As persulfate activator, Metal organic frameworks (MOFs) and derivatives are widely concerned in degradation of emerging environmental pollutants by advanced oxygen technology dominated by sulfate radical (▪) (SR-AOPs). However, the poor stability and low catalytic efficiency limit the performance of MOFs, requiring multiple strategies to further enhance their catalytic activity. The aim of this paper is to improve the catalytic activity of MOFs and their derivatives by physical and chemical enhancement strategies. Physical enhancement strategies mainly refer to the activation strategies including thermal activation, microwave activation and photoactivation. However, the physical enhancement strategies need energy consumption and require high stability of MOFs. As a substitute, chemical enhancement strategies are more widely used and represented by optimization, modification, composites and derivatives. In addition, the identification of reactive oxygen species, active site and electron distribution are important for distinguishing radical and non-radical pathways. Finally, as a new wastewater treatment technology exploration of unknown areas in SR-AOPs could better promote the technology development.

Microplastics (MPs), which are emerging environmental pollutants, remain uncertainties in their toxic mechanism. MPs have been linked to severe liver metabolic disorders and neurotoxicity, but it is still unknown whether the abnormal metabolites induced by MPs can affect brain tissue through the liver-brain axis. Exposed to MPs of chickens results in liver metabolic disorders and increased glutamine and glutamate synthesis. The relative expression of glutamine in the C group was −0.862, the L-PS group was 0.271, and the H-PS group was 0.592. The expression of tight junction proteins in the blood-brain barrier (BBB) was reduced by PS-MPs. Occludin protein expression decreased by 35.8%–41.2%. Claudin 3 decreased by 19.6%–42.3%, and ZO-1 decreased by 28.3%–44.6%. Excessive glutamine and glutamate cooperated with PS-MPs to inhibit the Nrf2-Keap1-HO-1/NQO1 signaling pathway and triggered autophagy-dependent ferroptosis and apoptosis. GPX protein expression decreased by 30.9%–38%. LC3II/LC3I increased by 54%, and Caspase 3 increased by 45%. Eventually, the number of Purkinje cells was reduced, causing neurological dysfunction. In conclusion, this study provides new insights for revealing the mechanism of nervous system damaged caused by PS-MPs exposed in chickens.

Vegetation plays an important role as both a sink of air pollutants via dry deposition and a source of biogenic VOC (BVOC) emissions which often provide the precursors of air pollutants. To identify the vegetation-driven offset between the deposition and formation of air pollutants, this study examines the responses of ozone and PM₂.₅ concentrations to changes in the leaf area index (LAI) over East Asia and its neighboring seas, using up-to-date satellite-derived LAI and green vegetation fraction (GVF) products. Two LAI scenarios that examine (1) table-prescribed LAI and GVF from 1992 to 1993 AVHRR and 2001 MODIS products and (2) reprocessed 2019 MODIS LAI and 2019 VIIRS GVF products were used in WRF-CMAQ modeling to simulate ozone and PM₂.₅ concentrations for June 2019. The use of up-to-date LAI and GVF products resulted in monthly mean LAI differences ranging from −56.20% to 96.81% over the study domain. The increase in LAI resulted in the differences in hourly mean ozone and PM₂.₅ concentrations over inland areas ranging from 0.27 ppbV to −7.17 ppbV and 0.89 μg/m³ to −2.65 μg/m³, and the differences of those over the adjacent sea surface ranging from 0.69 ppbV to −2.86 ppbV and 3.41 μg/m³ to −7.47 μg/m³. The decreases in inland ozone and PM₂.₅ concentrations were mainly the results of dry deposition accelerated by increases in LAI, which outweighed the ozone and PM₂.₅ formations via BVOC-driven chemistry. Some inland regions showed further decreases in PM₂.₅ concentrations due to reduced reactions of PM₂.₅ precursors with hydroxyl radicals depleted by BVOCs. The reductions in sea surface ozone and PM₂.₅ concentrations were accompanied by the reductions in those in upwind inland regions, which led to less ozone and PM₂.₅ inflows. The results suggest the importance of the selective use of vegetation parameters for air quality modeling.

The relationships and interactions between extracellular polymeric substances (EPS) and microplastics (MPs) in coral reef ecosystems were symmetrically investigated. The current study aims to investigate the responses of scleractinian coral (Goniopora columna) to exposure of model MPs, exemplified by polyethylene (PE), in the size range of 40–48 μm as affected by MPs concentration of MP in the range between 0 and 300 mg L⁻¹ for 14 days. The structure of EPS-associated microbial community was studied using a series of techniques including high-throughput sequencing of 16 S rRNA, transmission electron microscopy (TEM), hydrodynamic diameter, surface charge (via zeta potential), X-ray diffraction (XRD), attenuated total reflectance‒Fourier transform infrared (ATR‒FTIR) spectroscopy, X-ray photoelectron spectroscopy (XPS), and fluorescence excitation–emission matrix (FEEM) spectroscopy. Microbial interactions between PE-MPs and coral caused aggregation and formation of EPS matrix, which resulted in increase and decrease in the relative abundance of Donghicola (Proteobacteria phylum) and Marivita (Proteobacteria phylum) in PE-MP-associated EPS, respectively. Particle size, electrostatic interactions, and complexation with the functional groups of the EPS-based matrix affected the humification index. FEEM spectroscopy analyses suggested the presence of humic- and fulvic-like fluorophores in EPS and dissolved organic matter (DOM) in PE-MP-derived DOM. The findings provided insights into the potential environmental implications of coral-based EPS and co-existing microbial assemblages due to EPS-PE-MP-microbiome interactions throughout the dynamic PE-MP exposure process.

Current synthesis routes of bismuth oxide nanosheets (BiONS) are relatively complicated, requiring the use of halogens or metalloids. Herein, a facile method to synthesize BiONS without the addition of halogens or other metalloids was developed. The synthesized BiONS were identified to have flake-shaped structures (300–1000 nm in width) with the thickness of 6–10 nm, which were predominantly made of β-Bi₂O₃. Such BiONS were applied to modify the surface of screen-printed carbon electrodes (BiONS-SPCEs) for the development of a robust palladium (Pd²⁺) sensor. After optimizing the electrochemical parameters of the sensor, it was found that the linear sensor response range and limit of detection for Pd²⁺ were 40–400 and 1.4 ppb, respectively. The electrocatalytic activity of the Pd²⁺-sensor was validated in the competing environment of other metal and metalloid ions. Real samples collected during a Pd recovery process from pharmaceutical wastewater were used to verify the application of BiONS-SPCEs in control of palladium recovery process. The quantitative results of post recovery palladium concentrations obtained using BiONS-SPCEs in treated pharmaceutical wastewater samples were in good agreement with those obtained by inductively coupled plasma-optical emission spectrometry (ICP-OES). Thus, such Pd²⁺-sensor provided the possibility of on-site process control of complex industrial samples for obtaining near-instant information that would lead to better management of resources used in the process, and same time assure environmental standards for both recovered products and processed discharge.

With the dramatic increase in anthropogenic threats to the Pearl River Estuary (PRE), the population size of the Indo-Pacific humpback dolphins (Sousa chinensis) has significantly decreased over the past decade. To understand the impact and potential risks of intense human activities on these dolphins, factors related to the mortality of humpback dolphins in the PRE were investigated by a detailed examination of 343 dolphin specimens stranded during 2003–2017. There was a significant (p < 0.01) increasing trend for humpback dolphin stranding, reflecting the accelerating rate of the population decline. A large proportion of strandings (35.88%) were neonates. A low recruitment rate implies slow population growth, and hence, limited capacity to resist anthropogenic stress. The most commonly diagnosed causes of death were vessel collision and net entanglement. The concentrations of trace metals, polychlorinated biphenyl (PCB) congeners, dichlorodiphenyltrichloroethane, polycyclic aromatic hydrocarbons, and most of per- and polyfluoroalkyl substances (PFASs) in the dolphin samples were greater than those previously reported in cetaceans globally. Furthermore, Cu, PCB77, PCB169, PCB81, PCB37, and PFASs (excluding PFBA, PFPeA, PFHxA, PFHxDA, and PFODA) were the major pollutants accumulated in neonates. 67% of PCB, 78% of Cu, and 100% of perfluorooctane sulfonate concentrations in the neonates exceeded the threshold for toxicological effects in marine mammals, suggesting that these compounds could be important factors contributing to the low survival rate of calves in this area. This study revealed that vessel transportation, fishing activities, and pollutant bioaccumulation are the three major causes of humpback dolphin mortality in the PRE. These results highlight the need for more efforts to restrict anthropogenic activities, especially vessel traffic, the catching of these marine animals and fishing, and pollutant discharge, in order to prevent vulnerable species from continuous population decline and further extinction.

Recently, increasing attention has been paid to antibiotic resistance genes (ARGs) in urban stormwater runoff. However, there were little data on the diversity and distribution of ARGs associated with road sediments transported in runoff. The investigation of ARGs diversity showed that sulfonamide resistance genes (sul2 and sul3) occupied 61.7%–82.3% of total ARGs in runoff. The analysis of ARGs distribution in particulate matter (PM) implied that both tetQ and trbC existed mainly in PM with size of 150–300 μm, but other ARGs and mobile genetic elements (MGEs) were dominant in PM with size <75 μm. The discussion of potential hosts indicated that target genes (ermF, blaOXA1/blaOXA30, ermC, qnrA, sul2, tnpA-01, intI2, tetW, intI1, sul3, trbC) had the strongest subordinate relationship with Proteobacteria at phylum level and Enterobacter at genus level. The effect evaluation of ARGs distribution suggested that 13 kinds of ARGs were positively correlated with Pr/PS and Zeta potential, resulting in the more ARGs in PM with smaller size (<75 μm).

As a widely used pure elemental carbon in colloidal particles, carbon black was listed as a group 2B carcinogen by IARC in 2010. The most available mechanism information about carbon black and carcinogenesis are from in vivo or in vitro studies. However, few studies concerned the nanoparticle's real-ambient exposure causing systemic change and further affecting the target organ. Herein, we used an ex vivo biosensor assay to investigate the transcriptome change of primary bronchial epithelial cells after treatment with the plasma from workers with long-term occupational carbon black exposure history. Based on ex vivo biosensor assay and transcriptome sequencing, we found the effect of internal systemic environment on epithelial cells after carbon black exposure was an inflammatory response, which mainly activates cell cycle-related pathways. After exposure to carbon black, the internal systemic environment could activate cancer-related pathways like epithelial-mesenchymal transition, hypoxia, TNF-α signaling via NF-κB. The hub genes in the carbon black group (CDC20 and PLK1) and their correlation with the systemic environment were uncovered by constructing the protein-protein interaction network. Inflammatory cytokines, especially CRP, were strongly correlated with the expression of CDC20 and PLK1. Besides, we also find a strong correlation between CDC20 and cytokinesis-block micronucleus endpoints in peripheral blood (rho = 0.591, P < 0.001). Our results show that long-term carbon black exposure might activate cell cycle-related pathways through circulating inflammation and increase the risk of cancer, while the oxidative stress caused by diesel exhaust particles are mainly related to PAHs exposure. After exposure to carbon black, the systemic environment could activate cancer-related pathways like diesel exhaust particles, increasing the risk of lung cancer. These attempts might provide a further understanding of the indirect effect of chronic occupational inhaled carbon black exposure on pulmonary carcinogenesis.

Halogenated organic compounds are persistent pollutants, whose persistent contamination and rapid spread seriously threaten human health and the safety of ecosystems. It is difficult to remove them completely by traditional physicochemical techniques. In-situ remediation utilizing bioelectrochemical technology represents a promising strategy for degradation of halogenated organic compounds, which can be achieved through potential modulation. In this review, we summarize the reactor configuration of microbial electrochemical dehalogenation systems and relevant organohalide-respiring bacteria. We also highlight the mechanisms of electrode potential regulation of microbial dehalogenation and the role of extracellular electron transfer in dehalogenation process, and further discuss the application of bioelectrochemical technology in bioremediation of halogenated organic compounds. Therefore, this review summarizes the status of research on microbial electrochemical dehalogenation systems from macroscopic to microscopic levels, providing theoretical support for the development of rapid and efficient in situ bioremediation technologies for halogenated organic compounds contaminated sites, as well as insights for the removal of refractory fluorides.

This review summarizes the most relevant information on PBDEs’ occurrence and their impacts in cetaceans at global scale, with special attention on the species with the highest reported levels and therefore the most potentially impacted by the current and continuous release of these substances. This review also emphasizes the anthropogenic and environmental factors that could increase concentrations and associated risks for these species in the next future. High PBDE concentrations above the toxicity threshold and stationary trends have been related to continuous import of PBDE-containing products in cetaceans of Brazil and Australia, where PBDEs have never been produced. Non-decreasing levels documented in cetaceans from the Northwest Pacific Ocean might be linked to the increased e-waste import and ongoing production and use of deca-BDE that is still allowed in China. Moreover, high levels of PBDEs in some endangered species such as beluga whales (Delphinapterus leucas) in St. Lawrence Estuary and Southern Resident killer whales (Orcinus Orca) are influenced by the discharge of contaminated waters deriving from wastewater treatment plants. Climate change related processes such as enhanced long-range transport, re-emissions from secondary sources and shifts in migration habits could lead to greater exposure and accumulation of PBDEs in cetaceans, above all in those species living in the Arctic. In addition, increased rainfall could carry greater amount of contaminants to the marine environment, thereby, enhancing the exposure and accumulation especially for coastal species. Synergic effects of all these factors and ongoing emissions of PBDEs, expected to continue at least until 2050, could increase the degree of exposure and menace for cetacean populations. In this regard, it is necessary to improve current regulations on PBDEs and broader the knowledge about their toxicological effects, in order to assess health risks and support regulatory protection for cetacean species.