Fipronil, a broad-spectrum chiral insecticide, has been documented to induce significant neurotoxicity to nontarget aquatic species; however, whether its neurotoxicity behaves enantioselectively and what molecular mechanisms correspond to the neurotoxicity remain unanswered. To date, few investigations have focused on the genomic mechanisms responsible for the enantioselective toxicity of chiral pesticides. The epigenetic modifications, especially DNA methylation, caused by the pesticides are also blind spot of the research works. Video tracking showed that R-fipronil exhibited more intense neurotoxicity, as well as the induction of more severe anxiety-like behavior, such as boosted swimming speed and dysregulated photoperiodic locomotion, to embryonic and larval zebrafish compared with S-fipronil. The MeDIP-Seq analysis, combined with Gene Ontology and KEGG, revealed that R-fipronil disrupted five signaling pathways (MAPK, Calcium signaling, Neuroactive ligand-receptor interaction, Purine metabolism, and Endocytosis) to a greater extent than S-fipronil through the hypermethylation of several important neuro-related genes, whereas no significant alterations of global DNA methylation were observed on the two enantiomers. To summarize, our data indicated that the fipronil-conducted enantioselective neurotoxicity likely applied its enantioselectivity by the dysregulation of DNA methylation. Our study also provided novel epigenetic insights into the study of enantioselective biological effects and the relevant underlying mechanisms of chiral insecticide.

Recently, ground ozone has become one major airborne pollutant and the frequency of ozone-induced pollution episodes has increased rapidly across China. However, due to the lack of long-term observation data, relevant research on the characteristics and influencing factors of urban ozone concentrations remains limited. Based on ground ozone observation data during 2006–2016, we quantified the causality influence of individual meteorological factors on ozone concentrations in Beijing using a convergent cross mapping (CCM) method. The result indicated that the influence of each meteorological factor on ozone concentrations varied significantly across seasons and years. At the inter-annual scale, all-year meteorological influences on ozone concentrations were much more stable than seasonal meteorological influences. At the seasonal scale, meteorological influences on ozone concentrations were stronger in spring and autumn. Amongst multiple individual factors, temperature was the key meteorological influencing factor for ozone concentrations in all seasons except winter, when wind, humidity and SSD exerted major influences on ozone concentrations. In addition to temperature, air pressure was another meteorological factor that exerted strong influences on ozone concentrations. At both the inter-annual and seasonal scale, the influence of temperature and humidity on ozone concentrations was generally stable whilst that of other factors experienced large variations. Different from PM2.5, meteorological influences on ozone concentrations were relatively weak in summer, when ozone concentrations were the highest in Beijing. Given the generally stable meteorological influences on ozone concentrations and human-induced emissions of VOCs and NOx across seasons, warming induced notable increase in summertime biogenic emissions of VOCs and NOx can be a major driver for the increasing ozone pollution episodes. This research provides useful references for understanding long-term meteorological influences on ozone concentrations in mega cities in China.

The occurrence and distribution of 168 pharmaceutically active compounds (PhACs) in the surface seawater of Jiaozhou Bay (JZB) were investigated using ultra-high-performance liquid chromatography in tandem with a triple-quadrupole mass spectrometer equipped with an electrospray ionization source (UHPLC-ESI-MS-MS). Thirty-six compounds were detected, and 17 of these compounds were first detected in seawater, including sulfabenzamide, sulphacetamide, cephalonium, desacetyl-cefotaxime, cefminox, cefotaxime, cephradine, cefazolin, carprofen, nabumetone, glibenclamide, glimepiride, glipizide, prednisone, fluoromethalone, diazepam and amantadine. The total concentration of PhACs in the surface seawater ranged from 23.6 ng/L to 217 ng/L. The compounds found at the highest mean concentrations included amantadine (24.7 ng/L), lincomycin (8.55 ng/L), carprofen (8.30 ng/L), and tetracycline (7.48 ng/L). The PhAC concentration was higher in the inner bay than in the outside of the bay. In the inner bay, the eastern district showed higher concentrations of PhACs than the western district. Input from the Licun River may be the primary source of pollution. A statistically significant positive correlation was observed between nutrients and PhACs in seawater. Phosphate can be used to indicate the distribution of PhACs in JZB. Based on the individual risk quotient (RQ) values, lincomycin and ofloxacin posed high risks to the relevant aquatic organisms in JZB, especially in the eastern parts. Regular monitoring is required to evaluate the levels of PhACs as they are constantly released into JZB.

Sustainable remediation is a new way of thinking and acting in the management of contaminated sites. This research aims to identify and structure the state-of-the-art of sustainable remediation from the risk management and stakeholder involvement perspective. A systematic and bibliometric study of scientific production was performed on scientific papers indexed in the Scopus and Web of Science databases with the objectives: 1) to select a bibliographic portfolio that is aligned with the perception of the researchers in regard to theme, 2) to perform a bibliometric analysis of the selected bibliographic portfolio, and 3) to conduct a thematic synthesis and identify the integration of sustainable remediation from the risk management and stakeholder involvement perspective. The results indicated that although sustainable remediation is a recent theme it presents a promising field for development worldwide, verified by the growing number of publications in recent years. A change is observed in the way risk management is considered with the rise of sustainable remediation, demonstrated by different approaches in publications. Likewise, the involvement of stakeholders is widely discussed, and the importance of their participation in decision-making processes in the field of sustainable remediation is identified. This research brings several and new contributions as it provides with a detailed overview and guidance about the main characteristics and peculiarities as well as what already exists, the form to approach, the advances and what still needs to be improved so that the perception of stakeholders and risk management are better understood within the context of sustainable remediation.

In recent years, concerns about using Bisphenol A (BPA) in daily consume products and its effects in many chronic human diseases have prompted the removal of BPA. However, the widely used BPA alternatives, including Bisphenol S (BPS), have a high structural similarity with BPA, suggesting that they may have similar biological effects towards human beings. Indeed, BPS was also found to have endocrine-disrupting effects. Epigenetic mechanism was reported to be involved in BPA-induced biological effects in both in vitro and in vivo models. However, there is no assessment on whether BPS could cause epigenetic changes. In this work, we investigated the possible epigenetic effects of BPS that might induce in human breast cancer cell line MCF-7. We found that BPS could change DNA methylation level of transposons. Besides, methylation status in promoter of breast cancer related genes CDH1, SFN, TNFRSF10C were also changed, which implied that BPS might play a role in the development of breast cancer. Gene expression profiling showed that some genes related to breast cancer progression were upregulated, including THBS4, PPARGC1A, CREB5, COL5A3. Gene ontology (GO) analysis of the differentially expressed genes revealed the significantly changes in PI3K-Akt signaling pathway and extracellular matrix, which were related to the proliferation, migration and invasion of breast cancer cells. These results illustrated that BPS exposure might play roles in the progression of breast cancer.

Exposure to the emerging contaminant bisphenol A (BPA) is ubiquitous and associated with cardiovascular disorders. BPA effect as endocrine disruptor is widely known but other mechanisms underlying heart disease, such as epigenetic modifications, remain still unclear. A compound of green tea, epigallocatechin gallate (EGCG), may act both as anti-estrogen and as inhibitor of some epigenetic enzymes. The aims of this study were to analyze the molecular processes related to BPA impairment of heart development and to prove the potential ability of EGCG to neutralize the toxic effects caused by BPA on cardiac health. Zebrafish embryos were exposed to 2000 and 4000 μg/L BPA and treated with 50 and 100 μM EGCG. Heart malformations were assessed at histological level and by confocal imaging. Expression of genes involved in cardiac development, estrogen receptors and epigenetic enzymes was analyzed by qPCR whereas epigenetic modifications were evaluated by whole mount immunostaining. BPA embryonic exposure led to changes in cardiac phenotype, induced an overexpression of hand2, a crucial factor for cardiomyocyte differentiation, increased the expression of estrogen receptor (esr2b), promoted an overexpression of a histone acetyltransferase (kat6a) and also caused an increase in histone acetylation, both mechanisms being able to act in sinergy. EGCG treatment neutralized all the molecular alterations caused by BPA, allowing the embryos to go on with a proper heart development. Both molecular mechanisms of BPA action (estrogenic and epigenetic) likely lying behind cardiogenesis impairment were successfully counteracted by EGCG treatment.

Irrigation of crop plants with microcystins (MCs) contaminated water could be a threat to human health via bioaccumulation. Despite the fact MCs bioaccumulation in crop plants is well documented, MCs depuration, as well as the mechanism involved remains unclear. The objectives of the present study were to investigate the bioaccumulation and depuration of microcystin-LR (MC-LR) in lettuce (Lactuca sativa L.) and spinach (Spinacia oleracea L.), as well as to explore the role of glutathione (GSH) biosynthesis in MC-LR depuration. The tested plants were irrigated with deionized water containing 10 μg L⁻¹ MC-LR for 12 days (bioaccumulation), and subsequently, with either deionized water only or deionized water containing 0.5 mM buthionine sulfoximine (BSO, a specific inhibitor of GSH biosynthesis) for 12 days (depuration). After bioaccumulation period, highest concentrations of MC-LR found in lettuce and spinach were 114.4 and 138.5 μg kg⁻¹ dry weight (DW) respectively. Depuration rates of MC-LR in lettuce and spinach were 9.5 and 8.1 μg kg⁻¹ DW d⁻¹, which deceased to 3.7 and 4.6 μg kg⁻¹ DW d⁻¹ in treatments with BSO application. GSH content in both lettuce and spinach were not significantly affected during depuration without BSO; whereas after treatment with BSO, GSH content significantly decreased by 36.0% and 24.7% in lettuce and spinach on 15 d, and the decrease remained on 18 d and 21 d in lettuce. Moreover, during the bioaccumulation period, activities of glutathione reductase (GR) and glutathione S-transferase (GST) were enhanced in both plants. Our results suggested that GSH biosynthesis played an important role in MC-LR depuration in the tested plants. Concerning human health risk, most of the estimated daily intake (EDI) values during the bioaccumulation period exceeded the tolerable daily intake (TDI) guideline. However, the risk could be alleviated by irrigating with MCs-free water for a certain amount of time before harvest.

Cadmium is one of the most serious metal pollutants in the Bohai Sea. Previous studies revealed that mitochondrion might be the target organelle of Cd toxicity. However, there is a lack of a global view on the mitochondrial responses in marine animals to Cd. In this work, the mitochondrial responses were characterized in clams Ruditapes philippinarum treated with two concentrations (5 and 50 μg/L) of Cd for 5 weeks using tetraethylbenzimidazolylcarbocyanine iodide (JC-1) staining, ultrastructural observation and quantitative proteomic analysis. Basically, a significant decrease of mitochondrial membrane potential (△Ψm) was observed in clams treated with the high concentration (50 μg/L) of Cd. Cd treatments also induced specific morphological changes indicated by elongated mitochondria. Furthermore, iTRAQ-based mitochondrial proteomics showed that a total of 97 proteins were significantly altered in response to Cd treatment. These proteins were closely associated with multiple biological processes in mitochondria, including tricarboxylic acid (TCA) cycle, oxidative phosphorylation, fatty acid β-oxidation, stress resistance and apoptosis, and mitochondrial fission. These findings confirmed that mitochondrion was one of the key targets of Cd toxicity. Moreover, dynamical regulations, such as reconstruction of energy homeostasis, induction of stress resistance and apoptosis, and morphological alterations, in mitochondria might play essential roles in Cd tolerance. Overall, this work provided a deep insight into the mitochondrial toxicity of Cd in clams based on a global mitochondrial proteomic analysis.

Air pollutants accumulated in confined livestock barns could impact the health of animals and staff. Particulate matter (PM) and ammonia (NH3) concentrations are typically high in enclosed livestock houses with weak ventilation. The objective of this study was to investigate the distribution of PM in different size fractions and the levels of NH3 in a high-rise nursery (HN) barn and a high-rise fattening (HF) barn on a swine farm and to analyse the physicochemical properties of fine PM (PM2.5, PM with aerodynamic diameter ≤ 2.5 μm). The concentrations of total suspended particles (TSP, PM with aerodynamic diameter ≤ 100 μm), inhalable PM (PM10, PM with aerodynamic diameter ≤ 10 μm), PM2.5 and NH3 were monitored continuously for 6 d in each barn. The results showed that the concentrations of PM and NH3 varied with position, they were significantly higher inside the barns than outside (P < 0.01) and significantly higher in the forepart than at the rear of the two barns (P < 0.05). In the HF barn, the values of the two parameters were 0.777 ± 0.2 mg m−3 and 26.7 ± 7 mg m−3, respectively, significantly higher than the values observed in the HN barn at all monitored sites (P < 0.05). The PM concentrations increased markedly during feeding time in the two barns. Chemical characteristics analysis revealed that the main sources of PM2.5 in the two barns may have consisted of blowing dust, feed, mineral particles and smoke. In conclusion, the air quality at the forepart was worse than that at the rear of the barns. Activities such as feeding could increase the PM concentrations. The components of PM2.5 in the two barns were probably blowing dust, feed, mineral particles and smoke from outside.

Epidemiological evidence showed that the particulate matter exposure is associated with atherosclerotic plaque progression, which may be related to foam cell formation, but the mechanism is still unknown. The study was aimed to investigate the toxic effects and possible mechanism of PM2.5 on the formation of macrophage foam cells induced by oxidized low density lipoprotein (ox-LDL). Results showed that PM2.5 induced cytotoxicity by decreasing the cell viability and increasing the LDH level in macrophage foam cells. PM2.5 aggravated the lipid accumulation in ox-LDL-stimulated macrophage RAW264.7 within markedly increasing level of intracellular lipid by Oil red O staining. The level of ROS increased obivously after co-exposure to PM2.5 and ox-LDL than single exposure group. In addition, serious mitochondrial damage such as the mitochondrial swelling, cristae rupturing and disappearance were observed in macrophage foam cells. The loss of the mitochondrial membrane potential (MMP) further exacerbated the mitochondrial damage in PM2.5-induced macrophage foam cells. The apoptotic rate increased more severely via up-regulated protein level of Bax, Cyt C, Caspase-9, Caspase-3, and down-regulated that of Bcl-2, indicating that PM2.5 activated the mitochondrial-mediated apoptosis pathway. In summary, our results demonstrated that PM2.5 aggravated the lipid accumulation, mitochondrial damage and apoptosis in macrophage foam cells, suggesting that PM2.5 was a risk factor of atherosclerosis progression.