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Maternal exposure to ambient fine particulate matter (PM 2.5) during pregnancy has been associated with impaired neurobehavioral development in children. However, the specific mechanism remains unclear. Brain derived neurotrophic factor (BDNF) is an important growth factor in the nervous system. We evaluated the associations of maternal PM 2.5 exposures with fetal BDNF in the umbilical cord blood in a prospective cohort study. A total of 711 eligible mother-infant pairs from the Shanghai Birth Cohort were included in the current study. Daily maternal exposures to ambient PM 2.5 were assessed with a gap-filling approach at 1 * 1 km2 resolution based on self-reported home addresses. The concentrations of BDNF in the cord blood were measured by ELISA. A linear regression model was applied to evaluate the association of maternal ambient PM 2.5 exposure with fetal BDNF level at birth. The median concentration of BDNF was 13,403 pg/ml. Vaginal deliveries and female infants had higher BDNF levels than cesarean deliveries and male infants. One natural log (ln) unit increase in maternal PM 2.5 exposure during the second trimester was significantly associated with − 0.20 (95% CI: −0.36, −0.05) ln-unit decrease in BDNF level in all births. These effects were stronger and more significant in vaginal deliveries and in male infants. Our study suggests that BDNF in the cord blood may serve as a potential biomarker in assessing the neurodevelopmental effects of maternal PM 2.5 exposure. • Limited evidence is available on maternal PM 2.5 exposures and fetal BDNF levels. • Maternal PM 2.5 exposure was negatively associated with fetal BDNF level at birth. • Delivery modes and infant sex may modify the association. [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]

Accurate individual exposure assessment is crucial for evaluating the health effects of particulate matter (PM). Various portable monitors built upon low-cost optical sensors have emerged. However, the main challenge for their application is to guarantee accuracy of measurements. To assess the performance of a newly developed PM sensor, and to develop methods for post-hoc data calibration to optimize its data quality. We conducted a series of laboratory experiments and field evaluations to quantify the reproducibility within Plantower PM sensors 7003 (PMS 7003) and the consistency between sensors and two established PM 2.5 measurement methods [tapered element oscillating microbalances (TEOM) and gravimetric method (GM)]. Post-hoc data calibration methods for sensors were based on a multiple linear regression model (MLRM) and a random forest model (RFM). Ratios of raw and calibrated readings over the data of reference methods were calculated to examine the improvement after calibration. Strong correlations (≥0.82) and relatively small relative standard deviations (16–21%) between sensors were found during the laboratory and the field sampling. Compared with the reference methods, moderate to strong coefficients of determination (0.56–0.83) were observed; however, significant deviations were presented. After calibration, the ratios of PMS measurements over that of two reference methods both became convergent. Our study validated low-cost optical PM sensors under a wide range of PM 2.5 concentrations (8–167 μg/m3). Our findings indicated potential applicability of PM sensors in PM 2.5 exposure assessment, and confirmed a need of calibration. Linear calibration methods may be sufficient for ambient monitoring using TEOM as a reference, while nonlinear calibration methods may be more appropriate for indoor monitoring using GM as a reference. • We evaluated the performance of a low-cost optical particle matter sensor. • Sensitivity to potential source and high reproducibility within sensors were found. • Multiple linear regression and random forest models were developed for calibration. • Careful calibration ensures confident use of PMS 7003 in exposure assessment. [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]

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]

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]

[Display omitted] • This is the largest nationwide study to examine the associations of maternal PM 2.5 exposure with PROM in China. • Both acute and chronic maternal ambient PM 2.5 exposure increased the risk of PROM. • Women who were less educated, obese, or delivered in a cold season were more sensitive to PM 2.5 exposure. Prelabor rupture of the fetal membranes (PROM) is a major contributor to adverse perinatal outcomes. Some epidemiologic studies explored the association between maternal PM 2.5 exposure and PROM but failed to treat the labor induction and prelabor cesarean section as censored observations. We aimed to evaluated whether acute and chronic maternal ambient PM 2.5 exposure may increase the risk of PROM in China. This study was based on the China Labor and Delivery Survey, a nationwide multicenter investigation. Included in the current analysis were 45,879 singleton spontaneous births in 96 hospitals in mainland China from 2015 to 2017. Outcomes were PROM, preterm PROM (<37 weeks' gestation) and term PROM (≥37 weeks' gestation). Daily concentration of PM 2.5 at 1 km spatial resolution was estimated by gap-filling model. Generalized linear mixed model and mixed effects Cox model were applied to assess the associations of acute (from 0 to 4 days before delivery) and chronic (average gestational and trimester-specific) ambient PM 2.5 exposure with outcomes, respectively. Significant associations were found between acute PM 2.5 exposures (per interquartile range increase) and the risk of preterm PROM (OR = 1.11; 95 % CI: 1.03, 1.19 for PM 2.5 on delivery day; OR = 1.10; 95 % CI: 1.02, 1.18 for PM 2.5 1 day before delivery) but not for term PROM. An interquartile range increase in PM 2.5 during the second trimester was associated with elevated risks of PROM (HR = 1.14; 95 % CI: 1.07, 1.22), preterm PROM (HR = 1.22; 95 % CI: 1.02, 1.45) and term PROM (HR = 1.13; 95 % CI: 1.06, 1.22), respectively. Women who were less educated, obese, or gave birth in a cold season appeared to be more sensitive to ambient PM 2.5 exposure. Our findings suggest that both acute and chronic maternal exposures to ambient PM 2.5 during pregnancy are risk factors for PROM. [ABSTRACT FROM AUTHOR]

[Display omitted] • Exposure to PM 2.5 increased CVD mortality in a nationally representative cohort. • We provided one of the very few evidence on long-term CVD effects of PM 2.5 constituents. • BC, OM, NO 3 –, NH 4 + and SO 4 2− showed appreciably larger risks than PM 2.5 total mass. • Soil dust showed no cardiovascular risks. Few studies have evaluated long-term cardiovascular effects of fine particulate matter (PM 2.5) and its constituents in countries with high air pollution levels. We aimed to investigate the associations of long-term exposure to PM 2.5 and constituents with cardiovascular mortality in China. We conducted a prospective cohort study of 90,672 adults ≥ 18 years from 2010 to 2017 in 161 districts/counties across China. The residential annual-average exposure to PM 2.5 and 6 main components from 2011 to 2017 were estimated by satellite-based and chemical transport models. Associations of PM 2.5 and constituents with cardiovascular mortality were analyzed by competing-risk Cox proportional hazards regression. The average PM 2.5 exposure throughout the whole period was 46 ± 22 μg/m3. The hazard ratios of mortality (95% confidence intervals) per 10 μg/m3 increase in PM 2.5 concentrations were 1.02 (1.00, 1.05) for overall cardiovascular disease, 1.05 (1.01, 1.09) for ischemic heart disease, 1.03 (1.00, 1.06) for overall stroke, 0.99 (0.94, 1.04) for hemorrhagic stroke, and 1.11 (1.04, 1.19) for ischemic stroke. PM 2.5 constituents from fossil fuel combustion (i.e., black carbon, organic matter, nitrate, ammonium, and sulfate) showed larger hazard ratios than PM 2.5 total mass, while soil dust showed no risks. This nationwide cohort study demonstrated associations of long-term exposure to PM 2.5 and its constituents with increased risks of cardiovascular mortality in the general population of China. Our study highlighted the importance of PM 2.5 constituents from fossil fuel combustion in the long-term cardiovascular effects of PM 2.5 in China. [ABSTRACT FROM AUTHOR]

[Display omitted] • Evidence is scarce on PM 2.5 exposure and birth outcome in African countries. • Use of Satellite-derived PM 2.5 estimates and the Demographic Health and Surveys data. • PM 2.5 exposure was significantly associated with preterm birth (8%) and low birth weight (28%) • Associations were modified by region, and maternal, infant, household characteristics. Fine particulate matter (PM 2.5) exposure has been reported to adversely affect birth outcomes, but the evidence is limited, particularly in low- and middle-income countries (LMICs). We assessed the associations between maternal PM 2.5 exposure and low birth weight (LBW) and preterm birth (PTB) in Africa. We used standard Demographic and Health Surveys (DHS) data (2005–2015) from 15 countries in Africa to conduct a cross-sectional study. The study population was composed of 131,594 births with detailed information on maternal and household variables. LBW was defined as a birth weight of < 2500 g after 37 weeks, and PTB was defined as live birth occurring before 37 weeks of gestation. Average exposure to PM 2.5 during pregnancy was estimated using satellite-based models. Multivariable logistic regression models were constructed, and analyses of data by region (Western, Eastern, Central, and Southern Africa) and data stratified by potential effect modifiers were conducted. A total of 13,214 (10%) LBW and 4,377 (3.3%) PTB cases were identified. An interquartile range (IQR) (33.9 μg/m3) increase in PM 2.5 during pregnancy was associated with increased odds of LBW and PTB, with odds ratios (ORs) of 1.28 (95% CI: 1.23, 1.34) and 1.08 (95% CI: 1.01, 1.16), respectively. Region-specific analyses revealed significant associations between PM 2.5 and LBW in all regions, and significant associations between PM 2.5 and PTB in Western and Southern Africa. Subgroup analyses revealed that the association between PM 2.5 and LBW was present in all subgroups, and stronger associations were observed in female infants, while the association between PM 2.5 and PTB was larger in subgroups of older individuals living in urban areas. This multicountry study in Africa demonstrated significant associations between maternal exposure to PM 2.5 and higher odds of LBW and PTB. Our findings may facilitate air quality control strategies that address adverse birth outcomes in LMICs. [ABSTRACT FROM AUTHOR]

[Display omitted] • Limited evidence on short-term exposure to PM 2.5 and under-5 mortality in China. • A national case-crossover study and use of satellite-based exposure model. • PM 2.5 was associated a 1.15% (95%CI: 0.65%, 1.65%) increase in under-5 mortality. • Cause-specific mortality from diarrhea, pneumonia, digestive diseases, and preterm birth. • Supra-linear concentration-response curve with steeper slope in lower concentrations. Under-5 mortality rate is an important indicator in Millennium Development Goals and Sustainable Development Goals. To date, no nationally representative studies have examined the effects of fine particulate matter (PM 2.5) air pollution on under-5 mortality. To investigate the association of short-term exposure to PM 2.5 with under-5 mortality from total and specific causes in China. We used the national Maternal and Child Health Surveillance System to identify under-5 mortality cases during the study period of 2009 to 2019. We adopted a time-stratified case-crossover study design at the individual level to capture the effect of short-term exposure to daily PM 2.5 on under-5 mortality, using conditional logistic regression models. A total of 61,464 under-5 mortality cases were included. A 10 μg/m3 increase in concentrations of PM 2.5 on lag 0–1 d was significantly associated with a 1.15% (95%confidence interval: 0.65%, 1.65%) increase in under-5 mortality. Mortality from diarrhea, pneumonia, digestive diseases, and preterm birth were significantly associated with exposure to PM 2.5. The effect estimates were larger for neonatal mortality (<28 days), female children, and in warm seasons. We observed steeper slopes in lower ranges (<50 μg/m3) of the concentration-response curve between PM 2.5 and under-5 mortality, and positive associations remained below the 24-h PM 2.5 concentration limit recommended by WHO Air Quality Guidelines and China Air Quality Standards. This nationwide case-crossover study in China demonstrated that acute exposure to PM 2.5 may significantly increase the risk of under-5 mortality, with larger effects for neonates, female children, and during warm seasons. Relevant control strategies are needed to remove this roadblock to achieving under-5 mortality targets in developing countries. [ABSTRACT FROM AUTHOR]

[Display omitted] • This is the largest and multicenter study of particulate matter and ABPM. • Transient exposure to PM 2.5 elevated blood pressure within the first 12 h. • Exposure-response curves were almost linear without thresholds. • PM 2.5–10 did not show significant association with blood pressure. Epidemiological evidence from ambulatory blood pressure monitoring is needed to clarify the associations of particulate air pollution with blood pressure and potential lag patterns. We examined the associations of fine and coarse particulate matter (PM 2.5 , PM 2.5–10) with ambulatory blood pressure among 7108 non-hypertensive participants from 7 Chinese cities between April 2016 and November 2020. Hourly concentrations of PM 2.5 and PM 2.5–10 were obtained from the nearest monitoring stations. We measured four blood pressure indicators, including systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP). Linear mixed-effect models combined with distributed lag models were applied to analyze the data. Generally, very short-term exposure to PM 2.5 was significantly associated with elevated blood pressure. These effects occurred on the same hour of blood pressure measurement, attenuated gradually, and became insignificant approximately at lag 12 h. An interquartile range (IQR, 33 μg/m3) increase of PM 2.5 was significantly associated with cumulative increments of 0.58 mmHg for SBP, 0.31 mmHg for DBP, 0.38 mmHg for MAP, and 0.33 mmHg for PP over lag 0 to 12 h. The exposure–response relationship curves were almost linear without thresholds, but tended to be flat at very high concentrations. No significant associations were observed for PM 2.5–10. Our study provides independent and robust associations between transient PM 2.5 exposure and elevated blood pressure within the first 12 h, and reinforces the evidence for a linear and non-threshold exposure–response relationship, which may have implications for blood pressure management and hypertension prevention in susceptible population. [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]

• Limited evidence on the PM 2.5 constituents - infant mortality association in developing countries. • A multi-country cross-sectional study based on the Demographic and Health Surveys in Africa. • PM 2.5 was associated with increased infant mortality across 15 countries in Africa. • PM 2.5 carbonaceous fractions and sulfate play a major important role in infant mortality. Few studies have investigated the association between exposure to fine particulate matter (PM 2.5) and infant mortality in developing countries, especially for the health effects of specific PM 2.5 constituents. We aimed to examine the association of long-term exposure to specific PM 2.5 constituents with infant mortality in 15 African countries from 2005 to 2015. Based on the Demographic and Health Surveys (DHS) dataset, we included birth history records from 15 countries in Africa and conducted a multicountry cross-sectional study to examine the associations between specific PM 2.5 constituents and infant mortality. We estimated annual residential exposure using satellite-derived PM 2.5 for mass and a chemical transport model (GEOS-Chem) for its six constituents, including organic matter (OM), black carbon (BC), sulfate (SO 4 2−), nitrate (NO 3 −), ammonium (NH 4 +), and soil dust (DUST). Multivariable logistic regression analysis was employed by fitting single-constituent models, the constituent-PM 2.5 models, and the constituent-residual models. We also conducted stratified analyses by potential effect modifiers and examined the specific associations for each country. We found positive and significant associations between PM 2.5 total mass and most of its constituents with infant mortality. In the single-constituent model, for an IQR increase in pollutant concentrations, the odds ratio (OR) of infant mortality was 1.03 (95 %CI; 1.01, 1.06) for PM 2.5 total mass, and was 1.04 (95 %CI: 1.02, 1.06), 1.04 (95 %CI: 1.02, 1.05), 1.02 (95 %CI: 1.00, 1.03), 1.04 (1.01, 1.06) for BC, OM, SO 4 2−, and DUST, respectively. The associations of BC, OM, and SO 4 2− remained significant in the other two models. We observed larger estimates in subgroups with older maternal age, living in urban areas, using unclean cooking energy, and with access to piped water. The associations varied among countries, and by different constituents. The carbonaceous fractions and sulfate play a major important role among PM 2.5 constituents on infant mortality. Our findings have certain policy implications for implementing effective measures for targeted reduction in specific sources (fossil fuel combustion and biomass burning) of PM 2.5 constituents against the risk of infant mortality. [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]

Systemic inflammation is considered one of the key mechanisms in the development of cardiovascular diseases induced by fine particulate matter (PM 2.5) air pollution. However, evidence concerning the effects of various PM 2.5 constituents on circulating inflammatory biomarkers were limited and inconsistent. To evaluate the associations of short-term exposure to a variety of PM 2.5 constituents with circulating inflammatory biomarkers. We conducted a panel study from May to October 2016 among 40 healthy adults in Shanghai, China. We monitored the concentrations of 27 constituents of PM 2.5. We applied linear mixed-effect models to analyze the associations of PM 2.5 and its constituents with 7 inflammatory biomarkers, and further assessed the robustness of the associations by fitting models adjusting for PM 2.5 mass and/or their collinearity. Benjamini-Hochberg false discovery rate was used to correct for multiple comparisons. The associations of PM 2.5 were strongest at lag 0 d with tumor necrosis factor- α (TNF-α), at lag 1 d with interleukin-6, interleukin-8, and interleukin-17A, at lag 02 d with monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1). After correcting for multiple comparisons in all models, Cl−, K+, Si, K, As, and Pb were significantly associated with interleukin-8; SO 4 2− and Se were marginally significantly associated with interleukin-8; SO 4 2−, As, and Se were marginally significantly associated with TNF- α ; and Si, K, Zn, As, Se, and Pb were marginally significantly associated with MCP-1. Our results suggested that some constituents (SO 4 2−, Cl−, K+, and some elements) might be mainly responsible for systemic inflammation triggered by short-term PM 2.5 exposure. Unlabelled Image • It remains unclear how PM 2.5 constituents affect systemic inflammation differently. • 27 constituents and 7 inflammatory biomarkers were evaluated in Shanghai, China. • SO 4 2−, Cl−, K+ and some elements may be responsible for inflammation. [ABSTRACT FROM AUTHOR]