Agricultural plastic mulching films are the main source of plastic pollution in farmlands. Long-term exposure to light radiation may cause their aging and degradation, and precipitation and irrigation further promote the release of additives into the water, posing a potential threat to the ecological environment. This study systematically investigated the changes in the physical and chemical properties of the film during aging and the neurotoxic effects of its leachate. The results showed that light radiation promoted the presence of oxygen-containing functional groups, increasing with the degree of aging, which facilitated the release of plastic additives. The toxicity assessment using the Caenorhabditis elegans model indicated that high concentrations of leachate could significantly inhibit the locomotion ability of the nematode. It is notable that the exudates from the photoaging film had a stronger inhibitory effect on the locomotion behavior of the nematode. Further analysis revealed that the aged film leachate reduced the content of key neurotransmitters in the nematode. Molecular biology studies showed that this neurotoxic effect was closely related to the expression inhibition of neurotransmission-related genes (dop-3, eat-4, mod-1, and unc-47). This study provides important scientific evidence for assessing the environmental risks of agricultural plastic mulching film pollution.

Microplastics (MPs) are known to induce diverse toxic effects across biological systems; however, how environmentally photoaged MPs influence organismal aging and the underlying mechanisms remain poorly understood. Here, virgin polystyrene (PS-0) and 45-day photoaged polystyrene (PS-45) were evaluated at environmentally relevant concentrations (0-100 μg/L) to assess aging-related effects and molecular pathways in Caenorhabditis elegans. Photoaging markedly altered PS physicochemical properties, including surface morphology, crystallinity, and functional groups. Exposure to 100 μg/L PS-0 or PS-45 significantly shortened lifespan, impaired physiological behaviors, and increased lipofuscin accumulation, whereas PS-45 at 10-100 μg/L elicited substantially stronger pro-aging effects. These enhanced toxicities were driven by particle-associated processes, particularly elevated environmentally persistent free radical generation and increased particle accumulation in nematodes. Mechanistically, PS-45 inhibited DAF-16 nuclear translocation and dysregulated insulin/IGF-1 signaling genes (daf-2, age-1, pdk-1, akt-1, and daf-16). Concurrently, PS-45 induced ferroptosis, as evidenced by increased Fe2+ and malondialdehyde levels, glutathione depletion, and suppression of ftn-1; these effects were alleviated by the ferroptosis inhibitor ferrostatin-1. Mutations in daf-2, age-1, pdk-1, akt-1, daf-16, and ftn-1 significantly altered PS-45-induced aging phenotypes and ferroptotic stress, identifying the DAF-2-AGE-1-PDK-1-AKT-DAF-16-FTN-1 axis as a central regulatory pathway. Collectively, this study reveals a mechanistic link between insulin signaling and ferroptosis in MPs-induced aging and highlights the elevated environmental health risks posed by photoaged MPs.

Natural iron (oxyhydr)oxides are increasingly recognized as important regulators of microplastics (MPs) transformation, yet their mechanistic influence on polymer photodegradation remains poorly understood. Here, we investigated how goethite (α-FeOOH) alters the photodegradation of polystyrene microplastics derived from disposable plastic spoons (Spoon-MPs) under simulated sunlight. Goethite increased Spoon-MP mass loss from 14.41% under light-only conditions to 21.78% after 12 d and increased the apparent degradation rate constant. Photodegradation induced pronounced physicochemical changes, including surface erosion, loss of structural order, molecular-weight reduction, and enhanced surface oxidation. Time-resolved FTIR and 2D-COS revealed distinct transformation sequences: aromatic-associated bands responded earlier under light-only conditions, whereas backbone C–H-associated bands responded earlier in the presence of goethite. EPR and scavenger experiments further showed enhanced generation of multiple reactive species, particularly •OH, supporting a greater contribution of hydrogen-abstraction-driven oxidation in the goethite system. GC–MS revealed increased relative abundances of low-molecular-weight oxygenated products, including ketone- and ester-containing compounds. DFT calculations identified aromatic and benzylic regions as intrinsically reactive sites, complementing the experimentally observed transformation patterns. Collectively, these findings demonstrate that goethite not only accelerates PS photodegradation but also alters the temporal sequence and relative importance of oxidative pathways, providing mechanistic insight into mineral-mediated transformation of microplastics in aquatic environments.

Microplastics (MPs) have emerged as ubiquitous environmental contaminants, while thallium (Tl), a highly toxic metalloid, is gaining attention as a novel pollutant due to its increasing release from electronic waste and mining activities. These pollutants frequently coexist in aquatic environments; however, their combined effects at environmentally relevant concentrations remain poorly understood. In this study, the adsorption behavior and joint neurotoxicity of polystyrene (PS) microplastics and Tl were systematically evaluated using Caenorhabditis elegans as a model organism. Adsorption kinetics followed both pseudo-first-order and pseudo-second-order models, yielding maximum Tl adsorption capacities of 66.682 µg/g and 67.981 µg/g, respectively. Adsorption efficiency declined with increasing salinity but was enhanced by higher pH, temperature, and humic acid (HA) concentrations. Neurotoxicity assays were conducted using Tl at 0.01 and 0.1 μg/L, along with PS at corresponding Tl-saturated adsorption concentrations (147 and 1470 μg/L). Behavioral analysis revealed that PS significantly amplified Tl-induced neurotoxicity, as evidenced by reductions in head thrashes and body bends. Co-exposure led to pronounced neurodegeneration and altered fluorescence intensity in serotonergic, GABAergic, and glutamatergic neurons in transgenic nematodes. Additionally, neurotransmitter levels were markedly decreased, and the expression of key neurofunctional genes (e.g., mod-1, tph-1, and unc-46) was significantly dysregulated. Collectively, these findings demonstrate that PS microplastics potentiate the neurotoxic effects of Tl by disrupting multiple neurotransmission pathways, underscoring the ecological risks associated with the co-occurrence of MPs and heavy metals in the environment.

Microplastics are pervasive environmental contaminants found across diverse ecosystems, inducing toxic effects in a wide range of organisms. However, the neurotoxic effects of thermally degraded polystyrene (T-PS) and its underlying mechanisms remain poorly unexplored. In this study, Caenorhabditis elegans was exposed to environmentally relevant concentrations of T-PS (0.1-100 μg/L), and endpoints including locomotion behaviors, neuronal development, neurotransmitter levels, and gene expression were assessed. Significant alterations in morphology, crystallinity, elemental composition, and functional groups were observed in T-PS compared to virgin polystyrene (V-PS), indicating that thermal degradation modifies the physicochemical properties of V-PS. Exposure to 10-100 μg/L T-PS resulted in a more pronounced decrease in head thrashes, body bends, forward turns, and backward turns compared to V-PS. In transgenic nematodes, T-PS exposure significantly impacted fluorescence intensity and the percentage of worms exhibiting neurodegeneration in serotonergic, cholinergic, dopaminergic, and γ-aminobutyric acid (GABA) neurons. Correspondingly, marked reductions were observed in the levels of dopamine, serotonin, GABA, and choline neurotransmitters, alongside significant declines in neurotransmitter-related gene expression (e.g., dat-1, tph-1, unc-30, and cha-1). Pearson's correlation analysis revealed a significant positive association between these genes and locomotion behaviors. Furthermore, the absence of locomotion behavior impairment in dat-1 (ok157), tph-1 (mg280), unc-30 (e191), and cha-1 (e1152) mutants highlights the pivotal roles of these genes in mediating T-PS-induced neurotoxicity in C. elegans. This study enhances our understanding of the neurotoxic mechanisms of T-PS at environmental concentrations, providing valuable insights into its potential environmental health risks.

Benzotriazole UV stabilizer-329 (UV-329), a novel stabilizer used in polymers, has been detected in various environmental matrices and organisms, where it exerts toxic effects. However, the neurotoxic effects and underlying mechanisms of UV-329 remain largely unexplored. In this study, Caenorhabditis elegans was used as a model organism to investigate the neurotoxicity of UV-329 at environmental concentrations (0.1-100 μg/L) following a 24-h exposure. The accumulation of UV-329 in nematodes was confirmed through quantitative analysis. Acute exposure to UV-329 at concentrations of 10-100 μg/L significantly impaired locomotive behaviors, suggesting potential neurotoxicity in C. elegans. Significant alterations in fluorescence intensity and the neurodegeneration of dopaminergic, serotonergic, and GABAergic neurons were also observed. Additionally, exposure to UV-329 significantly reduced levels of dopamine, serotonin, and γ-aminobutyric acid (GABA), accompanied by a marked decrease in the expression of dop-3, mod-1, and unc-25 genes. The strong binding affinity of UV-329 to DOP-3, MOD-1, and UNC-25 proteins was also demonstrated. Neurotoxic effects on locomotion behavior were absent in dop-3(vs106), mod-1(ok103), and unc-25(e156) mutants. Thus, UV-329 exerts neurotoxicity by disrupting dopamine, serotonin, and GABA neurotransmission, with dop-3, mod-1, and unc-25 playing pivotal roles in mediating this neurotoxicity. This study enhances our understanding of neurotoxic mechanisms of UV-329 at environmental concentrations, providing valuable insights into its environmental health risks.

Triphenyl phosphate (TPHP) is widely used as a flame retardant and plasticizer in consumer products and is frequently detected in the environment. TPHP competitively binds to estrogen receptors, exhibiting both estrogenic and anti-estrogenic effects, leading to ongoing debate about its role. This study demonstrates that TPHP shows a higher affinity for the estrogen receptor NHR-14 in Caenorhabditis elegans (C. elegans) compared to the typical estrogen estradiol (E2) and the estrogen antagonist 4-hydroxytamoxifen (4-HT). The study also examines the production, distribution, and transport of the estrogen biomarker Vitellogenin family member 2 (VIT-2) following exposure to TPHP, E2, and 4-HT. Environmentally-relevant concentrations of TPHP significantly increased VIT-2 transcription and protein expression levels in C. elegans during early pregnancy, similar to the effects observed with E2. However, during peak pregnancy, TPHP exposure led to abnormal accumulation of VIT-2, primarily due to an increase in the Gibbs Free Energy of the VIT-2_RME-2 complex, which reduced their affinity and subsequently impaired the normal transport of VIT-2. These findings provide novel insights into the toxic mechanisms of TPHP in oviparous animals, highlighting its broader environmental impacts and emphasizing the urgency for further research and regulatory actions to mitigate its risks.

Microplastics (MPs), particularly microbeads used in shower gel products, have garnered increasing attention due to their widespread presence in the aquatic environment and associated ecological risks. However, the photoaging behavior and toxicity of shower gel-derived microbeads (SGMBs) remain poorly understood. In this study, we investigated the aging characteristics and photoaging-induced neurotoxicity of microbeads isolated from shower gel products. The results demonstrated that the physicochemical properties of SGMBs changed progressively during photooxidation, accompanied by the generation of three environmentally persistent free radicals (alkyl, alkoxyl, and peroxyl radicals) and three reactive oxygen species (•OH, O2•-, and 1O2). Toxicity assays using Caenorhabditis elegans as a model organism revealed a significant decline in nematode motility upon exposure to 60-day photoaged SGMBs (SGMB-60), compared to those exposed to unaged SGMBs. Moreover, SGMB-60 exposure impaired serotonergic, glutamatergic, and GABAergic neurons, reduced the levels of serotonin, glutamate, and γ-aminobutyric acid (GABA), and downregulated the expression of neurotransmission-related genes mod-1, eat-4, unc-30, unc-46, and unc-49. Correlation analyses indicated that the expression of mod-1, eat-4, unc-30, and unc-49 was significantly associated with neurotransmitter levels and locomotor behaviors, underscoring the critical roles of these genes in SGMB-60-induced neurotoxicity. This study advances our understanding of the photoaging behavior and neurotoxic potential of microbeads in natural environments.

Tetrabromobisphenol-A-bis(2,3-dibromopropyl ether) (TBBPA-BDBPE), a novel additive brominated flame retardant, is being developed for use in polyolefin and copolymers. Despite its emerging application, the neurotoxicity and mechanisms of action of TBBPA-BDBPE remain unexplored. Caenorhabditis elegans was utilized as the model organism to study the neurotoxic effects of TBBPA-BDBPE across environmental concentrations ranging from 0 to 100 mu g/L. This investigation focused on various toxicological endpoints such as locomotive behavior, neuronal injury, neurotransmitter transmission, and the regulation of nervous system-related gene expression. Acute exposure to TBBPA-BDBPE at concentrations of 10-100 mu g/L significantly impaired nematode movement, indicating potential neurotoxicity. In transgenic nematodes, this exposure also caused damage to gamma-aminobutyric acid (GABAergic) and serotonergic neurons, along with notable changes in the levels of GABAergic and serotonergic neurotransmitters. Further molecular studies indicated alterations in neurotransmission-related genes (cat-4, mod-1, unc-25, and unc-47). Molecular docking analysis confirmed the binding affinity of TBBPA-BDBPE to key neurotransmission proteins-CAT-4, MOD-1, UNC-25, and UNC-47. These findings demonstrate that TBBPA-BDBPE exerts neurotoxic effects by impacting GABAergic and serotonergic neurotransmission in nematodes. This study provides new insights into the potential environmental risks of TBBPA-BDBPE.

Tire wear particles (TWP) are a prevalent form of microplastics (MPs) extensively distributed in the environment, raising concerns about their environmental behaviors and risks. However, knowledge regarding the properties and toxicity of these particles at environmentally relevant concentrations, specifically regarding the role of environmentally persistent free radicals (EPFRs) generated during TWP photoaging, remains limited. In this study, the evolution of EPFRs on TWP under different photoaging times and their adverse effects on Caenorhabditis elegans were systematically investigated. The photoaging process primarily resulted in the formation of EPFRs and reactive oxygen species (O2•−, ⋅OH, and 1O2), altering the physicochemical properties of TWP. The exposure of nematodes to 100 μg/L of TWP-50 (TWP with a photoaging time of 50 d) led to a significant decrease in locomotory behaviors (e.g., head thrashes, body bends, and wavelength) and neurotransmitter contents (e.g., dopamine, glutamate, and serotonin). Similarly, the expression of neurotransmission-related genes was reduced in nematodes exposed to TWP-50. Furthermore, the addition of free-radical inhibitors significantly suppressed TWP-induced neurotoxicity. Notably, correlation analysis revealed a significantly negative correlation between EPFRs levels and the locomotory behaviors and neurotransmitter contents of nematodes. Thus, it was concluded that EPFRs on photoaged TWP induce neurotoxicity by affecting neurotransmission. These findings elucidate the toxicity effects and mechanisms of EPFRs, emphasizing the importance of considering their contributions when evaluating the environmental risks associated with TWP.

Microplastics (MPs) are ubiquitous environmental contaminants that exert multiple toxicological effects. Current studies have mainly focused on modeled or unaged MPs, which lack environmental relevance. The generation and toxicity of environmentally persistent free radicals (EPFRs) on photoaging polystyrene (PS) have not been well studied, and the role of EPFRs on the toxic effects of photoaged PS is easily ignored. Photoaging primarily produces EPFRs, followed by an increase in reactive oxygen species (ROS) content and oxidative potential, which alter the physicochemical properties of photoaged PS. The mean lifespan and lipofuscin content were significantly altered after acute exposure to photoaged PS for 45 d (PS-45) and 60 d (PS-60) in Caenorhabditis elegans. Intestinal ROS and gst-4::GFP expression were enhanced, concomitant with the upregulation of associated genes. Treatment with N-acetyl-L-cysteine by radical quenching test significantly decreased EPFRs levels on the aged PS and inhibited the acceleration of the aging and oxidative stress response in nematodes. Pearson’s correlation analysis also indicated that the EPFRs levels were significantly associated with these factors. Thus, the EPFRs generated on photoaged PS contribute to the acceleration of aging by oxidative stress. This study provides new insights into the potential toxicity and highlights the need to consider the role of EPFRs in the toxicity assessment of photoaged PS.

Sediment is the ultimate sink of environmental pollutants. A total of 128 surface sediment samples were collected from 8 rivers and 3 reservoirs in Maoming City, Guangdong Province. This study assessed the content and distribution of brominated flame retardants in sediments. The acute toxicity effects of tetrabromobisphenol A (TBBPA) and hexabromocyclododecane (HBCDs) in sediments were evaluated using Caenorhabditis elegans as model organisms. The concentration of TBBPA in sediments ranged from not detected (ND) to 12.59 pg/kg and was mainly distributed in the central area, which was affected by the emission of TBBPA from residential and factory. The concentration of HBCDs ranged from ND to 6.31 pg/kg, and the diastereoisomer distribution was consistent, showing a trend close to the South China Sea. The composition pattem of HBCDs in the surface sediments from rivers were 41.73%62.33%, 7.89%-25.54%, and 18.76%-40.65% for a-, /3-, and y-HBCD, respectively, and in the sediments from reservoirs were 26.15%-45.52%, 7.44%-19.23%, and 47.04%-61.89% for a-, /3-, and y-HBCD, respectively. When the sum of concentrations of TBBPA and HBCD in sediments were above high levels, reactive oxygen species in nematodes significantly increased, resulting in an oxidative stress response. Intestinal permeability was also enhanced, causing intestinal damage. In addition, in terms of this study, TBBPA had a greater impact on biotoxicity compared to HBCDs, and more attention should be paid to the toxic effects of the river ecosystem organisms in Maoming City, Guangdong Province. This study can complement the pollution database in the study area and provide basic data for pollution control. (c) 2024 The Research Center for Eco-Environmental Sciences, Chinese Academy of

Nanopolystyrene (NPS), a frequently employed nanoplastic, is an emerging environmental contaminant known to cause neurotoxicity in various organisms. However, the potential for transgenerational neurotoxic effects, especially from photoaged NPS (P-NPS), remains underexplored. This study investigated the aging of virgin NPS (V-NPS) under a xenon lamp to simulate natural sunlight exposure, which altered the physicochemical characteristics of the NPS. The parental generation (P0) of Caenorhabditis elegans was exposed to environmental concentrations (0.1-100 mu g/L) of V-NPS and P-NPS, with subsequent offspring (F1-F4 generations) cultured under NPS-free conditions. Exposure to 100 mu g/L P-NPS resulted in more pronounced deterioration in locomotion behavior in the P0 generation compared to V-NPS; this deterioration persisted into the F1-F2 generations but returned to normal in the F3-F4 generations. Additionally, maternal exposure to P-NPS damaged dopaminergic, glutamatergic, and serotonergic neurons in subsequent generations. Correspondingly, there was a significant decrease in the levels of dopamine, glutamate, and serotonin, associated with reduced expression of neurotransmission-related genes dat-1, eat-4, and tph-1 in the P0 and F1-F2 generations. Further analysis showed that the effects of P-NPS on locomotion behavior were absent in subsequent generations of eat-4(ad572), tph-1(mg280), and dat-1(ok157) mutants, highlighting the pivotal roles of these genes in mediating P-NPS-induced transgenerational neurotoxicity. These findings emphasize the crucial role of neurotransmission in the transgenerational effects of P-NPS on locomotion behavior, providing new insights into the environmental risks associated with exposure to photoaged nanoplastics.

Although polystyrene microplastics (PS-MPs) could induce toxic effects on environmental organisms, the toxicity of aged PS-MPs with H2O2 on soil organisms remains unclear. Our study utilized Caenorhabditis elegans as model organism to examine the reproductive toxicity of pristine PS-MPs (pPS-MPs) and aged PS-MPs (aPS-MPs) at environmentally relevant concentrations (0.1–100 μg/L). Acute exposure to aPS-MPs could induce greater reproductive impairment compared to pPS-MPs, as evidenced by changes in brood size and egg release. Assessment of gonad development using the number of mitotic cells, length of gonad arm, and relative area of gonad arm as parameters revealed a high reproductive toxicity caused by aPS-MPs exposure. Furthermore, aPS-MPs exposure promoted substantial germline apoptosis. Additionally, exposure to aPS-MPs (100 μg/L) markedly altered the expression of DNA damage-induced apoptosis-related genes (e.g., egl-1, cep-1, clk-2, ced-3, -4, and -9). Alterations in germline apoptosis caused by aPS-MPs were observed in mutants of cep-1, hus-1, egl-1, ced-3, -4, and -9. Consequently, the augmentation of reproductive toxicity resulting from aPS-MPs exposure was attributed to DNA damage-triggered cellular apoptosis. Additionally, the EGL-1-CEP-1-HUS-1-CED-3-CED-4-CED-9 signaling pathway was identified as a key regulator of germline apoptosis in nematodes. Our study provides insights into potential environmental risk of aPS-MPs with H2O2 on environmental organisms.

Microplastics (MPs) are emerging pollutants widely distributed in the environment, inducing toxic effects in various organisms. However, the neurotoxicity and underlying mechanisms of simulated sunlight-aged MPs have rarely been investigated. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant concentrations (0, 0.1, 1, 10, and 100 μg/L) of virgin polystyrene (V-PS) and aged polystyrene (A-PS) for 120 hpf to evaluate the neurotoxicity. The results demonstrated that simulated sunlight irradiation altered the physicochemical properties (morphology, functional groups, and chemical composition) of V-PS. Exposure to A-PS causes greater toxicity on locomotor ability in larval zebrafish than V-PS. Motor neuron development was disrupted by transgenic (hb9-GFP) zebrafish larvae exposed to A-PS, with significant alterations in neurotransmitter levels (ACh, DA, 5-HT, and GABA) and enzyme activity (AChE, ChAT, and ChE). Further investigation found that exposure to A-PS had a significantly impact on the expression of neurotransmission and neurodevelopment-related genes in zebrafish. These findings suggest that A-PS induces neurotoxicity by its effects on neurotransmission and neurodevelopment. This study highlights the neurotoxic effects and mechanisms of simulated sunlight irradiation of MPs, providing new insights for assessing the ecological risks of photoaged MPs in the environment.

Tetrachlorobisphenol A (TCBPA) has been used as an alternative flame retardant in various fields. However, the long-term effects of TCBPA on the nervous system remain unclear. Thus, Caenorhabditis elegans (L4 larvae) were selected as a model animal to investigate the neurotoxic effects and underlying mechanisms after 10 d of TCBPA exposure. Exposure to TCBPA (0.01–100 μg/L) decreased locomotive behavior in a concentration-dependent manner. In addition, reactive oxygen species (ROS) formation and lipofuscin accumulation were significantly increased, and the expression of sod-3 was upregulated in the exposed nematodes, indicating that TCBPA exposure induced oxidative damage. Furthermore, 100 μg/L TCBPA exposure caused a reduction in dopamine and serotonin levels, and damage in dopaminergic and serotoninergic neurons, which was further confirmed by the downregulated expression of related genes (e.g., dop-1, dop-3, cat-1, and mod-1). Molecular docking analysis demonstrated the potential of TCBPA to bind to the neurotransmitter receptor proteins DOP-1, DOP-3, and MOD-1. These results indicate that chronic exposure to TCBPA induces neurotoxic effects on locomotive behavior, which is associated with oxidative stress and damage to dopaminergic and serotoninergic neurons.

Microplastics, recognized as emerging contaminants, are commonly observed to be charged in the environment, potentially exerting toxic effects on various organisms. However, the transgenerational reproductive toxicity and underlying mechanisms of polystyrene (PS), particularly carboxyl-modified PS (PS-COOH) and amino-modified PS (PS-NH2), remain largely unexplored. In this study, the parental generation (P0) of Caenorhabditis elegans was subjected to environmental concentrations (0.1-100 mu g/L) of PS, PS-COOH, and PS-NH2, with subsequent generations (F1-F4) cultured under normal conditions. Exposure to PS-NH2 at concentrations of 10-100 mu g/L exhibited more pronounced reproductive toxicity compared to PS or PS-COOH, resulting in decreased brood size, egg ejection rate, number of fertilized eggs, and cell corpses per gonad. Similarly, maternal exposure to 100 mu g/L of PS-NH2 induced more severe transgenerational reproductive effects in C. elegans. Significant increases in H3 on lysine 4 dimethylation (H3K4me2) and H3 on lysine 9 trimethylation (H3K9me3) levels were observed in the subsequent generation, concurrent with the transgenerational upregulation of set-30 and met-2 following parental exposure to PS, PS-COOH, and PS-NH2. Correlation analyses revealed significant associations between the expression of these genes with the reproductive ability. Molecular docking studies suggested that PS-NH2 exhibited higher affinity for SET-30 and MET-2. Further analysis demonstrated that transgenerational effects on reproduction were absent in set-30(gk315) and met-2(n4256) mutants, highlighting the pivotal role of set-30 and met-2 in mediating the transgenerational effect. This study provides novel insights into the environmental risks associated with negatively and positively charged microplastics.

Neonicotinoid insecticides (NNIs) are extensively used in agricultural production in China due to their selective neurotoxicity towards target insects. In recent years, the rapid development of agriculture has increased the use and residue of NNIs. Consequently, the sediment environment, serving as the ultimate sink, is significantly impacted by NNIs. Upon release into the environment, NNIs can enter the human body through the food chain, posing potential ecological and human health risks. This study analyzed 79 sediment samples from two major river basins in North and South China, the Liaohe River basin in Liaoning Province and the Jianjiang River basin in Guangdong Province. The content, composition, distribution, and source of eight NNIs were analyzed, and assess the ecological and human health risks of the target compounds in these regions. The results indicated that the average concentration of NNIs in the sediments of the Jianjiang River basin (2.34 μg/kg) is slightly higher than that of the Liaohe River basin (2.32 μg/kg), and the sources of NNIs in the two areas were different, with differences in the sources of NNIs likely attributable to varying types of agricultural production. The risk assessment revealed that the ecotoxicological and public health risks were more pronounced in the Jianjiang River basin compared to the Liaohe River basin, underscoring the critical need for surveillance and management of hazardous substances like NNIs. The insights findings from this study can provide scientific guidance for the risk evaluation and environmental management of NNIs.

The impact of primary metabolites of organophosphate triesters (tri-OPEs), namely, organophosphate diesters (di-OPEs), on the ecology, environment, and humans cannot be ignored. While extensive studies have been conducted on tri-OPEs, research on the environmental occurrence, toxicity, and health risks of di-OPEs is still in the preliminary stage. Understanding the current research status of di-OPEs is crucial for directing future investigations on the production, distribution, and risks associated with environmental organophosphate esters (OPEs). This paper specifically reviews the metabolization process from tri-OPEs to di-OPEs and the occurrence of di-OPEs in environmental media and organisms, proposes typical di-OPEs in different media, and classifies their toxicological and epidemiological findings. Through a comprehensive analysis, six di-OPEs were identified as typical di-OPEs that require prioritized research. These include di-n-butyl phosphate (DNBP), bis(2-butoxyethyl) phosphate (BBOEP), bis(1,3-dichloro-2-propyl) phosphate (BDCIPP), bis(2-chloroethyl) phosphate (BCEP), bis(1-chloro-2-propyl) phosphate (BCIPP), and diphenyl phosphate (DPHP). This review provides new insights for subsequent toxicological studies on these typical di-OPEs, aiming to improve our understanding of their current status and provide guidance and ideas for research on the toxicity and health risks of di-OPEs. Ultimately, this review aims to enhance the risk warning system of environmental OPEs.

Polystyrene nanoplastics (PS-NPs) are emerging environmental contaminants that are ubiquitously detected in various environments and have toxic effects on various organisms. Nevertheless, the transgenerational reproductive toxicity and underlying mechanisms of PS-NPs remain largely unknown, especially for photoaged PS-NPs under ultraviolet irradiation. In this study, only the parental generation (P0) was exposed to virgin and aged PS-NPs at environmentally relevant concentrations (0.1-100 μg/L), and subsequent generations (F1-F4) were cultured under normal conditions. Ultraviolet irradiation induced the generation of environmentally persistent free radicals and reactive oxygen species, which altered the physical and chemical characteristics of PS-NPs. The results of toxicity testing suggested that exposure to aged PS-NPs caused a more severe decrease in brood size, egg ejection rate, number of fertilized eggs, and hatchability than did the virgin PS-NPs in the P0, F1, and F2 generations. Additionally, a single maternal exposure to aged PS-NPs resulted in transgenerational effects on fertility in the F1 and F2 generations. Increased levels of H3K4 and H3K9 methylation were observed in the F1 and F2 generations, which were concomitant with the transgenerational downregulation of the expression of associated genes, such as spr-5, set-17, and met-2. On the basis of correlation analyses, the levels of histone methylation and the expression of these genes were significantly correlated to transgenerational reproductive effects. Further research showed that transgenerational effects on fertility were not observed in spr-5(by134), met-2(n4256), and set-17(n5017) mutants. Overall, maternal exposure to aged PS-NPs induced transgenerational reproductive effects via H3K4 and H3K9 methylation, and the spr-5, met-2, and set-17 genes were involved in the regulation of transgenerational toxicity. This study provides new insights into the potential risks of photoaging PS-NPs in the environment.