While extreme high temperatures are an important aspect of global warming, their effects on organisms are relatively understudied, especially in ecotoxicology. Sequential exposure to heat spikes and pesticides is a realistic scenario as both are typically transient stressors and are expected to further increase in frequency under global warming. We tested the effects of exposure to a lethal heat spike and subsequently to an ecologically relevant lethal pulse exposure of the pesticide chlorpyrifos in the larvae of mosquito Culex pipiens. The heat spike caused direct and delayed mortality, and resulted in a higher heat tolerance and activity of acetylcholinesterase, and a lower fat content in the survivors. The chlorpyrifos exposure caused mortality, accelerated growth rate, and decreased the heat tolerance and the activity of acetylcholinesterase. The preceding heat spike did not change how chlorpyrifos reduced the heat tolerance. Notably, the preceding heat spike did lower the lethal effect of the pesticide, which makes an important novel finding at the interface of ecotoxicology and global change biology, and adds a new dimension to the “climate-induced toxicant sensitivity” (CITS) concept. This may be due to both survival selection and cross-tolerance, and therefore likely a widespread phenomenon. Our results emphasize the importance of including extreme high temperatures as an important transient global change stressor in ecotoxicology.

Microplastic (MP) pollution and its potential to concentrate and transport organic contaminants in environments have recently gained widespread attention. Compared to traditional nonpolar plastics such as polypropylene (PP) and polyethylene (PE), study about the environmental behavior of polyurethane (PT), polyuria (PU) and urea-formaldehyde resin (UF), which are typically used as shell materials for pesticide microcapsules and have polar structure is scarce. In the present study, we investigated the sorption capacities and binding mechanisms of PT, PU and UF for three polycyclic aromatic hydrocarbons (PAHs, naphthalene, phenanthrene (PHE), and pyrene) and two PHE derivates (ethylphenanthrene-2-carboxylate (2-CPHE) and 2-methylphenathrene (2-MPHE)) selected as the model compounds, and the effects of salinity and UV and/or H₂O₂ aging treatments on PHE sorption to MPs. The results showed that PT, PU and UF had negative surface charges, micron-scaled sizes and abundant polar functional groups containing O and N elements. PT, PU and UF could sorb PAHs efficiently with sorption coefficients (Kd) being in the range of 8.11 × 10³–9.53 × 10⁵ (L/Kg) and partitioning was the main sorption mechanism with polar interactions (H-boning and p/π-π EDA interactions) also contributing. The sorption capacity of the three MPs changed mainly depending on their glass transition temperatures (Tg). Furthermore, high salinity decreased the surface zeta-potential of the MPs and enhanced PHE sorption to MPs. In addition, aging treatments with UV and/or H₂O₂ markedly decreased the Tg of PT and enhanced its sorption capacity for PHE, while opposite results were obtained for PU. The findings on the sorption mechanisms of PAHs to agricultural MPs are useful for predicting the transport, fate and persistence of the co-existing HOCs in agricultural ecosystems and provide a scientific basis for the comprehensive risk assessment of agricultural MPs.

Pesticides pollution has caused serious environmental problems in recent years, and mounting evidence has shown that more and more insecticides have serious risk in human health. Emamectin Benzoate formally regarded as a highly safety insecticide based on its exclusive targets, but the cytotoxicity to human lung was ignored for a long time. In the present study, bioassay experiments were used to assess the toxicity of the Emamectin Benzoatein on human non-target cells including cell viability assay, DNA damage assay, flow cytometer assay and western blotting assay. The results indicated that Emamectin Benzoatecan cause the inhibition of the proliferation, cytochrome c release, activation of caspase-3/9 and increase Bax/Bcl-2 ratio, which means it induced the cytotoxicity on 16HBE cells associated with the mitochondrial apoptosis. Besides, the DNA damge caused by the Emamectin Benzoate suggest it has a potential genotoxic effect on human lung cells.

The aquatic ecosystem is seriously damaged because of the heavy use of pesticides and antibiotics. Fish is the indispensable link between environmental pollution and human health. However, the toxic effects of environment-related concentrations of pesticides and antibiotics in fish have not been thoroughly studied. In this study, grass carps exposed to cypermethrin (CMN, 0.651 μg/L) or/and sulfamethoxazole (SMZ, 0.3 μg/L) for 42 days caused oxidative stress, apoptosis and immunodeficiency in the spleen of grass carps. CMN or/and SMZ exposure led to oxidative damage (consumption of antioxidant enzymes (superoxide dismutase and catalase)) and lipid peroxidation (accumulation of malondialdehyde), induced apoptosis (increases in TUNEL index, Bax/bcl-2, p53, puma and Caspase family expression). In addition, the levels of immunoglobulin M (IgM), complement 3 (C3) were significantly decreased in all treatment groups, which trend was also found in C-reactive protein in CMN and MIX group, and lysozyme in MIX group. Transcription of almost all genes involved in the Toll-like receptors (TLR) signaling pathway was up-regulated under CMN or/and SMZ exposure. However, when subsequently attacked by Aeromonas hydrophila for 2 days, the TLR pathway was inhibited in spleens of all treatment groups accompanied by higher mortality. Overall, the environmentally relevant concentration of CMN and SMZ damages the immune system, triggering oxidative stress and apoptosis in carps. And by affecting the conduction of TLR signaling pathway, CMN or/and SMZ exposure inhibits the innate immune response of fish and reducing their disease resistance. This study highlights the importance of rational and regulated use of these pesticides and antibiotics.

Current study deals with the surface modification of acid activated carbon (prepared from Pongamia pinnata shells) with Cetyltrimethylammonium bromide (CTAB) and its role as an adsorbent in eliminating anionic azo dyes viz. Congo red (CR) and Direct blue 6 (DB) from single and binary adsorptive systems. Binary adsorptive system involved the synergistic and antagonistic influence of one dye over the adsorption of other dye. Physico-chemical alterations due to surfactant modification and post adsorption were studied using atomic force microscopy (AFM), Zeta Potential, scanning electron microscopy (SEM), Energy-dispersive X-ray spectroscopy (EDS), surface area analysis and Fourier-transformed infrared spectroscopy (FTIR). Process parameters influencing efficient adsorption of CR and DB species viz. initial pH of dye solution, adsorbent dosage, incubation temperature and initial concentration of dye species were optimised. Sorbate-sorbent interaction studies for single adsorptive system revealed sorbate’s monolayer formation over adsorbent’s surface and the involvement of chemisorption, as verified by Langmuir isotherm model and pseudo-second order model, respectively. Langmuir maximum adsorption capacity of the adsorbent was 555.56 mg/g for CR and 625.00 mg/g for DB. Meanwhile, for binary adsorptive system, competitive Langmuir model verified both CR and DB had antagonistic/competitive effect over each other’s adsorption. Thermodynamic analysis revealed the adsorptive process as exothermic, spontaneous and thermodynamically favourable with an elevated degree of dis-orderedness. Co-existing cations and anions has nominal effect on the adsorption capacity of dyes. Recyclability studies verified a modest efficiency of 62.52% for CR and 50.47% for DB species after the end of 4th adsorption-desorption cycle; thus affirming its recyclability potential. Phytotoxic assay affirmed the effectivity of the adsorbent in adsorbing dye species from aqueous solutions using Vigna mungo seeds as the model.

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.