Nickel and cobalt are essential elements that become toxic at high concentrations. Little is known about nickel and cobalt toxicity in aquatic animals. This study aimed to investigate acute and chronic toxicity of nickel and cobalt in Japanese flounder (Paralichthys olivaceous), with emphasis on oxidative stress reactions, histopathological changes, and differences in gene expression. The lethal concentration for 50% mortality (LC₅₀) in 3 and 8 cm Japanese flounder exposed to nickel for 96 h was found to be 86.2 ± 0.018 and 151.3 ± 0.039 mg/L; for cobalt exposure, LC₅₀ was 47.5 ± 0.015 and 180.4 ± 0.034 mg/L, respectively. Chronic nickel and cobalt exposure caused different degrees of oxidative enzyme activity changes in gill, liver, and muscle tissues. Erythrocyte deformations were detected after acute or chronic exposure to nickel and cobalt. the nickel and cobalt exposure also caused pathological changes such as spherical swelling over other gill patches, rod-like proliferations in the gill patch epithelial cell layer, and disorder in hepatocyte arrangement, cell swelling, and cytoplasm loosening. RNA-Seq indicated that there were 184 upregulated and 185 downregulated genes in the liver of Japanese flounder exposed to 15 mg/L nickel for 28 d. For cobalt, 920 upregulated and 457 downregulated genes were detected. Among these differentially expressed genes, 162 were shared by both nickel and cobalt exposure. In both nickel and cobalt, pathways including fatty acid elongation, steroid biosynthesis, unsaturated fatty acid biosynthesis, fatty acid metabolism, PPAR signaling, and ferroptosis were significantly enriched. Taken together, these results aided our understanding of the toxicity of nickel and cobalt in aquatic animals.

Because oil spills frequently occur in coastal regions that serve as spawning habitat, characterizing the effects of oil in estuarine fish carries both economic and environmental importance. There is a breadth of research investigating the effects of crude oil on fish, however few studies have addressed how transcriptional responses to oil change throughout development or how these responses might be conserved across taxa. To investigate these effects, we performed RNA-seq and pathway analysis following oil exposure 1) in a single estuarine species (Cyprinodon variegatus) at three developmental time points (embryos, yolk-sack larvae, free-feeding larvae), and 2) in two ecologically similar species (C. variegatus and Fundulus grandis), immediately post-hatch (yolk-sack stage). Our results indicate that C. variegatus embryos mount a diminished transcriptional response to oil compared to later stages, and that few transcriptional responses are conserved throughout development. Pathway analysis of larval C. variegatus revealed dysregulation of similar biological processes at later larval stages, including alteration of cholesterol biosynthesis pathways, cardiac development processes, and immune functions. Our cross-species comparison showed that F. grandis exhibited a reduced transcriptional response compared to C. variegatus. Pathway analysis revealed that the two species shared similar immune and cardiac responses, however pathways related to cholesterol biosynthesis exhibited a divergent response as they were activated in C. variegatus but inhibited in F. grandis. Our results suggest that examination of larval stages may provide a more sensitive estimate of oil-impacts than examination of embryos, and challenge assumptions that ecologically comparable species respond to oil similarly.

Decabromodiphenyl ether (DecaBDE) is a brominated flame retardant belonging to the group of polybrominated diphenyl ethers. DecaBDE has been widely used for various applications, such as plastics, textiles, and building and construction materials. Limited information on DecaBDE production and usage inventory has been elaborated, however. Therefore, this work aimed to produce a preliminary emissions inventory of DecaBDE in mainland China by estimating production and consumption amounts of DecaBDE, and characterizing its emission factors during production and usage, based on industrial investigation and theoretical prediction. It was indicated that the total production of DecaBDE reached 464.68 thousand metric tons (kt), of which 62.72 kt were exported, since the beginning of its production. Shandong and Jiangsu provinces dominate the production, with proportions of 77.95% and 18.45%, respectively. The production stage releases most of the DecaBDE to the atmosphere, with an emissions factor of 23 ± 1.9 kg/t, followed by 20 ± 0.9 kg/t DecaBDE to waste water and 16 ± 1.0 kg/t DecaBDE as solid residue. DecaBDE emissions in the consumption stage—namely the plastic production process—are 0.17 ± 0.06–0.23 ± 0.08 kg DecaBDE to the atmosphere and 1.72 ± 0.58–2.29 ± 0.77 kg DecaBDE to solid residue, for each metric ton of plastic produced. The total annual DecaBDE emissions to waste water are 93.98–1140.9 mg—negligible. The results showed that the sources of DecaBDE environmental pollution are its manufacturing and flame-retardant plastic modification plants, which are easily overlooked by both the government and the public. Yet DecaBDE emissions elimination and the environmentally sound management of the DecaBDE waste generated from these two processes are crucial for environmental protection.

We investigated the levels and distribution patterns of α- and β-endosulfan and endosulfan sulfate in air, soil, water, and sediment samples collected from the South Korean persistent organic pollutants (POPs) monitoring networks. In the air samples, the highest concentrations of the total (Σ₃) endosulfan (50.3–611 pg/m³, mean: 274 pg/m³) were observed during summer. Spearman analysis revealed a good correlation between agricultural land area and atmospheric concentrations of Σ₃ endosulfan except during winter. Regardless of the season, the ratio of the two isomers (α/β) was 3.6–4.9 in the air samples, higher than that observed in technical mixtures (2.0–2.3), possibly due to the higher volatility of α-endosulfan, compared to β-endosulfan. Concentrations of Σ₃ endosulfan in the soil samples (n.d.−13.4 ng/g, mean: 0.8 ng/g) were not significantly different except at some stations adjacent to large areas of farmland. The average levels of Σ₃ endosulfan in the water and sediment samples were 2.1 ng/L and 0.1 ng/g dw, respectively. In analyzing the four largest rivers, it was observed that a few water stations during spring and fall and sediment stations in fall had high concentrations of the two isomers and endosulfan sulfate, particularly around the Yeoungsan and Nakdong Rivers near large areas of agricultural land. Endosulfan sulfate was dominant at most water and sediment sampling stations. This study demonstrates that the endosulfan found in most environmental compartments most probably derives from agricultural areas despite its ban as a pesticide. On the other hand, given that it was also detected in industrial and urban areas, in which pesticide application does not occur, it can be conjectured that endosulfan is aerially transported at higher temperatures and continuously circulates within the environment.

Soils, especially permafrost in the Arctic and the Tibetan Plateau, are one of the largest reservoirs of mercury (Hg) in the global environment. The Hg concentration in the grassland soils over the Tibetan Plateau and its driving factors have been less studied. This study analyzes soil total mercury (STHg) concentrations and its vertical distribution in grassland soil samples collected from the Tibetan Plateau. We adopt a nested-grid high-resolution GEOS-Chem model to simulate atmospheric Hg deposition. The relationship between STHg and soil organic carbon (SOC), as well as atmospheric deposition, are explored. Our results show that the STHg concentrations in the Tibetan Plateau are 19.8 ± 12.2 ng/g. The concentrations are higher in the south and lower in the north in the Tibetan Plateau, consistent with the previous results. Our model shows that the average deposition flux of Hg is 3.3 μg m⁻² yr⁻¹, with 57% contributed by dry deposition of elemental mercury (Hg⁰), followed by dry (19%) and wet (24%) deposition of divalent mercury. We calculate the Hg to carbon ratio (RHg:C) as 5.6 ± 6.5 μg Hg/g C, and the estimated STHg is 86.6 ± 101.2 Gg in alpine grasslands in the Tibetan Plateau. We find a positive relationship between STHg and SOC in the Tibetan Plateau (r² = 0.36) and a similar positive relationship between STHg and atmospheric total Hg deposition (r² = 0.24). A multiple linear regression involving both variables better model the observed STHg (r² = 0.42). We conclude that SOC and atmospheric deposition influence STHg simultaneously in this region. The data provides information to quantify the size of the soil Hg pool in the Tibetan Plateau further, which has important implications for the Hg cycles in the permafrost regions as well as on the global scale.

Fluoride has been considered as a risk factor of cardiovascular disease due to its endothelial toxicology. However, the mechanism underlying the endothelial toxicity of fluoride has not been clearly illustrated. MiR-200c-3p was strongly linked with endothelial function and its level is increased in serum of fluorosis patients, but it is unclear the role of miR-200c-3p in the fluoride induced endothelial dysfunction. In this study, we confirmed that fluoride exposure induced the apoptosis of endothelial cells both in established rats model and cultured human umbilical vein endothelial cells (HUVECs). And miR-200c-3p was found to be upregulated in NaF treated HUVECs. Fluoride stimulation increased caspase-dependent apoptosis through miR-200c-3p upregulation, with repressing expression of its target gene Fas-associated phosphatase 1 (Fap-1), which functioned as Fas inhibitor. This resulted in activation of Fas-associated extrinsic apoptosis via interaction with increased Fas, Fadd, Cleaved Caspase-8 and Cleaved Caspase-3. The activation of Fas-associated extrinsic apoptosis was abrogated by miR-200c-3p inhibitor. Furthermore, the antiapoptotic effect of downregulated miR-200c-3p was restored by Fap-1 siRNA. These results suggested a determinant role of the miR-200c-3p/Fap-1 axis in fluoride induced endothelial apoptosis.

We propose a methodology to estimate single and multiple emission sources of atmospheric contaminants. It combines hybrid metaheuristic/gradient-descent optimization techniques and Tikhonov-type regularization. The dispersion problem is solved by the Galerkin/Least-squares finite element formulation, which allows more realistic modeling. The accuracy of the proposed inversion model is tested under different contexts with experimental data. To identify single and multiple emissions, we use experimental field data. We consider different configurations for both the Tikhonov-type functional and optimization techniques. Several single and composite data misfit functions are tested. We also use a discrepancy-based choice rule for the regularization parameter. The resulting inversion tool is highly versatile and presents accurate results under different contexts with a competitive computational cost.

Glyphosate is one of the most used herbicides in the world. The fate of glyphosate in tropical soils may be different from that in soils from temperate regions. In particular, the amounts and types of non-extractable residues (NER) may differ considerably, resulting in different relative contributions of xenoNER (sorbed and sequestered parent compound) and bioNER (biomass residues of degraders). In addition, environmental conditions and agricultural practices leading to total organic carbon (TOC) or pH variation can alter the degradation of glyphosate. The aim of this study is thus to investigate how the glyphosate degradation and turnover are influenced by varying temperature, pH and TOC of sandy loam soil from Colombia. The pH or TOC of a Colombian soil was modified to yield five treatments: control (pH 7.0, TOC 3%), 4% TOC, 5% TOC, pH 6.5, and pH 5.5. Each treatment received 50 mg kg⁻¹ of ¹³C₃¹⁵N-glyphosate and was incubated at 10 °C, 20 °C and 30 °C for 40 days. Rising temperature increased the mineralization of ¹³C₃¹⁵N-glyphosate from 13 to 20% (10 °C) to 32–39% (20 °C) and 41–51% (30 °C) and decreased the amounts of extractable ¹³C₃¹⁵N-glyphosate after 40 days of incubation from 13 to 26% (10 °C) to 4.6–12% (20 °C) and 1.2–3.2% (30 °C). Extractable ¹³C₃¹⁵N-glyphosate increased with higher TOC and higher pH. Total ¹³C-NER were similar in all treatments and at all temperatures (47%–60%), indicating that none of the factors studied affected the amount of total ¹³C-NER. However, ¹³C-bioNER dominated within the ¹³C-NER pool in the control and the 4% TOC treatment (76–88% of total ¹³C-NER at 20 °C and 30 °C), whereas in soil with 5% TOC and pH 6.5 or 5.5 ¹³C-bioNER were lower (47–61% at 20 °C and 30 °C). In contrast, the ¹⁵N-bioNER pool was small (between 14 and 39% of the ¹⁵N-NER). Thus, more than 60% of ¹⁵N-NER is potentially hazardous xenobiotic NER which need careful attention in the future.

In recent years, numerous studies paid more attention to the molecular mechanisms associated with fluoride toxicity. However, the detailed mechanisms of fluoride immunotoxicity in bovine neutrophils remain unclear. Neutrophil extracellular traps (NETs) is a novel immune mechanism of neutrophils. We hypothesized that sodium fluoride (NaF) can trigger NETs activation and release, and investigate the related molecular mechanisms during the process. We exposed peripheral blood neutrophils to 1 mM NaF for 120 min in bovine neutrophils. The results showed that NaF exposure triggered NET-like structures decorated with histones and granule proteins. Quantitative measurement of NETs content correlated positively with the concentration of NaF. Mechanistically, NaF exposure increased reactive oxygen species (ROS) levels and phosphorylation levels of ERK, p38, whereas inhibiting the activities of superoxide dismutase (SOD) and catalase (CAT) compared with control neutrophils. NETs formation is induced by NaF and this effect was inhibited by the inhibitors diphenyleneiodonium chloride (DPI), U0126 and SB202190. Our findings described the potential importance of NaF-triggered NETs related molecules, which might help to extend the current understanding of NaF immunotoxicity.

Di-(2-ethylhexyl) phthalate (DEHP) has been classified as a priority pollutant which increased the healthy risk to human and animals dramatically. Hence, a novel biochemical system combined by DEHP-resistant bacterial flora (B) and a green oxidant of persulfate (PS) activated by Nano-Fe₃O₄ was applied to degrade DEHP in contaminated soil. In this study, the resistant bacterial flora was screened from activated sludge and immobilized by sodium alginate (SAB). Nano-Fe₃O₄ was coated on biochar (BC@Fe₃O₄) to prevent agglomerating in soil. X-ray diffraction (XRD) and scanning electron microscope (SEM) were utilized to characterize BC@Fe₃O₄. Results demonstrated that the treatment of biochemical system (SAB + BC@Fe₃O₄ + PS) presented the maximum degradation rate about 92.56% within 24 days of incubation and improved soil microecology. The 16S rDNA sequences analysis of soil microorganisms showed a significantly different abundance and a similar diversity among different treatments. Kyoto Encyclopedia of Genes and Genomes (KEGG) functional genes difference analysis showed that some metabolic pathways, such as metabolism of cofactors and vitamins, energy metabolism, cell growth and death, replication and repair, were associated with the biodegradation of DEHP. Besides, DEHP was converted to MEHP and PA by biodegradation, while DEHP was converted to DBP and PA by persulfate and BC@Fe₃O₄, and then ultimately degraded to CO₂ and H₂O.