Ppm O3 Research Articles

Deep oxidation of NO via catalytic ozonation

ABSTRACT In addition to selective catalytic reduction (SCR) and selective non-catalytic reduction (SNCR) which are available to remove NOx from flue gas, oxidation method is receiving more and more attention because this method makes it possible to remove NOx and SO2 from flue gas simultaneously by wet scrubbing. O3 as a strong oxidant has a high oxidation capacity and it can oxide NO to N2O5 which has a higher water solubility compared with NO2. However, it needs a long reaction time and the escape of unreacted ozone may cause secondary pollution. In this study, FeMnCo/Al2O3 catalyst and FeMnCe/Al2O3 catalyst were prepared and applied to enhance the deep oxidation of NOx with ozone and reduce O3 slip. Effects of various operating parameters such as O3/NO ratio, gas residence time and operating temperature were evaluated and the results demonstrate that N2O5 began to generate when O3/NO ratio was higher than 1.0 and increased with increasing O3/NO ratio. Little residual O3 was formed in the presence of catalyst while 350 ppm O3 was measured at the outlet gas when O3/NO ratio was controlled at 2.0. The N2O5 conversion efficiency increased with increasing gas residence time, operating temperature and the highest N2O5 conversion efficiency was achieved at 100°C. Furthermore, the conversion efficiency remained around 90% during 20 h operation over FeMnCe/Al2O3 catalyst with an O3/NO ratio of 1.73, a gas residence time of 1.2 s, and a temperature of 100°C. On the other hand, the N2O5 conversion efficiency remained around 80% during 3 h operation over FeMnCo/Al2O3 catalyst. Overall, FeMnCe/Al2O3 catalyst reveals good potential for deep oxidation of NO by O3 and can be further developed as a viable catalyst for reducing NO emission from industries.

Modification of gut and airway microbiota on ozone-induced airway inflammation

Ground-level ozone (O3) has been shown to induce airway inflammation, the underlying mechanisms remain unclear. The aim of this study was to determine whether gut and airway microbiota dysbiosis, and airway metabolic alterations were associated with O3-induced airway inflammation. Thirty-six 8-week-old male C57BL/6 N mice were divided into 2 groups: sterile water group and broad-spectrum antibiotics group (Abx). Each group was further divided into two subgroups, filtered air group (Air) and O3 group (O3), with 9 mice in each subgroup. Mice in the Air and O3 groups were exposed to filtered air or 1 ppm O3, 4 h/d for 5 consecutive days, respectively. Mice in Abx + Air and Abx + O3 groups were exposed to filtered air or O3, respectively, after drinking broad-spectrum Abx. 24 h after the final O3 exposure, mouse feces and bronchoalveolar lavage fluids (BALF) were collected and subjected to measurements of airway oxidative stress and inflammation biomarkers, 16S rRNA sequencing and metabolite profiling. Hematoxylin-eosin staining of lung tissues was applied to examine the pathological changes of lung tissue. The results showed that O3 exposure resulted in airway oxidative stress and inflammation, as well as gut and airway microbiota dysbiosis, and airway metabolism alteration. Abx pre-treatment markedly changed gut and airway microbiota and promoted O3-induced metabolic disorder and airway inflammation. Spearman correlation analyses indicated that inter-related gut and airway microbiota dysbiosis and airway metabolic disorder were associated with O3-induced airway inflammation. Together, inhaled O3 causes airway inflammation, which may implicate gut and airway microbiota dysbiosis and airway metabolic alterations.

Fatty acids metabolism in ozone-induced pulmonary inflammatory injury: Evidence, mechanism and prevention

Ozone (O3) is a major air pollutant that directly threatens the respiratory system, lung fatty acid metabolism disorder is an important molecular event in pulmonary inflammatory diseases. Liver kinase B1 (LKB1) and nucleotide-binding domain leucine-rich repeat-containing protein 3 (NLRP3) inflammasome not only regulate inflammation, but also have close relationship with fatty acid metabolism. However, the role and mechanism of LKB1 and NLRP3 inflammasome in lung fatty acid metabolism, which may contribute to ozone-induced lung inflammation, remain unclear, and effective strategy for preventing O3-induced pulmonary inflammatory injury is lacking. To explore these, mice were exposed to 1.00 ppm O3 (3 h/d, 5 days), and pulmonary inflammation was determined by airway hyperresponsiveness, histopathological examination, total cells and cytokines in bronchoalveolar lavage fluid (BALF). Targeted fatty acids metabolomics was used to detect medium and long fatty acid in lung tissue. Then, using LKB1-overexpressing adenovirus and NLRP3 knockout (NLRP3−/−) mice to explore the mechanism of O3-induced lung fatty acid metabolism disorder. Results demonstrated that O3 exposure caused pulmonary inflammatory injury and lung medium and long chain fatty acids metabolism disorder, especially decreased dihomo-γ-linolenic acid (DGLA). Meanwhile, LKB1 expression was decreased, and NLRP3 inflammasome was activated in lung of mice after O3 exposure. Additionally, LKB1 overexpression alleviated O3-induced lung inflammation and inhibited the activation of NLRP3 inflammasome. And we found that pulmonary fatty acid metabolism disorder was ameliorated of NLRP3 −/− mice compared with those in wide type mice after O3 exposure. Furthermore, administrating DGLA intratracheally prior to O3 exposure significantly attenuated O3-induced pulmonary inflammatory injury. Taken together, these findings suggest that fatty acids metabolism disorder is involved in O3-induced pulmonary inflammation, which is regulated by LKB1-mediated NLRP3 pathway, DGLA supplement could be a useful preventive strategy to ameliorate ozone-associated lung inflammatory injury.

Highly stable flexible ozone gas sensors using Mn3O4 nanoparticles-decorated IGZO thin films through the SILAR method

Metal or semiconductor nanoparticles (NPs) can enhance the device performance of gas sensors due to their high surface area and unique electronic properties. However, this method requires additional thermal bonding with high temperatures to secure the NPs, making it unsuitable for flexible substrates. In this study, we develop a room-temperature flexible ozone (O3) gas sensor using Mn3O4 NPs on an amorphous InGaZnO (a-IGZO) film. The Mn3O4 NPs are synthesized by a successive ionic layer adsorption and reaction (SILAR) method at low temperatures. The sensor with Mn3O4 NPs exhibits a gas response of 4.06 against 5 ppm O3 gas at room temperature, which is much higher than that of its pristine counterpart. It also shows excellent selectivity for O3 over toxic gases and maintains stability over 60 days, with reproducible folding even after 500 bending cycles. Thus, the combination of SILAR-synthesized Mn3O4 NPs and a-IGZO films provides an effective way to fabricate flexible O3 gas sensors.

Ozone decomposition by mesoporous LnOx/MnOx catalysts derived from Mn-BTC under humid conditions

Mesoporous MnOx-Y and LnOx/MnOx ozone decomposition catalysts were prepared by calcination of Mn-BTC (BTC = 1,3,5-benzentricarboxylate) and doping of lanthanide elements (Ln = La, Ce, Sm, Eu, Er). Compared to MnOx-Y catalysts, the LnOx/MnOx catalysts showed higher ozone catalytic activity, the mutual conversion between Lnn+ and Mnn+ was helpful to improve ozone decomposition. The CeOx/MnOx catalyst showed the highest catalytic that showed 93% conversion of 40 ppm O3 in the relative humidity (RH) = 65% after 360 min, which was attributed to the largest specific surface area, more oxygen vacancies, Mn3+ and Oads. In addition, the CeOx/MnOx catalyst was loaded into the non-woven fabric to obtain CeOx/MnOx-NWF catalyst, which showed a highly efficient and stable ozone conversion under the RH range from less than 5%–85%. This work will promote the practical application of Mn-BTC derived catalysts.

Space-confined manganese oxides nanosheets for efficient catalytic decomposition of ozone

Ground-level ozone has long posed a substantial menace to human well-being and the ecological milieu. The widely reported manganese-based catalysts for ozone decomposition still facing the persisting issues encompass inefficiency and instability. To surmount these challenges, we developed a mesoporous silica thin films with perpendicular nanochannels (SBA(⊥)) confined Mn3O4 catalyst (Mn3O4@SBA(⊥)). Under a weight hourly space velocity (WHSV) of 500,000 mL g−1 h−1, the Mn3O4@SBA(⊥) catalyst exhibited 100% ozone decomposition efficiency in 5 h and stability across a wide humidity range, which exceed the performance of bulk Mn3O4 and Mn3O4 confine in commonly reported SBA-15. Rapidly decompose 20 ppm O3 to a safety level below 100 μg m−3 in the presence of dust in smog chamber (60 × 60 × 60 cm) was also realized. This prominent catalytic performance can be attributed to the unique confined structure engenders the highly exposed active sites, facilitate the reactant-active sites contact and impeded the water accumulation on the active sites. This work offers new insights into the design of confined structure catalysts for air purification.

Exposure to Ozone Downregulates Bcl-2 and Increases Executing Caspases-3 and -8 in the Hippocampus, Frontal Cortex, and Cerebellum of Rats.

Introduction Ozone (O3) is one of the most prevalent atmospheric pollutants, arising from a photochemical reaction between volatile organic compounds (VOC), nitrogen oxides (NOx), and sunlight.O3 triggers oxidative stress, resulting in lipid oxidation, inflammation, alterations in metabolic and cellular signaling, and potentially initiating cell death in vulnerable brain regions.Inflammation and oxidative stress are recognized for their ability to induce cell death, primarily through the apoptosis pathway, involving various proteins that participate in this process via two pathways: intrinsic and extrinsic. Objective This study aims to identify the expression of pro-apoptotic proteins and Bcl-2 in the frontal cortex, cerebellum, and hippocampus of rats exposed to O3 acutely. Methods Two groups of 20 Wistar rodents (250-300 g) were established. The control group (n=10) was exposed to unrestricted polluted air for 12 hours, while the experimental group (n=10) was exposed to 1 ppm of O3. After exposure, the animals were sacrificed for immunofluorescence and Western blot analysis. Using a t-test, the arbitrary units of pro-apoptotic proteins and Bcl-2 were compared between the two groups. Results Significant increases in caspase-8 and caspase-3 activation were found in the O3-exposedgroup compared to the control group, specifically in the frontal cortex, cerebellum, and hippocampus. Additionally, notable changes in Bcl-2 expression were observed in these brain regions. The TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay further indicated significant differences in immunopositivity between the groups in the same areas. However, intrinsic apoptotic proteins such as Bax, VDAC1, and cytochrome-c did not show significant differences between the groups within these structures. Western blotanalyses aligned with the immunofluorescence results, showing statistically significant concentrations of caspase-8 in the cerebellum, caspase-3 in the hippocampus, and Bcl-2 in the frontal cortex in the O3exposed group. Conversely, proteins like Bax, cytochrome-c, and VDAC1 did not exhibit significant differences in all analyzed structures. Conclusions This study demonstrates that acute exposure to 1 ppm of ozone can trigger neuronal apoptosis in the frontal cortex, hippocampus, and cerebellum of rats, primarily through the activation of the extrinsic apoptosis pathway via caspase-8 and caspase-3. Additionally, it causes a reduction in Bcl-2 expression, an essential antiapoptotic protein. Despite not observing the activation of intrinsic pathway proteins like BAX, VDAC, or cytochrome-c, the study suggests that chronic O3 exposure might promote cell death by activating this pathway, requiring further long-term research.

Vitamin C compounds mixture prevents skin barrier alterations and inflammatory responses upon real life multi pollutant exposure.

Cutaneous tissues is among the main target of outdoor stressors such as ozone (O3 ), particulate matter (PM), and ultraviolet radiation (UV) all involved in inducing extrinsic skin aging. Only a few reports have studied the multipollutant interaction and its effect on skin damage. In the present work, we intended to evaluate the ability of pollutants such as O3 and PM to further aggravate cutaneous UV damage. In addition, the preventive properties of a cosmeceutical formulation mixture (AOX mix) containing 15% vitamin C (L-ascorbic acid), 1% vitamin E (α-tocopherol) and 0.5% ferulic acid was also investigated. Skin explants obtained from three different subjects were exposed to 200 mJ UV light, 0.25 ppm O3 for 2 h, and 30 min of diesel engine exhaust (DEE), alone or in combination for 4 days (time point D1 and D4). The results showed a clear additive effect of O3 and DEE in combination with UV in terms of keratin 10, Desmocollin and Claudin loss. In addition, the multipollutant exposure significantly induced the inflammatory response measured as NLRP1/ASC co-localization suggesting the activation of the inflammasome machinery. Finally, the loss of Aquaporin3 was also affected by the combined outdoor stressors. Furthermore, daily topical pre-treatment with the AOX Mix significantly prevented the cutaneous changes induced by the multipollutants. In conclusion, this study is among the first to investigate the combined effects of three of the most harmful outdoor stressors on human skin and confirms that daily topical of an antioxidant application may prevent pollution-induced skin damage.

Multi-Omics analysis reveals molecular insights into the effects of acute ozone exposure on lung tissues of normal and obese male mice

Certain sub-groups, including men and obese individuals, are more susceptible to ozone (O3) exposure, but the underlying molecular mechanisms remain unclear. In this study, the male mice were divided into two dietary groups: one fed a high-fat diet (HFD), mimicking obesity conditions, and the other fed a normal diet (ND), then exposed to 0.5 ppm and 2 ppm O3 for 4 h per day over two days. The HFD mice exhibited significantly higher body weight and serum lipid biochemical indicators compared to the ND mice. Obese mice also exhibited more severe pulmonary inflammation and oxidative stress. Using a multi-omics approach including proteomics, metabolomics, and lipidomics, we observed that O3 exposure induced significant pulmonary molecular changes in both obese and normal mice, primarily arachidonic acid metabolism and lipid metabolism. Different molecular biomarker responses to acute O3 exposure were also observed between two dietary groups, with immune-related proteins impacted in obese mice and PPAR pathway-related proteins affected in normal mice. Furthermore, although not statistically significant, O3 exposure tended to aggravate HFD-induced disturbances in lung glycerophospholipid metabolism. Overall, this study provides valuable molecular insights into the responses of lung to O3 exposure and highlights the potential impact of O3 on obesity-induced metabolic changes.

High temperature exacerbates ozone-induced airway inflammation: Implication of airway microbiota and metabolites

Short-term exposure to ozone (O3) has been associated with airway inflammation. Given that high temperature (HT) accelerates O3 production, it is of significance to determine whether co-exposure to HT exacerbates O3-induced airway inflammation. The aim of this study was to examine the possible promotive effect of HT on O3-induced airway inflammation and underlying mechanisms. Forty-eight C57BL/6 N male mice were randomly divided into four groups: filtered air (control), O3, HT, and HT + O3 (co-exposure) groups. Mice in control and O3 groups were exposed to filtered air or 1 ppm O3 at 24 °C, respectively, while mice in HT and co-exposure groups were exposed to filtered air or 1 ppm O3 at 36 °C, respectively. The exposure scenario for four groups was 4 h/d for 5 consecutive days. Bronchoalveolar lavage fluids (BALF) were collected 24 h after the last exposure and subjected to examinations of oxidative stress and inflammation biomarkers, 16S rRNA sequencing, and metabolic profiling. Lung tissues were processed for H&E histological staining. The results showed that O3 inhalation triggered oxidative stress and inflammation in the airways, which was worsen by co-exposure to HT. Further studies revealed that co-exposure to HT strengthened O3-induced decline in Firmicutes and Allobaculum in airways. Moreover, co-exposure to HT promoted O3-induced airway metabolic disorder. Spearman correlation analysis revealed correlations among microbiota dysbiosis, metabolic disorder, oxidative stress and inflammation induced by co-exposure to HT and O3. Taken together, HT exposure aggravates O3-induced airway oxidative stress and inflammation, possibly through modulation of microbiota and metabolism of the airways.

An experimental and modeling study on the ozone-assisted low-temperature ignition of methylcyclohexane in an RCM

Methylcyclohexane (MCH) is a significant component of practical fuels and has garnered significant research interest in recent years. However, due to the low reactivity of MCH, ignition data below the temperature of 680 K are still lacking. To extend the experimental condition of MCH ignition to a lower temperature range, ozone (O3) was used as an active additive to assist in the kinetic investigation of the low-temperature ignition chemistry of MCH. Ignition delay times (IDTs) and the first-stage IDTs for MCH containing varying concentrations of O3 (0, 100, and 500 ppm) were determined in a rapid compression machine (RCM) under the pressure of 20 bar, equivalence ratios of 1.0 and 1.5, and temperatures in the range of 616–864 K. Species profiles during the auto-ignition of MCH at 615 K and 795 K were recorded using a fast sampling system combined with the gas chromatography (GC) technique. A kinetic model for MCH ignition with O3 addition was developed with some key reaction rates updated based on our newly obtained data. The promotional effects of O3 on the ignition of MCH were observed through both the IDTs and species evolutions. The negative temperature coefficient (NTC) behavior of MCH ignition disappeared in the presence of 500 ppm O3. The production of intermediate species displayed varying tendencies, with the formation of acetaldehyde (CH3CHO) being favored over other small alkenes. Moreover, the production of ethane (C2H6) was detected under 615 K with 500 ppm O3 addition, which was not reported in previous works concerning MCH combustion. Model analysis revealed that the oxidation pathways for ROO radicals of MCH altered because the addition of O3 shifted the onset of the oxidation temperature to a lower region, making the generation of RO radicals significantly favored. Therefore, the experimental species profiles can provide additional kinetic information for the low-temperature oxidation chemistry of MCH, and the corresponding data effectively highlighted and constrained the reaction rates of ROO radicals yielding RO radicals. Further model simulation indicated that the intramolecular hydrogen immigration of ROO radicals and the following secondary O2 addition oxidation pathways of MCH can be nearly frozen if the onset oxidation temperature is shifted as low as 550 K with 1000 ppm O3.

Cation Substitution Induced d‐Band Center Modulation on Cobalt‐Based Spinel Oxides for Catalytic Ozonation

AbstractCo3O4 spinel is a promising transition metal oxide (TMO) catalyst for the catalytic ozonation of volatile organic compounds (VOCs). Herein, metal–organic frameworks (MOFs)‐derived Ni‐ and Mg‐ substituted Co3O4 catalysts retain similar spinel structures, but display improved and reduced ozonation performance of methyl mercaptan (CH3SH), respectively. Remarkably, the NiCo2O4 catalyst can still ≈90% removal of CH3SH after running for 20 h at room temperature under an initial concentration of 50 ppm CH3SH and 40 ppm O3, relative humidity of 60%, and space velocity of 300 000 mL h−1 g−1, exceeding the reported values. Experimental characterizations have unveiled that the substitution of Ni and Mg into the Co3O4 spinel altered surface acidity, oxygen species mobility, and Co2+/Co3+ ratio. The in situ Raman spectra reveal the dynamic formation Co(III)‐Oad* via the transformation of O3 into surface atomic oxygen (Oad*) and peroxide species (O2*). Theoretical calculations verify that Ni‐substitution increases nonuniform charges and Fermi density, leading to a moderate increase in d‐band center energy levels, thereby promoting O3 specific adsorption/activation to convert Oad*/O2* and •OH/1O2/•O2−, which contributes to eliminate CH3SH and prevent poisoning. The concept of tuning the d‐band center can provide valuable insights for the design of other catalysts for catalytic ozonation.

Plasma sterols and vitamin D are correlates and predictors of ozone-induced inflammation in the lung: A pilot study.

Ozone (O3) exposure causes respiratory effects including lung function decrements, increased lung permeability, and airway inflammation. Additionally, baseline metabolic state can predispose individuals to adverse health effects from O3. For this reason, we conducted an exploratory study to examine the effect of O3 exposure on derivatives of cholesterol biosynthesis: sterols, oxysterols, and secosteroid (25-hydroxyvitamin D) not only in the lung, but also in circulation. We obtained plasma and induced sputum samples from non-asthmatic (n = 12) and asthmatic (n = 12) adult volunteers 6 hours following exposure to 0.4ppm O3 for 2 hours. We quantified the concentrations of 24 cholesterol precursors and derivatives by UPLC-MS and 30 cytokines by ELISA. We use computational analyses including machine learning to determine whether baseline plasma sterols are predictive of O3 responsiveness. We observed an overall decrease in the concentration of cholesterol precursors and derivatives (e.g. 27-hydroxycholesterol) and an increase in concentration of autooxidation products (e.g. secosterol-B) in sputum samples. In plasma, we saw a significant increase in the concentration of secosterol-B after O3 exposure. Machine learning algorithms showed that plasma cholesterol was a top predictor of O3 responder status based on decrease in FEV1 (>5%). Further, 25-hydroxyvitamin D was positively associated with lung function in non-asthmatic subjects and with sputum uteroglobin, whereas it was inversely associated with sputum myeloperoxidase and neutrophil counts. This study highlights alterations in sterol metabolites in the airway and circulation as potential contributors to systemic health outcomes and predictors of pulmonary and inflammatory responsiveness following O3 exposure.

Photochemically-Activated p-Type CuGaO2 Thin Films for Highly-Stable Room-Temperature Gas Sensors

The photochemical activation process is a promising way to operate metal oxide gas sensors at room temperature. However, this technique is only used in n-type semiconductors. In this study, we report a highly stable p-type copper gallium oxide (CuGaO2) gas sensor fabricated through the facile sol-gel process. The sensor is capable of detecting O3 gas at room temperature, and its gas response can be further enhanced by ultraviolet (UV) activation. The highest gas response of 7.12 to 5 ppm O3 gas at a UV intensity of 10 mW cm−2 is achieved at room-temperature. In addition, the CuGaO2 sensor shows excellent long-term stability, with a degradation of approximately 3% over 90 days. These results strongly support the solution-processed CuGaO2 as a good candidate for room-temperature gas sensors.

Mesoporous CeOx/MnOx catalyst derived from Mn-BTC for ozone catalytic decomposition

Mesoporous 10CeOx/MnOx-Y catalysts were successfully prepared by doping Ce and calcining Mn-BTC (BTC = 1,3,5-benzenetricarboxylate) for ozone catalytic decomposition. The 10CeOx/MnOx-300 catalyst exhibited the highest catalytic activity under the relative humidity (RH) range from less than 5–65 %, giving 100 % conversion of 40 ppm O3 after 6 h. Series of physicochemical characterizations including XRD, TG, SEM, HR-TEM, ICP-OES, BET, XPS and H2-TPR were introduced the relationship of calcination temperature, catalysts structure and ozone catalytic performance. The results demonstrated that the 10CeOx/MnOx-300 catalyst had the highest Mn3+/Mn4+ and Oads/Olatt ratios and the largest specific surface compared with those of other samples, which are crucial to decompose ozone. In addition, better dispersion of crystals, larger pore volume, more oxygen vacancies, and better low-temperature reducibility are also conducive to ozone decomposition. This research establishes the basis for the application of manganese-based MOFs for ozone decomposition.

The impact of subchronic ozone exposure on serum metabolome and the mechanisms of abnormal bile acid and arachidonic acid metabolisms in the liver

Ambient ozone (O3) pollution can induce respiratory and cardiovascular toxicity. However, its impact on the metabolome and the underlying mechanisms remain unclear. This study first investigated the serum metabolite changes in rats exposed to 0.5 ppm O3 for 3 months using untargeted metabolomic approach. Results showed chronic ozone exposure significantly altered the serum levels of 34 metabolites with potential increased risk of digestive, respiratory and cardiovascular disease. Moreover, bile acid synthesis and secretion, and arachidonic acid (AA) metabolism became the most prominent affected metabolic pathways after O3 exposure. Further studies on the mechanisms found that the elevated serum toxic bile acid was not due to the increased biosynthesis in the liver, but the reduced reuptake from the portal vein to hepatocytes owing to repressed Ntcp and Oatp1a1, and the decreased bile acid efflux in hepatocytes as a results of inhibited Bsep, Ostalpha and Ostbeta. Meanwhile, decreased expressions of detoxification enzyme of SULT2A1 and the important regulators of FXR, PXR and HNF4α also contributed to the abnormal bile acids. In addition, O3 promoted the conversion of AA into thromboxane A2 (TXA2) and 20-hydroxyarachidonic acid (20-HETE) in the liver by up-regulation of Fads2, Cyp4a and Tbxas1 which resulting in decreased AA and linoleic acid (LA), and increased thromboxane B2 (TXB2) and 20-HETE in the serum. Furthermore, apparent hepatic chronic inflammation, fibrosis and abnormal function were found in ozone-exposed rats. These results indicated chronic ozone exposure could alter serum metabolites by interfering their metabolism in the liver, and inducing liver injury to aggravate metabolic disorders.

Effects of Ozone on Sickness and Depressive-like Behavioral and Biochemical Phenotypes and Their Regulation by Serum Amyloid A in Mice.

Ozone (O3) is an air pollutant that primarily damages the lungs, but growing evidence supports the idea that O3 also harms the brain; acute exposure to O3 has been linked to central nervous system (CNS) symptoms such as depressed mood and sickness behaviors. However, the mechanisms by which O3 inhalation causes neurobehavioral changes are limited. One hypothesis is that factors in the circulation bridge communication between the lungs and brain following O3 exposure. In this study, our goals were to characterize neurobehavioral endpoints of O3 exposure as they relate to markers of systemic and pulmonary inflammation, with a particular focus on serum amyloid A (SAA) and kynurenine as candidate mediators of O3 behavioral effects. We evaluated O3-induced dose-, time- and sex-dependent changes in pulmonary inflammation, circulating SAA and kynurenine and its metabolic enzymes, and sickness and depressive-like behaviors in Balb/c and CD-1 mice. We found that 3 parts per million (ppm) O3, but not 2 or 1 ppm O3, increased circulating SAA and lung inflammation, which were resolved by 48 h and was worse in females. We also found that indoleamine 2,3-dioxygenase (Ido1) mRNA expression was increased in the brain and spleen 24 h after 3 ppm O3 and that kynurenine was increased in blood. Sickness and depressive-like behaviors were observed at all O3 doses (1-3 ppm), suggesting that behavioral responses to O3 can occur independently of increased SAA or neutrophils in the lungs. Using SAA knockout mice, we found that SAA did not contribute to O3-induced pulmonary damage or inflammation, systemic increases in kynurenine post-O3, or depressive-like behavior but did contribute to weight loss. Together, these findings indicate that acute O3 exposure induces transient symptoms of sickness and depressive-like behaviors that may occur in the presence or absence of overt pulmonary neutrophilia and systemic increases of SAA. SAA does not appear to contribute to pulmonary inflammation induced by O3, although it may contribute to other aspects of sickness behavior, as reflected by a modest effect on weight loss.

Effect of Fe and Al based coagulants and disinfectants on polyethylene microplastics removal in coagulation process through response surface methodology.

Microplastic (MP) pollution has been rising as a threatening risk and recently has appealed to the attention of more researchers. In this study, influential parameters affecting the removal rate of polyethylene microplastics (PEMPs) were optimized through response surface methodology (RSM). In Box Behnken Design (BBD), independent parameters were pH, PEMP size, coagulant dosage and polyacrylamide dosage. Two experimental sets were conducted, one with ferric chloride and the second with poly aluminum chloride as two commonly applied coagulants in drinking water treatment plants (DWTPs). Comparing the results of optimized parameters, PAC was a better coagulant with the predicted removal rate of 58.19%, while the removal rate with ferric chloride as a coagulant was predicted to be 56.37%. Moreover, some experiments were conducted to analyze the effect of ozone gas and sodium hypochlorite as disinfectants on removal rate. The highest removal rate was observed when 2 ppm of O3 was added to the solution coagulated with optimal dosage of PAC, reaching the removal rate of 76.8%.

A kinetic investigation on low-temperature ignition of propane with ozone addition in an RCM

To extend the temperature for propane ignition to a lower region (< 680 K), ozone (O3) was used as an ignition promoter to investigate the low-temperature chemistry of propane. Ignition delay times for propane containing varying concentrations of O3 (0, 100, and 1000 ppm) were measured at 25 bar, 654–882 K, and equivalence ratios of 0.5 and 1.0 in a rapid compression machine (RCM). Species profiles during propane ignition with varying O3 concentrations were recorded using a fast sampling system combined with a gas chromatograph (GC). A kinetic model for propane ignition with O3 was developed. O3 shortened ignition delay times of propane significantly, and the NTC behavior was weakened. O atoms released from O3 reacted with propane through hydrogen abstraction reactions, which led to the fast production of OH radicals. The following oxidation of fuel radicals generated additional OH radicals. Consequently, the inhibition caused by the slow chemistry of hydrogen peroxide (H2O2) in the NTC region was weakened in the presence of O3. Experimental results with O3 addition can provide extra constraints on the low-temperature chemistry of propane. Species profiles during propane ignition at 730 K with 1000 ppm O3 addition showed the production of propanal (C2H5CHO), acetone (CH3COCH3), and acetaldehyde (CH3CHO) was promoted significantly. Model analyses indicated that O3 shifted the oxidation temperature of propane to a lower region, in which reactions of ROO radicals (NC3H7O2 and IC3H7O2) tend to generate RO radicals (NC3H7O and IC3H7O). The promotion of RO radicals led to the fast production of C2H5CHO, CH3COCH3, and CH3CHO. The corresponding species profile highlighted the reaction relevant to ROO and RO radicals (NC3H7O + O2 = C2H5CHO + HO2 and 2 IC3H7O2 = 2 IC3H7O + O2). Rate constants of these reactions were updated, which can potentially improve the performance of the core mechanism under lower temperatures and provide references for model development of larger hydrocarbons.

Sensitive and selective ozone sensor based on CuCo2O4 synthesized by a facile solution combustion method

In this study, p-type spinel CuCo2O4 nanomaterials with abundant oxygen vacancies were synthesized by a facile one-step solution combustion method, and their sensing characteristics have been investigated. The p-type CuCo2O4 sensor shows a high response of 11 to 1 ppm O3 and low responses (< 2) to various interference gases (100 ppm NH3, NO2, SO2, and 500 ppm ethanol, methanol and acetone) at 90 °C in dry air, indicating a superior selectivity. The sensor also possesses a wide O3 detection range from 10 to 3000 ppb and good repeatability. More importantly, the relative humidity (RH) could promote the electrical response to O3, and the response to 1 ppm O3 only deviates from 24 to 27 as the RH increases from 50% to 90%, benefitting for practical applications in ambient humid air atmospheres. The humidity enhanced response for p-type CuCo2O4 could be ascribed to the competition of hole carrier reduction, O2− active sites reduction and O3 decomposition promotion induced by the hydroxyl groups.