Design of novel chiral self-assembling peptides to explore the efficiency and mechanism of mRNA-FIPV vaccine delivery vehicles.

The enhancement of conventional liposome and lipid nanoparticle (LNP) methodologies in the formulation and deployment of messenger RNA (mRNA) vaccines necessitates further refinement to augment both their effectiveness and biosafety profiles. Additionally, researching these innovative delivery carrier materials represents both a prominent focus and a significant challenge in the current scientific landscape. Here we designed new chiral self-assembling peptides as the delivery carrier for RNA vaccines to study the underlying mechanisms in the feline infectious peritonitis virus (FIPV) model system. Firstly, we successfully transcribed mature enhanced green fluorescent protein (EGFP) mRNA and feline infectious peritonitis virus nucleocapsid (FIPV N) mRNA in vitro from optimized vectors. Subsequently, we developed chiral self-assembling peptide-1 (CSP-1) and chiral self-assembling peptide-2 (CSP-2) peptides, taking into account the physical and chemical characteristics of nucleic acid molecules as well as the principles of self-assembling peptides, with the aim of improving the delivery efficiency of mRNA molecule complexes. We determined the optimal coating ratio between CSP and mRNA by electrophoretic mobility shift assay. We found that the peptides and mRNA complexes can protect the mRNA from RNase A enzyme and efficiently deliver mRNA into cells for target antigen proteins expression. Animal experiments confirmed that CSP-1/mRNA complex can effectively trigger immune response mechanisms involving IFN-γ and T cell activation. It can also stimulate CD4+ and CD8+ T cell proliferation and induce serum antibody titers up to 10,000 times higher. And no pathological changes were observed by immunohistochemistry in liver, spleen, and kidney, indicating that CSP-1 may be a safe and promising delivery system for mRNA vaccines. Methodologically, this research represents a novel endeavor in the utilization of chiral self-assembling peptides within the realm of mRNA vaccines. This approach not only introduces fresh prospects for employing such nanomaterials in various mRNA vaccines but also expands the potential for developing small molecules, proteins, and antibodies. Furthermore, it paves the way for new clinical applications of existing pharmaceuticals.

Associations between atmospheric PM2.5 exposure and carcinogenic health risks: Surveillance data from the year of lowest recorded levels in Beijing, China.

Scant research has pinpointed the year of minimum PM2.5 concentration through extensive, uninterrupted monitoring, nor has it thoroughly assessed carcinogenic risks associated with analyzing numerous components during this nadir in Beijing. This study endeavored to delineate the atmospheric PM2.5 pollution in Beijing from 2015 to 2022 and to undertake comprehensive evaluation of carcinogenic risks associated with the composition of atmospheric PM2.5 during the year exhibiting the lowest concentration. PM2.5 concentrations were monitored gradually in 9 districts of Beijing for 7 consecutive days per month from 2015 to 2022, and 32 kinds of PM2.5 components collected in the lowest PM2.5 concentration year were analyzed. This comprehensive dataset served as the basis for carcinogenic risk assessment using Monte Carlo simulation. And we applied the Positive Matrix Factorization (PMF) method to identity the sources of atmospheric PM2.5. Furthermore, we integrated this source appointment model with risk assessment model to discern the origins of these risks. The findings revealed that the annual average PM2.5 concentration in 2022 stood at 43.1 µg/m3, marking the lowest level recorded. The mean carcinogenic risks of atmospheric PM2.5 exposure calculated at 6.30E-6 (empirical 95% CI 1.09E-6 to 2.25E-5) in 2022. The PMF model suggested that secondary sources (35.4%), coal combustion (25.6%), resuspended dust (15.1%), biomass combustion (14.1%), vehicle emissions (7.1%), industrial emissions (2.0%) and others (0.7%) were the main sources of atmospheric PM2.5 in Beijing. The mixed model revealed that coal combustion (2.41E-6), vehicle emissions (1.90E-6) and industrial emissions (1.32E-6) were the main sources of carcinogenic risks with caution. Despite a continual decrease in atmospheric PM2.5 concentration in recent years, the lowest concentration levels still pose non-negligible carcinogenic risks. Notably, the carcinogenic risks associated with metals and metalloids exceeded that of PAHs. And the distribution of risk sources did not align proportionally with the distribution of PM2.5 mass concentration.

Construction of a three-dimensional inflammation model of human bronchial epithelial cells BEAS-2B by using the self-assembling D-form peptide Sciobio-â ¢.

Human bronchial epithelial cells in the airway system, as the primary barrier between humans and the surrounding environment, assume a crucial function in orchestrating the processes of airway inflammation. Target to develop a new three-dimensional (3D) inflammatory model to airway system, and here we report a strategy by using self-assembling D-form peptide to cover the process. By testing physicochemical properties and biocompatibility of Sciobio-Ⅲ, we confirmed that it can rapidly self-assembles under the trigger of ions to form a 3D nanonetwork-like scaffold, which supports 3D cell culture including the cell strains like BEAS-2B cells. Subsequently, inflammation model was established by lipopolysaccharide (LPS), the expression of some markers of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), and interleukin-8 (IL-8), the levels of relevant inflammatory factors were measured by RT-qPCR and the secretion profile of inflammatory cytokines by ELISA, are obtained the quite difference effects in 2D and 3D microenvironment, which suggested Sciobio-Ⅲ hydrogel is an ideal scaffold that create the microenvironment for 3D cell culture. Here we are success to establish a 3D inflammation model for airway system. This innovative model allows for rapid and accurate evaluation of drug metabolism and toxicological side effects, hope to use in drug screening for airway inflammatory diseases and beyond.

Association between serum AMH levels and IVF/ICSI outcomes in patients with polycystic ovary syndrome: a systematic review and meta-analysis.

CONTEXT: Anti-Müllerian hormone (AMH) levels are increased in polycystic ovary syndrome (PCOS) patients and are associated with PCOS severity. OBJECTIVE: To evaluate the associations between serum AMH levels and in vitro fertilization (IVF)/ intracytoplasmic sperm injection (ICSI) outcomes in patients with PCOS. DATA SOURCES: PubMed, Embase, and the Cochrane Library were searched on 11 July 2022. STUDY SELECTION: Studies reporting the association between serum AMH levels and IVF/ICSI outcomes in PCOS patients were considered for inclusion. The primary outcomes were clinical pregnancy, live birth, and ovarian hyperstimulation syndrome. DATA EXTRACTION: Data were extracted using a standardized data extraction form. Study quality was assessed independently by two groups of researchers. DATA SYNTHESIS: Nineteen studies were included in this review. Meta-analyses demonstrated that PCOS patients with a serum AMH level within the 75-100th percentile had a decreased odds of clinical pregnancy (OR: 0.77, 95% CI: 0.63-0.93) and livebirth (OR: 0.71; 95% CI: 0.58-0.87) compared to those within the 0-25th percentile. An increased AMH level was also correlated with an increased number of oocytes retrieved (SMD: 0.90, 95% CI: 0.30-1.51) and a lower odds of fertilization (OR: 0.92, 95% CI: 0.87-0.98). There was no significant difference in the number of MII oocytes (SMD: 1.85, 95% CI: -1.07-4.78), E2 on the day of hCG (SMD: 0.12; 95% CI: -0.98-1.23), or implantation (OR: 0.82, 95% CI: 0.28-2.39) between the two groups. In addition, we found significant dose-response associations between serum AMH level and clinical pregnancy, live birth, number of oocytes retrieved, and fertilization in PCOS patients. CONCLUSION: AMH may have clinical utility in counseling regarding IVF/ICSI outcomes among women with PCOS who wish to undergo fertility treatment. More large-scale, high-quality cohort studies are needed to confirm these findings.

Carbon nanotubes: a powerful bridge for conductivity and flexibility in electrochemical glucose sensors.

The utilization of nanomaterials in the biosensor field has garnered substantial attention in recent years. Initially, the emphasis was on enhancing the sensor current rather than material interactions. However, carbon nanotubes (CNTs) have gained prominence in glucose sensors due to their high aspect ratio, remarkable chemical stability, and notable optical and electronic attributes. The diverse nanostructures and metal surface designs of CNTs, coupled with their exceptional physical and chemical properties, have led to diverse applications in electrochemical glucose sensor research. Substantial progress has been achieved, particularly in constructing flexible interfaces based on CNTs. This review focuses on CNT-based sensor design, manufacturing advancements, material synergy effects, and minimally invasive/noninvasive glucose monitoring devices. The review also discusses the trend toward simultaneous detection of multiple markers in glucose sensors and the pivotal role played by CNTs in this trend. Furthermore, the latest applications of CNTs in electrochemical glucose sensors are explored, accompanied by an overview of the current status, challenges, and future prospects of CNT-based sensors and their potential applications.

Preparation of Carbon Dots@r-GO Nanocomposite with an Enhanced Pseudo-Capacitance.

Carbon materials with pseudocapacitive performance have attracted emerging interest in the energy storage and conversion field. Reduced graphene oxide (r-GO) with superior conductivity and electrochemical stability has been extensively investigated as an efficient capacitive electrode material. In this study, three-dimensional carbon dots (CDs)@r-GO hydrogel electrode was successfully in situ prepared by the one-pot method, where the CDs play a critical role in serving as both reduction agent and electrochemical active sites. With prolonged reaction time, the oxygen content of the CDs@r-GO nanocomposite material could be effectively reduced to ensure better electric conductivity, and the nitrogen content, which provides pseudocapacitance, was gradually increased. The representative two pairs of fast and reversible current peaks appeared in cyclic voltammetry curves, with around three times higher specific capacitance of CDs@r-GO hydrogel electrode (290 F g-1 at the current density of 1 A g-1 in 1 M H2SO4 electrolyte). This simple and mild approach is promising and it is believed it will shed more light on the preparation of high-efficiency and high-performance energy storage materials based on functional reductive CDs.

A Self-Assembling Peptide as a Model for Detection of Colorectal Cancer.

Patient-derived organoid (PDO) models have been widely used in precision medicine. The inability to standardize organoid creation in pre-clinical models has become apparent. The common mouse-derived extracellular matrix can no longer meet the requirements for the establishment of PDO models. Therefore, in order to develop effective methods for 3D cultures of organoids, we designed a self-assembling peptide, namely DRF3, which can be self-assembled into ordered fibrous scaffold structures. Here, we used the co-assembly of self-assembling peptide (SAP) and collagen type I, fibronectin, and laminin (SAP-Matrix) to co-simulate the extracellular matrix, which significantly reduced the culture time of PDO, improved the culture efficiency, and increased the self-assembly ability of cells. Compared with the results from the 2D cell line, the PDO showed a more significant expression of cancer-related genes. During organoid self-assembly, the expression of cancer-related genes is increased. These findings provide a theoretical basis for the establishment of precision molecular modeling platforms in the future.

Identification of MT1E as a novel tumor suppressor in hepatocellular carcinoma.

BACKGROUND: Metallothioneins (MTs) involves in the tumorigenesis and prognosis of various cancers. The biological function and methylation status of MT1E in hepatocellular carcinoma (HCC) remain to be elucidated. METHODS: We analyzed differentially expressed genes (DEGs) in tumor tissue samples and normal samples from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) database, and identified the expression levels of MT1E in the HCC. Then, the expression levels and methylation status of MT1E in HCC tissues and cells were validated by qRT-PCR and methylation-specific PCR (MSP). Also, MTT, colony formation, transwell assays, and flow cytometry, as well as xenograft model, were used to assess the biological roles of MT1E in HCC. RESULTS: Downregulated expression of MT1E was found in HCC tissues, and was notably correlated with an aberrant methylation level of the gene promoter. Moreover, our study verified that MT1E suppressed cell growth in vitro and vivo. Further study demonstrated that MT1E could induce apoptosis and suppress the metastasis of HCC cells. CONCLUSIONS: Our results suggested that epigenetic silencing of MT1E due to promoter hypermethylation could play a vital role in HCC.

Association of emergency room visits for respiratory diseases with sources of ambient PM2.5.

Previous studies have reported associations of short-term exposure to different sources of ambient fine particulate matter (PM2.5) and increased mortality or hospitalizations for respiratory diseases. Few studies, however, have focused on the short-term effects of source-specific PM2.5 on emergency room visits (ERVs) of respiratory diseases. Source apportionment for PM2.5 was performed with Positive Matrix Factorization (PMF) and generalized additive model was applied to estimate associations between source-specific PM2.5 and respiratory disease ERVs. The association of PM2.5 and total respiratory ERVs was found on lag4 (RR = 1.011, 95%CI: 1.002, 1.020) per interquartile range (76 µg/m3) increase. We found PM2.5 to be significantly associated with asthma, bronchitis and chronic obstructive pulmonary disease (COPD) ERVs, with the strongest effects on lag5 (RR = 1.072, 95%CI: 1.024, 1.119), lag4 (RR = 1.104, 95%CI: 1.032, 1.176) and lag3 (RR = 1.091, 95%CI: 1.047, 1.135), respectively. The estimated effects of PM2.5 changed little after adjusting for different air pollutants. Six primary PM2.5 sources were identified using PMF analysis, including dust/soil (6.7%), industry emission (4.5%), secondary aerosols (30.3%), metal processing (3.2%), coal combustion (37.5%) and traffic-related source (17.8%). Some of the sources were identified to have effects on ERVs of total respiratory diseases (dust/soil, secondary aerosols, metal processing, coal combustion and traffic-related source), bronchitis ERVs (dust/soil) and COPD ERVs (traffic-related source, industry emission and secondary aerosols). Different sources of PM2.5 contribute to increased risk of respiratory ERVs to different extents, which may provide potential implications for the decision making of air quality related policies, rational emission control and public health welfare.

A novel case of endometrial dedifferentiated adenocarcinoma associated with MLH1 promotor hypermethylation and microsatellite instability.

Endometrial dedifferentiated carcinoma is a rare, malignant tumor whose molecular alterations have not been clarified yet. We report a novel case of a 61-year old woman who presented with irregular vaginal bleeding after menopause and a 3 cm uterus mass. Histology revealed endometrial dedifferentiated adenocarcinoma, a rare subtype comprised of undifferentiated adenocarcinoma. The patient still survived 1 year after surgery without chemotherapy and radiotherapy. Immunohistochemistry revealed loss of MLH1/PMS2 expression and retained MSH2/MSH6 expression. Consistently, microsatellite instability was detected indicative of high microsatellite instability (MSI-H). No BRAF V600E, KRAS and POLE mutations were identified. Remarkably, the promoter regions of mutL homolog 1(MLH1) were methylated. Furthermore, several tumor cells were PD-L1 positive in this case with a concentration at the infiltrating tumor edge indicating MSI-H in endometrial dedifferentiated adenocarcinoma is a potential predictive factor for response to immunotherapy targeting the PD-1 or its ligand PD-L1.

The burden of ozone pollution on years of life lost from chronic obstructive pulmonary disease in a city of Yangtze River Delta, China.

OBJECTIVE: Ambient ozone is one of the most important air pollutants with respect to its impacts on human health and its increasing concentrations globally. However, studies which explored the burden of ozone pollution on chronic obstructive pulmonary disease (COPD) and estimated the relevant economic loss were rare. OBJECTIVE: We explored the relationships between ambient ozone exposure and years of life lost (YLL) from COPD mortality and estimated the relevant economic loss in Ningbo, in the Yangtze River Delta of China, 2011-2015. METHODS: A time-series study was conducted to explore the effects of ozone on YLL from COPD. Seasonal stratified analyses were performed, and the effect modification of demographic factors was estimated. In addition, the related economic loss was calculated using the method of the value per statistical life year (VSLY). RESULTS: Averaged daily mean maximum 8-h average ozone concentration was 40.90 ppb in Ningbo, China, 2011-2015. The effect of short term ambient ozone exposure on COPD YLL was more pronounced in the cool season than in the warm season, with 10 ppb increment of ozone corresponding to 7.09(95%CI: 3.41, 10.78) years increase in the cool season and 0.31 (95%CI: -2.15, 2.77) years change in the warm season. The effect was higher in the elderly than the young. Economic loss due to excess COPD YLL related to ozone exposure accounted for 7.30% of the total economic loss due to COPD YLL in Ningbo during the study period. CONCLUSIONS: Our findings highlight that ozone exposure was related to tremendous disease burden of COPD in Ningbo, China. The effects were more pronounced in the cool season, and the elderly were more susceptible populations.

The burden of ischemic heart disease related to ambient air pollution exposure in a coastal city in South China.

OBJECTIVE: Air pollution is considered one of the most important risk factors for ischemic heart disease (IHD), which is a major public health concern. The disease burden of IHD has continued to rise in China in the past two decades. However, epidemiological studies examining the associations between air pollution and IHD have been scarce in China, and the only studies were conducted in severe air pollution areas, where air pollution levels seriously exceed the World Health Organization Air Quality Guidelines. Whether the influence of air pollution on IHD in areas with relatively low levels of air pollution differs from the influence of high pollution levels in heavily studied areas was unknown until now. Furthermore, the estimation of the disease burden of IHD related to air pollution has been very limited. METHODS: We conducted a time-series study to estimate the short-term burden of ambient air pollution on IHD using the indicator of years of life lost (YLL), based on 10 322 IHD deaths from 2011 to 2015 in Ningbo, a coastal city in South China. RESULTS: The mean concentrations of fine particle (PM2.5), sulfur dioxide (SO2) and nitrogen dioxide (NO2) were 49.58 µg/m3, 21.34 µg/m3 and 43.41 µg/m3, respectively. A 10 µg/m3 increase in PM2.5, SO2 and NO2 was associated with changes in YLL of 0.71 (95%CI: - 0.21,1.64), 3.31 (95%CI: 0.78, 5.84), and 2.27 (95%CI: 0.26, 4.28) years, respectively. Relatively stronger impacts were found for gaseous pollutants than PM2.5. A larger increase in YLL was found in the younger population than in the older population for NO2 exposure. In addition, estimations of the effects of SO2 and NO2 on YLL were higher for males than females. SO2 exposure was positively associated with YLL in widowed group. CONCLUSIONS: The findings highlighted the importance of stringent air pollution control, especially for gaseous pollutants. Furthermore, using the indicator of YLL, considering the occurrence of death at different ages, provided more information for resource allocation and protection of vulnerable populations.

Silencing of vacuolar ATPase c subunit ATP6V0C inhibits the invasion of prostate cancer cells through a LASS2/TMSG1-independent manner.

Vacuolar ATPase (V-ATPase), widespread in eukaryotic cells, is extensively expressed in many highly metastatic tumors, of which the V-ATPase c subunit ATP6V0C is particularly associated with the invasion and metastasis of cancer. ATP6V0C was directly found to interact with LASS2/TMSG1 which is a new tumor metastasis inhibitory gene identified by our laboratory in 1999. In order to study the role of ATP6V0C, we generated small interference RNA (siRNA) targeting ATP6V0C and investigated its function on the invasion of human prostate cancer cell line PC-3M-1E8 with high metastatic potential and its interplay with LASS2/TMSG1. We found that the expression of ATP6V0C was higher in prostate cancer cell lines PC-3M-1E8 and PC-3M with high metastatic potential than that from cell lines PC-3M-2B4 and PC-3 with low metastatic potential, indicating that ATP6V0C enhanced metastatic capacity in prostate cancer cells. Furthermore, silencing of ATP6V0C in PC-3M-1E8 cells inhibited V-ATPase activity (by ~5-fold), decreased extracellular hydrogen ion concentration and successively decreased activation of secreted MMP-9 (by ~3.6-fold), which coincided with the inhibition of cell migration and invasion in vitro, as well as a marked decrease in the expression of LASS2/TMSG1 probably through positive feedback. Thus we concluded that silencing of the ATP6V0C gene effectively suppressed the migration and invasion of prostate carcinoma cells through the inhibition of the function of V-ATPase, not through a LASS2/TMSG1-dependent manner. Therefore ATP6V0C inhibitors are promising therapeutic targets for advanced prostate cancer.

Temporal variation in associations between temperature and years of life lost in a southern China city with typical subtropical climate.

Though some studies have explored the association between temperature and years of life lost (YLL), limited evidence is available regarding the effect of temporal variation on the temperature-YLL relationship, especially in developing countries. We explored temporal variation in the associations between temperature and YLL before and after 2013 heat waves (period I: Jan 2008 to Sep 2013, period II: Oct 2013 to Dec 2015) in Ningbo, a southern China city with typical subtropical climate. The heat associations showed an increasing trend. The number of YLL due to heat-related respiratory mortality was significantly higher in period II (46.03, 95% CI: 11.97, 80.08) than in period I (7.21, 95% CI: -10.04, 24.46) among married individuals. In contrast, the cold associations presented an attenuating trend, and the number of YLL due to non-accidental mortality was significantly lower in period II (262.32, 95% CI: -304.18, 828.83) than in period I (916.78, 95% CI: 596.05, 1237.51). These results indicate more effort still needed to be made to reduce heat-related YLL even after periods of extreme heat. Furthermore, using YLL provided complementary information for identifying vulnerable subgroups, which has important implications for the planning of public health interventions.

The short term burden of ambient fine particulate matter on chronic obstructive pulmonary disease in Ningbo, China.

BACKGROUND: Numerous studies have found associations between ambient fine particulate matter (PM2.5) and increased mortality risk. However, little evidence is available on associations between PM2.5 and years of life lost (YLL). We aimed to estimate the YLL due to chronic obstructive pulmonary disease (COPD) mortality related to ambient PM2.5 exposure. METHODS: A time-series study was conducted based on the data on air pollutants, meteorological conditions and 18,472 registered COPD deaths in Ningbo, China, 2011-2015. The effects of PM2.5 on YLL and daily death of COPD were estimated, after controlling long term trend, meteorological index and other confounders. RESULTS: The impact of PM2.5 on YLL due to COPD lasted for 5 days (lag 0-4). Per 10 µg/m3 increase in PM2.5 was associated with 0.91 (95%CI: 0.16, 1.66) years increase in YLL. The excess YLL of COPD mortality were 8206 years, and 0.38 day per person in Ningbo from 2011 to 2015. The exposure-response curve of PM2.5 and YLL due to COPD showed a non-linear pattern, with relatively steep at low levels and flattened out at higher exposures.. Furthermore, the effects were significantly higher in the elderly than those in the younger. CONCLUSIONS: Our findings explored burden of PM2.5 on YLL due to COPD and highlight the importance and urgency of ambient PM2.5 pollution control and protection of the vulnerable populations.

Impact of Air Pollutants on Outpatient Visits for Acute Respiratory Outcomes.

The air pollution in China is a severe problem. The aim of our study was to investigate the impact of air pollutants on acute respiratory outcomes in outpatients. Outpatient data from 2 December 2013 to 1 December 2014 were collected, as well as air pollutant data including ozone (O3), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and particulate matter (PM2.5 and PM10). We screened six categories of acute respiratory outcomes and analyzed their associations with different air pollutant exposures, including upper respiratory tract infection (URTI), acute bronchitis (AB), community-acquired pneumonia (CAP), acute exacerbation of chronic obstructive pulmonary disease (AECOPD), acute exacerbation of asthma (AE-asthma), and acute exacerbation of bronchiectasis (AEBX). A case-crossover design with a bidirectional control sampling approach was used for statistical analysis. A total of 57,144 patients were enrolled for analysis. PM2.5, PM10, NO2, SO2, and CO exposures were positively associated with outpatient visits for URTI, AB, CAP, and AEBX. PM10, SO2, and CO exposures were positively associated with outpatient visits for AECOPD. Exposure to O3 was positively associated with outpatient visits for AE-asthma, but negatively associated with outpatient visits for URTI, CAP, and AEBX. In conclusion, air pollutants had acute effects on outpatient visits for acute respiratory outcomes, with specific outcomes associated with specific pollutants.

Efficiency of Emission Control Measures on Particulate Matter-Related Health Impacts and Economic Cost during the 2014 Asia-Pacific Economic Cooperation Meeting in Beijing.

Background: The Asia-Pacific Economic Cooperation (APEC) meeting was held from 5 November to 11 November 2014 in Beijing, and comprehensive emission control measures were implemented. The efficiency of these measures on particulate matter-related health impacts and economic cost need to be evaluated. Methods: The influences of emission control measures during APEC on particulate matter were evaluated, and health economic effects were assessed. Results: Average concentrations of PM2.5 and PM10 during APEC were reduced by 57.0%, and 50.6% respectively, compared with pre-APEC period. However, the concentrations of particulate matter rebounded after APEC. Compared with the pre-APEC and post-APEC periods, the estimated number of deaths caused by non-accidental, cardiovascular and respiratory diseases that could be attributed to PM2.5 and PM10 during the APEC were the lowest. The economic cost associated with mortality caused by PM2.5 and PM10 during the APEC were reduced by (61.3% and 66.6%) and (50.3% and 60.8%) respectively, compared with pre-APEC and post-APEC. Conclusions: The emission control measures were effective in improving short term air quality and reducing health risks and medical expenses during 2014 APEC, but more efforts is needed for long term and continuous air quality improvement and health protection.

Acute effects on pulmonary function in young healthy adults exposed to traffic-related air pollution in semi-closed transport hub in Beijing.

OBJECTIVES: Transport hub is an important part of urban comprehensive transportation system. Traffic-related air pollution can reach high level because of difficulty of diffusion and increase of emission in transport hub. However, whether exposure in this semi-closed traffic micro-environment causes acute changes in pulmonary function of commuters still needs to be explored. METHODS: Forty young healthy adults participated in this randomized, crossover study. Each participant underwent 2 h exposure in a designated transport hub and, on a separate occasion, in an appointed park. Personal exposures to fine particulate matter (PM2.5), black carbon (BC) and carbon monoxide (CO) were measured. Forced expiratory volume in 1 s (FEV1) and peak expiratory flow (PEF) were assessed pre-, during and post-exposure. Mixed linear models were used to analyze the pulmonary effects of traffic-related air pollutants. RESULTS: Participants had significantly higher exposures to PM2.5, BC and CO in the transport hub than in the park. Exposure in transport hub induced significant reductions in FEV1 and PEF compared with the park during exposure 1 and 2 h. The reductions were significant associated with traffic-related air pollutants. For instance, per 10 µg/m3 increment in PM2.5 was associated with -0.15 % (95 % CI -0.28, -0.02 %) reduction in FEV1 during exposure 2 h. However, effects became attenuate after 2 h exposure. CONCLUSIONS: Short-term exposure in transport hub had acute reduction effects on pulmonary function. More attention should be paid to the health effects of exposure in the semi-closed traffic micro-environment.