Quantification for photochemical loss of volatile organic compounds upon ozone formation chemistry at an industrial city (Zibo) in North China Plain.

Volatile organic compounds (VOCs) are consumed by photochemical reactions during transport, leading to inaccuracies in estimating the local ozone (O3) formation mechanism and its subsequent strategy for O3 attainment. To comprehensively quantify the deviations in O3 formation mechanism by consumed VOCs (C-VOCs), a 5-month field campaign was conducted in a typical industrial city in Northern China over incorporating a 0-D box model (implemented with MCMv3.3.1). The averaged C-VOCs concentration was 6.8 ppbv during entire period, and Alkenes accounted for 62% dominantly. Without considering C-VOCs, the relative incremental reactivity (RIR) of anthropogenic VOCs (AVOC, overestimated by 68%-75%) and NOx (underestimated by 137%-527%) demonstrated deviations at multiple scenarios, and the RIR deviations for precursors in High-O3-periods (HOP) were lower than Low-O3-periods (LOP). The RIR deviations from individual species involved C-VOCs calculation did not impact the identification for the high-ranking-RIR AVOC species but non-negligible. Monthly comparisons showed that higher C-VOCs concentrations would lead to higher RIR deviations. The daily maximum of net Ox production rate (P(Ox)) and the regional transport Ox (Trans(Ox)) without C-VOCs were underestimated by 56%-194% and 81%-243%, respectively. After considering C-VOCs, the contribution of HO2+NO for Ox gross production (G(Ox)) decreased by 7% (LOP) and 7% (HOP), but OH + NO2 for Ox destruction (D(Ox)) decreased by 16% (LOP) and 23% (HOP), and alkenes + O3 increased for D(Ox) by 12% (LOP) and 22% (HOP). This implies that VOCs-NOx-O3 sensitivity was deviated between with/without C-VOCs, and severe O3 pollution rendered deviations in O3 formation, especially via NOx-driving chemistry. Based on RIR(NOx)/RIR(AVOC) with/without C-VOCs, the sensitivity regime shifted from VOCs-limited (-0.93) to transition (1.38) at LOP, and from VOCs-limited (0.19) to NOx-limited (3.79) at HOP. Our results reflected that the NOx limitation degree was underestimated without constraint C-VOCs, especially HOP, and provided implication to more precise O3 pollution control strategies.

Reducing Indoor Particulate Air Pollution Improves Student Test Scores: A Randomized Double-Blind Crossover Study.

Short-term exposure to air pollution is associated with a decline in cognitive function. Standardized test scores have been employed to evaluate the effects of air pollution exposure on cognitive performance. Few studies aimed to prove whether air pollution is responsible for reduced test scores; none have implemented a "gold-standard" method for assessing the association such as a randomized, double-blind intervention. This study used a "gold-standard" method─randomized, double-blind crossover─to assess whether reducing short-term indoor particle concentrations results in improved test scores in college students in Tianjin, China. Participants (n = 162) were randomly assigned to one of two similar classrooms and completed a standardized English test on two consecutive weekends. Air purifiers with active or sham (i.e., filter removed) particle filtration were placed in each classroom. The filtration mode was switched between the two test days. Linear mixed-effect models were used to evaluate the effect of the intervention mode on the test scores. The results show that air purification (i.e., reducing PM) was significantly associated with increases in the z score for combined (0.11 [95%CI: 0.02, 0.21]) and reading (0.11 [95%CI: 0.00, 0.22]) components. In conclusion, a short-term reduction in indoor particle concentration led to improved test scores in students, suggesting an improvement in cognitive function.

Personal Exposure to Source-Specific Particulate Polycyclic Aromatic Hydrocarbons and Systemic Inflammation: A Cross-Sectional Study of Urban-Dwelling Older Adults in China.

Environmental exposure to ambient polycyclic aromatic hydrocarbons (PAHs) can disturb the immune response. However, the evidence on adverse health effects caused by exposure to PAHs emitted from specific sources among different vulnerable subpopulations is limited. In this cross-sectional study, we aimed to evaluate whether exposure to source-specific PAHs could increase systemic inflammation in older adults. The present study included community-dwelling older adults and collected filter samples of personal exposure to PM2.5 during the winter of 2011. Blood samples were collected after the PM2.5 sample collection. We analyzed PM2.5 bound PAHs and serum inflammatory cytokines (interleukin (IL)1ß, IL6, and tumor necrosis factor alpha levels. The Positive Matrix Factorization model was used to identify PAH sources. We used a linear regression model to assess the relative effects of source-specific PM2.5 bound PAHs on the levels of measured inflammatory cytokines. After controlling for confounders, exposure to PAHs emitted from biomass burning or diesel vehicle emission was significantly associated with increased serum inflammatory cytokines and systemic inflammation. These findings highlight the importance of considering exposure sources in epidemiological studies and controlling exposures to organic materials from specific sources.

The impact of high-glucose or high-fat diets on the metabolomic profiling of mice.

Objective: Diets high in glucose or fat contribute to an increased prevalence of the diseases. Therefore, the objective of the current research was to observe and evaluate the impact of dietary components on different metabolomic profiles in primary tissues of mice. Methods: For 8 weeks, diet with high-glucose or-fat was given to C57BL/6 J mice. The levels of metabolites in the primary tissues of mice were studied using gas chromatography-mass spectrometry (GC-MS) and analyzed using multivariate statistics. Results: By comparing the metabolic profiles between the two diet groups and control group in mice main tissues, our study revealed 32 metabolites in the high-glucose diet (HGD) group and 28 metabolites in the high-fat diet (HFD) group. The most significantly altered metabolites were amino acids (AAs; L-alanine, L-valine, glycine, L-aspartic acid, L-isoleucine, L-leucine, L-threonine, L-glutamic acid, phenylalanine, tyrosine, serine, proline, and lysine), fatty acids (FAs; propanoic acid, 9,12-octadecadienoic acid, pentadecanoic acid, hexanoic acid, and myristic acid), and organic compounds (succinic acid, malic acid, citric acid, L-(+)-lactic acid, myo-inositol, and urea). These metabolites are implicated in many metabolic pathways related to energy, AAs, and lipids metabolism. Conclusion: We systematically analyzed the metabolic changes underlying high-glucose or high-fat diet. The two divergent diets induced patent changes in AA and lipid metabolism in the main tissues, and helped identify metabolic pathways in a mouse model.

Integrating ambient carbonyl compounds provides insight into the constrained ozone formation chemistry in Zibo city of the North China Plain.

Quantifying the impact of carbonyl compounds (carbonyls) on ozone (O3) photochemical formation is crucial to formulating targeted O3 mitigation strategies. To investigate the emission source of ambient carbonyls and their integrated observational constraint on the impact of O3 formation chemistry, a field campaign was conducted in an industrial city (Zibo) of the North China Plain from August to September 2020. The site-to-site variations of OH reactivity for carbonyls were in accordance with the sequence of Beijiao (BJ, urban, 4.4 s-1) > Xindian (XD, suburban, 4.2 s-1) > Tianzhen (TZ, suburban, 1.6 s-1). A 0-D box model (MCMv3.3.1) was applied to assess the O3-precursor relationship influenced by measured carbonyls. It was found that without carbonyls constraint, the O3 photochemical production of the three sites was underestimated to varying degrees, and the biases of overestimating the VOC-limited degree were also identified through a sensitivity test to NOx emission changes, which may be associated with the reactivity of carbonyls. In addition, the results of the positive matrix factorization (PMF) model indicated that the main source of aldehydes and ketones was secondary formation and background (81.6% for aldehydes, 76.8% for ketones), followed by traffic emission (11.0% for aldehydes, 14.0% for ketones). Incorporated with the box model, we found that biogenic emission contributed the most to the O3 production at the three sites, followed by traffic emission as well as industry and solvent usage. Meanwhile, the relative incremental reactivity (RIR) values of O3 precursor groups from diverse VOC emission sources featured consistencies and differences at the three sites, which further highlights the importance of the synergetic mitigation of target O3 precursors at regional and local scales. This study will help to provide targeted policy-guiding O3 control strategies for other regions.

[Characteristics and Reactivity of VOCs in a Typical Industrial City in Summer].

To investigate the ambient pollution caused by volatile organic compounds (VOCs) in a typical industrial city in summer, the characteristics and chemical reactivity from VOCs and the causes of ozone (O3) pollution were analyzed using online VOCs measurements during polluted and non-polluted periods in Zibo city in July 2020. The results showed that the average hourly concentration of total volatile organic compounds (TVOC) during the polluted period[(50.6±28.3)] µg·m-3 was 32.5% higher than that during the non-polluted period[(38.2±24.9) µg·m-3]. The contribution of all VOCs categories were as follows:alkanes>aromatics>alkenes>alkynes, and the diurnal averages of TVOC and O3 concentrations were opposite during the polluted and non-polluted period. Ozone formation potential (OFP),·OH radical loss rate (L·OH), and secondary organic aerosol formation potential (SOAp) during the polluted period were higher than those during the non-polluted period. Alkenes contributed most to OFP and L·OH, whereas aromatics contributed most to SOAp. The tendency of the diurnal average of OFP and SOAp was overall consistent with that of TVOC. The priority species of OFP, L·OH, and SOAp were alkenes and aromatics. The VOCs/NOx method was applied to identify the O3-VOC-NOx sensitivity during the polluted and non-polluted periods, and the results showed that the photochemical regimes were VOCs-limited and transition regions. In addition, the smog production model (SPM) was employed to identify the O3 formation regime, and the results showed that those during the polluted period were identified as VOCs-limited and transition regions from 08:00 to 16:00, whereas the non-polluted period was mainly considered to be VOCs-limited. To mitigate the O3 pollution in summertime, the synergistic control of VOCs (especially alkenes and aromatics) and NOx emissions should be enforced.

Short-term effects of the toxic component of traffic-related air pollution (TRAP) on lung function in healthy adults using a powered air purifying respirator (PAPR).

Short-term exposure to traffic-related air pollution (TRAP) are associated with reduced lung function. However, TRAP is a mixture of various gaseous pollutants and particulate matter (PM), and therefore it is unknown that which components of TRAP are responsible for the respiratory toxicity. Using a powered air-purifying respirator (PAPR), we conducted a randomized, double-blind, crossover trial in which 40 adults were exposed to TRAP for 2 h at the sidewalk of a busy road. During the exposure, the participants wore the PAPR fitted with a PM filter, a PM and volatile organic compounds (VOCs) filter, or a sham filter (no filtration, Sham mode). The participants were blinded to the type of filter in their PAPR, and experienced three exposures, once for each intervention mode in random order. We measured two lung function measures (forced expiratory volume in 1 s [FEV1] and forced vital capacity [FVC]) and an airway inflammation marker (fraction of exhaled nitric oxide [FENO]) before and immediately after each exposure, and further measured them at different time periods after exposure. We applied linear mixed effect models to estimate the effects of the interventions on the changes of lung function from baseline values after controlling for other covariates. Compared to baseline, exposing to TRAP decreased FEV1 and FVC, and increased FEV1/FVC and FENO in all three intervention modes. The mixed models showed that with the sham mode as reference, lung function and airway inflammation post exposure were significantly improved by filtering both PM and VOCs, but marginally affected by filtering only PM. In conclusion, the VOCs component of TRAP is responsible for the reduction in lung function caused by short-term exposure to TRAP. However, the result needs to be interpreted cautiously before further verified by laboratory experiment using purely isolated component(s) of TRAP.

Characteristics, Source Contributions, and Source-Specific Health Risks of PM2.5-Bound Polycyclic Aromatic Hydrocarbons for Senior Citizens during the Heating Season in Tianjin, China.

Polycyclic aromatic hydrocarbons (PAHs) have carcinogenic impacts on human health. However, limited studies are available on the characteristics, sources, and source-specific health risks of PM2.5-bound PAHs based on personal exposure data, and comparisons of the contributions of indoor and outdoor sources are also lacking. We recruited 101 senior citizens in the winter of 2011 for personal PM2.5 sample collection. Fourteen PAHs were analyzed, potential sources were apportioned using positive matrix factorization (PMF), and inhalational carcinogenic risks of each source were estimated. Six emission sources were identified, including coal combustion, gasoline emission, diesel emission, biomass burning, cooking, and environmental tobacco smoking (ETS). The contribution to carcinogenic risk of each source occurred in the following sequence: biomass burning > diesel emission > gasoline emission > ETS > coal combustion > cooking. Moreover, the contributions of biomass burning, diesel emission, ETS, and indoor sources (sum of cooking and ETS) to PAH-induced carcinogenic risk were higher than those to the PAH mass concentration, suggesting severe carcinogenic risk per unit contribution. This study revealed the contribution of indoor and outdoor sources to mass concentration and carcinogenic risk of PM2.5-bound PAHs, which could act as a guide to mitigate the exposure level and risk of PM2.5-bound PAHs.

[Comparison of VOCs Pollution Characteristics Between an Urban Site and a Background Site in Summer in Zibo].

To study the differences in volatile organic compound (VOCs) pollution characteristics between an urban site and a background site in summer, ambient VOCs were monitored using an online gas chromatograph (GC) at an urban site and a background site (Mt. Lu) in Zibo in July 2020. The VOCs pollution characteristics and chemical reactivity were analyzed, and the sources of VOCs were identified using the positive matrix factorization model(PMF). The results showed that ρ(TVOC) and ρ(NOx) were higher at the urban site, but ρ(O3) was higher at the background site. Diurnal average characteristics of ρ(TVOC) and ρ(NOx) were high at night and low during the day at the urban site, and there were no obvious variation characteristics at the background site. The diurnal average characteristics of ρ(O3) were consistent at the urban and background sites, showing low level at night and high level during the day; however, the peak in the background site was later than that at the urban site. The average ρ(TVOC) at the urban site and background site were (44.9±27.5) µg·m-3 and (17.3±9.1) µg·m-3, respectively, and the mass fraction of each component was ordered as alkanes>aromatics>alkenes>alkynes in both sites. The average ozone formation potentials(OFP)were (115.5±63.1) µg·m-3 and (38.0±20.2) µg·m-3, and the contribution of each component was ordered as alkenes>aromatics>alkanes>alkynes. The respective average values of·OH radical loss rate(L·OH) were (3.9±2.3) s-1 and (1.0±0.6) s-1, with the highest contribution of alkenes and the lowest contribution of alkynes in both sites. The average values of secondary organic aerosol formation potential(SOAp) were (0.5±0.3) µg·m-3 and (0.2±0.06) µg·m-3, respectively, with aromatic being the most abundant group. According to the source appointment by the PMF model, the main source of VOCs in the urban site was traffic sources (52.4%), followed by petroleum evaporation (19.2%), solvent evaporation (17.3%), and oil and biological sources (11.1%). The source of VOCs in the background site mainly came from traffic sources (40.2%), followed by solvent evaporation (31.3%), combustion sources (19.3%), and biological sources (9.2%). Zibo City should strengthen the management and control of motor vehicle emissions, petroleum evaporation, and the use of industrial solvents.

A Comprehensive 2018-Based Vehicle Emission Inventory and Its Spatial-Temporal Characteristics in the Central Liaoning Urban Agglomeration, China.

Rapid economic expansion and urbanisation have seriously affected the atmospheric environmental quality of the Central Liaoning Urban Agglomeration (CLUA). This study aimed to establish a detailed vehicle emission inventory of the CLUA with a 3 km × 3 km gridded spatiotemporal distribution. A top-down methodology using vehicle kilometres travelled annually, emission factors, and activity data of each city was established. Carbon monoxide (CO), nitrogen oxides (NOx), sulfur dioxide (SO2), ammonia (NH3), volatile organic compounds (VOCs), particulate matter with an aerodynamic diameter less than 2.5 µm (PM2.5), particulate matter with an aerodynamic diameter less than 10 µm (PM10), Black Carbon (BC), and organic carbon (OC) emissions were 291.0, 221.8, 3.6, 2.2, 42.8, 9.3, 10.3, 5.2, and 1.6 Gg in 2018, respectively. The contribution of diesel heavy-duty trucks to NOx, SO2, PM2.5, PM10, BC, and OC emissions was greater than 54.5%, the largest contribution of all vehicles. Gasoline small passenger vehicles were the primary contributor to CO, VOC, and NH3 emissions, contributing 37.3%, 39.5%, and 75.3% of total emissions, respectively. For emission standards, Pre-China 1 vehicles were the largest contributor to CO and VOC emissions and China 3 vehicles contributed the largest amount of NOx, SO2, PM2.5, PM10, BC, and OC emissions. The spatial distribution of pollutants showed "obvious lines" and grids with high emissions were concentrated in expressways, national highways, and provincial highways. The temporal variation showed morning-evening peaks during diurnal variations, which was consistent with resident behaviour. This work can help us understand vehicular emission characteristics of the CLUA and provide basic data for air quality modelling. Future research should investigate traffic flow by vehicle types and emission factors at a local level, which will be helpful for transport management planning.

Associations of Exposure to Fine Particulate Matter Mass and Constituents with Systemic Inflammation: A Cross-Sectional Study of Urban Older Adults in China.

Systemic inflammation is a key mechanism in the development of cardiovascular diseases induced by exposure to fine particles (particles with aerodynamic diameter ≤2.5 µm [PM2.5]). However, little is known about the effects of chemical constituents of PM2.5 on systemic inflammation. In this cross-sectional study, filter samples of personal exposure to PM2.5 were collected from community-dwelling older adults in Tianjin, China, and the chemical constituents of PM2.5 were analyzed. Blood samples were collected immediately after the PM2.5 sample collection. Seventeen cytokines were measured as targets. A linear regression model was applied to estimate the relative effects of PM2.5 and its chemical constituents on the measured cytokines. A positive matrix factorization model was employed to distinguish the sources of PM2.5. The calculated source contributions were used to estimate their effects on cytokines. After adjusting for other covariates, higher PM2.5-bound copper was significantly associated with increased levels of interleukin (IL)1ß, IL6, IL10, and IL17 levels. Source analysis showed that an increase in PM2.5 concentration that originated from tire/brake wear and cooking emissions was significantly associated with enhanced levels of IL1ß, IL6, tumor necrosis factor alpha (TNFα), and IL17. In summary, personal exposure to some PM2.5 constituents and specific sources could increase systemic inflammation in older adults. These findings may explain the cardiopulmonary effects of specific particulate chemical constituents of urban air pollution.

Activation of angiotensin-converting enzyme 2/angiotensin (1-7)/mas receptor axis triggers autophagy and suppresses microglia proinflammatory polarization via forkhead box class O1 signaling.

Brain renin-angiotensin (Ang) system (RAS) is implicated in neuroinflammation, a major characteristic of aging process. Angiotensin (Ang) II, produced by angiotensin-converting enzyme (ACE), activates immune system via angiotensin type 1 receptor (AT1), whereas Ang(1-7), generated by ACE2, binds with Mas receptor (MasR) to restrain excessive inflammatory response. Therefore, the present study aims to explore the relationship between RAS and neuroinflammation. We found that repeated lipopolysaccharide (LPS) treatment shifted the balance between ACE/Ang II/AT1 and ACE2/Ang(1-7)/MasR axis to the deleterious side and treatment with either MasR agonist, AVE0991 (AVE) or ACE2 activator, diminazene aceturate, exhibited strong neuroprotective actions. Mechanically, activation of ACE2/Ang(1-7)/MasR axis triggered the Forkhead box class O1 (FOXO1)-autophagy pathway and induced superoxide dismutase (SOD) and catalase (CAT), the FOXO1-targeted antioxidant enzymes. Meanwhile, knockdown of MasR or FOXO1 in BV2 cells, or using the selective FOXO1 inhibitor, AS1842856, in animals, suppressed FOXO1 translocation and compromised the autophagic process induced by MasR activation. We further used chloroquine (CQ) to block autophagy and showed that suppressing either FOXO1 or autophagy abrogated the anti-inflammatory action of AVE. Likewise, Ang(1-7) also induced FOXO1 signaling and autophagic flux following LPS treatment in BV2 cells. Cotreatment with AS1842856 or CQ all led to autophagic inhibition and thereby abolished Ang(1-7)-induced remission on NLRP3 inflammasome activation caused by LPS exposure, shifting the microglial polarization from M1 to M2 phenotype. Collectively, these results firstly illustrated the mechanism of ACE2/Ang(1-7)/MasR axis in neuroinflammation, strongly indicating the involvement of FOXO1-mediated autophagy in the neuroimmune-modulating effects triggered by MasR activation.

Acute cardiovascular effects of traffic-related air pollution (TRAP) exposure in healthy adults: A randomized, blinded, crossover intervention study.

Exposure to traffic-related air pollution (TRAP) may enhance the risk of cardiovascular disease. However, the short-term effects of TRAP components on the cardiovascular system are not well understood. We conducted a randomized, double-blinded, crossover intervention study in which 39 healthy university students spent 2 h next to a busy road. Participants wore a powered air-purifying respirator (PAPR) or an N95 mask. PAPRs were equipped with a filter for particulate matter (PM), a PM and volatile organic compounds (VOCs) filter or a sham filter. Participants were blinded to PAPR filter type and underwent randomized exposures four times, once for each intervention mode. Blood pressure (BP), heart rate (HR) and heart rate variability (HRV) were measured before, during and for 6 h after the roadside exposure. Linear mixed-effect models were used to evaluate the effects of the interventions relative to baseline controlling for other covariates. All HRV measures increased during and following exposure for all intervention modes. Some HRV measures (SDNN and rMSSD during exposure and SDNN after exposure) were marginally affected by PM filtration. Wearing the N95 mask affected VLF power and rMSSD responses to traffic exposure differently than the PAPR interventions. Both systolic and diastolic BP increased slightly during exposure, but then were generally lower than baseline after exposure for the sham and filter interventions. HR, which fell during exposure and mostly remained lower than baseline after exposure, was lower yet with all filter interventions compared to the sham mode following exposure. Therefore, short-term exposure to traffic acutely affects HRV, BP and HR, but N95 mask and PAPR interventions generally show little efficacy in reducing these effects. Removing the PM component of TRAP has some limited effects on HRV responses to exposure but exaggerates the traffic-related decrease in HR. HRV findings from N95 mask interventions need to be interpreted cautiously.

Systematic Metabolic Profiling of Mice with Dextran Sulfate Sodium-Induced Colitis.

PURPOSE: Inflammatory bowel diseases (IBD) are a chronic inflammatory disease, which affects almost all tissues in the body. Previous studies mainly focused on breathing, fecal, and urine samples of patients with IBD. However, there is no comprehensive metabolomic analysis of the serum, colon, heart, liver, kidney, cortex, hippocampus, and brown fat tissues. Therefore, the aim of our study is to evaluate the utility metabolomic analysis of target tissues in the pathogenesis of IBD in exploring new biomarkers for early diagnosis and treatment. METHODS: Male Sprague-Dawley rats were randomly allocated to control and DSS-treated groups (n = 7). Dextran sulfate sodium (DSS) was orally administered for 6 weeks. Gas chromatography-mass spectrometry (GC-MS) was used for metabolite determination, multivariate statistical analysis was used to identify metabolites that were differentially expressed in two groups. RESULTS: Our results showed that 3, 11, 12, 6, 5, 13, 13, and 11 metabolites were differentially expressed between the DSS treatment group and the control group in the serum, colon, heart, liver, kidney, cortex, hippocampus, and brown fat tissues, respectively. The most significant change of metabolites in the study was amino acid (L-alanine, L-glutamic acid, L-phenylalanine, L-proline, L-lysine, L-isoleucine, L-tryptophan, L-norleucine, L-valine, glycine, serine, L-threonine), organic acid (citric acid, 3-hydroxybutyric acid, propanoic acid), glucide (D-arabinose, D-fructose) and purine (9H-purin-6-ol, D-ribose) profiles. Several pathways were affected according to the integrated pathway analysis. These pathways ranged from amino acid metabolism (such as alanine, aspartate, and glutamate metabolism, glutathione metabolism) to purine metabolism (aminoacyl-tRNA biosynthesis). CONCLUSION: Using GC-MS-based profiling of metabolite changes, these results may provide a more comprehensive view for IBD and IBD-related diseases and improve the understanding of IBD pathogenesis.

Comprehensive analysis of metabolic changes in rats exposed to acrylamide.

Acrylamide (ACR) is a widely used environmentally hazardous compound that is known to be neurotoxic, genotoxic, carcinogenic, and reproductive toxicity. It is widely present in soil, water, agents used in chemical industries, and food. It can be distributed to all organs and tissues, and can cause damage to various human systems and those of other animals. Previous metabolomics studies have mainly focused on metabolites in serum and urine, but have lacked comprehensive analysis of major organs and tissues. In the current study, a gas chromatography-massspectrometry method was used to investigate mechanisms underlying organ toxicity, in an effort to identify potentially sensitive biomarkers in the main target tissues of rats after ACR exposure. Male Sprague-Dawley rats were assigned to two groups; a control group and a group treated with 20 mg kg-1 ACR intragastrically for 6 weeks. Metabolite changes in the two groups were statistically analyzed. The respective numbers of altered metabolites in the hippocampus, cortex, kidney, serum, heart, liver, and kidney fat were 21, 21, 17, 5, 15, 14, and 6. There were 14 metabolic pathways related to amino acid, fatty acid, purine, and energy metabolism, revealing that the toxic mechanism of ACR may involve oxidative stress, inflammation, and amino acid metabolism and energy disorders.

[Source and Health Risk Assessment of PM2.5-Bound Metallic Elements in Road Dust in Zibo City].

To study the pollution characteristics, sources, and ecological and health risk of PM2.5-bound metallic elements in road dust in Zibo City, a total of 97 dust samples were collected in eight districts between October 2016 and May 2017, and particles smaller than 2.5 µm were suspended filtered using a resuspension system. Inductively coupled plasma mass spectrometry (ICP-MS) and optical emission spectrometry (ICP-OES) were used to investigate 18 metal elements within the dust samples. The results showed that the mass fraction of Ca[ω(Ca)] was highest with an average of 120307.7 mg·kg-1, which was 7.2 times higher than the soil background values for Shandong Province. The mean values of ω(Zn), ω(Cu), ω(Sb), and ω(Cd) were 13.9, 11.7, 13.3, and 29.6 times higher than the background values, respectively. The geo-accumulation index (Igeo) indicated high levels of Cd, Zn, Cu, and Sb pollution, especially in winter. Enrichment factors (EFs) also indicated high concentrations of Cd, Zn, Sb, and Cu in the road dust, which were notably affected by human activities. Principal component analysis (PCA) showed that biomass combustion, coal burning, vehicle emissions, iron and steel smelting, and soil dust are the five main sources of metal elements in road dust in Zibo City. The potential ecological risk of Cd and the total potential risk were extremely high during three seasons and was highest in winter. Health risk assessment showed that As and Pb had a non-carcinogenic risk for children, while Cr presents a carcinogenic risk. In conclusion, pollution from PM2.5-bound metallic elements in road dust in Zibo City is derived from anthropogenic sources and is most severe during winter. Importantly, the levels of pollution detected represent potential ecological risk as well as some non-carcinogenic and carcinogenic risks for children. Therefore, the source control of road dust requires particular attention.

Aircraft-based observation of gaseous pollutants in the lower troposphere over the Beijing-Tianjin-Hebei region.

To investigate the spatial and vertical distribution of atmospheric pollutants (SO2, NOx, CO and O3), aircraft-based measurements (model: Yun-12, 12 flights, 27 h total flight time) were conducted from near the surface up to 2400 m over the Beijing-Tianjin-Hebei (BTH) region between June 17th and July 22nd 2016. The results showed that high concentrations of primary gaseous pollutants (SO2, NOx, CO) were generally present in Beijing, Tianjin, Langfang and Tangshan areas, while high values of O3 frequently appeared in areas far from the city. The flights at noon and dusk measured higher O3 concentrations at 600 m and lower O3 concentrations at higher altitudes, implying a strong influence by photochemical production. Back trajectory analysis suggested that the high levels of gaseous pollutants, especially at 600 m, were associated with pollution sources transported from the southerly direction during the observation period. The first simultaneous vertical distribution measurements using aircraft and tethered balloon were conducted in Gaocun (a rural site between Beijing and Tianjin) on June 17th. The results indicated that an inversion layer at the top of the planetary boundary layer (PBL) significantly suppressed vertical exchange through the PBL and resulted in a "two-layer" vertical distribution of pollutants above and below the PBL. Additionally, a residual high O3 layer (79.9 ± 2.5 ppb, 500-1000 m) was observed above the PBL, and it contributed to the surface peak O3 level at noon through downward transport along with the opening up of the PBL. These results indicate that coupled effects of horizontal and vertical transport should be investigated in future studies to improve the chemical transport models used to study the vertical distribution and regional transport over the BTH region.

Systematic Evaluations of Doxorubicin-Induced Toxicity in Rats Based on Metabolomics.

Doxorubicin (DOX) is widely used to treat solid tumors, but its use is limited by its severe cardiotoxicity, nephrotoxicity, hepatotoxicity, and neurotoxicity. Metabolomic studies on DOX-induced toxicity are mainly focused on alterations in the heart and kidney, but systematic research on multiple matrices (serum, heart, liver, brain, and kidney) is rare. Thus, in our study, gas chromatography-mass spectrometry analysis of main targeted tissues (serum, heart, liver, brain, and kidney) was used to systemically evaluate the toxicity of DOX. Multivariate analyses, including orthogonal projections to the latent structure and t-test, revealed 21 metabolites in the serum, including cholesterol, d-glucose, d-lactic acid, glycine, l-alanine, l-glutamic acid, l-isoleucine, l-leucine, l-proline, l-serine, l-tryptophan, l-tyrosine, l-valine, MG (0:0/18:0/0:0), MG (16:0/0:0/0:0), N-methylphenylethanolamine, oleamide, palmitic acid, pyroglutamic acid, stearic acid, and urea. In the heart, perturbed metabolites included 3-methyl-1-pentanol, cholesterol, d-glucose, d-lactic acid, glycerol, glycine, l-alanine, l-valine, MG (16:0/0:0/0:0), palmitic acid, phenol, propanoic acid, and stearic acid. For the liver, DOX exposure caused alterations of acetamide, acetic acid, d-glucose, glycerol, l-threonine, palmitic acid, palmitoleic acid, stearic acid, and urea. In the brain, metabolic changes involved 2-butanol, carbamic acid, cholesterol, desmosterol, d-lactic acid, l-valine, MG (16:0/0:0/0:0), palmitic acid, and stearic acid. In the kidney, disturbed metabolites were involved in cholesterol, glycerol, glycine, l-alanine, MG (0:0/18:0/0:0), MG (16:0/0:0/0:0), and squalene. Complementary evidence by multiple matrices revealed disturbed pathways concerning amino acid metabolism, energy metabolism, and lipid metabolism. Our results may help to systematically elucidate the metabolic changes of DOX-induced toxicity and clarify the underlying mechanisms.

Circulating sortilin levels are associated with inflammation in patients with moyamoya disease.

BACKGROUND: Systemic inflammation has been implicated in the pathogenesis of moyamoya disease (MMD). Sortilin is a critical regulator of proinflammatory cytokine secretion in several cell types. The present study investigated the association between circulating sortilin and proinflammatory cytokine levels and the occurrence of MMD. METHODS: Forty-two MMD cases and 76 age- and sex-matched controls were enrolled in this study between January 2018 and June 2019 at the Affiliated Hospital of Jining Medical University. The demographic and clinical characteristics were evaluated, and the circulating serum and cerebrospinal fluid (CSF) levels of sortilin, sortilin-related receptor with A-type repeats (SorLA), and proinflammatory cytokines including C-reactive protein (CRP), interleukin (IL)-6, interferon (IFN)-γ were measured by enzyme-linked immunosorbent assay. Linear regression and correlation analyses were used to estimate the associations between sortilin, SorLA, and proinflammatory cytokine levels. RESULTS: MMD patients had higher serum levels of sortilin (P = 0.012), CRP (P = 0.013), IL-6 (P = 0.004), and IFN-γ (P = 0.033) than healthy controls. In MMD patients, serum sortilin was positively correlated with serum proinflammatory cytokines (CRP: r = 0.459, P = 0.0022; IL-6: r = 0.445, P = 0.0032; and IFN-γ: r = 0.448, P = 0.0029) and CSF sortilin (r = 0.440, P = 0.0035); the latter was positively correlated with CSF levels of CRP (r = 0.542, P = 0.0002), IL-6 (r = 0.440, P = 0.0036), and IFN-γ (r = 0.443, P = 0.0033). CONCLUSIONS: Elevated sortilin level is associated MMD onset and may be a clinically useful biomarker along with proinflammatory cytokine levels.

Comprehensive Evaluation of Lipopolysaccharide-Induced Changes in Rats Based on Metabolomics.

PURPOSE: Substantial evidence indicates that lipopolysaccharide (LPS) exposure can lead to systemic inflammatory response syndrome (SIRS) and multiple organ failure. Previous metabolomic studies have mainly focused on LPS-induced depression or hepatic and renal effects. However, no comprehensive metabolomics-based analysis of the serum, liver, kidney, hippocampus, and heart following exposure to LPS has been undertaken to date. MATERIAL AND METHODS: Male Sprague-Dawley rats were randomly allocated to a control and a LPS-treated group (n=8). LPS for 2 weeks (0.5 mg/kg every other day) was given via intraperitoneal injection. Gas chromatography-mass spectrometry (GC-MS) was used for metabolite determination, while multivariate statistical analysis was performed to identify differentially expressed metabolites between the two groups. RESULTS: Our study revealed that 24, 13, 12, 7, and 12 metabolites were differentially expressed between the LPS treatment group and the control group in the serum, liver, kidney, hippocampus, and heart, respectively. We further identified that these metabolic changes were mainly involved with aminoacyl-tRNA biosynthesis; glutathione metabolism; glyoxylate and dicarboxylate metabolism; glycine, serine, and threonine metabolism; arginine biosynthesis; bile acid biosynthesis; and glycerolipid metabolism. CONCLUSION: We have systematically elucidated the metabolic changes underlying LPS-induced SIRS, thereby providing insight into the mechanisms associated with these alterations.