In order to investigate the effectiveness of diagnostic ratios in polycyclic aromatic hydrocarbon (PAH) source discrimination, semi-open pyrolysis experiments have been performed on an organic-rich, immature shale from the Winnipegosis Formation in southeastern Saskatchewan, Western Canada Sedimentary Basin. The concentrations and distributions of PAHs in expelled oils and residual extracts change drastically with increasing pyrolysis temperatures. The difficulty and inconsistency commonly encountered by using diagnostic ratios for PAH source identification in environmental samples seem to be rooted in the great variation of the diagnostic ratios themselves under different formation temperatures. No single diagnostic ratio allows a simple segregation of PAHs into petrogenic or pyrogenic sources. Some diagnostic ratios such as anthracene/phenanthrene and benz[a]anthracene/chrysene compound pairs are mostly effective for low-temperature pyrolysis, whereas indeno[1,2,3-cd]pyrene/benzo[ghi]perylene, aromatic hydrocarbon ring number distribution and degree of alkylation are mainly valid for high-temperature pyrolysis. The diagnostic ratios based on fluoranthene/pyrene, benzo[bk]fluoranthene/benz[a]pyrene compound pairs enjoy limited validity over a narrow pyrolysis range, whereas parameters derived from aromatic hydrocarbon ring number distribution, degree of alkylation and 1,7-/(2,6- + 1,7-dimentylphenanthrene) may be undistinguishable between petrogenesis and low-temperature pyrolysis. The apparent temperature-related variability must be taken into account when using the diagnostic ratios for source identification purposes. Multiple molecular markers need to be carefully selected to confirm the results obtained with PAH diagnostic ratios. Mechanical use of diagnostic ratios most likely leads to misinterpretation of environmental samples.

Risk assessment for molecular toxicity endpoints of environmental matrices may be a pressing issue. Here, we combined chemical analysis with species sensitivity distributions (SSD) and in silico docking for multi-species estrogen receptor mediated-risk assessment in water from Dongjiang River, China. The water contains high levels of phenolic endocrine-disrupting chemicals (PEDCs) and phthalic acid esters (PAEs). The concentration of ∑₄PEDCs and ∑₆PAEs ranged from 2202 to 3404 ng/L and 834–4368 ng/L, with an average of 3241 and 2215 ng/L, respectively. The SSD approach showed that 4-NP, BPA, E2 of PEDCs, and DBP, DOP, and DEHP could severely threaten the aquatic ecosystems, while most other target compounds posed low-to-medium risks. Moreover, binding affinities from molecular docking among PEDCs, PAEs, and estrogen receptors (ERα, Erβ, and GPER) were applied as toxic equivalency factors. Estrogen receptor-mediated risk suggested that PEDCs were the main contributors, containing 53.37–69.79% of total risk. They potentially pose more severe estrogen-receptor toxicity to zebrafish, turtles, and frogs. ERβ was the major contributor, followed by ERα and GPER. This study is the first attempt to assess the estrogen receptor-mediated risk of river water in multiple aquatic organisms. The in silico simulation approach could complement toxic effect evaluations in molecular endpoints.

Around the world, green tides are happening with increasing frequency because of the dual effects of increasingly intense human activity and climate change; this leads to significant impacts on marine ecology and economies. In the last decade, the world's largest green tide, which is formed by Ulva/Enteromorpha porifera, has become a recurrent phenomenon every year in the southern Yellow Sea (China), and it has been getting worse. To alleviate the impacts of such green tide outbreaks, multiple measures need to be developed. Among these approaches, biotechnology plays important roles in revealing the outbreak mechanism (e.g., molecular identification technology for algal genotypes), controlling and preventing outbreaks at the origin sites (e.g., technology to inhibit propagation), and utilizing valuable algal biomass. This review focuses on the various previously used biotechnological approaches that may be applicable to worldwide seaweed blooms that result from global climate change and environmental degradation.

Bakelite, the first synthetic plastic, is a rather unexplored material in the field of ecotoxicology, despite its long production and use. The aim of this study was to investigate the ecotoxicity of Bakelite microplastics (before and after leaching) and its leachates on four aquatic organisms: the crustacean Daphnia magna, the plant Lemna minor, the bacterium Allivibrio fischeri and the alga Pseudokirchneriella subcapitata. Bakelite microplastics before and after leaching and leachates affected all organisms, but to varying degrees. Leachates showed increased ecotoxicity to Daphnia magna, while Pseudokirchneriella subcapitata was more affected by particles. For Lemna minor and Allivibrio fischeri, the effects of particles before leaching and leachate were comparable, while the negative effect of particles after leaching was minimal or not present. All leachates were analysed, and phenol and phenol-like compounds were the predominant organics found. In addition, bioadhesion of Bakelite microplastics to the surface of Daphnia magna and Lemna minor was confirmed, but the particles were mainly weakly adhered. Results of this study suggest that, in addition to the recently studied microplastics from consumer products (e.g. from polyethylene and polystyrene), microplastics from industrial plastics such as Bakelite may be of increasing concern, primarily due to leaching of toxic chemicals.

Lung cancer is the most common cancer in China and second worldwide, of which the incidence of lung adenocarcinoma is rising. As an independent factor, air pollution has drawn the attention of the public. An increasing body of studies has focused on the effect of PM₂.₅ on lung adenocarcinoma; however, the mechanism remains unclear. We collected the PM₂.₅ in two megacities, Beijing (BPM) and Shijiazhuang (SPM), located in the capital of China, and compared the different components and sources of PM₂.₅ in the two cities. Vehicle emissions are the primary sources of BPM, whereas SPM is industrial emissions. We found that chronic exposure to PM₂.₅ promotes the tumorigenesis and metastasis of lung adenocarcinoma in patient-derived xenograft (PDX) models, as well as the migration and invasion of lung adenocarcinoma cell lines. SPM has more severe effects in vivo and in vitro. The underlying mechanisms are related to the stem cell properties of cancer cells, the epithelial-mesenchymal transition (EMT) process, and the corresponding miRNAs. It is hopeful to provide a theoretical basis for improving air pollution in China, especially in the capital area, and is of the significance of long-term survival of lung cancer patients.

The resource utilization of sewage sludge can solve its disposal issue essentially. Meanwhile the removal of diclofenac (DCF) in wastewater is an emerging environmental problem. In this study, a novel strategy of sludge utilizing via hydrothermal - peroxydisulfate (PDS) dewatering coupled pyrolysis process was proposed. The obtained sludge-derived biochar (HSC) could be as candidate to activate PDS to degrade DCF. Results indicated that exceed 90% of DCF was eliminated within 30 min in HSC-PDS/DCF ternary system under the optimized condition (0.6 mmol/L PDS and 0.5 mg/L HSC, without temperature and pH pre-adjusting). The inner mechanism of HSC-PDS/DCF system was revealed as follows: (1) Major: CO in quinones and ketone structure in HSC accelerated the degradation of DCF via non-radical pathway (electron transfer and ¹O₂). (2) Minor: Graphitic N structure accelerated the electron transfer and O₂•⁻ originated from defective sites involved into the redox. Several by-products were identified and two tentative degradation pathways of DCF (eg. dechlorination and C–N cleavage) were proposed.

This study investigated the distribution of moss species, physiological parameters (superoxide dismutase, peroxide, catalase, and total chlorophyll), and concentrations of potentially toxic elements (Mn, Cr, Zn, Cu, Pb, and Cd) in moss communities and topsoil at the Huayuan manganese mine, Xiangjiang manganese mine, and Nancha manganese mine (Southern China). Partial least squares path modeling (PLS-PM) was then performed to determine the relationship between the indicators. Cd, Mn, and Zn were the main topsoil pollutants, followed by Pb, Cr, and Cu. A total of 73 moss species, comprising 31 genera from 17 families, and 8 community functional groups were identified. The most dominant families were Pottiaceae (30.14%) and Bryaceae (21.92%). PLS-PM revealed that increasing topsoil Mn, Cr, Zn, Cu, Pb, and Cd significantly reduced species diversity and functional diversity. These potentially toxic elements in the topsoil impeded vegetation growth by deteriorating soil conditions and subsequently altering the microenvironment of the moss communities. The community-weighted means demonstrated that functional traits of turfs and warty leaves were the adaptation of the moss communities to an increasingly dry and exposed microenvironment. Moss species with curly and narrow leaves were used to reduce contact with particulate pollutants. PLS-PM also indicated that Mn, Cr, Pb, and Cd may have a detrimental effect on superoxide dismutase, peroxide, catalase, and total chlorophyll, although further validation studies are needed.

Wastewater treatment plants (WWTPs) are among the main hotspots of antibiotic resistance genes (ARGs) in the environment. Previously, we demonstrated that, by increasing anthropogenic pollution, the antibiotic resistome persisted in the microbial community of rivers and lakes, independently by changes in community composition. In this study, we reanalysed the data to test for the relation of metal resistance genes (MRGs), plasmids, and integrons to the persistence of the antibiotic resistome. The experiment consisted in replicated co-cultures of riverine or lacustrine microbial communities and WWTP effluents in different proportions. Samples before (T0) and after a short period of incubation (TF) were collected and community metagenomic data were obtained by shotgun sequencing. The data were processed to annotate MRGs, plasmids, and integrases. The integrases stabilized in the aquatic environment following the degree of contamination with effluent water (in particular in one site), whereas MRGs and plasmids showed stochastic trajectories. These results confirm the potential correlation between integrons and anthropogenic pollution, and the reliability of intI1 as a pollution marker. Only in one site MRGs, plasmids, and ARGs were correlated, highlighting their partial contribution to the persistence of ARGs in surface waters.

Through a literature survey and meta-data analysis, monitoring methods and contamination levels of marine micro- and macroplastics in seawater were compared between the North Pacific and the world's other ocean basins. The minimum cut-off size in sampling and/or analysis of microplastics was crucial to the comparison of monitoring data. The North Pacific was most actively monitored for microplastics and showed comparatively high levels in the global context, while the Mediterranean Sea was most frequently monitored for macroplastics. Of the 65 extracted mean abundances of microplastics in seawater from the North Pacific, two (3.1%) exceeded the lowest predicted no-effect concentration (PNEC) proposed thus far. However, in the context of business-as-usual conditions, the PNEC exceedance probability may be expected to reach 27.7% in the North Pacific in 2100. The abundance of marine plastics in seawater, which reflects the current pollution status and marine organisms' waterborne exposure levels, is a useful indicator for marine plastic pollution. For regional and global assessments of pollution status across space and time, as well as assessment of ecological risk, two microplastic monitoring approaches are recommended along with their key aspects. Although microplastic pollution is closely linked with macroplastics, the monitoring data available for floating macroplastics and more extent to mesoplastics in most ocean basins are limited. A more specific framework for visual macroplastic survey (e.g. fixed minimum cut-off size, along with survey transect width and length according to survey vessel class) is required to facilitate data comparison. With the implementation of standardised methods, increased efforts are required to gather monitoring data for microplastics and—more importantly—floating macroplastics in seawater worldwide.

Epidemiological studies have indicated that exposure to ambient air-borne fine particulate matter (PM2.5) is associated with many cardiopulmonary diseases; however, the underlying pathological mechanisms of PM2.5-induced lung injury remain unknown. In this study, we aimed to assess the impact of acute or prolonged exposure to water-insoluble fractions of PM2.5 (PM2.5 particulate) on lung injury and its molecular mechanisms. Balb/c mice were randomly exposed to PM2.5 once (acute exposure) or once every three days for a total of 6 times (prolonged exposure). Lung, BALF and blood samples were collected, and pulmonary pathophysiological alterations were analyzed. Nrf2 knockout mice were adapted to assess the involvement of Nrf2 in lung injury, and transcriptomic analysis was performed to delineate the mechanisms. Through transcriptomic analysis and validation of Nrf2 knockout mice, we found that acute exposure to PM2.5 insoluble particulates induced neutrophil infiltration-mediated airway inflammation, whereas prolonged exposure to PM2.5 insoluble particulate triggered lung fibrosis by decreasing the transcriptional activity of Nrf2, which resulted in the downregulated expression of antioxidant-related genes. In response to secondary LPS exposure, prolonged PM2.5 exposure induced more severe lung injury, indicating that prolonged PM2.5 exposure induced Nrf2 inhibition weakened its antioxidative defense capacity against oxidative stress injury, leading to the formation of pulmonary fibrosis and increasing its susceptibility to secondary bacterial infection.