Multiple stable isotopic approaches for tracing nitrate contamination sources: Implications for nitrogen management in complex watersheds.

Nitrate (NO3-) contamination of surface water is a global environmental problem that has serious consequences for watershed ecosystems and endangers human health. It is crucial to identify influences of different sources of NO3-, especially the incoming water from upper reaches. A combination of hydrochemistry and multi-isotope tracers (δ11B, δ15N-NO3-, and δ18O-NO3-) were used to determine NO3- sources and their transformation the North Jiulong River (NJLR), Southeast China. The findings revealed that NO3-, which accounted for an average of 87.1% of dissolved inorganic nitrogen (DIN), was the main chemical form of nitrogen species. The integration of dual stable isotopes of NO3-, δ11B, and hydrochemistry showed that NO3- was primarily contributed by sewage, soil nitrogen (SN), and ammonium (NH4+) via precipitation or fertilizers. The contributions from the sewage and soil nitrate source were almost equivalent and much higher than those from other sources in the NJLR watershed. The contributions from diverse sources varied seasonally and spatially. Manure and sewage (M&S) were the leading sources in the summer and autumn, accounting for 60.9 ± 8.5% and 47.3 ± 7.9%, respectively. However, NO3- fertilizers were the predominant source in the spring and winter. The NO3- inflow from upper reaches was proposed as an additional end-member to identify its contribution in the midstream and downstream in this study. The contributions of NO3- from the upper reaches were significant sources in the midstream and downstream, accounting for 27.2 ± 17.8% and 42.9 ± 21.9%, respectively. The obvious decline in local NO3-contribution shares from midstream to downstream implied structural changes in pollutant sources and regional environmental responsibility. Therefore, tracing nitrate sources and quantifying their contributions is critical for clarifying environmental responsibilities for precise local nitrogen management in watersheds.

Occurrence and Risk Assessment of Perfluorooctanoate (PFOA) and Perfluorooctane Sulfonate (PFOS) in Surface Water, Groundwater and Sediments of the Jin River Basin, Southeastern China.

Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) levels were determined in surface water, groundwater and sediments of the Jin River Basin, southeastern China. PFOA was detected in most of the samples, and its concentrations ranged from 0.53 to 8.77 ng/L, 0.26 to 15.1 ng/L and not detected (ND) to 23.9 ng/g in surface water, groundwater and sediments, respectively. Unlike PFOA, the detection frequency of PFOS was lower than 32%, and its concentrations ranged from ND to 2.56 ng/L, ND to 7.01 ng/L, ND to 11.1 ng/g in surface water, groundwater and sediments, respectively. The environmental risk assessment showed that PFOA could pose a high risk to surface water and groundwater, and both PFOA and PFOS posed a high risk to sediments. Moreover, the adults living in the Jin River Basin were at insignificant health risk to exposure to PFOA and PFOS through water consumption.

Sirtuin 1 alleviates neuroinflammation-induced apoptosis after traumatic brain injury.

Sirtuin 1 (SIRT1) plays a very important role in a wide range of biological responses, such as metabolism, inflammation and cell apoptosis. Changes in the levels of SIRT1 have been detected in the brain after traumatic brain injury (TBI). Further, SIRT1 has shown a neuroprotective effect in some models of neuronal death; however, its role and working mechanisms are not well understood in the model of TBI. This study aimed to address this issue. SIRT1-specific inhibitor (sirtinol) and activator (A3) were introduced to explore the role of SIRT1 in cell apoptosis. Results of the study suggest that SIRT1 plays an important role in neuronal apoptosis after TBI by inhibiting NF-κB, IL-6 and TNF-α deacetylation and the apoptotic pathway sequentially, possibly by alleviating neuroinflammation.

Causal association of adipokines with osteoarthritis: a Mendelian randomization study.

OBJECTIVE: This two-sample Mendelian randomization study aimed to delve into the effects of genetically predicted adipokine levels on OA. METHODS: Summary statistic data for OA originated from a meta-analysis of a genome-wide association study with an overall 50 508 subjects of European ancestry. Publicly available summary data from four genome-wide association studies were exploited to respectively identify instrumental variables of adiponectin, leptin, resistin, chemerin and retinol-blinding protein 4. Subsequently, Mendelian randomization analyses were conducted with inverse variance weighted (IVW), weighted median and Mendelian randomization-Egger regression. Furthermore, sensitivity analyses were then conducted to assess the robustness of our results. RESULTS: The positive causality between genetically predicted leptin level and risk of total OA was indicated by IVW [odds ratio (OR): 2.40, 95% CI: 1.13-5.09] and weighted median (OR: 2.94, 95% CI: 1.23-6.99). In subgroup analyses, evidence of potential harmful effects of higher level of adiponectin (OR: 1.28, 95% CI: 1.01-1.61 using IVW), leptin (OR: 3.44, 95% CI: 1.18-10.03 using IVW) and resistin (OR: 1.18, 95% CI: 1.03-1.36 using IVW) on risk of knee OA were acquired. However, the mentioned effects on risk of hip OA were not statistically significant. Slight evidence was identified supporting causality of chemerin and retinol-blinding protein 4 for OA. The findings of this study were verified by the results from sensitivity analysis. CONCLUSIONS: An association between genetically predicted leptin level and risk of total OA was identified. Furthermore, association of genetically predicted levels of adiponectin, leptin and resistin with risk of knee OA were reported.

Characteristics of ozone pollution and the sensitivity to precursors during early summer in central plain, China.

In this study, we conducted an observation experiment from May 1 to June 30, 2018 in Zhengzhou, a major city in central China, where ground ozone (O3) pollution has become serious in recent years. The concentrations of O3 and its precursors, as well as H2O2 and meteorological data were obtained from the urban site (Yanchang, YC), suburban (Zhengzhou University, ZZU) and background sites (Ganglishuiku, GLSK). Result showed that the rates of O3 concentration exceeded Chinese National Air Quality Standard Grade II (93.3 ppbv) were 59.0%, 52.5%, and 55.7% at the above three sites with good consistency, respectively, indicating that O3 pollution is a regional problem in Zhengzhou. The daily peak O3 appeared at 15:00-16:00, which was opposite to VOCs, NOx, and CO and consistent with H2O2. The exhaustive statistical analysis of meteorological factors and chemical effects on O3 formation at YC was advanced. The high concentration of precursors, high temperature, low relative humidity, and moderately high wind speed together with the wind direction dominated by south and southeast wind contribute to urban O3 episodes in Zhengzhou. O3 formation analysis showed that reactive alkenes such as isoprene and cis-2-butene contributed most to O3 formation. The VOCs/NOx ratio and smog production model were used to determine O3-VOC-NOx sensitivity. The O3 formation in Zhengzhou during early summer was mainly under VOC-limited and transition regions alternately, which implies that the simultaneous emission reduction of alkenes and NOx is effective in reducing O3 pollution in Zhengzhou.

Valproic acid attenuates traumatic spinal cord injury-induced inflammation via STAT1 and NF-κB pathway dependent of HDAC3.

BACKGROUND: Microglial polarization with M1/M2 phenotype shifts and the subsequent neuroinflammatory responses are vital contributing factors for spinal cord injury (SCI)-induced secondary injury. Nuclear factor-κB (NF-κB) is considered the central transcription factor of inflammatory mediators, which plays a crucial role in microglial activation. Lysine acetylation of STAT1 seems necessary for NF-kB pathway activity, as it is regulated by histone deacetylases (HDACs). There have been no studies that have explained if HDAC inhibition by valproic acid (VPA) affects the NF-κB pathway via acetylation of STAT1 dependent of HDAC activity in the microglia-mediated central inflammation following SCI. We investigated the potential molecular mechanisms that focus on the phenotypic transition of microglia and the STAT1-mediated NF-κB acetylation after a VPA treatment. METHODS: The Basso-Beattie-Bresnahan locomotion scale, the inclined plane test, the blood-spinal cord barrier, and Nissl staining were employed to determine the neuroprotective effects of VPA treatment after SCI. Assessment of microglia polarization and pro-inflammatory markers, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, and interferon (INF)-γ was used to evaluate the neuroinflammatory responses and the anti-inflammatory effects of VPA treatment. Immunofluorescent staining and Western blot analysis were used to detect HDAC3 nuclear translocation, activity, and NF-κB signaling pathway activation to evaluate the effects of VPA treatment. The impact of STAT1 acetylation on NF-kB pathway and the interaction between STAT1 and NF-kB were assessed to evaluate anti-inflammation effects of VPA treatment and also whether these effects were dependent on a STAT1/NF-κB pathway to gain further insight into the mechanisms underlying the development of the neuroinflammatory response after SCI. RESULTS: The results showed that the VPA treatment promoted the phenotypic shift of microglia from M1 to M2 phenotype and inhibited microglial activation, thus reducing the SCI-induced inflammatory factors. The VPA treatment upregulation of the acetylation of STAT1/NF-κB pathway was likely caused by the HDAC3 translocation to the nucleus and activity. These results indicated that the treatment with the VPA suppressed the expression and the activity of HDAC3 and enhanced STAT1, as well as NF-κB p65 acetylation following a SCI. The acetylation status of NF-kB p65 and the complex with NF-κB p65 and STAT1 inhibited the NF-kB p65 transcriptional activity and attenuated the microglia-mediated central inflammatory response following SCI. CONCLUSIONS: These results suggested that the VPA treatment attenuated the inflammatory response by modulating microglia polarization through STAT1-mediated acetylation of the NF-κB pathway, dependent of HDAC3 activity. These effects led to neuroprotective effects following SCI.

Omega-3 polyunsaturated fatty acid attenuates traumatic brain injury-induced neuronal apoptosis by inducing autophagy through the upregulation of SIRT1-mediated deacetylation of Beclin-1.

BACKGROUND: Enhancing autophagy after traumatic brain injury (TBI) may decrease the expression of neuronal apoptosis-related molecules. Autophagy-mediated neuronal survival is regulated by the sirtuin family of proteins (SIRT). Omega-3 polyunsaturated fatty acids (ω-3 PUFA) are known to have antioxidative and anti-inflammatory effects. We previously demonstrated that ω-3 PUFA supplementation attenuated neuronal apoptosis by modulating the neuroinflammatory response through SIRT1-mediated deacetylation of the HMGB1/NF-κB pathway, leading to neuroprotective effects following experimental traumatic brain injury (TBI). However, no studies have elucidated if the neuroprotective effects of ω-3 PUFAs against TBI-induced neuronal apoptosis are modulated by SIRT1-mediated deacetylation of the autophagy pathway. METHODS: The Feeney DM TBI model was adopted to induce TBI rats. Modified neurological severity scores, the rotarod test, brain water content, and Nissl staining were employed to determine the neuroprotective effects of ω-3 PUFA supplementation. Immunofluorescent staining and western blot analysis were used to detect Beclin-1 nuclear translocation and autophagy pathway activation. The impact of SIRT1 deacetylase activity on Beclin-1 acetylation and the interaction between cytoplasmic Beclin-1 and Bcl-2 were assessed to evaluate the neuroprotective effects of ω-3 PUFAs and to determine if these effects were dependent on SIRT1-mediated deacetylation of the autophagy pathway in order to gain further insight into the mechanisms underlying the development of neuroprotection after TBI. RESULTS: ω-3 PUFA supplementation protected neurons against TBI-induced neuronal apoptosis via enhancement of the autophagy pathway. We also found that treatment with ω-3 PUFA significantly increased the NAD+/NADH ratio and SIRT1 activity following TBI. In addition, ω-3 PUFA supplementation increased Beclin-1 deacetylation and its nuclear export and induced direct interactions between cytoplasmic Beclin-1 and Bcl-2 by increasing SIRT1 activity following TBI. These events led to the inhibition of neuronal apoptosis and to neuroprotective effects through enhancing autophagy after TBI, possibly due to elevated SIRT1. CONCLUSIONS: ω-3 PUFA supplementation attenuated TBI-induced neuronal apoptosis by inducing the autophagy pathway through the upregulation of SIRT1-mediated deacetylation of Beclin-1.

Omega-3 polyunsaturated fatty acid attenuates the inflammatory response by modulating microglia polarization through SIRT1-mediated deacetylation of the HMGB1/NF-κB pathway following experimental traumatic brain injury.

BACKGROUND: Microglial polarization and the subsequent neuroinflammatory response are contributing factors for traumatic brain injury (TBI)-induced secondary injury. High mobile group box 1 (HMGB1) mediates the activation of the NF-κB pathway, and it is considered to be pivotal in the late neuroinflammatory response. Activation of the HMGB1/NF-κB pathway is closely related to HMGB1 acetylation, which is regulated by the sirtuin (SIRT) family of proteins. Omega-3 polyunsaturated fatty acids (ω-3 PUFA) are known to have antioxidative and anti-inflammatory effects. We previously demonstrated that ω-3 PUFA inhibited TBI-induced microglial activation and the subsequent neuroinflammatory response by regulating the HMGB1/NF-κB signaling pathway. However, no studies have elucidated if ω-3 PUFA affects the HMGB1/NF-κB pathway in a HMGB1 deacetylation of dependent SIRT1 manner, thus regulating microglial polarization and the subsequent neuroinflammatory response. METHODS: The Feeney DM TBI model was adopted to induce brain injury in rats. Modified neurological severity scores, rotarod test, brain water content, and Nissl staining were employed to determine the neuroprotective effects of ω-3 PUFA supplementation. Assessment of microglia polarization and pro-inflammatory markers, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, and HMGB1, were used to evaluate the neuroinflammatory responses and the anti-inflammatory effects of ω-3 PUFA supplementation. Immunofluorescent staining and western blot analysis were used to detect HMGB1 nuclear translocation, secretion, and HMGB1/NF-κB signaling pathway activation to evaluate the effects of ω-3 PUFA supplementation. The impact of SIRT1 deacetylase activity on HMGB1 acetylation and the interaction between HMGB1 and SIRT1 were assessed to evaluate anti-inflammation effects of ω-3 PUFAs, and also, whether these effects were dependent on a SIRT1-HMGB1/NF-κB axis to gain further insight into the mechanisms underlying the development of the neuroinflammatory response after TBI. RESULTS: The results of our study showed that ω-3 PUFA supplementation promoted a shift from the M1 microglial phenotype to the M2 microglial phenotype and inhibited microglial activation, thus reducing TBI-induced inflammatory factors. In addition, ω-3 PUFA-mediated downregulation of HMGB1 acetylation and its extracellular secretion was found to be likely due to increased SIRT1 activity. We also found that treatment with ω-3 PUFA inhibited HMGB1 acetylation and induced direct interactions between SIRT1 and HMGB1 by elevating SIRT1 activity following TBI. These events lead to inhibition of HMGB1 nucleocytoplasmic translocation/extracellular secretion and alleviated HMGB1-mediated activation of the NF-κB pathway following TBI-induced microglial activation, thus inhibiting the subsequent inflammatory response. CONCLUSIONS: The results of this study suggest that ω-3 PUFA supplementation attenuates the inflammatory response by modulating microglial polarization through SIRT1-mediated deacetylation of the HMGB1/NF-κB pathway, leading to neuroprotective effects following experimental traumatic brain injury.

Tetrahydrocurcumin Provides Neuroprotection in Experimental Traumatic Brain Injury and the Nrf2 Signaling Pathway as a Potential Mechanism.

The protective effect of tetrahydrocurcumin (THC) after experimental traumatic brain injury (TBI) has been demonstrated, as demonstrated by the inhibition of oxidative stress, mitochondrial dysfunction, and apoptosis. However, the mechanisms underlying this effect are still not well understood. This study was to investigate the neuroprotective effects of THC, and its potential mechanisms, in a rat model of TBI. To this end, rats were divided into 4 groups: the sham group, the TBI group, the TBI + vehicle (V) group, and the TBI + THC group. THC or V was administered via intraperitoneal injection to rats in the TBI + V and TBI + THC groups 30 min after TBI. After euthanasia (24 h after TBI), neurological scores, brain water content, and neuronal cell death in the cerebral cortex were recorded. Brain samples were collected after neurological scoring for further analysis. THC treatment alleviated brain edema, attenuated TBI-induced neuronal cell apoptosis, and improved neurobehavioral function. In addition, NFE2-related factor 2 (Nrf2) expression was upregulated following TBI. These results suggest that THC improves neurological outcome after TBI, possibly by activating the Nrf2 signaling pathway.

Response of microbial communities to roxarsone under different culture conditions.

Roxarsone is a feed additive widely used in the broiler and swine industries that has the potential to contaminate the environment, mainly via the use of poultry manure as fertilizer, which results in release of inorganic arsenic to the soil and water. This study was conducted to investigate roxarsone degradation and the response of the microbial community under different culture conditions using high-throughput sequencing technology. Poultry litter was incubated for 288 h in the presence of roxarsone under light aerobic, dark aerobic, or dark anaerobic conditions. The results showed that roxarsone was completely degraded after 48 h of dark anaerobic incubation, while 79.9% and 94.5% of roxarsone was degraded after 288 h of dark aerobic and light aerobic incubation, respectively. Under dark aerobic conditions with microbial inhibitor sodium azide, roxarsone was rarely degraded during the 288 h of incubation, illustrating that microorganisms play an important role in roxarsone degradation. Microbial community structure was significantly different among various culture conditions. Olivibacter, Sphingobacterium, and Proteiniphilum were the top 3 genera in the control samples. Sphingobacterium and Alishewanella dominated the light aerobic samples, while the dominant microflora of the dark aerobic samples were Acinetobacter spp. Pseudomonas and Advenella were the predominant genera of dark anaerobic samples. This study emphasizes the potential importance of microbes in roxarsone degradation and expands our current understanding of microbial ecology during roxarsone degradation under different environmental conditions.

Response of soil microbial communities to roxarsone pollution along a concentration gradient.

The extensive use of roxarsone (3-nitro-4-hydroxyphenylarsonic acid) as a feed additive in the broiler poultry industry can lead to environmental arsenic contamination. This study was conducted to reveal the response of soil microbial communities to roxarsone pollution along a concentration gradient. To explore the degradation process and degradation kinetics of roxarsone concentration gradients in soil, the concentration shift of roxarsone at initial concentrations of 0, 50, 100, and 200 mg/kg, as well as that of the arsenic derivatives, was detected. The soil microbial community composition and structure accompanying roxarsone degradation were investigated by high-throughput sequencing. The results showed that roxarsone degradation was inhibited by a biological inhibitor, confirming that soil microbes were absolutely essential to its degradation. Moreover, soil microbes had considerable potential to degrade roxarsone, as a high initial concentration of roxarsone resulted in a substantially increased degradation rate. The concentrations of the degradation products HAPA (3-amino-4-hydroxyphenylarsonic acid), AS(III), and AS(V) in soils were significantly positively correlated. The soil microbial community composition and structure changed significantly across the roxarsone contamination gradient, and the addition of roxarsone decreased the microbial diversity. Some bacteria tended to be inhibited by roxarsone, while Bacillus, Paenibacillus, Arthrobacter, Lysobacter, and Alkaliphilus played important roles in roxarsone degradation. Moreover, HAPA, AS(III), and AS(V) were significantly positively correlated with Symbiobacterium, which dominated soils containing roxarsone, and their abundance increased with increasing initial roxarsone concentration. Accordingly, Symbiobacterium could serve as indicator of arsenic derivatives released by roxarsone as well as the initial roxarsone concentration. This is the first investigation of microbes closely related to roxarsone degradation.

Anaerobic oxidation of methane driven by different electron acceptors: A review.

Methane, the most significant reduced form of carbon on Earth, acts as a crucial fuel and greenhouse gas. Globally, microbial methane sinks encompass both aerobic oxidation of methane (AeOM), conducted by oxygen-utilizing methanotrophs, and anaerobic oxidation of methane (AOM), performed by anaerobic methanotrophs employing various alternative electron acceptors. These electron acceptors involved in AOM include sulfate, nitrate/nitrite, humic substances, and diverse metal oxides. The known anaerobic methanotrophic pathways comprise the internal aerobic oxidation pathway found in NC10 bacteria and the reverse methanogenesis pathway utilized by anaerobic methanotrophic archaea (ANME). Diverse anaerobic methanotrophs can perform AOM independently or in cooperation with symbiotic partners through several extracellular electron transfer (EET) pathways. AOM has been documented in various environments, including seafloor methane seepages, coastal wetlands, freshwater lakes, soils, and even extreme environments like hydrothermal vents. The environmental activities of AOM processes, driven by different electron acceptors, primarily depend on the energy yields, availability of electron acceptors, and environmental adaptability of methanotrophs. It has been suggested that different electron acceptors driving AOM may occur across a wider range of habitats than previously recognized. Additionally, it is proposed that methanotrophs have evolved flexible metabolic strategies to adapt to complex environmental conditions. This review primarily focuses on AOM, driven by different electron acceptors, discussing the associated reaction mechanisms and the habitats where these processes are active. Furthermore, it emphasizes the pivotal role of AOM in mitigating methane emissions.

Influence of dissolved organic matter on the anaerobic biotransformation of roxarsone accompanying microbial community response.

Roxarsone (ROX), commonly employed as a livestock feed additive, largely remains unmetabolized and is subsequently excreted via feces. ROX could cause serious environmental risks due to its rapid transformation and high mobility in the anaerobic subsurface environment. Dissolved organic matter (DOM) is an important constituent of fecal organics in livestock waste and could affect the ROX biotransformation. Nonetheless, the underlying mechanisms governing the interaction between DOM and ROX biotransformation have not yet been elucidated in the anaerobic environment. In this study, the changes of ROX, metabolites, and microbial biomass in the solutions with varying DOM concentrations (0, 50, 100, 200, and 400 mg/L) under anaerobic environments were investigated during the ROX (200 mg/L) degradation. EEM-PARAFAC and metagenomic sequencing were combined to identify the dynamic shifts of DOM components and the functional microbial populations responsible for ROX degradation. Results indicated that DOM facilitated the anaerobic biotransformation of ROX and 200 mg/L ROX could be degraded completely in 28 h. The tryptophan-like within DOM functioned as a carbon source to promote the growth of microorganisms, thus accelerating the degradation of ROX. The mixed microflora involved in ROX anaerobic degrading contained genes associated with arsenic metabolism (arsR, arsC, acr3, arsA, nfnB, and arsB), and arsR, arsC, acr3 exhibited high microbial diversity. Variations in DOM concentrations significantly impacted the population dynamics of microorganisms involved in arsenic metabolism (Proteiniclasticum, Exiguobacterium, Clostridium, Proteiniphilum, Alkaliphilus, and Corynebacterium spp.), which in turn affected the transformation of ROX and its derivatives. This study reveals the mechanism of ROX degradation influenced by the varying concentrations of DOM under anaerobic environments, which is important for the prevention of arsenic contamination with elevated levels of organic matter.

Genome-wide characterization of extrachromosomal circular DNA in SLE and functional analysis reveal their association with apoptosis.

Extrachromosomal circular DNA (eccDNA) derived from linear chromosomes, are showed typical nucleosomal ladder pattern in agarose gel which as a known feature of apoptosis and demonstrated to be immunogenicity. In systemic lupus erythematosus (SLE) patients, elevated levels of cell-free DNA (cfDNA) can be found in either linear forms or circular forms, while circular ones are much less common and harder to detect. The molecular characteristics and function of circular forms in plasma SLE patients remains elusive. Herein, we characterized the hallmarks of plasma eccDNA in SLE patients, including the lower normalized number and GC content of eccDNA in SLE plasma than in the healthy, and SLE eccDNA number positively correlated with C3 and negatively with anti-dsDNA antibodies. The differential eccGenes (eccDNAs carrying the protein coding gene sequence) of SLE was significantly enriched in apoptosis-related pathways. The artificially synthesized eccDNA with sequences of the PRF1 exon region could promote transcriptional expression of PRF1, IFNA and IFIT3 and inhibit early-stage apoptosis. Plasma eccDNA can serve as a novel autoantigen in the pathogenesis of SLE.

Deciphering the seasonal dynamics of multifaceted aerosol-ozone interplay: Implications for air quality management in Eastern China.

We employed an enhanced WRF-Chem to investigate the discrete mechanisms of aerosol-radiation-feedback (ARF), extinction-photochemistry (AEP), and heterogeneous-reactions (AHR) across different seasons in eastern China, aiming to assess the synergistic effects arising from the simultaneous operation of multiple processes on O3 and PM2.5. Our findings demonstrated that ARF fostered the accumulation of pollutants and moisture, initiating two distinct feedback mechanisms concerning O3. The elevation in the NO/NO2 ratio amplified O3 consumption. Increased near-surface moisture diminished upper-level cloud formation, thereby enhancing photolysis rates and O3 photochemical production. The pronounced impact of heightened NO/NO2 on O3 led to a decrease of 0.1-2.7 ppb. When decoupled from ARF, AEP led to a more significant reduction in photolysis rates, resulting in declines in both O3 and PM2.5, except for an anomalous increase observed in summer, with O3 increasing by 1.6 ppb and PM2.5 by 2.5 µg m-3. The heterogeneous absorption of hydroxides in spring, autumn, and winter predominantly governed the AHR-induced variation of O3, leading to a decrease in O3 by 0.7-1 ppb. Conversely, O3 variations in summer were primarily dictated by O3-sensitive chemistry, with heterogeneous absorption of NOy catalyzing a decrease of 2.4 ppb in O3. Furthermore, AHR accentuated PM2.5 by facilitating the formation of fine sulfates and ammonium while impeding nitrate formation. In summer, the collective impact of ARF, AEP, and AHR (ALL) led to a substantial reduction of 6.2 ppb in O3, alleviating the secondary oxidation of PM2.5 and leading to a decrease of 0.3 µg m-3 in PM2.5. Conversely, albeit aerosol substantially depleted O3 by 0.4-4 ppb through their interactions except for summer, aerosol feedback on PM2.5 was more pronounced, resulting in a significant increase of 1.7-6.1 µg m-3 in PM2.5. Our study underscored the seasonal disparities in the ramifications of multifaceted aerosol-ozone interplay on air quality.

Evolution of groundwater hydrochemical characteristics and formation mechanism during groundwater recharge: A case study in the Hutuo River alluvial-pluvial fan, North China Plain.

A pilot project for groundwater recharge from rivers is currently being carried out in North China Plain. To investigate the influence of river recharge on groundwater hydrochemical characteristics, dynamic monitoring and analysis of groundwater samples were conducted at a typical recharge site in the Hutuo River alluvial-pluvial fan in the North China Plain from 2019 to 2021. Hydrochemical, isotopic, and multivariate statistical analyses were used to systematically reveal the spatiotemporal variation of groundwater chemistry and its driving factors during groundwater recharge process. The results showed that the groundwater hydrochemical types and characteristics in different recharge areas and recharge periods exhibited obvious spatiotemporal differences. The groundwater type varied from HCO3·SO4-Na·Mg to HCO3·SO4-Ca·Mg in an upstream ecological area, while the groundwater type changed from SO4·HCO3-Mg·Ca to HCO3·SO4-Ca·Mg in the downstream impacted by reclaimed water. Changes in the contents of Ca2+, Mg2+ and HCO3- were mostly controlled by the water-rock interactions and mixing-dilution of recharge water, while the increases in Na+, NO3-, Cl-, SO42- and NO3- contents were mainly due to the infiltration of reclaimed water. Nitrogen and oxygen isotope (δ15N and δ18O) tests and the Bayesian isotope mixing model results further demonstrated that nitrate pollution mainly originated from anthropogenic sources, and the major contribution came from manure and sewage, with an average proportion of 64.6 %. Principal component analysis indicated that water-rock interactions, river-groundwater mixing and redox environment alternation were dominant factors controlling groundwater chemical evolution in groundwater recharge process.

Predicting the speciation of ionizable antibiotic ciprofloxacin by biochars with varying carbonization degrees.

Sorption mechanisms of ionizable organic pollutants by biochars and approaches for the prediction of sorption are still unclear. In this study, batch experiments were conducted to explore the sorption mechanisms of woodchip-derived biochars prepared at 200-700 °C (referred as WC200-WC700) for cationic, zwitterionic and anionic species of ciprofloxacin (referred as CIP+, CIP± and CIP-, respectively). The results revealed that the sorption affinity of WC200 for different CIP species was in the order of CIP± > CIP+ > CIP-, while that of WC300-WC700 remained the order of CIP+ > CIP± > CIP-. WC200 exhibited a strong sorption ability, which could be attributed to hydrogen bonding and electrostatic attraction with CIP+, electrostatic attraction with CIP±, and charge-assisted hydrogen bonding with CIP-. Pore filling and π-π interactions contributed to the sorption of WC300-WC700 for CIP+, CIP± and CIP-. Rising temperature facilitated CIP sorption to WC400 as verified by site energy distribution analysis. Proposed models including the proportion of the three CIP species and sorbent aromaticity index (H/C) can quantitatively predict CIP sorption to biochars with varying carbonization degrees. These findings are vital to elucidating the sorption behaviors of ionizable antibiotics to biochars and exploring potential sorbents for environmental remediation.

Effects of dissolved organic matter derived from chicken manure on the biotransformation of roxarsone in soil.

Roxarsone (3-nitro-4-hydroxyphenylarsonic acid, ROX), widely used as a livestock feed additive, is excreted untransformed in large concentrations. Accumulation of this manure in the open environment increases dissolved organic matter (DOM) and ROX in soil within the aeration zone. And microbial action plays a dominant role in the transformation of ROX. However, the specific effect of DOM on the biotransformation of ROX is not known. In this paper, we investigated the transformation rate, metabolite content, and microbial community response of ROX in soils with different DOM concentrations (71.61, 100, 200, 500, and 800 mg L-1). The transformation of ROX was consistent with first-order transformation kinetics. DOM promoted the transformation of ROX, and with high DOM (DOM ≥200 mg L-1), ROX was transformed almost completely within two days. In this case, DOM provided nutrients to microorganisms and promoted their growth, accelerating the transformation of ROX. Also, the solubility of ROX was enhanced by DOM to increase its bioavailability. The microbial diversity was negatively correlated with DOM concentration and ROX transformation time; during the transformation of ROX, Bacillus, Arthrobacter, Enterococcus, Acinetobacter, and Pseudomonas became dominant in the soil with anomalously high levels of DOM. This study demonstrates the transformation process of ROX under actual environmental conditions where organic matter coexists with ROX, and this understanding is important for the prevention and control of arsenic pollution in soil within the aeration zone with anomalously high levels of DOM.

Spatio-temporal analysis of the sources and transformations of anthropogenic nitrogen in a highly degraded coastal basin in Southeast China.

Nitrogen transport from terrestrial to aquatic environments could cause water quality deterioration and eutrophication. By sampling in the high- and low-flow periods in a highly disturbed coastal basin of Southeast China, hydrochemical characteristics, nitrate stable isotope composition, estimation of potential nitrogen source input fluxes, and the Bayesian mixing model were combined to determine the sources and transformation of nitrogen. Nitrate was the main form of nitrogen. Nitrification, nitrate assimilation, and NH4+ volatilization were the main nitrogen transformation processes, whereas denitrification was limited due to the high flow rate and unsuitable physicochemical properties. For both sampling periods, non-point source pollution from the upper to the middle reaches was the main source of nitrogen, especially in the high-flow period. In addition to synthetic fertilizer, atmospheric deposition and sewage and manure input were also major nitrate sources in the low-flow period. Hydrological condition was the main factor determining nitrate transformation in this coastal basin, despite the high degree of urbanization and the high volume of sewage discharge in the middle to the lower reaches. The findings of this study highlight that the control of agricultural non-point contamination sources is essential to pollution and eutrophication alleviation, especially for watersheds that receive high amounts of annual precipitation.