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Background Exposure to bisphenols may affect fetal growth and development. The trimester-specific effects of bisphenols on repeated measures of fetal growth remain unknown. Our objective was to assess the associations of maternal bisphenol urine concentrations with fetal growth measures and birth outcomes and identify potential critical exposure periods. Methods In a population-based prospective cohort study among 1379 pregnant women, we measured maternal bisphenol A, S and F urine concentrations in the first, second and third trimester. Fetal head circumference, length and weight were measured in the second and third trimester by ultrasound and at birth. Results An interquartile range increase in maternal pregnancy-averaged bisphenol S concentrations was associated with larger fetal head circumference (difference 0.18 (95% confidence interval (CI) 0.01 to 0.34) standard deviation scores (SDS), p -value< 0.05) across pregnancy. When focusing on specific critical exposure periods, any detection of first trimester bisphenol S was associated with larger second and third trimester fetal head circumference (difference 0.15 (95% CI 0.05 to 0.26) and 0.12 (95% CI 0.02 to 0.23) SDS, respectively) and fetal weight (difference 0.12 (95% CI 0.02 to 0.22) and 0.16 (95% CI 0.06 to 0.26) SDS, respectively). The other bisphenols were not consistently associated with fetal growth outcomes. Any detection of bisphenol S and bisphenol F in first trimester was also associated with a lower risk of being born small size for gestational age (Odds Ratio 0.56 (95% CI 0.38 to 0.74) and 0.55 (95% CI 0.36 to 0.85), respectively). Bisphenols were not associated with risk of preterm birth. Conclusions Higher maternal bisphenol S urine concentrations, especially in the first trimester, seem to be related with larger fetal head circumference, higher weight and a lower risk of being small size for gestational age at birth.

Bisphenol A (BPA) is an industrial chemical identified as a vertebrate endocrine disruptor. Numerous alternatives have been developed, for which toxicity data are lacking. The present study assessed the toxicity of BPA and its replacement products bisphenol F (BPF), bisphenol S (BPS), and bisphenol AF (BPAF) in freshwater snail ( Planorbella pilsbryi ) embryos and adults. The chronic toxicity of BPA and BPAF was further characterized in 28-day tests with adult snails, followed by 21-day assessments of hatching and survival of embryos produced at the end of the test (F1 generation). In acute tests, BPAF was the most toxic of the substances tested (maximum acceptable toxicant concentration [MATC], 136 µg/L), followed by BPA (MATC, 1404 µg/L), BPF (MATC, 1525 µg/L), and BPS (MATC > 8590 µg/L). In the chronic test with BPA, although we observed no significant effects on adult snails up to 479 µg/L, the hatching and survival of juveniles from the F1 generation decreased (MATC, 13 µg/L), and was delayed by 7.5 days, on average. In contrast, we did not observe any decrease in hatching or survival of juveniles from the F1 generation during exposure to BPAF. Effects were observed at concentrations above most reported environmental exposure concentrations, although there was an overlap between exposure and effect concentrations. Given that concentrations of alternative substances are expected to increase, and in the absence of data on potential effects of mixtures, further research is needed.

Given its simplicity, Caenorhabditis elegans appears to be a promising model for future research on endocrine disruptors, including bisphenol A and its supposedly safer alternatives. The aim of this study was to investigate the impact of embryonic exposure of C. elegans to different concentrations (0.5, 1.0, and 5 µM) of bisphenol A and its analogs (bisphenol S, bisphenol F, and bisphenol AF) on selected biological characteristics of the nematode C. elegans and to compare them with an unexposed control group. Embryonal exposure of C. elegans to bisphenol A, as well as bisphenol S, F, and AF at concentrations of 0.5, 1.0, and 5 µM resulted in a significant influence on the percentage of hatched eggs and habituation to anterior stimuli (with significant results ranging from p ≤ 0.05 to p ≤ 0.001). The growth of C. elegans was also significantly impaired by bisphenol A, S, and AF in some concentrations (with p-values ranging from p ≤ 0.05 to p ≤ 0.001). Our findings confirm prior research that bisphenol A and its supposedly safer analogs exert a detrimental effect on diverse biological processes. Therefore, bisphenol A analogs should be employed with caution, particularly until a comprehensive risk assessment has been conducted.

As benthic filter feeders, bivalve mollusks serve as ideal biological indicators. Bisphenol A (BPA) and its substitutes (BPS, BPF, and BPAF) are endocrine disruptors with reproductive toxicity, targeting estrogen receptors (ERs). However, their binding sites and affinity for shellfish ERs remain unclear. This study aims to identify ER binding sites of BPA and its substitutes, compare toxicity via molecular docking, and validate results through exposure experiments. The full-length cDNA of Corbicula fluminea ER was cloned using the RACE technique for the first time, the sequence length is 2138bp. Homologous models of LBD sequences from Danio rerio, C. fluminea, Azumapecten farreri, and Ruditapes philippinarum ERs were constructed via homology modeling and screened for optimal fit. Hydrogen bonds were observed during the docking process, with interaction sites including Glu-66, Arg-177, and other amino acid residues. Exposure experiments (1, 10, and 100 μg/L) showed an enhancement in ER mRNA expression. Based on the docking energies and results of the exposure experiments, it was concluded that the toxicity of BPA and BPS is similar and greater than that of BPF and BPAF. This study provides data for a reproductive risk assessment and aquatic toxicological monitoring of bisphenols.

Background Global infertility rates have noticeably increased in recent decades. The effects of environmental exposures on human fertility have been well-noted. However, Evidence on couple-based preconception exposure to bisphenols (BPs), particularly emerging substitutes, and fecundity remains limited. This study aimed to investigate the exposure profiles of 14 classic and emerging BPs in the preconception period as well as their impacts on couple fecundity, to assess both the individual effects of specific compounds and the combined effects of mixtures in males and females, and to evaluate the health risks induced by BPs exposure after tolerable daily intake (TDI) value was tightened in 2023. Methods This nested case-control study involved 1934 preconception individuals in two research sites of China, from October 2016 to May 2025. The case and control groups were comprised of 318 and 649 couples with time to pregnancy (TTP) > 12 and ≤ 12 menstrual cycles, respectively. BPs were quantified in preconception urine samples using ultra-performance liquid chromatography-tandem mass spectrometry, including novel substitutes that had not been measured and reported in human beings, such as 2,2’-diallyl bisphenol A (DBA) and 4-hydroxy-4’-isopropoxydiphenylsulfone (D8). Generalized linear, weighted quantile sum and Bayesian kernel machine regression models were employed to assess individual and mixture effects of BPs on subfecundity. Results The positive associations of BPs and subfecundity risks were observed in both females and males. Mixed BPs were positively correlated with subfecundity in females (OR = 2.84, 95% CI: 2.23–3.61), males (OR = 4.21, 95% CI: 3.24–5.47), and couples (OR = 6.73, 95% CI: 4.81–9.41), with DBA and bisphenol AF (BPAF) identified as major contributors. Health risk assessment indicated that although few participants had an estimated daily intake (EDI) exceeding the 2015 TDI (4000 ng/kg bw/day), most (81.8%-100%) surpassed the 2023 TDI (0.2 ng/kg bw/day). Conclusions This study provides the first evidence linking novel bisphenols, BPAF and DBA, to increased subfecundity risk and highlights significant health risks in a population with an intention to conceive, underscoring the urgency to regulate a broader range of bisphenols to protect reproductive health.

Purpose Bisphenols (BPs), including bisphenol A (BPA) and its analogs BPB, BPF, BPS, and BPAF, are essential industrial raw materials used in the production of consumer goods but pose significant public health risks. Bisphenols contribute to carcinogenesis due to their endocrine-disrupting properties, particularly in breast cancer. However, the relationship between BPs exposure and putative cancer risk, as well as the underlying molecular mechanisms, remains poorly understood. Methods This study employed network toxicology, molecular docking, molecular dynamics simulation, machine learning, and bioinformatics to systematically investigate the molecular mechanisms and potential targets associated with carcinogenic risks of five BPs. Results The findings revealed that BPs exposure increases cancer risk by targeting 26 core proteins, including RXRA, AKT2, and CYCS, leading to oxidative stress and modulation of cancer-related signaling pathways such as MAPK, PI3K/AKT, Ras, and VEGF. Molecular docking and dynamics simulations demonstrated stable binding interactions between RXRA and all five BPs. Analysis of the TCM database indicated that Ginseng , Turmeric , and Salvia miltiorrhiza can mitigate BPs-induced cancer risk by targeting these core proteins. Pan-cancer analysis showed that kidney renal clear cell carcinoma (KIRC) and low-grade glioma (LGG) are most strongly associated with BPs exposure. Diagnostic and prognostic models based on core targets exhibited high predictive accuracy, offering valuable clinical decision support. Single-cell sequencing revealed that core targets are primarily localized in immune cells in KIRC and glioma cells in LGG. Conclusion This study provides a theoretical foundation for evaluating cancer risk associated with BPs exposure and establishes a novel framework for understanding the pathogenesis and potential therapeutic strategies for environmental pollutants.

Bisphenol A (BPA) has long been used in plastics, resins, and food packaging materials; however, extensive research has demonstrated its reproductive, developmental, and endocrine-disrupting effects. Consequently, BPA has been increasingly restricted and replaced with structural analogues. Among these, tetramethyl bisphenol F (TMBPF) has emerged as one of the most widely used substitutes, particularly in epoxy resins and food-can coatings. Although initially regarded as a safer alternative, accumulating evidence suggests that TMBPF may exert multiple toxicological effects, raising concerns about its potential developmental neurotoxicity. The present study aimed to investigate the neurodevelopmental effects of TMBPF using both in vitro and in vivo approaches. First, a developmental neurotoxicity assay employing Sox1−GFP mouse embryonic stem cells was used to evaluate cytotoxicity using the cell counting kit-8 assay and neural differentiation based on green fluorescent protein (GFP) fluorescence intensity. The results indicated developmental neurotoxic potential according to the established discrimination index. Subsequently, pregnant and lactating mice were exposed to TMBPF daily from gestational day 10.5 to postnatal day 20, and their offspring were assessed for behavioral performance as well as changes in the expression of neurodevelopment-related genes in the brain. Behavioral analyses encompassed multiple domains, including memory and learning, social behavior, anxiety-related responses, and spontaneous locomotor activity, suggesting alterations in these functional outcomes. Molecular analyses further demonstrated changes associated with dopaminergic and cholinergic signaling, synaptic plasticity, neuronal activity markers, neuropeptides, and inflammatory pathways. Collectively, these findings provide the first evidence in a mammalian model that maternal exposure to TMBPF may influence offspring neurodevelopment. These findings suggest potential implications for human exposure to TMBPF, particularly through food-contact materials, and warrant further mechanistic and dose–response studies.

This study assessed bisphenol exposure in preterm infants (born before 35 weeks of gestation) hospitalized in a neonatal intensive care unit (NICU), along with associated prenatal exposure. Fifty-eight infants and 48 mothers were included. Bisphenol A (BPA) and bisphenol F (BPF) levels were measured in maternal urine, cord blood, and infant urine samples using high-performance liquid chromatography (HPLC). There was a significant negative association between maternal urine BPF (MuBPF) and the newborn’s birth weight percentile. A significant positive correlation was found between the BPA levels of the infant’s urine taken on the first day (NuBPA1) and the second sample taken on the last day (NuBPA2) in the NICU. There was a significant negative association between tertile levels of cord BPA (cBPA) and stretched penile length (SPL). NuBPF1 levels in the first-born babies were significantly higher compared to the later-borns. Detectable NuBPF1 levels and decreased NuBPF2 compared to NuBPF1 levels were observed more frequently in males. Cord BPA (cBPA) and BPF (cBPF) levels did not significantly correlate with maternal or infant urinary levels. No association was found between NICU procedures and BPA or BPF exposure levels. The absence of significant associations between neonatal urine BPA levels and both maternal urine and cord blood BPA, as well as NICU procedures, suggests that newborns may be exposed to these chemicals through other, unpredictable sources that were not captured in this study. The study highlights the need to minimize BPA and BPF exposure, especially during pregnancy and NICU stays, to protect fetal health and prevent future issues.

Bisphenol F (BPF), a primary substitute for bisphenol A (BPA), is widely utilized in industrial production and daily life. However, its widespread environmental presence has raised concerns regarding potential health risks. This study aims to investigate the potential toxic targets of BPF in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Initially, potential target genes of BPF were identified using the ChEMBL, STITCH, and SWISS databases. NAFLD-related genes were obtained from the OMIM and GeneCards databases, yielding a preliminary set of 28 overlapping candidate targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were subsequently performed to elucidate the biological processes and signaling pathways potentially affected by BPF. Differential expression analysis of transcriptomic data from NAFLD and normal liver tissues obtained from the GEO database (GSE260666) revealed that CYP2C19 and SHBG were significantly upregulated in NAFLD samples, suggesting their potential as key targets of BPF. Molecular docking simulations using AutoDock demonstrated stable binding conformations between BPF and both CYP2C19 and SHBG proteins, with favorable binding free energies indicating strong interactions. Furthermore, molecular dynamics simulations confirmed the structural stability of the protein-ligand complexes under simulated physiological conditions. These findings provide a theoretical basis for understanding the toxic targets and mechanisms of BPF in NAFLD pathogenesis and offer insights for the prevention and treatment of NAFLD associated with BPF exposure from plastic products.

Due to the estrogenic behavior of bisphenol (BP) A, industries have developed many substitutes, such as BPS and BPF. However, due to their structural similarities, adverse effects on reproduction are currently observed in various organisms, including fish. Even if new results have shown impacts of these bisphenols on many other physiological functions, their mode of action remains unclear. In this context, we proposed to better understand the impact of BPA, BPS, and BPF on immune responses (leucocyte sub-populations, cell death, respiratory burst, lysosomal presence, and phagocytic activity) and on biomarkers of metabolic detoxification (ethoxyresorufin-O-deethylase, EROD, and glutathione S-transferase, GST) and oxidative stress (glutathione peroxidase, GPx, and lipid peroxidation with thiobarbituric acid reactive substance method, TBARS) in an adult sentinel fish species, the three-spined stickleback. In order to enhance our understanding of how biomarkers change over time, it is essential to determine the internal concentration responsible for the observed responses. Therefore, it is necessary to explore the toxicokinetics of bisphenols. Thus, sticklebacks were exposed either to 100 μg/L of BPA, BPF or BPS for 21 days, or for seven days to 10 and 100 μg/L of BPA or BPS followed by seven days of depuration. Although BPS has very different TK, due to its lower bioaccumulation compared to BPA and BPF, BPS affect oxidative stress and phagocytic activity in the same way. For those reasons, the replacement of BPA by any substitute should be made carefully in terms of risk assessment on aquatic ecosystems.