Weiping Liu

Engineered nanomaterials (ENMs) are used or investigated in sports for mechanical reinforcement, friction regulation, thermal management, biosensing, energy harvesting, and tissue repair. This critical review examines their applications, environmental release, transformation, exposure pathways, biological interactions, and end-of-life management, distinguishing field measurements, laboratory tests, models, and proposed pathways. ENMs are deliberately engineered for nanoscale functionality; microplastics (MPs) and nanoplastics (NPs) are classified by polymer composition and size. Micro(nano)plastics (MNPs) are not inherently nanomaterials; nanoscale polymer particles may be engineered or incidental. MNPs from synthetic turf, polymeric infill, running tracks, footwear, and apparel are assessed as degradation products, potential carriers of embedded ENMs, and co-occurring contaminants. Field evidence is stronger for turf-derived MP release than for sports-related free ENM or NP release. Abrasion, oxidation, and weathering modify particle size, surface chemistry, and sorption capacity, while hydrological runoff, wind transport, and human activities redistribute particles. Athlete exposure through inhalation, ingestion, and dermal contact is plausible, but limited longitudinal biomonitoring warrants cautious interpretation of health risks. Laboratory ecotoxicological studies identify material- and preparation-dependent hazards to terrestrial and aquatic biota, but do not establish effects at measured sports-field drainage concentrations. Sustainability requires low-emission material design, effective physical containment, advanced drainage treatment, environmentally realistic exposure testing, transparent material disclosure, and robust end-of-life recovery systems. Circularity metrics must incorporate diffuse particulate and chemical emissions into life-cycle exposure and ecosystem risk assessments. Comparative synthesis links material properties, release identity, analytical limits, and pathway confidence; a minimum reporting framework identifies the measurements needed for quantitative exposure and risk assessment.

Per- and polyfluoroalkyl substances (PFASs) are widely used, with significant environmental and health impacts. PFASs often exist as isomers with distinct physicochemical properties that influence their environmental fate and toxicity. This study advances PFAS analysis through isomeric resolution of 41 linear and 39 branched congeners by liquid chromatography-ion mobility-high-resolution mass spectrometry (LC-IM-HRMS), reporting the largest collision cross-section (CCS) data set for PFAS structural isomers to date, including the first reported drift-tube ion mobility (DTIM)-derived DTCCSN2 values for PFNA and PFNS isomers. The workflow was successfully applied to 41 great and blue tit egg samples collected near a contaminated industrial site in Belgium, where 20 linear and 34 branched PFAS isomer features were detected. Correlation analysis between the number of isomers detected for each PFAS in bird eggs revealed distinct co-occurrence patterns among branched PFAS isomers, with PFBS and PFDoDA showing unique behavior compared with other PFAS classes. A significant difference in PFOS isomer profiles was identified between the two species, which may be related to differences in foraging behavior and species-specific accumulation. The results demonstrate that LC-IM-HRMS is a useful tool for confidence-enhanced PFAS isomer identification in complex biological samples despite the limited availability of single-branched isomer standards and highlight the value of isomer-resolved analysis for environmental biomonitoring and exposure characterization.

Chlorinated paraffins (CPs) are recognized as a novel class of persistent organic pollutants (POPs) and are categorized into short- (SCCPs, C_10–13), medium- (MCCPs, C1_4–17), and long- (LCCPs, C_≥18) chain CPs considering the carbon-chain length. Among them, SCCPs possess lower molecular weights, higher vapor pressures, and greater water solubilities compared to their longer-chain counterparts (MCCPs and LCCPs), which promote their environmental release. Consequently, SCCPs were designated as POPs of concern under the Stockholm Convention in 2017. This review concludes the recent research progress of SCCPs in China from 2015 to present, and we present a comprehensive overview of SCCP concentrations, encompassing diverse environmental matrices and human tissues, for example, air, water, soil, sediments, biota, food, human placenta, breast milk, blood, and organs (fat, kidney, liver, brain, bone, etc.). Whereafter, we summarize the development of SCCPs determination methods, benefiting from quantifying relative carbon-chain length and chlorine content of SCCPs correctly. Moreover, toxicity, toxicokinetics, and adverse health effects of SCCPs in humans from China are concluded and discussed. Meanwhile, we review the existing control and treatment technologies for SCCPs. Lastly, we describe some noteworthy and prospective issues that are worthy of further study. In the future, the relevant studies are still necessary to keep up with consecutive monitoring and evaluation of SCCP levels and relative potential health impacts in China.

Tropical coastal waters are increasingly recognized as critical reservoirs for virulent, antibiotic-resistant enteric pathogens, yet seasonal dynamics governing their spatial distribution remain poorly characterized. We hypothesized that hydrological shifts and anthropogenic nutrient enrichment drive the seasonal distribution, virulence profiles, and antimicrobial resistance (AMR) of Escherichia coli, Salmonella spp., and Shigella spp. in the Jaffna Peninsula, Sri Lanka. Across 25 coastal sites during dry and transitional seasons, we integrated physicochemical water quality assessment, culture-based enumeration, PCR-based virulence gene profiling, Minimum Inhibitory Concentration (MIC) assays, GIS mapping, and statistical analyses. Key water quality parameters, including ammonium, nitrite, and total phosphorus, showed significant seasonal variation (p < 0.05), reflecting distinct hydrological regimes across seasons. A total of 220 E. coli, 200 Salmonella spp., and 100 Shigella spp. isolates were examined for virulence gene profiles and antibiotic tolerance. E. coli was detected at 80–88% of sites, Salmonella spp. at 72–88%, and Shigella spp. at 32–48%. Among E. coli isolates, stx1 was detected at 20–28% of sites and eae at 16% across both seasons. The stn gene was detected in Salmonella spp. at 12–28% of sites seasonally. Virulence profiling confirmed STEC harbouring stx1, stx2, and eae; Salmonella spp. carried stn; and Shigella spp. possessed invasion-associated genes. Trimethoprim–sulfamethoxazole resistance was recorded in 63.2% of E. coli, 33.0% of Salmonella spp., and 31.0% of Shigella spp. isolates at the lowest tested concentration of 4 µg/mL., while ciprofloxacin and piperacillin–tazobactam retained greater efficacy. Correlation analyses revealed significant associations among faecal contamination, nutrient enrichment, and virulence gene prevalence, implicating untreated sewage discharge and eutrophication as likely ecological factors associated with pathogen occurrence. These findings designate the Jaffna coastal zone as a significant reservoir of virulent AMR enteric pathogens, underscoring the urgent need for integrated One Health surveillance and seasonally adaptive coastal water quality management.

The toxicity of radioactive metals arises from both chemical toxicity and radiotoxicity. ²¹⁰Pb(II) is a long-lived radionuclide in the decay chain of natural uranium series ²³⁸U and exhibits extremely high toxicity. Both ²¹⁰Pb(II) and Pb(II) are widely present in natural water bodies. However, their combined toxicity remains unclear. Based on this, this study used zebrafish embryos as model organisms to investigate developmental toxicity, behavioral toxicity, and thyroid disruption effects, through single and combined exposure to Pb(II) (0, 1, 10, 100 μg/L) and ²¹⁰Pb(II) (0, 100, 1000 Bq/L) for 120 h by comparing the radiotoxicity of ²¹⁰Pb(II) with the chemical toxicity of Pb(II) and further exploring their combined effects. The results showed that following exposure to different environmental concentrations of Pb(II) and environmental activity levels of ²¹⁰Pb(II), exposure to Pb(II) alone caused an increase in the malformation rate of zebrafish embryos, a decrease in locomotor activity, and significant upregulation of thyroid-related genes, including thyroid hormone receptor beta (TRβ) and corticotropin-releasing hormone (CRH) in the larvae. Exposure to ²¹⁰Pb(II) alone had no significant effects on zebrafish embryos. Notably, compared with the individual exposure groups, the toxic effects in the combined exposure group of Pb(II) and ²¹⁰Pb(II) were further significantly enhanced. Furthermore, correlation analysis indicated a positive correlation between malformations in zebrafish embryos and the expression of key genes in the hypothalamic–pituitary–thyroid (HPT) axis. These findings suggest that under combined exposure, the chemical toxicity of Pb(II) plays a dominant role, while the radioactive component ²¹⁰Pb(II) exerts a synergistic amplification effect. This study provides important scientific evidence for improving the environmental risk assessment of radioactive metals.

Triethylamine (TEA) is extensively used in industry, and its aquatic ecological risks have attracted regulatory attention. This study assessed TEA occurrence in groundwater and surface water within a chemical industrial park and evaluated its toxicity and mechanisms in zebrafish embryo-larvae. The results revealed elevated TEA concentrations, reaching 41.200 mg/L in groundwater and 0.377 mg/L in surface water, both of which substantially exceeded the groundwater drinking water risk screening reference value in US EPA Regional Screening Levels (0.015 mg/L). Toxicity assessments showed reduced heart rate, abnormal behavior, and increased malformations in zebrafish exposed to 0.015–10.00 mg/L TEA. Mechanistically, TEA induced significant oxidative stress, evidenced by elevated catalase (CAT) activity and glutathione (GSH) content, with non-linear changes in malondialdehyde (MDA) content and superoxide dismutase (SOD) activity, and a marked increase in hepatic aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) activities. Additionally, TEA exposure significantly reduced the levels of thyroid hormone T3 and T4 and altered expression of hypothalamus-pituitary-thyroid (HPT) axis genes including TTR, UGT1ab, and TSHβ. Correlations revealed significant associations among T3, T4, and HPT axis gene expression with oxidative stress markers and hepatic enzymes, whereas molecular docking revealed no strong binding between TEA and HPT axis proteins. Collectively, this study reveals the high-risk occurrence of TEA in a chemical industrial park and its multifaceted toxicity in zebrafish embryos, and elucidates the key mechanism of TEA-induced thyroid disruption mediated by oxidative stress and liver injury. These findings provide a key scientific basis for the ecological and environmental risk management of TEA.

Microplastics (MPs) have become pervasive contaminants. This is due to plastic mulching, wastewater irrigation, and sludge application. Concentrations of MPs in intensive farming regions have been recorded at 41,741 particles/kg. MPs are absorbed by crop roots and leaves and then travel to reproductive organs. In these organs, they cause oxidative stress, genotoxicity, and toxicity, which disrupts nutrient uptake, photosynthesis, and crop yield. This review summarizes 20 years (2003-2024) of studies on MP-distribution in soil-crop systems and their phytotoxicity mechanisms, highlighting the pioneering role of multiomics methods. Genomic analyses show that MPs cause DNA damage and change the expression levels of stress-response genes. Transcriptomics identifies disrupted pathways. These pathways are in carbohydrate metabolism, plant hormones, and antioxidant defense. Proteomics uncovers post-translational modifications. These affect nutrient transporters. Metabolomics further highlights disturbances in glycolysis, amino acid synthesis, and ROS-scavenging metabolites. Despite these advances, integrating multiomics data sets to elucidate systemic "gene-protein-metabolite" networks remains challenging. Key knowledge gaps include MP-protein binding mechanisms, the development of crop-specific biomarkers, and the interaction of MPs with costressors. Future research should prioritize integrated transcriptomic-metabolomic profiling to identify stress-response pathways, use X-ray crystallography to map MP-protein interactions, and develop MP-resilient crop varieties. Multiomics integration is essential for decoding the toxicity of the MPs and formulating mitigation strategies to safeguard the sustainability of agriculture.

The chiral herbicide glufosinate-ammonium (racemic-GLA) is banned in the European Union due to developmental toxicity. Its herbicidally active l-enantiomer (l-GLA), marketed as a potential safer alternative, lacks developmental toxicity assessment. This study investigated the reproductive/developmental toxicity of l-GLA and racemic-GLA in pregnant mice at 13 and 130 μg/kg/day, achieving serum concentrations below or comparable to those reported in humans. Prenatal exposure to l-GLA and racemic-GLA at both doses caused fetal growth restriction (FGR), an approximate 10% reduction in placental weight, and structural abnormalities, including a smaller labyrinth zone, underdeveloped junctional zone, and increased apoptosis. l-GLA or racemic-GLA exposure impaired placental putrescine metabolism by downregulating arginase 1 (Arg1) and upregulating amine oxidase copper containing 1 (Aoc1) and monoamine oxidase A (Maoa) gene expression, resulted in reduced putrescine concentrations. Furthermore, impaired pyruvate metabolism, likely from 4-hydroxy-2-oxoglutarate aldolase 1 (Hoga1) downregulation, depleted pyruvate and increased lactate in the placenta. In human placental trophoblast cells, putrescine or pyruvate supplementation rescued impaired celluar migration and invasion caused by l-GLA or racemic-GLA. These results indicate that environmentally relevant doses of l-GLA/racemic-GLA impair trophoblast function via putrescine/pyruvate-mediated metabolic reprogramming, leading to placental dysfunction and FGR. These findings challenge the presumed safety of l-GLA as a racemic-GLA alternative.