Identify organic contaminants of high-concern based on non-targeted toxicity testing and non-targeted LC-HRMS analysis in tap water and source water along the Yangtze River.

Many organic pollutants were detected in tap water (TW) and source water (SW) along the Yangtze River. However, the potential toxic effects and the high-concern organics (HCOs) which drive the effect are still unknown. Here, a non-targeted toxicity testing method based on the concentration-dependent transcriptome and non-targeted LC-HRMS analysis combining tiered filtering were used to reveal the overall biological effects and chemical information. Subsequently, we developed a qualitative pathway-structure relationship (QPSR) model to effectively match the biological and chemical information and successfully identified HCOs in TW and SW along the Yangtze River by potential substructures of HCOs. Non-targeted toxicity testing found that the biological potency of both TW and SW was stronger in the downstream of the Yangtze River, and disruption of the endocrine system and cancer were the main drivers of the effect. In addition, non-targeted LC-HRMS analysis combined with retention time prediction results identified 3220 and 631 high-confidence compound structures in positive and negative ion modes, respectively. Then, QPSR model was further implied and identified a total of 103 HCOs, containing 35 industrial chemicals, 30 PPCPs, 26 pesticides, and 12 hormones in TW and SW, respectively. Among them, the neuroactive and hormonal compounds oxoamide, 8-iso-16-cyclohexyl-tetranor prostaglandin E2, E Keppra, and Tocris-0788 showed the highest frequency of detection, which were identified in more than 1/3 of the samples. The strategy of combining non-targeted toxicity testing and non-targeted LC-HRMS analysis will support comprehensive biological effect assessment, identification of HCOs, and risk control of mixtures.

Immunotoxicity Evaluation of Trihalophenolic Disinfection By-Products in Mouse and Human Mononuclear Macrophage Systems: The Role of RNA Epitranscriptomic Modification in Mammalian Immunity.

BACKGROUND: 2,4,6-Trichlorophenol (TCP), 2,4,6-tribromophenol (TBP) and 2,4,6-triiodophenol (TIP) are three widely detected trihalophenolic disinfection by-products (DBPs). Previous studies have mainly focused on the carcinogenic risk and developmental toxicity of 2,4,6-trihalophenols. Very little is known about their immunotoxicity in mammals. OBJECTIVES: We investigated the effects of 2,4,6-trihalophenols on mammalian immunity using a mouse macrophage model infected with bacteria or intracellular parasites and aimed to elucidate the underlying mechanisms from an epitranscriptomic perspective. The identified mechanisms were further validated in human peripheral blood mononuclear cells (PBMCs). METHODS: The mouse macrophage cell line RAW264.7 and primary mouse peritoneal macrophages were exposed to different concentrations of TCP, TBP, and TIP. The pro-inflammatory marker Ly6C, the survival of the bacterium Escherichia coli (E. coli), and the parasite burden of Toxoplasma gondii (T. gondii) were assessed. Furthermore, the global gene expression profiling of macrophages following exposure to 2,4,6-trihalophenols was obtained through RNA-sequencing (RNA-seq). The effects of 2,4,6-trihalophenols on RNA N6-methyladenosine (m6A) methyltransferases and total RNA m6A levels were evaluated using Western blotting and dot blot, respectively. Transcriptome-wide m6A methylome was analyzed by m6A-seq. In addition, expression of m6A regulators and total RNA m6A levels in human PBMCs exposed to 2,4,6-trihalophenols were detected using quantitative reverse transcriptase polymerase chain reaction and dot blot, respectively. RESULTS: Mouse macrophages exposed to TCP, TBP, or TIP had lower expression of the pro-inflammatory marker Ly6C, with a greater difference from control observed for TIP-exposed cells. Consistently, macrophages exposed to such DBPs, especially TIP, were susceptible to infection with the bacterium E. coli and the intracellular parasite T. gondii, indicating a compromised ability of macrophages to defend against pathogens. Intriguingly, macrophages exposed to TIP had significantly greater m6A levels, which correlated with the greater expression levels of m6A methyltransferases. Macrophages exposed to each of the three 2,4,6-trihalophenols exhibited transcriptome-wide redistribution of m6A. In particular, the m6A peaks in genes associated with immune-related pathways were altered after exposure. In addition, differences in m6A were also observed in human PBMCs after exposure to 2,4,6-trihalophenols. DISCUSSION: These findings suggest that 2,4,6-trihalophenol exposure impaired the ability of macrophages to defend against pathogens. This response might be associated with notable differences in m6A after exposure. To the best of our knowledge, this study presents the first m6A landscape across the transcriptome of immune cells exposed to pollutants. However, significant challenges remain in elucidating the mechanisms by which m6A mediates immune dysregulation in infected macrophages after 2,4,6-trihalophenol exposure. https://doi.org/10.1289/EHP11329.

Toxoplasma gondii microneme protein MIC3 induces macrophage TNF-α production and Ly6C expression via TLR11/MyD88 pathway.

Toxoplasma gondii is the most successful parasite worldwide. It is of great interest to understand how T. gondii induce different immune responses in different hosts. In this study, we found that a peptide of T. gondii microneme protein MIC3 induced TNF-α production, NF-κB phosphorylation, iNOS transcription and Ly6C expression in mouse macrophage RAW264.7 cells. MyD88 inhibition, small interfering RNA against Tlr11 and CRISPR/Cas9-mediated knock-out of Tlr11 all reduced MIC3-induced TNF-α production, NF-κB phosphorylation, iNOS transcription and Ly6C expression. Additionally, we determined the location of MIC3 peptide in mouse macrophages using immunofluorescence. MIC3 could both adhere to the cell membrane of mouse macrophages and enter the cells. These results suggest that MIC3 triggered the immune responses in mouse macrophages via TLR11/MyD88/NF-κB pathway. It is known that human macrophages lacking TLR11. We predicted that the immune responses induced by MIC3 in human macrophages were significantly different from those in mouse macrophages. As expected, MIC3 peptide failed to induce TNF-α expression, iNOS expression and NF-κB phosphorylation in human THP-1 derived macrophages. MIC3 induced macrophage immune responses via TLR11. Intriguingly, the amino acid sequence of MIC3 is completely different from the well-known TLR11 ligand profilin, which generates a potent IL-12p40, TNF-α and IL-6 response. In marked contrast to profilin, MIC3 could not induce IL-12p40 expression in both mouse RAW264.7 cells and human THP-1 derived macrophages. Furthermore, the simulated tertiary structure of MIC3 peptide shows poor similarity with the crystal structure of profilin, suggesting that MIC3 might be a different ligand from profilin. These findings about MIC3 and TLR11 will provide us with important insights into the pathogenesis of toxoplasmosis and coevolution during host-parasite interaction.

Peritoneal GATA6+ macrophage drives hepatic immunopathogenesis and maintains the Treg cell niche in the liver.

The source of macrophages that contribute to human liver disease remains poorly understood. The purpose of this study is to investigate the functional mechanism of peritoneal macrophages in the development of hepatic immunopathology. By performing the natural infection with the blood fluke Schistosoma japonicum (S. japonicum) and the chemically carbon tetrachloride (CCl4 )-induced liver injured mouse model, we identified the peritoneal cavity as an essential source of hepatic macrophages. Here, we show that a large number of F4/80+ macrophages was accumulated in the peritoneal cavity during liver injury. An unknown source population of macrophages, which highly expressed GATA6 that is specific to peritoneal macrophages, was found to exist in the injured livers. Peritoneal macrophage deletion by injection with clodronate-containing liposomes led to an attenuated hepatic pathology and the inflammatory microenvironment, while adoptive transfer of macrophages into the abdominal cavity, by contrast, results in restoring liver pathology. Importantly, there are set genes of monocyte chemoattractant protein (MCP)-1, -2, and -3 that are highly related to recruit GATA6+ macrophages during S. japonicum infection, while administration of bindarit, a selective inhibitor of MCPs synthesis, dramatically decreased the hepatic expression of GATA6+ macrophages and thus attenuated hepatic pathology. Furthermore, in vivo study showed that peritoneal macrophages promote hepatic immunopathology is dependent on the accumulation of regulatory T cells (Tregs) in the liver. Altogether, these data provide the first clear evidence that GATA6+ peritoneal macrophages play critical roles in both the formation of hepatic immunopathology and the accumulation of Tregs cells.

In vivo toxicity evaluations of halophenolic disinfection byproducts in drinking water: A multi-omics analysis of toxic mechanisms.

Halophenolic disinfection byproducts (DBPs) in drinking water have attracted considerable concerns in recent years due to their wide occurrence and high toxicity. The liver has been demonstrated as a major target organ for several halophenolic DBPs. However, little is known about the underlying mechanisms of liver damage caused by halophenolic DBPs. In this study, 2,4,6-trichlorophenol (TCP), 2,4,6-tribromophenol (TBP) and 2,4,6-triiodiophenol (TIP) were selected as representative halophenolic DBPs and exposed to C57BL/6 mice at an environmentally-relevant concentration (0.5 µg/L) and two toxicological concentrations (10 and 200 µg/L) for 12 weeks. Then, a combination of histopathologic and biochemical examination, liver transcriptome, serum metabolome, and gut microbiome was adopted. It was found that trihalophenol exposure significantly elevated the serum levels of alkaline phosphatase and albumin. Liver inflammation was observed at toxicological concentrations in the histopathological examination. Transcriptome results showed that the three trihalophenols could impact immune-related pathways at 0.5 µg/L, which further contributed to the disturbance of pathways in infectious diseases and cancers. Notably, TBP and TIP had higher immunosuppressive effects than TCP, which might lead to uncontrolled infection and cancer. In terms of serum metabolic profiles, energy metabolism pathway of citrate cycle and amino acid metabolism pathways of valine, leucine, and isoleucine were also significantly affected. Integration of the metabolomic and transcriptomic data suggested that a 12-week trihalophenol exposure could prominently disturb the glutathione metabolism pathway, indicating the impaired antioxidation and detoxification abilities in liver. Moreover, the disorder of the intestinal flora could interfere with immune regulation and host metabolism. This study reveals the toxic effects of halophenolic DBPs on mammalian liver and provides novel insights into the underlying mechanisms of hepatotoxicity.

Detection, transformation, and toxicity of indole-derivative nonsteroidal anti-inflammatory drugs during chlorine disinfection.

As important emerging contaminants, nonsteroidal anti-inflammatory drugs (NSAIDs) are the most intensively prescribed pharmaceuticals introduced to drinking water due to their incomplete removal in wastewater treatment. While concentrations of NSAIDs in drinking water are generally low, they have been attracting increasing concern as a result of their disinfection byproducts (DBPs) generated in drinking water disinfection. In this work, detection methods were set up for four representative indole-derivative NSAIDs (indomethacin, acemetacin, sulindac, and etodolac) using ultra performance liquid chromatography/electrospray ionization-triple quadruple mass spectrometry (UPLC/ESI-tqMS). ESI+ was better for detection of indomethacin and sulindac, whereas ESI- was suitable to detection of acemetacin and etodolac. With optimized MS parameters, the instrument detection and quantitation limits of the four indole derivatives were achieved to be 1.1-24.6 ng/L and 3.7-41.0 ng/L, respectively. During chlorination, indomethacin and acemetacin could undergo five major reaction types (chlorine substitution, hydrolysis, decarboxylation, C-C coupling, and C-N cleavage) to form a series of DBPs, among which 19 were proposed/identified with structures. Based on the revealed structures of DBPs, transformation pathways of indomethacin and acemetacin in chlorination were partially elucidated. Notably, individual and mixture toxicity of indomethacin and acemetacin before/after chlorination were evaluated using a well-established acute toxicity assessment and a Hep G2 cell cytotoxicity assay, respectively. Results showed that the predicted acute toxicity of a few chlorination DBPs were higher than their precursors; chlorination substantially enhanced the mixture cytotoxicity of indomethacin by over 10 times and slightly increased the mixture cytotoxicity of acemetacin.

Praziquantel ameliorates CCl4 -induced liver fibrosis in mice by inhibiting TGF-ß/Smad signalling via up-regulating Smad7 in hepatic stellate cells.

BACKGROUND AND PURPOSE: Praziquantel is a schistosomicide, which has been used for more than 30 years due to its efficiency, safety, and mild side effects. Previous studies showed that prolonged treatment with praziquantel suppressed the development of liver fibrosis in mice with schistosomiasis. In this study, we investigated the potential mechanisms underlying the antifibrotic effects of praziquantel. EXPERIMENTAL APPROACH: To avoid the effect of schistosomicidal activity of praziquantel against liver fibrosis induced by Schistosoma japonicum infection, we established a mouse model of carbon tetrachloride (CCl4 )-induced liver fibrosis for in vivo studies and used TGF-ß1-stimulated human hepatic stellate cell line (LX-2) in addition to other fibroblast-like cell line (MES13) and fibroblast cell line (NIH3T3) in vitro. Western blotting, immunohistochemistry, quantitative real-time PCR, siRNA, and immunofluorescence staining were utilized to assess the expression of key molecules in liver fibrosis and the TGF-ß/Smad pathway. KEY RESULTS: Praziquantel significantly attenuated CCl4 -induced liver fibrosis by inhibiting the activation of hepatic stellate cells (HSCs) and expression of collagen matrix via enhancement of Smad7 expression, which were confirmed in LX-2, MES13, and NIH3T3 cells in vitro. In contrast, knockdown of Smad7 in LX-2 cells prevented praziquantel-mediated inhibition of LX-2 cell activation and TGF-ß1-mediated collagen type I α1 induction, revealing the critical role of Smad7 in the antifibrotic effect of praziquantel during liver fibrosis. CONCLUSIONS AND IMPLICATIONS: PZQ exhibited a strong efficacy against liver fibrosis by inhibiting activation of HSCs via Smad7 up-regulation, suggesting potential broad utility in treatment of diseases characterized by liver fibrosis.

A comparative evaluation of the immunotoxicity and immunomodulatory effects on macrophages exposed to aromatic trihalogenated DBPs.

Objective: 2,4,6-trichlorophenol (TCP), 2,4,6-tribromophenol (TBP), and 2,4,6-triiodophenol (TIP) are three aromatic halogenated disinfection byproducts (DBPs) identified in chlorinated saline effluents. This study aimed to evaluate and compare their immunotoxicity and immunomodulatory effects on macrophages. Materials and methods: CCK-8 assay was used to evaluate cytotoxicity of TCP, TBP, and TIP in mouse macrophage RAW264.7 cells. A light microscope and digital camera were used to record the morphological changes of RAW264.7 cells. qRT-PCR was used to measure the mRNA levels of polarization markers and secreted cytokines. Cytokine production was also detected by ELISA. Flow cytometry was performed to analyze the expression of M1 and M2 markers on macrophages. Results: TCP, TBP, and TIP had different cytotoxic effects on macrophages. The rank order of cytotoxicity was TIP > TBP > TCP. Furthermore, the three halogenated DBPs displayed different preferences for macrophage polarization. Intriguingly, 200 µM TIP remarkably induced the M2-dominant polarization of macrophages, while 200 µM TCP induced an M1-dominant polarization of macrophages. TBP has a moderate ability in inducing M1 and M2 polarization compared with TCP and TIP. Conclusions: TIP displayed higher cytotoxicity against macrophages than TBP and TCP, its brominated and chlorinated analogs. Since M1 and M2 macrophages facilitate the inflammatory and anti-inflammatory responses, respectively, the discrepancy of TCP, TBP, and TIP in inducing macrophage polarization may lead to distinct immunomodulatory and toxicological outcomes, thus giving rise to different types of diseases. This finding may provide novel insights into evaluating the toxicity of environmental pollutants on the immune system.

Research on the effect and mechanism of antimicrobial peptides HPRP-A1/A2 work against Toxoplasma gondii infection.

With increasing antibiotic resistance and drug safety concerns, novel therapeutics are urgently needed. Antimicrobial peptides are promising candidates that could address the spread of multidrug-resistant pathogens. HPRP-A1/A2 are known to display antimicrobial activity against gram-negative bacteria, gram-positive bacteria and some pathogenic fungi, but whether HPRP-A1/A2 work on Toxoplasma gondii (T gondii) is unknown. In this study, we found that the viability of tachyzoites that received HPRP-A1/A2 treatment was significantly decreased, and there was a reduction in the adhesion to and invasion of macrophages by tachyzoites after HPRP-A1/A2 treatment. HPRP-A1/A2 damaged the integrity of tachyzoite membranes, as characterized by membrane disorganization in and cytoplasm outflow from tachyzoites. In addition, in vivo injection with HPRP-A1/A2 resulted in a significantly decreased number of tachyzoites and an accelerated Th1/Tc1 response, and elicited pro-inflammatory cytokines in T gondii-infected mice. Furthermore, HPRP-A1/A2-treated splenocytes exhibited a significantly increased Tc1/Th1 response, and HPRP-A1/A2-stimulated macrophages inhibited the growth of carboxyfluorescein succinimidyl amino ester (CFSE)-labelled tachyzoites, which had higher TNF-α/IL-12 mRNA levels. Altogether, these results imply that HPRP-A1/A2 are effective against T gondii through damaging the structure of tachyzoites and inducing a protective immune response, which could offer an alternative approach against T gondii infection.

Estradiol Attenuates the Severity of Primary Toxoplasma gondii Infection-Induced Adverse Pregnancy Outcomes Through the Regulation of Tregs in a Dose-Dependent Manner.

Estradiol (E2) plays a crucial and intricate role during pregnancy to mediate several aspects of the pregnancy process. A perplexing phenomenon in congenital toxoplasmosis is that the severity of Toxoplasma gondii (T. gondii)-mediated adverse pregnancy outcome is closely related with time of primary maternal infection during pregnancy. In this study, the results showed that T. gondii infection in early pregnancy was more likely to induce miscarriage in mice than in late pregnancy, which may be related to inflammation of the maternal-fetal interface. Meanwhile, the T. gondii infection-induced-apoptotic rate of Tregs was higher and the expression of programmed death-1 (PD-1) on Tregs was lower in early pregnancy than in late pregnancy. As the level of E2 in mouse serum gradually increased with the development of pregnancy, we proposed that E2 may contribute to the discrepancy of Tregs at different stages of pregnancy. Thus, we investigated in vitro and in vivo effects of E2 in regulating Tregs. We found that E2 in vitro could protect Tregs against apoptosis and upregulate the expression of PD-1 on Tregs in a dose-dependent manner through ERα. Likewise, the simulated mid-pregnancy level of E2 in nonpregnant mice also alleviated the T. gondii infection-induced apoptosis of Tregs and potentiated the PD-1 expression on Tregs. Therefore, in the pathogenesis of T. gondii-induced abnormal pregnancy, E2 helped maintain the immune balance and improve the pregnancy outcome through regulating Tregs. This finding illustrates the intricate working of hormone-immune system interaction in infection-induced abnormal pregnancy.

Toxicological and chemical insights into representative source and drinking water in eastern China.

Drinking water safety is continuously threatened by the emergence of numerous toxic organic pollutants (TOPs) in environmental waters. In this study, an approach integrating in vitro bioassays and chemical analyses was performed to explore toxicological profiles of representative source and drinking water from waterworks of the Yangtze River (Yz), Taihu Lake (Th), and the Huaihe River (Hh) basins in eastern China. Overall, 34 of 96 TOPs were detected in all water samples, with higher concentrations in both source and drinking water samples of Hh, and pollutant profiles also differed across different river basins. Non-specific bioassays indicated that source water samples of Hh waterworks showed higher genotoxicity and mutagenicity than samples of Yz and Th. An EROD assay demonstrated dioxin-like toxicity which was detected in 5 of 7 source water samples, with toxin concentration levels ranging from 62.40 to 115.51 picograms TCDD equivalents per liter of water (eq./L). PAHs and PCBs were not the main contributors to observed dioxin-like toxicity in detected samples. All source water samples induced estrogenic activities of 8.00-129.00 nanograms 17ß-estradiol eq./L, and estrogens, including 17α-ethinylestradiol and estriol, contributed 40.38-84.15% of the observed activities in examined samples. While drinking water treatments efficiently removed TOPs and their toxic effects, and estrogenic activity was still observed in drinking water samples of Hh. Altogether, this study indicated that the representative source water in eastern China, especially that found in Hh, may negatively affect human health, a finding that demonstrates an urgent requirement for advanced drinking water treatments.

Praziquantel Targets M1 Macrophages and Ameliorates Splenomegaly in Chronic Schistosomiasis.

Splenomegaly is a common feature of many infectious diseases, including schistosomiasis japonica. However, the immunopathogenesis and the treatment of splenomegaly due to schistosomiasis have been largely neglected. Praziquantel (PZQ), a classical schistosomicide, has been demonstrated by us and others to have antifibrotic and anti-inflammatory activities against schistosomiasis. In this study, we investigated the effect of PZQ on alleviating the splenomegaly caused by Schistosoma japonicum infection in mice. The results showed that the number of macrophages, especially the number of M1 macrophages, was significantly increased in the enlarged spleens of infected mice (P < 0.001). After PZQ treatment for 4 weeks, the number of splenic macrophages, especially the number of M1 macrophages, was significantly reduced (P < 0.001) by the way of apoptosis, and another schistosomicide, mefloquine, had no effect either on the splenomegaly or on reducing the number of macrophages. Furthermore, by using the murine macrophage line RAW 264.7, we found that PZQ could inhibit the formation of the NLRP3 inflammasome and attenuate phagocytic activity in M1 macrophages. Thus, our studies suggest that PZQ plays a powerful role in ameliorating the splenomegaly caused by S. japonicum infection, which presents a new strategy for the therapy of splenomegaly resulting from other pathological conditions.

Vascular endothelial growth factor promotes the activation of hepatic stellate cells in chronic schistosomiasis.

The activation of hepatic stellate cells (HSCs) is a key event in fibrotic pathogenesis. However, the mechanism involving activation of HSCs in chronic schistosomiasis is not entirely clear. Human HSC LX-2 and human umbilical vein endothelial cells (ECs) were cultured with Schistosoma japonicum antigens (SA) in vitro. Fibrosis-associated genes and cell proliferation were analyzed. HSCs were isolated from mice of chronic schistosomiasis with or without praziquantel (PZQ) treatment, followed by the microarray analysis for the liver fibrosis-associated pathways. Although SA inhibited the activation and proliferation of HSCs, it induced the EC proliferation and vascular endothelial growth factor-a (VEGF) production. VEGF significantly increased the proliferation of HSCs and upregulated the expression of collagen and α-smooth muscle actin. For in vivo study, we found that several fibrosis-associated pathways were involved in the HSCs during the reversal of liver fibrosis caused by schistosomiasis, including VEGF, platelet-derived growth factor, tumor necrosis factor and endothelin-1 pathways. The Ingenuity Pathway Analysis showed that VEGF directly regulated several pro-fibrotic and immune cytokine genes in HSCs, including integrin, fibronectin, interferon-γ, interleukin (IL)-6 and IL-10. Our data indicated the critical role of VEGF signaling in HSC activation in chronic schistosomiasis and highlighted several promising genes and pathways in HSCs as potential targets for therapeutic treatment of liver fibrosis.

Identification of a TNF-α inducer MIC3 originating from the microneme of non-cystogenic, virulent Toxoplasma gondii.

Toxoplasma gondii is an opportunistic parasite with avirulent cystogenic and highly virulent non-cystogenic isolates. Although non-cystogenic strains are considered the most virulent, there are also marked genetic and virulence differences among these strains. Excretory-secretory antigens (ESAs) of T. gondii are critical for the invasion process and the immune response of the host. To better understand the differences in virulence between non-cystogenic T. gondii isolates, we studied ESAs of the RH strain (Type I), and the very prevalent in China, but less virulent TgCtwh3 strain (Chinese 1). ESAs of RH and TgCtwh3 triggered different levels of TNF-α production and macrophage M1 polarization. Using iTRAQ analysis, 27 differentially expressed proteins originating from secretory organelles and surface were quantified. Of these proteins, 11 microneme-associated proteins (MICs), 6 rhoptry proteins, 2 dense granule proteins and 5 surface proteins were more abundant in RH than in TgCtwh3. The protein-protein correlation network was employed to identify the important functional node protein MIC3, which was upregulated 5-fold in RH compared with TgCtwh3. MIC3 was experimentally confirmed to evoke a TNF-α secretory response, and it also induced macrophage M1 polarization. This result suggests that MIC3 is a potentially useful immunomodulator that induces TNF-α secretion and macrophage M1 polarization.

Development of a magnetic solid-phase extraction coupled with gas chromatography and mass spectrometry method for the analysis of semivolatile organic compounds.

Semivolatile organic compounds are a category of organic micropollutants including phthalate esters, polycyclic aromatic hydrocarbons and so on, which are commonly analyzed by solid-phase extraction followed by gas chromatography with mass spectrometry. In this work, a highly sensitive and feasible method of magnetic solid-phase extraction combined with gas chromatography with mass spectrometry was established for the determination of semivolatile organic compounds in water. The novel method was based on a permanent magnetic resin with uniform particle size and high surface area (1154.3 m2 /g). The results demonstrated that the extraction efficiency of the resin was superior to that of a C18 cartridge. The method was proved to be of satisfactory recoveries (75-115.7%) and limits of detection and quantification (0.063-6.524 and 0.212-21.745 µg/L, respectively). The method was applied to the analysis of semivolatile organic compounds in the midstream Huai River. It was observed that polychlorinated biphenyls exceeded current water standards. To further illustrate the potential effects on human health, health risk assessment was conducted based on the obtained data. The existence of health risk was proved, with hexachlorobenzene and 2,2',4,4'-tetrachlorobiphenyl as the major causes. The method possesses the characteristics of high efficiency and rapid analysis, offering a good prospect of applications in large quantities of practical water.