Identification of pollution point source in rivers is strenuous due to accidental chemical spills or unmanaged wastewater discharges. It is crucial to take physical characteristics into account in the estimation of pollution sources. In this study, an integrated inverse modeling framework is developed to identify a point source of accidental water pollution based on the contaminant concentrations observed at monitoring sites in time series. The modeling approach includes a Markov chain Monte Carlo method based on Bayesian inference (Bayesian-MCMC) inverse model and a genetic algorithm (GA) inverse model. Both inverse models can estimate the pollution sources, including the emission mass quantity, release time, and release position in an accidental river pollution event. The developed model is first tested for a hypothetical case with field river conditions. The results show that the source parameters identified by the Bayesian-MCMC inverse model are very close to the true values with relative errors of 0.02% or less; the GA inverse model also works with relative errors in the range of 2%–7%. Additionally, the uncertainties associated with model parameters are analyzed based on global sensitive analysis (GSA) in this study. It is also found that the emission mass of pollution source positively correlates with the dispersion coefficient and the river cross-sectional area, whereas the flow velocity significantly affects release position and release time. A real case study in the Fen River is further conducted to test the applicability of the developed inverse modeling approach. Results confirm that the Bayesian-MCMC model performs better than the GA model in terms of accuracy and stability for the field application. The findings of this study would support decision-making during emergency responses to river pollution incidents.

As a novel brominated flame retardant (NBFR), decabromodiphenyl ethane (DBDPE) has been poorly understood for the environmental fate and toxicity in terrestrial invertebrates. For the first time, the bioaccumulation, elimination, metabolism and detoxification of DBDPE in earthworms as well as its potential impacts on soil microbes were investigated. The results showed much higher DBDPE concentrations in casts than in earthworms. The bioaccumulation factor (BAF) and elimination rate constant (kₑ) values were 0.028–0.213 (gdw, worm/gdw, soil) and 0.323–0.452 (day⁻¹), respectively. The detoxifying enzymes (CYP450 and GST) could be induced by DBDPE within the range of exposure dosage, and the activities were significantly increased at 21 d (p < 0.05). The results were identified by GC-ECNI-MS, and it showed that at least eleven unknown peaks were separately observed in the earthworms, which were the biotransformation products of DBDPE in earthworms. Additionally, the damages, including skin shrinkage, setae impairment, and intercellular vacuolization, were clearly observed by SEM/TEM. Based on these data, DBDPE could accumulate in earthworms, yet, with low bioaccumulation ability. Moreover, DBDPE exposure resulted in minimal harmful impacts on microbial activities including microbial biomass C (MBC), Microbial basal respiration (MBR), Urease (US) activity and fluorescein diacetate hydrolase (FDA) activity (p < 0.05). Our findings would provide some essential information for interpreting the ecological risks of DBDPE in soil.

The historical air pollution with halogenated flame retardants (HFRs) in Germany was assessed by investigating tree leaf and shoot samples which have been archived in the German environmental specimen bank. Samples covered the period from 1985 to 2016. 43 HFRs comprising polybrominated diphenyl ethers as well as emerging brominated and chlorinated compounds such as Dechlorane Plus, DBDPE, or DPTE, were analysed in 115 samples from ten sub sites originating from six areas characterised by different land uses, including urban as well as a background site. HFRs were observed in each sample showing the widespread distribution of HFRs in Germany in tree leaves and shoots as bioindicators of past and present atmospheric pollution. Analytes observed at elevated concentrations were BDE 209, DBDPE and DPTE. Observed HFR-levels differed between analytes as well as sampling locations, particularly prior to the year 2000. They were typically highest at conurbation areas. Concentrations at the background site often belonged to the lowest ones observed, however, lowest values were not exclusively found there. The quantification frequencies appeared to decrease from the past to most recent samples. With few exceptions, atmospheric pollution of both, legacy and emerging HFRs, decreased significantly.

Deltamethrin is the most common type II synthetic pyrethroid insecticide, and has posed widespread residues to environment. However, whether deltamethrin has potential toxic effects on quail cerebrum remains greatly obscure. Accordingly, we investigated the impact of chronic exposure to deltamethrin on oxidative stress and apoptosis in quail cerebrum. Quails upon 12-week exposure of deltamethrin (0, 15, 30, or 45 mg/kg body weight intragastric administration) were used as a cerebrum injury model. The results showed that deltamethrin treatment led to cerebral injury dose-dependently through the weakened antioxidant defense by downregulating nuclear factor erythroid-2-related factor 2 (Nrf2) and its downstream proteins levels and mRNA expression. Furthermore, deltamethrin treatment induced apoptosis in cerebrum by decreasing B-cell lymphoma gene 2 (Bcl-2) level, as well as increasing Jun N-terminal kinase3, caspase-3, and Bcl-2-associated X protein levels. Simultaneously, toll-like receptor 4 (TLR4) downstream inflammation-related genes or proteins were significantly up-regulated by deltamethrin dose-dependently. Altogether, our study demonstrated that chronic exposure to deltamethrin induces inflammation and apoptosis in quail cerebrums by promoting oxidative stress linked to inhibition of the Nrf2/TLR4 signaling pathway. These results provide a novel knowledge on the chronic toxic effect of deltamethrin, and establish a theoretical foundation for the evaluation of pesticide-induced health risk.

Degradation of freshwater ecosystems by uncontrolled human activities is a growing concern in the tropics. In this regard, we aimed at testing an integrative framework based on the IFEQ index to assess freshwater ecosystem health of river basins impacted by intense livestock and agricultural activities, using the Muchacho River Basin (MRB) as a case study. The IFEQ combine multiple lines of evidence such as riverine hydromorphological analysis (LOE 1), physicochemical characterization using ions and pesticides (LOE 2), aquatic macroinvertebrate monitoring (LOE 3), and phytotoxicological essays with L. sativa (LOE 4). Overall, results showed an important reduction in streamflow and an elevated increase in ion concentrations along the MRB caused by deforestation and erosion linked to agricultural and livestock activities. Impacts of the high ion concentrations were evidenced in macroinvertebrate communities as pollution-tolerant families, associated with high conductivity levels, represented 92 % of the total abundance. Pollution produced by organophosphate pesticides (OPPs) was critical in the whole MRB, showing levels that exceeded 270-fold maximum threshold for malathion and 30-fold for parathion, the latter banned in Ecuador. OPPs concentrations were related to low germination percentages of Lactuca sativa in sediment phytotoxicity tests. The IEFQ index ranged from 44.4 to 25.6, indicating that freshwater ecosystem conditions were “bad” at the headwaters of the MRB and “critical” along the lowest reaches. Our results show strong evidence that intense agricultural and livestock activities generated significant impacts on the aquatic ecosystem of the MRB. This integrative approach better explains the cumulative effects of human impacts, and should be replicated in other basins with similar conditions to help decision-makers and concerned inhabitants generate adequate policies and strategies to mitigate the degradation of freshwater ecosystems.

Microbial-mediated Sb volatilization is a poorly understood part of the Sb biogeochemical cycle. This is mostly due to a lack of laboratory and field-deployable methods that are capable of quantifying low-level emissions of Sb from diffuse sources. In this study, we validated two methods using a H₂O₂ -HNO₃ liquid chemotrap and an activated coconut shell charcoal solid-phase trap, achieving an absolute limit of detection of 4.6 ng and below 2.0 ng Sb, respectively. The activated charcoal solid-phase trapping method, the most easily operated method, was then applied to contaminated shooting range soils. Four treatments were tested: 1) flooded, 2) manure amended + flooded, 3) 70 % water holding capacity, and 4) manure amendment +70 % water holding capacity, since agricultural practices and flooding events may contribute to Sb volatilization. Volatile Sb was only produced from flooded microcosms and manure amendment greatly influenced the onset and amount of volatile Sb produced. The highest amount of volatile Sb produced, up to 62.1 ng kg⁻¹ d⁻¹, was from the flooded manure amended soil. This suggests that anaerobic microorganisms may potentially be drivers of Sb volatilization. Our results show that polluted shooting range soils are a source of volatile Sb under flooded conditions, which may lead to an increase in the mobility of Sb. Some of these volatile Sb species are toxic and genotoxic, highlighting the role of Sb volatilization on environmental health, especially for individuals living in contaminated areas exposed to wetlands or flooded conditions (e.g., rice paddy agriculture surrounding mining areas). This work paves way for research on Sb volatilization in the environment.

Because most relevant studies have used small sample sizes, to date, representative atmospheric monitoring of persistent organic pollutants (POPs) on a regional scale has been very limited, which makes it difficult to precisely identify “hotspots” and possible pollution sources. In this study, an ultrahigh resolution monitoring technique was used to measure the atmospheric spatial variations in POP concentrations on a regional scale, throughout Campania, Italy. The occurrence of specific POPs—including polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), polycyclic aromatic hydrocarbons (PAHs), polybrominated diphenyl ethers (PBDEs) and phthalate esters (PAEs)—were investigated using polyurethane foam-based passive air samplers (PUF-PAS), which were deployed at 129 sites across the Campania Territory between April and July 2016. The results show that the highest POP levels occurred in the Naples metropolitan area (NMA), although there were other problematic spots throughout the Territory. More specifically, hotspot areas in the NMA that depict serious POP pollution were found in the Bagnoli brownfield site, Sarno River Basin, and parts of the northeastern NMA sector. The atmospheric POP contamination in Campania is jointly controlled by the contributions of local emissions and long-range atmospheric transport. Diffusion model was employed to identify the potential sources of various POPs. The simulation showed that all the POP sources are located in the NMA and are closely related to industrial sites. This study demonstrates the advantage of using large sample sizes to identify POP source locations and achieve geospatial visualization of POP concentration and risk assessment levels.

Research on the relationship between short-term exposure to fine particulate matter (PM₂.₅) and urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) is sparse in the nonoccupationally exposed populations. A quasi-experimental observation of haze events nested within a randomized crossover trial of alternative 1-week real or sham indoor air filtration was conducted to evaluate the associations of urinary monohydroxy-PAHs (OH-PAHs) with short-term exposure to PM₂.₅ and PM₂.₅-bound PAHs. The study was conducted among 57 healthy college students in Beijing, China. PM₂.₅-bound PAHs and urinary OH-PAHs were quantified using gas chromatography coupled with a triple-quadrupole tandem mass spectrometer. Linear mixed-effect models were applied to evaluate the association of urinary OH-PAHs with time-weighted personal PM₂.₅ and PM₂.₅-bound PAHs, controlling for potentially confounding variables. The results demonstrated that air filtration could markedly reduce external exposure to PM₂.₅ and PM₂.₅-bound parent, nitrated, and oxygenated PAHs. In the intervention trial, the urinary concentrations of 2-hydroxyfluorene (2-OH-FLU) and 9-hydroxyphenanthrene (9-OH-PHE) were elevated significantly by 16.5% (95% CI, 2.1%, 33.1%) and 37.9% (95% CI, 8.4%, 75.4%), respectively, in association with a doubling increase in personal PM₂.₅ exposure. Urinary 9-OH-PHE was also significantly positively associated with the increase in the sum of PM₂.₅-bound parent PAHs. Furthermore, the levels of urinary OH-PAHs such as 2-OH-FLU and 9-OH-PHE in the haze events were elevated by 31.1% (95% CI, 8.7%, 53.4%) and 73.5% (95% CI, 16.0%, 131.0%), respectively, in association with a doubling increase in personal PM₂.₅ exposure. The findings indicated that urinary 2-OH-FLU and 9-OH-PHE could serve as potential internal exposure biomarkers for assessing short-term PM₂.₅ exposure in nonoccupational populations.

Nitrate is a major pollutant component in ambient PM₂.₅. It is known that chronic exposure to PM₂.₅ NO₃⁻ damages respiratory functions. We aim to explore the underlying toxicological mechanism at single cell resolution.We systematically conducted exposure experiments on forty C57BL/6 mice, assessed respiratory functions, and profiled lung transcriptome. . Afterward, we estimated the cell type compositions from RNA-seq data using deconvolution analysis. The genes and pathways associated with respiratory function and dysregulated by to PM₂.₅ NO₃⁻ exposure were characterized at bulk-tissue and single-cell resolution.PM₂.₅ NO₃⁻ exposure did not significantly modify the cell type composition in lung, but profoundly altered the gene expression within each cell type. At ambient concentration (22 μg/m³), exposure significantly (FDR<10%) altered 95 genes’ expression. Among the genes associated with respiratory functions, a large fraction (74.6–91.7%) were significantly perturbed by PM₂.₅ NO₃⁻ exposure. For example, among the 764 genes associated with peak expiratory flow (PEF), 608 (79.6%) were affected by exposure (p = 1.92e-345). Pathways known to play role in lung disease pathogenesis, including circadian rhythms, sphingolipid metabolism, immune response and lysosome, were found significantly associated with respiratory functions and disrupted by PM₂.₅ NO₃⁻ exposure.This study extended our knowledge of PM₂.₅ NO₃⁻ exposure’s effect to the levels of lung gene expression, pathways, lung cell type composition and cell specific transcriptome. At single cell resolution, we provided insights in toxicological mechanism of PM₂.₅ NO₃⁻ exposure and subsequent pulmonary disease risks.

Hexafluoropropylene oxide dimer acid (HFPO-DA) is a perfluorooctanoic acid (PFOA) substitute. In the current study, potential developmental cardiotoxicity and hepatotoxicity following HFPO-DA exposure in chicken embryo has been investigated, focusing on the roles of peroxisome proliferator activated receptor alpha (PPARα), the major molecular target in PFOA-induced toxicities. HFPO-DA was exposed to fertile chicken eggs via air cell injection, morphology and function of the target organs (heart and liver) in hatchlings were investigated with histopathology and electrocardiography, and the serum levels of HFPO-DA had been measured with quadrupole-time of flight liquid chromatograph-mass spectrometer (Q-TOF LC/MS). Additionally, lentivirus-mediated in ovo PPARα silencing was used to assess the roles of PPARα in HFPO-DA induced developmental toxicities. The results indicated that developmental exposure to HFPO-DA induced developmental cardiotoxicity, including thinned right ventricular wall and elevated heart rates, similar to those observed with PFOA exposure, as well as developmental hepatotoxicity in the form of steatosis. Silencing of PPARα alleviated such effects, suggesting participation of PPARα in HFPO-DA induced developmental toxicities in chicken embryo. Moreover, enhanced expression of PPARα downstream genes, cluster of differentiation 36 (CD36) and enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase (EHHADH), were observed in HFPO-DA exposed animal heart tissues, which can be abolished by PPARα silencing. On the other hand, liver-type fatty acid binding protein (L-FABP) and CD36 expression were effectively enhanced in exposed liver tissues, but not EHHADH, suggesting differential mechanism of toxicity in heart and liver tissues. In summary, developmental exposure to HFPO-DA induced developmental cardiotoxicity and hepatotoxicity in hatchling chickens similar to PFOA, and PPARα still participates in such toxicities, with some differential downstream gene regulations in different organs. Further investigation on HFPO-DA-induced developmental toxicities is guaranteed.