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Although our previous studies have established the crucial role of RP105 in myocardial ischemia/reperfusion injury (MI/RI), its involvement in regulating oxidative stress induced by MI/RI remains unclear. To investigate this, we conducted experiments using a rat model of ischemia/reperfusion (I/R) injury. Adenovirus carrying RP105 was injected apically at multiple points, and after 72 h, the left anterior descending coronary artery was ligated for 30 min followed by 2 h of reperfusion. In vitro experiments were performed on H9C2 cells, which were transfected with recombinant adenoviral vectors for 48 h, subjected to 4 h of hypoxia, and then reoxygenated for 2 h. We measured oxidative stress markers, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, as well as malondialdehyde (MDA) concentration, using a microplate reader. The fluorescence intensity of reactive oxygen species (ROS) in myocardial tissue was measured using a DHE probe. We also investigated the upstream and downstream components of the signal transducer and activator of transcription 3 (STAT3). Upregulation of RP105 increased SOD and GSH-Px activities, reduced MDA concentration, and inhibited ROS production in response to I/R injury in vivo and hypoxia reoxygenation (H/R) stimulation in vitro. The overexpression of RP105 led to a decrease in the myocardial enzyme LDH in serum and cell culture supernatant, as well as a reduction in infarct size. Additionally, left ventricular fraction (LVEF) and fractional shortening (LVFS) were improved in the RP105 overexpression group compared to the control. Upregulation of RP105 promoted the expression of Lyn and Syk and further activated STAT phosphorylation, which was blocked by PP2 (a Lyn inhibitor). Our findings suggest that RP105 can inhibit MI/RI-induced oxidative stress by activating STAT3 via the Lyn/Syk signaling pathway., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: PM 2.5 is a harmful mixture of various chemical components that pose a challenge in determining their individual and combined health effects due to multicollinearity issues with traditional linear regression models. This study aimed to develop an analytical methodology combining traditional and novel machine learning models to evaluate PM 2.5 's combined effects on blood pressure (BP) and identify the most toxic components., Methods: We measured late-pregnancy BP of 1138 women from the Heshan cohort while simultaneously analyzing 31 PM 2.5 components. We utilized multiple linear regression modeling to establish the relationship between PM 2.5 components and late-pregnancy BP and applied Random Forest (RF) and generalized Weighted Quantile Sum (gWQS) regression to identify the most toxic components contributing to elevated BP and to quantitatively evaluate the cumulative effect of the PM 2.5 component mixtures., Results: The results revealed that 16 PM 2.5 components, such as EC, OC, Ti, Fe, Mn, Cu, Cd, Mg, K, Pb, Se, Na + , K + , Cl - , NO 3 - , and F - , contributed to elevated systolic blood pressure (SBP), while 26 components, including two carbon components (EC, OC), fourteen metallics (Ti, Fe, Mn, Cr, Mo, Co, Cu, Zn, Cd, Na, Mg, Al, K, Pb), one metalloid (Se), and nine water-soluble ions (Na + , K + , Mg 2+ , Ca 2+ , NH 4 + , Cl - , NO 3 - , SO 4 2- , F - ), contributed to elevated diastolic blood pressure (DBP). Mn and Cr were the most toxic components for elevated SBP and DBP, respectively, as analyzed by RF and gWQS models and verified against each other. Exposure to PM 2.5 component mixtures increased SBP by 1.04 mmHg (95% CI: 0.33-1.76) and DBP by 1.13 mmHg (95% CI: 0.47-1.78)., Conclusions: Our study highlights the effectiveness of combining traditional and novel models as an analytical strategy to quantify the health effects of PM 2.5 constituent mixtures., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Distinguishing the effects of different fine particulate matter components (PMCs) is crucial for mitigating their effects on human health. However, the sparse distribution of locations where PM is collected for component analysis makes it challenging to investigate the relevant health effects. This study aimed to investigate the agreement between data-fusion-enhanced exposure assessment and site monitoring data in estimating the effects of PMCs on gestational diabetes mellitus (GDM). We first improved the spatial resolution and accuracy of exposure assessment for five major PMCs (EC, OM, NO 3 - , NH 4 + , and SO 4 2- ) in the Pearl River Delta region by a data fusion model that combined inputs from multiple sources using a random forest model (10-fold cross-validation R 2 : 0.52 to 0.61; root mean square error: 0.55 to 2.26 μg/m 3 ). Next, we compared the associations between exposures to PMCs during pregnancy and GDM in a hospital-based cohort of 1148 pregnant women in Heshan, China, using both site monitoring data and data-fusion model estimates. The comparative analysis showed that the data-fusion-based exposure generated stronger estimates of identifying statistical disparities. This study suggests that data-fusion-enhanced estimates can improve exposure assessment and potentially mitigate the misclassification of population exposure arising from the utilization of site monitoring data.

As a transcriptional activator widely expressed in various tissues, nuclear factor of activated T cells (NFAT) is involved in the regulation of the immune system, the development of the heart and brain systems, and classically mediating pathological processes such as cardiac hypertrophy. Oxidative stress is an imbalance of intracellular redox status, characterized by excessive generation of reactive oxygen species, accompanied by mitochondrial dysfunction, calcium overload, and subsequent lipid peroxidation, inflammation, and apoptosis. Oxidative stress occurs during various pathological processes, such as chronic hypoxia, vascular smooth muscle cell phenotype switching, ischemia-reperfusion, and cardiac remodeling. Calcium overload leads to an increase in intracellular calcium concentration, while NFAT can be activated through calcium-calcineurin, which is also the main regulatory mode of NFAT factors. This review focuses on the effects of NFAT transcription factors on reactive oxygen species production, calcium overload, mitochondrial dysfunction, redox reactions, lipid peroxidation, inflammation, and apoptosis in response to oxidative stress. We hope to provide a reference for the functions and characteristics of NFAT involved in various stages of oxidative stress as well as related potential targets., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare., (Copyright © 2023. Published by Elsevier Ltd.)

Background: Feto-placental hemodynamic deterioration is a critical contributing factor to fetal growth restriction. Whether PM 2.5 oxidative potential (OP) affects feto-placental hemodynamics and what impact is on estimated fetal weight (EFW) have not been fully elucidated. We sought to evaluate the association of PM 2.5 OP with EFW and to explore whether feto-placental vascular impedance hemodynamic change is a possible mediator in this association., Methods: A repeated-measures study was conducted involving sixty pregnant women with at least 26 weeks of follow-up during pregnancy in Guangzhou, China, from September 2017 to October 2018. Daily filter-based PM 2.5 samples were prospectively collected from ground monitors, and estimates of OP for PM 2.5 and its metallic (OPv-metal) and non-metallic constituents (OPv-nonmental) were determined by dithiothreitol assay. Ultrasound data of fetal growth and umbilical arterial resistance, including estimated fetal weight (EFW), pulsatility index, resistance index, and systolic-to-diastolic ratio, were also obtained during gestation. Generalized estimating equations and polynomial distribution lag models were applied to analyze the associations of maternal exposure to PM 2.5 OP with EFW and umbilical artery indices. Causal mediation analysis was used to evaluate the mediating role of umbilical arterial resistance., Results: Prenatal exposure to ambient PM 2.5 OP was significantly inversely associated with EFW. The magnitudes of effects of OPv-nonmetal on EFW were larger than those of OPv-metal. Significant mediation for the relationship between PM 2.5 -related OP and EFW by increased impedance in the umbilical artery was observed, with the estimated percent mediated ranging from 31% to 61%. The estimated percent mediated for OPv-nonmetal was higher than those for OPv-metal., Conclusions: Findings suggest that increased impedance in the umbilical artery may be one of the potential mediators of the relationship between PM 2.5 oxidative potential exposure and low fetal weight., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Leucocyte immunoglobulin-like receptors subfamily B (LILRB) belongs to the type I transmembrane glycoproteins, which is the immunosuppressive receptor. LILRBs are widely expressed in bone marrow cells, hematopoietic stem cells, nerve cells and other body cells. Studies have found that LILRBs receptor can bind to a variety of ligands and has a variety of biological functions such as regulating inflammatory response, immune tolerance and cell differentiation. Inflammatory reaction plays a vital role in resisting microorganisms. The function of inhibitory immune receptors can recognize the signs of infection and promote the function of anti-microbial effect. The inflammatory response must be strictly regulated to prevent excessive inflammation and tissue damage. Therefore, it is of general interest to understand the role of LILRBs in the inflammatory response. Because they can inhibit the anti-microbial response of neutrophils, some human pathogens use these receptors to escape immunity. This article reviews the biological role of LILRBs in the inflammatory response. We focus on the known ligands of LILRBs, their different roles after binding with ligands, and how these receptors help to form neutrophil responses during infection. Recent studies have shown that LILRBs recruit phosphatases through intracellular tyrosine-based immunoreceptor inhibitory motifs to negatively regulate immune activation, thereby transmitting inflammation-related signals, suggesting that LILRBs may be an ideal target for the treatment of inflammatory diseases. Here, we describe in detail the regulation of LILRBs on the inflammatory response, its signal transduction mode in inflammation, and the progress in the treatment of inflammatory diseases, providing a reference for further research., (© 2023 John Wiley & Sons Ltd.)

Immune diseases are caused by the imbalance of immune regulation. This imbalance is regulated by many factors, both negative and positive. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is a member of leukocyte immunoglobulin-like receptors (LILRs). LILRs are expressed constitutively on the surface of multiple immune cells which associate with membrane adaptors to signal through multi- ple cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIMs) or immunoreceptor tyro-sine-based activation motifs (ITAMs). Through ITIM, LILRB4 could recruit the src homology domain type-2-containing tyrosine phosphatase 1 or 2 (SHP-1 or SHP-2) into the cell membrane. In addition, many factors can induce the expression of LILRB4, such as vitamin D, interferon and so on. Studies have demonstrated that LILRB4 had a negative regulatory role in various of immune diseases. The present review intends to expound the structure and function of LILRB4, as well as its regulators and receptors in the immune cells, so as to provide a theoretical basis for immune disease therapy., Competing Interests: The authors declare no conflict of interest., (Copyright © 2023 Termedia.)

Maternal exposure to PM 2.5 has been associated with abnormal glucose tolerance during pregnancy, but little is known about which constituents and sources are most relevant to glycemic effects. We conducted a retrospective cohort study of 1148 pregnant women to investigate associations of PM 2.5 chemical components with gestational diabetes mellitus (GDM) and impaired glucose tolerance (IGT) and to identify the most harmful sources in Heshan, China from January 2015 to July 2016. We measured PM 2.5 using filter-based method and analyzed them for 28 constituents, including carbonaceous species, water-soluble ions and metal elements. Contributions of PM 2.5 sources were assessed by positive matrix factorization (PMF). Logistic regression model was used to estimate composition-specific and source-specific effects on GDM/IGT. Random forest algorithm was applied to evaluate the relative importance of components to GDM and IGT. PM 2.5 total mass and several chemical constituents were associated with GDM and IGT across the early to mid-gestation periods, as were the PM 2.5 sources fossil fuel/oil combustion, road dust, metal smelting, construction dust, electronic waster, vehicular emissions and industrial emissions. The trimester-specific associations differed among pollutants and sources. The third and highest quartile of elemental carbon, ammonium (NH 4 + ), iron (Fe) and manganese (Mn) across gestation were consistently associated with higher odds of GDM/IGT. Maternal exposures to zinc (Zn), titanium (Ti) and vehicular emissions during the first trimester, and vanadium (V), nickel (Ni), road dust and fossil fuel/oil combustion during the second trimester were more important for GDM/IGT. This study provides important new evidence that maternal exposure to PM 2.5 components and sources is significantly related to elevated risk for abnormal glucose tolerance during pregnancy., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Abstract: Although inflammation plays an important role in myocardial ischemia/reperfusion injury (MI/RI), an anti-inflammatory treatment with a single target has little clinical efficacy because of the multifactorial disorders involved in MI/RI. MicroRNAs (miR-24) can achieve multitarget regulation in several diseases, suggesting that this factor may have ideal effects on alleviation of MI/RI. In the present study, bioinformatics method was used to screen potential therapeutic targets of miR-24 associated with MI/RI. Three days before ischemia/reperfusion surgery, rats in the ischemia/reperfusion, miR-24, and adenovirus-negative control groups were injected with saline, miR-24, and adenovirus-negative control (0.1 mL of 5 × 109 PFU/mL), respectively. Myocardial enzymes, myocardial infarct size, cardiac function, and the possible molecular mechanism were subsequently analyzed. In contrast to the level of S100A8, the level of miR-24 in myocardial tissue was significantly reduced after 30 minutes of ischemia followed by reperfusion for 2 hours. Overexpression of miR-24 reduced the myocardial infarction area and improved the heart function of rats 3 days after MI/RI. Moreover, miR-24 inhibited infiltration of inflammatory cells in the peri-infarction area and decreased creatine kinase myocardial band and lactate dehydrogenase release. Interestingly, miR-24 upregulation reduced S100A8 expression, followed by inhibition of toll-like receptor 4/MyD-88/nuclear factor-k-gene binding signaling activation. In conclusion, miR-24 can alleviate MI/RI via inactivation of the S100A8/toll-like receptor 4/MyD-88/nuclear factor-k-gene binding signaling pathway., Competing Interests: The authors report no conflicts of interest., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Quantification of source-specific health risks of PM 2.5 plays an essential role in health-oriented air pollution control. However, there is limited evidence supporting the source-based risk apportionment of particle-bound metals. In this study, source-specific cancer and non-cancer risk characterization of 12 particle-bound metals was performed in the Pearl River Delta (PRD) region, China. A combination of health risk assessment model and receptor-based source apportionment modeling with positive matrix factorization (PMF) was applied for characterizing the spatial-temporal patterns for inhalation health risks of particle-bound metals in three main city clusters, inland area and coastal area in the region from December 2014 through July 2016. Results showed that the carcinogenic risk of particle-bound metals for adults (4.13 × 10 -5 ) was higher than that for children (9.53 × 10 -6 ) in the PRD region. The highest and significant non-carcinogenic risk was found in the northwest city cluster. Industrial emission (63.3%) were the dominant contributors to the cancer risk, while the main contributors to the non-cancer risk were the vehicle emission source (33.2%) in the dry season and industrial emission (30.8%) in the wet season. Our results provide important evidence for spatial source-specific health risks with temporal characteristics of particle-bound metals in most densely populated areas in the southern China, and suggest that reduction of industrial and vehicle emissions could facilitate more cost-effective PM 2.5 control measures to improve human health., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Although miR-327 had a protective effect on cardiomyocytes as described previously, the potential mechanism still needs further exploration. The aim of this study was to investigate the role and mechanism of miR-327 on oxidative stress in myocardial ischemia/reperfusion injury (MI/RI) process. Oxidative stress and cardiomyocytes injury were detected in rat model of MI/RI, hypoxia/reoxygenation (H/R), and tert-butyl hydroperoxide (TBHP) model of H9c2 cells. In vitro , downregulation of miR-327 inhibited both H/R- and TBHP-induced oxidative stress, and suppressed apoptosis. Meanwhile, fibroblast growth factor 10(FGF10) was enhanced by miR-327 knocked down, followed by the activation of p-PI3K and p -Akt, and the translocation of Nrf2. However, miR-327 overexpression performed with opposite effects. Consistent with the results in vitro , downregulation of miR-327 attenuated reactive oxygen species (ROS) generation as well as intrinsic apoptosis, and alleviated I/R injury. In conclusion, inhibition of miR-327 improved antioxidative ability and myocardial cell survival via regulating the FGF10/Akt/Nrf2 pathway., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Zheng, Yang, Zhang, Yang, Fan, Li, Zhai, Liu and Yang.)

Background: Fasting blood glucose may capture the adverse effects of air pollution on pregnant women better than the incidence of gestational diabetes mellitus (GDM), but evidence on the association between air pollution and maternal glucose concentrations is limited., Objective: To investigate the associations between air pollutants, GDM and fasting blood glucose during pregnancy., Methods: We recruited 2326 pregnant women from two birth cohorts located in Guangzhou and Heshan, the Pearl River Delta region (PRD), China. PM 10 , PM 2.5 and black carbon (BC) exposure concentrations in the first and second trimesters of pregnancy were collected at fixed-site monitoring stations for each cohort. Multiple logistic regressions were employed to estimate the associations between particle pollution and GDM. Mixed-effects models were used to evaluate the associations of air pollutants with blood glucose levels. Restricted cubic spline functions were fitted to visualize the concentration-response relationships. Distributed lag non-linear models were used to estimate week-specific lag effects of particle pollution exposure on GDM and blood glucose. Unconstrained distributed lag models with lags of 0-3 weeks were used to examine potential cumulative effects., Results: We observed positive and significant associations of PM 10 , PM 2.5 and BC exposure with fasting glucose, particularly in the second trimester. PM 10 , PM 2.5 and BC were strongly correlated and displayed similar cumulative (lag 0-3 weeks) associations with fasting blood glucose. Exposure to particle pollution was not associated with 1-h or 2-h blood glucose. Models estimating the association between air pollutants and GDM were consistent with statistical insignificance., Conclusions: Based on the results of the present study, exposure to air pollution during pregnancy exerts cumulative, adverse effects on fasting glucose levels. This study provides preliminary support for the use of blood glucose levels to explore the potential health impact of air pollution on pregnant women., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

The Src-family protein tyrosine kinases (SFKs), a subfamily of non-receptor tyrosine kinases, are ubiquitously expressed in various cell types. Numerous studies have suggested that SFKs are related to signal transduction in major cardiac physiological and pathological processes, it is the activity of SFKs that is connected with the maintenance of cardiovascular homeostasis. Upon stimulation of various injury factors or stress, the phosphorylation state of SFKs is changed, which has been found to modulate different cardiac pathological conditions, such as hypertension, coronary heart disease, ischemic heart disease, myocardial ischemia-reperfusion injury, arrhythmia and cardiomyopathy via regulating cell growth, differentiation, movement and function, electrophysiologic signals. This review summarizes the basic information about SFKs, updates its role in the different processes underlying the development of multiple cardiovascular diseases (CVDs), and highlights their potential role as disease biomarkers and therapeutic targets, which would help understand the pathophysiology of CVDs and promote the further potential clinical adhibition., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

While several scientific studies have linked PM 2.5 to decreased lung function, there is still some degree of uncertainty regarding which particulate physicochemical properties are most harmful. We followed a panel of 57 healthy schoolchildren (857 person-days) to investigate the associations between a wide variety of PM 2.5 and lung function in Heshan, China in 2016 for three periods. We monitored the daily concentrations of mass, chemical composition, size, number, surface area, and volume of particulate mixture. Associations of lung function with various particle metrics were estimated using generalized estimating equations and unconstrained distributed lag models. Random forest model was used to compare the relative importance of exposure metrics. Immediate (lag 0) associations of PM 2.5 and carbonaceous aerosols with reduced FEV 1 and MMEF, and accumulation-mode particles with FEV 1 were found. Slightly delayed (lag 1, 2) effects on PEF were particularly prominent for Aitken-mode particles. Possible cumulative (lags 0-2) effects of PM 2.5 and carbonaceous aerosols on PEF and Aitken-mode particles on FEV 1 , MMEF, and PEF were observed. This study provides comprehensive evidence that the physicochemical properties of particulate mixtures are associated with reduced lung function in children. Organic carbon (OC) may be an important risk factor for the decreased lung function related to PM exposure.

Background: There is a significant lack of scientific knowledge on population exposure to ultrafine particles (UFP) in China to date. This paper quantifies and characterises school children's personal UFP exposure and exposure intensity against their indoor and outdoor activities during a school day (home, school and commuting) in the city of Heshan within the Pearl River Delta (PRD) region, southern China., Methods: Time-series of UFP number concentrations and average size were measured over 24 h for 24 children (9-13 years old), using personal monitors over two weeks in April 2016. Time-activity diaries and a questionnaire on the general home environment and potential sources of particles at home were also collected for each participating child. The analysis included concurrently measured size distributions of ambient UFP at a nearby fixed reference site (Heshan Supersite)., Results: Hourly average UFP concentrations exhibited three peaks in the morning, midday and evening. Time spent indoors at home was found to have the highest average exposure (1.26 × 10 4  cm - 3 during sleeping) and exposure intensity (2.41). While there is always infiltration of outdoor particles indoors (from nearby traffic and general urban background sources), indoor exposure at home was significantly higher than outdoor exposure. Based on the collected questionnaire data, this was considered to be driven predominantly by adults smoking and the use of mosquito repellent incense during the night. Outdoor activities at school were associated with the lowest average exposure (6.87 × 10 2  cm - 3 ) and exposure intensity (0.52)., Conclusion: Despite the small sample size, this study characterised, for the first time, children's personal UFP exposure in a city downwind of major pollution sources of the PRD region in China. Particularly, the results highlighted the impact of smoking at home on children's exposure. While the study could not apportion the specific contributions of second hand-smoking and mosquito coil burning, considering the prevalence of smokers among the parents who smoke at home, smoking is a very significant factor. Exposure to second-hand smoke is avoidable, and these findings point out to the crucial role of government authorities and public health educators in engaging with the community on the role of air quality on health, and the severity of the impact of second-hand smoke on children's health., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Black carbon (BC) caused by incomplete combustion of fossil and bio-fuel has a dual effect on health and climate. There is a need for systematic approaches to evaluation of health outcomes and climate impacts relevant to BC exposure., Objectives: We propose and illustrate for the first time, to our knowledge, an integrated analysis of a region-specific health model with climate change valuation module to quantify the health and climate consequences of BC exposure., Methods: Based on the data from regional air pollution monitoring stations from 2013 to 2014 in the Pearl River Delta region (PRD), China, we analyzed the carcinogenic and non-carcinogenic effects and the relative risk of cause-specific mortality due to BC exposure in three typical cities of the PRD (i.e. Guangzhou, Jiangmen and Huizhou). The radiative forcing (RF) and heating rate (HR) were calculated by the Fu-Liou-Gu (FLG) plane-parallel radiation model and the conversion of empirical formula. We further connected the health and climate impacts by calculating the excess mortalities attributed to climate warming due to BC., Results: Between 2013 and 2014, carcinogenic risks of adults and children due to BC exposure in the PRD were higher than the recommended limits (1 × 10 -6 to 1 × 10 -4 ), resulting in an excess of 4.82 cancer cases per 10,000 adults (4.82 × 10 -4 ) and an excess of 1.97 cancer cases per 10,000 children (1.97 × 10 -4 ). Non-carcinogenic risk caused by BC was not found. The relative risks of BC exposure on mortality were higher in winter and dry season. The atmospheric RFs of BC were 26.31 W m -2 , 26.41 W m -2 , and 22.45 W m -2 for Guangzhou, Jiangmen and Huizhou, leading to a warming of the atmosphere in the PRD. The estimated annual excess mortalities of climate warming due to BC were 5052 (95% CI: 1983, 8139), 5121 (95% CI: 2010, 8249) and 4363 (95% CI: 1712, 7032) for Guangzhou, Jiangmen and Huizhou, respectively., Conclusion: Our estimates suggest that current levels of BC exposure in the PRD region posed a considerable risk to human health and the climate. Reduction of BC emission could lead to substantial health and climate co-benefits., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Water-soluble organic matter (WSOM) represents a critical fraction of fine particles (PM 2.5 ) in the air, but its changing behaviors and formation mechanisms are not well understood yet, partly due to the lack of fast techniques for the ambient measurements. In this study, a novel system for the on-line measurement of water-soluble components in PM 2.5 , the particle-into-liquid sampler (PILS)-Nebulizer-aerosol chemical speciation monitor (ACSM), was developed by combining a PILS, a nebulizer, and an ACSM. High time resolution concentrations of WSOM, sulfate, nitrate, ammonium, and chloride, as well as mass spectra, can be obtained with satisfied quality control results. The system was firstly applied in China for field measurement of WSOM. The mass spectrum of WSOM was found to resemble that of oxygenated organic aerosol, and WSOM agreed well with secondary inorganic ions. All evidence collected in the field campaign demonstrated that WSOM could be a good surrogate of secondary organic aerosol (SOA). The PILS-Nebulizer-ACSM system can thus be a useful tool for intensive study of WSOM and SOA in PM 2.5 ., (Copyright © 2018. Published by Elsevier B.V.)