Nontargeted Analysis of Coumarins in Source Water and Their Formation of Chlorinated Coumarins as DBPs in Drinking Water.

Coumarin was detected as one of the most abundant compounds by nontargeted analysis of natural product components in actual water samples prior to disinfection. More importantly, prechlorination of humic acid generated 3-hydroxycoumarin and monohydroxy-monomethyl-substituted coumarin with a total yield of ≤10.1%, which suggested the humic substance in raw water is an important source of coumarins. 7-Hydroxycoumarin, 6-hydroxy-4-methylcoumarin, 6,7-dihydroxycoumarin, and 7-methoxy-4-methylcoumarin were identified in raw water by high-performance liquid chromatography-tandem high-resolution mass spectrometry because only some coumarin standards were commercially available. Their chlorination generated monochlorinated and polychlorinated coumarins, and their structures were confirmed by the synthesized standards. These products could form at various dosages of chlorine and pH levels, and some with a concentration of 600 ng/L can be stable in tap water for days. 3,6,8-Trichloro-7-hydroxycoumarin, 3-chloro-7-methoxy-4-methylcoumarin, and 3,6-dichloro-7-methoxy-4-methylcoumarin were first identified in finished water with concentrations of 0.0670, 78.1, and 14.7 ng/L, respectively, but not in source water, suggesting that they are new DBPs formed during disinfection. The cytotoxicity of 3-chloro-7-methoxy-4-methylcoumarin in CHO-K1 cells was comparable to those of 2,6-dibromo-1,4-benzoquinone and 2,6-dichloro-1,4-benzoquinone in TIC-Tox analyses, suggesting that further investigation of their occurrence and control in drinking water systems is warranted.

Analysis of direct drinking water quality and its influencing factors in primary and secondary schools in Nanjing City / 中国学校卫生

Objective@#To investigate the quality and influencing factors of direct drinking water in schools in Nanjing City, so as to provide basis for management of school drinking water.@*Methods@#From April to July 2023, direct drinking water equipment from 146 primary and secondary schools were selected from Nanjing City using a stratified random sampling method and tested for colony forming units (CFU) and permanganate index. Mann-Whitney U test was used to compare the differences between groups, and multiple linear regression was used to analyze the influencing factors.@*Results@#The CFU and permanganate levels of school direct drinking water in Nanjing City were 1.00(0.00,15.50)CFU/mL and 0.47(0.26, 0.75)mg/L, respectively. The CFU level increased when the filter replacement time exceeded 3 months and when the water source was piped, while the permanganate index increased when the filter replacement time exceeded 3 months and using activated carbon technology ( Z =-2.21, -3.92, -2.31, -8.45 , P <0.05). The results of multiple linear regression analysis showed that the replacement time of filter element exceeding 3 months was positively correlated with the CFU level, and the process type involving activated carbon, a laid pipe network and a filter replacement time exceeding 3 months were positively correlated with the permanganate index( β =167.08, 0.32, 0.35, 0.11, P ＜0.05).@*Conclusions@#There are certain problems with the water quality of primary and secondary school direct drinking water in Nanjing City. Schools should promptly replace the filter and maintain the drinking water equipment to ensure the hygiene and safety of campus water quality.

Efficacy of virtual reality training on motor performance, activity of daily living, and quality of life in patients with Parkinson's disease: an umbrella review comprising meta-analyses of randomized controlled trials.

OBJECTIVE: There are several meta-analyses of randomized controlled trials (RCTs) demonstrating the benefits of virtual reality (VR) training as an intervention for motor performance, activity of daily living (ADL) and quality of life (QoL) outcomes in patients with Parkinson's disease (PD). However, the aggregate evidence collected to date has not been thoroughly evaluated for strength, quality, and reproducibility. An umbrella review from published meta-analyses of RCTs was conducted to evaluate the strength and quality of existing evidence regarding the efficacy of VR training in improving the motor performance, ADL and QoL outcomes of patients with PD. METHODS: PubMed, PsychInfo, Web of Science, and Scopus were searched to identify relevant meta-analysis of RCTs examining the effects of VR training on motor performance and quality of life outcomes in PD patients. We recalculated the effect sizes (Hedges'g) for VR training using DerSimonian and Laird (DL) random effects models. We further assessed between-study heterogeneity, prediction interval (PI), publication bias, small-size studies, and whether the results of the observed positive studies were better than would be expected by chance. Based on these calculations, the quality of evidence for each outcome was assessed by using the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) criteria. RESULTS: Four meta-analysis with eight outcomes included in the umbrella review was recalculated effect size. Pooled results found VR training can large improve the basic balance ability, moderate improve the overall balance capacity and moderate improve the stride length in PD patients. For ADL and QoL, the effect sizes were pooled that suggested VR training can moderate improve ADL and QoL for PD patients. However, no statistically clear evidence was found in walking speed, motor function and gait function during VR training. The analyzed meta-analyses showed low-to-moderate methodological quality (AMSTAR2) as well as presented evidence of moderate-to-very low quality (GRADE). Tow adverse reactions were reported in the included meta-analyses. CONCLUSIONS: In this umbrella review, a beneficial correlation between VR and balance ability, stride length, ADL and QoL in PD patients was discovered, especially for the very positive effect of VR on balance because of two of the eight outcomes related to balance ability showed large effect size. The observations were accompanied by moderate- to very low-quality rating evidence, supporting VR training as a practical approach to rehabilitation.

Seasonal variability of the correlation network of antibiotics, antibiotic resistance determinants, and bacteria in a wastewater treatment plant and receiving water.

Sewage treatment plants are an essential source of antibiotics, antibiotic resistance determinants, and bacteria in environmental waters. However, it is still unclear whether they can maintain a relatively stable relationship in wastewater and environmental waters. This study analyzed the removal capacity of the above three pollutants in the sewage treatment plant in summer and their impact on environmental waters, and then examines the relationship between the three contaminants in the wastewater and environmental waters in summer and winter based on our previous study. The results found that the removal capacity of bacteria in summer was poor, the concentration of fluoroquinolone in the effluent was higher than that in influent, and the abundance of intI1, tetW, qnrB, and ermB increased after wastewater treatment. Proteobacteria and Bacteroides were the main bacteria that constitute the correlation network between bacteria, and they existed stably in summer and winter. However, fluoroquinolones occupied a significant position in the determinant network of antibiotics and antibiotic resistance in summer and winter. There are fewer correlation between antibiotics and antibiotics resistance determinants in winter. Interestingly, the relationship between bacteria, antibiotics, and antibiotic resistance determinants was a mainly positive correlation in summer and negative correlation in winter. This study analyzed the relationship between bacteria, antibiotics, and antibiotic resistance determinants that were stable in the wastewater and environmental waters and pointed out the direction for subsequent targeted seasonal control of novel pollutants in wastewater and environmental waters.

Urban fine particulate matter causes cardiac hypertrophy through calcium-mediated mitochondrial bioenergetics dysfunction in mice hearts and human cardiomyocytes.

In recent years, the cardiovascular toxicity of urban fine particulate matter (PM2.5) has sparked significant alarm. Mitochondria produce 90% of ATP and make up 30% of the volume of cardiomyocytes. Thus knowledge of myocardial mitochondrial dysfunction due to PM2.5 exposure is essential for further cardiotoxic effects. Here, the mechanism of PM2.5-induced cardiac hypertrophy through calcium overload and mitochondrial dysfunction was investigated in vivo and in vitro. Male and female BALB/c mice were given 1.28, 5.5, and 11 mg PM2.5/kg bodyweight weekly through oropharyngeal inhalation for four weeks and were assigned to low, medium, and high dose groups, respectively. PM2.5-induced myocardial edema and cardiac hypertrophy were detected in the high-dose group. Mitochondria were scattered and ruptured with abnormal ultrastructural morphology. In vitro experiments on human cardiomyocyte AC16 showed that exposure to PM2.5 for 24 h caused opened mitochondrial permeability transition pore --leading to excessive calcium production, decreased mitochondrial membrane potential, weakened mitochondrial respiratory metabolism capacity, and decreased ATP production. Nevertheless, the administration of calcium chelator ameliorated the mitochondrial damage in the PM2.5-treated group. Our in vivo and in vitro results confirmed that calcium overload under PM2.5 exposure triggered mTOR/AKT/GSK-3ß activation, leading to mitochondrial bioenergetics dysfunction and cardiac hypertrophy.

2,6-Dichloro-1,4-benzoquinone formation from chlorination of substituted aromatic antioxidants and its control by pre-ozonation in drinking water treatment plant.

Halobenzoquinones are frequently detected as disinfection by-products in drinking water. Among identified halobenzoquinones, 2,6-dichloro-1,4-benzoquinone (2,6-DCBQ) is particularly toxic and is frequently detected in drinking water. Synthetic aromatic antioxidants discharged to source water may increase the risk of 2,6-DCBQ formation, as many studies suggest that aromatic compounds are the most likely precursors to 2,6-DCBQ. Herein, we investigated the formation of 2,6-DCBQ from chlorination of three model aromatic antioxidants, including 3-tert-butyl-4-hydroxyanisole (BHA), 2,6-di-tert-butyl-4-methylphenol (BHT) and bis(4-tert-butylphenyl)amine (BBPA). Only BBPA produced 2,6-DCBQ under chlorination, while chlorination of BHA and BHT formed α, ß-unsaturated C4-dicarbonyl ring-opening products and phenolic compounds. Based on mass balance and intermediate transformation analysis, mechanisms for the formation of 2,6-DCBQ from BBPA chlorination involved hydrolysis, tert-butyl group cleavage, chlorine substitution, desamination and oxidation. Mitigating aromatic compounds will be an efficient method for 2,6-DCBQ control, such as pre-ozonation, because the intermediates involved in 2,6-DCBQ formation were aromatic compounds. Real water samples from two drinking water treatment plants (DWTPs), one with pre-ozonation (DWTP 2) and the other without pre-ozonation (DWTP1), were analyzed. The two DWTPs were built along the Yangtse river in Nanjing city. Raw water parameters from the two DWTPs, including dissolved organic carbon (DOC), UV absorbance at 254 nm (UV254) and NH3-N, indicated the water quality between these sources was similar. Pre-ozonation in DWTP 2 vanished 2,6-DCBQ in raw water. Concentrations of 2,6-DCBQ in finished water from DWTP 1 (5.69 ng/L) was higher than concentrations generated from DWTP 2 (1.31 ng/L). These results demonstrate that pre-ozonation, granular activated carbon (GAC) and quartz sand treatments at DWTP 2 remove more 2,6-DCBQ precursors than the conventional quartz sand and GAC treatments in DWTP 1. These results suggest the pre-ozonation, GAC and quartz sand treatments can help minimize concentrations of 2,6-DCBQ generated in DWTPs.

Intermittent exposure to airborne particulate matter induces subcellular dysfunction and aortic cell damage in BALB/c mice through multi-endpoint assessment at environmentally relevant concentrations.

Airborne particulate matter (PM) has been linked to cardiovascular diseases, but the underlying mechanisms remain unclear, especially at realistic exposure levels. In this study, both male and female BALB/c mice were employed to assess vascular homeostasis following a standard urban particulate matter, PM SRM1648a, via oropharyngeal aspiration at three environmentally relevant concentrations. The tested indicators included histopathological observation and lipid deposition, as well as redox biology and inflammatory responses. Furthermore, endothelial monolayer, vascular cell apoptosis and subcellular function were assessed to decipher whether episodic PM SRM1648a exposure leads to vascular damage after multiple periods of treatment, including subacute (4 weeks) and subchronic (8 weeks) durations. As a result, PM aspiration caused thickening of airways, leukocytes infiltration and adhesion to alveoli, with the spot of particles engulfed by pulmonary macrophages. Meanwhile, it induced local and systemic oxidative stress and inflammation, but limited pathological changes were captured throughout aortic tissues after either subacute or subchronic treatment. Furthermore, even in the absence of aortic impairment, vascular cell equilibrium has been disturbed by the characteristics of endothelial monolayer disintegration and cell apoptosis. Mechanistically, PM SRM1648a activated molecular markers of ER stress (BIP) and mitochondrial dynamics (DRP1) at both transcriptional and translational levels, which were strongly correlated to ox-inflammation and could serve as early checkpoints of hazardous events. In summary, our data basically indicate that episodic exposure of BALB/c mice to PM SRM1648a exerts limited effects on vascular histopathological alterations, but induces vascular cell apoptosis and subcellular dysfunction, to which local and systemic redox biology and inflammation are probably correlated.

NADPH oxidases regulate endothelial inflammatory injury induced by PM2.5 via AKT/eNOS/NO axis.

Fine particulate matter (PM2.5 )-induced detrimental cardiovascular effects have been widely concerned, especially for endothelial cells, which is the first barrier of the cardiovascular system. Among potential mechanisms involved, reactive oxidative species take up a crucial part. However, source of oxidative stress and its relationship with inflammatory response have been rarely studied in PM2.5 -induced endothelial injury. Here, as a key oxidase that catalyzes redox reactions, NADPH oxidase (NOX) was investigated. Human umbilical vein endothelial cells (EA.hy926) were exposed to Standard Reference Material 1648a of urban PM2.5 for 24 h, which resulted in NOX-sourced oxidative stress, endothelial dysfunction, and inflammation induction. These are manifested by the up-regulation of NOX, increase of superoxide anion and hydrogen peroxide, elevated endothelin-1 (ET-1) and asymmetric dimethylarginine (ADMA) level, reduced nitric oxide (NO) production, and down-regulation of phosphorylation of endothelial NO synthase (eNOS) with increased levels of inducible NO synthase, as well as the imbalance between tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor 1 (PAI-1), and changes in the levels of pro-inflammatory and anti-inflammatory factors. However, administration of NOX1/4 inhibitor GKT137831 alleviated PM2.5 -induced elevated endothelial dysfunction biomarkers (NO, ET-1, ADMA, iNOS, and tPA/PAI-1), inflammatory factors (IL-1ß, IL-10, and IL-18), and adhesion molecules (ICAM-1, VCAM-1, and P-selectin) and also passivated NOX-dependent AKT and eNOS phosphorylation that involved in endothelial activation. In summary, PM2.5 -induced NOX up-regulation is the source of ROS in EA.hy926, which activated AKT/eNOS/NO signal response leading to endothelial dysfunction and inflammatory damage in EA.hy926 cells.

The involvement of DRP1-mediated caspase-1 activation in inflammatory response by urban particulate matter in EA.hy926 human vascular endothelial cells.

Atmospheric particulate matter (PM) has been reported to be closely related to cardiovascular adverse events. However, the underlying mode of action remains to be elucidated. Previous studies have documented that PM induces mitochondrial damage and inflammation, the relation between these two biological outcomes is still unclear though. In this study, we used EA.hy926 human vascular endothelial cells and a standard PM, PM SRM1648a to study the potential effects of mitochondrial dysfunction on endothelial inflammatory responses. As a result, PM SRM1648a changes mitochondrial morphology and interrupts mitochondrial dynamics with a persistent tendency of fission in a dose-dependent manner. Additionally, the caspase-1/IL-1ß axis is involved in inflammatory responses but not cell pyroptosis in EA.hy926 cells following the exposure to PM SRM1648a. The activation of caspase-1 has implications in inflammation but not pyroptosis, because caspase-1-dependent pyroptosis is not the main modality of cell death in PM SRM1648a-treated EA.hy926 cells. With regard to the association between mitochondrial damage and inflammation in the case of particle stimulation, DRP1-mediated mitochondrial fission is responsible for inflammatory responses as a result of caspase-1 activation. The current study showed that PM SRM1648a has the ability to disturb mitochondrial dynamics, and trigger endothelial inflammation via DRP1/caspase-1/IL-1ß regulatory pathway. In a conclusion, mitochondrial fission enables EA.hy926 cells to facilitate caspase-1 activation in response to PM SRM1648a, which is a crucial step for inflammatory reaction in vascular endothelial cells.

Acute associations between air pollution on premature rupture of membranes in Hefei, China.

Numerous studies had focused on the association between air pollution and health outcomes in recent years. However, little evidence is available on associations between air pollutants and premature rupture of membranes (PROM). Therefore, we performed time-series analysis to evaluate the association between PROM and air pollution. The daily average concentrations of PM2.5, SO2 and NO2 were 54.58 µg/m3, 13.06 µg/m3 and 46.09 µg/m3, respectively, and daily maximum 8-h average O3 concentration was 95.67 µg/m3. The strongest effects of SO2, NO2 and O3 were found in lag4, lag06 and lag09, and an increase of 10 µg/m3 in SO2, NO2 and O3 was corresponding to increase in incidence of PROM of 8.74% (95% CI 2.12-15.79%), 3.09% (95% CI 0.64-5.59%) and 1.68% (95% CI 0.28-3.09%), respectively. There were no significant effects of PM2.5 on PROM. Season-specific analyses found that the effects of PM2.5, SO2 and O3 on PROM were more obvious in cold season, but the statistically significant effect of NO2 was observed in warm season. We also found the modifying effects by maternal age on PROM, and we found that the effects of SO2 and NO2 on PROM were higher among younger mothers (< 35 years) than advanced age mothers (≥ 35 years); however, ≥ 35 years group were more vulnerable to O3 than < 35 years group. This study indicates that air pollution exposure is an important risk factor for PROM and we wish this study could provide evidence to local government to take rigid approaches to control emissions of air pollutants.

Characterization of Urban Subway Microenvironment Exposure- A Case of Nanjing in China.

Environmental quality in public rail transit has recently raised great concern, with more attention paid to underground subway microenvironment. This research aimed to provide guidance for healthy urban subway microenvironments (sub-MEs) according to comprehensive micro-environmental categories, including thermal environment, air quality, lighting environment, and acoustic environment from both practical and regulation perspectives. Field sampling experiments were conducted in Nanjing Metro Line X (NMLX). Descriptive analysis, correlation analysis and one-way analysis of variance were used to investigate the status quo of urban sub-MEs. A paired samples t-test was then performed to compare among subway station halls, platforms, and in-cabin trains based on integrated sub-MEs. Results show that relative humidity, air velocity, respirable particulate matter (PM10) concentration, and illuminance dissatisfy the requirements in relevant national standards. Significant difference was observed in lighting environment between station hall and platform. It was detected platforms are warmer and more polluted than train cabins. Additionally, subway trains generate main noise on platform which is much louder when leaving than arriving. Protective strategies for sub-ME improvement as well as principles for updating standards were proposed from a proactive point of view. The findings are beneficial for moving towards healthy urban sub-MEs and more sustainable operation of subway systems.

Monitoring and exposure assessment of organophosphorus flame retardants in source and drinking water, Nanjing, China.

This study developed a new method to determine the residues of 13 organophosphorus flame retardants (OPFRs) in drinking water by gas chromatography-tandem mass spectrometry (GC-MS/MS) technique and investigated the chemical distribution in water samples from municipal plants along the Yangtze River in Nanjing. The linear calibration correlation coefficients R2 for all 13 OPFRs were at least 0.998 0. Three levels of spiked test were performed. Most of the recoveries were in the range of 80~120%, and the relative standard deviations (RSDs) for the 13 OPFRs were 2.1~17% (n = 6). Five OPFRs were 100% positively detected in the samples, and 3 OPFRs were positively detected in some samples. The concentrations of detected OPFR in the water ranged from 0.7 to 5780.0 ng L-1. The average concentrations of OPFRs in wet season were higher than those in dry season, and the contaminants mainly originated from the source water in the Yangtze River. The exposure assessments of individual and total OPFRs were investigated. The estimated daily intakes of total OPFRs via ingestion of drinking water reached up to 64.8 and 45.2 ng/kg bw/day in dry and wet season, respectively. This study demonstrates a profile of OPFR distribution in Nanjing municipal water and provides information on human exposure assessment via drinking water in the Nanjing District, China.

[Determination of three volatile N-nitrosamine in drinking water by solid phase extraction and gas chromatography-triple quadrupole mass spectrometry with programmable temperature vaporizer-based large volume injection].

A method had been developed for the determination of three N-nitrosamines, namely, N-nitrosodimethylamine (NDMA), N-nitrosomethylethylamine (NMEA), and N-nitrosodiethylamine (NDEA) in drinking water by solid phase extraction (SPE) and gas chromatography-triple quadrupole mass spectrometry (GC-QqQ-MS/MS) with programmable temperature vaporizer (PTV)-based large volume injection (LVI). The N-nitrosamine compounds were extracted from the water sample using a solid phase extraction (SPE) cartridge filled with coconut charcoal, and then eluted with 10 mL methylene chloride. The eluate was dried by anhydrous sodium sulfate and 10 µL was injected into the GC-MS/MS by PTV-LVI. The target compounds were detected by the multi-reaction monitoring (MRM) mode, and quantified with the external standard method. The results showed that the three compounds had good linearities in the range of 1-50 ng/L with correlation coefficients (r2) higher than 0.999. Drinking water samples were spiked with the target compounds at three concentration levels (10, 20, and 50 ng/L), and satisfactory recoveries (between 94.8% and 109%) and good reproductivities (relative standard deviation RSD<10%) were achieved. The limits of quantitation (LOQs) of the three N-nitrosamines were found to be in the range of 0.08-0.7 ng/L. The developed method was sensitive, accurate, convenient, and reliable for the determination of the three trace level N-nitrosamines in drinking water.

Identification of mRNA-miRNA crosstalk in human endothelial cells after exposure of PM2.5 through integrative transcriptome analysis.

PM2.5 has implications in cardiovascular adverse events, but the underlying mechanisms are still obscure. The aim of this study is to evaluate miRNA expression in endothelial cells in response to two realistic doses of PM2.5 and to identify the possible gene targets of deregulated miRNAs through microarray profiling and computational technology. As a result, there are 18 differentially expressed miRNAs between 2.5 µg/cm2 group and the control, of which 11 miRNAs are up-regulated and 7 miRNAs are down-regulated. Relative to the control group, 40 miRNAs are significantly changed in 10 µg/cm2 group with 21 miRNAs being upregulated and 19 miRNAs being downregulated. Interestingly, when two PM2.5-treated groups respectively compared with the control, the expressed trends of 12 miRNAs in 2.5 µg/cm2 group are the same as those in 10 µg/cm2 group, with 8 being upregulated and 4 miRNAs being simultaneously downregulated. Gene ontology (GO) analysis shows that the crucial functional categories of miRNA-targeted genes incorporate transcription-related process and intracellular signal transduction. Pathway analysis reveals that endocytosis, FoxO signaling pathway and PI3K-Akt signaling pathway are involved in the PM2.5-caused cardiotoxicity. Further confirmation by RT-qPCR indicates that PM2.5 could induce the down-regulation of hsa-miR-128-3p, hsa-miR-96-5p, hsa-miR-28-5p, hsa-miR-4478 and hsa-miR-6808-5p, which are in accordance with the results of array data. With the comprehensive analysis of mRNAs and miRNAs, a great number of pairs have been identified, suggesting abnormally expressed miRNAs have functions in the cardiotoxicity of PM2.5, and the function may be achieved through the post-transcriptional regulation of certain genes on the related pathways.

Genome-wide identification and functional analysis of long non-coding RNAs in human endothelial cell line after incubation with PM2.5.

Epidemiological studies and experimental research have illustrated that PM2.5 has an association with cardiovascular adverse events. However, the underlying mechanisms are still unknown. Long non-coding RNAs (lncRNAs) have been proposed to take part in diverse diseases. To comprehensively gain insight into the molecular toxicity of PM2.5, expression patterns are analyzed in EA.hy926 cell line through RNAs microarray. A total of 356 lncRNA transcripts are dysregulated in 2.5 µg/cm2 group, and there are 1283 lncRNAs differentially expressed in 10 µg/cm2 group. From functional analysis, several lncRNAs may be implicated in the bio-pathways of phagosome, TNF signaling pathway, chemokine signaling pathway and gap junction. Moreover, certain lncRNAs participate in the toxicity of PM2.5 through cis- and/or trans-regulation of their co-expressed genes. Therefore, lncRNAs may be used as new candidate biomarkers and potentially preventive targets in cardiotoxicity of PM2.5. Our study indicates that not limited to transcriptional regulation, post-transcriptional regulation plays a pivotal role in PM2.5-caused toxicity.

Risk Reduction Behaviors Regarding PM2.5 Exposure among Outdoor Exercisers in the Nanjing Metropolitan Area, China.

Aims: This study aimed to describe risk reduction behaviors regarding ambient particulate matter with a diameter of 2.5 µm or less (PM2.5) among outdoor exercisers and to explore potential factors influencing those behaviors in the urban area of Nanjing, China. Method: A cross-sectional convenience sample survey was conducted among 302 outdoor exercisers in May 2015. Descriptive analysis was used to describe demographics, outdoor physical activity patterns, knowledge of PM2.5 and risk reduction behaviors. Multivariate logistic regression analysis was then used to explore factors that influence the adoption of risk reduction behaviors. Results: The most common behavior to reduce PM2.5 exposure was minimizing the times for opening windows on hazy days (75.5%), and the least common one was using air purifiers (19.3%). Two thirds of respondents indicated that they wore face masks when going outside in the haze (59.5%), but only 13.6% of them would wear professional antismog face masks. Participants adopting risk reduction behaviors regarding PM2.5 exposure tended to be females, 50⁻60 year-olds, those with higher levels of knowledge about PM2.5 and those who had children. Conclusions: These findings indicate the importance of improving knowledge about PM2.5 among outdoor exercisers. Educational interventions should also be necessary to guide the public to take appropriate precautionary measures when undertaking outdoor exercise in high PM2.5 pollution areas.

Impact of Indoor Physical Environment on Learning Efficiency in Different Types of Tasks: A 3 × 4 × 3 Full Factorial Design Analysis.

Indoor physical environments appear to influence learning efficiency nowadays. For improvement in learning efficiency, environmental scenarios need to be designed when occupants engage in different learning tasks. However, how learning efficiency is affected by indoor physical environment based on task types are still not well understood. The present study aims to explore the impacts of three physical environmental factors (i.e., temperature, noise, and illuminance) on learning efficiency according to different types of tasks, including perception, memory, problem-solving, and attention-oriented tasks. A 3 × 4 × 3 full factorial design experiment was employed in a university classroom with 10 subjects recruited. Environmental scenarios were generated based on different levels of temperature (17 °C, 22 °C, and 27 °C), noise (40 dB(A), 50 dB(A), 60 dB(A), and 70 dB(A)) and illuminance (60 lx, 300 lx, and 2200 lx). Accuracy rate (AC), reaction time (RT), and the final performance indicator (PI) were used to quantify learning efficiency. The results showed ambient temperature, noise, and illuminance exerted significant main effect on learning efficiency based on four task types. Significant concurrent effects of the three factors on final learning efficiency was found in all tasks except problem-solving-oriented task. The optimal environmental scenarios for top learning efficiency were further identified under different environmental interactions. The highest learning efficiency came in thermoneutral, relatively quiet, and bright conditions in perception-oriented task. Subjects performed best under warm, relatively quiet, and moderately light exposure when recalling images in the memory-oriented task. Learning efficiency peaked to maxima in thermoneutral, fairly quiet, and moderately light environment in problem-solving process while in cool, fairly quiet and bright environment with regard to attention-oriented task. The study provides guidance for building users to conduct effective environmental intervention with simultaneous controls of ambient temperature, noise, and illuminance. It contributes to creating the most suitable indoor physical environment for improving occupants learning efficiency according to different task types. The findings could further supplement the present indoor environment-related standards or norms with providing empirical reference on environmental interactions.

Analysis of differentially changed gene expression in EA.hy926 human endothelial cell after exposure of fine particulate matter on the basis of microarray profile.

Epidemiological studies have illustrated that PM2.5 is closely related to cardiovascular disease (CVD), but underlying toxicological mechanisms are not yet clear. The main purpose of this study is to disclose the potential biological mechanisms responsible for PM2.5-dependent adverse cardiovascular outcomes through the appliance of genome-wide transcription microarray. From results, compared with the control group, there are 97 genes significantly altered in 2.5 µg/cm2 PM2.5 treated group and 440 differentially expressed genes in 10 µg/cm2 group. Of note, when 2.5 µg/cm2 and 10 µg/cm2 group were respectively compared with the control group, 46 significantly altered genes showed a consistent tendency in two treated groups, of which 31 genes were upregulated while 15 genes were meanwhile downregulated. Based on Gene Ontology (GO) annotation, altered genes are mainly gathered in functions of cellular processes and immune regulation. Pathway analysis indicated that TNF signaling pathway, NOD-like receptor (NLRs) signaling pathway, MAPK signaling pathway and gap junction are vital pathways involved in PM2.5-induced toxicity in EA.hy926. Moreover, results from RT-qPCR further corroborated that changed genes are implicated in oxidative stress, inflammation and metabolic disorder. In addition, metabolism of xenobiotics by cytochrome P450 pathway is the critical pathway which may serve as a target to prevent PM2.5-induced CVD. To sum up, our effort provides a fundamental data for further studies regarding mechanisms of PM2.5-induced cardiovascular toxicity on the basis of genome-wide screening.

Associations Between Air Quality Changes and Biomarkers of Systemic Inflammation During the 2014 Nanjing Youth Olympics: A Quasi-Experimental Study.

There is increasing interest in quasi-experimental research to evaluate whether actions taken to improve air quality will benefit public health. We conducted a quasi-experimental study to evaluate inflammatory response to changes in air quality during the 2014 Nanjing Youth Olympics in China. We repeatedly measured 8 biomarkers of systemic inflammation in 31 healthy adults and obtained hourly air pollutant concentrations from a nearby fixed-site monitoring station. We used linear mixed-effect models to examine the associations between air quality changes and blood biomarkers. Air pollutant concentrations decreased apparently during the Youth Olympics. Concomitantly, we observed significant decreases in levels of soluble cluster of differentiation 40 (CD40) ligand and interleukin 1ß (geometric means ratios were 0.45 and 0.24, respectively) from the pre-Olympic period to the intra-Olympic period. Afterwards, levels of C-reactive protein and vascular cell adhesion molecule 1 increased significantly (geometric means ratios were 2.22 and 1.29, respectively) in the post-Olympic period. Fine particulate matter and ozone were significantly associated with soluble CD40 ligand, P-selectin, interleukin 1ß, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1. Other pollutants showed positive but nonsignificant associations. Our study indicated that reduced air pollution, especially fine particulate matter and ozone, during the 2014 Nanjing Youth Olympics was associated with alleviated systemic inflammation in healthy adults.

Toxicity of inhaled particulate matter on the central nervous system: neuroinflammation, neuropsychological effects and neurodegenerative disease.

Particulate matter (PM) combined with meteorological factors cause the haze, which brings inconvenience to people's daily life and deeply endanger people's health. Accumulating literature, to date, reported that PM are closely related to cardiopulmonary disease. Outpatient visits and admissions as a result of asthma and heart attacks gradually increase with an elevated concentration of PM. Owing to its special physicochemical property, the brain could be a potential target beyond the cardiopulmonary system. Possible routes of PM to the brain via a direct route or stimulation of pro-inflammatory cytokines have been reported in several documents concerning toxicity of engineered nanoparticles in rodents. Recent studies have demonstrated that PM have implications in oxidative stress, inflammation, dysfunction of cellular organelles, as well as the disturbance of protein homeostasis, promoting neuron loss and exaggerating the burden of central nervous system (CNS). Moreover, the smallest particles (nano-sized particles), which were involved in inflammation, reactive oxygen species (ROS), microglial activation and neuron loss, may accelerate the process of the neurodevelopmental disorder and neurodegenerative disease. Potential or other undiscovered mechanisms are not mutually exclusive but complementary aspects of each other. Epidemiology studies have shown that exposure to PM could bring about neurotoxicity and play a significant role in the etiology of CNS disease, which has been gradually corroborated by in vivo and in vitro studies. This review highlights research advances on the health effects of PM with an emphasis on neurotoxicity. With the hope of enhancing awareness in the public and calling for prevention and protective measures, it is a critical topic that requires proceeding exploration. Copyright © 2017 John Wiley & Sons, Ltd.