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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.

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.

BackgroundEmerging studies suggest that endocrine disrupting chemicals (EDCs) in personal care and other consumer products are linked with various adverse health effects, including respiratory and reproductive effects. Despite Black persons using more personal care products than other demographic groups and having a high asthma burden, little is known regarding their consumer product use patterns and associated EDC exposures.ObjectiveTo examine the association between recent exposure to select EDCs with specific consumer products and behaviors in a cohort of 110 predominantly Black children with asthma, ages 8–17 years, living in Baltimore City, Maryland.MethodsWe quantified concentrations of bisphenol A (BPA), bisphenol S (BPS), bisphenol F, two dichlorophenols, four parabens, triclosan, benzophenone-3, and triclocarban in spot urine samples. Questionnaires were used to capture recent (last 24-h) consumer product use and behaviors. Associations between EDCs and consumer product uses/behaviors were assessed using multivariable linear regression, adjusting for age, gender, race/ethnicity, and caregiver income level. Effect estimates were expressed as geometric mean ratios of biomarker concentrations of product-users vs non-users.ResultsIncreased concentrations to select EDCs were associated with recent use of air freshener (ratios; BPA: 1.9, 95%CI 1.4–2; BPS 1.7, 95%CI 1–2.97; propyl paraben: 3.0, 95%CI 1.6–5.6), scented candles (methyl paraben: 2.6, 95%CI 1.1–6.1), and scented carpet powder (2,5-dichlorophenol: 2.8, 95%CI 1.2–6.3). Additionally, consuming canned food was associated with some increased biomarker concentrations (ratios: BPA: 1.7, 95%CI 1.2–2.4; BPS: 2.1, 95% CI: 1.2–3.6).SignificanceThese findings add to the body of evidence suggesting that recent use of select consumer products in Black children contributes to exposure of chemicals of concern and could potentially inform exposure mitigation interventions. Findings have broad potential health implications for pediatric populations and Black children who may face exposure and health disparities.ImpactLittle is known about how children’s personal care product use and consumer behaviors affect their exposures to endocrine disrupting chemicals (EDCs). This is particularly true for Black children who often experience a disparate exposure burden to many EDCs. This is a significant knowledge gap among children that are uniquely vulnerable to EDCs as they undergo critical windows of growth and development. Our findings show associations between consumer products and EDC exposures in predominantly Black children in low-income settings. Identifying EDC exposure determinants has broad health implications as many of these chemicals have been associated with adverse health risks.

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.

Bisphenol A (BPA) and bisphenol S (BPS) are frequently used in the plastic industry. Despite significant alimentary exposure, their effects on the gastrointestinal (GI) tract remain largely unknown. Cholinergic and/or purinergic neurotransmission facilitates GI tract motility and secretion, indirectly controlling the absorption and toxicity of xenobiotics. Hence, this study examined the neurochemical effects of BPA and BPS in the tripartite cholinergic myenteric synapse of CD1 mice colon. Short time exposure to both bisphenols showed a partial loss of VAChT-positive neurons and Ano-1-positive interstitial cells of Cajal (ICCs), without affecting the amount of glial cells labelled with S100β. Both bisphenols reduced the spontaneous myographic activity and the release of [3H]acetylcholine ([3H]ACh) and adenosine from stimulated myenteric neurons and pacemaker ICCs, respectively, without affecting the outflow of ATP. Overall data suggest that both bisphenols inhibit the cholinergic neurotransmission of CD1 mice colon by affecting the amount and/or function of ICCs at the tripartite myenteric synapse.

Considering the increased risk of cognitive deficits and mood disorders programming associated with bisphenol exposure, we used a preclinical model to identify short- and long-term effects of early exposure to Bisphenol A (BPA) and its replacement, Bisphenol S (BPS), on the central cholinergic and serotonergic systems. Wistar female and male rats born to dams exposed to BPA or BPS (both at 10 μg/kg/day or 50 μg/kg/day) during pregnancy and lactation were euthanized at weaning or adulthood. Cholinergic and serotonergic biomarkers were assessed in the frontal cortex and pons + medulla oblongata. BPA and BPS disrupted these systems, with outcomes depending on the specific bisphenol, biomarker, and time point. Effects also varied across brain regions and between sexes. The nicotinic cholinergic receptor showed more pronounced alterations than the presynaptic choline transporter. Both serotonergic receptors—5-HT1AR and 5-HT2R—were affected; however, the serotonergic transporter remained unchanged. Increased binding was the predominant effect for both systems. Maternal exposure to BPA, even at low doses, induces sex-dependent short- and long-term changes in the cholinergic and serotonergic systems of the progeny. BPS affects these same neurotransmitter systems, although leading to compound-specific outcomes. These results pose both BPA and BPS as neurotoxicants that compromise neurodevelopment and program disorders later in life.

Bisphenol A (BPA) is a well-known endocrine-disrupting chemical (EDC) used as a plastic enhancer in producing polycarbonate resins to manufacture hard plastics. Due to strict limitations on the manufacturing and utilization of BPA, several bisphenol substitutes, bisphenol F (BPF), bisphenol S (BPS), and bisphenol AF (BPAF), have been developed to replace it in various applications. Because of their widespread use in food containers, infant bottles, and reusable water bottles, bisphenols (BPs) have been identified in different environmental circumstances, including drinking water, seawater, industrial effluent, and endocrine systems such as human blood, urine, and breast milk. However, locating and analyzing them in different conditions has proven to be challenging. Therefore, there is a need to reduce the prevalence of BPs in the environment. The significance of advanced treatment options for treating and eliminating BPA and its alternatives from water bodies are reviewed. Also, the research gaps and future scopes are discussed in this review article. According to the literature survey, adsorption and photocatalytic degradation provide synergistic benefits for environmental challenges because of their substantial adsorption Q5 capacity, high oxidation capability, and low cost compared to alternative individual treatment options.

The introduction of bisphenol-S (BPS) in substitution of bisphenol-A (BPA) has become argumentative owing to their endocrine destructive properties and insufficient comparative ecotoxicity assessments. Thus, comparative effects of long-term, low-dose BPA and BPS exposure on the development of juvenile zebrafish ( Danio rerio ) were investigated. Juvenile zebrafish (age: 21 days; weight: ~ 61.5 mg; length: ~ 7.56 mm) were exposed to environmentally-relevant 50 µg/L of BPA, BPS, and control for ~ 60 days in triplicate. Both BPA and BPS significantly increased length (p  =  0.00) , weight (p  =  0.00) , specific growth rate (p  =  0.00) , female preponderance ( p  =  0.003 ), mortality ( p  =  0.017 ), ammonia excretion ( p  =  0.00 ), and aggression ( p  =  0.00 ) in zebrafish compared to control. Both bisphenols significantly reduced fish swimming speed in a comparable manner ( p  =  0.001 ). A notably higher female-biased-sex ratio was observed in BPS than in BPA ( p  =  0.003 ). The length gain ( p  =  0.014 ) and aggression ( p  =  0.032 ) were higher in BPA-treated fish than in BPS. However, a significant difference was not shown in body mass index ( p  =  0.295 ) and condition factor ( p  =  0.256 ) between bisphenols and control ( p  <  0.05 ). BPA and BPS exposure led to hyperplasia, mucous secretion, aneurism in fish gills, vacuolization and necrosis in liver. Therefore, BPS (~ 50 µg/L) also imposes noteworthy threats to aquatic wildlife, emphasizing the necessity of toxicity assessments and regular monitoring aiming at bespoken environmental standards for freshwater.