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Lipids have been found to modulate tumor biology, including proliferation, survival, and metastasis. With the new understanding of tumor immune escape that has developed in recent years, the influence of lipids on the cancer–immunity cycle has also been gradually discovered. First, regarding antigen presentation, cholesterol prevents tumor antigens from being identified by antigen presenting cells. Fatty acids reduce the expression of major histocompatibility complex class I and costimulatory factors in dendritic cells, impairing antigen presentation to T cells. Prostaglandin E2 (PGE2) reduce the accumulation of tumor-infiltrating dendritic cells. Regarding T-cell priming and activation, cholesterol destroys the structure of the T-cell receptor and reduces immunodetection. In contrast, cholesterol also promotes T-cell receptor clustering and relative signal transduction. PGE2 represses T-cell proliferation. Finally, regarding T-cell killing of cancer cells, PGE2 and cholesterol weaken granule-dependent cytotoxicity. Moreover, fatty acids, cholesterol, and PGE2 can improve the activity of immunosuppressive cells, increase the expression of immune checkpoints and promote the secretion of immunosuppressive cytokines. Given the regulatory role of lipids in the cancer–immunity cycle, drugs that modulate fatty acids, cholesterol and PGE2 have been envisioned as effective way in restoring antitumor immunity and synergizing with immunotherapy. These strategies have been studied in both preclinical and clinical studies. Lipids regulate cancer immunity cycle by affecting antigen presentation, T-cell priming and activation and T-cell killing of tumor, which in turn promotes immune surveillance escape. [Display omitted] [ABSTRACT FROM AUTHOR]

Compared with a disordered network, the ordered framework is more beneficial to improving the multifunctional properties (including thermal, electrical, and mechanical properties) of epoxy-based composites. However, current methods for building aligned structures are both energy and time-consuming on account of the tedious and lengthy lyophilization process. Herein, a new strategy is proposed to obtain low-density graphene aerogels (GAs) with long-range oriented structures through a lyophilization-free processes. Due to the minimum thermal boundary resistance, the prepared aligned graphene/epoxy composite exhibits an ultrahigh thermal conductivity of ∼11.6 W/(m·K) at a graphene content of 1.84 vol%, i.e., an enhancement efficiency of 3640% per 1 vol%. In addition, the compressive strength of the composite is increased by 2.6 times compared to epoxy (from 0.29 MPa to 0.76 MPa). Because the composite shows a modulus as low as 0.5–1.0 MPa, it has excellent deformability and compression performance. Moreover, the obtained 3-mm-thick composite achieves an electromagnetic interference shielding effectiveness (EMI SE) of 40 dB due to the interconnected graphene network structure, which meets the requirements of commercial EMI shielding applications. Hence, this strategy can be used to synthesize aligned graphene/epoxy composites with excellent multifunctional performances, which can be simultaneously used as elastic thermal interface materials (TIMs) and EMI shielding materials in the fields of advanced electronic packaging. [Display omitted] • Aligned graphene aerogel (GA) was fabricated by a lyophilization-free approach. • The compressive strength of the composite is increased by 2.6 times compared to epoxy (0.29 MPa to 0.76 MPa) and the composite shows a modulus as low as 0.48–1.0 MPa, exhibiting excellent deformability and compression performance. • The vertical pathways and high-quality give composite an ultrahigh thermal conductivity (∼11.6 W/m·K) with ultralow graphene loading (1.84 vol%), i.e., an enhancement efficiency of 3640% per 1 vol%. • The obtained 3-mm-thick composite achieves an electromagnetic interference shielding effectiveness of 40 dB due to the interconnected network structure. [ABSTRACT FROM AUTHOR]

Substantial evidence has linked short-term exposure to ambient fine particulate matter (PM 2.5 ) with increased cardiovascular mortality, however, the specific chemical constituent and emission source responsible for this effect remained largely unclear. A time series Poisson model was employed to quantify the association of cardiovascular mortality with two sets of shipping pollution emission: nickel (Ni), vanadium (V) (the indices of shipping emission) and estimated shipping emission using a source apportionment approach in Guangzhou, China in 2014. We observed that Ni, V, and estimated shipping emission in PM 2.5 were associated with increased cardiovascular mortality, an inter-quartile range (IQR) increase in lag 2 Ni was associated with 4.60% (95% CI: 0.14%, 9.26%) increase in overall cardiovascular mortality, and 13.35% (95% CI: 5.54%, 21.75%) increase in cerebrovascular mortality; each IQR increase of lag 1 V was correlated with 6.01% (95% CI: 1.83%, 10.37%) increase in overall cardiovascular mortality, and 11.02% (95% CI: 3.15%, 19.49%) increase in cerebrovascular mortality; and each IQR increase in lag 1 shipping emission was associated with 5.55% (95% CI: 0.78%, 10.54%) increase in overall cardiovascular mortality, and 10.39% (95% CI: 1.43%, 20.14%) increase in cerebrovascular mortality. The results remained robust to adjustment for PM 2.5 mass and gaseous air pollutants. This study suggests that shipping emission is an important detrimental factor of cardiovascular mortality, and should be emphasized in air pollution control and management in order to protect the public health in Guangzhou, China. [ABSTRACT FROM AUTHOR]

While increasing evidence suggested that PM 2.5 is the most harmful fraction of the particle pollutants, the health effects of coarse particles (PM 10–2.5 ) have been inconclusive, especially on cerebrovascular diseases, we thus evaluated the effects of PM 10 , PM 2.5 , and PM 10–2.5 on stroke mortality in six Chinese subtropical cities using generalized additive models. We also conducted random-effects meta-analyses to estimate the overall effects across the six cities. We found that PM 10 , PM 2.5 , and PM 10-2.5 were significantly associated with stroke mortality. Each 10 μg/m 3 increase of PM 10 , PM 2.5 and PM 10-2.5 (lag03) was associated with an increase of 1.88% (95% CI: 1.37%, 2.39%), 3.07% (95% CI: 2.35%, 3.79%), and 5.72% (95% CI: 3.82%, 7.65%) in overall stroke mortality. Using the World Health Organization's guideline as reference concentration, we estimated that 3.21% (95% CI: 1.65%, 3.01%) of stroke mortality (corresponding to 1743 stroke mortalities, 95% CI: 896, 1633) were attributed to PM 10 , 5.57% (95% CI: 0.50%, 1.23%) stroke mortality (3019, 95% CI: 2286, 3777) were attributed to PM 2.5 , and 2.02% (95% CI: 1.85%, 3.08%) of stroke mortality (1097, 95% CI: 1005, 1673) could be attributed to PM 10-2.5 . Our analysis indicates that both PM 2.5 and PM 10-2.5 are important risk factors of stroke mortality and should be considered in the prevention and control of stroke in the study area. [ABSTRACT FROM AUTHOR]

Until menopause, women have a lower propensity to develop metabolic diseases than men, suggestive of a protective role for sex hormones. Although a functional synergy between central actions of estrogens and leptin has been demonstrated to protect against metabolic disturbances, the underlying cellular and molecular mechanisms mediating this crosstalk have remained elusive. By using a series of embryonic, adult-onset, and tissue/cell-specific loss-of-function mouse models, we document an unprecedented role of hypothalamic Cbp/P300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 1 (Cited1) in mediating estradiol (E2)-dependent leptin actions that control feeding specifically in pro-opiomelanocortin (Pomc) neurons. We reveal that within arcuate Pomc neurons, Cited1 drives leptin's anorectic effects by acting as a co-factor converging E2 and leptin signaling via direct Cited1-ERα-Stat3 interactions. Together, these results provide new insights on how melanocortin neurons integrate endocrine inputs from gonadal and adipose axes via Cited1, thereby contributing to the sexual dimorphism in diet-induced obesity. [Display omitted] • Global and hypothalamic Cited1 loss exacerbates diet-induced obesity in female mice • Cited1 is highly enriched in estradiol-sensitive melanocortin neurons • Hypothalamic Cited1 molecularly links the effects of E2 and leptin on food intake • Cited1 in PomcARC neurons acts as a downstream co-factor for E2-leptin signaling Estradiol regulates energy homeostasis by altering feeding behavior, but how this sex hormone converges with the melanocortin system is not fully understood. Here, González-García et al. discover that Cited1 acts as a crucial hypothalamic co-factor mediating the anti-obesity effects of estradiol through potentiation of leptin's anorectic actions. This neuroendocrine mechanism represents a mode by which melanocortin neurons integrate energy stores with reproductive signals for metabolic adaptation in diet-induced obesity. [ABSTRACT FROM AUTHOR]

Though significant associations between particulate matter (PM) air pollution and cardiovascular diseases have been widely reported, it remains unclear what characteristics, such as particle size and chemical constituents, may be responsible for the effects. A time-series model was applied to examine the cardiovascular effects of particle size (for the period of 2009–2011) and chemical constituents (2007–2010) in Guangzhou, we controlled for potential confounders in the model, such as time trends, day of the week, public holidays, meteorological factors and influenza epidemic. We found significant associations of cardiovascular mortality with PM 10 , PM 2.5 and PM 1 ; the excess risk (ER) was 6.10% (95% CI: 1.76%, 10.64%), 6.11% (95% CI: 1.76%, 10.64%) and 6.48% (95% CI: 2.10%, 11.06%) for per IQR increase in PM 10 , PM 2.5 and PM 1 at moving averages for the current day and the previous 3 days (lag 03 ), respectively. We did not find significant effects of PM 2.5-10 and PM 1-2.5 . For PM 2.5 constituents, we found that organic carbon, elemental carbon, sulfate, nitrate and ammonium were significantly associated with cardiovascular mortality, the corresponding ER for an IQR concentration increase at lag 03 was 1.13% (95% CI: 0.10%, 2.17%), 2.77% (95% CI: 0.72%, 4.86%), 2.21% (95% CI: 1.05%, 3.38%), 1.98% (95% CI: 0.54%, 3.44%), and 3.38% (95% CI: 1.56%, 5.23%), respectively. These results were robust to adjustment of other air pollutants and they remained consistent in various sensitivity analyses by changing model parameters. Our study suggests that PM 1 and constituents from combustion and secondary aerosols might be important characteristics of PM pollution associated with cardiovascular mortality in Guangzhou. [ABSTRACT FROM AUTHOR]

The short-term effects of ambient temperature on mortality have been widely investigated. However, the epidemiological evidence on the long-term effects of temperature on mortality is rare. In present study, we conducted a nationwide quasi-experimental design, which based on a variant of difference-in-differences (DID) approach, to examine the association between long-term exposure to ambient temperature and mortality risk in China, and to analyze the effect modification of population characteristics and socioeconomic status. Data on mortality were collected from 364 communities across China during 2006–2017, and environmental data were obtained for the same period. We estimated a 2.93 % (95 % CI: 2.68 %, 3.18 %) increase in mortality risk per 1 °C decreases in annual temperature, the greater effects were observed on respiratory diseases (5.16 %, 95 % CI: 4.53 %, 5.79 %) than cardiovascular diseases (3.43 %, 95 % CI: 3.06 %, 3.80 %), and on younger people (4.21 %, 95 % CI: 3.73 %, 4.68 %) than the elderly (2.36 %, 95 % CI: 2.06 %, 2.65 %). In seasonal analysis, per 1 °C decreases in average temperature was associated with 1.55 % (95 % CI: 1.23 %, 1.87 %), −0.53 % (95 % CI: −0.89 %, −0.16 %), 2.88 % (95 % CI: 2.45 %, 3.31 %) and 4.21 % (95 % CI: 3.98 %, 4.43 %) mortality change in spring, summer, autumn and winter, respectively. The effects of long-term temperature on total mortality were more pronounced among the communities with low urbanization, low education attainment, and low GDP per capita. In total, the decrease of average temperature in summer decreased mortality risk, while increased mortality risk in other seasons, and the associations were modified by demographic characteristics and socioeconomic status. Our findings suggest that populations with disadvantaged characteristics and socioeconomic status are vulnerable to long-term exposure of temperature, and targeted policies should be formulated to strengthen the response to the health threats of temperature exposure. [Display omitted] • Long-term effect of temperature on health was assessed by a quasi-experiment study. • The decreased summer temperature was associated with decreased mortality risks. • The average winter temperature is negatively correlated with mortality risks. • People with respiratory diseases and the young are more susceptible to temperature. • The temperature risk are more prominent in areas with low socioeconomic status. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To describe the epidemiological characteristics of nonfatal child pedestrian injuries and provide information to help understand an important public-health problem. Methods: This was a school-based, cross-sectional questionnaire survey. The sample (42 750 children) was obtained from two urban cities of Guangdong Province, China, using multi-stage randomized sampling. Information was collected by the respondents self-reporting in the classroom. Results: The incidence rate of nonfatal child pedestrian injuries in the cities was 2.0%. Boys had a higher incidence rate (2.6%) than girls (1.4%). Compared to other children, those aged 10 years are at the highest risk. The primary places of occurrence were sidewalks, residential roads, and crosswalks. High-risk behavior of the children immediately prior to injury included mid-block crossings, playing on roads, and crossing on red lights. The major vehicles that caused pedestrian injuries were bicycles, car or vans, and motorcycles. Bruises, fractures, and injuries to the internal organs were the top three types of injuries. Almost 40% of victims were hospitalized, and nearly 30% of the victims suffered long-term disabilities. Conclusion: This study shows that nonfatal child pedestrian injuries are a very serious public-health problem in the urban cities of Guangdong. Based on the epidemiological characteristics, prevention strategies and further research should be carried out to reduce the occurrence of injuries. [Copyright &y& Elsevier]

The small naphthoquinone molecules modified reduced-graphene oxide with chemical absorption of polysulfides based on the abundant keto functional groups, leads to the significantly improved cycling performance for Li-S batteries. • Organic NQ molecule-decorated rGO was applied as host for Li-S batteries. • Chemical absorption of polysulfides/sulfur can be achieved. • The S/NQ-rGO electrode delivers outstanding electrochemical performance. Graphene-based materials are explored to be promising candidates for lithium-sulfur batteries based on their unique two-dimensional geometry structure and excellent electric conductivity. However, the inferior ability to confine polysulfides results in quick capacity fading and poor cycling stability of graphene-related electrode materials. Herein, small organic naphthoquinone (NQ) molecules with redox active properties are introduced to the reduced graphene oxide (rGO) as an advanced sulfur host to significantly prolong cycle life for Li-S batteries. The effective combination between small NQ organic molecules and rGO successfully leads to the conductive composite network, where the keto groups from NQ play the key role in promoting the chemical absorption of polysulfides/sulfur by forming the S O interaction. Notably, the NQ-rGO composite shows superior lithium polysulfides absorptivity with a sulfur loading of 65.3%. The S/NQ-rGO displays outstanding electrochemical performances for lithium-sulfur batteries, in terms of large reversible capacities with excellent cycling stability (936 mAh g−1 after 200 cycles at 0.1C and 670 mAh g−1 after 500 cycles at 1C) and superior rate ability (525 mAh g−1 at 5C). [ABSTRACT FROM AUTHOR]

Background & Aims We aimed to identify long noncoding RNAs (lncRNAs) that are up-regulated in gastric cancer tissues from patients and study their function in gastric tumor metastasis. Methods We collected gastric tumor and nontumor tissues from patients in China and analyzed levels of lncRNAs by microarray analysis, proteins by immunohistochemistry, and RNAs by quantitative reverse-transcription polymerase chain reaction; we compared these with survival times of patients and tumor progression. RNA levels were knocked down or knocked out in BGC-823, SGC-7901, and MKN45 cell lines using small interfering or short hairpin RNAs or clustered regularly interspaced short palindromic repeats (ie, CRISPR)/CRISPR associated protein 9 (ie, Cas9) vectors. Genes were overexpressed from transfected plasmids in HGC-27 cells. Cells were analyzed by Northern blot and immunoblot, polysome profiling assay, and cell invasion assay. Cells were injected into the tail veins or spleens of nude mice or SCID mice; lung and liver tissues were collected, and metastases were counted. lncRNAs were cloned by using rapid amplification of complementary DNA ends. Their interactions with other genes were determined by RNA pulldown and mapping assays. Results In microarray analyses, we identified 151 lncRNAs expressed at significantly higher levels in gastric tumor vs nontumor tissues. Levels of an lncRNA that we called gastric cancer metastasis associated long noncoding RNA (GMAN) were increased in gastric tumor tissues, compared with nontumor tissues; its up-regulation was associated with tumor metastasis and shorter survival times of patients. The GMAN gene overlaps with the ephrin A1 gene (EFNA1) and was highly expressed in BGC-823 and MKN45 cells. Knockdown of GMAN in these cells did not affect proliferation, colony formation, or adhesion but did reduce their invasive activity in Transwell assays. Ectopic expression of GMAN increased the invasive activity of HGC-27 cells. BGC-823 and MKN45 cells with knockdown of GMAN formed fewer metastases after injection into tail veins of nude mice. Knockdown or knockout of GMAN also reduced levels of ephrin A1 protein in cells. We found that GMAN promoted translation of ephrin A1 messenger RNA into protein by binding to the antisense GMAN RNA (GMAN-AS)—this antisense sequence is also complementary to that of ephrin A1 mRNA. Levels of ephrin A1 protein were also increased in gastric tumors from patients with metastases than in those without metastases. Knockout of ephrin A1 in BGC-823 cells reduced their invasive activity in Transwell assays and ability to form metastases after injection into SCID mice. Ectopic expression of ephrin A1 in BGC-823 cells with knockdown or knockout of GMAN restored their invasive activities and ability form metastases in nude or SCID mice. A CRISPR/Cas9-based strategy to disrupt the GMAN gene significantly reduced the numbers of metastases formed from SGC-7901 cells in mice. Conclusions We identified an lncRNA, which we call GMAN , that is increased in gastric tumors from patients and associated with survival and formation of metastases. It regulates translation of ephrin A1 mRNA by binding competitively to GMAN-AS. Knockdown or knockout of GMAN or ephrin A1 in gastric cancer cell lines reduces their invasive activity and ability to form metastases after injection into mice. These genes might be targeted to prevent or reduce gastric cancer metastasis. [ABSTRACT FROM AUTHOR]

Abstract The World Health Organization sets up the Ambient Air Quality Guidelines mainly based on short-term and long-term health effects of air pollution. Previous studies, however, have generally revealed a non-threshold concentration-response relationship between air pollution and health, making it difficult to determine a concentration, below which no obvious health effects can be observed. Here we proposed a novel approach based on the concept of "number needed to treat", specifically, we calculated the reduction in air pollution concentrations needed to avoid one death corresponding to different hypothetical concentration standards; the one with the smallest value would be the most practical concentration standard. As an example, we applied this approach to the daily standard of ambient PM 2.5 (particulate matter with aerodynamic diameter ≤2.5 μm) in four Chinese cities. The calculation was based on the association between daily mortality and ambient PM 2.5 , which was examined by a generalized additive model with adjustment of important covariates. Significant associations were observed between PM 2.5 and mortality. Our analyses suggested that it is appropriate to have 50 μg/m3 as the daily standard of ambient PM 2.5 for the study area, compared to the current standard of which were directly adopted from the national standard of 75 μg/m3. This novel approach should be considered when planning and/or revising the ambient air quality guidelines/standards. Highlights • There is limited method for air pollution standard formulation. • The "number needed to treat" was proposed as one potential method. • We examined the acute association between PM 2.5 and mortality in four Chinese cities. • We then calculated the reduction in air pollution concentrations needed to avoid one death. • Finally, we suggested that 50 μg/m3 should be considered as daily standard of ambient PM 2.5 in the study area. Capsule This study proposes a new "number needed to treat" approach to help establish or revise daily ambient air quality standards. [ABSTRACT FROM AUTHOR]

Three bacterial strains capable of transforming pyrazosulfuron-ethyl, designated as D61, D66, and D713, were isolated from pyrazosulfuron-ethyl contaminated soils. According to the sequence analysis of the partial 16S rRNA gene, it is found that the strains D61 and D66 belong to Pseudomonas sp., and the strain D713 belongs to Bacillus sp. The effects of pyrazosulfuron-ethyl concentration, pH and temperature on biodegradation were examined. At a concentration of 10.0mgL−1, pyrazosulfuron-ethyl was completely degraded by Pseudomonas sp. D61 after 2d and by Pseudomonas sp. D66 after 5d. At a concentration of 90.0mgL−1, pyrazosulfuron-ethyl can be completely degraded by Pseudomonas sp. D66 and D61 after 12d. More than 85.9% degradation rate was observed with Bacillus sp. D713 after 12d. The growth of these three strains was inhibited at low pH buffers. The abiotic degradation occurs much faster at low pH than at neutral and basic pH conditions. The degradation rate of pyrazosulfuron-ethyl at 28°C was faster than those at 20°C and 37°C by these strains, except the highest degradation rate of Bacillus sp. D713 was obtained at 37°C. The pyrazosulfuron-ethyl biodegradation products were identified by liquid chromatography–mass spectroscopy with positive/negative modes and tandem MS–MS techniques. The main degradation product was detected and identified as 5-(N-(4,6-dimethoxypyrimidin-2-ylcarbamoyl)sulfamoyl)-1-methyl-1H-pyrazole-4-carboxylic acid based on mass spectral data and fragmentation patterns. [Copyright &y& Elsevier]

Previous research has reported the effects of long-term fine particulate matter (PM 2.5) pollution on years of life lost (YLL), but these effects may not represent the full impact. This study aims to estimate potential benefits in life time from adhering to daily ambient PM 2.5 concentration standards/guidelines. This study evaluated the relationship between daily ambient PM 2.5 level and YLL using a two-stage approach with generalized additive models and meta-analysis. Potential life expectancy gains were then estimated by presuming that daily PM 2.5 levels were in compliance with the Chinese and WHO standards. In addition, the attributable fraction of YLL due to excess PM 2.5 exposure was also calculated. During 2013–2016, 459,468 non-accidental deaths were recorded in the six cities of Pearl River Delta, China. Each 10 μg/m3 increment in four-day average (lag 03) level of PM 2.5 was related to an increment of 13.31 [95% confidence interval (CI): 5.74, 20.87] years of life lost. Implementation of the WHO guidelines might avoid 180,980.83 YLLs (95% CI: 78,116.07, 283,845.60), which corresponded to 0.39 (95% CI: 0.17, 0.62) years of increased life time per death. Additionally, an estimated 0.15% (95% CI: 0.06%, 0.23%) or 2.04% (95% CI: 0.88%, 3.20%) of YLLs could be attributed to PM 2.5 exposures higher than the Chinese or WHO guidelines, respectively. This study suggests that people might live longer by controlling daily PM 2.5 concentration and highlights the need to adopt stricter standards in China. • We estimated the life time gain by attaining daily PM 2.5 standards. • Life time might increase by 0.39 years for each death by attaining WHO's guideline. • Up to 2.04% of YLL could be ascribed to PM 2.5 exposure higher than WHO's guideline. • More ambitious target for PM 2.5 control should be employed to improve public health. [ABSTRACT FROM AUTHOR]

Experimental studies have indicated that alterations in the gut microbiota might play a role in the pathway of diabetes induction resulting from particulate matter pollution with aerodynamic diameters < 2.5 μm (PM 2.5). However, few human studies have examined such experimental findings. Here, we examine the mediating effects of gut microbial dysbiosis on the associations between PM 2.5 and particulate matter pollution with aerodynamic diameters < 1 μm (PM 1) on diabetes using the Guangdong Gut Microbiome Project (GGMP) dataset. A multistage cluster sampling method was employed to recruit adult participants from communities in Guangdong. Each participant was interviewed using a questionnaire, fasting blood and stool samples were collected, and the exposure to air pollutants was assessed using a spatiotemporal land-use regression model. The mediation analysis was conducted to estimate the associations among air pollutants, gut microbiota diversity and diabetes. Both PM 2.5 and PM 1 were positively associated with the risks of impaired fasting glucose (IFG) or type 2 diabetes and negatively associated with alpha diversity indices of the gut microbiota. The mediation analyses indicated that the associations of PM 2.5 and PM 1 with the risk of type 2 diabetes were partially mediated by the decrease in gut microbiota diversity. Moreover, we found that 79 (PM 2.5 on IFG), 84 (PM 2.5 on type 2 diabetes), 83 (PM 1 on IFG) and 89 (PM 1 on type 2 diabetes) bacterial taxa could partially mediate the associations of PM 2.5 and PM 1 with IFG and type 2 diabetes, respectively. The relative abundance of most Firmicutes , Proteobacteria and Verrucomicrobia bacteria were negatively associated with particulate matter (PM) concentrations and the risks of diabetes. Long-term exposure to PM may increase the risk of diabetes, and alterations in the gut microbiota partially explained these associations. Unlabelled Image • Long-term exposure to PM may increase the risks of IFG and T2DM, and decrease the diversity of gut microbiota. • The alternations of gut microbiota diversity could partially mediate the associations of PM with diabetes risk. • Bacterial taxa could partially mediate the effects of PM 2·5 and PM 1 on IFG and T2DM. [ABSTRACT FROM AUTHOR]

Background Daily mean concentration cannot fully address the hourly variations of air pollution within one day. As such, we proposed a new indicator, daily exceedance concentration hours (DECH), to explore the acute cardiovascular effects of ambient PM 2.5 (particles with aerodynamic diameters less than 2.5 μm). The DECH in PM 2.5 was defined as daily total concentration-hours > 25 μg/m 3 . Methods A generalized additive model with a quasi-Poisson link was applied to estimate the associations between day-to-day variation in PM 2.5 DECH and day-to-day variation in cardiovascular mortality in six subtropical cities in Guangdong Province, China. Results The analysis revealed significant associations between PM 2.5 DECHs and cardiovascular mortality. A 500 μg/m 3 ∗ h increase in PM 2.5 DECHs at lag 03 was associated with an increase of 4.55% (95% confidence interval (CI): 3.59%, 5.52%) in cardiovascular mortality, 4.45% (95% CI: 2.81%, 6.12%) in ischemic cardiovascular mortality, 5.02% (95% CI: 3.41%, 6.65%) in cerebrovascular mortality, and 3.00% (95% CI: 1.13%, 4.90%) in acute myocardial infarction mortality. We further observed a greater mortality burden using PM 2.5 DECHs than daily mean PM 2.5 (6478 (95% CI: 5071, 7917) VS 5136 (95% CI: 3990, 6305)). Conclusion This study reveals that PM 2.5 DECH is one important exposure indicator of ambient PM 2.5 to measure its cardiovascular mortality effects in Pearl River Delta region; and that using daily mean concentration could under-estimate the mortality burden compared with this new indicator. [ABSTRACT FROM AUTHOR]

Compared with daily mean concentration of air pollution, hourly peak concentration may be more directly relevant to the acute health effects due to the high concentration levels, however, few have analyzed the acute mortality effects of hourly peak levels of air pollution. We examined the associations of hourly peak concentration of fine particulate matter air pollution (PM 2.5 ) with mortality in six cities in Pearl River Delta, China. We used generalized additive Poisson models to examine the associations with adjustment for potential confounders in each city. We further applied random-effects meta-analyses to estimate the regional overall effects. We further estimated the mortality burden attributable to hourly peak and daily mean PM 2.5 . We observed significant associations between hourly peak PM 2.5 and mortality. Each 10 μg/m3 increase in 4-day averaged (lag 03 ) hourly peak PM 2.5 corresponded to a 0.9% [95% confidence interval (CI): 0.7%, 1.1%] increase in total mortality, 1.2% (95% CI: 1.0%, 1.5%) in cardiovascular mortality, and 0.7% (95% CI: 0.2%, 1.1%) in respiratory mortality. We observed a greater mortality burden using hourly peak PM 2.5 than daily mean PM 2.5 , with an estimated 12915 (95% CI: 9922, 15949) premature deaths attributable to hourly peak PM 2.5 , and 7951 (95% CI: 5067, 10890) to daily mean PM 2.5 in the Pearl River Delta (PRD) region during the study period. This study suggests that hourly peak PM 2.5 might be one important risk factor of mortality in PRD region of China; the finding provides important information for future air pollution management and epidemiological studies. [ABSTRACT FROM AUTHOR]

Background Epidemiological studies have reported significant association between ambient fine particulate matter air pollution (PM 2.5 ) and mortality, however, few studies have investigated the relationship of mortality with PM 2.5 and associated mortality burden in China, especially in a multicity setting. Methods We investigated the PM 2.5 -mortality association in six cities of the Pearl River Delta region from 2013 to 2015. We used generalized additive Poisson models incorporating penalized smoothing splines to control for temporal trend, temperature, and relative humidity. We applied meta-analyses using random-effects models to pool the effect estimates in the six cities. We also examined these associations in stratified analyses by sex, age group, education level and location of death. We further estimated the mortality burden (attributable fraction and attributable mortality) due to ambient PM 2.5 exposures. Results During the study period, a total of 316,305 deaths were recorded in the study area. The analysis revealed a significant association between PM 2.5 and mortality. Specifically, a 10 μg/m 3 increase in 4-day averaged (lag 03 ) PM 2.5 concentration corresponded to a 1.76% (95% confidence interval (CI): 1.47%, 2.06%) increase in total mortality, 2.19% (95% CI: 1.80%, 2.59%) in cardiovascular mortality, and 1.68% (95% CI: 1.00%, 2.37%) in respiratory mortality. The results were generally robust to model specifications and adjustment of gaseous air pollutants. We estimated that 0.56% (95% CI: 0.47%, 0.66%) and 3.79% (95% CI: 3.14%, 4.45%) of all-cause mortalities were attributable to PM 2.5 using China's and WHO's air quality standards as the reference, corresponding to 1661 (95% CI: 1379, 1946) and 11,176 (95% CI: 9261, 13,120) attributable premature mortalities, respectively. Conclusion This analysis adds to the growing body of evidence linking PM 2.5 with daily mortality, and mortality burdens, particularly in one Chinese region with high levels of air pollution. [ABSTRACT FROM AUTHOR]

In 2012, Chinese Environmental Bureau modified its National Ambient Air Quality Standards to include fine particulate matter (PM 2.5 ). Recent air pollution monitoring data shows that numerous locations have exceeded this standard, which may have resulted in avoidable adverse health effects. For example, among the 74 Chinese cities with PM 2.5 monitoring data in 2013, only three cities attained the annual air quality standard (35 μg/m 3 ). This study aimed to quantify the potential short- and long-term health benefits from achieving the Chinese ambient air quality standard and WHO’s air quality objectives. A generalized additive model was used to estimate the short-term association of mortality with changes in daily PM 2.5 concentrations, based on which we estimated the potential premature mortality reduction that would have been achieved during the period of 2012–2015 if the daily air quality standard had been met in Guangzhou, China; we also estimated the avoidable deaths if attaining the annual air quality standard using the relative risk obtained from a previous cohort study. During the study period, there were 160 days exceeding the national daily PM 2.5 standard (75 μg/m 3 ) in Guangzhou, and the annual average concentration (47.7 μg/m 3 ) was higher than the air quality standard of 35 μg/m 3 . Significant associations between PM 2.5 and mortality were observed. An increase of 10 μg/m 3 in PM 2.5 was associated with increases in daily death counts of 0.95% (95% CI: 0.56%, 1.34%) in natural mortality, 1.31% (95% CI: 0.75%, 1.87%) in cardiovascular mortality, and 1.06% (95% CI: 0.19%, 1.94%) in respiratory mortality. The health benefits of attaining the national daily air quality standard of PM 2.5 (75 μg/m 3 ) would have prevented 143 [95% confidence interval (CI): 84, 203] fewer natural deaths, including 84 (95% CI: 48, 121) fewer cardiovascular deaths and 27 (95% CI: 5, 49) fewer respiratory deaths. Had the annual PM 2.5 levels been reduced to 35 μg/m 3 , an estimated 3875 (95% CI: 1852, 6074) natural deaths, 2378 (95% CI: 800, 4230) cardiovascular deaths, and 227 (95% CI: -437, 1033) respiratory deaths could have been prevented. Even greater substantial mortality reductions could be achieved if the WHO’s air quality objectives were met. Our study suggests that air pollution is significantly associated with mortality in Guangzhou, and more stringent air quality standards would significantly reduce air pollution-related premature mortality. [ABSTRACT FROM AUTHOR]

Heavy metals play an important role in inducing fine particulate matter (PM 2.5) related cardiovascular disease (CVD). However, most of the past researches concerned the associations between CVD mortality and the PM 2.5 mass, which may not reveal the CVD mortality risk contributed by heavy metals in PM 2.5. This study explored the correlations between individual heavy metals in PM 2.5 and CVD mortality, identified the heavy metals that significantly contribute to PM 2.5 -related CVD, heart disease (HD), and cerebrovascular disease (CEV) mortality, and attempted to establish corresponding source control measures. Over a 2-year study period, PM 2.5 was sampled daily in Guangzhou, China and analyzed for heavy metals. The airborne pollution and weather data, along with CVD, HD, and CEV mortality, were obtained at the same time. The excess risk (ER) of mortality was linked to the individual heavy metals using a distributed lag non-linear model. PM 2.5 and most heavy metals showed significant correlations with the CVD, HD, and CEV mortality; the largest cumulative ER (LCER) values of CVD mortality associated with an interquartile range increase in the levels of lead, cadmium, arsenic, selenium, antimony, nickel, thallium, aluminum, iron, and PM 2.5 were 2.43%, 2.23%, 1.66%, 2.39%, 1.19%, 1.21%, 2.69%, 3.29%, 1.74%, and 2.40%, respectively. Most heavy metals showed comparable LCER values of HD and CEV mortality. Heavy metals with the addition of PM 2.5 were divided into three groups following their LCER values; lead, cadmium, arsenic, antimony, thallium, zinc, aluminum, and iron, whose contributions were greater than or equal to the average effect of the PM 2.5 components, should be limited on a priority basis. These findings indicated that heavy metals play roles in the CVD, HD, and CEV mortality risk of PM 2.5 , and specific control measures which aimed at the emission sources should be taken to reduce the CVD mortality risk of PM 2.5. [Display omitted] • Daily levels of heavy metals in PM 2.5 were analyzed from a 2-year sampling. • Nine heavy metals in PM 2.5 were significantly associated with CVD mortality. • Precise source control of Pb, Cd, Se, Sb, Tl, Zn, Al, and Fe should be conducted. [ABSTRACT FROM AUTHOR]

Abstract: Though increased particulate air pollution has been consistently associated with elevated mortality, evidence regarding whether diminished particulate air pollution would lead to mortality reduction is limited. Citywide air pollution mitigation program during the 2010 Asian Games in Guangzhou, China, provided such an opportunity. Daily mortality from non-accidental, cardiovascular and respiratory diseases was compared for 51 intervention days (November 1–December 21) in 2010 with the same calendar date of baseline years (2006–2009 and 2011). Relative risk (RR) and 95% confidence interval (95% CI) were estimated using a time series Poisson model, adjusting for day of week, public holidays, daily mean temperature and relative humidity. Daily PM10 (particle with aerodynamic diameter less than 10 μm) decreased from 88.64 μg/m3 during the baseline period to 80.61 μg/m3 during the Asian Games period. Other measured air pollutants and weather variables did not differ substantially. Daily mortality from non-accidental, cardiovascular and respiratory diseases decreased from 32, 11 and 6 during the baseline period to 25, 8 and 5 during the Games period, the corresponding RR for the Games period compared with the baseline period was 0.79 (95% CI: 0.73–0.86), 0.77 (95% CI: 0.66–0.89) and 0.68 (95% CI: 0.57–0.80), respectively. No significant decreases were observed in other months of 2010 in Guangzhou and intervention period in two control cities. This finding supports the efforts to reduce air pollution and improve public health through transportation restriction and industrial emission control. [Copyright &y& Elsevier]