Journal of hazardous materials最新文献

Rhizosphere microbiome are pivotal for plant adaptation to extreme environments. However, the regulatory mechanisms underlying their control of the ecological adaptation of native woody plants in mining areas remain unclear. Here, we integrated metagenomic and transcriptomic analyses to elucidate how the rhizosphere microbiome facilitates Betula luminifera adaptation to antimony (Sb) mining sites. Under sterile conditions, B. luminifera from mining sites prioritized shoot growth, whereas control-origin seedlings favored root development. Microbial inoculation mitigated this growth dichotomy, balancing above- and belowground biomass allocation. Notably, B. luminifera from control sites upregulated antioxidant biosynthesis genes (α- and β-tocopherol pathways), while B. luminifera from mining sites enhanced lignin synthesis under Sb stress. After inoculation with rhizosphere microbiome from the mining-site, genes related to Sb/As resistance (ACR3, arsB/C) and soil nutrient cycle (narG, phnM) were significantly enriched in the rhizosphere of B. luminifera, which were contributed by Proteobacteria and Actinobacteria. Transcriptional profiling revealed that microbial inoculation triggered systemic upregulation of phytohormone-related genes (auxin, cytokinin, abscisic acid), enhancing stress resilience and growth. These findings unveil a synergistic plant-microbe adaptation mechanism in Sb polluted soils in mining sites, highlighting microbial-mediated trait trade-offs and transcriptional plasticity as drivers of ecological success in extreme environments.

Perfluorooctane sulfonate (PFOS), a pervasive environmental contaminant, is ubiquitously detected in water, air, soil, and food chains. Emerging evidence has implicated PFOS in the pathogenesis of cardiovascular diseases, particularly atherosclerosis - the fundamental pathological process underlying diverse cardiovascular and cerebrovascular disorders. A previous study demonstrated that PFOS exacerbates atherosclerosis in apolipoprotein E-deficient (ApoE^-/-) mice through pro-inflammatory M1 macrophage polarization. However, the effects of PFOS on vascular smooth muscle cells (VSMCs) and their contribution to intimal hyperplasia and atherosclerosis remain unexplored. Our in vitro investigations revealed that PFOS potentiates proliferation, migration, and phenotypic switching in primary human aortic smooth muscle cells (HASMCs). Moreover, we also demonstrated that PFOS exposure aggravated neointimal formation in a femoral artery injury model and promoted atherosclerosis. To elucidate the role of VSMCs in these processes in vivo, we established a VSMCs lineage-tracing model utilizing Myh11-Cre/ERT2; R26-tdTomato; ApoE^-/- mice. Following 16 weeks of PFOS exposure, atherosclerotic plaque progression exhibited a positive correlation with intraplaque VSMCs accumulation. RNA sequencing analysis and subsequent validation confirmed PFOS-induced tissue plasminogen activator (tPA) upregulation in VSMCs at both transcriptional and translational levels. Notably, tPA knockdown abrogated PFOS-driven proliferation, migration, and phenotypic switching in HASMCs. Mechanistic studies revealed ERK signaling pathway activation as the primary mediator of PFOS-induced tPA expression. Collectively, these findings provide novel mechanistic insights into how PFOS aggravates intimal hyperplasia and atherosclerosis, highlighting its role in exacerbating cardiovascular pathogenesis. They further suggest that ERK inhibitors may mitigate the detrimental effects of PFOS on the vasculature.

The contamination of groundwater by sulfate (SO₄²⁻) and iron (Fe) in mining regions has become an increasingly critical environmental issue. However, the complex interplay between sulfur and iron biogeochemical cycles under mining disturbances remains poorly constrained. This study employs a novel multi-isotope approach (Sr-Fe-S-O-H) combined with Positive Matrix Factorization (PMF) modeling to unravel the iron mobilization mechanisms coupled with sulfur cycling in groundwater systems of a historic deep coal mining area. Key findings reveal that mining-induced pyrite oxidation serves as the predominant source of both SO₄²⁻ and Fe, whereas sulfate evolution in low-flow zones is governed by gypsum dissolution and cation exchange. Iron transformation occurs through oxidation of aqueous Fe(II) to Fe(III) hydroxides with subsequent pore precipitation, concurrent with Fe(II) resorption. Notably, Mn-Fe oxides (MnO₂/FeOOH) facilitate bacterial disproportionation of sulfur intermediates (BDSI), yielding characteristic oxygen-sulfur isotope fractionation (Δδ³⁴S/Δδ¹⁸O ≈ 0.60). Along hydraulic gradients, bacterial sulfate reduction (BSR) emerges as the dominant process, generating sulfides that reduce Fe(III) hydroxides and synergistically with BDSI drive Fe(II) remobilization. Our results demonstrate that the tripartite coupling of BDSI, BSR, and biotic/abiotic iron reduction collectively regulates iron and sulfur cycling and mobilization of Fe and SO₄. These insights advance our understanding of anthropogenic impacts on subsurface iron-sulfur coupling and provide a scientific basis for developing targeted groundwater remediation strategies in mining-affected aquifers.

Background chloride (Cl^-) can inhibit the degradation of emerging contaminants such as carbamazepine (CBZ) by some peroxides-based advanced oxidation processes. This study was aimed at developing a Cl^-/dithionite (DTN)/NaClO system, leveraging in-situ Cl^- and DTN (S₂O₄^2-) to activate sodium hypochlorite (NaClO), a commonly used disinfectant in water treatment. Compared with the Cl^--free DTN/NaClO system, the presence of Cl^- enhanced the CBZ degradation rate constant by approximately 8-fold (0.4280 min^-1) and reduced dependence on dissolved oxygen. Quenching tests and electron paramagnetic resonance spectroscopy confirmed the presence of both reactive chlorine species (RCS) and reactive oxygen species (ROS) in the system. However, Cl^- selectively amplified RCS formation while minimally affecting ROS generation, establishing the dominance of RCS in CBZ degradation. Computational potential energy surface analysis corroborated the role of RCS as the governing species. Effective CBZ degradation occurred across mildly acidic to weakly alkaline conditions. The low activation energy (Ea = 20.29 kJ·mol^-1) indicated the avoidance of high-energy transition states commonly encountered in the degradation of emerging contaminants. Plausible degradation pathways included hydroxyl substitution, skeletal rearrangement, RCS addition/oxidation, and chloro-hydroxyl synergy. The treatment mitigated CBZ developmental toxicity, mutagenicity, and lethality to Daphnia magna. Based on the concept of "waste treating waste", this work offers a novel strategy leveraging in situ Cl^- for effective contaminant control, particularly in Cl^--rich waters.

Microalgae-based remediation of emerging contaminants (dimethyl phthalate, DMP) represents a promising strategy for green, low-carbon development within a circular economy. However, the limited knowledge of the toxicity mechanisms underlying DMP-induced algal apoptosis has constrained its broader application under high pollutant loads. To address this challenge, microalgae were cultured in DMP-containing media under blue-light illumination, and proteomic analysis was employed to elucidate the molecular mechanisms governing toxicity response and photoregulation. The results showed that exposure to 100 mg/L DMP under blue-light antagonism exerted no significant effect on microalgal growth, whereas 500 mg/L DMP induced significant growth inhibition (58.76 %). The redox imbalance led to increases in antioxidant levels by 2.37-fold (carotenoids), 61.67 % (SOD), and 25.91 % (CAT). Concurrently, high-dose DMP significantly compromised cell membrane integrity (31.80 %) and decreased mitochondrial membrane potential (22.40 %), which was associated with Cytochrome C-mediated activation of downstream caspase cascades, leading to programmed cell death. In contrast, low DMP concentrations promoted carotenoid biosynthesis under blue light to mitigate reactive oxygen species accumulation and circumvent redox disorder-induced cell death. These findings reveal the key regulatory mechanisms of DMP-coupled blue light on the apoptosis and metabolic reprogramming in microalgae and provide a theoretical and practical basis for developing efficient and tunable algal-based bioremediation strategies.

Fine particulate matter is prone to serving as a carrier for toxic air pollutants and can harm health through exposure processes such as inhalation. We analyzed the PM_2.5 concentration at different operation points in the welding workshop, as well as the exposure levels of metal elements and polycyclic aromatic hydrocarbons (PAHs) carried by PM_2.5 to explore the health risks of PAHs and harmful metal elements from the perspective of occupational populations. The results showed that the average PM_2.5 concentrations at the two points exceeded the national secondary air quality standard (75 μg/m³). The contents of Fe and Zn were the highest, both exceeding 10 %. The total PAHs concentration at the manual repair point (MRP)was 14.17 ng/m³, and that at the welding point (WP)was 14.44 ng/m³. The correlation analysis results showed that Ni exposure was associated with elevated blood pressure, Li affected lipid metabolism. BbF and Chr were negatively correlated with red blood cell count. Phe, and BaA were positively correlated with hemoglobin. The incremental lifetime cancer risk (ILCR) of Cr at the WP (2.14 ×10^-4) exceeded the safety threshold, while the carcinogenic risks of other elements such as As and Ni were within the acceptable range (10⁻⁶-10⁻⁴). The hazard quotient (HQ) of all elements was less than 1, and the ILCR (10⁻⁶-10⁻⁴) and HQ (<1) of PAHs exposure at the two points were at a relatively low level. The results provide a scientific basis for the monitoring of welding fumes and reduce occupational hazards caused by welding fume exposure.

This study developed a long-wave ultraviolet (UVA)/nitrite (NO₂^-) system to degrade antibiotics in aquaculture wastewater, using NO₂^- as a treatment agent in line with the "waste-to-treat-waste" approach. It further advanced the understanding of reactive nitrogen species (RNSs)-mediated oxidation by quantifying radical dynamics, assessing transformation product ecotoxicity, and evaluating system performance under varying environmental conditions. The degradation of sulfamethoxazole (SMX), a model antibiotic, was primarily driven by RNSs, with nitric oxide radicals (NO•) emerging as the most impactful species. Steady-state analysis revealed that the RNSs concentration ([RNSs]_SS = 1.79 × 10^-13 M) was significantly higher than that of hydroxyl radical (•OH) ([•OH]_SS = 2.25 × 10^-14 M). Among RNSs, NO• was dominant ([NO•]_SS = 1.51 × 10^-13 M), followed by nitrogen dioxide radicals (NO₂•, [NO₂•]_SS = 2.76 × 10^-14 M) and peroxynitrite (ONOO⁻, [ONOO⁻]_SS = 4.19 × 10^-18 M). RNSs contributed 55.97 % to SMX degradation, surpassing UVA (3.23 %) and •OH (40.80 %). Furthermore, ten transformation products were identified, showing relatively low toxicity and minimal ecological impact. Additionally, the UVA/NO₂⁻ system remained stable across varying temperatures and anion concentrations, making it promising for real-world wastewater treatment. This study establishes a quantified methodology for RNSs, providing critical insights into their kinetic behavior and role in antibiotic degradation.

Organochlorine pesticides (OCPs), notably dichlorodiphenyltrichloroethane (DDT) and hexachlorocyclohexane (HCH) isomers, persist in agricultural soils. This study compared the dissipation dynamics of DDT metabolites and HCH isomers in legacy contaminated and freshly spiked soils. To assess the phytoremediation potential of C4 perennial grass Miscanthus × giganteus (Mxg), dormant rhizomes were planted into contaminated and uncontaminated soils in glasshouse pot experiments. Initial and final DDT and HCH concentrations were measured via headspace solid-phase microextraction gas chromatography-mass spectrometry. In freshly spiked soils, α-HCH showed the highest dissipation (from 98 to 8 µg/kg, 92 %) and β-HCH the lowest (from 9 to 4 µg/kg, 50 %). In legacy soil, δ-HCH had the highest dissipation (from 103.2 to 2.1 µg/kg, 98 %), but β-HCH concentrations increased from 0.7 to 28.5 µg/kg, indicating possible isomerization. DDT transformation products (DDE and DDD) were prominent in legacy soil, but not in the freshly spiked soil. In the contaminated non-plant treatment, ∑HCH and ∑DDT decreased 71 % and 45 %, respectively. The root-to-soil ratio indicated OCP uptake, but these compounds proved highly toxic to this Miscanthus clone. Future research should explore other genotypes in polluted areas with localised amendments like biochar to reduce toxicity, enhance uptake, and stimulate transformations.

Diesel exhaust (DE) entering the environment poses a significant risk to public health, but the molecular mechanisms of DE-induced metabolic disorders remain largely unknown. Here we elucidated the impacts of DE exposure on hepatic lipid metabolism using a range of cohort, in vivo, and in vitro approaches. The cohort study revealed altered liver function indices of diesel engine testers (DETs) compared to those of non-DETs and with increasing exposure duration. Mice exposed to DE via whole-body exposure system developed hepatic steatosis, which coincided with an upregulation of the fatty acid transporter CD36, and a marked increase in long-chain fatty acids. Mechanistically, enhanced CD36 expression was predominantly related to the activation of aryl hydrocarbon receptor (AHR). Notably, treatment with organic extract of diesel exhaust particulate (DEP-OE) up-regulated the AHR/CD36 signaling pathway, and led to lipid accumulation in primary mouse hepatocytes. Both effects were markedly diminished by AHR and CD36 knockdown. Finally, we show that targeted inhibition of AHR alleviated DE-induced steatosis in mouse liver. Together, we demonstrate that the organic components of DE cause hepatic steatosis by activating the AHR/CD36 signaling pathway. Our research elucidates DE exposure risks and sheds new insights into the early prevention of diseases in DE-exposed populations.

Humic acid (HA), a redox-active soil and groundwater compound rich in functional groups (e.g., carboxyl, phenolic hydroxyl, and quinyl group), can complex with Fe(II) to form HA-Fe(II). While HA significantly influences contaminant behavior, the mechanisms it regulates Fe(II) structure-reactivity relationships remain unclear. This study demonstrates that HA content critically controls the Fe(II)-mediated reductive dechlorination of carbon tetrachloride (CT), exhibiting a dual regulatory effect: dechlorination is initially suppressed at lower HA concentrations but enhanced at higher concentrations. Macroscopically, HA mediates the exposure of Fe(OH)₂ (100) facets via a concentration-dependent threshold mechanism, directly modulating the electron-donating capacity of surface Fe(II) sites. HA content tunes Fe(II)'s electron-donating capacity at the electronic-structure level by synergistically altering Fe-O bond lengths, octahedral distortion, and the internal electric field. This regulation stems from HA's role as a weak-field ligand, which modifies the electronic occupancy of Fe(II) complexes' antibonding e_g* orbitals, thereby impacting electron transfer efficiency. HA content modulates the Schikorr reaction, providing insights into complex iron-based reduction processes. Through multi-scale analysis, this work elucidates the structure-activity relationship between natural organic matter and iron minerals in pollutant degradation, offering a theoretical foundation for designing environmental remediation materials.