Smoke from plastic waste incineration in an open air travels worldwide and is a major source of air pollution particulate matter (PM) that is very withstand to degradation and hazard to human health. Suspension of smoke aerosol components in water occurs during rains and fire extinguishing. Here, water-suspended plastic smoke aerosol (WPS) preparations suitable for biotesting were synthesized. It has been revealed using dynamic light scattering that WPS contained major nano-sized (∼30 nm) PM fraction, and this result was confirmed by electron microscopy. Optical absorption of WPS was in the UV region and an increase in λₑₓ led to a red-shift in fluorescence emission with a corresponding decrease in fluorescence intensity. WPS was analyzed in neurotoxicity studies in vitro using presynaptic rat cortex nerve terminals (synaptosomes). Generation of spontaneous reactive oxygen species (ROS) detected using fluorescent dye 2′,7-dichlorofluorescein in nerve terminals was decreased by WPS (10–50 μg/ml) in a dose-dependent manner. WPS also reduced the H₂O₂-evoked ROS production in synaptosomes, thereby influencing cellular oxidative processes and this effect was similar to that for carbon nanodots. WPS (0.1 mg/ml) decreased the synaptosomal membrane potential and synaptic vesicle acidification in fluorimetric experiments. WPS (1.0 mg/ml) attenuated the synaptosomal transporter-mediated uptake of excitatory and inhibitory neurotransmitters, L-[¹⁴C]glutamate and [³H]GABA, respectively. This can lead to an excessive increase in the glutamate concentration in the synaptic cleft and neurotoxicity via over activation of ionotropic glutamate receptors. Therefore, WPS was neurotoxic and provoked presynaptic malfunction through changes of oxidative activity, reduction of the membrane potential, synaptic vesicle acidification, and transporter-mediated uptake of excitatory and inhibitory neurotransmitters in nerve terminals. In summary, synthesis and emission to the environment of ultrafine PM occur during combustion of plastics, thereby polluting air and water resources, and possibly triggering development of neuropathologies.

Environmental pollution by heavy metals (HMs) has raised considerable attention due to their toxic impacts on plants, animals and human beings. Thus, the environmental cleanup of these toxic (HMs) is extremely urgent both from the environmental and biological point of view. To remediate HMs-polluted environment, several nanoparticles (NPs) such as metals and its oxides, carbon materials, zeolites, and bimetallic NPs have been documented. Among these, Fe-based NPs have emerged as an effective choice for remediating environmental contamination, due to infinite size, high reactivity, and adsorption properties. This review summarizes the utilization of various Fe-based NPs such as nano zero-valent iron (NZVI), modified-NZVI, supported-NZVI, doped-NZVI, and Fe oxides and hydroxides in remediating the HMs-polluted environment. It presents a comprehensive elaboration on the possible reaction mechanisms between the Fe-based NPs and heavy metals, including adsorption, oxidation/reduction, and precipitation. Subsequently, the environmental factors (e.g., pH, organic matter, and redox) affecting the reactivity of the Fe-based NPs with heavy metals are also highlighted in the current study. Research shows that Fe-based NPs can be toxic to living organisms. In this context, this review points out the environmental hazards associated with the application of Fe-based NPs and proposes future recommendations for the utilization of these NPs.

Polybrominated diphenyl ethers (PBDEs) are a family where each congener possesses different physicochemical properties, persistence and/or toxicity. Biodegradation can selectively change the abundance of congeners. These warrant modeling of individual congeners by considering biodegradation pathways together with fate and transport (F&T) mechanisms. Accordingly, this study aims to develop a F&T model (Fate and Transport model for Hydrophobic Pollutants - FTHP) that integrates congener specific biodegradation of PBDEs in sediments. The model is tested using sediment data from a location representing the Lower South Bay of San Francisco. Results demonstrated settling, resuspension, and biodegradation as important mechanisms. FTHP is then used to predict congener concentrations in a period of 20 years for two cases (constant and time-dependent water column concentrations) and four alternative scenarios: no intervention (i.e., natural attenuation, also serves as the base case), no degradation, dredging and biostimulation. The greatest impact on the reduction of total PBDE concentrations was achieved by a reduction in water column concentrations, i.e. source control, and dredging. On the other hand, biostimulation coupled with source control was the most effective in reducing bioaccumulative PBDE congener concentrations and almost as effective as dredging for the rest of congeners. Proposed FTHP model can distinguish between congeners and help devise informed management plans which focus on decreasing risks associated with persistent and bioaccumulative compounds in contaminated sediments.

Some studies have indicated that formaldehyde, a ubiquitous environmental pollutant, can induce or aggravate allergic asthma. Epidemiological studies have also shown that the relative humidity indoors may be an independent and a key factor associated with the aggravation of allergic asthma. However, the synergy of humidity and formaldehyde on allergic asthma and the mechanism underlying this effect remain largely unknown. In this study, we aim to determine the effect of high relative humidity and/or formaldehyde exposure on allergic asthma and explore the underlying mechanisms. Male Balb/c mice were modeled with ovalbumin (OVA) and exposure to 0.5 mg/m3 formaldehyde and/or different relative humidity (60%/75%/90%). Histopathological changes, pulmonary function, Th1/Th2 balance, the status of mucus hypersecretion and the levels of inflammatory factors were detected to assess the exacerbation of allergic asthma. The levels of the transient receptor potential vanilloid 4 (TRPV4), calcium ion and the activation of p38 mitogen-activated protein kinases (p38 MAPK) were detected to explore the underlying mechanisms. The results showed that exposure to high relative humidity or to 0.5 mg/m3 formaldehyde alone had a slight, but not significant, affect on allergic asthma. However, the pathological response and airway hyperresponsiveness (AHR) were greatly aggravated by simultaneous exposure to 0.5 mg/m3 formaldehyde and 90% relative humidity. Blocking TRPV4or p38 MAPK using HC-067047 and SB203580 respectively, effectively alleviated the exacerbation of allergic asthma induced by this simultaneous exposure to formaldehyde and high relative humidity. The results show that when formaldehyde and high relative humidity are present this can enhance the activation of the TRPV4 ion channel in the lung leading to the aggravation of the p38 MAPK activation, resulting in the exacerbation of inflammation and hypersecretion of mucus in the airways.

The ecological risk assessment guidance of virtually all federal and state agencies, private companies, and other interests can be traced to that of the essential design of the U.S. Environmental Protection Agency (EPA). The EPA ecological risk assessment paradigm has remained unchanged for all intents and purposes since its inception 30 years ago, this despite criticism expressed repeatedly by some, for many years. Despite the discipline's name, a core paradigm shortcoming is its inability to express risk, the probability of a receptor-of-concern at a contaminated site developing a toxicological endpoint (e.g., reproductive impairment). Further, common site context and biological realities (e.g., site sizes; home ranges of receptors-of concern) allow for the supported challenges that risk assessments aren't needed altogether, and instances of ecological damage at sites being unknown. This commentary is an open appeal to the EPA to replace the paradigm it has set forth, dispensing with failed processes (e.g., endeavoring to assess risk potential at 75 year-old sites; endeavoring to assess risk potential to wide-ranging species at one-acre properties). The commentary invites the EPA to respond, not with counter-arguments, but rather with explanations for the Agency's resistance to acknowledging problems with its guidance, followed by the Agency commitment to sorely needed ERA reform.

Glyphosate, introduced by Monsanto Company under the commercial name Roundup in 1974, became the extensively used herbicide worldwide in the last few decades. Glyphosate has excellent properties of fast sorption in soil, biodegradation and less toxicity to nontarget organisms. However, glyphosate has been reported to increase the risk of cancer, endocrine-disruption, celiac disease, autism, effect on erythrocytes, leaky-gut syndrome, etc. The reclassification of glyphosate in 2015 as ‘probably carcinogenic’ under Group 2A by the International Agency for Research on Cancer has been broadly circulated by anti-chemical and environmental advocacy groups claiming for restricted use or ban of glyphosate. In contrast, some comprehensive epidemiological studies involving farmers with long-time exposure to glyphosate in USA and elsewhere coupled with available toxicological data showed no correlation with any kind of carcinogenic or genotoxic threat to humans. Moreover, several investigations confirmed that the surfactant, polyethoxylated tallow amine (POEA), contained in the formulations of glyphosate like Roundup, is responsible for the established adverse impacts on human and ecological health. Subsequent to the evolution of genetically modified glyphosate-resistant crops and the extensive use of glyphosate over the last 45 years, about 38 weed species developed resistance to this herbicide. Consequently, its use in the recent years has been either restricted or banned in 20 countries. This critical review on glyphosate provides an overview of its behaviour, fate, detrimental impacts on ecological and human health, and the development of resistance in weeds and pathogens. Thus, the ultimate objective is to help the authorities and agencies concerned in resolving the existing controversies and in providing the necessary regulations for safer use of the herbicide. In our opinion, glyphosate can be judiciously used in agriculture with the inclusion of safer surfactants in commercial formulations sine POEA, which is toxic by itself is likely to increase the toxicity of glyphosate.

Textile microfibers are one of the most important sources within primary microplastics. These have raised environmental concerns since its recent identification as pollutants. However, there are still no accurate models to assess their contribution to the microplastic pollution. Hence, in this study, a method to estimate the mass flow of microfibers detached from household laundry that reaches aquatic environments has been developed. The method considers a set of parameters related to the detachment of microfibers, which are, basically: (1) the detachment rate of microfibers from different textile garments, (2) the volume of laundry effluents, (3) the percentage of municipal water that has been treated, (4) the type of used-water treatment applied, and, (5) the proportion of front- versus top-loading washing machines. In this way, 0.28 million tons of microfibers per year were estimated to reach aquatic environments, which is approximately half than the last published valuation. Finally, hypothetical situations were simulated to evaluate the reduction of microfibers by the modification of some of the parameters at different levels (consumer, government entities, and industry). Thus, depending on the implanted alternatives, microfibers that reach the aquatic environments could be reduced between 30% and 65%.

A series of phosphorus containing ZnO (P–ZnO) photocatalysts with various percentages of phosphorus were successfully synthesized using the hydrothermal method. The structural, physical and optical properties of the obtained microparticles were investigated using diverse techniques such as X-ray diffraction (XRD), Fourier transform infrared (FT-IR) spectroscopy, ultraviolet–visible diffusion reflectance spectroscopy (UV–Vis DRS), photoluminescence (PL) spectroscopy, transmission electron microscopy (TEM), energy dispersive X-ray spectroscopy (EDS) and N₂ adsorption-desorption analysis. The photocatalytic activities of the pure and P–ZnO samples were evaluated for the degradation of Rhodamine B (RhB) under visible light irradiation. The parameters such as pH, catalyst dosage, contaminant concentration and effect of persulfate as an oxidant were studied. It was found that the P–ZnO1.8% photocatalyst could destroy 99% of RhB (5 ppm) in 180 min at pH = 7; furthermore, it degraded ∼100% of 5 and 10 ppm of the RhB pollutant in 120 and 180 min, respectively, only by adding 0.01 g of persulfate into the reaction solution. To determine the photocatalytic mechanism, 2-propanol, benzoquinone and EDTA were used and it was indicated that hydroxyl radicals, superoxide ions and holes, all had major roles in the photocatalytic degradation but the hydroxyl radical effect was the most significant. The phenol degradation was also investigated using the P–ZnO1.8% optimum photocatalyst which could destroy 53% of the phenol (5 ppm) in 180 min. According to the reusability test, it was proved that after 5 cycles, the catalyst activity was not highly changed and it was potentially capable of pollutant degradation.

The study aimed to investigate temporal trends of “old” and “new” persistent halogenated organic pollutants (HOPs) in Taihu Lake, the third largest freshwater lake in China, and the associated health risks. Five fish species were consecutively collected from the lake every year during 2011–2018. HOPs including 37 polychlorinated biphenyls (PCBs), 10 organochlorine pesticides (OCPs), short- and medium-chain chlorinated paraffins (SCCPs and MCCPs), 19 polybrominated diphenyl ethers (PBDEs), and 10 new brominated flame retardants (NBFRs), were measured. The results showed that all the HOPs were detected, with MCCPs and NBFRs showing the highest and lowest concentrations, respectively. The levels of SCCPs and MCCPs were several orders of magnitude higher than those of the other HOPs. There were obvious increasing trends for SCCPs, MCCPs, and hexachlorobenzene, but a decreasing trend for PBDEs. No obvious increasing or decreasing trends were observed for the other HOPs. The present study indicated that the use of NBFRs to replace PBDEs was not yet clearly observed. Fish consumption did not result in non-carcinogenic risks, but posed low carcinogenic risks, with PCBs and DDTs being the highest-risk contaminants because of historical residues. This is the first study for the temporal variations of the HOPs in the lake.

Previous in vitro studies have indicated that 2,3,3′,4,4′,5-hexachlorobiphenyl (PCB 156) may be a new contributor to metabolic disruption and may further cause the occurrence of nonalcoholic fatty liver disease (NAFLD). However, no study has clarified the specific contributions of PCB 156 to NAFLD progression by constructing an in vivo model. Herein, we evaluated the effects of PCB 156 treatment (55 mg/kg, i.p.) on the livers of C57BL/6 mice fed a control diet (CD) or a high-fat diet (HFD). The results showed that PCB 156 administration increased intra-abdominal fat mass, hepatic lipid levels and dyslipidemia in the CD-fed group and aggravated NAFLD in HFD-fed group. By using transcriptomics studies and biological methods, we found that the genes expression involved in lipid metabolism pathways, such as lipogenesis, lipid accumulation and lipid β-oxidation, was greatly altered in liver tissues exposed to PCB 156. In addition, the cytochrome P450 pathway, peroxisome proliferator-activated receptors (PPARs) and the glutathione metabolism pathway were significantly activated following exposure to PCB 156. Furthermore, PCB 156 exposure increased serum transaminase levels and lipid peroxidation, and the redox-related genes were significantly dysregulated in liver tissue. In conclusion, our data suggested that PCB 156 could promote NAFLD development by altering the expression of genes related to lipid metabolism and inducing oxidative stress.