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Organophosphates esters (OPEs) have become a preferred alternative in nail polish as plasticizers due to health concerns over previously used additives like dibutyl phthalate. However, the true extent of nail technicians' exposure to OPEs is largely unknown. This study shows that nail salon workers are significant exposed to OPEs, with varied concentrations found in air, dust, masks, and urine. The total concentrations of 11 OPEs in ultrasonic personal air samplers (UPAS) ranged from 251 to 1007 ng/m³, and in air conditioner filter dust from 371 to 14473 ng/g. Triphenyl phosphate (TPHP) was the most abundant compound found in the nail polishes used in these salons. On average, the concentrations of TPHP and diphenyl phosphate (DPHP) in workers' urine after work were 5.2 and 1.8 times higher than those before work, respectively. Two nail salons that had the highest nail polish usage also had very high concentrations of TPHP in surgical masks, dust, and UPAS. TPHP concentrations in workers' urine after work were 19 and 13 times those before work, respectively, in these two salons. Human internal exposure assessment showed that the average exposure dose of TPHP after work was 1.8 times higher than that before work. On average, use of masks reduced OPEs in urine by 77%. In conclusion, frequent mask replacement is highly recommended, especially in long working circumstances. Without regular replacement, masks may accumulate OPEs from the air, potentially becoming another source of human exposure to OPEs. Therefore, more attention should be paid to the occupational exposure of nail salon workers to OPEs, particularly considering that most practitioners in this industry are young women of reproductive age.

BackgroundOrganic phosphate flame retardants are emerging environmental pollutants. While there have been multiple toxicities reported following organic phosphate flame retardants exposure, few studies focus on their potential developmental toxicities. It is necessary to elucidate these developmental toxicological effects and underlying mechanisms to improve risk assessments and better protect sensitive populations. ObjectiveTo evaluate potential developmental toxicities in early chicken embryos following exposure to triphenyl phosphate (TPhP) or cresyl diphenyl phosphate (CDP), to reveal TPhP and CDP’s capabilities to activate peroxisome proliferator-activated receptor γ (PPARγ) in vivo in an established chicken embryo gene reporter system, and to investigate the roles of PPARγ in TPhP/CDP-induced developmental toxicities with lentivirus-mediated in vivo gene silencing. MethodsFirstly, diverse doses of TPhP and CDP were injected into the air sacs of fertilized eggs to assess the development of chicken embryos after 6 d of incubation, and an optimal dose was chosen for subsequent experiments. Subsequently, the report gene system was employed to evaluate the intraembryonic activation of PPARγ by TPhP and CDP. Eventually, PPARγ was silenced using lentivirus, and the embryos were co-treated with TPhP and CDP to further disclose the roles of PPARγ in the observed developmental toxicity. ResultsFollowing developmental exposure to TPhP or CDP, significantly lower chicken embryo weights (normalized with egg weights) were observed in the 6 d embryos (10, 30 mg·kg−1 TPhP and 3, 10, 30 mg·kg−1 CDP), indicating that both chemicals have general developmental toxicities and CDP is more potent. Additionally, exposure to CDP also resulted in remarkably increased sagittal brain area (normalized to embryo weights) and decreased sagittal eye area (normalized to embryo weights) (P CDP > TPhP. The lentivirus microinjection successfully achieved in vivo silencing of PPARγ in developing chicken embryos, and the estimated silencing efficacy was approximately 55% according to the real-time quantitative polymerase chain reaction (qRT-PCR) results. The in vivo silencing of PPARγ effectively alleviated TPhP or CDP-induced decrease of embryo weights (P

Triphenyl phosphate (TPHP) - a widely used organophosphate-based flame retardant - blocks cardiac looping during zebrafish development in a concentration-dependent manner, a phenotype that is dependent on disruption of embryonic osmoregulation and pericardial edema formation. However, its currently unclear whether (1) TPHP-induced effects on osmoregulation are driven by direct TPHP-induced injury to the embryonic epidermis and (2) whether TPHP-induced pericardial edema is reversible or irreversible following cessation of exposure. Therefore, the objectives of this study were to determine whether TPHP-induced pericardial edema is reversible and whether TPHP causes injury to the embryonic epidermis by quantifying the number of DAPI-positive epidermal cells and analyzing the morphology of the yolk sac epithelium using scanning electron microscopy. First, we found that exposure to 5 μM TPHP from 24-72 h post-fertilization (hpf) did not increase prolactin - a hormone that regulates ions and water levels - in embryonic zebrafish, whereas high ionic strength exposure media was associated with elevated levels of prolactin. Second, we found that exposure to 5 μM TPHP from 24-72 hpf did not decrease DAPI-positive epidermal cells within the embryonic epithelium, and that co-exposure with 2.14 μM fenretinide - a synthetic retinoid that promotes epithelial wound repair - from 24-72 hpf did not mitigate the prevalence of TPHP-induced epidermal folds within the yolk sac epithelium when embryos were exposed within high ionic strength exposure media. Finally, we found that the pericardial area and body length of embryos exposed to 5 μM TPHP from 24-72 hpf were similar to vehicle-treated embryos at 120 hpf following transfer to clean water and depuration of TPHP from 72-120 hpf. Overall, our findings suggest that (1) the ionic strength of exposure media may influence the baseline physiology of zebrafish embryos; (2) TPHP does not cause direct injury to the embryonic epidermis; and (3) TPHP-induced effects on pericardial area and body length are reversible 48 h after transferring embryos to clean water.

Triphenyl phosphate (TPhP) is an organophosphate flame retardant and plasticizer that is added to a wide variety of consumer and industrial products. It is also a ubiquitous environmental pollutant. Exposure to TPhP has been shown to alter gene expression in metabolic and estrogenic signaling pathways in in vitro and in vivo models of a variety of species, and as such, is considered to be an endocrine disrupting chemical. Exposure to endocrine disrupting chemicals is increasingly being associated with changes to the epigenome, especially during embryonic development. The aim of this study was to evaluate whether TPhP exposure in aquatic ecosystems has the ability to alter the epigenome in two immortal cell lines derived from trout (Oncorhynchus mykiss). This study assessed whether 24 h exposure to TPhP resulted in changes to histone modification and DNA methylation profiles in steelhead trout embryonic cells and rainbow trout gill epithelial cells. Results show that several epigenetic modifications on histone H3 and DNA methylation are altered in the embryonic cells following TPhP exposure, but not in the gill epithelial cells. Specifically, histone H3 acetylation, histone H3 mono‐methylation and global DNA methylation were found to be reduced. The alterations of these epigenetic modification profiles in the embryonic cells suggest that exposure to TPhP during fetal development may alter gene expression in the developing embryo, likely in metabolic and estrogenic pathways. The impacts to the epigenome determined in this study may even carry multigenerational detrimental effects on human and ecosystem health, which requires further investigation. Triphenyl phosphate (TPhP) is an organophosphate flame retardant, ubiquitous environmental pollutant and endocrine disrupting chemical. This study evaluated whether TPhP exposure caused changes to posttranslational histone modifications and DNA methylation profiles in steelhead trout embryonic cells and rainbow trout gill epithelial cells. Histone H3 acetylation, histone H3 mono‐methylation and global DNA methylation were reduced in TPhP‐exposed embryonic cells but not gill epithelial cells. Results suggest that exposure to TPhP during fetal development may alter gene expression in the developing embryo. [ABSTRACT FROM AUTHOR]

Triphenyl phosphate (TPhP), a chemical commonly found in human placenta and breast milk, has been shown to disturb the endocrine system. Our previous study confirmed that TPhP could accumulate in the placenta and interference with placental lipid metabolism and steroid hormone synthesis, as well as induce endoplasmic reticulum (ER) stress through PPARγ in human placental trophoblast JEG‐3 cells. However, the molecular mechanism underlying this disruption remains unknown. Our study aimed to identify the role of the PPARγ/CD36 pathway in TPhP‐induced steroid hormone disruption. We found that TPhP increased lipid accumulation, total cholesterol, low‐ and high‐density protein cholesterol, progesterone, estradiol, glucocorticoid, and aldosterone levels, and genes related to steroid hormones synthesis, including 3βHSD1, 17βHSD1, CYP11A, CYP19, and CYP21. These effects were largely blocked by co‐exposure with either a PPARγ antagonist GW9662 or knockdown of CD36 using siRNA (siCD36). Furthermore, an ER stress inhibitor 4‐PBA attenuated the effect of TPhP on progesterone and glucocorticoid levels, and siCD36 reduced ER stress‐related protein levels induced by TPhP, including BiP, PERK, and CHOP. These findings suggest that ER stress may also play a role in the disruption of steroid hormone synthesis by TPhP. As our study has shed light on the PPARγ/CD36 pathway's involvement in the disturbance of steroid hormone biosynthesis by TPhP in the JEG‐3 cells, further investigations of the potential impacts on the placental function and following birth outcome are warranted. [ABSTRACT FROM AUTHOR]

Pericardial edema is commonly observed in zebrafish embryo-based chemical toxicity screens, and a mechanism underlying edema may be disruption of embryonic osmoregulation. Therefore, the objective of this study was to identify whether triphenyl phosphate (TPHP) - a widely used aryl phosphate ester-based flame retardant - induces pericardial edema via impacts on osmoregulation within embryonic zebrafish. In addition to an increase in TPHP-induced microridges in the embryonic yolk sac epithelium, an increase in ionic strength of exposure media exacerbated TPHP-induced pericardial edema when embryos were exposed from 24 to 72 h post-fertilization (hpf). However, there was no difference in embryonic sodium concentrations in situ within TPHP-exposed embryos relative to embryos exposed to vehicle (0.1% DMSO) from 24 to 72 hpf. Interestingly, increasing the osmolarity of exposure media with mannitol (an osmotic diuretic which mitigates TPHP-induced pericardial edema) and increasing the ionic strength of the exposure media (which exacerbates TPHP-induced pericardial edema) did not affect embryonic doses of TPHP, suggesting that TPHP uptake was not altered under these varying experimental conditions. Overall, our findings suggest that TPHP-induced pericardial edema within zebrafish embryos is dependent on the ionic strength of exposure media, underscoring the importance of further standardization of exposure media and embryo rearing protocols in zebrafish-based chemical toxicity screening assays.

A common flame-retardant and plasticizer, triphenyl phosphate (TPhP) is an aryl phosphate ester found in many aquatic environments at nM concentrations. Yet, most studies interrogating its toxicity have used µM concentrations. In this study, we used the model organism zebrafish (Danio rerio) to uncover the developmental impact of nM exposures to TPhP at the phenotypic and molecular levels. At concentrations of 1.5–15 nM (0.5 µg/L–5 µg/L), chronically dosed 5dpf larvae were shorter in length and had pericardial edema phenotypes that had been previously reported for exposures in the µM range. Cardiotoxicity was observed but did not present as cardiac looping defects as previously reported for µM concentrations. The RXR pathway does not seem to be involved at nM concentrations, but the tbx5a transcription factor cascade including natriuretic peptides (nppa and nppb) and bone morphogenetic protein 4 (bmp4) were dysregulated and could be contributing to the cardiac phenotypes. We also demonstrate that TPhP is a weak pro-oxidant, as it increases the oxidative stress response within hours of exposure. Overall, our data indicate that TPhP can affect animal development at environmentally relevant concentrations and its mode of action involves multiple pathways. [ABSTRACT FROM AUTHOR]

Background: Gastric cancer is a leading cause of cancer-related deaths influenced by both genetic and environmental factors. Triphenyl phosphate (TPP) is a prevalent flame retardant, but its health implications remain to be thoroughly understood. Objective: To explore the link between TPP exposure and gastric cancer by examining gene expression patterns and developing a predictive model. Methods: Gene expression data were sourced from The Cancer Genome Atlas (TCGA) and the Comparative Toxicogenomics Database (CTD). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were employed for analysis. Single-sample Gene Set Enrichment Analysis (ssGSEA) was used to obtain phosphate flame retardant-related scores. A predictive model was constructed through differential analysis, univariate COX regression, and LASSO regression. Molecular docking was performed to assess protein interactions with TPP. Results: ssGSEA identified scores related to phosphate flame retardants in gastric cancer, which had a strong association with immune-related traits. Several genes associated with TPP were identified and used to develop a prognostic model that has clinical significance. Molecular docking showed a high binding affinity of TPP with MTTP, a gene related to lipid metabolism. Pathway analysis indicated that TPP exposure contributes to gastric cancer through lipid metabolic processes. Conclusion: The study establishes a potential correlation between TPP exposure and gastric cancer onset, pinpointing key genes and pathways involved. This underscores the significance of environmental factors in gastric cancer research and presents a potential diagnostic tool for clinical application.

Combined toxicity is a critical concern during the risk assessment of environmental pollutants. Due to the characteristics of strong hydrophobicity and large specific surface area, microplastics (MPs) and nanoplastics (NPs) have become potential carriers of organic pollutants that may pose a health risk to humans. The co-occurrence of organic pollutants and MPs would cause adverse effects on aquatic organism, while the information about combined toxicity induced by organophosphorus flame retardants and MPs on human cells was limited. This study aimed to reveal the toxicity effects of co-exposure to triphenyl phosphate (TPHP) and polystyrene (PS) particles with micron-size/nano-size on HepG2 cell line. The adsorption behaviors of TPHP on PS particles was observed, with the PS-NP exhibiting a higher adsorption capacity. The reactive oxygen species generation, mitochondrial membrane potential depolarization, lactate dehydrogenase release and cell apoptosis proved that PS-NPs/MPs exacerbated TPHP-induced cytotoxicity. The particle size of PS would affect the toxicity to HepG2 cells that PS-NP (0.07 μm) exhibited more pronounced combined toxicity than PS-MP (1 μm) with equivalent concentrations of TPHP. This study provides fundamental insights into the co-toxicity of TPHP and PS micro/nanoplastics in HepG2 cells, which is crucial for validating the potential risk of combined toxicity in humans.

Organophosphorus flame retardants, such as triphenyl phosphate (TPhP), exist ubiquitously in various environments owing to their widespread usage. Potential toxic effects of residual flame retardants on cultured non-fish species are not concerned commonly. TPhP-induced physiological and biochemical effects in an aquatic turtle were evaluated here by systematically investigating the changes in growth and locomotor performance, hepatic antioxidant ability and metabolite, and intestinal microbiota composition of turtle hatchlings after exposure to different TPhP concentrations. Reduced locomotor ability and antioxidant activity were only observed in the highest concentration group. Several metabolic perturbations that involved in amino acid, energy and nucleotide metabolism, in exposed turtles were revealed by metabolite profiles. No significant among-group difference in intestinal bacterial diversity was observed, but the composition was changed markedly in exposed turtles. Increased relative abundances of some bacterial genera (e.g., Staphylococcus, Vogesella and Lawsonella) probably indicated adverse outcomes of TPhP exposure. Despite having only limited impacts of exposure at environmentally relevant levels, our results revealed potential ecotoxicological risks of residual TPhP for aquatic turtles considering TPhP-induced metabolic perturbations and intestinal bacterial changes.

The drying process of polymeric coatings, particularly in the presence of surfactants, poses a complex challenge due to its intricate dynamics involving simultaneous heat and mass transfer. This study addresses the inherent complexity by employing Artificial Neural Networks (ANNs) to model the surfactant-enhanced drying of poly(styrene)-p-xylene coatings. A substantial dataset of 16,258 experimentally obtained samples forms the basis for training the ANN model, showcasing the suitability of this approach when ample training data is available. The chosen single-layer feed-forward network with backpropagation adeptly captures the non-linear relationships within the drying data, providing a predictive tool with exceptional accuracy. Our results demonstrate that the developed ANN model achieves a precision level exceeding 99% in predicting coating weight loss for specified input values of time, surfactant amount, and initial coating thickness. The model's robust generalization capability eliminates the need for additional experiments, offering reliable predictions for both familiar and novel conditions. Comparative analysis reveals the superiority of the ANN over the regression tree, emphasizing its efficacy in handling the intricate dynamics of polymeric coating drying processes. In conclusion, this study contributes a valuable tool for optimizing polymeric coating processes, reducing production defects, and enhancing overall manufacturing quality and cost-effectiveness. [ABSTRACT FROM AUTHOR]

Triphenyl phosphate (TPhP) is the predominant compound of organophosphate flame retardants (OPFRs), which can elicit a toxicological effect on physiological response and tissue development of fish. In this study, we investigated the effect of TPhP exposure on cell viability, antioxidant capacities, and apoptosis in EPC cells. Current study revealed that TPhP exposure could decrease cell viability and promote intracellular oxidative stress in EPC cells. In addition, high-dose TPhP exposure could facilitate antioxidant insults and cause mitochondrial collapse in a dose-dependent manner, along with increased gene expressions involved in apoptosis and unfolded protein response (UPR). These results indicated that reactive oxygen species (ROS)-induced cytotoxic stress and cell death were involved in antioxidant insults and apoptotic activation in TPhP-exposed fish cells. [ABSTRACT FROM AUTHOR]

Copyright of Lubrication Engineering (0254-0150) is the property of Editorial Office of LUBRICATION ENGINEERING and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: Triphenyl phosphate (TPHP) is a widely used organophosphate flame retardant, which can be transformed in vivo into diphenyl phosphate (DPHP) and 4-hydroxyphenyl phosphate (diphenyl) ester (OH-TPHP) through biotransformation process. Accumulation of TPHP and its derivatives in biological tissues makes it necessary to investigate their toxicity and molecular mechanism. Methods: The present study evaluated the cellular effects of TPHP, DPHP, and OH‐TPHP on cell survival, cell membrane damage, oxidative damage, and cell apoptosis using HeLa cells as in vitro model. RNA sequencing and bioinformatics analysis were conducted to monitor the differently expressed genes, and then RT-qPCR and Western bolt were used to identify potential molecular mechanisms and key hub genes. Results: Results showed that OH-TPHP had the most significant cytotoxic effect in HeLa cells, followed by TPHP; and no significant cytotoxic effects were observed for DPHP exposure within the experimental concentrations. Biological function enrichment analysis suggested that TPHP and OH-TPHP exposure may induce endoplasmic reticulum stress (ERS) and cell apoptosis. The nodes filtering revealed that ERS and apoptosis related genes were involved in biological effects induced by TPHP and OH-TPHP, which may be mediated through the eukaryotic translation initiation factor 2α/activating transcription factor 4 (ATF4)/ATF3- CCAAT/ enhancer-binding protein homologous protein (CHOP) cascade pathway and death receptor 5 (DR5) /P53 signaling axis. Conclusion: Above all, these findings indicated that ERS-mediated apoptosis might be one of potential mechanisms for cytotoxicity of TPHP and OH-TPHP. Graphical Abstract [ABSTRACT FROM AUTHOR]

Triphenyl phosphate (TPhP), a widely used organophosphate-flame retardant, is ubiquitously found in household environments and may adversely affect human health. Evidence indicates that TPhP exposure causes metabolic dysfunctions in vivo; however, the underlying mechanism of such adverse effects has not been comprehensively investigated. Herein, we utilized two in vitro models including mouse and human preadipocytes to delineate adipogenic mechanisms of TPhP. The results revealed that both mouse and human preadipocytes exposed to TPhP concentration-dependently accumulated more fat through a significant upregulation of epidermal growth factor receptor (EGFR). We demonstrated that TPhP significantly promoted adipogenesis through the activation of EGFR/ERK/AKT signaling pathway as evident by a drastic reduction in adipogenesis of preadipocytes cotreated with inhibitors of EGFR and its major effectors. Furthermore, we confirmed the mechanism of TPhP-induced metabolic dysfunctions in vivo. We observed that male mice perinatally exposed to TPhP had a significant increase in adiposity, hepatic triglycerides, insulin resistance, plasma insulin levels, hypotension, and phosphorylated EGFR in gonadal fat. Interestingly, an administration of a potent and selective EGFR inhibitor significantly ameliorated the adverse metabolic effects caused by TPhP. Our findings uncovered a potential mechanism of TPhP-induced metabolic dysfunctions and provided implications on toxic metabolic effects posed by environmental chemicals.

In recent years, organophosphate ester flame retardants (OPFRs) have emerged as preferred alternatives to brominated flame retardants (BFRs) in materials such as building supplies, textiles, and furnishings. Simultaneously, a notable surge in bladder cancer incidences has been observed globally, particularly in developed nations, placing it as the 10th most prevalent cancer type. Among the extensive OPFRs, the linkage between triphenyl phosphate (TPP) and bladder cancer remains inadequately investigated. Hence, our study endeavors to elucidate this potential association. We sourced transcriptome profiles and TPP-related data from The Cancer Genome Atlas and Comparative Toxicogenomics databases. Using the ssGSEA algorithm, we established TPP-correlated scores within the bladder cancer cohort. Differentially expressed analysis enabled us to identify key genes in bladder cancer patients. We utilized the LASSO regression analysis, along with univariate and multivariate COX regression analyses to construct a prognostic prediction model. To uncover critical pathways involving key genes, we employed GSEA and GSVA enrichment analyses. Molecular docking analysis was performed to determine the binding capability between TPP and proteins. Our findings reveal that the TPP-centric risk model offers valuable prediction for bladder cancer cohorts. Furthermore, the reliability of this TPP-influenced risk model was verified through ROC curve analysis and survival studies. Intriguingly, TPP exposure appears to bolster the proliferation and invasiveness of bladder cancer cells. This study furnishes new insights into the possible benefits of minimizing TPP exposure for hindering bladder cancer progression. [ABSTRACT FROM AUTHOR]

Copyright of Environmental Science & Technology (10036504) is the property of Editorial Board of Environmental Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Triphenyl phosphate (TPHP) is one of the most widely used organic phosphorus flame retardants and is ubiquitous in the environment. Studies have been reported that TPHP may lead to obesity, neurotoxicity and reproductive toxicity, but its impact on the immune system is almost blank. The present study was aimed to investigate the potential immunotoxicity of TPHP on macrophages and its underlying mechanism. The results demonstrated for the first time that TPHP (12.5, 25, and 50 μM)‐induced F4/80+CD11c+ phenotype of RAW 264.7 macrophages, accompanied by increased mRNA levels of inflammatory mediators, antigen‐presenting genes (Cd80, Cd86, and H2‐Aa), and significantly enhanced the phagocytosis of macrophage. Meanwhile, TPHP increased the expression of Toll‐like receptor 4 (TLR4), and its co‐receptor CD14, leading to significant activation of the downstream ERK/NF‐κB pathway. However, co‐exposure of cells to TAK‐242, a TLR4 inhibitor, suppressed TPHP‐induced F4/80+CD11c+ phenotype, and down‐regulated inflammatory mediators and antigen‐presentation related genes, via blocked the TLR4/ERK/NF‐κB pathway. Taken together, our results suggested that TPHP could induce macrophage dysfunction through activating TLR4‐mediated ERK/NF‐κB signaling pathway, and it may be the potential reason for health‐threatening consequences. [ABSTRACT FROM AUTHOR]

Recent studies have identified the ability of plants to uptake and translocate organophosphate esters (OPEs) within cells. In response to the increasing interest in OPEs and their occurrence in paddy fields and rice, the current study aimed to present an effective and sensitive GC–MS based methodology for quantitative determination of 11 OPEs with octanol–water coefficients ranging from 1.6 to 10. Rice was sonicated with hexane and dichloromethane, and fractionated on two columns: one consisting of neutral alumina, and neutral silica, and the other consisting of graphitized carbon black. Method precision was validated using spiked rice (n = 30) and procedural blanks (n = 9). The mean recovery of matrix spikes for all target OPEs were within 78–110% with relative standard deviation lower than 25%, with a few exceptions. This method was applied to process the wild rice (O. sativa) in which tri-n-propyl phosphate was the dominant targeted OPE. The recoveries of surrogate standards were 81 ± 17% for d12- tris(2-chloroethyl) phosphate and 95 ± 8.8% for 13C12- triphenyl phosphate. The developed method was further used to examine the recoveries of target OPEs in the subcellular structure of rice tissues, including cell wall, cell organelles, cell water-soluble fractions, and cell residue. Recoveries of most target OPEs were in the range of 50–150%; however, ion enhancement was observed for four OPEs in root and shoot tissues. Hydrophobic OPEs accumulated in the cell wall, cell residue, and cell organelles while chlorinated OPEs mainly distributed in the cell water-soluble fraction. These results provide new insight for the ecological risk assessment of OPEs in an important food staple. [ABSTRACT FROM AUTHOR]

Waterborne polyvinyl alcohol (PVA) films show lower environmental impact but render high residual solvent on account of hydrophilicity of PVA and low volatility of water. Plasticizers have shown high potential to act as drying enhancers in some recent studies. Plasticizers triphenyl phosphate (TPP) and polyethylene glycol (PEG400) with their favorable chemical structures and relatively low molar masses are promising options. Their performances in drying waterborne PVA films are compared with the plasticizers used in earlier works, at different initial wet film thicknesses, polymer contents, enhancer contents, and enhancer molar masses. Films were solvent casted by drying PVA‐water solutions in a substrate. TPP causes maximum lowering of the residual solvent and does this at high drying rate corresponding to low initial wet film thickness and PVA content. The least value of residual solvent is 0.20% at optimum TPP loading. The next best residual solvent results of 0.21% and 0.59% are, respectively, exhibited by PEG400 and PEG6000, but at low drying rate for high wet film thickness, for both the enhancers; however, at high drying rate for low wet film thickness anomalous skinning increased the residual solvent. At 0.51%, Capstone FS‐63 also gives good results and at high drying rate. Their relative performances are correlated to the viscosity of cast solutions, glass transition temperature of films (DSC), and chemical structures of the polymer and enhancers. TPP thus proved to be most effective. SEM showed dense films and disappearance of defects with optimum loading of TPP, and TGA/DTG showed thermally stable coatings. In spite of the higher cost of TPP it can have useful specialized applications that exploit its excellent flame retardance features. [ABSTRACT FROM AUTHOR]

A common flame-retardant and plasticizer, triphenyl phosphate (TPhP) is an aryl phosphate ester found in many aquatic environments at nM concentrations. Yet, most studies interrogating its toxicity have used µM concentrations. In this study, we used the model organism zebrafish (Danio rerio) to uncover the developmental impact of nM exposures to TPhP at the phenotypic and molecular levels. At concentrations of 1.5–15 nM (0.5 µg/L–5 µg/L), chronically dosed 5dpf larvae were shorter in length and had pericardial edema phenotypes that had been previously reported for exposures in the µM range. Cardiotoxicity was observed but did not present as cardiac looping defects as previously reported for µM concentrations. The RXR pathway does not seem to be involved at nM concentrations, but the tbx5a transcription factor cascade including natriuretic peptides (nppa and nppb) and bone morphogenetic protein 4 (bmp4) were dysregulated and could be contributing to the cardiac phenotypes. We also demonstrate that TPhP is a weak pro-oxidant, as it increases the oxidative stress response within hours of exposure. Overall, our data indicate that TPhP can affect animal development at environmentally relevant concentrations and its mode of action involves multiple pathways.

Triphenyl phosphate (TPHP) is a commonly used organophosphate flame retardant and plasticizer in the United States. Using zebrafish as a model, the overall objective of this study was to identify potential organs that might be targeted by TPHP during embryonic development. Based on mRNA-sequencing, TPHP exposure from 24 to 30 h post fertilization (hpf) and 24 to 48 hpf significantly affected the abundance of 305 and 274 transcripts, respectively, relative to vehicle (0.1% DMSO) controls. In addition to minor effects on cardiotoxicity- and nephrotoxicity-related pathways, ingenuity pathway analysis (IPA) of significantly affected transcripts within 30- and 48-hpf embryos revealed that hepatotoxicity-related pathways were strongly affected following exposure to TPHP-alone. Moreover, although pretreatment with fenretinide (a retinoic acid receptor agonist) mitigated TPHP-induced pericardial edema and liver enlargement at 72 and 128 hpf, respectively, IPA revealed that fenretinide was unable to block TPHP-induced effects on cardiotoxicity-, nephrotoxicity-, and hepatotoxicity-related pathways at 48 hpf, suggesting that TPHP-induced effects on the transcriptome were not associated with toxicity later in development. In addition, based on Oil Red O staining, we found that exposure to TPHP nearly abolished neutral lipids from the embryonic head and trunk and, based on metabolomics, significantly decreased the total abundance of metabolites-including betaine, a known osmoprotectant-at 48 and 72 hpf. Overall, our data suggest that, in addition to the heart, TPHP exposure during early development results in adverse effects on the liver, lipid utilization, and osmoregulation within embryonic zebrafish.

Objective Triphenyl phosphate (TPHP) is one of the most commonly used organophosphorus flame retardants that may accumulate in the environment. However, its effects on human reproductive organs have not been well studied. We aimed to investigate the in vitro effects of TPHP in human Ishikawa endometrial cancer cells to elucidate how TPHP exposure disrupts intracellular signaling and cell proliferation in reproductive tissues. Methods Human Ishikawa endometrial cancer cells were exposed to TPHP. Results Exposure to TPHP elevated the levels of estrogen receptor (ER) α and progesterone receptor-B and reduced ER β in human Ishikawa endometrial cancer cells. TPHP stimulated phosphoinositide 3-kinase/protein kinase B and mitogen-activated protein kinase/extracellular signal-regulated kinases 1/2 kinase signaling, which may contribute to the activation of ER function and induce nuclear translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in human Ishikawa endometrial cancer cells. Activated ER and NF-κB stimulate the expression of cyclin D1/cyclin-dependent kinase (CDK) 4/CDK6, indicating cell cycle progression and proliferation. Conclusion This report may provide new information on the molecular mechanisms underlying how TPHP exposure dysregulates the cellular physiology of the human endometrium.

Microbiological contamination of cinematographic films can cause damage and loss of image information. A large part of the films is made with the base of cellulose triacetate, which has been used from the 1940s until today. Cellulose triacetate is relatively resistant to common organic solvents, but some types of microorganisms can contribute to its faster degradation. In this work, we tested four types of disinfectants suitable for mass disinfection and sufficiently effective against various types of microorganisms. Butanol vapours, a commercial mixture of alcohols (Bacillol® AF), Septonex® (an aqueous solution of [1-(ethoxycarbonyl)pentadecyl] trimethylammonium bromide) and ethylene oxide applied as a gas mixed with carbon dioxide were tested. Samples of a commercial film made of cellulose triacetate were disinfected. The samples were aged for 56 days at 70 °C and 55% RH. Changes in optical, mechanical and chemical properties were studied. None of the disinfectants affected the change in the degree of substitution. For samples disinfected with Bacillol® AF (alcohol mixture), part of the plasticiser (triphenyl phosphate) was extracted and the intrinsic viscosity of the cellulose triacetate solution was reduced after ageing. A slight decrease in intrinsic viscosity also occurred after disinfection with ethylene oxide. Compared to the non-disinfected samples, butanol vapours and Septonex® appear to be the most gentle disinfectants for the cellulose triacetate film base, within the studied parameters. [ABSTRACT FROM AUTHOR]

Copyright of Asian Journals of Ecotoxicology is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The Expert Panel for Cosmetic Ingredient Safety (Panel) assessed the safety of Triphenyl Phosphate, which is reported to function as a plasticizer in manicuring products. The Panel reviewed the available data to determine the safety of this ingredient. The Panel concluded that Triphenyl Phosphate is safe in cosmetics in the present practices of use and concentration described in this safety assessment. [ABSTRACT FROM AUTHOR]

Waste baijiu distillers' grains (BDGs) are one kind of low-value-added biomass originated from Chinese baijiu industry. Considering the large quantity and abundance in carbon element, conversion of waste BDGs to biochar as functional material is of great potential for the sustainable development of baijiu industry. In this study, with the assistance of potassium acetate as activation agent, waste BDGs were converted to highly porous biochar materials through a pyrolysis procedure. Taking the advantages of large specific surface area, well-developed micro- and mesopores, partially graphitized carbon with thin layer structure and abundant surface functional groups, the waste BDGs-derived biochar performed well for the removal of typical organophosphate esters (OPEs) in water, e.g., a maximum adsorption capacity for triphenyl phosphate (TPhP) reached 752.95 mg g−1 over biochar sample of BC 1:3–900. Although the adsorption equilibrium needed up to 10 h to reach, over 50 % effective adsorption was completed in the first 30 min. The adsorption behavior of TPhP on biochar was identified as an exothermic and mono-layer adsorption process, including both fast surface adsorption and relatively slow intra-particle diffusion steps. Solution pH did not affect TPhP adsorption much, but environmental temperature showed great influence on TPhP adsorption capacity. The developed biochar of BC 1:3–900 was still effective for TPhP removal from natural water bodies. Further studies indicated that π-π electron-donor-acceptor (EDA) interaction, hydrogen bonding, σ bonding as well as pore filling effect were the main adsorption mechanisms, contributing to the good adsorption performance of biochar. Besides of aromatic OPEs of TPhP and tricresyl phosphate (TCP), the optimized biochar material was also efficient in removing alkyl and halogenated OPEs, i.e., tributyl phosphate (TBP) and tris(2-chloroethyl) phosphate (TCEP). The facile preparation procedure of biochar material and their good adsorption performance bring a possible alternative for the treatment of OPEs-containing water/wastewater. [Display omitted] • Waste baijiu distillers' grains was converted to biochar by molten salt-assisted pyrolysis. • Biochar held a high adsorption capacity of 752.95 mg g-1 for triphenyl phosphate. • π-π electron-donor-accepter interaction, H-bonding, σ-bonding dominated adsorption process. [ABSTRACT FROM AUTHOR]

Triphenyl phosphate (TPHP) is a widely used organophosphate flame retardant and has biological toxicity. Previous studies showed TPHP can restrain testosterone biosynthesis in Leydig cells, while the underlying mechanisms remain unclear. In this study, C57BL/6J male mice were exposed to 0, 5, 50, and 200 mg/kg B.W. of TPHP for 30 d by oral, as well as TM3 cells were treated with 0, 50, 100, and 200 μM of TPHP for 24 h. Results showed that TPHP induced testes damage, including spermatogenesis disorders and testosterone synthesis inhibition. Meanwhile, TPHP can cause apoptosis in testicular Leydig cells and TM3 cells, as evidenced by the increased apoptosis rate and decreased Bcl-2/Bax ratio. Moreover, TPHP disrupted mitochondrial ultrastructure of testicular Leydig cells and TM3 cells, reduced healthy mitochondria content and depressed mitochondrial membrane potential of TM3 cells, as well as inhibited mitochondrial fusion proteins mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and optic atrophy 1 (Opa1) expression, without effect on mitochondrial fission proteins dynamin-related protein 1 (Drp1) and fission 1 (Fis1) in testicular tissue and/or TM3 cells. Then, the mitochondrial fusion promoter M1 was used to pre-treat TPHP-exposed TM3 cells to determine the roles of mitochondrial fusion inhibition in TPHP-induced Leydig cells apoptosis. The results showed M1 pretreatment alleviated the above changes and further mitigated TM3 cells apoptosis and testosterone levels decreased, indicating TPHP induced TM3 cells apoptosis by inhibited mitochondrial fusion. Intriguingly, the intervention experiment of N-acetylcysteine (NAC) showed that TPHP-induced mitochondrial fusion inhibition is ROS dependent, because inhibition of ROS overproduction alleviated mitochondrial fusion inhibition, and subsequently relieved TPHP-induced apoptosis in TM3 cells. In summary, above data revealed that apoptosis is a specific mechanism for TPHP-induced male reproductive toxicity, and that ROS-mediated mitochondrial fusion inhibition is responsible for Leydig cells apoptosis caused by TPHP.

Background: Human exposures to organophosphate flame retardants result from their use as additives in numerous consumer products. These agents are replacements for brominated flame retardants but have not yet faced similar scrutiny for developmental neurotoxicity. We examined a representative organophosphate flame retardant, triphenyl phosphate (TPP) and its potential effects on behavioral development and dopaminergic function. Methods: Female Sprague–Dawley rats were given low doses of TPP (16 or 32 mg kg−1 day−1) via subcutaneous osmotic minipumps, begun preconception and continued into the early postnatal period. Offspring were administered a battery of behavioral tests from adolescence into adulthood, and littermates were used to evaluate dopaminergic synaptic function. Results: Offspring with TPP exposures showed increased latency to begin eating in the novelty‐suppressed feeding test, impaired object recognition memory, impaired choice accuracy in the visual signal detection test, and sex‐selective effects on locomotor activity in adolescence (males) but not adulthood. Male, but not female, offspring showed marked increases in dopamine utilization in the striatum, evidenced by an increase in the ratio of the primary dopamine metabolite (3,4‐dihydroxyphenylacetic acid) relative to dopamine levels. Conclusions: These results indicate that TPP has adverse effects that are similar in some respects to those of organophosphate pesticides, which were restricted because of their developmental neurotoxicity. [ABSTRACT FROM AUTHOR]

Introduction: Triphenyl phosphate (TPHP) is a chemical flame retardant and plasticizer which is added to consumer and industrial products. The developmental origins of health and disease hypothesis postulate that in utero exposures can have later‐in‐life effects on the developing fetus and can alter fetal gene expression. This study aimed to determine whether epigenetic modifications occurred following in utero TPHP exposure in mice and whether these changes were dose and/or sex‐dependent. Methods: Pregnant C57Bl/6 mice were treated with 0, 5, 25, or 50 mg/kg of TPHP on gestational days (GD) 8, 10, 12, and 14 via intraperitoneal injection and fetal livers were collected on GD 19. Changes in the levels of acetylation of H3 and H4, as well as methylation of H3K9 and global DNA methylation were assessed in the fetal livers by western blot. Results: Results showed that there was a significant decrease in fetal DNA methylation following in utero exposure to 50 mg/kg TPHP compared to the control (0 mg/kg) independent of the sex of the fetus. While there were no significant alterations compared to controls in any histone modifications at any dose or sex following in utero TPHP exposure, we did note a decrease (t test, p =.025) in the levels of acetylated H3 in males versus females following a maternal dose of 25 mg/kg. The monomethylated H3K9 levels were also increased in females versus males following exposure to TPHP at 5 mg/kg (p =.018) and 25 mg/kg (p =.027) when analyzed via unpaired t tests, although not significantly different from controls. Discussion: The results suggest that gestational TPHP exposure can induce epigenetic modifications in murine fetal tissue. Specifically, global DNA methylation levels were downregulated in response to TPHP. Additionally, males appear to be more sensitive to TPHP‐induced histone modifications than females. These data support the need for further studies investigating the impacts of gestational TPHP exposure on the developing fetus. [ABSTRACT FROM AUTHOR]

The reliability of relative quantification RT-qPCR depends upon the gene of interest being normalized to one or more reference genes, with the assumption that the chosen reference genes do not experience altered expression with experimental conditions. The correct choice of stable reference genes is critical when investigating alterations to gene transcript levels following exposure to endocrine and metabolic disrupting chemicals, such as the flame retardant triphenyl phosphate (TPhP). This study assessed the stability of eight reference genes following TPhP exposure in embryonic cells derived from rainbow trout (Oncorhynchus mykiss). The genes β-actin (actb) and 18s rRNA (18s) were stable, while glyceraldehyde-3-phosphate dehydrogenase (gapdh) relative expression was found to be increased. gapdh is a popular reference gene and has been previously used in the literature for investigating TPhP exposure in teleost fish models. We discuss the implications of gapdh upregulation in the context of TPhP as a metabolic disrupting chemical. Furthermore, we quantified the expression of the tumor suppressor gene p53 following TPhP exposure in relation to different reference genes to use as an example to report on how discrepancies in findings might arise depending on the stability of the chosen reference gene., (© 2024 The Author(s). Journal of Applied Toxicology published by John Wiley & Sons Ltd.)

Organophosphates esters (OPEs) have become a preferred alternative in nail polish as plasticizers due to health concerns over previously used additives like dibutyl phthalate. However, the true extent of nail technicians' exposure to OPEs is largely unknown. This study shows that nail salon workers are significant exposed to OPEs, with varied concentrations found in air, dust, masks, and urine. The total concentrations of 11 OPEs in ultrasonic personal air samplers (UPAS) ranged from 251 to 1007 ng/m³, and in air conditioner filter dust from 371 to 14473 ng/g. Triphenyl phosphate (TPHP) was the most abundant compound found in the nail polishes used in these salons. On average, the concentrations of TPHP and diphenyl phosphate (DPHP) in workers' urine after work were 5.2 and 1.8 times higher than those before work, respectively. Two nail salons that had the highest nail polish usage also had very high concentrations of TPHP in surgical masks, dust, and UPAS. TPHP concentrations in workers' urine after work were 19 and 13 times those before work, respectively, in these two salons. Human internal exposure assessment showed that the average exposure dose of TPHP after work was 1.8 times higher than that before work. On average, use of masks reduced OPEs in urine by 77%. In conclusion, frequent mask replacement is highly recommended, especially in long working circumstances. Without regular replacement, masks may accumulate OPEs from the air, potentially becoming another source of human exposure to OPEs. Therefore, more attention should be paid to the occupational exposure of nail salon workers to OPEs, particularly considering that most practitioners in this industry are young women of reproductive age., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Pericardial edema is commonly observed in zebrafish embryo-based chemical toxicity screens, and a mechanism underlying edema may be disruption of embryonic osmoregulation. Therefore, the objective of this study was to identify whether triphenyl phosphate (TPHP) – a widely used aryl phosphate ester-based flame retardant – induces pericardial edema via impacts on osmoregulation within embryonic zebrafish. In addition to an increase in TPHP-induced microridges in the embryonic yolk sac epithelium, an increase in ionic strength of exposure media exacerbated TPHP-induced pericardial edema when embryos were exposed from 24 to 72 h post-fertilization (hpf). However, there was no difference in embryonic sodium concentrations in situ within TPHP-exposed embryos relative to embryos exposed to vehicle (0.1% DMSO) from 24 to 72 hpf. Interestingly, increasing the osmolarity of exposure media with mannitol (an osmotic diuretic which mitigates TPHP-induced pericardial edema) and increasing the ionic strength of the exposure media (which exacerbates TPHP-induced pericardial edema) did not affect embryonic doses of TPHP, suggesting that TPHP uptake was not altered under these varying experimental conditions. Overall, our findings suggest that TPHP-induced pericardial edema within zebrafish embryos is dependent on the ionic strength of exposure media, underscoring the importance of further standardization of exposure media and embryo rearing protocols in zebrafish-based chemical toxicity screening assays.

Triphenyl phosphate (TPHP) is a widely used flame retardant and plasticizer and has been detected extensively in environmental media, wildlife and human bodies. Several epidemiological and animal studies have revealed that TPHP exposure is positively associated with glucose homeostasis disruption and diabetes. However, the effects of TPHP on hepatic glucose homeostasis and the underlying mechanisms remain unclear. The present work aimed to investigate the cytotoxicity and glucose metabolism disruption of TPHP and its metabolite diphenyl phosphate (DPHP) within hepatocytes. The cell viability assay undertaken on human normal liver (L02) cells showed that TPHP exhibited more potent hepatotoxicity than DPHP. RNA sequencing (RNA-seq) data showed that TPHP and DPHP presented different modes of toxic action. Insulin resistance is one of the predominant toxicities for TPHP, but not for DPHP. The insulin-stimulated glucose uptake and glycogen synthesis were impaired by TPHP, while DPHP exhibited no significant impairment on these factors. TPHP exposure induced endoplasmic reticulum (ER) stress, and the ER stress antagonist 4-PBA restored the impairment of insulin-stimulated glucose uptake and glycogen synthesis induced by TPHP. TPHP could also induce liver ER stress and insulin resistance in mice. Taken together, the results suggested that TPHP induces more potent insulin resistance through ER stress than its metabolite DPHP.

As BFRs have gradually been banned recently, organophosphorus flame retardants (OPFRs) have been manufactured and used in their place. Although OPFRs are considered the better alternatives to BFRs, many studies have discovered that OPFRs may be associated with various cancers, including prostate cancer, bladder cancer, hepatocellular carcinoma, and colorectal cancer. However, few studies have examined the relationship between OPFRs and gliomas. This study investigated the relationship between triphenyl phosphate (TPP) and glioma using bioinformatics analysis approaches. The comparative toxicogenomics database (CTD) and The Cancer Genome Atlas (TCGA) databases were accessed for TPP-related genes and gene expression data from glioma patients. The Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses show that TPP might be closely related to many pathways. Further, the analysis of protein-protein interactions revealed strong intrinsic relationships between TPP-related genes. In addition, the TPP-based prognostic prediction model demonstrated promising results in predicting the prognosis of patients with gliomas. Several TPP-related genes were closely related to glioma patients' overall survival rates. The proliferation and migration abilities of glioma cells were further demonstrated to be significantly enhanced by TPP. In a bioinformatics analysis, we also discovered that melatonin is highly correlated with the presence of TPP and gliomas. According to the cell proliferation and migration assays, exposure to melatonin and TPP inhibited the ability of glioma cells to invade compared with the TPP group.

Organophosphate flame retardants (OPFRs) have been widely used due to their unique properties. The OPFRs are mainly metabolized in the liver. However, whether the plasma level of OPFRs was involved in the progression of liver cancer remains unclear. Triphenyl phosphate (TPP) is one of the OPFRs that are mostly detected in environment. In this study, we performed CCK8, ATP, and EdU analyses to evaluate the effect of TPP at the concentrations at 0.025–12.8 μM on the proliferation, invasion, and migration of Hep3B, a hepatocellular carcinoma (HCC) cell line. Tumor‐bearing mouse model was used for in vivo validation. The results showed that low concentrations of TPP at (0.025–0.1 μM), which are obtained in the plasma of patients with cancers, remarkably promoted cell invasion and migration of Hep3B cells. Animal experiments confirmed that TPP treatment significantly enhanced tumor growth in the xenograft HCC model. To explore the possible molecular mechanisms that might mediate the actions of TPP on Hep3B cells, we profiled gene expression in groups treated with or without TPP at the concentrations of 0.05 and 0.1 μM using transcriptional sequencing. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and Protein–protein interaction (PPI) analyses demonstrated that pathways affected by differentially expressed genes (DEGs) were mainly in nuclear‐transcribed mRNA catabolic processes, cytosolic ribosome, and ATPase activity. A 0.05 and 0.1 μM TPP led to up‐regulation of a series of genes including EREG, DNPH1, SAMD9, DUSP5, PFN1, CKB, MICAL2, SCUBE3, and CXCL8, but suppressed the expression of MCC. These genes have been shown to be associated with proliferation and movement of cells. Taken together, our findings suggest that low concentration of TPP could fuel the proliferation, invasion, and migration of HCC cells. Thus, TPP is a risk factor in the progression of HCC in human beings. [ABSTRACT FROM AUTHOR]

Triphenyl phosphate (TPhP) is a non-halogenated organophosphorus flame retardant, and there is a higher exposure risk in children. TPhP has been found to be neurotoxic upon developmental exposure, yet the specific mechanism remains unclear. To characterize the cellular responses underlying TPhP-induced developmental neurotoxicity, we administered TPhP (0.5, 5 or 50 mg/kg/day) to neonatal mice from postnatal day 10 (P10)–P70. A total of 17,229 cells and 26,338 genes were identified in cortical samples from control and low-dose (the internal doses of metabolite DPhP comparable to human exposure level) groups using single-cell RNA sequencing (scRNA-seq). TPhP exposure led to heterogeneous transcriptional alterations and intercellular crosstalk among neurons, neural stem/progenitor cells (NSPCs), endothelial cells, and immunocytes. Deprivation of NSPCs, loss of mature neurons, and concomitant neuroinflammation mediated by extrinsic and intrinsic immunocytes were found in TPhP-exposed cortices. In addition, we observed blood–brain barrier destruction prior to the anxiety/depression-like neurobehavioral changes. These results reveal the distinctive cellular processes in TPhP's neurodevelopmental toxicity and uncover that the impeded neurogenesis, disrupted vascular barrier, and concomitant neuroinflammation are the sensitive responses to TPhP exposure. Our study paves the way for the application of scRNA-seq in toxicity assessments for emerging neurotoxic pollutants. [ABSTRACT FROM AUTHOR]

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BackgroundChildren are exposed to flame retardants from the built environment. Brominated diphenyl ethers (BDE) and organophosphate-based flame retardants (OPFRs) are associated with poorer neurocognitive functioning in children. Less is known, however, about the association between these classes of compounds and children's emotional and social behaviors. The objective of this study was to determine if flame retardant exposure was associated with measurable differences in social behaviors among children ages 3-5 years.MethodsWe examined teacher-rated social behaviors measured using the Social Skills Improvement Rating Scale (SSIS) and personal exposure to flame retardants in children aged 3-5 years who attended preschool (n = 72). Silicone passive samplers worn for 7 days were used to assess personal exposure to 41 compounds using gas chromatography-mass spectrophotometer. These concentrations were then summed into total BDE and total OPFR exposure prior to natural log transformation. Separate generalized additive models were used to evaluate the relationship between seven subscales of the SSIS and lnΣBDE or lnΣOPFR adjusting for other age, sex, adverse social experiences, and family context.ResultsAll children were exposed to a mixture of flame retardant compounds. We observed a dose dependent relationship between lnΣOPFR and two subscales where children with higher exposures were rated by their preschool teachers as having less responsible behavior (p = 0.07) and more externalizing behavior problems (p = 0.03). Additionally, children with higher lnΣBDE exposure were rated by teachers as less assertive (p = 0.007).ConclusionsWe observed a cross-sectional association between children's exposure to flame retardant compounds and teacher-rated social behaviors among preschool-aged children. Children with higher flame retardant exposures exhibited poorer social skills in three domains that play an important role in a child's ability to succeed academically and socially.