Environmental Pollution最新文献

Benzo (k) fluoranthene (BkF) has adverse effects on male reproduction, but its specific mechanism of action is still unclear. This study focused on the role of RNA reading protein YTHDF2 and its mechanism in BkF induced male reproductive injury. Mouse GC-2 spermatocytes were exposed to 0, 40, 80, 160 μM BkF. It was found that BkF significantly increased the apoptosis of GC-2 cell and decreased its survival rate. BCL2 in spermatocytes decreased significantly, while the expression of P53 and BAX exhibited a notable increase. Interestingly, the expression of RNA reading protein YTHDF2 progressively rose in tandem with the escalating BkF exposure dosage. Overexpression of YTHDF2 significantly reduced the viability of cells and increased the apoptosis rate. Meanwhile, there was a substantial increase in the expression of P53 and BAX, BCL2 was significantly down-regulated. On the contrary, interfering with YTHDF2 increased cell proliferation and reduced cell apoptosis. Furthermore, YTHDF2 overexpression exacerbated the decrease in cell viability under BkF exposure, while YTHDF2 knockdown was the opposite. The results from the RIP assay demonstrated a significant enhancement in the interaction of YTHDF2 protein with BCL2 mRNA following the overexpression of YTHDF2. In addition, animal experiments showed that there was an increase in apoptosis and a decrease in proliferation of testicular cells in mice in the high-dose (30 mg/kg) BkF group by TUNEL staining and Ki67 staining. Immunohistochemical analysis showed that BCL2 levels were significantly lower in the high-dose group than in the control group, while YTHDF2, P53 and BAX were dramatically increased. In summary, our study suggests that YTHDF2 has been implicated in BkF-induced male reproductive injury by promoting the degradation of BCL2.

Faced with worldwide mercury (Hg) contamination in groundwater, efficient in situ remediation technologies are urgently needed. Carboxymethyl cellulose (CMC) stabilized iron sulfide (CMC-FeS) nanoparticles have been found effective for immobilizing mercury in water and soil. Yet, the potential use of the nanoparticles for creating an in situ reactive zone (ISRZ) in porous geo-media has not been explored. This study assessed the transport and deliverability of CMC-FeS in sand media towards creating an ISRZ. The nanoparticles were deliverable through the saturated sand bed and the particle breakthrough/deposition profiles depended on the injection pore velocity, initial CMC-FeS concentration, and ionic strength. The transport data were well interpreted using an advection-dispersion transport model combined with the classical filtration theory. The resulting ISRZ effectively removed mercury from contaminated groundwater under typical subsurface conditions. While the operating conditions are yet to be optimized, the Hg breakthrough time can be affected by groundwater velocity, influent mercury concentration, dissolved organic matter, and co-existing metals/metalloids. The one-dimensional advection-dispersion equation well simulated the Hg breakthrough data. CMC-FeS-laden ISRZ effectively converted the more easily available Hg species to stable species. These findings reveal the potential of creating an ISRZ using CMC-FeS for in situ remediation of Hg contaminated soil and groundwater.

Air pollution from transport hubs is a recognised health concern for local urban inhabitants. Within the domain of transport hubs, significant attention has been given to larger airport and port settings, however concerns have been raised about emissions from urban railway hubs, especially those with diesel trains. This paper presents an approach that adopts low-cost monitoring (LCM) for fixed site monitoring (FSM) to quantify and disaggregate PM_2.5 and NO₂ contributions from railway station and road traffic on air quality in the vicinity of railway station in Dublin, Ireland. The NO₂ sensor showed larger discrepancies than the PM_2.5 sensor when compared to the reference monitor. Machine learning models (XGBoost and Random Forest (RF) regression) were applied to calibrate the LCM devices, with the XGBoost model (NO_2, R² = 0.8 and RSME = 9.1 μg/m³ & PM_2.5, R² = 0.92 and RSME = 2.2 μg/m³) deemed more appropriate than the RF model. Local wind conditions, pressure, PM_2.5 concentrations, and road traffic significantly impacted NO₂ model results, while raw PM_2.5 sensor readings greatly influenced the PM_2.5 model output. This highlights that the NO₂ sensor requires more input data for accurate calibration, unlike the PM_2.5 sensor. The monitoring results from the one-month monitoring campaign from May 25, 2023 to June 25, 2023 presented elevated NO₂ and PM_2.5 concentrations measured at the railway station, which translated to exceedances of the annual WHO limits (PM_2.5 = 5 μg/m³, NO₂ = 10 μg/m³) by 1.6-1.8 and 3.2-5.2 times respectively at the study site. A subsequent data filtering technique based on wind orientation, revealed that the railway station was the main PM_2.5 source and road traffic was the main NO₂ source when winds come from the railway station. This study highlights the value of LCM devices alongside robust machine learning techniques to capture air quality in urban settings.

There is mounting evidence implicating the potential neurotoxic effects of PM2.5 during brain development, as it has been observed to traverse both the placental barrier and the fetal blood-brain barrier. However, the current utilization of 2D cell culture and animal models falls short in providing an accurate representation of human brain development. Consequently, the precise mechanisms underlying PM2.5-induced developmental neurotoxicity in humans remain obscure. To address this research gap, we constructed three-dimensional (3D) cortical organoids that faithfully recapitulate the initial stages of human cerebral cortex development. Our goal is to investigate the mechanisms of PM2.5-induced neurotoxicity using 3D brain organoids that express cortical layer proteins. Our findings demonstrate that exposure to PM2.5 concentrations of 5 μg/mL and 50 μg/mL induces neuronal apoptosis and disrupts normal neural differentiation, thereby suggesting a detrimental impact on neurodevelopment. Furthermore, transcriptomic analysis revealed PM2.5 exposure induced aberrations in mitochondrial complex I functionality, which is reminiscent of Parkinson's syndrome, potentially mediated by misguided axon guidance and compromised synaptic maintenance. This study is a pioneering assessment of the neurotoxicity of PM2.5 pollution on human brain tissues based on 3D cortical organoids, and the results are of great significance in guiding the formulation of the next air pollution prevention and control policies in China to achieve the sustainable improvement of air quality and to formulate pollution abatement strategies that can maximize the benefits to public health.