Direct utilization of waste polyethylene terephthalate (PET) from the environment to form highly porous aerogel technology for oil absorption is an attractive approach from the view point of green chemistry. However, the oil absorption reaction is limited by low oil absorption capacity and less stability. For now, silica aerogel are used to solve these problem. Our goal is to substitute to these silica aerogel with PET aerogel technology. Herein, we have prepared an environmental waste PET based aerogel with 1.0:0.5 wt% PET, polyvinyl alcohol (PVA), and glutaraldehyde (GA) 0.2% v/v were dispersed in 10 mL DI water, followed by homogenization (30 min), sonication (10 min), and ageing (2 h) at 70 °C. To escape macroscopic cracking, cooling (8 h) at 4 °C was followed by freezing (6 h), freeze drying at −80 °C, and 5 mTorr for 18 h. The hybrid PET aerogel displays excellent performance towards oil absorption. Notably it showed high absorption capacity towards the different oils about 21–40 times its own weight, depending on the viscosity and density of the oil and solvents within 15–35 s, 25 °C, and 2 × 2 cm aerogel size. In addition, the aerogel shows there is no change in structure after several recycles due to high mechanical strength. Furthermore, because of the PET aerogel's high porosity (99.74%) and low density (0.0311 g/cm³), close bonding between PET-PVA occurs. Therefore, aerogel shows hydrophobic nature, good mechanical strength, high thermal stability, arrangement of the interconnected fibrillar pore network offers a high surface to volume ratio, low surface energy, high surface roughness, and more reusability. All these parameters are responsible for high oil absorption.

Increasing chloride concentrations from road salt applications are an emerging threat to freshwater diversity in cold weather regions. Few studies have focused on how road salt affects freshwater biota and even fewer have focused on how the rate of exposure alters organism responses. We hypothesized that road salt concentrations delivered gradually would result in slower population declines and more rapid rebounds due to evolved tolerance. To test this hypothesis, we examined the responses of freshwater lake organisms to four environmentally relevant salt concentrations (100, 230, 860, and 1600 mg Cl⁻/L) that differed in application rate (abrupt vs. gradual). We used outdoor aquatic mesocosms containing zooplankton, filamentous algae, phytoplankton, periphyton, and macroinvertebrates. We found negative effects of road salt on zooplankton and macroinvertebrate abundance, but positive effects on phytoplankton and periphyton, likely resulting from reduced grazing. Only rarely did we detect a difference between abrupt vs gradual salt applications and the directions of those differences were not consistent. This affirms the need for additional research on how road salt pollution entering ecosystems at different frequencies and magnitudes will alter freshwater communities.

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.

Pollution damages ecosystems around the globe and some forms of pollution, like oil pollution, can be either man-made or derived from natural sources. Despite the pervasiveness of oil pollution, certain organisms are able to colonise polluted or toxic environments, yet we only have a limited understanding of how they are affected by it. Here, we analysed phenotypic responses to oil pollution in guppies (Poecilia reticulata) living in oil-polluted habitats across southern Trinidad. We analysed body-shape and life-history traits for 352 individuals from 11 independent populations, six living in oil-polluted environments (including the naturally oil-polluted Pitch Lake), and five stemming from non-polluted habitats. Based on theory of, and previous studies on, responses to environmental stressors, we predicted guppies from oil-polluted waters to have larger heads and shallower bodies, to be smaller, to invest more into reproduction, and to produce more but smaller offspring compared to guppies from non-polluted habitats. Contrary to most of our predictions, we uncovered strong population-specific variation regardless of the presence of oil pollution. Moreover, guppies from oil-polluted habitats were characterised by increased body size; rounder, deeper bodies with increased head size; and increased offspring size, when compared to their counterparts from non-polluted sites. This suggests that guppies in oil-polluted environments are not only subject to the direct negative effects of oil pollution, but might gain some (indirect) benefits from other concomitant environmental factors, such as reduced predation and reduced parasite load. Our results extend our knowledge of organismal responses to oil pollution and highlight the importance of anthropogenic pollution as a source of environmental variation. They also emphasise the understudied ecological heterogeneity of extreme environments.

The presence of manufactured nano-objects (MNOs) in various consumer or their (future large-scale) use as nanoagrochemical have increased with the rapid development of nanotechnology and therefore, concerns associated with its possible ecotoxicological effects are also arising. MNOs are releasing along the product life cycle, consequently accumulating in soils and other environmental matrices, and potentially leading to adverse effects on soil biota and their associated processes. Earthworms, of the group of Oligochaetes, are an ecologically significant group of organisms and play an important role in soil remediation, as well as acting as a potential vector for trophic transfer of MNOs through the food chain. This review presents a comprehensive and critical overview of toxic effects of MNOs on earthworms in soil system. We reviewed pathways of MNOs in agriculture soil environment with its expected production, release, and bioaccumulation. Furthermore, we thoroughly examined scientific literature from last ten years and critically evaluated the potential ecotoxicity of 16 different metal oxide or carbon-based MNO types. Various adverse effects on the different earthworm life stages have been reported, including reduction in growth rate, changes in biochemical and molecular markers, reproduction and survival rate. Importantly, this literature review reveals the scarcity of long-term toxicological data needed to actually characterize MNOs risks, as well as an understanding of mechanisms causing toxicity to earthworm species. This review sheds light on this knowledge gap as investigating bio-nano interplay in soil environment improves our major understanding for safer applications of MNOs in the agriculture environment.

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.

6:2 Cl-PFESA is a polyfluoroalkyl ether with high environmental persistence that has been confirmed to have significant adverse effects on animals. In this study, 6-week-old female C57BL/6 mice were exposed to 0, 1, 3 and 10 μg/L 6:2 Cl-PFESA for 10 weeks to estimate the hepatotoxicity of 6:2 Cl-PFESA and explore its underlying molecular mechanism. The results indicated that 6:2 Cl-PFESA preferentially bioaccumulated in the liver and induced hepatic cytoplasmic vacuolation and hepatomegaly in mice. In addition, serum metabolic profiling showed that 6:2 Cl-PFESA exposure caused an abnormal increase in amino acids and an abnormal decrease in acyl-carnitine, which interfered with fatty acid transport and increased the risk of metabolic diseases. Further experiments showed that 6:2 Cl-PFESA formed more hydrogen bonds with PPAR-γ than PFOS, Rosi and GW9662, and the binding affinity of 6:2 Cl-PFESA toward PPAR-γ was the highest among the ligands. 6:2 Cl-PFESA promoted the differentiation of 3T3-L1 cells by increasing PPAR-γ expression. Therefore, our results showed that 6:2 Cl-PFESA has the potential to induce liver damage and dysfunction in female mice, and this effect was achieved through PPAR-γ. This study is the first to reveal the hepatic toxicity of 6:2 Cl-PFESA in female mammals and provides new insights for subsequent in-depth research.

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.

The removal of halogenated dye and sensing of pharmaceutical products in the water bodies with quick purification time is of high need due to the scarcity of drinking water. The present work reported on the preparation of graphitic carbon nitride (g-C₃N₄) for quick time water contaminant adsorption, followed by synthesizing silver nanoparticles decorated graphitic carbon nitride for pharmaceutical product sensing using in-situ SERS technique. The prepared graphitic carbon nitride is used to study the adsorption behavior of water contaminants at room temperature, in the presence of methylene blue (MB) as an adsorbate model. The water-soluble graphitic carbon nitride, even at low concentration, possesses an excellent ability to adsorb halogenated organic dye. As a result, the dyes are found to adsorb within ∼5s even without any additional physical or chemical activation. From the UV–Vis absorption investigations, it has been perceived that in the presence of graphitic carbon nitride (g-C₃N₄) the dye adsorption efficacy is observed nearly 80% with the well fitted linearly of R² = 0.9731. Effective in-situ surface-enhanced Raman scattering (SERS) studies for Ag nanoparticles decorated graphitic carbon nitride has been carried out and the obtained result shows good sensing performance of the material towards acetaminophen drug. This method opens the possibility of the Nobel metal decorated graphitic carbon nitride for real-time sensing of SERS-based drug products along with the development of high-performance sensing of the target analyte in the future.

The trace element fluoride can be beneficial for oral health by preventing dental caries. However, fluoride is also known as an environmental pollutant. Fluoride pollution can lead to fluoride over-ingestion and can cause health issues, including dental fluorosis. Curcumin attenuated fluoride-induced toxicity in animal models, however the molecular mechanisms of how curcumin affects fluoride toxicity remain to be elucidated. We hypothesized that curcumin attenuates fluoride toxicity through modulation of Ac-p53. Here we investigated how curcumin affects the p53-p21 pathway in fluoride toxicity.LS8 cells were treated with NaF with/without curcumin. Curcumin significantly increased phosphorylation of Akt [Thr308] and attenuated fluoride-mediated caspase-3 cleavage and DNA damage marker γH2AX expression. Curcumin-mediated attenuation of caspase-3 activation was reversed by Akt inhibitor LY294002 (LY). However, LY did not alter curcumin-mediated γH2AX suppression. These results suggest that curcumin inhibited fluoride-mediated apoptosis via Akt activation, but DNA damage was suppressed by other pathways. Curcumin did not suppress/alter fluoride-mediated Ac-p53. However, curcumin itself significantly increased Ac-p53 and upregulated p21 protein levels to suppress cell proliferation in a dose-dependent manner. Curcumin suppressed fluoride-induced phosphorylation of p21 and increased p21 levels within the nuclear fraction. However, curcumin did not reverse fluoride-mediated cell growth inhibition. These results suggest that curcumin-induced Ac-p53 and p21 led to cell cycle arrest, while curcumin attenuated fluoride-mediated apoptosis via activation of Akt and suppressed fluoride-mediated DNA damage.By inhibiting DNA damage and apoptosis, curcumin may potentially alleviate health issues caused by fluoride pollution. Further studies are required to better understand the mechanism of curcumin-induced biological effects on fluoride toxicity.