Pollution Characteristics and Health Risk Assessment of Phthalate Esters in PSW Recycling Sites: A Typical Case Study.

The concentrations of six priority phthalate esters (PAEs) in 700 soil samples and 110 sediment samples from an area in China containing plastic solid waste (PSW) recycling sites were determined. The total concentrations of the six PAEs in soil and sediment were not detected - 274 and not detected - 597 mg kg-1, respectively, and the mean concentrations in soil and sediment were 14.4 and 31.7 mg kg-1, respectively. The dominant PAEs were di(2-ethylhexyl) phthalate and di-n-butyl phthalate. PAEs were detected in soil collected from the surface to 0.5 m below ground level around the PSW recycling sites, and the concentrations were markedly higher in these areas than at other polluted sites. PSW recycling is an important source of PAEs to soil and sediment. The di(2-ethylhexyl)phthalate concentrations in soil were higher than the relevant concentrations that pose environmental risks for sensitive land uses and non-sensitive land uses (42 and 121 mg kg-1, respectively), indicating emissions of PAEs from PSW recycling sites may pose environmental risks. The results indicate that PAE pollution at PSW sites needs to be better controlled and managed.

Bioaccessibility and Toxicity Assessment of Polycyclic Aromatic Hydrocarbons in Two Contaminated Sites.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous soil contaminants, and their bioaccessibility determines their environmental risks in contaminated land. In the present study, the residual concentrations of PAHs in the soils of two industrial sites were determined, and their bioaccessibility was estimated by the hydroxypropyl-ß-cyclodextrin extraction (HPCD) extraction method. The results showed heavy PAH contamination at both site S1 (0.38-3342.5 mg kg-1) and site S2 (0.2-138.18 mg kg-1), of which high molecular weight (HMW) PAHs (4-, 5-, and 6-ring compounds) accounted for approximately 80%. The average bioaccessibility of PAHs at sites S1 and S2 was 52.02% and 29.28%, respectively. The bioaccessibility of certain PAH compounds decreased with increasing ring number of the molecule. Lower PAH bioaccessibility was detected in loamy and silty soil textures than in sandy soil. Moreover, among the soil properties, the dissolved organic matter, total organic carbon, total potassium, and total manganese concentrations had significant effects on the bioaccessibility of PAHs. The toxicity analysis showed that the composition and bioaccessibility of PAHs could affect their potential toxicity in soil. We suggest that bioaccessibility should be taken into consideration when assessing the toxicity of PAHs in soil, and more attention should be given to low-ring PAHs with high bioaccessibility.

Multi-pathway assessment of human health risk posed by polycyclic aromatic hydrocarbons.

To assess aggregate exposure to polycyclic aromatic hydrocarbons (PAHs) via several environmental media and pathways, a probabilistic framework for multi-pathway health risk assessment that integrates PAHs potency equivalence factors, risk estimation modeling, and Monte Carlo simulation was applied to a case study in Nanjing, which is an important industrial city in China. Incremental lifetime risk of additional cancers posed by exposure to 16 USEPA priority PAHs in air, water, soil, and fish was assessed. Risks to three age groups, infants, children, and adults, through various exposure pathways, including oral ingestion, dermal absorption, and inhalation, were estimated. Results of the analysis of risk indicated that B[a]P, B[b]F, and BA were the predominant PAHs pollutants in Nanjing. Risk of additional cancer for local adults was on average 2.62 × 10(-5). The risks were primarily due to ingestion of fish and inhalation, which contributed 99 % of the total risks. By contrast, risk to infants was essentially negligible. Results of a sensitivity analysis indicated that the input variables of concentration of PAHs in fish (C f), the body weight (BW), and the ingestion rate of fish (IRf) were the major influences on estimates of risks.

Two-phase system model to predict hydrophobic organic compound partition to heterogeneous soil dissolved organic matter across China.

Soil dissolved organic matter (SDOM) is an important part of the DOM pool in terrestrial systems, influencing the transport and fate of many pollutants. In this study, SDOMs from different regions across China were compared by a series of spectroscopic methods, including UV-vis spectroscopy, fluorescence spectroscopy, and Fourier transform infrared (FTIR) spectroscopy, and the hydrophobicity was quantified by partition coefficients of SDOM in the aqueous two-phase system (KATPS). The molecular weight, aromaticity, and hydrophobicity of SDOM from different regions exhibited strong heterogeneity, KATPS combined with UV-vis and fluorescence indices can be readily used for differentiating heterogeneous SDOM, and SDOMs were compositionally and structurally different from DOMs in aquatic systems based on spectral characterization. Importantly, the two-phase system (TPS) model has only been validated by DOMs in freshwater systems, and good organic carbon‒water partition coefficient (KOC) predictive power (RMSE = 0.11) could be provided by the TPS model when applied to heterogeneous SDOM without calibration, showing its broad applicability. Our results demonstrate the applicability of the TPS model for predicting the sorption behavior of terrestrial DOM, broadening the application scope of the TPS model and indicating its potential as a routine model for the risk assessment of hydrophobic organic compounds (HOCs) in organic contaminated sites.

Identification of trace organic pollutants in drinking water and the associated human health risks in Jiangsu Province, China.

Organochlorine pesticides (OCPs), polycyclic aromatic hydrocarbons (PAHs), dibutyl phthalate (DNBP) and di-2-ethylhexyl phthalate (DEHP) were all detectable in surface water in Jiangsu Province, China. Concentrations of OCPs ranged from 5.13 to 8.15 ng/L. PAHs were found ranging from 14.7 to 24.5 ng/L. Concentrations of DNBP and DEHP ranged from 16 to 5,857.5 ng/L and 556 to 15,670.7 ng/L, respectively. Greater than 70 % of chemicals were removed in water treatment processes. The carcinogenic risks posed by trace organic pollutants through tap water ingestion were lower than 10(-6), and the noncarcinogenic risks were less than 10(-5).

Detection of the SARS-CoV-2 Delta Variant in the Transboundary Rivers of Yunnan, China.

Ruili and Longchuan, two border counties in southwestern China, are facing epidemic control challenges due to the high rate of COVID-19 infections originating from neighboring Myanmar. Here, we aimed to establish the applicability of wastewater and environmental water surveillance of SARS-CoV-2 and conduct whole-genome sequencing (WGS) to trace the possible infection origin. In August 2021, total 72 wastewater and river water samples were collected from 32 sampling sites. SARS-CoV-2 ORF1ab and N genes were measured by RT-qPCR. We found that 19 samples (26.39%) were positive, and the viral loads of ORF1ab and N genes were 6.62 × 102-2.55×105 and 1.86 × 103-2.32 × 105 copies/L, respectively. WGS further indicated the sequences in two transboundary river samples, and one hospital wastewater sample belonged to the delta variant, suggesting that the infection source might be areas with high COVID-19 delta variant incidence in Southeast Asia (e.g., Myanmar). We reported for the first time the detection and quantification of SARS-CoV-2 RNA in the transboundary rivers of Myanmar-China. Our findings demonstrate that wastewater and environmental water may provide independent and nonintrusive surveillance points to monitor the global spread of emerging COVID-19 variants of concern, particularly in high-risk regions or border areas with considerable epidemic challenges and poor wastewater treatment facilities.

MRI evaluation of axonal reorganization after bone marrow stromal cell treatment of traumatic brain injury.

We treated traumatic brain injury (TBI) with human bone marrow stromal cells (hMSCs) and evaluated the effect of treatment on white matter reorganization using MRI. We subjected male Wistar rats (n = 17) to controlled cortical impact and either withheld treatment (controls; n = 9) or inserted collagen scaffolds containing hMSCs (n = 8). Six weeks later, the rats were sacrificed and MRI revealed selective migration of grafted neural progenitor cells towards the white matter reorganized boundary of the TBI-induced lesion. Histology confirmed that the white matter had been reorganized, associated with increased fractional anisotropy (FA; p < 0.01) in the recovery regions relative to the injured core region in both treated and control groups. Treatment with hMSCs increased FA in the recovery regions, lowered T(2) in the core region, decreased lesion volume and improved functional recovery relative to untreated controls. Immunoreactive staining showed axonal projections emanating from neurons and extruding from the corpus callosum into the ipsilateral cortex at the boundary of the lesion. Fiber tracking (FT) maps derived from diffusion tensor imaging confirmed the immunohistological data and provided information on axonal rewiring. The apparent kurtosis coefficient (AKC) detected additional axonal remodeling regions with crossing axons, confirmed by immunohistological staining, compared with FA. Our data demonstrate that AKC, FA, FT and T(2) can be used to evaluate treatment-induced white matter recovery, which may facilitate restorative therapy in patients with TBI.

New insights into the responses of soil microorganisms to polycyclic aromatic hydrocarbon stress by combining enzyme activity and sequencing analysis with metabolomics.

Polycyclic aromatic hydrocarbons (PAHs), some of the most widespread organic contaminants, are highly toxic to soil microorganisms. Whether long-term polluted soils can still respond to the fresh input of pollutants is unknown. In this study, the soil enzyme activity, soil microbial community structure and function and microbial metabolism pathways were examined to systematically investigate the responses of soil microorganisms to fresh PAH stress. Microbial activity as determined by soil dehydrogenase and urease activity was inhibited upon microbe exposure to PAH stress. In addition, the soil microbial community and function were obviously shifted under PAH stress. Both microbial diversity and richness were decreased by PAH stress. Rhizobacter, Sphingobium, Mycobacterium, Massilia, Bacillus and Pseudarthrobacter were significantly affected by PAH stress and can be considered important indicators of PAH contamination in agricultural soils. Moreover, the majority of microbial metabolic function predicted to respond to PAH stress were affected adversely. Finally, soil metabolomics further revealed specific inhibition of soil metabolism pathways associated with fatty acids, carbohydrates and amino acids. Therefore, the soil metabolic composition distinctively changed, reflecting a change in the soil metabolism. In summary, fresh contaminant introduction into long-term polluted soils inhibited microbial activity and metabolism, which might profoundly affect the whole soil quality.

Simvastatin-mediated upregulation of VEGF and BDNF, activation of the PI3K/Akt pathway, and increase of neurogenesis are associated with therapeutic improvement after traumatic brain injury.

This study was undertaken to evaluate the effect of simvastatin, a cholesterol-lowering agent, on the Akt-mediated signaling pathway and neurogenesis in the dentate gyrus (DG) of the hippocampus in rats after traumatic brain injury (TBI). Adult male Wistar rats were divided into three groups: (1) sham group (n = 8); (2) saline control group (n = 40); and (3) simvastatin-treated group (n = 40). Controlled cortical impact (CCI) injury was performed over the left parietal lobe. Simvastatin was administered orally at a dose of 1 mg/kg starting at day 1 after TBI and then daily for 14 days. Bromodeoxyuridine (BrdU) was injected intraperitoneally into rats. A modified Morris Water Maze (WM) task was performed between 31 and 35 days after treatment to test spatial memory (n = 8/group). Animals were sacrificed at 1, 3, 7, 14, and 35 days after treatment (n = 8/group/time point). Western blot was utilized to investigate the changes in the Akt-mediated signaling pathway. Enzyme-linked immunosorbent assay (ELISA) analyses were employed to measure vascular endothelial growth factor (VEGF) and brain-derived neurotrophin factor (BDNF) expression. Immunohistochemical and fluorescent staining were performed to detect the BrdU- and neuronal nuclei (NeuN)/BrdU-positive cells. Our data show that simvastatin treatment increases phosphorylation of v-akt murine thymoma viral oncogene homolog (Akt), glycogen synthase kinase-3beta (GSK-3beta), and cAMP response element-binding proteins (CREB); elevates the expression of BDNF and VEGF in the DG; increases cell proliferation and differentiation in the DG; and enhances the recovery of spatial learning. These data suggest that the neurorestorative effect of simvastatin may be mediated through activation of the Akt-mediated signaling pathway, subsequently upregulating expression of growth factors and inducing neurogenesis in the DG of the hippocampus, thereby leading to restoration of cognitive function after TBI in rats.

Long-lasting benefits after treatment of traumatic brain injury (TBI) in rats with combination therapy of marrow stromal cells (MSCs) and simvastatin.

This study was designed to investigate the beneficial effects of combination therapy of simvastatin and marrow stromal cells (MSCs) in improving functional outcome after traumatic brain injury (TBI) in rats. Adult female Wistar rats (n=72 and 8, per group) were injured with controlled cortical impact and treated either with monotherapy of MSCs or simvastatin or a combination therapy of these two agents. Different combination doses were tested, and nine groups of animals were studied. Neurological function was evaluated using Modified Neurological Severity Score (MNSS), and animals were sacrificed 3 months after injury. Coronal brain sections were stained with standard hematoxylin and eosin immunohistochemistry. Our results showed that, though functional improvement was seen with monotherapies of MSCs and simvastatin, the combination therapy when used in optimal doses was significantly better in improving functional outcome. This improvement was long lasting and persisted until the end of the trial (3 months). The optimum combination dose was 0.5mg of simvastatin combined with 2 x 10(6) MSCs. Post mortem analysis showed the presence of donor MSCs within the injured cortex. Endogenous cellular proliferation induced by the neurorestorative treatments was also observed in the lesion boundary zone. Our data show that MSCs and simvastatin have a synergistic effect in improving functional outcome after TBI.

Treatment of traumatic brain injury in mice with marrow stromal cells.

This study was designed to investigate the potential beneficial effects of bone marrow stromal cell (MSC) treatment of traumatic brain injury (TBI) in mice. Twelve female C57BL/6J mice (weight, 21-26 g) were injured with controlled cortical impact and divided into 2 groups (n=6 each). The experimental group was injected with MSCs (0.3x10(6)) intravenously one day after TBI, whereas the control group was injected with saline. MSCs were harvested from male mice, and male to female transplantation was performed to identify male donor cells within female recipient animals. This was achieved by localizing Y chromosomes within the female mice. Neurological function was assessed using the Morris water maze and foot fault tests. All mice were sacrificed 35 days after TBI. Brain sections were stained using in situ hybridization and immunohistochemistry to identify MSCs as well as to analyze vascular density following MSC treatment. Both modalities of testing demonstrated significant improvement in neurological function in the MSC-treated group compared to the saline-treated control group (p<0.05). Histologically, Y chromosome labeled MSCs were easily identified in the injured brain, localized primarily around the lesion boundary zone. There was also a significant increase in vascular density in the lesion boundary zone and hippocampus of MSC-treated mice compared to control mice. This is the first study to show beneficial effects of MSC treatment after TBI in mice.

Histological and functional outcomes after traumatic brain injury in mice null for the erythropoietin receptor in the central nervous system.

Erythropoietin (EPO) and its receptor (EPOR), essential for erythropoiesis, are expressed in the nervous system. Recombinant human EPO treatment promotes functional outcome after traumatic brain injury (TBI) and stroke, suggesting that the endogenous EPO/EPOR system plays an important role in neuroprotection and neurorestoration. This study was designed to investigate effects of the EPOR on histological and functional outcomes after TBI. Experimental TBI was induced in adult EPOR-null and wild-type mice by controlled cortical impact. Neurological function was assessed using the modified Morris Water Maze and footfault tests. Animals were sacrificed 35 days after injury and brain sections stained for immunohistochemistry. As compared to the wild-type injured mice, EPOR-null mice did not exhibit higher susceptibility to TBI as exemplified by tissue loss in the cortex, cell loss in the dentate gyrus, impaired spatial learning, angiogenesis and cell proliferation. We observed that less cortical neurogenesis occurred and that sensorimotor function (i.e., footfault) was more impaired in the EPOR-null mice after TBI. Co-accumulation of amyloid precursor protein (axonal injury marker) and calcium was observed in the ipsilateral thalamus in both EPOR-null and wild-type mice after TBI with more calcium deposits present in the wild-type mice. This study demonstrates for the first time that EPOR null in the nervous system aggravates sensorimotor deficits, impairs cortical neurogenesis and reduces thalamic calcium precipitation after TBI.

Effects of erythropoietin on reducing brain damage and improving functional outcome after traumatic brain injury in mice.

OBJECT: This study was designed to investigate the beneficial effects of recombinant human erythropoietin (rhEPO) treatment of traumatic brain injury (TBI) in mice. METHODS: Adult male C57BL/6 mice were divided into 3 groups: 1) the saline group (TBI and saline [13 mice]); 2) EPO group (TBI and rhEPO [12]); and 3) sham group (sham and rhEPO [8]). Traumatic brain injury was induced by controlled cortical impact. Bromodeoxyuridine (100 mg/kg) was injected daily for 10 days, starting 1 day after injury, for labeling proliferating cells. Recombinant human erythropoietin was administered intraperitoneally at 6 hours and at 3 and 7 days post-TBI (5000 U/kg body weight, total dosage 15,000 U/kg). Neurological function was assessed using the Morris water maze and footfault tests. Animals were killed 35 days after injury, and brain sections were stained for immunohistochemical evaluation. RESULTS: Traumatic brain injury caused tissue loss in the cortex and cell loss in the dentate gyrus (DG) as well as impairment of sensorimotor function (footfault testing) and spatial learning (Morris water maze). Traumatic brain injury alone stimulated cell proliferation and angiogenesis. Compared with saline treatment, rhEPO significantly reduced lesion volume in the cortex and cell loss in the DG after TBI and substantially improved recovery of sensorimotor function and spatial learning performance. It enhanced neurogenesis in the injured cortex and the DG. CONCLUSIONS: Recombinant human erythropoietin initiated 6 hours post-TBI provided neuroprotection by decreasing lesion volume and cell loss as well as neurorestoration by enhancing neurogenesis, subsequently improving sensorimotor and spatial learning function. It is a promising neuroprotective and neurorestorative agent for TBI and warrants further investigation.

Increase in phosphorylation of Akt and its downstream signaling targets and suppression of apoptosis by simvastatin after traumatic brain injury.

OBJECT: In their previous studies, the authors found that simvastatin treatment of traumatic brain injury (TBI) in rats had beneficial effects on spatial learning functions. In the current study they wanted to determine whether simvastatin suppressed neuronal cell apoptosis after TBI, and if so, they wanted to examine the underlying mechanisms of this process. METHODS: Saline or simvastatin (1 mg/kg) was administered orally to rats starting on Day 1 after TBI and then daily for 14 days. Modified Neurological Severity Scores were used to evaluate the sensory motor functional recovery. Rats were killed at 1, 3, 7, 14, and 35 days after treatment, and brain tissue was harvested for terminal deoxynucleotidyl nick-end labeling (TUNEL) staining, caspase-3 activity assay, and Western blot analysis. RESULTS: Simvastatin significantly decreased the modified Neurological Severity Scores from Days 7 to 35 after TBI, significantly reduced the number of TUNEL-positive cells at Day 3, suppressed the caspase-3 activity at Days 1 and 3 after TBI, and increased phosphorylation of Akt as well as Forkhead transcription factor 1, inhibitory-kappaB, and endothelial nitric oxide synthase, which are the downstream targets of the prosurvival Akt signaling protein. CONCLUSIONS: These data suggested that simvastatin reduces the apoptosis in neuronal cells and improves the sensory motor function recovery after TBI. These beneficial effects of simvastatin may be mediated through activation of Akt, Forkhead transcription factor 1 and nuclear factor-kappaB signaling pathways, which suppress the activation of caspase-3 and apoptotic cell death, and thereby, lead to neuronal function recovery after TBI.

Concentrations, spatial distributions, and congener profiles of polychlorinated dibenzo-p-dioxins and dibenzofurans around original plastic solid waste recovery sites in China.

The concentrations, profiles, and spatial distributions of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) in soil and sediment samples from several typical plastic solid waste (PSW) recovery sites (particularly from areas in which PSW is burned openly) in China were investigated. The results showed that burning PSW directly influenced PCDD/F concentrations immediately around the burning area. All of the samples in which soil contained black burning residue, collected from immediately around burning areas, had PCDD/F concentrations (mean 21708 ng kg-1) and toxic equivalent (TEQ) concentrations (mean 2140 ng I-TEQ kg-1 or 1877 ng WHO2006-TEQ kg-1) more than 100 times higher than the concentrations in samples collected away from burning areas (mean 222 ng kg-1, 8.75 ng I-TEQ kg-1, 7.96 ng WHO2006-TEQ kg-1). Principal component analysis and hierarchical cluster analysis indicated that the PCDD/F concentrations in seven soil samples from near PSW burning areas were influenced by PSW burning but that the PCDD/Fs in these soil samples may have had other or multiple sources. PCDD/F distributions at PSW recovery sites have been investigated in few previous studies. The results presented here indicate that appropriate measures should be taken to decrease the ecological risks posed by PSW recovery and to prevent, control, and remediate PCDD/F and other chemical contamination caused by PSW recovery.

Spatial distribution, risk and potential sources of lead in soils in the vicinity of a historic industrial site.

Because of measures taken by local and national government agencies to control releases of metals, former industrial sites in China that are contaminated with lead (Pb) in soils have been abandoned. Compared with historic sites themselves, little attention has been paid to contamination with Pb in areas surrounding these sites. In this study, a method by integrating sequential extraction and isotopic fingerprinting was proposed to reveal the key fractions of Pb contaminants in soils, trace their sources and determine the subject of liability for remediation. Topsoils from near a historic site, where lead oxide was produced, were found to be contaminated. Concentrations of Pb in soils were inversely proportional to distances from the industrial site and depth in soils. The predominant form of Pb was the Fe/Mn-oxide-bound fraction (FM3), which accounted for from 53.39% to 82.07% of total concentrations of Pb. Concentrations of Pb in vegetables produced on contaminated soils exceeded those allowed in food for consumption by humans. An assessment of hazards and risks posed by consumption of vegetables grown on these soils indicated relatively high potential for adverse effects on local residents around the closed plant. By use of isotopic finger printing for Pb, the abandoned factory was determined to be the most likely source of Pb in topsoils, especially fraction FM3. To mitigate exposures of people to Pb via consumption of locally produced food, recommended strategies should target legacy sources of Pb to soils in the vicinity of this historic industrial site.

Statins increase neurogenesis in the dentate gyrus, reduce delayed neuronal death in the hippocampal CA3 region, and improve spatial learning in rat after traumatic brain injury.

Traumatic brain injury (TBI) remains a major public health problem globally. Presently, there is no way to restore cognitive deficits caused by TBI. In this study, we seek to evaluate the effect of statins (simvastatin and atorvastatin) on the spatial learning and neurogenesis in rats subjected to controlled cortical impact. Rats were treated with atorvastatin and simvastatin 1 day after TBI and daily for 14 days. Morris water maze tests were performed during weeks 2 and 5 after TBI. Bromodeoxyuridine (BrdU; 50 mg/kg) was intraperitoneally injected 1 day after TBI and daily for 14 days. Brain tissue was processed for immunohistochemical staining to identify newly generated cells and vessels. Our data show that (1) treatment of TBI with statins improves spatial learning on days 31-35 after onset of TBI; (2) in the non-neurogenic region of the hippocampal CA3 region, statin treatment reduces the neuronal loss after TBI, demonstrating the neuroprotective effect of statins; (3) in the neurogenic region of the dentate gyrus, treatment of TBI with statins enhances neurogenesis; (4) statin treatment augments TBI-induced angiogenesis; and (5) treatment with simvastatin at the same dose provides a therapeutic effect superior to treatment with atorvastatin. These results suggest that statins may be candidates for treatment of TBI.