Toxic mechanism in Daphnia magna due to phthalic acid esters and CuO nanoparticles co-exposure: The insight of physiological, microbiomic and metabolomic profiles.

Various phthalic acid esters (PAEs) such as dibutyl phthalate (DBP) and butyl benzyl phthalate (BBP) co-exist with nanopollutants in aquatic environment. In this study, Daphnia magna was exposed to nano-CuO and DBP or BBP at environmental relevant concentrations for 21-days to investigate these combined toxic effects. Acute EC50 values (48 h) of nano-CuO, DBP, and BBP were 12.572 mg/L, 8.978 mg/L, and 4.785 mg/L, respectively. Results showed that co-exposure with nano-CuO (500 µg/L) for 21 days significantly enhanced the toxicity of DBP (100 µg/L) and BBP (100 µg/L) to Daphnia magna by 18.37% and 18.11%, respectively. The activities of superoxide dismutase, catalase, and glutathione S-transferase were enhanced by 10.95% and 14.07%, 25.63% and 25.91%, and 39.93% and 35.01% in nano-CuO+DBP and nano-CuO+BBP treatments as compared to the individual exposure groups, verifying that antioxidative defense responses were activated. Furthermore, the co-exposure of nano-CuO and PAEs decreased the population richness and diversity microbiota, and changed the microbial community composition in Daphnia magna. Metabolomic analysis elucidated that nano-CuO + PAEs exposure induced stronger disturbance on metabolic network and molecular function, including amino acid, nucleotides, and lipid metabolism-related metabolic pathways, as comparison to PAEs single exposure treatments. In summary, the integration of physiological, microflora, and untargeted metabolomics analysis offers a fresh perspective into the potential ecological risk associated with nanopollutants and phthalate pollution in aquatic ecosystems.

Phthalate acid esters: A review of aquatic environmental occurrence and their interactions with plants.

The increasing use of phthalate acid esters (PAEs) in various applications has inevitably led to their widespread presence in the aquatic environment. This presents a considerable threat to plants. However, the interactions between PAEs and plants in the aquatic environment have not yet been comprehensively reviewed. In this review, the properties, occurrence, uptake, transformation, and toxic effects of PAEs on plants in the aquatic environment are summarized. PAEs have been prevalently detected in the aquatic environment, including surface water, groundwater, seawater, and sediment, with concentrations ranging from the ng/L or ng/kg to the mg/L or mg/kg range. PAEs in the aquatic environment can be uptake, translocated, and metabolized by plants. Exposure to PAEs induces multiple adverse effects in aquatic plants, including growth perturbation, structural damage, disruption of photosynthesis, oxidative damage, and potential genotoxicity. High-throughput omics techniques further reveal the underlying toxicity molecular mechanisms of how PAEs disrupt plants on the transcription, protein, and metabolism levels. Finally, this review proposes that future studies should evaluate the interactions between plants and PAEs with a focus on long-term exposure to environmental PAE concentrations, the effects of PAE alternatives, and human health risks via the intake of plant-based foods.

3-Monochloropropane-1,2-diol esters induce HepG2 cells necroptosis via CTSB/TFAM/ROS pathway.

3-monochloropropane-1,2-diol esters (3-MCPDE) are toxic substances that form in food thermal processing and have a diverse range of toxicities. In this study, we found that 3-MCPDE triggered necroptosis by RIPK1/RIPK3/MLKL pathway in HepG2 cells. Previous studies have shown that ROS is an important activator of RIPK1 and RIPK3. The data showed that 3-MCPDE induced excessive ROS production through mitochondrial damage. After treatment with ROS inhibitor N-acetylcysteine (NAC), 3-MCPDE-induced necroptosis was relieved. Further, we explored how 3-MCPDE destroys mitochondria. The data suggested that 3-MCPDE induced mitochondrial dysfunction through the CTSB/TFAM pathway. Overall, the results indicated that 3-MCPDE induced necroptosis through CTSB/TFAM/ROS pathway in HepG2 cells. Our study provided a new mechanism for 3-MCPDE hepatotoxicity.

Prediction of HC5s for phthalate esters by use of the QSAR-ICE model and ecological risk assessment in Chinese surface waters.

Due to their endocrine-disrupting effects and the risks posed in surface waters, in particular by chronic low-dose exposure to aquatic organisms, phthalate esters (PAEs) have received significant attention. However, most assessments of risks posed by PAEs were performed at a selection level, and thus limited by empirical data on toxic effects and potencies. A quantitative structure activity relationship (QSAR) and interspecies correlation estimation (ICE) model was constructed to estimate hazardous concentrations (HCs) of selected PAEs to aquatic organisms, then they were used to conduct a multiple-level environmental risk assessment for PAEs in surface waters of China. Values of hazardous concentration for 5% of species (HC5s), based on acute lethality, estimated by use of the QSAR-ICE model were within 1.25-fold of HC5 values derived from empirical data on toxic potency, indicating that the QSAR-ICE model predicts the toxicity of these three PAEs with sufficient accuracy. The five selected PAEs may be commonly measured in China surface waters at concentrations between ng/L and µg/L. Risk quotients according to median concentrations of the five PAEs ranged from 3.24 for di(2-ethylhexhyl) phthalate (DEHP) to 4.10 × 10-3 for dimethyl phthalate (DMP). DEHP and dibutyl phthalate (DBP) had risks to the most vulnerable aquatic biota, with the frequency of exceedances of the predicted no-effect concentration (PNECs) of 75.5% and 38.0%, respectively. DEHP and DBP were identified as having "high" or "moderate" risks. Results of the joint probability curves (JPC) method indicated DEHP posed "intermediate" risk to freshwater species with a maximum risk product of 5.98%. The multiple level system introduced in this study can be used to prioritize chemicals and other new pollutant in the aquatic ecological.

Global environmental and toxicological impacts of polybrominated diphenyl ethers versus organophosphate esters: A comparative analysis and regrettable substitution dilemma.

The prevalence of organophosphate esters (OPEs) in the global environment is increasing, which aligns with the decline in the usage of polybrominated diphenyl ethers (PBDEs). PBDEs, a category of flame retardants, were banned and classified as persistent organic pollutants (POPs) through the Stockholm Convention due to their toxic and persistent properties. Despite a lack of comprehensive understanding of their ecological and health consequences, OPEs were adopted as replacements for PBDEs. This research aims to offer a comparative assessment of PBDEs and OPEs in various domains, specifically focusing on their persistence, bioaccumulation, and toxicity (PBT) properties. This study explored physicochemical properties (such as molecular weight, octanol-water partition coefficient, octanol-air partition coefficient, Henry's law constant, and vapor pressures), environmental behaviors, global concentrations in environmental matrices (air, water, and soil), toxicities, bioaccumulation, and trophic transfer mechanisms of both groups of compounds. Based on the comparison and analysis of environmental and toxicological data, we evaluate whether OPEs represent another instance of regrettable substitution and global contamination as much as PBDEs. Our findings indicate that the physical and chemical characteristics, environmental behaviors, and global concentrations of PBDEs and OPEs, are similar and overlap in many instances. Notably, OPE concentrations have even surged by orders of several magnitude compared to PBDEs in certain pristine regions like the Arctic and Antarctic, implying long-range transport. In many instances, air and water concentrations of OPEs have been increased than PBDEs. While the bioaccumulation factors (BAFs) of PBDEs (ranging from 4.8 to 7.5) are slightly elevated compared to OPEs (-0.5 to 5.36) in aquatic environments, both groups of compounds exhibit BAF values beyond the threshold of 5000 L/kg (log10 BAF > 3.7). Similarly, the trophic magnification factors (TMFs) for PBDEs (ranging from 0.39 to 4.44) slightly surpass those for OPEs (ranging from 1.06 to 3.5) in all cases. Metabolic biotransformation rates (LogKM) and hydrophobicity are potentially major factors deciding their trophic magnification potential. However, many compounds of PBDEs and OPEs show TMF values higher than 1, indicating biomagnification potential. Collectively, all data suggest that PBDEs and OPEs have the potential to bioaccumulate and transfer through the food chain. OPEs and PBDEs present a myriad of toxicity endpoints, with notable overlaps encompassing reproductive issues, oxidative stress, developmental defects, liver dysfunction, DNA damage, neurological toxicity, reproductive anomalies, carcinogenic effects, and behavior changes. Based on our investigation and comparative analysis, we conclude that substituting PBDEs with OPEs is regrettable based on PBT properties, underscoring the urgency for policy reforms and effective management strategies. Addressing this predicament before an exacerbation of global contamination is imperative.

Grouping of esters of 4-hydroxybenzoic acid for hazard assessment.

Hazardous properties of a large number of esters of 4-hydroxybenzoic acid (parabens) have been proposed by ECHA to be assessed as a group. We recommend to restrict the grouping approach to short chain esters, i.e. methyl, ethyl, propyl and butyl paraben which are very similar in chemical structures, physicochemical properties, toxicokinetics, and hazardous properties. While these parabens show a weak estrogenicity in some in vitro or in vivo screening assays, they do not induce estrogen-receptor-mediated adverse effects in intact animals. Therefore, there is no support regarding classification and labeling of endocrine disruption or reproductive toxicity of these parabens.

Typical neonicotinoids and organophosphate esters, but not their metabolites, adversely impact early human development by activating BMP4 signaling.

Recent studies have highlighted the presence of potentially harmful chemicals, such as neonicotinoids (NEOs) and organophosphate esters (OPEs), in everyday items. Despite their potential threats to human health, these dangers are often overlooked. In a previous study, we discovered that NEOs and OPEs can negatively impact development, but liver metabolism can help mitigate their harmful effects. In our current research, our objective was to investigate the toxicity mechanisms associated with NEOs, OPEs, and their liver metabolites using a human embryonic stem cell-based differentiation model that mimics early embryonic development. Our transcriptomics data revealed that NEOs and OPEs significantly influenced the expression of hundreds of genes, disrupted around 100 biological processes, and affected two signaling pathways. Notably, the BMP4 signaling pathway emerged as a key player in the disruption caused by exposure to these pollutants. Both NEOs and OPEs activated BMP4 signaling, potentially impacting early embryonic development. Interestingly, we observed that treatment with a human liver S9 fraction, which mimics liver metabolism, effectively reduced the toxic effects of these pollutants. Most importantly, it reversed the adverse effects dependent on the BMP4 pathway. These findings suggest that normal liver function plays a crucial role in detoxifying environmental pollutants and provides valuable experimental insights for addressing this issue.

Elucidating the toxicity mechanisms of organophosphate esters by adverse outcome pathway network.

With the widespread use of organophosphate esters (OPEs), the accumulation and toxicity effect of OPEs in biota are attracting more and more concern. In order to clarify the mechanism of toxicity of OPEs to organisms, this study reviewed the OPEs toxicity and systematically identified the mechanism of OPEs toxicity under the framework of adverse outcome pathway (AOP). OPEs were divided into three groups (alkyl-OPEs, aryl-OPEs, and halogenated-OPEs) and biota was divided into aquatic organism and mammals. The results showed that tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) and triphenyl phosphate (TPHP) mainly caused neurotoxicity, reproductive, and hepatotoxicity in different mechanisms. According to the constructed AOP network, the toxicity mechanism of OPEs on aquatic organisms and mammals is different, which is mainly attributed to the different biological metabolic systems of aquatic organisms and mammals. Interestingly, our results indicate that the toxicity effect of the three kinds of OPEs on aquatic organisms is different, while there was no obvious difference in the mechanism of toxicity of OPEs on mammals. This study provides a theoretical basis for OPEs risk assessment in the future.

Emerging organophosphate ester resorcinol bis(diphenyl phosphate) exerts estrogenic effects via estrogen receptor pathways.

Environmental occurrence and human exposure of emerging organophosphate esters (eOPEs) have increased significantly in recent years. Resorcinol bis(diphenyl) phosphate (RDP) is one of the major eOPEs detected in indoor dust, but the knowledge on its toxicities and health risks is rather limited. In this study, we investigated the in vitro estrogenic effects and underlying mechanism of RDP in comparison with a legacy OPE triphenyl phosphate (TPHP). Our results showed that RDP promoted MCF-7 cell proliferation with the lowest effect concentration of 2.5 µM, and the maximum enhancement of 1.6 folds is greater than that of TPHP (1.3 folds). The effect was inhibited completely by an estrogen receptor (ER) antagonist, suggesting that ER activation was responsible for the enhancement. In luciferase reporter gene assays both RDP and TPHP activated ER transcriptional activity at 2.5 µM, but RDP activity was higher than TPHP. Competitive fluorescence binding assays showed that RDP bound to ER with an IC10 of 0.26 µM, which is 20 folds lower than TPHP (5.6 µM). Molecular docking simulation revealed that both RDP and TPHP interacted with ER at the binding pocket of estradiol, although the hydrogen bonds were different. Taken together, RDP exerted stronger estrogenic effects than TPHP through ER-mediated pathways and may pose more health risks.

Combined cytotoxicity of phthalate esters on HepG2 cells: A comprehensive analysis of transcriptomics and metabolomics.

Phthalate esters (PAEs), widely used as plasticizers, may pose a potential environmental and human hazard. The aim of this study was to compare the cytotoxicity of di(2-ethylhexyl) phthalates (DEHP) and dibutyl phthalate (DBP)) after their exposure to HepG2 cells alone or in combination. HepG2 cells treated with individual/combined DEHP and DBP at a dose of 10-2 M for 24 h were selected for metabolome and transcriptome analysis. The results demonstrated that exposure to the mixtures of DEHP and DBP caused enhanced or reduced toxic effects regarding 8 pathways with 1065 downregulated genes and 643 upregulated genes, in comparison with those of single chemicals. The combined toxicity of mixture revealed both synergistic and antagonistic interactions between DEHP and DBP. Besides, combined exposure to DEHP and DBP promoted TCA cycle, pyrimidine, and purine metabolism, while an antagonistic effect on fatty acid derangement should require further investigation. To summarize, our results suggest that DEHP exposed alone or combined with DBP caused a variety of metabolic disorders, and the type of combination effects varied among metabolic pathways.

Multi-level biological effects of diverse alkyl chains phthalate esters on cotton seedlings (Gossypium hirsutum L.): Insights into individual, physiological-biochemical and molecular perspectives.

Phthalate esters (PAEs) are organic contaminants that pose environmental threat and safety risks to soil health and crop production. However, the ecological toxicity of different PAEs to cotton and the underlying mechanisms are not clear. This study investigated the ecotoxic effects and potential mechanisms of different alkyl-chain PAEs, including dioctyl phthalate (DOP), dibutyl phthalate (DBP), and diethyl phthalate (DEP) on cotton seedlings at multiple levels. The results showed that PAEs significantly hindered the growth and development of cotton. The chlorophyll content decreased by 1.87-31.66 %, accompanied by non-stomatal photosynthetic inhibition. The antioxidant system was activated by the three PAEs in cotton seedlings, while the osmotic potential was boosted intracellularly. Additionally, PAEs significantly interfered with functional gene expression and exhibited genotoxicity. Risk assessment results indicated that the ecotoxicity was DOP >DBP >DEP, with a "dose-response" relationship. The affinity between the three PAEs and catalase increased as the alkyl chain length increased, further supporting the toxicity sequence. Surprisingly, the bioconcentration factors of short-chain DEP were 8.07 ± 5.89 times and 1837.49 ± 826.83 times higher than those of long-chain DBP and DOP, respectively. These results support the ecological risk assessment of PAEs in cotton and provide new insights into determining the toxicity levels of different PAEs.

Established and emerging organophosphate esters (OPEs) and the expansion of an environmental contamination issue: A review and future directions.

The list of organophosphate esters (OPEs) reported in the environment continues to expand as evidenced by the increasing number of OPE studies in the literature. However, there remains a general dearth of information on more recently produced and used OPEs that are proving to be emerging environmental contaminants. The present review summarizes the available studies in a systematic framework of the current state of knowledge on the analysis, environmental fate, and behavior of emerging OPEs. This review also details future directions to better understand emerging OPEs in the environment. Firstly, we make recommendations that the current structural/practical abbreviations and naming of OPEs be revised and updated. A chemical database (CDB) containing 114 OPEs is presently established based on the suspect list from the current scientific literature. There are 12 established OPEs and a total of 83 emerging OPEs that have been reported in human and/or biota samples. Of the emerging OPEs more than 80% have nearly 100% detection frequencies in samples of certain environmental media including indoor air, wastewater treatment plants, sediment, and fish. In contrast to OPEs considered established contaminants, most emerging OPEs have been identified more recently due to the more pervasive use of high-resolution mass spectrometry (HRMS) based approaches and especially gas or liquid chromatography coupled with HRMS-based non-target analysis (NTA) of environmental sample fractions. Intentional/unintentional industrial use and non-industrial formation are sources of emerging OPEs in the environment. Predicted physical-chemical properties in silico of newer, molecularly larger and more oligomeric OPEs strongly suggest that some compounds such as bisphenol A diphenyl phosphate (BPA-DPP) are highly persistent, bioaccumulative and/or toxic. Limited information on laboratory-based toxicity data has shown that some emerging OPEs elicit harmful effects such as cytotoxicity, development toxicity, hepatotoxicity, and endocrine disruption in exposed humans and mammals. Established, and to a much lesser degree emerging OPEs, have also been shown to transform and degrade in biota and possibly alter their toxicological effects. Research on emerging OPE contaminants is presently limited and more study is warranted on sample analysis methods, source apportionment, transformation processes, environmental behavior, biomarkers of exposure and toxicity.

Phthalate acid esters contribute to the cytotoxicity of mask leachate: Cell-based assay for toxicity assessment.

After the COVID-19 outbreak, masks have become an essential part of people lives. Although several studies have been conducted to determine the release of hazardous substances from masks, how their co-presence poses a potential exposure risk to human health remains unexplored. In this study, we quantitatively compared the leaching of substances from six different common types of masks, including phthalate acid esters (PAEs), metals, and microplastics (MPs), and comprehensively evaluated the potential cytotoxicity of different leachates. MPs smaller than 3 µm were quantified by Py-GC-MS, and reusable masks showed greater releasing potentials up to 1504 µg/g. We also detected the prevalence of PAEs in masks, with the highest release reaching 42 µg/g, with dibutyl phthalate (DBP), diisobutyl phthalate (DiBP) and bis (2-ethylhexyl) phthalate (DEHP) being the predominant types. Moreover, the antimicrobial cloth masks released 173.0 µg of Cu or 4.5 µg of Ag, representing 2.7% and 0.04% of the original masks, respectively. Our cell-based assay results demonstrated for the first time that mask leachate induced nuclear condensation with DNA damage, and simultaneously triggered high levels of glutathione and reactive oxidative stress production, which exacerbated mitochondrial fragmentation, eventually leading to cell death. Combined with substance identification and correlation analysis, PAEs were found to be the contributors to cytotoxicity. Masks containing Cu or Ag led to acidification of lysosomes and alkalinization of cells. These results strongly suggested that the levels of PAEs in the production of regulatory masks should be strictly controlled.

Safety Assessment of Polyglyceryl Fatty Acid Esters as Used in Cosmetics.

The Expert Panel for Cosmetic Ingredient Safety (Panel) assessed the safety of 274 polyglyceryl fatty acid esters. Each of the esters in this group is a polyether comprising 2 to 20 glyceryl residues, end-capped by esterification with simple carboxylic acids, such as fatty acids. Most of these ingredients are reported to function in cosmetics as skin-conditioning agents and/or surfactants. The Panel reviewed the available data and considered conclusions from their relevant previous reports, and determined that these ingredients are safe in cosmetics in the present practices of use and concentration described in this safety assessment when formulated to be non-irritating.

Phthalate esters: occurrence, toxicity, bioremediation, and advanced oxidation processes.

Phthalic acid esters are emerging pollutants, commonly used as plasticizers that are categorized as hazardous endocrine-disrupting chemicals (EDCs). A rise in anthropogenic activities leads to an increase in phthalate concentration in the environment which leads to various adverse environmental effects and health issues in humans and other aquatic organisms. This paper gives an overview of the research related to phthalate ester contamination and degradation methods by conducting a bibliometric analysis with VOS Viewer. Ecotoxicity analysis requires an understanding of the current status of phthalate pollution, health impacts, exposure routes, and their sources. This review covers five toxic phthalates, occurrences in the aquatic environment, toxicity studies, biodegradation studies, and degradation pathways. It highlights the various advanced oxidation processes like photocatalysis, Fenton processes, ozonation, sonolysis, and modified AOPs used for phthalate removal from the environment.

Toxicology of 3-monochloropropane-1,2-diol and its esters: a narrative review.

3-Monochloropropane-1,2-diol (3-MCPD) is a chiral molecule naturally existing as a racemic mixture of (R)- and (S)-enantiomers. It was thoroughly investigated during the 1970s as a male antifertility drug until research was abandoned because of the side effects observed in toxicity studies. More than 20 years later, 3-MCPD, both in the free form and esterified to the fatty acids, was detected in vegetable oil and discovered to be a widespread contaminant in different processed foods. This review summarises the main toxicological studies on 3-MCPD and its esters. Current knowledge shows that the kidney and reproductive system are the primary targets of 3-MCPD toxicity, followed by neurological and immune systems. Despite uncertainties, in vivo studies suggest that renal and reproductive toxicity is mediated by toxic metabolites, leading to inhibition of glycolysis and energy depletion. Few acute, short-term, and subchronic toxicity studies have investigated the 3-MCPD esters. The pattern of toxicity was similar to that of free 3-MCPD. Some evidence suggests that the toxicity of 3-MCPD diesters may be milder than 3-MCPD, likely because of an incomplete enzymatic hydrolysis in the equivalent free form in the gastrointestinal tract. Further research to clarify absorption, metabolism, and long-term toxicity of 3-MCPD esters would be pivotal to improve the risk assessment of these compounds via food.

Aryl-, halogenated- and alkyl- organophosphate esters induced oxidative stress, endoplasmic reticulum stress and NLRP3 inflammasome activation in HepG2 cells.

Organophosphate esters (OPEs) are a group of extensively used man-made chemicals with diverse substituents that are ubiquitously detected in human-related samples including serum, breastmilk, food and house dust. The understanding of their toxicological effects and potential mechanisms on hepatocytes is still limited. In this study, nine most frequently detected OPEs were selected and divided into three subgroups (aryl-, halogenated- and alkyl-OPEs) based on their substituents. The cytotoxicity, apoptosis, oxidative stress, endoplasmic reticulum (ER) stress and NLRP3 inflammasome activation induced by OPEs were evaluated in human hepatocellular carcinomas HepG2 cells. All OPEs induced apoptosis likely through a caspase-dependent apoptotic pathway. The activities of anti-oxidative enzyme SOD and CAT exhibited sensitive responses after OPEs treatment for 6 h. The OPEs induced ROS overproduction, DNA damage, endoplasmic reticulum (ER) stress and NLRP3 inflammasome activation varied among aryl-, halogenated- and alkyl-OPEs. Halogenated- and alkyl- OPEs induced overproduction of ROS and DNA damage, and elevated ER stress and NLRP3 inflammasome activation are observed aryl-OPEs induced cytotoxicity.

Reproductive and developmental toxicity following exposure to organophosphate ester flame retardants and plasticizers, triphenyl phosphate and isopropylated phenyl phosphate, in Sprague Dawley rats.

Two organophosphate esters used as flame retardants and plasticizers, triphenyl phosphate (TPHP) and isopropylated phenyl phosphate (IPP), have been detected in environmental samples around the world. Human exposure primarily occurs via oral ingestion with reported higher concentrations in children. Currently, there are no data to evaluate potential risk from exposure to either TPHP or IPP during fetal development. These short-term perinatal studies in rats provide preliminary toxicity data for TPHP and IPP, including information on transfer to fetus/offspring and across the pup blood-brain barrier. In separate experiments, TPHP or IPP were administered via dosed feed at concentrations 0, 1000, 3000, 10 000, 15 000, or 30 000 ppm to time-mated Hsd:Sprague Dawley SD rats from gestation day (GD) 6 through postnatal day (PND) 28; offspring were provided dosed feed at the same concentration as their dam (PND 28-PND 56). TPHP- and IPP-related toxicity resulted in removal of both 30 000 ppm groups on GD 12 and 15 000 ppm IPP group after parturition. Body weight and organ weights were impacted with exposure in remaining dams. Reproductive performance was perturbed at ≥10 000 ppm TPHP and all IPP exposure groups. In offspring, both TPHP- and IPP-related toxicity was noted in pups at ≥10 000 ppm as well as reduction in bodyweights, delays in pubertal endpoints, and/or reduced cholinesterase enzyme activity starting at 1000 ppm TPHP or IPP. Preliminary internal dose assessment indicated gestational and lactational transfer following exposure to TPHP or IPP. These findings demonstrate that offspring development is sensitive to 1000 ppm TPHP or IPP exposure.

Insights into the geographical distribution, bioaccumulation characteristics, and ecological risks of organophosphate esters.

Organophosphate esters (OPEs), as flame retardants and plasticizers, have been numerously explored regarding the occurrence and ecotoxicology. Given their toxicity, persistency and bio-accumulative potential, however, they may pose negative effects on ecosystems, regarding which is a growing global concern. Accordingly, the present review systematically analyses the recent literature to (1) elucidate their worldwide distribution, bioaccumulation, and biomagnification potential, (2) determine their interim water quality criteria (i.e., effect thresholds), and (3) preliminarily assess the ecological risks for 32 OPEs in aquatic ecosystems. The results showed that the spatiotemporal distribution of OPEs was geographically specific and closely related to human activities (i.e., megacities), especially halogenated-OPEs. We also found that precipitation of airborne particulates could affect the concentrations of OPEs in soil, and there was a positive correlation between the bioaccumulation and hydrophobicity of OPEs. Tris(2-ethylhexyl) phosphate may exhibit high bioaccumulation in aquatic organisms. A substantial difference was found among interim water quality criteria for OPEs, partly attributable to the variation of their available toxicity data. Tris(phenyl) phosphate (TPHP) and tris(1,3-dichloroisopropyl) phosphate with the lowest predicted no-effect concentration showed the strongest toxicity of growth and reproduction. Through the application of the risk quotient and joint probability curve, TPHP and tris(chloroethyl) phosphate tended to pose moderate risks, which should receive more attention for risk management. Future research should focus on knowledge gaps in the mechanism of biomagnification, derivation of water quality criteria, and more precise assessment of ecological risks for OPEs.

Toxicity and larvicidal activity on Aedes aegypti of citronella essential oil submitted to enzymatic esterification / Toxicidade e atividade larvicida sobre Aedes aegypti de óleo essencial de citronella submetido à esterificação enzimática

The essential oil of citronella (Cymbopogon winterianus) has several biological activities, among them the insect repellent action. Some studies showed that cinnamic acid esters can be applied as natural pesticides, insecticides and fungicides. In this context, the objective of the present work was to evaluate the production of esters from citronella essential oil with cinnamic acid via enzymatic esterification. Besides, the essential oil toxicity before and after esterification against Artemia salina and larvicidal action on Aedes aegypti was investigated. Esters were produced using cinnamic acid as the acylating agent and citronella essential oil (3:1) in heptane and 15 wt% NS 88011 enzyme as biocatalysts, at 70 °C and 150 rpm. Conversion rates of citronellyl and geranyl cinnamates were 58.7 and 69.0% for NS 88011, respectively. For the toxicity to Artemia salina LC50 results of 5.29 μg mL-¹ were obtained for the essential oil and 4.36 μg mL-¹ for the esterified oils obtained with NS 88011. In the insecticidal activity against Aedes aegypti larvae, was obtained LC50 of 111.84 μg mL-¹ for the essential oil of citronella and 86.30 μg mL-¹ for the esterified oils obtained with the enzyme NS 88011, indicating high toxicity of the esters. The results demonstrated that the evaluated samples present potential of application as bioinsecticide.

O óleo essencial de citronela (Cymbopogon winterianus) possui diversas atividades biológicas, entre elas a ação repelente a insetos. Alguns estudos mostraram que os ésteres do ácido cinâmico podem ser aplicados como pesticidas naturais, inseticidas e fungicidas. Nesse contexto, o objetivo do presente trabalho foi avaliar a produção de ésteres a partir do óleo essencial de citronela com ácido cinâmico via esterificação enzimática. Além disso, foi investigada a toxicidade do óleo essencial antes e após a esterificação contra Artemia salina e a ação larvicida sobre Aedes aegypti. Os ésteres foram produzidos utilizando ácido cinâmico como agente acilante e óleo essencial de citronela (3: 1) em heptano e 15% em peso da enzima NS 88011 como biocatalisadores, a 70 ° C e 150 rpm. As taxas de conversão de cinamatos de citronelil e geranil foram 58,7 e 69,0% para NS 88011, respectivamente. Para a toxicidade sobre Artemia salina foram obtidos CL50 de 5,29 μg mL-¹ para o óleo essencial e 4,36 μg mL-¹ para os óleos esterificados com NS 88011. Na atividade inseticida contra larvas de Aedes aegypti, obteve-se CL50 de 111,84 μg mL-¹ para o óleo essencial de citronela e 86,30 μg mL-¹ para os óleos esterificados com a enzima NS 88011, indicando alta toxicidade dos ésteres. Os resultados demonstraram que as amostras avaliadas apresentam potencial de aplicação como bioinseticida.