Journal of hazardous materials最新文献

Microplastics (MPs) are emerging environmental contaminants, yet their impact on autoimmune diseases such as rheumatoid arthritis (RA) remains unclear. We report that polystyrene microplastics (PS-MPs) are detectable in synovial fluid samples from RA patients and that exposure to 5 μm PS-MPs directly promotes the pathogenic activation of RA fibroblast-like synoviocytes (RA-FLSs), key effector cells in synovial inflammation and joint destruction. High-resolution imaging confirmed PS-MPs internalization into the cytoplasm of RA-FLSs, accompanied by cytoskeletal changes and mitochondrial cristae disruption indicative of intracellular stress. PS-MPs exposure activated NF-κB and MAPK (JNK/p38) signaling and induced the expression of IL-6, IL-8, CCL2, MMP3, MMP9, NAMPT, and TWIST1. These changes coincided with enhanced migration, invasion, and monocyte adhesion via increased VCAM-1 and ICAM-1. In vivo, chronic PS-MPs exposure aggravated inflammation in CFA-induced arthritis, with fluorescent particles accumulating in inflamed synovium. In humanized SCID co-implantation model, PS-MPs-treated RA-FLSs triggered greater cartilage erosion and macrophage infiltration. Importantly, pharmacologic inhibition of NF-κB and p38, as well as treatment with Ginsenoside Compound K (GCK), significantly reduced PS-MPs-induced cytokine production in vitro. Together, these findings demonstrate that MPs can directly activate synovial fibroblasts and aggravate RA pathology. This study identifies MPs as a previously unrecognized environmental cofactor in autoimmune joint disease.

Micro-nanoplastics (MNPs) ubiquitously occurring in various ecosystems can accumulate in the human gastrointestinal tract via multiple exposure routes, and threaten the intestinal homeostasis. However, clarifying whether and how these contaminants cause the physio-toxicity to intestinal probiotics remains elusive. Using Lacticaseibacillus rhamnosus as a case study and an in vitro digestion (IVD) system to simulate MNPs digestion, we found that MNPs inhibit bacterial growth and the synthesis of extracellular polymeric substances (EPS) and lactic acid (LA). This toxicity depended on material composition (polyethylene terephthalate, PET > polystyrene > polyvinyl chloride), was enhanced at the nanoscale, and was exacerbated by high concentrations. Under the strongest inhibitory condition (150.0 nm 250.0 mg/L IVD-treated PET; PET-NPs), scanning electron microscopy reveals that EPS secreted by L. rhamnosus under PET-NPs stimulation binds to the particles and adheres to the bacterial surface, potentially causing physical obstruction and membrane damage. Integrated transcriptomics and metabolomics demonstrated that IVD-treated PET-NPs significantly down-regulated core genes (e.g., galK, log₂FC = -5.40; bglA, log₂FC = -6.58), and reduced metabolite levels in central carbon metabolism pathways (e.g., phosphotransferase system, glycolysis, TCA cycle, pentose phosphate pathway, oxidative phosphorylation), impairing glucose uptake/metabolism and energy generation, and thus limiting precursor supply for EPS and LA synthesis. Although exogenous glucose partially restored function, upstream metabolic damage persisted. The findings indicate that MNPs disrupt the glucose metabolism-product synthesis axis by inhibiting central carbon metabolism, providing clear evidence of MNP-mediated impairment of metabolism and efficacy in probiotics and mechanistic insights into the potential health impacts of MNPs contaminants.

Despite growing evidence regarding the effects of copper hydroxide (Cu(OH)₂) nanopesticides on soil microbes and enzyme activity, its effects on root exudates, microbial communities and enzyme activities at the plant-soil interface remain unclear. This study investigated alterations in enzyme activities, root exudates and bacterial communities in wheat rhizosphere soil treated with a commercial Cu(OH)₂ nanopesticide formulation (NPF), its nanosized active ingredient (AI), or its ionic analog (CuSO₄). At 70 mg/kg Cu, representing short-term use, the changes in enzyme activity were negligible. At 500 mg/kg Cu, representing long-term accumulation, NPF, AI and CuSO₄ increased fluorescein diacetate hydrolase activity, reduced N-acetylglucosaminidase and leucine aminopeptidase activities, and had minimal effects on urease activity. These treatments also affected the root exudation profiles, increasing the excretion of benzoxazinoids and chemoeffectors such as xanthine. Furthermore, microbial diversity decreased, whereas the relative abundance of metal-tolerant and nitrogen-cycling bacteria, including Brevundimonas and Cupriavidus, increased. Correlation analysis suggested that the modified exudation patterns under Cu(OH)₂ nanopesticide exposure may facilitate the recruitment of these bacteria, which may impact soil enzyme activity. Notably, in the NPF treatment, this response was predominantly triggered by the nanosized Cu(OH)₂. These findings highlight the potential long-term ecological effects of Cu(OH)₂ nanopesticides at the soil-plant interface.

Disinfection byproducts (DBPs) inevitably form during municipal wastewater disinfection, posing potential threats to human and ecological health. While UV-based advanced oxidation/reduction processes (UV-AOPs/ARPs) show promise in eliminating DBP precursors, their efficacy and mechanisms for controlling both known and unknown DBPs remain unclear. This study systemically investigated dissolved organic matter (DOM) transformation and DBP mitigation during pre-treatments of actual municipal wastewater using UV, UV/Peroxydisulfate (UV/PS), UV/H₂O₂, and UV/Sulfite. Combining spectroscopy, chromatography, and Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR-MS) analyses, the results demonstrated that UV/PS and UV/H₂O₂ were more effective than UV/Sulfite at degrading aromatic and fluorescent compounds. All pre-treatments significantly reduced total organic chlorine and known DBPs versus direct chlorination, with UV/Sulfite achieving the highest reduction (80.42% and 60.98%). Unknown DBP molecules decreased by 31.54-53.04% (UV < UV/Sulfite < UV/PS < UV/H₂O₂). Specifically, UV/PS and UV/H₂O₂ preferentially controlled CHOSCl and CHONCl compounds, and 1Cl-DBPs, whereas UV/Sulfite excelled at reducing multi-chlorinated DBPs. Additionally, all pre-treatments reduced the calculated cytotoxicity of known DBPs by 49.89-81.25%, most notably for UV/Sulfite. These findings demonstrate the effectiveness of UV-AOPs/ARPs for comprehensive DBP control and provide practical guidance for selecting an optimal pre-treatment strategy based on target DBP profiles in wastewater applications.

The practical application of hydrogel-based polymer membranes in separating emulsified oily wastewater is hindered by their dynamic interfacial instability and insufficient inherent self-cleaning capacity. Herein, the polyvinyl alcohol-tannic acid (PVA-TA) hydrogel decorated polyacrylonitrile (PAN) nanofiber composite membrane with super-wetting and photothermal-catalytic self-cleaning features was constructed via hydrogen bond crosslinking and nano-reinforcement of thorn ball-like Bi₁₉Br₃S₂₇-PDA-Bi₄O₅Br₂ core@double-shell nanohybrid (BB@PAN). The oil repellence test, density functional theory calculation, and molecular dynamics simulation verified the super-wettable and ultra-low oil adhesion behavior of BB@PAN composite membrane, resulting in highly efficient separation of oil-in-water emulsions (Flux: 1943-2626 L m^-2 h^-1, oil rejection rate: 99.19-99.57 %). Owing to the nano-enhancement and multiple hydrogen bonds, the BB@PAN membrane retained its structural integrity and separation stability under extreme conditions. The broad-spectrum response and high light absorption efficiency of 3D core@double-shell structure (BOB-PDA-BBS) endowed the membrane with efficient photothermal conversion (temperature reached 62.56 °C within 24 min), enabling rapid volatilization of adhered light oils and effectively preventing a decline in permeation flux. With the support of PDA-mediated electron transfer bridge, the BB@PAN composite membrane achieved outstanding photocatalytic self-cleaning efficiency, as evidenced by its high degradation rate for various dyes. Therefore, the photothermal-catalytic double-mode self-cleaning mechanism tremendously addresses the complicated membrane fouling issues caused by oils and organic pollutants.

The Atrato River basin in western Colombia, one of the most biodiverse regions globally, faces severe mercury (Hg) contamination from artisanal gold mining. This study assessed the hematological effects of Hg exposure in 601 residents (aged 15-89 years) from four localities with different exposure levels. Blood mercury concentrations (HgB) were used to classify participants into high (HHgB >5.0 µg/L; n = 507) and low (LHgB <5.0 µg/L; n = 94) exposure groups. Alarmingly, the median HgB was 14.95 µg/L, and 84.3 % of samples exceeded the safety threshold of 5.0 µg/L. Males consistently showed higher HgB levels than females, particularly in adult and older age groups. Significant hematological alterations were observed in associations with Hg exposure. A considerable proportion of HHgB participants showed anemia: 14.7 % of young males and 21.2 % of young females had low hemoglobin; 6.9 % of adult males and 19.1 % of adult females had reduced hematocrit. Gender- and age-based differences were detected in multiple hematological parameters (HGB, HCT, RBC, MCHC, LYMPH, and PLT) measured using an Abbott Cell-Dyn Sapphire Analyzer, showing distinct patterns between HHgB and LHgB groups. Positive correlations were found between HgB and HGB or MCV in young males, and between HgB and neutrophils in young females with neutropenia, suggesting Hg-related disruption of red and white blood cell profiles. Comparisons between exposure groups also revealed differences in basophils, monocytes, and lymphocytes, especially among adults and olders. Despite regulations banning mercury use, continued exposure remains a major public health concern. These findings highlight the urgent need for targeted policies to strengthen enforcement of mercury regulations, increase monitoring, and implement community-based health interventions in gold mining regions.

Phthalate esters (PAEs) are typically released from agricultural plastic films and veterinary antibiotics introduced through livestock manure. They often accumulate in agricultural soils, posing complex ecological risks and severe biological effects that are not yet fully understood. Therefore, this study investigated the ecotoxicity and risks of di(2-ethylhexyl) phthalate (DEHP), sulfadiazine (SDZ), and their co-exposure on earthworms. DEHP, SDZ, and their co-exposure was found to significantly impair earthworm growth and reproduction, induced oxidative stress, and altered the expression of functional genes (tctp, ann, sod, cat, hsp70, er). Both DEHP and SDZ strongly bound to key earthworm proteins (SOD and TCTP), further supporting the evidence of oxidative stress and adverse effects on growth and development. Risk assessment revealed that DEHP exacerbated the reproductive and oxidative stress compared to SDZ and the co-exposure. Furthermore, histopathological and flow cytometric results suggested antagonistic interactions between DEHP and SDZ during co-exposure. Transcriptomics data demonstrated that SDZ activated pathways related to oxidative stress repair (peroxisome pathways) and detoxification (glutathione metabolism) in earthworms, which explains the relatively lower toxicity of co-exposure. Overall, these findings provide multi-level insights into the antagonistic effects of compound pollution in soil ecosystems and support the ecological risk assessment of PAEs and antibiotics.

Cylindrospermopsin (CYN) is a toxic substance produced by cyanobacteria. It has attracted much attention due to its widespread global distribution, bioaccumulation and multi organ toxicity. This study aims to explore the negative effects of environmentally relevant concentrations (0.5-2000 μg/L) of CYN using different life stages of zebrafish. We found that CYN exposure decreased the spontaneous movement of embryos, reduced the swimming distance and average speed of larvae post 6-days exposure, and interfered with the courtship performance of adult fish after 14 days exposure with effective concentration of 100 and 0.5 μg/L respectively. These behavioral changes were companied by slowed embryonic heart rate, decreased body length in hatched larvae and reduced spawning, fertilization rates, abnormal level of sex hormone in adults. Further analysis indicated a high association between inhibited courtship behaviors and reproductive effects induced by CYN. Transcriptomic analysis of zebrafish larvae showed that genes related to heart development, cytoskeletal structure in muscle cells, and energy metabolism were significantly altered after CYN exposure. These transcriptional changes are consistent with the observed phenotypic symptoms. These findings offer a comprehensive understanding of the toxic effects of CYN exposure on zebrafish from a behavioral perspective.

Acrolein is a common environmental and metabolic toxicant, and natural products that counteract its toxicity can benefit human health. This review interprets the effects of 34 miRNAs and 33 targets involved in acrolein toxicity and explores the acrolein-counteracting functions of 31 natural products. Since the natural products, miRNAs, and targets involved in acrolein toxicity have yet to be systematically evaluated, their integrated relationships are examined via the target-target interaction bioinformatics tool STRING using information retrieved from Google Scholar. Moreover, the interplay between these natural products and miRNAs is explored in detail and integrated into the STRING target network, with 169 target-target interactions. Overall, this review presents a novel natural-product-miRNA-target axis against acrolein toxicity. It sheds light on a number of viable research directions for understanding the effects of acrolein toxicity, as well as the molecular mechanisms underlying its alleviation, via a systematic analysis of natural products, miRNAs, and target interactions.

This study provides a global review of per- and polyfluoroalkyl substances (PFAS) occurrence in industrial wastewater from six key industrial sectors and critically evaluates the performance of currently employed treatment processes for removing PFAS from wastewater. The analysis incorporates publicly available data (2006.11-2025.02) from 205 industrial sites across Asia, Europe, and North America. The dataset includes 1635 concentration records from targeted analysis (77 PFAS) and 137 records from non-targeted analysis (31 PFAS). The results revealed pronounced sectoral clustering in terms of data availability: fluorochemical, electronics, textile, and electroplating wastewater data accounted for over 85 % of the dataset, while PFAS data remaining were limited for pharmaceuticals and food processing. PFAS concentrations spanned ∼12 orders of magnitude in industrial wastewater (2.1 ×10^-3 to 1.7 ×10⁹ ng/L). Fluorochemical wastewater exhibited the highest diversity (73 PFAS), dominated by short-chain and emerging PFAS. Electronics industry wastewater showed a shift toward short- and ultrashort-chain PFAS, while textile wastewater featured overall lower PFAS concentrations but was enriched in long-chain PFAS and ether-based alternatives. Electroplating effluents contained elevated levels of perfluorooctane sulfonate (PFOS) and its replacement (perfluoro (2-(6-chlorohexyl) oxy) ethanesulfonic acid and 6:2 fluorotelomer sulfonic acid). Analysis of 734 PFAS data records from 21 full-scale industrial wastewater treatment plants (WWTPs) showed that advanced processes such as adsorption, membrane technology, and the Fenton process achieved removal rates exceeding 90 % for long-chain PFAS (e.g., PFOS), which is substantially higher than the < 50 % removal typically observed for traditional processes. This study highlights the complexity and persistence of industrial PFAS pollution, calling for enhanced monitoring of PFAS and their precursors, development of effective and sustainable treatment technologies, and implementation of life-cycle-based regulatory frameworks to reduce environmental and health risks.