites. Decreases in biliverdin and bilirubin, heme catabolites with antioxidant properties, were detected in ozone‐exposed male and female offspring fed the CD but not the HFD, suggesting that the maternal diet may impact heme metabolism in offspring. Increases in free polyunsaturated fatty acids (PUFAs) were observed in ozone‐exposed male rats whereas in the female HFD ozone group, decreases in free PUFAs and monounsaturated fatty acids were apparent. Moreover, exposure to ozone led to increased levels of glucose in male rats regardless of maternal diet; however, in female offspring, pyruvate levels were elevated suggesting an increase in glucose utilization. This is supported by an ozone‐induced increase in the TCA cycle intermediates citrate and isocitrate in the female offspring of the HFD group. Collectively, the dataset suggest that ozone exposure elicits greater metabolic impact in juvenile female than male rats, and that maternal diet may further potentiate this effect. These results represent the basis to study the effects of maternal HFD on offspring sensitivity towards environmental factors and clearly suggest that susceptibility to ozone‐induced injury is sex‐dependent. (This abstract does not reflect US EPA Policy)Support or Funding InformationThis work was supported by US EPA funds.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Photolysis and photooxidation of typical gaseous VOCs by UV Irradiation: Removal performance and mechanisms

Photodegradation by ultraviolet irradiation (UV) is increasingly applied in volatile organic compound (VOC) and odor gas treatments. In this study, 27 typical VOCs, including 11 hydrocarbons and 16 hydrocarbon derivatives, at 150–200 ppm in air and nitrogen gas were treated by a laboratory-scale UV reactor with 185/254 nm irradiation to systematically investigate their removal and conversion by UV irradiation. For the tested 27 VOCs, the VOC removal efficiencies in air were within the range of 13%–97% (with an average of 80%) at a retention time of 53 s, which showed a moderate positive correlation with the molecular weight of the VOCs (R = 0.53). The respective contributions of photolysis and photooxidation to VOC removal were identified for each VOC. According to the CO2 results, the mineralization rate of the tested VOCs was within the range of 9%–90%, with an average of 41% and were negatively correlated to the molecular weight (R = −0.63). Many of the tested VOCs exhibited high concentration particulate matters in the off-gases with a 3–283 mg/m3 PM10 range and a 2–40 mg/m3 PM2.5 range. The carbon balance of each VOC during UVirradiation was analyzed based on the VOC, CO2 and PM10 concentrations. Certain organic intermediates and 23–218 ppm ozone were also identified in the off-gases. Although the UV technique exhibited a high VOC removal efficiency, its drawbacks, specifically low mineralization, particulate matters production, and ozone emission, must be considered prior to its application in VOC gas treatments.

&amp;lt;i&amp;gt;α&amp;lt;/i&amp;gt;-Pinene secondary organic aerosol at low temperature: chemical composition and implications for particle viscosity

Abstract. Chemical composition, size distributions, and degree of oligomerization of secondary organic aerosol (SOA) from α-pinene (C10H16) ozonolysis were investigated for low-temperature conditions (223 K). Two types of experiments were performed using two simulation chambers at the Karlsruhe Institute of Technology: the Aerosol Preparation and Characterization (APC) chamber, and the Aerosol Interaction and Dynamics in the Atmosphere (AIDA) chamber. Experiment type 1 simulated SOA formation at upper tropospheric conditions: SOA was generated in the AIDA chamber directly at 223 K at 61 % relative humidity (RH; experiment termed “cold humid”, CH) and for comparison at 6 % RH (experiment termed “cold dry”, CD) conditions. Experiment type 2 simulated SOA uplifting: SOA was formed in the APC chamber at room temperature (296 K) and &lt; 1 % RH (experiment termed “warm dry”, WD) or 21 % RH (experiment termed “warm humid”, WH) conditions, and then partially transferred to the AIDA chamber kept at 223 K, and 61 % RH (WDtoCH) or 30 % RH (WHtoCH), respectively. Precursor concentrations varied between 0.7 and 2.2 ppm α-pinene, and between 2.3 and 1.8 ppm ozone for type 1 and type 2 experiments, respectively. Among other instrumentation, a chemical ionization mass spectrometer (CIMS) coupled to a filter inlet for gases and aerosols (FIGAERO), deploying I− as reagent ion, was used for SOA chemical composition analysis. For type 1 experiments with lower α-pinene concentrations and cold SOA formation temperature (223 K), smaller particles of 100–300 nm vacuum aerodynamic diameter (dva) and higher mass fractions (&gt; 40 %) of adducts (molecules with more than 10 carbon atoms) of α-pinene oxidation products were observed. For type 2 experiments with higher α-pinene concentrations and warm SOA formation temperature (296 K), larger particles (∼ 500 nm dva) with smaller mass fractions of adducts (&lt; 35 %) were produced. We also observed differences (up to 20 ∘C) in maximum desorption temperature (Tmax) of individual compounds desorbing from the particles deposited on the FIGAERO Teflon filter for different experiments, indicating that Tmax is not purely a function of a compound's vapor pressure or volatility, but is also influenced by diffusion limitations within the particles (particle viscosity), interactions between particles deposited on the filter (particle matrix), and/or particle mass on the filter. Highest Tmax were observed for SOA under dry conditions and with higher adduct mass fraction; lowest Tmax were observed for SOA under humid conditions and with lower adduct mass fraction. The observations indicate that particle viscosity may be influenced by intra- and inter-molecular hydrogen bonding between oligomers, and particle water uptake, even under such low-temperature conditions. Our results suggest that particle physicochemical properties such as viscosity and oligomer content mutually influence each other, and that variation in Tmax of particle desorptions may have implications for particle viscosity and particle matrix effects. The differences in particle physicochemical properties observed between our different experiments demonstrate the importance of taking experimental conditions into consideration when interpreting data from laboratory studies or using them as input in climate models.

Changes in Metabolites Present in Lung-Lining Fluid Following Exposure of Humans to Ozone.

Controlled human exposure to the oxidant air pollutant ozone causes decrements in lung function and increased inflammation as evidenced by neutrophil influx into the lung and increased levels of proinflammatory cytokines in the airways. Here we describe a targeted metabolomics evaluation of human bronchoalveolar lavage fluid (BALF) following controlled in vivo exposure to ozone to gain greater insight into its pulmonary effects. In a 2-arm cross-over study, each healthy adult human volunteer was randomly exposed to filtered air (FA) and to 0.3 ppm ozone for 2 h while undergoing intermittent exercise with a minimum of 4 weeks between exposures. Bronchoscopy was performed and BALF obtained at 1 (n = 9) or 24 (n = 23) h postexposure. Metabolites were detected using ultrahigh performance liquid chromatography-tandem mass spectroscopy. At 1-h postexposure, a total of 28 metabolites were differentially expressed (DE) (p < .05) following ozone exposure compared with FA-exposure. These changes were associated with increased glycolysis and antioxidant responses, suggesting rapid increased energy utilization as part of the cellular response to oxidative stress. At 24-h postexposure, 41 metabolites were DE. Many of the changes were in amino acids and linked with enhanced proteolysis. Changes associated with increased lipid membrane turnover were also observed. These later-stage changes were consistent with ongoing repair of airway tissues. There were 1.37 times as many metabolites were differentially expressed at 24 h compared with 1-h postexposure. The changes at 1 h reflect responses to oxidative stress while the changes at 24 h indicate a broader set of responses consistent with tissue repair. These results illustrate the ability of metabolomic analysis to identify mechanistic features of ozone toxicity and aspects of the subsequent tissue response.

Ozone assisted oxidation of gaseous PCDD/Fs over CNTs-containing composite catalysts at low temperature

Ozone assisted carbon nanotubes (CNTs) supported vanadium oxide/titanium dioxide (V/Ti-CNTs) or vanadium oxide-manganese oxide/titanium dioxide (V-Mn/Ti-CNTs) catalysts towards gaseous PCDD/Fs (polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans) catalytic oxidations at low temperature (150 °C) were investigated. The removal efficiency (RE) and decomposition efficiency (DE) of PCDD/Fs achieved with V-Mn/Ti-CNTs alone were 95% and 45% at 150 °C under a space velocity (SV) of 14000 h−1; yet, these values reached 99% and 91% when catalyst and low concentration (50 ppm) ozone were used in combined. The ozone promotion effect on catalytic activity was further enhanced with the addition of manganese oxide (MnOx) and CNTs. Adding MnOx and CNTs in V/Ti catalysts facilitated the ozone decomposition (creating more active species on catalyst surface), thus, improved ozone utilization (demanding relatively lower ozone addition concentration). On the other hand, this study threw light upon ozone promotion mechanism based on the comparison of catalyst properties (i.e. components, surface area, surface acidity, redox ability and oxidation state) before and after ozone treatment. The experimental results indicate that a synergistic effect exists between catalyst and ozone: ozone is captured and decomposed on catalyst surface; meanwhile, the catalyst properties are changed by ozone in return. Reactive oxygen species from ozone decomposition and the accompanied catalyst properties optimization are crucial reasons for catalyst activation at low temperature.

Ozone modifies the metabolic and endocrine response to glucose: Reproduction of effects with the stress hormone corticosterone

Air pollution is associated with increased incidence of metabolic disease (e.g. metabolic syndrome, obesity, diabetes); however, underlying mechanisms are poorly understood. Air pollutants increase the release of stress hormones (human cortisol, rodent corticosterone), which could contribute to metabolic dysregulation. We assessed acute effects of ozone, and stress axis involvement, on glucose tolerance and on the metabolic (triglyceride), endocrine/energy regulation (insulin, glucagon, GLP-1, leptin, ghrelin, corticosterone), and inflammatory/endothelial (TNF, IL-6, VEGF, PAI-1) response to exogenous glucose. Male Fischer-344 rats were exposed to clean air or 0.8 ppm ozone for 4 h in whole body chambers. Hypothalamic-pituitary-adrenal (HPA) axis involvement in ozone effects was tested through subcutaneous administration of the glucocorticoid synthesis inhibitor metyrapone (50 mg/kg body weight), corticosterone (10 mg/kg body weight), or vehicle (40% propylene glycol) prior to exposure. A glucose tolerance test (2 g/kg body weight glucose) was conducted immediately after exposure, with blood samples collected at 0, 30, 60, 90, and 120 min. Ozone exposure impaired glucose tolerance, an effect accompanied by increased plasma triglycerides but no impairment of insulin release. Ozone diminished glucagon, GLP-1, and ghrelin responses to glucose, but did not significantly impact inflammatory/endothelial analytes. Metyrapone reduced corticosterone but increased glucose and triglycerides, complicating evaluation of the impact of glucocorticoid inhibition. However, administration of corticosterone reproduced the profile of ozone effects, supporting a role for the HPA axis. The results show that ozone-dependent changes in glucose tolerance are accompanied by altered metabolic and endocrine responses to glucose challenge that are reproduced by exogenous stress hormone.

LuminoTox as a tool to optimize ozone doses for the removal of contaminants and their associated toxicity

New treatment technologies and quality monitoring tools are needed for Contaminants of Emerging Concern (CECs) in wastewater. The purpose of this work was to assess the LuminoTox as a monitoring tool for CEC-associated toxicity in municipal wastewater during ozone treatment, and to evaluate the impact of different ozone feed concentrations at equivalent ozone doses for removing toxicity. The LuminoTox was sensitive at monitoring changes in toxicity of atrazine (ATZ) in synthetic wastewater (SWW) and in a 14 CECs mix in secondary effluent (SE) during ozone treatment. In both experiments, a decrease in toxicity was observed with increasing transferred ozone dose, which corresponded to a decrease in CEC concentration. For ATZ in SWW, a 5 ppm ozone feed showed better toxicity removal, up to 25% and 35% inhibition for LuminoTox algae biosensors SAPS I and SAPS II, respectively, for statistically equivalent ozone dose pairs of 43 mg (5 ppm ozone feed) and 36 mg (15 ppm ozone feed). The opposite was true for the 14 CECs in SE; the 15 ppm ozone feed showed better toxicity removal, up to a reduction of 37% and 40% for SAPS I and SAPS II inhibition, respectively, for statistically equivalent ozone dose pairs of 42 mg (5 ppm ozone feed) and 42 mg (15 ppm ozone feed). Different feed applications had an impact on the efficiency of toxicity removal for equivalent ozone doses; this efficiency appears to depend on the type of contaminants and/or wastewater matrix.

Uterine Artery Flow and Offspring Growth in Long-Evans Rats following Maternal Exposure to Ozone during Implantation.

Background:Epidemiological studies suggest that increased ozone exposure during gestation may compromise fetal growth. In particular, the implantation stage of pregnancy is considered a key window of susceptibility for this outcome.Objectives:The main goals of this study were to investigate the effects of short-term ozone inhalation during implantation on fetal growth outcomes and to explore the potential for alterations in uterine arterial flow as a contributing mechanism.Methods:Pregnant Long-Evans rats were exposed to filtered air, ozone, or ozone for 4 h/d during implantation, on gestation days (GD) 5 and 6. Tail cuff blood pressure and uterine artery Doppler ultrasound were measured on GD 15, 19, and 21. To assess whether peri-implantation ozone exposure resulted in sustained pulmonary or systemic health effects, bronchoalveolar lavage fluid, serum metabolic and inflammatory end points, and kidney histopathology were evaluated in dams at GD 21. Growth parameters assessed in GD 21 offspring included fetal weight, length, and body composition.Results:Measures of maternal uterine arterial flow, including resistance index and mean velocity, indicated that resistance increased between GD 15 and GD 21 in dams but decreased in controls, although absolute values were similar in both groups on GD 21. Ozone-exposed dams also had lower serum glucose and higher free fatty acid concentrations than controls on GD 21. On GD 21, both male and female offspring had lower body weight than controls, and pooled subsets of 3 male and 3 female fetuses from litters exposed to ozone had lower lean mass and fat mass than pooled control offspring.Conclusions:Findings from our experimental model suggest that the offspring of dams exposed to ozone during implantation had reduced growth compared with controls, possibly as a consequence of ozone-induced vascular dysfunction. https://doi.org/10.1289/EHP2019

Heterogeneous ozonation reactions of PAHs and fatty acid methyl esters in biodiesel particulate matter

Numerous studies have examined the oxidation of PAHs found in diesel particulate matter (PM) by ozone, but no studies have investigated the ozone oxidation of biodiesel exhaust PM. Fatty acid methyl esters (FAMEs), found in high abundance in biodiesel PM, can potentially alter the kinetics of the reactions between atmospheric oxidants such as ozone and particle-phase PAHs. In this study, the heterogeneous reactivity of 16 EPA PAHs upon 24 h exposure to 0.4 ppm ozone in the presence (PAH + FAMES) and absence (PAH-only) of FAMEs was investigated at room temperature and 50% relative humidity. The ozone-reactivity of the PAHs detected in 20% biodiesel (B20) exhaust PM was also investigated. In the absence of FAMEs, the pseudo-first order ozone reaction rate constant, kO3,of PAHs varied from 0.086 ± 0.030 hr−1 (chrysene) to 0.184 ± 0.078 hr−1 (anthracene). In the presence of FAMEs, kO3 of the PAHs varied between 0.013 ± 0.012 hr−1 (benzo[b]fluoranthene) and 0.168 ± 0.028 hr−1 (benzo[a]pyrene), and with the exception of benzo[a]pyrene, the kO3of PAHs were 1.2–8 times lower compared to those obtained during the PAH-only ozone exposure. Only one PAH, benzo[a]pyrene (BaP), did not show a significant change in kO3 with addition of FAMEs. Phenanthrene, fluoranthene, and pyrene, the only PAHs detected in the B20 PM, had kO3 values about 4 times lower in B20 PM than those obtained when spiked PAHs-only were exposed to ozone. The kO3 values of phenanthrene and fluoranthene in the B20 PM were 2 times higher than rates obtained when the PAH mix was exposed to ozone in the presence of the FAMEs. In contrast, pyrene's kO3 in the B20 PM was about 2 times lower than that obtained for the PAH + FAMEs exposure. Observed differences in PAH behavior demonstrate individual PAH heterogeneous reactivity with gas-phase ozone is sensitive to PAH (vapor pressure, solubility/sorption to matrix components, chemical reactivity) as well as substrate properties (PAH and O3 diffusivity in the matrix that may evolve with reaction progress). Saturated FAMEs were not reactive with ozone (kO3 range = 0.004 ± 0.003 to 0.012 ± 0.026 hr−1), but compared to PAHs, up to two times higher kO3 was measured for the unsaturated FAMEs (range 0.087 ± 0.015 to 0.329 ± 0.023 hr−1) during PAH + FAMEs exposures. These changes in substrate composition during atmospheric aging would be expected to affect PAH diffusivity and therefore heterogeneous reactivity over time. The factor of 1.2–8 decreased heterogeneous reactivity of PAHs in the presence of the FAMEs mix and the B20 PM matrix suggests that the presence of FAMEs in the diesel fuel supply may lead to increased PAH atmospheric lifetimes and longer range PAH transport. Predictive methods to quantify changes in PAH reactivity with gas-phase oxidants as a function of substrate composition and characteristics (viscosity, polarity, degree of unsaturation) are needed as biodiesel is increasingly present in our diesel engine fuel supply from a variety of feedstocks at different blend ratios.

Efficacy of Ozone Against the Life Stages of Oryzaephilus mercator (Coleoptera: Silvanidae)

Ozone is a highly oxidizing gas with insecticidal activity and it is a potential alternative to conventional fumigants, such as phosphine and methyl bromide, for managing stored product insects. Susceptibility of the merchant grain beetle, Oryzaephilus mercator (Fauvel; Coleoptera: Silvanidae), an important pest of stored products, to ozone treatments is unknown. In this study, we investigated the efficacy of ozone for controlling O. mercator. We determined concentration-mortality relationships for all stages of O. mercator exposed to 100-400 ppm for 1 h (1 g/m3 = 467 ppm). We also determined time-mortality relationships for adults exposed to 100 ppm for 1-6 h. Mortality was recorded as percentages of eggs that failed to hatch 10 days after treatment (DAT), larvae or pupae that failed to develop into adults 20 or 15 DAT, respectively, and adults that died 2 DAT. Generally, mortality increased with an increase in ozone concentration. Mortality was higher when insects were treated without food. When food was not provided, a minimum of 11030 ppm for 1 h is required to kill 99% of eggs, the most tolerant stage, whereas 500 ppm for 1 h is required to kill 99% of larvae, the least tolerant. When provided with food, adults were the most tolerant and larvae the least tolerant. Adults require exposure time of 7.7 h of 100 ppm ozone to kill 99% of insects in the absence of food. The work reported suggests that ozone could be an alternative fumigant for the management of all O. mercator life stages.

Responses of cucumber (Cucumissativus L.) to ozonated water under varying drought stress intensities

ABSTRACTThis study explores the effect of drought stress and ozone on cucumber. A factorial experiment with complete randomized design was carried out in a greenhouse. Experimental treatments were drought stress, including three levels 100% (control), 80%, and 60% of the field capacity (FC) and three ozone concentrations of 0, 0.5, and 1 ppm. The drought stress (80% and 60% of the FC) significantly reduced fruit length, weight, and yield, leaf area, and number of fruits. Across the levels of drought stress, the statistical analysis showed significant increments in the fruit weight with the increasing in the ozone concentrations. An enhancement in the total suspended solids values was obtained with the increase in the drought stress level. The height, dry, and fresh weights of plant decreased with the increase in the drought stress level. The highest leaf area, dry, and fresh weights were observed in the 0.5 ppm ozone and 100% FC.

Rapid detection of trace ozone in TiO2–In2O3 materials by using the differential method

TiO2–In2O3 composites were fabricated for detecting trace amounts of gaseous ozone and were characterized using transmission electron microscopy, X-ray diffraction, and ultraviolet–visible spectrophotometry. The fabricated TiO2–In2O3 composites exhibited a high ozone gas sensor response of 56.5–2.0ppm at room temperature (25±2°C) under irradiation at 405nm using a light-emitting diode. The differential function dR/dt (R, sensor resistance; t, time) was used to analyze ozone concentrations from 40 to 2000ppb, and a favorable regression coefficient of R2=0.997 was obtained. In addition, the results revealed that the ozone sensor exhibited a rapid response rate of 30s and favorable short-term stability to 2.0ppm ozone. A possible sensing mechanism was proposed.

Structural Changes of Amyloid Beta in Hippocampus of Rats Exposed to Ozone: A Raman Spectroscopy Study

The aim of this work was to study the effect of oxidative stress on the structural changes of the secondary peptide structure of amyloid beta 1–42 (Aβ 1–42), in the dentate gyrus of hippocampus of rats exposed to low doses of ozone. The animals were exposed to ozone-free air (control group) and 0.25 ppm ozone during 7, 15, 30, 60, and 90 days, respectively. The samples were studied by: (1) Raman spectroscopy to detect the global conformational changes in peptides with α-helix and β-sheet secondary structure, following the deconvolution profile of the amide I band; and (2) immunohistochemistry against Aβ 1–42. The results of the deconvolutions of the amide I band indicate that, ozone exposure causes a progressively decrease in the abundance percentage of α-helix secondary structure. Furthermore, the β-sheet secondary structure increases its abundance percentage. After 60 days of ozone exposure, the β-sheet band is identified in a similar wavenumber of the Aβ 1–42 peptide standard. Immunohistochemistry assays show an increase of Aβ 1–42 immunoreactivity, coinciding with the conformational changes observed in the Raman spectroscopy of Aβ 1–42 at 60 and 90 days. In conclusion, oxidative stress produces changes in the folding process of amyloid beta peptide structure in the dentate gyrus, leading to its conformational change in a final β-sheet structure. This is associated to an increase in Aβ 1–42 expression, similar to the one that happens in the brain of Alzheimer’s Disease (AD) patients.

Peri‐implantation Ozone Exposure Alters Uterine Artery Flow and Induces Fetal Growth Restriction in Rats

Epidemiological studies suggest a relationship between air pollutant exposures and various adverse pregnancy outcomes. Exposure to elevated ambient ozone levels during the first and second trimesters has been associated with increased risk for preeclampsia, gestational diabetes, and intrauterine growth restriction. As many of the adverse pregnancy outcomes are hypothesized to initiate from poor implantation, we sought to determine if an acute exposure to ozone during the implantation period would generate such outcomes later in pregnancy. Timed‐pregnant, Long‐Evans female rats were exposed to filtered air, 0.4ppm, or 0.8ppm ozone for 4 hours on each morning of gestational days 5 and 6. Tail cuff blood pressure and Doppler ultrasound of the uterine artery were measured following the phase of arterial remodeling on gestational days 15, 19, and 21. Rats were euthanized on gestational day 21 and offspring growth parameters were measured. While ozone exposure failed to impact maternal blood pressure at the times measured, multiple indices of blood flow in the uterine artery were adversely impacted as a result of early ozone exposure. Rats exposed to 0.8ppm ozone had increased uterine artery resistance index, systolic to diastolic ratio, pulsatile index, and end diastolic notching as pregnancy advanced compared to air controls. There was no evidence of systemic inflammation or kidney markers of preeclampsia in the dams. Ozone exposure decreased male and female offspring total weight, fat mass, and lean mass at the end of gestation. Further, 7 out of 9 dams exposed to 0.8ppm ozone during implantation had an average female offspring weight under the 10th percentile of air control pregnancies, suggestive of severe intrauterine growth restriction. Together these data suggest that peri‐implantation exposure to ozone adversely impacts uterine artery flow, which may have contributed to blunted fetal growth. These findings suggest a plausible biological mechanism for the epidemiological findings linking air pollutant exposure and adverse pregnancy outcomes. This abstract does not reflect US EPA Policy.Support or Funding InformationThis work was funded by the US EPA.