22 research outputs found

    Recent trends in gas-phase ammonia and PM<sub>2.5</sub> ammonium in the Southeast United States

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    <div><p>Ammonia measurements from the Southeastern Aerosol Research and Characterization (SEARCH) study network were analyzed for trends over 9 yr (2004–2012) of observations. Total ammonia concentrations, defined as the sum of gas-phase ammonia and fine particle ammonium, were found to be decreasing by 1–4% yr<sup>−1</sup> and were qualitatively consistent with ammonia emission estimates for the SEARCH states of Alabama, Georgia, Mississippi, and Florida. On the other hand, gas-phase ammonia mixing ratios were found to be slightly rising or steady over the region, leading to the observation that the gas-phase fraction of total ammonia has steadily increased over 2004–2012 as a result of declining emissions of the strong acid precursor species sulfur dioxide (SO<sub>2</sub>) and nitrogen oxides (NO<sub>x</sub>) and consequent reduced partitioning of ammonia to the fine particle phase. Because gas-phase ammonia is removed from the atmosphere more rapidly than fine particle ammonium, an increase in the gas-phase fraction of total ammonia may result in shifted deposition patterns as more ammonia is deposited closer to sources rather than transported downwind in fine particles. Additional long-term measurements and modeling studies are needed to determine if similar transitions of total ammonia to the gas phase are occurring outside of the Southeast and to assess if these changes are impacting plants and ecosystems near major ammonia sources. Unusually high ammonia concentrations observed in 2007 in the SEARCH measurements are hypothesized to be linked to emissions from wildfires that were much more prevalent across the Southeast during that year due to elevated temperatures and widespread drought. Although wildfires are currently estimated to be a relatively small fraction (3–10%) of total ammonia emissions in the Southeast, the projected increased incidence of wildfires in this region as a result of global climate change may lead to this source’s increased importance over the rest of the 21st century.</p><p>Implications: <i>Ammonia concentrations from the Southeastern Aerosol Research and Characterization study (SEARCH) network are analyzed over the 9-yr period 2004–2012. Total ammonia (gaseous ammonia + PM<sub>2.5</sub> ammonium) concentrations declined at a rate of 1–4% yr<sup>−1</sup>, consistent with U.S. Environmental Protection Agency (EPA) emission estimates for the Southeast United States, but the fraction of ammonia in the gas phase has risen steadily (+1–3% yr<sup>−1</sup>) over the time period. Declining emissions of SO<sub>2</sub> and NO<sub>x</sub> resulting from imposed air quality regulations have resulted in decreased atmospheric strong acids and less ammonia partitioning to the particle phase, which may impact the amount and overall pattern of ammonia deposition.</i></p></div

    Ozone Trends Across the United States over a Period of Decreasing NOx and VOC Emissions

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    In this work, we evaluate ambient ozone trends at urban, suburban, and rural monitoring sites across the United States over a period of decreasing NOx and VOC emissions (1998–2013). We find that decreasing ozone trends generally occur in the summer, in less urbanized areas, and at the upper end of the ozone distribution. Conversely, increasing ozone trends generally occur in the winter, in more urbanized areas, and at the lower end of the ozone distribution. The 95<sup>th</sup> percentile ozone concentrations decreased at urban, suburban, and rural monitors by 1–2 ppb/yr in the summer and 0.5–1 ppb/yr in the winter. In the summer, there are both increasing and decreasing trends in fifth percentile ozone concentrations of less than 0.5 ppb/yr at urban and suburban monitors, while fifth percentile ozone concentrations at rural monitors decreased by up to 1 ppb/yr. In the winter, fifth percentile ozone concentrations generally increased by 0.1–1 ppb/yr. These results demonstrate the large scale success of U.S. control strategies targeted at decreasing peak ozone concentrations. In addition, they indicate that as anthropogenic NOx emissions have decreased, the ozone distribution has been compressed, leading to less spatial and temporal variability

    DataSheet1_Efficacy and safety of the Chinese herbal medicine Xiao Yao San for treating anxiety: a systematic review with meta-analysis and trial sequential analysis.docx

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    Introduction: The effectiveness and safety of the Chinese herbal medicine (CHM) Xiao Yao San (XYS) used for treating anxiety disorders are still unknown. Thus, we conducted this systematic review with meta-analysis and trial sequential analysis (TSA) to determine its safety and efficacy.Methods: We searched 12 databases for relevant studies from the inception of each database till 10 August 2023. We selected randomized controlled trials to compare the efficacy and safety of XYS (including XYS only and XYS + anxiolytics) to those of anxiolytics in patients with anxiety.Results: We found 14 trials with 1,256 patients in total that met the requirements for inclusion. We assessed the majority of studies (8 out of 14) as being at high risk of bias; 6 were assessed as having a moderate risk of bias. Three trials compared oral XYS to anxiolytic medication, and 11 trials compared oral XYS plus anxiolytics to anxiolytic treatment alone. The pooled results showed that the efficacy of treatment in the XYS + anxiolytics groups was significantly higher than that of the anxiolytics alone group (RR = 1.19; 95% CI: [1.13, 1.26]; p 2 = 0) and the adverse event rates in the XYS + anxiolytics groups were significantly lower than those in the anxiolytics alone group (RR = 0.44; 95% CI: [0.28, 0.82]; p = 0.001 2 = 13). The efficacy of treatment in the XYS alone groups was also significantly higher than that of the anxiolytics alone groups (RR = 5.41; 95% CI: [2.23, 13.11]; p 2 = 0). However, there was no statistical difference between the adverse events of the XYS alone group and the anxiolytics alone group, although the incidence of adverse events in the XYS alone group was lower than that in the anxiolytics alone group. The results of the TSA confirmed the above findings.Conclusion: The use of XYS combined with anxiolytics for treating anxiety was found to be safe and effective. However, although XYS alone is effective in the treatment of anxiety disorder, more large-scale research is needed to investigate adverse events.Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=350358, identifier CRD42022350358.</p

    Soil Acidification in China: Is Controlling SO<sub>2</sub> Emissions Enough?

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    Facing challenges of increased energy consumption and related regional air pollution, China has been aggressively implementing flue gas desulfurization (FGD) and phasing out small inefficient units in the power sector in order to achieve the national goal of 10% reduction in sulfur dioxide (SO2) emissions from 2005 to 2010. In this paper, the effect of these measures on soil acidification is explored. An integrated methodology is used, combining emission inventory data, emission forecasts, air quality modeling, and ecological sensitivities indicated by critical load. National emissions of SO2, oxides of nitrogen (NOX), particulate matter (PM), and ammonia (NH3) in 2005 were estimated to be 30.7, 19.6, 31.3, and 16.6 Mt, respectively. Implementation of existing policy will lead to reductions in SO2 and PM emissions, while those of NOX and NH3 will continue to rise, even under tentatively proposed control measures. In 2005, the critical load for soil acidification caused by sulfur (S) deposition was exceeded in 28% of the country’s territory, mainly in eastern and south-central China. The area in exceedance will decrease to 26% and 20% in 2010 and 2020, respectively, given implementation of current plans for emission reductions. However, the exceedance of the critical load for nitrogen (N, combining effects of eutrophication and acidification) will double from 2005 to 2020 due to increased NOX and NH3 emissions. Combining the acidification effects of S and N, the benefits of SO2 reductions during 2005−2010 will almost be negated by increased N emissions. Therefore abatement of N emissions (NOX and NH3) and deposition will be a major challenge to China, requiring policy development and technology investments. To mitigate acidification in the future, China needs a multipollutant control strategy that integrates measures to reduce S, N, and PM

    Impact Assessment of Ammonia Emissions on Inorganic Aerosols in East China Using Response Surface Modeling Technique

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    Ammonia (NH<sub>3</sub>) is one important precursor of inorganic fine particles; however, knowledge of the impacts of NH<sub>3</sub> emissions on aerosol formation in China is very limited. In this study, we have developed China’s NH<sub>3</sub> emission inventory for 2005 and applied the Response Surface Modeling (RSM) technique upon a widely used regional air quality model, the Community Multi-Scale Air Quality Model (CMAQ). The purpose was to analyze the impacts of NH<sub>3</sub> emissions on fine particles for January, April, July, and October over east China, especially those most developed regions including the North China Plain (NCP), Yangtze River delta (YRD), and the Pearl River delta (PRD). The results indicate that NH<sub>3</sub> emissions contribute to 8–11% of PM<sub>2.5</sub> concentrations in these three regions, comparable with the contributions of SO<sub>2</sub> (9–11%) and NO<sub><i>x</i></sub> (5–11%) emissions. However, NH<sub>3</sub>, SO<sub>2</sub>, and NO<sub><i>x</i></sub> emissions present significant nonlinear impacts; the PM<sub>2.5</sub> responses to their emissions increase when more control efforts are taken mainly because of the transition between NH<sub>3</sub>-rich and NH<sub>3</sub>-poor conditions. Nitrate aerosol (NO<sub>3</sub><sup>–</sup>) concentration is more sensitive to NO<sub><i>x</i></sub> emissions in NCP and YRD because of the abundant NH<sub>3</sub> emissions in the two regions, but it is equally or even more sensitive to NH<sub>3</sub> emissions in the PRD. In high NO<sub>3</sub><sup>–</sup> pollution areas such as NCP and YRD, NH<sub>3</sub> is sufficiently abundant to neutralize extra nitric acid produced by an additional 25% of NO<sub><i>x</i></sub> emissions. The 90% increase of NH<sub>3</sub> emissions during 1990–2005 resulted in about 50–60% increases of NO<sub>3</sub><sup>–</sup> and SO<sub>4</sub><sup>2‑</sup> aerosol concentrations. If no control measures are taken for NH<sub>3</sub> emissions, NO<sub>3</sub><sup>–</sup> will be further enhanced in the future. Control of NH<sub>3</sub> emissions in winter, spring, and fall will benefit PM<sub>2.5</sub> reduction for most regions. However, to improve regional air quality and avoid exacerbating the acidity of aerosols, a more effective pathway is to adopt a multipollutant strategy to control NH<sub>3</sub> emissions in parallel with current SO<sub>2</sub> and NO<sub><i>x</i></sub> controls in China

    Optimization of a NO<i><sub>x</sub></i> and VOC Cooperative Control Strategy Based on Clean Air Benefits

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    Serious ambient PM2.5 and O3 pollution is one of the most important environmental challenges of China, necessitating an urgent cost-effective cocontrol strategy. Herein, we introduced a novel integrated assessment system to optimize a NOx and volatile organic compound (VOC) control strategy for the synergistic reduction of ambient PM2.5 and O3 pollution. Focusing on the Beijing–Tianjin–Hebei cities and their surrounding regions, which are experiencing the most serious PM2.5 and O3 pollution in China, we found that NOx emission reduction (64–81%) is essential to attain the air quality standard no matter how much VOC emission is reduced. However, the synergistic VOC control is strongly recommended considering its substantially human health and crop production benefits, which are estimated up to 163 (PM2.5-related) and 101 (O3-related) billion CHY during the reduction of considerable emissions. Notably, such benefits will be greatly reduced if the synergistic VOC reduction is delayed. This study also highlights the necessity of simultaneous VOC and NOx emission control in winter while enhancing the NOx control in the summer, which is contrary to the current control strategy adopted in China. These findings point out the right pathways for future policy making on comitigating PM2.5 and O3 pollution in China and other countries

    Image_3_A-Lipoic Acid Alleviates Folic Acid-Induced Renal Damage Through Inhibition of Ferroptosis.JPEG

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    Folic acid (FA)-induced acute kidney injury (AKI) is characterized by the disturbance of redox homeostasis, resulting in massive tubular necrosis and inflammation. Α-lipoic acid (LA), as an antioxidant, has been reported to play an important role in renal protection, but the underlying mechanism remains poorly explored. The aim of this study is to investigate the protective effect of LA on FA-induced renal damage. Our findings showed that LA could ameliorate renal dysfunction and histopathologic damage induced by FA overdose injection. Moreover, FA injection induced severe inflammation, indicated by increased release of pro-inflammatory cytokines tumor necrosis factor (TNF)-α and IL-1β, as well as infiltration of macrophage, which can be alleviated by LA supplementation. In addition, LA not only reduced the cellular iron overload by upregulating the expressions of Ferritin and ferroportin (FPN), but also mitigated reactive oxygen species (ROS) accumulation and lipid peroxidation by increasing the levels of antioxidant glutathione (GSH) and glutathione peroxidase-4 (GPX4). More importantly, we found that LA supplementation could reduce the number of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive tubular cells caused by FA, indicating that the tubular cell death mediated by ferroptosis may be inhibited. Further study demonstrated that LA supplementation could reverse the decreased expression of cystine/glutamate antiporter xCT (SLC7A11), which mediated GSH synthesis. What is more, mechanistic study indicated that p53 activation was involved in the inhibitory effect of SLC7A11 induced by FA administration, which could be suppressed by LA supplementation. Taken together, our findings indicated that LA played the protective effect on FA-induced renal damage mainly by inhibiting ferroptosis.</p

    Image_3_A-Lipoic Acid Alleviates Folic Acid-Induced Renal Damage Through Inhibition of Ferroptosis.jpg

    No full text
    Folic acid (FA)-induced acute kidney injury (AKI) is characterized by the disturbance of redox homeostasis, resulting in massive tubular necrosis and inflammation. Α-lipoic acid (LA), as an antioxidant, has been reported to play an important role in renal protection, but the underlying mechanism remains poorly explored. The aim of this study is to investigate the protective effect of LA on FA-induced renal damage. Our findings showed that LA could ameliorate renal dysfunction and histopathologic damage induced by FA overdose injection. Moreover, FA injection induced severe inflammation, indicated by increased release of pro-inflammatory cytokines tumor necrosis factor (TNF)-α and IL-1β, as well as infiltration of macrophage, which can be alleviated by LA supplementation. In addition, LA not only reduced the cellular iron overload by upregulating the expressions of Ferritin and ferroportin (FPN), but also mitigated reactive oxygen species (ROS) accumulation and lipid peroxidation by increasing the levels of antioxidant glutathione (GSH) and glutathione peroxidase-4 (GPX4). More importantly, we found that LA supplementation could reduce the number of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive tubular cells caused by FA, indicating that the tubular cell death mediated by ferroptosis may be inhibited. Further study demonstrated that LA supplementation could reverse the decreased expression of cystine/glutamate antiporter xCT (SLC7A11), which mediated GSH synthesis. What is more, mechanistic study indicated that p53 activation was involved in the inhibitory effect of SLC7A11 induced by FA administration, which could be suppressed by LA supplementation. Taken together, our findings indicated that LA played the protective effect on FA-induced renal damage mainly by inhibiting ferroptosis.</p

    Image_2_A-Lipoic Acid Alleviates Folic Acid-Induced Renal Damage Through Inhibition of Ferroptosis.jpg

    No full text
    Folic acid (FA)-induced acute kidney injury (AKI) is characterized by the disturbance of redox homeostasis, resulting in massive tubular necrosis and inflammation. Α-lipoic acid (LA), as an antioxidant, has been reported to play an important role in renal protection, but the underlying mechanism remains poorly explored. The aim of this study is to investigate the protective effect of LA on FA-induced renal damage. Our findings showed that LA could ameliorate renal dysfunction and histopathologic damage induced by FA overdose injection. Moreover, FA injection induced severe inflammation, indicated by increased release of pro-inflammatory cytokines tumor necrosis factor (TNF)-α and IL-1β, as well as infiltration of macrophage, which can be alleviated by LA supplementation. In addition, LA not only reduced the cellular iron overload by upregulating the expressions of Ferritin and ferroportin (FPN), but also mitigated reactive oxygen species (ROS) accumulation and lipid peroxidation by increasing the levels of antioxidant glutathione (GSH) and glutathione peroxidase-4 (GPX4). More importantly, we found that LA supplementation could reduce the number of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive tubular cells caused by FA, indicating that the tubular cell death mediated by ferroptosis may be inhibited. Further study demonstrated that LA supplementation could reverse the decreased expression of cystine/glutamate antiporter xCT (SLC7A11), which mediated GSH synthesis. What is more, mechanistic study indicated that p53 activation was involved in the inhibitory effect of SLC7A11 induced by FA administration, which could be suppressed by LA supplementation. Taken together, our findings indicated that LA played the protective effect on FA-induced renal damage mainly by inhibiting ferroptosis.</p

    Image_2_A-Lipoic Acid Alleviates Folic Acid-Induced Renal Damage Through Inhibition of Ferroptosis.JPEG

    No full text
    Folic acid (FA)-induced acute kidney injury (AKI) is characterized by the disturbance of redox homeostasis, resulting in massive tubular necrosis and inflammation. Α-lipoic acid (LA), as an antioxidant, has been reported to play an important role in renal protection, but the underlying mechanism remains poorly explored. The aim of this study is to investigate the protective effect of LA on FA-induced renal damage. Our findings showed that LA could ameliorate renal dysfunction and histopathologic damage induced by FA overdose injection. Moreover, FA injection induced severe inflammation, indicated by increased release of pro-inflammatory cytokines tumor necrosis factor (TNF)-α and IL-1β, as well as infiltration of macrophage, which can be alleviated by LA supplementation. In addition, LA not only reduced the cellular iron overload by upregulating the expressions of Ferritin and ferroportin (FPN), but also mitigated reactive oxygen species (ROS) accumulation and lipid peroxidation by increasing the levels of antioxidant glutathione (GSH) and glutathione peroxidase-4 (GPX4). More importantly, we found that LA supplementation could reduce the number of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive tubular cells caused by FA, indicating that the tubular cell death mediated by ferroptosis may be inhibited. Further study demonstrated that LA supplementation could reverse the decreased expression of cystine/glutamate antiporter xCT (SLC7A11), which mediated GSH synthesis. What is more, mechanistic study indicated that p53 activation was involved in the inhibitory effect of SLC7A11 induced by FA administration, which could be suppressed by LA supplementation. Taken together, our findings indicated that LA played the protective effect on FA-induced renal damage mainly by inhibiting ferroptosis.</p
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