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Guoqiang Cai is a Chinese artist and designer known for his designs that use gunpowder blasting to explore society, culture, and nature. The work mixes art, design, and Chinese culture. Unknown world The universe and the unknown world have always been important themes in Guoqiang Cai's design. By drawing on and absorbing elements of traditional Chinese culture and contemporary art language forms, he deconstructs art materials and simulates the elements of time and space in his work; he deconstructs the duality of Chinese and Western art and builds an innovative art and design language. [Extracted from the article]

Pre-bored precast piles with an enlarged base (PPEB piles) have been increasingly used in China over the past 5 years. However, the distributions of the shaft and toe resistance of the pile are still unclear. In order to reveal the ultimate bearing capacity and load transfer mechanism of PPEB piles in clay, three full-scale ultimate static loading tests were carried out in Shanghai. The test piles were instrumented with vibrating wire strain gauges to enable accurate measurement of the local shaft resistance along the pile shaft during the loading tests. The tests results revealed that about 75% of the pile bearing capacity was provided by shaft resistance when the ultimate load was applied and the majority of the shaft resistance was mobilised along the lower part of the test piles. After load testing, the soils around the test piles were excavated to evaluate the reliability and constructability of PPEB piles. The applicability of conventional methods (α-method and β-method) in estimating shaft resistance was assessed. In comparison with instrumented bored piles, the local shaft resistance of the PPEB piles in the lower stiff clays was significantly higher. [ABSTRACT FROM AUTHOR]

Exposure to fine particulate matter (PM 2.5) during pregnancy has been linked to the risk of gestational diabetes mellitus (GDM), while conclusions are inconsistent. In this study we aimed to estimate the effects of prenatal PM 2.5 exposure with blood glucose in early pregnancy and the GDM risk. Participants were recruited from the SH-IPMCH-BTH cohort (n = 41,929), a study of air pollution and birth outcome. All participants provided serum samples for analyses of fasting blood glucose (FBG) and HbA1c during early pregnancy. GDM was diagnosed using an oral glucose tolerance test (OGTT) with the time interval of 1 h. Prenatal exposure to PM 2.5 was estimated using gap-filled satellite exposure assessments in Shanghai, China. Both FBG and HbA1c levels were significantly and positively associated with PM 2.5 exposure during early pregnancy. A 10 μg/m3 increase of PM 2.5 exposure from early to middle pregnancy was associated with the risk of GDM (first trimester OR=1.09, 95% CI: 1.02, 1.16; second trimester OR=1.09, 95% CI: 1.03, 1.16; first two trimester OR=1.15, 95%CI: 1.04, 1.28). The combined effects were greater among elevated FBG and HbA1c women with higher PM 2.5 exposure in middle trimester (P for interaction=0.037 and 0.001, respectively). This study found that exposure to PM 2.5 exposure in the 1st and 2nd trimesters was related to GDM. FBG and HbA1c played roles in the relationship between PM 2.5 exposure in the 2nd trimester and GDM. [Display omitted] • PM 2.5 exposure in early trimester is associated with blood glucose impairment. • Higher early- and middle- pregnancy PM 2.5 exposure is associated with GDM. • FBG and HbA1c are effect modifiers of PM 2.5 exposure in the second trimester and GDM. [ABSTRACT FROM AUTHOR]

Limited evidence is available for the associations between fine particulate matter (PM 2.5) constituents and daily cardiovascular disease (CVD) mortality in China. In present study, a time-series analysis was conducted to evaluate the associations of PM 2.5 constituents (two carbonaceous fractions, eight water-soluble inorganic ions and fifteen elements) with daily CVD mortality in Pudong New Area of Shanghai, China, from 2014 to 2016. Results showed that the effect estimates for the associations of PM 2.5 and its constituents with CVD mortality were generally strongest when using the exposures of the previous two day concentrations. The associations of organic carbon, sulfate, ammonia, potassium, copper, arsenic, and lead with daily CVD mortality were robust to the adjustment of PM 2.5 total mass, their collinearity with PM 2.5 total mass, and criteria gaseous air pollutants. An interquartile range increase in the previous two day concentrations of PM 2.5 , organic carbon, sulfate, ammonia, potassium, copper, arsenic, and lead were associated with significant increments of 2.21% (95% confidence interval [95%CI]: 0.54%, 3.88%), 2.83% (95% CIs: 1.16%, 4.50%), 1.90% (95% CIs: 0.35%, 3.45%), 2.29% (95% CIs: 0.80%, 3.77%), 0.94% (95% CIs: 0.13%, 1.75%), 1.53% (95% CIs: 0.37%, 2.69%), 2.08% (95% CIs: 0.49%, 3.68%) and 1.98% (95% CIs: 0.49%, 3.47%) in daily CVD mortality, respectively, in single-pollutant models. In conclusion, this study suggested that organic carbon, sulfate, ammonia, potassium, copper, arsenic, and lead might be mainly responsible for the associations between short-term PM 2.5 exposures and increased CVD mortality in Shanghai, China. Image 1 • Limited evidence is available on PM 2.5 constituents and daily CVD mortality in China. • Significant associations were found between PM 2.5 and CVD mortality in Shanghai. • OC, SO 4 2−, NH 4 +, K, Cu, As and Pb might be mainly responsible for the associations. [ABSTRACT FROM AUTHOR]

Combined atmospheric oxidant capacity (O x), represented by the sum of nitrogen dioxide (NO 2) and ozone (O 3), is an important hazardous property of outdoor air pollution mixture. It remains unknown whether its adverse effects can be ameliorated by dietary fish-oil supplementation. To assess the effects of fish-oil supplementation against oxidative stress induced by acute O x exposure. We conducted a randomized, double-blinded and placebo-controlled study among 65 young adults in Shanghai, China between September 2017 and January 2018. We randomly assigned participants to receive either 2.5 g/day of fish oil or placebo, and conducted four repeated physical examinations during the last two months of treatments. O x concentrations were calculated as the sum of hourly measurements of NO 2 and O 3. We measured six biomarkers on systemic oxidative stress and antioxidant activity. Linear mixed-effect models were used to assess the short-term effects of O x on biomarkers in each group. During our study period, the 72-h average O x concentration was 93.6 μg/m3. Short-term exposure to O x led to weaker changes in all biomarkers in the fish oil group than in the placebo group. Compared with the placebo group, for a 10-μg/m3 increase in O x , there were smaller decrements in myeloperoxidase (MPO, difference = 5.92%, lag = 0–2 d, p = 0.03) and malondialdehyde (MDA, difference = 5.00%, lag = 1 d, p = 0.04) in the fish-oil group; there were also larger increments in total antioxidant capacity (TAC, difference = 16.33%, lag = 2 d, p = 0.02) and in glutathione peroxidase (GSH-Px, difference = 8.89%, lag = 0–2 d, p = 0.03) in the fish-oil group. The estimated differences for MPO were robust to adjustment for all co-pollutants and the differences for other biomarkers remained for some co-pollutants. This trial provides first-hand evidence that dietary fish-oil supplementation may alleviate the systemic oxidative stress induced by O x. • Combined atmospheric oxidant capacity (O x) exposure induced oxidative stress. • We provided the first-hand evidence on the effects of fish-oil against O x exposure. • Fish-oil supplementation could mitigate systemic oxidative stress response to O x. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM 2.5) has been widely associated with airway inflammation represented by increased fractional concentration of exhaled nitric oxide (FeNO). However, it remains unclear whether various PM 2.5 constituents have different impacts on FeNO and its production process from the arginase (ARG)–nitric oxide synthase (NOS) pathway. To investigate the acute effects of PM 2.5 constituents on FeNO and DNA methylation of genes involved. We conducted a longitudinal panel study among 43 young adults in Shanghai, China from May to October in 2016. We monitored the concentrations of 25 constituents of PM 2.5. We applied the linear mixed-effect model to evaluate the associations of PM 2.5 constituents with FeNO and DNA methylation of the ARG2 and NOS2A genes. Following PM 2.5 exposure, NOS2A methylation decreased and ARG2 methylation increased only on the concurrent day, whereas FeNO increased most prominently on the second day. Nine constituents (OC, EC, K, Fe, Zn, Ba, Cr, Se, and Pb) showed consistent associations with elevated FeNO and decreased NOS2A methylation or increased ARG2 methylation in single-constituent models and models adjusting for PM 2.5 total mass and collinearity. An interquartile range increase of these constituents was associated with respective decrements of 0.27–1.20 in NOS2A methylation (%5mC); increments of 0.48–1.56 in ARG2 methylation (%5mC); and increments of 7.12%–17.54% in FeNO. Our results suggested that OC, EC, and some metallic elements may be mainly responsible for the development and epigenetic regulation of airway inflammatory response induced by short-term PM 2.5 exposure. • It remains unclear how PM 2.5 constituents affect airway inflammation differently. • We evaluated the effects of 25 constituents in a panel study in Shanghai, China. • PM 2.5 was associated with increased FeNO and altered methylation for genes involved. • OC, EC and some metallic elements may be responsible for airway inflammation. [ABSTRACT FROM AUTHOR]

[Display omitted] • We developed a noise LUR model in Shanghai based on a purpose-designed monitoring network. • Common road-related variables and social activity-related variables are important factors affecting noise levels in Shanghai. • The model explained 79% of spatial variability of urban noise. • This study provides solutions for epidemiological studies of noise. Urban environment noise has been linked with wide adverse effects on health; however, noise epidemiological researches are hindered by the lack of large-scale population-based exposure assessment. We aimed to measure noise levels over multiple seasons and to establish an LUR model to assess the spatial variability of intra-urban noise and identify its potential sources in Shanghai, China. Forty-minute (L Aeq, 40 min) measurements of environmental noise were collected at 144 fixed sites, and each was visited three times (morning, afternoon, and evening) in winter, spring, and summer in 2019. Noise measurements were then integrated with land-use types, road networks, socioeconomic variables, and geographic information systems to construct LUR models. Ten-fold cross-validation was used to test the model performance. A total of 1296 measurements and 29 predicting variables were used to estimate the spatial variation in environmental noise. The annual mean (±standard deviation) of L Aeq, 40min , was 62 ± 8 dB (A). Significant variations were observed among monitoring sites but not between seasons or time of day. The LUR model explained 79% of the spatial variability of the noise, and the R2 of the ten-fold cross-validation was 0.75. The most contributory predictors of noise level were road-related variables all within the 50-m buffers, followed by urban area within a 50-m buffer, total area of buildings within a 1000-m buffer, and number of restaurant clusters within a 50-m buffer. Farmland area within a 100-m buffer was the only negative variable in the model. A 50-m resolution noise prediction map was produced and suggested high noise level in urban areas and near traffic arteries. LUR can be a robust method for reflecting noise variability in megacities such as Shanghai and may provide an efficient solution for noise exposure assessment in areas where noise maps are not available. [ABSTRACT FROM AUTHOR]

Prenatal exposure to ambient levels of air pollution has been reported to adversely affect birth outcomes, yet few studies have investigated refined susceptible windows for adverse birth outcomes. The study aimed at estimating associations between maternal exposure to ambient fine particulate matter (PM 2.5; particles with an aerodynamic diameter ≤ 2.5 μm) and birth outcomes, including birth weight, low birth weight (LBW) and preterm birth (PTB), and identify specific susceptible windows. A total of 3692 singleton live births were enrolled between 2013 and 2016 in Shanghai Birth Cohort, China. Based on mothers' residential addresses, weekly mean concentrations of PM 2.5 over gestation were estimated based on an incorporated evaluating approach combining satellite-based estimates and ground-level measurements. Distributed lag non-liner models (DLNMs) were fitted by incorporating with multiple liner models and Cox proportional hazard models to evaluate weekly-as well as trimester-exposure-lag-response associations between average PM 2.5 level and birth weight, LBW and PTB, and to identify critical windows. In this study, gestational exposure to PM 2.5 was associated with adverse birth outcomes in infants, and critical windows were identified as 31st–34th gestational weeks for reduced birth weight, 38th–42 nd weeks for LBW and 27th–30th weeks for PTB, respectively. Trimester-specific associations were found for all birth outcomes during the third trimester. Ambient PM 2.5 exposure exhibited adverse impacts on multiple outcomes including reduced birth weight, LBW and PTB in the late pregnancy. The study provides further evidence supporting harmful effects of maternal PM 2.5 exposure on birth outcomes and identifying critical windows. • The Shanghai birth cohort study is a large prospective cohort study in Shanghai, China. • We considered indoor air pollution indicators adjustment. • Individual prenatal exposure to PM 2.5 exerts adverse effects on birth outcomes including birth weight and gestational age. • Refined critical windows in late pregnancy are identified for multiple adverse birth outcomes. [ABSTRACT FROM AUTHOR]

Background: Few studies have evaluated the health benefits of omega-3 fatty acid supplementation against fine particulate matter (aerodynamic diameter <2.5 μm [PM2.5]) exposure in highly polluted areas.Objectives: The authors sought to evaluate whether dietary fish-oil supplementation protects cardiovascular health against PM2.5 exposure in China.Methods: This is a randomized, double-blinded, and placebo-controlled trial among 65 healthy college students in Shanghai, China. Participants were randomly assigned to either the placebo group or the intervention group with dietary fish-oil supplementation of 2.5 g/day from September 2017 to January 2018, and received 4 rounds of health examinations in the last 2 months of treatments. Fixed-site PM2.5 concentrations on campus were measured in real time. The authors measured blood pressure and 18 biomarkers of systematic inflammation, coagulation, endothelial function, oxidative stress, antioxidant activity, cardiometabolism, and neuroendocrine stress response. Acute effects of PM2.5 on these outcomes were evaluated within each group using linear mixed-effect models.Results: The average PM2.5 level was 38 μg/m3 during the study period. Compared with the placebo group, the fish-oil group showed relatively stable levels of most biomarkers in response to changes in PM2.5 exposure. Between-group differences associated with PM2.5 exposure varied by biomarkers and by lags of exposure. The authors observed beneficial effects of fish-oil supplementation on 5 biomarkers of blood inflammation, coagulation, endothelial function, oxidative stress, and neuroendocrine stress response in the fish-oil group at a false discovery rate of <0.05.Conclusions: This trial shows that omega-3 fatty acid supplementation is associated with short-term subclinical cardiovascular benefits against PM2.5 exposure among healthy young adults in China. (Effect of Dietary Supplemental Fish Oil in Alleviating Health Hazards Associated With Air Pollution; NCT03255187). [ABSTRACT FROM AUTHOR]

It remains unclear whether carbon content in airway macrophages (AM) can predict personal short-term exposure to fine particulate matter (PM 2.5) air pollution and its respiratory health effects. We aimed to evaluate the pathway from personal PM 2.5 exposure to adverse respiratory outcomes through AM carbon content. We designed a longitudinal panel study with 3 scheduled follow-ups among 113 non-smoking patients of chronic obstructive pulmonary disease in Shanghai, China, from April 2017 to January 2019. We quantified AM carbon content from induced sputum by image analysis, tested lung function and measured sputum levels of 4 pro-inflammatory cytokines and 2 anti-inflammatory cytokines. We applied the "meet in the middle" approach incorporating linear mixed-effect models to evaluate the associations from external PM 2.5 exposure to respiratory outcomes through AM carbon content. Our results indicated that personal exposure to PM 2.5 within 24 h was significantly associated with decreased forced expiratory volume in 1s and anti-inflammatory cytokines, as well as increased macrophages and pro-inflammatory cytokines. These changes were accompanied by increased areas of AM carbon and higher percentage of AM area occupied by carbon, both of which were associated with increased levels of pro-inflammatory cytokines and decreased levels of anti-inflammatory cytokines. Exposure to ambient black carbon and organic carbon in PM 2.5 within 2 days was significantly associated with increased AM carbon area and percentage of AM area occupied by carbon. Our findings reinforced the causality in respiratory health effects of PM 2.5 in which increased AM carbon content might serve as a valid exposure biomarker. • Acute PM 2.5 exposure increases AM carbon content and leads to respiratory effects. • The percentage of carbon area in AM may be a better exposure biomarker of PM 2.5. • This study reinforces the causality for the acute respiratory effects of PM 2.5. [ABSTRACT FROM AUTHOR]

Non-invasive bio-samples, such as saliva and urine, are promising tools for assessment of inflammation and oxidative stress biomarkers. Few studies have investigated potential responses of those biomarkers towards short-term PM 2.5 exposure. We conducted a longitudinal study with 4 repeated examinations among 40 healthy, nonsmoking adults in Shanghai, China. Personal samplings were performed for PM 2.5 exposure assessment. Then, five biomarkers, including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), alpha-1 antitrypsin (A1AT) in saliva and 8-Iso-Prostaglanding F 2α (8-iso-PGF 2α), total antioxidant capacity (TAC) in urine, were measured. We fitted linear mixed-effect models to evaluate short-term effect of personal PM 2.5 exposure on salivary and urinary biomarkers, adjusting for potential confounders of meteorology, sociodemographic characteristics and biomarker detection. We also explored sensitive time windows of exposure for different biomarkers. We found robust associations of salivary CRP, TNF-α, and urinary 8-iso-PGF 2α with PM 2.5 exposure, and responses of salivary inflammatory markers occurred more acutely than urinary oxidative stress markers. For instance, a 10 μg/m3 increase in PM 2.5 was associated with an elevation of 5.49% (95% CI: 1.17%, 9.99%) in CRP and 7.05% (95% CI: 1.29%, 13.13%) in TNF-α both at lag 12 h, and 6.97% (95% CI: 1.33%, 12.92%) in 8-iso-PGF 2α at lag 01 d. Based on non-invasive samples, this study provided evidence on effect of PM 2.5 exposure on responses of systematic inflammation and oxidative stress. Sub-daily (6–12 h) and daily (≥24 h) period after PM 2.5 exposure might be sensitive time window to detect the responses of salivary (i.e. CRP, TNF) and urinary biomarkers (i.e. 8-iso-PGF 2α), respectively. • PM 2.5 was associated with elevated inflammatory saliva markers (CRP&TNF-α). • Sub-daily period (6–12 h) is critical window to detect salivary CRP&TNF-α response. • PM 2.5 was associated with elevated urine oxidative stress marker (8-iso-PGF 2α). • Daily period (≥24 h) is critical window to detect urinary 8-iso-PGF 2α response. [ABSTRACT FROM AUTHOR]

Few studies have investigated respiratory effects of particulate matter air pollution using a full range of particle size distribution. To explore the short-term associations between size-fractionated particle number concentration (PNC) and chronic obstructive pulmonary disease (COPD) mortality. We conducted a time-series study to explore the associations between size-fractionated PNC and daily COPD mortality in the Pudong New Area of Shanghai, China, from 2014 to 2016. We evaluated particle size distribution from 0.01 μm to 10 μm, which was segregated into 7 ranges to better explore the size-dependent associations. We used over-dispersed generalized additive models to estimate the associations after controlling for time trends, temperature, humidity, day of the week and holidays. A total of 5430 deaths due to COPD were identified during the study period. For size ranges from 2.5 – 10 μm, 1–2.5 μm to 0.3–1 μm, there were stronger associations between PNC and COPD mortality, but the associations were statistically insignificant. However, for the smaller size ranges from 0.3 to 0.01 μm, the associations became statistically significant and the magnitude of association remained stable. An interquartile range increase in PNC at lag 0–1 day for size ranges 0.01–0.03 μm, 0.03–0.05 μm, 0.05–0.1 μm and 0.1–0.3 μm was associated with increments of 4.44% (95% CI: 1.16%, 7.73%), 4.31% (95% CI: 1.16%, 7.47%), 4.22% (95% CI: 1.05%, 7.40%), and 4.28% (95% CI: 0.48%, 8.09%) in COPD mortality, respectively. This study suggested that particles below 0.3 μm in diameter might be mainly responsible for the adverse effect of particulate air pollution on CDPD mortality in Shanghai, China. • A study linking a full range of particle size distribution and COPD mortality. • The associations generally increased with smaller particle size. • Particles below 0.3 μm in diameter may be mainly responsible for the associations. • Particles above 0.3 μm in diameter showed no significant associations. [ABSTRACT FROM AUTHOR]

Few epidemiological studies have evaluated the respiratory effects of personal exposure to nitrogen dioxide (NO 2), a major traffic-related air pollutant. The biological pathway for these effects remains unknown. To evaluate the short-term effects of personal NO 2 exposure on lung function, fractional exhaled nitric oxide (FeNO) and DNA methylation of genes involved. We conducted a longitudinal panel study among 40 college students with four repeated measurements in Shanghai from May to October in 2016. We measured DNA methylation of the key encoding genes of inducible nitric oxide synthase (NOS2A) and arginase (ARG2). We applied linear mixed-effect models to assess the effects of NO 2 on respiratory outcomes. Personal exposure to NO 2 was 27.39 ± 23.20 ppb on average. In response to a 10-ppb increase in NO 2 exposure, NOS2A methylation (%5 mC) decreased 0.19 at lag 0 d, ARG2 methylation (%5 mC) increased 0.21 and FeNO levels increased 2.82% at lag 1 d; and at lag 2 d the percentage of forced vital capacity, forced expiratory volume in 1 s and peak expiratory flow in predicted values decreased 0.12, 0.37 and 0.67, respectively. The model performance was better compared with those estimated using fixed-site measurements. These effects were robust to the adjustment for co-pollutants and weather conditions. Our study suggests that short-term personal exposure to NO 2 is associated with NOS2A hypomethylation, ARG2 hypermethylation, respiratory inflammation and lung function impairment. The use of personal measurements may better predict the respiratory effects of NO 2. • Personal NO 2 exposure may decrease NOS2A methylation and increase ARG2 methylation. • Personal exposure to NO 2 could elevate FeNO and reduce lung function. • Use of personal measurements may better predict the respiratory effects of NO 2. • Results are robust to the adjustment for co-pollutants and weather conditions. [ABSTRACT FROM AUTHOR]