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[Display omitted] • Particles release from erasers and pen grips upon dermal contact. • Particles derived from erasers and pen grips are mainly smaller than 1 μm. • Migrated particles mediate dermal contact of plasticizers to erasers and pen grips. Dermal exposure to chemicals released from daily consumer products is a rising concern, particularly for children who are susceptible to unintentional hand-to-mouth transfer and related chemical exposure risk. However, chemical transfer induced by tiny particles of intact products has yet to be adequately addressed. The objective of the present study was to determine the potentiality of particles release from intact erasers and pen grips upon dermal contact by measuring the migration rates of the embedded plasticizers (phthalates and its alternatives). The results showed that billions of particles were released from erasers (0.6–1.2 × 109) and pen grips (0.2–1.6 × 108) upon dermal contact at ambient temperature, with sizes mainly smaller than 1 μm. The composition of eraser leachates was identical to that of the corresponding bulk eraser, as confirmed by Fourier-transform infrared spectroscopy and pyrolysis. Migrated hydrophobic plasticizers may be used as indicators of particle release from erasers and pen grips. The potentiality of particle release was negatively correlated with the total plasticizer contents (r = −0.51; p < 0.05) for both erasers and pen grips. These findings indicated that particles directly released from school supplies and accessories could be a non-negligible source of human exposure to plasticizers. [ABSTRACT FROM AUTHOR]

[Display omitted] • From 26 different countries, on four continents (Africa, America, Asia and Europe), >60% of the toys and consumer products analysed in this study by chemical (GC-HRMS) and effect-based analysis (DR CALUX) for polyhalogenated dioxins, showed higher levels than the proposed limit value for toxic waste (>1000 TEQ pg/g) (Basel Convention, 2019). • We measured high levels of PBDD/Fs in these black plastic parts by using DR CALUX (from 110 to 17,000 pg BEQ/g) and by GC-HRMS (levels up to 13,900 pg TEQ/g). • High TBBPA levels were measured by using TTR-TRβ CALUX (up to 410 µg/g) and by chemical analysis (up to 836 µg/g) indicating thyroid hormone disruption activities. • Effect-based CALUX bioassay for dioxin- and thyroid hormone-like activities picked-out all elevated toxic products showing that in vitro toxicity analysis of total PBDD/F and TBBPA is a promising and suitable strategy to cover complex mixtures of BFRs and to assess BFRs in consumer products in general. • This study add further evidence that current limits for both trace contamination and the definition of POPs waste set in the EU POPs Regulation (European Parliament and the Council of the European Union, 2019 and 2022) and for the total content of PBDEs are too weak (500 ppm) to protect human health. It will allow a large number of such contaminated products to enter the market. Children and consumers are exposed to increasingly complex mixtures of known and as-yet-unknown toxic chemicals from toys and products. However traditional chemical analysis methods only evaluate a small number of chemicals at a time thereby restricting consumer awareness of the full range of potentially harmful chemicals in products. We used high-throughput effect-based non-animal methods to investigate exposures to complex chemical mixtures of several kinds of brominated flame retardants (BFRs) for their dioxin- and thyroid hormone-like activities in various kinds of consumer products and toys from 26 different countries, on four continents (Africa, America, Asia and Europe) in combination with chemical analysis of various polybrominated flame retardants (BFRs) and their impurities (such as polyhalogenated PCDD/Fs and PBDD/Fs). We found high levels of polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) in toys and now, for the first time, also in consumer products that are manufactured from black plastics containing certain brominated flame retardants (BFRs). The presence of PBDD/PBDFs as well as other BFRs in various black plastic materials from additional countries as well as additional kinds of consumer products as confirmed by effect-based in vitro reporter gene DR CALUX and TTR-TRβ CALUX assays as well as congener-specific chemical analysis. We compared total Toxicity Equivalent (TEQ) levels of PBDD/F-TEQs analysed by chemical analysis to by CALUX bioassay measured Biological equivalence (BEQ) concentrations (for further info see at ISO 23196, ISO, 2022). In the case of TBBPA, both chemical and TTR-TRβ CALUX analysis measure direct the amount of TBBPA. Finally, the daily ingestion of 2,3,7,8-TCDD equivalents from PBDD/Fs-contaminated plastic toys by child mouthing habits have been related to our earlier study (Budin et al., 2020). Interaction of children with such contaminated plastics may significantly contribute to the daily uptake of dioxin- and thyroid hormone transport disrupting-like compounds. Effect-based bioassays for dioxin- and thyroid hormone-like activities are relevant to pick-out such complex mixtures of known and yet unknown (and therefore not regulated) substances for safer and more sustainable plastics. Low POPs Content Levels and other mechanisms set under the Basel and Stockholm Conventions are set far too high to prevent a significant flow of BFRs and PBDD/Fs into consumer products. [ABSTRACT FROM AUTHOR]

[Display omitted] • Estrogenic and non-estrogenic effects of BPA in zebrafish have been reviewed. • The mechanisms of action of BPA in zebrafish have been summarized. • The effects of BPA should take into account the interplay of multiple complex processes. • Zebrafish have both technical and practical advantages for investigating the effects of BPA, as well as other EDCs. Bisphenol A (BPA) is the most simple and predominant component of the Bisphenol family. BPA is widely present in the environment and the human body as a result of its extensive usage in the plastic and epoxy resins of consumer goods like water bottles, food containers, and tableware. Since the 1930s, when BPA's estrogenic activity was first observed, and it was labeled as a "mimic hormone of E2", studies on the endocrine-disrupting effects of BPA then have been widely conducted. As a top vertebrate model for genetic and developmental studies, the zebrafish has caught tremendous attention in the past two decades. By using the zebrafish, the negative effects of BPA either through estrogenic signaling pathways or non-estrogenic signaling pathways were largely found. In this review, we tried to draw a full picture of the current state of knowledge on the estrogenic and non-estrogenic effects of BPA with their mechanisms of action through the zebrafish model of the past two decades, which may help to fully understand the endocrine-disrupting effects of BPA and its action mechanism, and give a direction for the future studies. [ABSTRACT FROM AUTHOR]

Higher exposure risk from emerging BPSs along with BPA and BPAs should be underlined for female, younger and abnormal-weighted children from an e-waste recycling city. [Display omitted] Emerging bisphenol S analogues (BPSs) have gained their application perspectives to replace bisphenol A (BPA) and BPA analogues (BPAs). However, the extent of human exposure and potential health risk from BPSs is rarely known yet. We hypothesized that children living in Shantou, China, a well-known e-waste recycling city, may expose to emerging BPSs together with BPA and BPAs. In this study, BPA, six commonly used BPAs and 11 emerging BPSs were determined simultaneously in 240 urine samples collected from children residing in Shantou. BPA, BPS, bisphenol F, bisphenol AF and three BPSs of 2,4′-bis(hydroxyphenyl)sulfone, 4-((4-(allyloxy)phenyl)sulfonyl)phenol and diphenylsulfone (DPS) were the urinary predominant bisphenols with detection frequencies of 67–100% in the children. BPA was found at the highest median concentration (3.36 µg/g creatinine) followed by BPS (0.313) and DPS (0.187). It is interesting to find that the girls and children in the younger group (2 ≤ age < 5) had consistently higher concentrations of the seven dominant bisphenols than the boys and these of the older group (5 ≤ age ≤ 10), respectively. The children with under/overweight suffered higher burdens of bisphenol exposure based on medians of estimated daily intakes. Association analysis results indicated that the Shantou children exposed themselves to multiple BPSs along with BPA and BPAs from assumed consumer products and/or contaminated environments. [ABSTRACT FROM AUTHOR]

• A China total diet study on exposure to nine BDGEs was comprehensively assessed. • BADGE and BADGE·2H 2 O is exposure of greater concern compared to BFDGEs. • Meats, eggs, and aquatic products are the main source of dietary exposure. • Current BDGEs exposure levels do not pose risks to general population. Despite the widespread use of bisphenol A diglycidyl ether (BADGE) and bisphenol F diglycidyl ether (BFDGE) in various consumer products as protective plasticizer, studies on human dietary exposure to these compounds are scare. In this study, nine bisphenol diglycidyl ethers (BDGEs) including BADGE, BFDGE, and seven of their derivatives were determined in the Chinese adult population based on composite dietary samples collected from the sixth (2016–2019) China total diet study (TDS). Contamination level of nine BDGEs was determined in 288 composite dietary samples from 24 provinces in China. BADGE·2H 2 O and BADGE are the most frequently detected and BADGE·2H 2 O presented the highest mean concentration (2.402 μg/kg). The most contaminated food composite is meats, with a mean ∑ 9 B D G E s of 8.203 μg/kg, followed by aquatic products (4.255 μg/kg), eggs (4.045 μg/kg), and dairy products (3.256 μg/kg). The estimated daily intake (EDI) of ∑ 9 B D G E s based on the mean and 95th percentile concentrations are 121.27 ng/kg bw/day and 249.71 ng/kg bw/day. Meats, eggs, and aquatic products are the main source of dietary exposure. Notably, beverages and water, alcohols were the main contributors of dietary exposure to BADGE and BADGE·2H 2 O, followed by animal-derived foods. Dietary exposure assessment demonstrated that human dietary BDGEs do not pose risks to general population based on the mean and 95th percentile hazard index with < 1. This is the first comprehensive national dietary exposure assessment of BDGEs in Chinese general population. [ABSTRACT FROM AUTHOR]

• We evaluated class-specific mixtures of phenol, phthalate, and organophosphate ester biomarkers in maternal urine. • We assessed the bioactive lipids called oxylipins from several biosynthetic pathways in maternal plasma. • Higher consumer product chemicals were associated with certain pro-inflammatory oxylipins. • Consumer product chemicals may promote inflammation related to lipid metabolism during pregnancy. Exposure to consumer product chemicals during pregnancy may increase susceptibility to pregnancy disorders by influencing maternal inflammation. However, effects on specific inflammatory pathways have not been well characterized. Oxylipins are a diverse class of lipids that act as important mediators and biomarkers of several biological pathways that regulate inflammation. Adverse pregnancy outcomes have been associated with circulating oxylipin levels in pregnancy. In this study, we aimed to determine the longitudinal associations between plasma oxylipins and urinary biomarkers of three classes of consumer product chemicals among pregnant women. Data come from a study of 90 pregnant women nested within the LIFECODES cohort. Maternal plasma and urine were collected at three prenatal visits. Plasma was analyzed for 61 oxylipins, which were grouped according to biosynthetic pathways that we defined by upstream: 1) fatty acid precursor, including linoleic, arachidonic, docosahexaenoic, or eicosapentaenoic acid; and 2) enzyme pathway, including cyclooxygenase (COX), lipoxygenase (LOX), or cytochrome P450 (CYP). Urine was analyzed for 12 phenol, 12 phthalate, and 9 organophosphate ester (OPE) biomarkers. Linear mixed effect models were used for single-pollutant analyses. We implemented a novel extension of quantile g-computation for longitudinal data to examine the joint effect of class-specific chemical mixtures on individual plasma oxylipin concentrations. We found that urinary biomarkers of consumer product chemicals were positively associated with pro-inflammatory oxylipins from several biosynthetic pathways. Importantly, these associations depended upon the chemical class of exposure biomarker. We estimated positive associations between urinary phenol biomarkers and oxylipins produced from arachidonic acid by LOX enzymes, including several important pro-inflammatory hydroxyeicosatetraenoic acids (HETEs). On average, mean concentrations of oxylipin produced from the arachidonic acid/LOX pathway were 48%–71% higher per quartile increase in the phenol biomarker mixture. For example, a simultaneous quartile increase in all urinary phenols was associated with 53% higher (95% confidence interval [CI]: 11%, 111%) concentrations of 12-HETE. The positive associations among phenols were primarily driven by methyl paraben, 2,5-dichlorophenol, and triclosan. Additionally, we observed that phthalate and OPE metabolites were associated with higher concentrations of oxylipins produced from linoleic acid by CYP enzymes, including the pro-inflammatory dihydroxy-octadecenoic acids (DiHOMEs). Associations among DiHOME oxylipins were driven by metabolites of benzylbutyl and di-isodecyl phthalate, and by the metabolite of tris(1,3-dichloro-2-propyl) phosphate among OPEs. We also observed inverse associations between phthalate and OPE metabolites and oxylipins produced from other pathways; however, adjusting for a plasma indicator of dietary fatty acid intake attenuated those results. Our findings support the hypothesis that consumer product chemicals may have diverse impacts on inflammation processes in pregnancy. Certain pro-inflammatory oxylipins were generally higher among participants with higher urinary chemical biomarker concentrations. Associations varied by class of chemical and by the biosynthetic pathway of oxylipin production, indicating potential specificity in the inflammatory effects of these environmental chemicals during pregnancy that warrant investigation in larger studies. [ABSTRACT FROM AUTHOR]

• Method demonstrates how GxE interaction potential differs for chemical exposures. • Different consumer product classes are high risk for varied disease associations. • Different consumer product classes implicate different genetic regions in diseases. • Genetic variants and pathways implicated in diseases differ depending on exposure. Interactions between environmental factors and genetics underlie the majority of chronic human diseases. Chemical exposures are likely an underestimated contributor, yet gene-environment (GxE) interaction studies rarely assess their modifying effects. Here, we describe a novel method to profile the human genome and identify regions associated with differential population susceptibility to chemical exposures. Single nucleotide polymorphisms (SNPs) implicated in enriched chemical-disease intersections were identified and validated for three chemical classes with expected GxE interaction potential (neuroactive, hepatoactive, and cardioactive compounds). The same approach was then used to characterize consumer product classes with unknown risk for GxE interactions (washing products, cosmetics, and adhesives). Additionally, high-risk variant sets that may confer differential population susceptibility were identified for these consumer product groups through frequent itemset mining and pathway analysis. A dataset of 2454 consumer product chemical-disease linkages, with risk values, SNPs, and pathways for each association was developed, describing the interplay between environmental factors and genetics in human disease progression. We found that genetic hotspots implicated in GxE interactions differ across chemical classes (e.g., washing products had high-risk SNPs implicated in nervous system disease) and illustrate how this approach can discover new associations (e.g., washing product n-butoxyethanol implicated SNPs in the PI3K-Akt signaling pathway for Alzheimer's disease). Hence, our approach can predict high-risk genetic regions for differential population susceptibility to chemical exposures and characterize chemical modifying factors in specific diseases. These methods show promise for describing how chemical exposures can lead to varied health outcomes in a population and for incorporating inter-individual variability into chemical risk assessment. [ABSTRACT FROM AUTHOR]