Phenolic environmental estrogens (PEEs) are a common class of endocrine-disrupting chemicals widely found in daily products. They competitively bind to estrogen receptors, thereby disrupting endocrine function. PEEs appear to play a role in the development of gestational diabetes mellitus (GDM). Earlier findings by our group indicated that 2-tert-octylphenol (2-t-OP) showed a positive correlation with GDM whereas nonylphenol (NP) showed an inverse association. However, the specific molecular mechanisms underlying this relationship remained largely unexplored. To address this gap, we performed comprehensive urinary PEEs quantification and metabolomic profiling in a cohort of 387 pregnant mothers, employing a meet-in-metabolite analysis to identify potential metabolic biomarkers between PEEs exposure and GDM. Our analysis uncovered 11 key metabolites that showed significant associations with both PEEs and GDM. Among these, the abundances of 8 metabolites (kynurenic acid, 11-Ketoetiocholanolone, N-Acetylneuraminic acid, α-Linolenoyl ethanolamide, uric acid, butylparaben, uracil, and N6,N6,N6-Trimethyl-L-lysine) were higher, while 3 (3′-Sialyllactose, thiosulfate, and phosphoroselenoic acid) were lower in the women with higher level of PEEs exposure. Notably, we found that 3′-Sialyllactose, uric acid, 11-Ketoetiocholanolone and phosphoroselenoic acid may impact the positive association of 2-t-OP with GDM, while 3′-Sialyllactose, 11-Ketoetiocholanolone and phosphoroselenoic acid appear to mediate the negative association for NP. Considering the relevant biological pathways, we propose that 2-t-OP and NP may inversely influence GDM risk by interfering with purine, steroid hormone and amino acid metabolism in pregnancy. By shining a light on these metabolic disruptions, our findings open up new avenues for understanding how PEEs exposure contribute to GDM.
Achieving synergy between pollutants treatment and corresponding greenhouse gas (GHG) emissions was critical for sustainable development of iron and steel industry. This study systematically quantified the three-phase pollutants emission characteristics and treatment-induced GHG emissions in both long and short process steelmaking. Furthermore, this study evaluated GHG emissions associated with 158,760 combinations of pollutant treatment technology. Results indicated that while the long-process steelmaking was characterized by dispersed and massive pollutant emissions, the short-process steelmaking had an advantage in pollutants source reduction. A trade-off existed in pollutants treatment. Air pollutants and wastewater treatment inevitably acted as carbon sources. Conversely, resource utilization of solid waste was the decisive factor for achieving carbon neutrality in pollutants treatment. Specifically, cascade utilization of blast furnace slag through heat recovery and cement substitution achieved an exceptional GHG reduction of -244.99 kg CO2e/t crude steel. Notably, under optimal synergistic scenarios, the long-process steelmaking could achieve a negative GHG emissions of -275.26 kg CO2e/t crude steel for three-phase pollutants treatment. These findings suggested that while transitioning to short-process steelmaking was essential for pollutants reduction, maximizing the resource utilization of solid waste in long-process steelmaking remained indispensable for offsetting unavoidable GHG emissions and achieving decarbonization in pollutants treatment.
The growing emphasis on sustainable remediation has increased demand for integrated risk management at contaminated sites. Evaluation should not only focus on pollution reduction but also comprehensively assess socioeconomic and environmental benefits. With strong policy support, China is undertaking extensive risk management and remediation of contaminated sites. There is an urgent need to establish an economic analysis framework for contaminated site risk control to support policy formulation and decision-making optimization. This study developed a framework for cost–benefit analysis of contaminated site risk management in China, focusing on costs, benefits, and socioeconomic impacts, and applied it to a chemical plant case. The framework monetizes remediation investments, health improvements, ecological services, land appreciation, and macroeconomic effects. Results show that although substantial capital input is required, risk management generates significant co-benefits. Improvements in soil environmental quality reduce disease and cancer risks for surrounding residents. Redevelopment into an urban park enhances ecological service values, including temperature reduction, carbon dioxide sequestration, flood regulation, tourism and leisure, and natural landscape premiums. The benefit–cost ratio is 1.13. Additionally, risk management positively stimulates the regional economy, with each 10,000 Chinese Yuan (CNY) invested estimated to generate a Gross Domestic Product increase of 13,000 CNY. Uncertainty analysis reveals that engineering cost parameters and land value-related parameters exhibit relatively high sensitivity to the outcomes. This study demonstrates the feasibility of the framework for assessing the economic sustainability of contaminated site risk management and provides support for evidence-based policies and strategies.
As a novel organophosphate ester widely distributed in airborne particulate matters, tris(2,4-di-tert-butylphenyl) phosphate (AO168=O) would pose a great hazard for the respiratory system. However, the underlying toxic mechanism of AO168=O on the lung organ, especially pulmonary malignant transformation, remained elusive. Hence, our study paid attention to the deleterious impact of AO168=O on malignant transformation of human bronchial epithelial (BEAS-2B) cells, identifying whether inflammation-coupled cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway mediated by TAR DNA-binding protein 43 (TDP-43) was involved in this process. Herein, we have observed that BEAS-2B cells were malignantly transformed upon exposure to AO168=O for 96 h, manifested by the increased mutation frequency at the Hprt locus, the enhanced anchorage-independent growth, the elevated migratory and invasive capabilities. Moreover, transcriptome sequencing, Western blot, quantitative PCR and immunofluorescence assay were adopted to show that the mitochondrial localization of TDP-43 could activate cGAS/STING pathway and inflammatory response upon exposure to 1000 ng/mL AO168=O for 96 h, thereby promoting epithelial-mesenchymal transition (EMT) in BEAS-2B cells deficient in homologous recombination repair. Furthermore, the blockage of inflammation-coupled cGAS/STING pathway reversed EMT and malignant transformation of BEAS-2B cells exposed to 1000 ng/mL AO168=O for 96 h. Collectively, our findings suggested that AO168=O promoted malignant progression of BEAS-2B cells, which was partially linked to the EMT process mediated by the mitochondrial localization of TDP-43. This also provided a valuable insight into the intervention for AO168=O-caused malignant transformation of human bronchial epithelial cells.
Coastal bays are semi-enclosed reactors regulating carbon cycling and increasingly subjected to anthropogenic nitrogen (N) and phosphorus (P) inputs. However, how inorganic nitrogen and/or phosphorus supply regulates dissolved organic matter (DOM) stability and assembly mechanisms remains poorly understood. We conducted large-scale mesocosm experiments (∼10.8 m³ each) in Daya Bay under four treatments: an unamended control and daily N, P, or combined N and P additions. Although phytoplankton blooms occurred only under N and combined N and P additions, Fourier transform ion cyclotron resonance mass spectrometry revealed all nutrient additions shifted DOM toward more labile forms, with lower molecular weight, aromaticity, and carbon chain length. N addition enhanced autotrophic production, releasing aliphatic-rich phytoplankton exudates, whereas P addition stimulated heterotrophic processing of pre-existing refractory DOM. Combined N and P addition intensified both processes, driving maximal destabilization, with the greatest relative enrichment of lipid- and carbohydrate-like compounds and relative decreases in recalcitrant carboxyl-rich alicyclic molecules and island-of-stability components. Null model and network analyses indicated enhanced deterministic selection and increased network vulnerability under combined nitrogen and phosphorus addition, with vulnerability increasing from 0.05 in the control to 0.13 in the combined treatment and modularity decreasing from 0.70 to 0.38, reflecting weakened network stability. Collectively, N and P enrichment induced convergent shifts toward DOM lability through distinct pathways associated with autotrophic substrate supply and heterotrophic DOM reworking. Notably, phosphorus addition alone caused detectable molecular labilization of DOM without a significant chlorophyll a response, indicating a decoupling between visible bloom indicators and molecular-level DOM stability.
Pyraclostrobin is one of the most widely used fungicides globally; however, the mechanisms underlying its hepatotoxicity at environmentally relevant concentrations remain poorly understood. This study demonstrates that exposure to pyraclostrobin at environmentally relevant concentrations (15 and 30 μg/L) induces liver injury in zebrafish by disrupting the homeostasis of the gut-liver axis and bile acid metabolism. The results showed that aquatic exposure to pyraclostrobin at these concentrations leads to the substantial accumulation in the liver and gut tissues of zebrafish. This accumulation caused hepatic vacuolation and dysfunction, intestinal villi defects, impaired gut barrier function, and a significant upregulation of proinflammatory cytokines, including TNF-alpha and IL-1 beta. Integrated multi-omics analysis revealed that pyraclostrobin exposure disrupted arachidonic acid metabolism and steroid hormone biosynthesis in the liver, induced gut microbiota dysbiosis, and exacerbated hepatic immune and metabolic dysfunction by modulating bile acid cycling through the gut-liver axis. Molecular docking studies suggested possible interactions between pyraclostrobin and both the rate-limiting enzyme in bile acid synthesis (cholesterol 7α-hydroxylase; CYP7A1) and the bile salt export pump (BSEP), potentially contributing to bile acid metabolic disorders. This study identifies a novel mechanism through which environmentally relevant concentrations of pyraclostrobin induce liver injury via bile acid accumulation and inflammatory responses through the gut-liver axis. It highlights the necessity of assessing the long-term exposure risks of pyraclostrobin to nontarget organisms at realistic environmental concentrations.
Intensive agricultural practices increasingly expose soils to complex mixtures of agrochemicals, yet their synergistic ecological consequences remain poorly understood. This study investigates the combined impacts of nitrogen fertilizer, pesticide (imidacloprid), and antibiotic (erythromycin) on soil microbial community assembly, antibiotic resistance gene (ARG) dissemination, and nitrogen metabolism within a soil–plant microcosm. The findings reveal that co-exposure to these chemicals significantly restructured microbial diversity, intensified the soil resistome, and altered key nitrogen metabolic pathways. The rhizosphere emerged as a critical ecological hotspot where root exudates modulated contaminant bioavailability, selected for distinct microbial taxa, and drove elevated ARG and mobile genetic element abundances compared with bulk soil and the endosphere. Single nitrogen fertilization stimulated canonical nitrification and denitrification pathways linked to elevated N₂O emission potential, whereas co-contaminant exposure shifted functional profiles toward dissimilatory nitrate reduction and biological nitrogen fixation, a shift predominantly mediated by rhizosphere microbiota. Additionally, resistome evolution was closely coupled with community compositional turnover and nitrogen-cycling gene profiles, indicating strong co-selection under rhizosphere-specific selective pressures. Importantly, metagenomic binning revealed that the potential co-dissemination of ARGs and metabolism related genes through horizontal gene transfer within the microbial communities could amplify its adaptability to mixed-contamination pressures. These findings demonstrate that agrochemical co-pollution exerts intricate mixture effects on microbial ecology and resistance evolution, highlighting the necessity to consider multi-contaminant and rhizosphere effects in risk assessments.
Industrial thermal processes unintentionally produce chlorinated and brominated persistent organic pollutants (POPs). With the progressive phase-out and centralized disposal of brominated flame retardants, increasing attention has shifted toward the emissions and control of polybrominated dibenzo-p-dioxins/dibenzofurans (PBDD/Fs) and polyhalogenated dibenzo-p-dioxins/dibenzofurans (PXDD/Fs). This review systematically compares the emission levels and congener distribution profiles of multiple chlorinated and brominated POPs across typical industrial thermal processes. Current understanding of the formation pathways of these pollutants is critically synthesized, emphasizing the mechanistic similarities and differences between chlorinated and brominated systems, with implications for the development of source-specific emission mitigation strategies. Building upon established radical-based formation mechanisms for polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs), the review further explores the free-radical mediated formation pathways of PBDD/Fs and PXDD/Fs. These insights contribute to a refined molecular-level framework for polyhalogenated POPs formation and provide a theoretical foundation for the synergistic control of chlorinated and brominated POPs in industrial thermal processes.
