Cadmium (Cd) is a ubiquitous toxic heavy metal derived mainly from industrial processes. In industrialized societies, individuals are exposed to a plethora of sources of Cd pollution. Cd can trigger serious diseases such as rheumatoid arthritis (RA) and chronic obstructive pulmonary disease (COPD) by the over-activating immune system. As an effector mechanism in innate immunity, neutrophil extracellular traps (NETs) not only play an important role in defending against infection but also lead to tissue damage. However, the role of NETs in Cd-induced lung damage process has not been previously studied. In this study, we aimed to investigate the potential effects of Cd-induced NETs on lung injury in vivo and further to clarify the molecular mechanisms of Cd-induced NETs formation. In vivo, Cd treatment destroyed the structural integrity of lung tissue and significantly increased the levels of NETs in the bronchoalveolar lavage fluid (BALF). The known NETs inhibitor DNase I ameliorated pathologic changes and significantly decreased levels of NETs in BALF, which suggesting the curial role of NETs in Cd-induced lung injury. Further investigation showed that Cd could significantly trigger NETs formation, which is composed of DNA backbone decorated with histones (H3) and neutrophils elastase (NE). The inhibitors of NADPH oxidase, ERK1/2 and p38 MAPK-signaling pathways significantly reduced the formation of NETs, and western blotting analysis also showed that Cd significantly increased the phosphorylation of p38 and ERK1/2 signaling pathways. Above results confirmed that NADPH oxidase, ERK1/2 and p38 MAPK-signaling pathways were related to Cd-induced NETs formation. In conclusion, NETs was involved in Cd-induced lung injury, and the mechanisms of Cd-induced NETs formation was via activating NADPH oxidase, ERK1/2 and p38 MAPK-signaling pathways, which might provide a new perspective in Cd-induced lung injury.

Microplastic (MP) pollution is potentially a major threat to many aquatic organisms. Yet we currently know very little about the mechanisms responsible for the effects of small MPs on phenotypes, and the extent to which effects of MPs are modified by genetic and environmental factors. Using a multivariate approach, we studied the effects of 500 nm polystyrene microspheres on the life history and immunity of eight clones of the freshwater cladoceran Daphnia magna reared at two temperatures (18 °C/24 °C). MP exposure altered multivariate phenotypes in half of the clones we studied but had no effect on others. In the clones that were affected, individuals exposed to MPs had smaller offspring at both temperatures, and more offspring at high temperature. Differences in response to MP exposure were unrelated to differences in particle uptake, but were instead linked to an upregulation of haemocytes, particularly at high temperature. The clone-specific, context-dependent nature of our results demonstrates the importance of incorporating genetic variation and environmental context into assessments of the impact of plastic particle exposure. Our results identify immunity as an important mechanism underpinning genetically variable responses to MP pollution and may have major implications for predicting consequences of MP pollution.

Microalgae can excrete exopolymer substances (EPS) with a potential to form hetero-aggregates with microplastic particles. In this work, two freshwater (Microcystis panniformis and Scenedesmus sp.) and two marine (Tetraselmis sp. and Gloeocapsa sp.) EPS producing microalgae were exposed to different microplastics. In this study, the influence of the microplastic particles type, size and density in the production of EPS and hetero-aggregates potential was studied. Most microalgae contaminated with microplastics displayed a cell abundance decrease (of up to 42%) in the cultures. The results showed that the formed aggregates were composed of microalgae and EPS (homo-aggregates) or a combination of microalgae, EPS and microplastics (hetero-aggregates). The hetero-aggregation was dependent on the size and yield production of EPS, which was species specific. Microcystis panniformis and Scenedesmus sp. exhibited small EPS, with a higher propension to disaggregate, and consequently lower capabilities to aggregate microplastics. Tetraselmis sp. displayed a higher ability to aggregate both low and high-density microplastics, being partially limited by the size of the microplastics. Gloeocapsa sp. had an outstanding EPS production and presented excellent microplastic aggregation capabilities (adhered onto the surface and also incorporated into the EPS). The results highlight the potential of microalgae to produce EPS and flocculate microplastics, contributing to their vertical transport and consequent deposition. Thus, this work shows the potential of microalgae as biocompatible solutions to water microplastics treatment.

Manufactured nanoparticles (MNPs) undergo transformation immediately after they enter wastewater treatment streams and during their partitioning to sewage sludge, which is applied to agricultural soils in form of biosolids. We examined toxicogenomic responses of the model nematode Caenorhabditis elegans to pristine and transformed ZnO-MNPs (phosphatized pZnO- and sulfidized sZnO-MNPs). To account for the toxicity due to dissolved Zn, a ZnSO₄ treatment was included. Transformation of ZnO-MNPs reduced their toxicity by nearly ten-fold, while there was almost no difference in the toxicity of pristine ZnO-MNPs and ZnSO₄. This combined with the fact that far more dissolved Zn was released from ZnO- compared to pZnO- or sZnO-MNPs, suggests that dissolution of pristine ZnO-MNPs is one of the main drivers of their toxicity. Transcriptomic responses at the EC₃₀ for reproduction resulted in a total of 1161 differentially expressed genes. Fifty percent of the genes differentially expressed in the ZnSO₄ treatment, including the three metal responsive genes (mtl-1, mtl-2 and numr-1), were shared among all treatments, suggesting that responses to all forms of Zn could be partially attributed to dissolved Zn. However, the toxicity and transcriptomic responses in all MNP treatments cannot be fully explained by dissolved Zn. Two of the biological pathways identified, one essential for protein biosynthesis (Aminoacyl-tRNA biosynthesis) and another associated with detoxification (ABC transporters), were shared among pristine and one or both transformed ZnO-MNPs, but not ZnSO₄. When comparing pristine and transformed ZnO-MNPs, 66% and 40% of genes were shared between ZnO-MNPs and sZnO-MNPs or pZnO-MNPs, respectively. This suggests greater similarity in transcriptomic responses between ZnO-MNPs and sZnO-MNPs, while toxicity mechanisms are more distinct for pZnO-MNPs, where 13 unique biological pathways were identified. Based on these pathways, the toxicity of pZnO-MNPs is likely to be associated with their adverse effect on digestion and metabolism.

Water diversion projects have been continuously used to alleviate water quality issues that arise during urbanization. However, studies about whether it has possible effects on the status of pharmaceutical and personal care products (PPCPs) are limited. In this study, the occurrence trends and spatial-temporal distribution characteristics of 50 PPCPs were investigated in surface water, suspended particulate matter (SPM) and sediments in Nanjing urban rivers under the background of the water diversion project from the Yangtze River to the Qinhuai River. In the four field campaigns that were embarked on April to July 2018, a total of 40, 38 and 24 PPCPs were detected in surface water, SPM and sediments, respectively, with overall concentrations of 138–1990 ng/L, 3214–33701 ng/g and 12.1–109 ng/g dry weight (dw) among nine sampling sites. The excessive concentration of caffeine (20.6–905 ng/L) may be evidence of the direct discharge of untreated sewage and an obvious indicator of the overall concentrations of PPCPs. The PPCPs contamination levels in surface water were increased along with the direction of the water diversion in urban runoff, and decreased by 8–31% due to the increase in volume attributable to the water diversion. The distribution coefficients (Kd) of pollutants in the SPM-water phases (3.0–5.6 L/kg) were two orders of magnitude higher than those in the sediment-water phases (0.3–3.3 L/kg). And the positive correlations between their log Kow and SPM-water log Kd values indicated SPM was the important carrier determining the fate of organic UV filters. Furthermore, the results of ecological risk assessment demonstrated that although the increase in the volume of water caused by the water diversion reduced the overall ecological risks of PPCPs in urban rivers, the current contamination level still represents high risks to algae and fish.

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.

Estrogenic endocrine disrupting chemicals (EDCs) are natural hormones, synthetic compounds or industrial chemicals that mimic estrogens due to their structural similarity with estrogen's functional moieties. They typically enter aquatic environments through wastewater treatment plant effluents or runoff from intensive livestock operations. Globally, most natural and synthetic estrogens in receiving aquatic environments are in the low ng/L range, while industrial chemicals (such as bisphenol A, nonylphenol and octylphenol) are present in the μg to low mg/L range. These environmental concentrations often exceed laboratory-based predicted no effect concentrations (PNECs) and have been evidenced to cause negative reproductive impacts on resident aquatic biota. In vertebrates, such as fish, a well-established indicator of estrogen-mediated endocrine disruption is overexpression of the egg yolk protein precursor vitellogenin (Vtg) in males. Although the vertebrate Vtg has high sensitivity and specificity to estrogens, and the molecular basis of its estrogen inducibility has been well studied, there is growing ethical concern over the use of vertebrate animals for contaminant monitoring. The potential utility of the invertebrate Vtg as a biomonitor for environmental estrogens has therefore gained increasing attention. Here we review evidence providing support that the molluscan Vtg holds promise as an invertebrate biomarker for exposure to estrogens. Unlike vertebrates, estrogen signalling in invertebrates remains largely unclarified and the classical genomic pathway only partially explains estrogen-mediated activation of Vtg. In light of this, in the latter part of this review, we summarise recent progress towards understanding the molecular mechanisms underlying the activation of the molluscan Vtg gene by estrogens and present a hypothetical model of the interplay between genomic and non-genomic pathways in the transcriptional regulation of the gene.

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.

The phenylpyrazole insecticide, fipronil, isused for the eradication of insects in agriculture, which also exposes various non-target groups such as birds and animals. Our aim was to assess the cardiac and pulmonary consequences of sub-acute administration of fipronil (¹∕₅ LD₅₀; 2.26 mg/kg) in the Japanese quail for fifteen days and to determine the tissue recovery over a period of 60 days. Fipronil exposure led to a significant decrease in the body weight of the treated birds. Its exposure also induced cardiac and pulmonary damage of varying degrees. Fipronil increased the lipid peroxide (LPO) and nitric oxide (NO) contents as well as indices of tissue injury in the serum of exposed birds. Furthermore, it decreased the antioxidant indices in both the organs. Most of these changes gradually reversed and the histological changes, particularly of the heart, reversed completely by day-60 of recovery. Furthermore, alterations in the mRNA gene expressions of Nuclear factor kappa B (NF-κB), Interleukin 6 (IL-6), and Tumor necrosis factor-alpha (TNF-α) were monitored by quantitative polymerase chain reaction (RT-PCR). In both the tissues, a significant up-regulation of the transcripts was recorded after fipronil administration, which was reversed during the recovery period in the heart tissue except for TNF-α, while the transcripts in the lung tissue declined non-significantly. This study showed that the exposure of Japanese quail to fipronil has a profound negative impact on heart and lung including oxidative injury and tissue inflammation. Fipronil can induce the activity of NF-κB inflammatory -signaling pathway that play a role in the associated tissue inflammation. Although most of the cardiac changes could be reversed after a recovery period of sixty days, the pulmonary changes did not reverse much.

Biomass burning (BB), such as, crop field burning during the post-harvest season, emits large amounts of air pollutants (e.g., PM₂.₅) that severely impact human health. However, it is challenging to evaluate the impact of BB on PM₂.₅ due to uncertainties in the size and location of sources as well as their temporal and spatial variability. This study focused on the impacts of BB on local pollution as well as the long-range transport of PM₂.₅ in Northeast Asia resulting from a huge field BB event in Northeast China during the autumn of 2014. Air quality simulations using the Community Multiscale Air Quality (CMAQ) model were conducted in the year 2014 over the horizontal domains covering Northeast Asia, including the Japanese mainland. In the baseline simulation (Base), field BB emissions were derived from Fire INventory from NCAR (FINN) v1.5 for the year 2014. The model reasonably captured the daily mean PM₂.₅ mass concentrations, however, it underestimated concentrations in autumn around Northeast China where irregular field BB following the harvest occurred frequently. To address the underestimation of emissions from BB sources in China, another simulation with boosted BB sources from cropland area (FINN20_crop) was conducted in addition to the Base simulation. The model performance of FINN20_crop was significantly improved and showed smaller biases and higher indices of agreement between simulated and observed values in comparison to those of Base. To evaluate long-range transport of PM₂.₅ from BB sources in China towards Japan, CMAQ with brute-force method (CMAQ/BFM)-estimated BB contributions for Base and FINN20_crop cases were compared with Positive Matrix Factorization (PMF)-estimated BB contributions at Noto Peninsula in Japan. The CMAQ/BFM-estimated contributions from FINN20_crop were in greater agreement with the PMF-estimated contributions. The comparison of BB contributions estimated by the two contrasting models also indicated large underestimations in the current BB emission estimates.