Rhizosphere processes strongly regulate antimony (Sb) bioavailability and root uptake in paddy soils, but whether organic nitrogen substitution induces divergent Sb transformation pathways across rhizosphere remains unclear. Here, by separating bulk soil, rhizosphere soil, and root iron plaque, we identified a soil-rhizosphere-plaque continuum that determines Sb mobilization, retention, and root uptake under organic nitrogen substitution. Organic nitrogen substitution exerted contrasting, rhizosphere-dependent effects on bioavailable Sb fractions, including non-specifically adsorbed Sb and specifically adsorbed Sb. These fractions decreased in bulk soil by 5.07-26.79% via humic acid complexation and sulfide precipitation, but increased in the rhizosphere by up to 31.45% through competitive adsorption by root-derived low-molecular-weight organic acids, phosphate, and dissolved organic matter. At the root surface, organic nitrogen substitution markedly promoted iron plaque formation by 32.41-75.63%, with amorphous iron (hydr)oxides dominating Sb retention and accounting for 86.31-89.08% of plaque-associated Sb. Iron plaque significantly reduced shoot Sb content by intercepting rhizosphere-mobilized Sb, leading to a 24.48-41.02% decrease in shoot Sb content. Finally, we propose a compartment-specific mechanism of Sb fate in which organic nitrogen substitution drives bulk-soil stabilization, rhizosphere mobilization, and root-surface interception of Sb, supporting organic nitrogen management as a strategy to mitigate rice Sb accumulation and sustain rice growth. SYNOPSIS: By distinguishing the rhizosphere from bulk soil, this study reveals that organic nitrogen substitution creates opposing effects on antimony bioavailability across soil compartments, while root iron plaque limits antimony uptake by rice. These findings advance our understanding of antimony cycling in paddy soils and inform safer rice production strategies.

Spatial exposure modelling for hazardous mineral fibres is constrained by sparse, biased datasets and poorly understood exposure pathways. This study applies six regression frameworks (OLS, ridge, LASSO, geographically weighted regression (GWR), random forest, and XGBoost) to two contrasting datasets: airborne asbestos in El Dorado Hills, California (n = 238) and mordenite in Ngakuru, New Zealand (n = 22). Performance was assessed using cross-validated R² and RMSE, with predictor importance scored across methods. In El Dorado Hills, cross-validated performance was moderate (R² = 0.25-0.36), with tree-based ensembles performing best; activity surfaces, canopy cover, and disturbance proximity were dominant predictors. In Ngakuru, penalised linear models performed strongest (R² = 0.83-0.87), driven by rock sample concentration and soil type, though high in-sample fit indicates overfitting risk given the small sample size. GWR was unstable, producing negative cross-validated R² in El Dorado Hills and in Ngakuru fixed-predictor models. Model complexity did not improve predictive performance at either site; source geology, land use, and land cover formed a transferable predictor framework, though dominant predictors differed by site. These findings indicate that targeted sampling and in-situ predictor measurement will advance exposure modelling for hazardous mineral fibres more than increased model complexity.

The toxicity of Tire and Road Wear Particles (TRWP) is mainly linked to organic additives and their transformation products. This study used a dual approach: controlled lab experiments on root uptake in clover, and paired soil-plant sampling from roadside environments, to assess contamination patterns and exposure routes. In soils spiked with 1% tire wear particles, clover roots absorbed tire-related additives and translocated them to leaves, with total concentrations of 15 additives reaching 621 ± 209 ng/g d.w. Roadside soils and plants were also significantly impacted, with concentrations declining exponentially with distance from the road-ranging from 72 to 0.7 ng/g d.w in soils and 777-73 ng/g d.w in plants between 1 m and 10 m. Notably, in pot experiments soil concentrations exceeded plant concentrations, whereas at roadside sites, plants showed much higher concentrations than soil. This contrast suggests that atmospheric deposition, rather than root uptake, is the dominant pathway by which tire-derived additives contaminate plants in real-world conditions. These findings offer key insights into the widespread occurrence of tire-derived compounds in terrestrial environments near roads, and underscore the need for further research to accurately assess the environmental and human health risks posed by this contamination.

Organophosphate esters (OPEs) frequently co-occur in human exposure, yet their combined hazards cannot be reliably inferred from single-compound toxicity. How individual OPEs reshape non-additive effects across compositions and effect levels remains unclear. Here, we investigated interaction patterns and associated biological responses of representative OPE mixtures, including tributyl phosphate (TNBP), triphenyl phosphate (TPHP), and tris(1,3-dichloro-2-propyl) phosphate (TDCIPP), using human keratinocytes as a dermal exposure model. Combination index (CI) analysis revealed composition- and effect-level-dependent interactions. Ternary mixtures exhibited distinct composition-dependent CI-Fa trajectories, with some compositions trending toward additivity at higher effect levels, whereas TPHP-rich mixtures showed progressively stronger synergism. Binary mixtures showed pair-dependent interactions, with TPHP-TDCIPP and TNBP-TDCIPP exhibiting contrasting interaction modes. At total nominal molar concentrations of 0.1, 1, and 10 μM for the 1:1:1 ternary mixture, co-exposure modestly increased HaCaT monolayer permeability, reaching statistical significance at 10 μM, and altered differentiation-related gene expression, revealing barrier-associated effects. Untargeted metabolomics of individual and mixture exposures further revealed distinct lipid remodeling patterns, including interaction-associated differences in glycerophospholipid responses. Collectively, OPE mixture hazards depend not only on individual toxicity but also on the capacity of specific components to modify combined effects, supporting improved mixture hazard characterization and prioritization of interaction-modifying contaminants.

Chemical insecticides can persist at sublethal concentrations after field application, posing reproductive risks to natural enemies. However, the mechanisms underlying insecticide-induced male reproductive toxicity remain poorly defined. Here, sublethal lambda-cyhalothrin (λ-Cy) exposure during the second larval instar severely impaired male reproduction in the lacewing Chrysoperla sinica, causing testicular enlargement, disordered spermatogenesis, accessory-gland atrophy, and reduced sperm production. Consequently, mating treated males with untreated females decreased female fecundity and egg hatchability by 42.9% and 35.0%, respectively. Mechanistically, λ-Cy induced acute larval Ca[2 +] overload, upregulating the Na[+]/Ca[2+] exchanger NCX3. Compensatory NCX3 overexpression drove excessive Ca[2+] extrusion, leading to Ca[2+] depletion in the corpora allata and testes during pupal and adult stages. This imbalance suppressed juvenile hormone and 20-hydroxyecdysone biosynthesis via Ca[2+]-CREB signaling. RNA interference, pharmacological assays, dual-luciferase reporter assays, and electrophoretic mobility shift assays validated this cascade. RNAi CsMet or CsEcR phenocopied λ-Cy-induced reproductive defects. These findings identify NCX3-mediated Ca[2+] depletion as a key mechanism of pyrethroid-induced endocrine disruption and male reproductive toxicity.

The intensity and frequency of wildfires have increased worldwide. The health impact of wildfire emitted particulate matter (WFPM) has been considered an emerging field in air pollution research. This review presents the state of toxicological science related to WFPM for the 2005-2025 period. We found 46 peer-reviewed in vitro and in vivo studies, excluding clinical, epidemiological, and ecotoxicological studies. Environmental WFPM collected during active wildfires was used to model exposure in only 42% of in vitro and 27% of in vivo studies. Most in vitro studies investigate effects on the pulmonary system (50%) and on macrophages (17%), with all other biological systems corresponding to 33%. Mechanisms of toxicity focused mostly on inflammatory and stress response, and DNA damage/mutation. Inhalation studies evaluated lung (46%), cardiovascular (15%) and brain (15%) effects, with the remaining 24% addressing reproductive, genetic or immune effects. WFPM induced significant toxicity with distinct mechanisms as a function of concentration, particle-size, biomass type and burning conditions. Knowledge gaps included: lack of a comprehensive physicochemical characterization of WFPM to achieve robust structure-activity conclusions, use of realistic concentrations representing human exposure scenarios, chronic exposure studies, evaluation of systemic effects and toxicokinetic studies, potential synergistic effects with other anthropogenic air pollution sources.

Calcium (Ca) amendments are widely used to restrict cadmium (Cd) accumulation in rice; however, the mechanisms governing competitive adsorption between Ca and Cd in iron plaque (IP) of rice roots remain poorly understood. Here, hydroponic and adsorption experiments using detached roots and goethite (Gt), a simulant for IP, were conducted to investigate these interactions. Results showed that exogenous Ca did not affect IP formation but decreased Cd concentrations in IP, roots, and shoots by 21%-28%, 11%-25%, and 17%-27%, respectively. Detached-root adsorption experiments showed that Ca reduced Cd adsorption in IP by 70% when the Ca: Cd ratio reached 20, with root Cd uptake declining by 50% compared with the Ca-free treatment. Gt experiments introduced competitive mechanisms through a dual-pathway model. First, Ca adsorption shifted the point of zero charge of Gt towards higher pH, weakening electrostatic attraction for Cd. Second, spectroscopic evidence supported that Ca bound to surface hydroxyl groups (Fe-OH) through ligand exchange to form inner-sphere complexes (Fe-O-Ca), competitively occupying surface binding sites. This study not only revealed molecular-scale mechanisms of Ca/Cd competition in roots IP, but also provided new insight into quantitatively estimating Ca detoxification when optimizing Ca compound strategies in Cd-contaminated paddy soils beyond pH effects.

Small fishponds embedded within rural farmland are directly affected by surrounding agricultural activities and may therefore serve as important interfaces for the input, transformation, and redistribution of pesticides. However, the occurrence, transformation-product patterns, and cross-media distribution of parent neonicotinoid insecticides (pNNIs) and their transformation products (TPNNIs) among environmental media in farmland-fishpond systems (FFS) remain poorly understood. In this study, pNNIs and TPNNIs were simultaneously analyzed in farmland soil, fishpond water, and sediment collected from FFS. Results showed that both pNNIs and TPNNIs were detected in all three media. The median concentrations of pNNIs were 66.9 ng/L in fishpond water, 46.2 ng/g in farmland soil, and 0.6 ng/g in sediment, while the corresponding concentrations of TPNNIs were 44.2 ng/L, 2.4 ng/g, and 0.3 ng/g, respectively. The compositional profiles of pNNIs were broadly similar among the three media and were dominated by clothianidin, thiamethoxam, and imidacloprid, whereas the compositional profiles of TPNNIs and TPNNIs/pNNIs ratios differed markedly among media. Environmental factors, including pH and total organic carbon, were significantly associated with residue levels of pNNIs and TPNNIs, relationships between pNNIs and their TPNNIs, and partitioning among media. Ecological risk screening indicated that clothianidin may pose risks to non-target organisms in both soil and water, while imidacloprid may also pose risks in water at some sites.

Catalytic hydrogenation over supported Ru catalysts offers an effective way for perchlorate (ClO4[-]) decomposition in water to Cl[-]; however, the role of catalyst supports in determining catalytic performance remains poorly understood. In this study, Ru catalysts supported on five oxide supports were evaluated for ClO4[-] reduction with H2. Among them, Ru/CeO2 and Ru/ZrO2 showed markedly higher activities than Ru/SiO2, Ru/Al2O3, and Ru/TiO2. The catalytic activity generally correlated with Ru dispersion and the electronic state of Ru. In particular, Ru/ZrO2 contained highly dispersed Ru species and electron-rich Ru sites, both of which contributed to its high activity. In contrast, Ru/CeO2 deviated from this trend. Kinetic analysis revealed that the exceptional activity of Ru/CeO2 originated from enhanced activation of adsorbed ClO4[-] rather than from H2 activation. Systematic variation of the CeO2 source and pre-calcination temperature further showed that spectroscopic features associated with the local Ru-CeO2 interfacial environment correlated with turnover frequency, whereas no single oxygen-defect descriptor alone accounted for the activity variation. These findings highlight the important role of the specific Ru-CeO2 interfacial environment in promoting ClO4[-] activation.

The threat posed by antibiotic contamination to agricultural ecosystems requires effective alleviation strategies. This study characterized the multi-level regulatory network by which Fe3O4 nanoparticles (NPs) restore soybean carbon metabolism under florfenicol stress. In a pot experiment across three growth stages (VE, V1, V2), florfenicol suppressed photosynthetic systems, reducing chlorophyll content by 19-65%, Fv/Fm by 30-56%, and Rubisco activity by 31-36%. Fe3O4-NPs treatment (40-80 mg/kg) reversed these effects, increasing chlorophyll content (up to 88%), enhancing chlorophyll fluorescence parameters (Fv/Fm, Y(II), ETR), and reducing non-photochemical energy dissipation (Y(NO)). Mechanistically, Fe3O4-NPs up-regulated key genes involved in chlorophyll synthesis, photosystem II, Rubisco subunits, sucrose synthesis, and sugar transport; and restored Rubisco, sucrose phosphate synthase, sucrose synthase, and amylase activities. Metabolomic and KEGG analyses revealed enrichment of metabolites in pathways related to core carbon metabolism and defense-related signaling, with potential involvement of hormone signaling pathways in leaves. Fe3O4-NPs restored the accumulation of key nutrients-which serve as cofactors for Rubisco (Mg), glycolytic enzymes (K), electron transport (Cu, Fe), and antioxidant defense (Cu, Zn)-linking nutrient homeostasis to photosynthetic carbon assimilation and energy metabolism. These findings establish a multi-level regulatory framework for Fe3O4-NP-mediated alleviation of antibiotic stress, offering a potential strategy for safeguarding crop productivity in antibiotic-contaminated soils.

The cooking fumes from frying carry highly toxic polycyclic aromatic hydrocarbons (PAHs), which pose a serious threat to human health. This study utilized the stable isotope PAH4-d12 to simulate the migration of PAH4 from frying oil into cooking fumes, and characterized the process through physicochemical analysis of oils, single particle aerosol mass spectrometry, GC-MS, and quantum chemical calculations. The results indicate that the concentration of PAH4-d12 in cooking fumes increases linearly with cooking time, and that it accumulates preferentially in fine particles with an aerodynamic diameter of less than 1.1 μm. The migration of PAH4-d12 increases significantly with the degree of lipid oxidation. The radical-mediated oxidation of unsaturated fatty acids is the key driving force behind PAH4 migration. The abundance of oxygen-containing functional groups on the surface of cooking fume particles further enhances the carrier capacity. Carbonyl compounds are key components responsible for carrying PAH4, their binding to PAH4 is primarily governed by intermolecular van der Waals forces, while the strength of π-π stacking and C-H-π interactions depends on the structure. These findings reveal that lipid oxidation and particle properties jointly regulate the migration of PAHs, and provide insights at molecular level for pollution control.

Tire pyrolysis oil (TPO) has physicochemical properties similar to diesel and can be regarded as a promising alternative fuel for diesel engines. This study employed a suspended-droplet evaporation apparatus to capture the evaporation process of TPO-diesel-blended fuel droplets and investigated the effects of TPO blending ratio and initial droplet volume on the bubble nucleation mechanism and the micro-explosion mode transition. The results show that the evaporation process of the blended fuel droplets can be divided into three stages: fluctuation evaporation, intense micro-explosion, and stable evaporation. Surface pit nucleation is the primary bubble nucleation mode, while raft-interface nucleation serves as a secondary mechanism, together facilitating the initial formation of bubbles within the droplet. As the TPO blending ratio increases, the bubble nucleation mode changes from multi-point nucleation to single-point nucleation, the nucleation location shifts from the droplet surface toward the center, and the maximum micro-explosion intensity increases. The blended fuel with a 20% TPO exhibits the shortest droplet lifetime. Variations in the initial droplet size can not alter the bubble nucleation mode or micro-explosion mode, but can increase the degree of droplet expansion. Increasing the initial droplet size effectively enhanced the micro-explosion intensity, but had no significant effect on droplet lifetime.

Amino acids and peptides in wastewater are key precursors of highly toxic nitrogenous disinfection byproducts (N-DBPs) during chlor(am)ination. The UV/chlor(am)ine processes have been increasingly employed for toxicity control, yet their efficacy against peptide precursors remains poorly understood. This study evaluated the toxicity control of UV/chlor(am)ine on tyrosyl-L-phenylalanine (Tyr-Phe), its monomers (Phe, Tyr), and real secondary effluents. At a UV dose of 1200 mJ·cm[-2], 5 mg-Cl2·L[-1] disinfectant and 4 mg-C·L[-1] precursor, UV/chlorine reduced the cytotoxicity and genotoxicity of Tyr-Phe by 75.7% and 82.8%, respectively (UV/chloramine: 55.5% and 64.4%). Total organic chlorine (TOCl) and Tyr-Phe-derived byproduct counts decreased by > 70% and > 30%, accompanied by a shift toward higher oxidation states and lower aromaticity. Four low molecular weight DBPs (trichloromethane, dichloroacetonitrile, trichloroacetaldehyde, and chloroacetone) and seven identified emerging aromatic DBPs were also significantly reduced. Similar trends were observed for Phe, Tyr, and real secondary effluents. Radical quenching coupled with TOCl measurements indicated that ·OH and ·Cl, individually or together, contribute to the suppression of DBP formation. Collectively, these findings demonstrate that UV/chlor(am)ine effectively controls DBP formation and associated toxicity from aromatic peptides and their monomers in wastewater disinfection.

Freshwater cyanophages has been shown to co-exploit host cellular resources to meet their energy and material requirements, which is in contrast with marine cyanophages that in many cases actively reprogram host metabolism via auxiliary metabolic genes (AMGs). Here, we investigated the infection of Microcystis aeruginosa by the cyanophage LMM01 (previously Ma-LMM01), integrating physiological, proteomic, and metabolomic analyses. Consistent with the previous infection transcriptome analysis, we observed no changes in host protein abundance during viral DNA replication. Metabolome profiling, however, revealed significant phage-induced modulation of M. aeruginosa metabolism. Photosynthetic activity remained largely stable until the major cell lysis event (up to 48 h post infection, hpi) pointing toward the absence of physiological stress during infection. The observed slight photoinhibition and altered electron transport dynamics suggests enhanced cyclic electron flow, potentially sustaining ATP supply for viral replication. Together, the LMM01 infection, characterized by a stable proteome, induced however significant changes in metabolic flux and metabolite pool sizes. This suggests that LMM01 achieves its resource requirement through post-translational modulation with resource co-exploitation and re-allocation rather than transcriptional or translational reprogramming. Such in-depth understanding the cyanophage impact on the physiology of infected population expands the current knowledge of how viruses alter host metabolism in ecologically important cyanobacteria.

T-2 toxin is a widely distributed dietary mycotoxin and a key environmental driver of Kashin-Beck disease (KBD), yet the molecular events linking exposure to cartilage injury remain incompletely defined. We examined the chondrotoxic mechanism of T-2 toxin through a MALAT1/miR-15b-5p/MAP2K3 competing endogenous RNA (ceRNA) axis across cellular, animal and human levels. Rat models of graded T-2 toxin exposure, combined with mRNA and miRNA sequencing identified affected pathways and candidate non-coding RNAs. In C28/I2 human chondrocytes, dual-luciferase and rescue experiments characterized the targeting relationships and functional consequences of the axis. The p38 inhibitor BIRB796 and exogenous insulin were administered to rats, and a 1:1:1 frequency-matched case-control study in a KBD-endemic area assessed clinical relevance. T-2 toxin increased chondrocyte MALAT1, which sponged miR-15b-5p and relieved its repression of MAP2K3, leading to sustained p38 MAPK hyperactivation and concurrent extracellular matrix degradation and glycometabolic reprogramming. p38 inhibition or insulin supplementation attenuated T-2 toxin-induced cartilage degeneration and glucose dysregulation in rats. In humans, elevated serum lactate and peripheral-blood MALAT1 were independently associated with both KBD and osteoarthritis. These findings expand the molecular network underlying T-2 toxin chondrotoxicity and provide candidate biomarkers for the health-risk assessment of mycotoxin exposure and prevention of environment-related osteoarthropathy.