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This study assessed three powdered activated carbons (BETM, COCO, and SIAL) commercialized in Brazil at the bench scale in agitated reactors, analyzing their kinetic behavior and adsorptive capacity for BPS and BPA in ultrapure water. BETM exhibited the highest adsorption capacities (Q0max) for BPS and BPA at 260.62 and 264.64 mg/g, respectively, followed by SIAL, with a Q0max of 248.25 mg/g for BPS and for 231.20 mg/g BPA, and COCO, with a Q0max of 136.51 mg/g for BPS and 150.03 mg/g for BPA. The Langmuir isotherm model can describe the processes well. A pseudo-second-order model can describe the adsorption kinetics, and SIAL carbon had the highest rate constants (7.45 × 10-3 mg/g/min for BPS and 2.84 × 10-3 mg/g/min for BPA). The Weber-Morris intraparticle diffusion model suggests intraparticle diffusion as the rate-limiting step of all adsorption processes. Boyd's model confirmed more than the mechanism actuating in the bisphenol adsorption. The results suggest that adsorbents with basic surfaces, high specific surface areas, and high mesopore volumes tend to remove BPS and BPA efficiently. Therefore, activated carbons can effectively complement the existing treatment in Brazilian water treatment plants (WTPs).

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Exposure to phenols and parabens may contribute to increased maternal inflammation and adverse birth outcomes, but these effects are not well-studied in humans. This study aimed to investigate relationships between concentrations of 8 phenols and 4 parabens with 6 inflammatory biomarkers (C-reactive protein (CRP); matrix metalloproteinases (MMP) 1, 2, and 9; intercellular adhesion molecule-1 (ICAM-1); and vascular cell adhesion molecule-1 (VCAM-1)) measured at two time points in pregnancy in the PROTECT birth cohort in Puerto Rico. Linear mixed models were used, adjusting for covariates of interest. Results are expressed as the percent change in outcome per interquartile range (IQR) increase in exposure. Particularly among phenols, numerous significant negative associations were found, for example, between benzophenone-3 and CRP (-11.21 %, 95 % CI: -17.82, -4.07) and triclocarban and MMP2 (-9.87 %, 95 % CI: -14.05, -5.5). However, significant positive associations were also detected, for instance, between bisphenol-A (BPA) and CRP (9.77 %, 95 % CI: 0.67, 19.68) and methyl-paraben and MMP1 (10.78 %, 95 % CI: 2.17, 20.11). Significant interactions with female fetal sex and the later study visit (at 24-28 weeks gestation) showed more positive associations compared to male fetal sex and the earlier study visit (16-20 weeks gestation). Our results suggest that phenols and parabens may disrupt inflammatory processes pertaining to uterine remodeling and endothelial function, with important implications for pregnancy outcomes. More research is needed to further understand maternal inflammatory status in an effort to improve reproductive and developmental outcomes.

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A laccase-based catalytic reactor was developed into a polydimethylsiloxane (PDMS) microfluidic device, allowing the degradation of different concentrations of the emergent pollutant, Bisphenol-A (BPA), at a rate similar to free enzyme. Among the immobilizing agents used, 1-Ethyl-3-(3-dimethylaminopropyl) carbodiimide (EDC) was capable of immobilizing a more significant amount of the laccase enzyme in comparison to glutaraldehyde (GA), and the passive method (2989, 1537, and 1905 U/mL, respectively). The immobilized enzyme inside the microfluidic device could degrade 55 ppm of BPA at a reaction rate of 0.5309 U/mL*min with a contaminant initial concentration of 100 ppm at room temperature. In conclusion, the design of a microfluidic device and the immobilization of the laccase enzyme successfully allowed a high capacity of BPA degradation.

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Bisphenol A is one of the most used components of the polycarbonate plastic industry in the word. This contaminant has disrupting effect in cells in in vitro and in vivo in fish. This study evaluated for the first time the cytotoxicity, oxidative stress and apoptosis induced by bisphenol A (BPA) in head-kidney and spleen leukocytes isolated from Pacific red snapper Lutjanus peru. Head-kidney and spleen leukocytes were exposed to 100, 1000 and 10,000 µg/mL of BPA at 2 and 24 h. Results showed cytotoxicity of BPA at 1000 and 10,000 µg/mL. Cell viability > 80% was observed in leukocytes exposed to 100 µg/mL for 2 h; thus, this concentration was selected for the remainder of the study. Reactive oxygen species (ROS) production, analyzed by DCF-DA and NBT assays, significantly increased in those leukocytes exposed to BPA compared to controls after 2 or 24 h. Superoxide dismutase and catalase activities increased in head-kidney leukocytes after 24 h of BPA exposure. Apoptosis was inferred from caspase (casp-1 and casp-3), granzyme A (granz-A) and perforin 1 (perf-1) gene expression, which was significantly up-regulated, at 2 h BPA exposure in head-kidney leukocytes, and from granz-A and perf-1, which were up-regulated, after 24 h BPA exposure in spleen leukocytes. Short cytoplasmic prolongations and membrane blebs, suggestive of apoptosis, were observed by scanning electron microscopy. These data suggest that BPA at 100 µg/mL induces cytotoxicity, oxidative stress, apoptosis in Pacific red snapper head-kidney and spleen leukocytes.

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BACKGROUND: Polycystic ovary syndrome (PCOS) is an endocrine disorder characterized by anovulation, hyperandrogenism, and polycystic ovarian morphology. Its etiology is uncertain and one of the hypotheses is that environmental factors, such as the bisphenol A (BPA) endocrine disruptor, may be involved. OBJECTIVE: To investigate the association between exposure to BPA and PCOS. SEARCH STRATEGY: Research was conducted focusing on studies published in English, Portuguese, and Spanish from January 2001 to March 2023 and available in Embase, Medline/PubMed, Rima, Lilacs, Scielo, Google academic, and SCI databases. SELECTION CRITERIA: Studies in humans that evaluated the association between exposure to BPA and a diagnosis of PCOS. DATA COLLECTION AND ANALYSIS: Following PRISMA guidelines, study characteristics and relevant data were extracted. MAIN RESULTS: Selection of 15 case-control and 7 cross-sectional studies with a total of 1682 PCOS patients. The studies were carried out in China, Poland, Turkey, Japan, Greece, Italy, the USA, Iran, Iraq, Egypt, India, Czechia, and Slovakia. A positive relationship between exposure to BPA and PCOS was described in19 studies (1391 [82.70%] of the PCOS patients). The fluids used in the studies were serum, urine, plasma, and follicular fluid. BPA was measured by ELISA and by chromatography (HPLC, HPLC-MS/MS, GC-MS, and GC-MS/MS). Diagnosis of PCOS used Rotterdam criteria in 15, NIH 1999 in 3, AE&PCOS Society in 2, similar to the Rotterdam criteria in 1, and criteria not informed in 1. Androgens were measured in 16 studies; in 12, hyperandrogenism was positively associated with BPA. BPA level was related to body mass index (BMI) in studies. In 15 studies independently of BMI, women with PCOS had higher BPA levels. Carbohydrate metabolism disorders were evaluated in 12 studies and in 6 a positive correlation was found with BPA levels. Lipid profile was evaluated in seven studies and in only one the correlation between lipid profile and BPA levels was present. CONCLUSIONS: Exposure to BPA is positively associated with PCOS, mainly with the hyperandrogenism.

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Plastics are everywhere. They are in many goods that we use every day. However, they are also a source of pollution. In 2022, at the resumed fifth session of the United Nations Environment Assembly, a historic resolution was adopted with the aim of convening an Intergovernmental Negotiating Committee to develop an international legally binding instrument on plastic pollution, including in the marine environment, with the intention to focus on the entire life cycle of plastics. Plastics, in essence, are composed of chemicals. According to a recent report from the secretariat of the Basel, Rotterdam, and Stockholm conventions, around 13 000 chemicals are associated with plastics and plastic pollution. Many of these chemicals are endocrine-disrupting chemicals and, according to reports by members of the Endocrine Society and others, exposure to some of these chemicals causes enormous costs due to the development of preventable diseases. The global plastics treaty brings the opportunity for harmonized, international regulation of chemicals with endocrine disrupting properties present in plastic products.

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PCOS is an endocrine disorder characterized by chronic anovulation, hyperandrogenism, and polycystic ovaries. Its etiology is uncertain. It is debated whether BPA would be a component of the environmental factor in the etiology of PCOS. Contamination by BPA can occur from food packaging (exposure during the diet) and through skin absorption and/or inhalation. It can be transferred to the fetus via the placenta or to the infant via breast milk, and it can be found in follicular fluid, fetal serum, and amniotic fluid. The phenolic structure of BPA allows it to interact with Estrogen Receptors (ERs) through genomic signaling, in which BPA binds to nuclear ERα or Erß, or through nongenomic signaling by binding to membrane ERs, prompting a rapid and intense response. With daily and constant exposure, BPA's tendency to bioaccumulate and its ability to activate nongenomic signaling pathways can alter women's metabolic and reproductive function, leading to hyperandrogenism, insulin resistance, obesity, atherogenic dyslipidemia, chronic inflammatory state, and anovulation and favoring PCOS. The harmful changes caused by BPA can be passed on to future generations without the need for additional exposure because of epigenetic modifications. Not only high BPA levels can produce harmful effects, but at low levels, BPA may be harmful when exposure occurs during the most vulnerable periods, such as the fetal and neonatal periods, as well as during the prepubertal age causing an early accumulation of BPA in the body. Learning how BPA participates in the pathogenesis of PCOS poses a challenge and further studies should be conducted.

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Phthalates and bisphenol A (BPA) are compounds widely used as raw materials in the production of plastics, making them ubiquitous in our daily lives. This results in widespread human exposure and human health hazards. Although efforts have been conducted to evaluate the risk of these compounds in diverse regions around the world, data scattering may mask important trends that could be useful for updating current guidelines and regulations. This study offers a comprehensive global assessment of human exposure levels to these chemicals, considering dietary and nondietary ingestion, and evaluates the associated risk. Overall, the exposure daily intake (EDI) values of phthalates and BPA reported worldwide ranged from 1.11 × 10-7 to 3 700 µg kg bw-1 d-1 and from 3.00 × 10-5 to 6.56 µg kg bw-1 d-1, respectively. Nevertheless, the dose-additive effect of phthalates has been shown to increase the EDI up to 5 100 µg kg bw-1 d-1, representing a high risk in terms of noncarcinogenic (HQ) and carcinogenic (CR) effects. The worldwide HQ values of phthalates and BPA ranged from 2.25 × 10-7 to 3.66 and from 2.74 × 10-7 to 9.72 × 10-2, respectively. Meanwhile, a significant number of studies exhibit high CR values for benzyl butyl phthalate (BBP) and di(2-ethylhexyl) phthalate (DEHP). Moreover, DEHP has shown the highest maximum mean CR values for humans in numerous studies, up to 179-fold higher than BBP. Despite mounting evidence of the harmful effects of these chemicals at low-dose exposure on animals and humans, most regulations have not been updated. Thus, this article emphasizes the need for updating guidelines and public policies considering compelling evidence for the adverse effects of low-dose exposure, and it cautions against the use of alternative plasticizers as substitutes for phthalates and BPA because of the significant gaps in their safety.

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Bisphenol A (BPA) is an endocrine-disrupting chemical with a potential role in endocrine cancers. However, the effects of BPA on the salivary glands have been barely explored. We investigated the impact of in vivo sub-chronic exposure to BPA and its in vitro effects on human salivary gland mucoepidermoid carcinoma cell lines. Male and female mice were exposed to BPA (30 mg/kg/day). Sublingual and submandibular salivary glands from an estrogen-deficiency model were also analyzed. BPA concentration in salivary glands was evaluated by gas chromatography coupled to ion trap mass spectrometry. Immunohistochemical analysis using anti-p63 and anti-α-SMA antibodies was performed on mouse salivary gland tissues. Gene expression of estrogen receptors alpha and beta, P63 and α-SMA was quantified in mouse salivary gland and/or mucoepidermoid (UM-HMC-1 and UM-HMC-3A) cell lines. Cell viability, p63 and Ki-67 immunostaining were evaluated in vitro. BPA disrupted the tissue architecture of the submandibular and sublingual glands, particularly in female mice, and increased the expression of estrogen receptors and p63, effects that were accompanied by significant BPA accumulation in these tissues. Conversely, ovariectomy slightly impacted BPA-induced morphological changes. In vitro, BPA did not affect the proliferation of neoplastic cells, but augmented the expression of p63 and estrogen receptors. The present data highlight a potential harmful effect of BPA on salivary gland tissues, particularly in female mice, and salivary gland tumor cells. Our findings suggest that estrogen-dependent pathways may orchestrate the effects of BPA in salivary glands.

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This systematic review provides an update on the effect of nanofibers as reinforcement on resin-based dental materials. A bibliographic search was conducted in MEDLINEPubMed, Embase, Web of Science, Scopus, BVS (LILACS, BBO e IBECS), Cochrane, LIVIVO, and gray literature (BDTD) to identify relevant articles up to May 2021. In vitro studies that evaluated and compared the mechanical properties of nanofibers resin-based composite materials, were eligible. No publication year or language restriction was applied, and methodological quality was assessed using two methods. In a total of 6100 potentially eligible studies, 81 were selected for full-text analysis and 35 were included for qualitative analysis. Of the 35 included studies, a total of 29 studies evaluated the flexural strength (FS) of the materials. These groups were distinguished according to the resin-based materials tested and nanofiber types. Most of the studies evaluated materials composed of glass fibers and demonstrated higher values of FS when compared to resin-based materials without nanofibers. The incorporation of nanofibers into resin-based dental materials improved the mechanical properties compared to resin-based materials without nanofibers, suggesting better performance of these materials in high-stressbearing application areas. Further clinical studies are required to confirm the efficacy of resin-based materials with nanofibers.

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Triple negative breast cancer (TNBC) is a subtype of breast tumor characterized for the absence of estrogen and progesterone receptors expression and low HER2/neu expression. Bisphenol A (BPA) is an endocrine disrupting chemical with estrogenic activity that has been associated with increasing rates of breast cancer. Moreover, BPA is a solid organic synthetic chemical employed in the manufacture of many consumer products, epoxy resins and polycarbonate plastics including baby bottles, containers for food and beverages, and the lining of beverage cans. The G-protein-coupled estrogen receptor (GPER) is activated by endogenous hormones and synthetic ligands, such as BPA. GPER is expressed in TNBC cells and its expression is associated with larger tumor size, metastasis and worse survival prognosis. In breast cancer cells, BPA induces activation of signal transduction pathways that mediates migration and invasion via GPER in human TNBC MDA-MB-231 cells. In this study, we demonstrate that BPA induces an increase of GPER expression and its translocation from cytosol to cytoplasmic membrane, metalloproteinase (MMP)-2 and MMP-9 secretion, migration and invasion in murine TNBC 4T1 cells. In a murine TNBC model "in vivo" using 4T1 cells, BPA induces the formation of mammary tumors with more weight and volume, and an increase in the number of mice with metastasis to lung and nodules in lung compared with tumors and metastasis to lung of untreated Balb/cJ mice. In conclusion, our findings demonstrate that BPA mediates the growth of mammary primary tumors and metastasis to lung in a murine model of breast cancer.

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The current industrial and human activities scenario has accelerated the widespread use of endocrine-disrupting compounds (EDCs), which can be found in everyday products, including plastic containers, bottles, toys, cosmetics, etc., but can pose a severe risk to human health and the environment. In this regard, fungal bioremediation appears as a green and cost-effective approach to removing pollutants from water resources. Besides, immobilizing fungal cells onto nanofibrous membranes appears as an innovative strategy to improve remediation performance by allowing the adsorption and degradation to occur simultaneously. Herein, we developed a novel nanostructured bioremediation platform based on polyacrylonitrile nanofibrous membrane (PAN NFM) as supporting material for immobilizing an endophytic fungus to remove bisphenol A (BPA), a typical EDC. The endophytic strain was isolated from Handroanthus impetiginosus leaves and identified as Phanerochaete sp. H2 by molecular methods. The successful assembly of fungus onto the PAN NFM surface was confirmed by scanning electron microscopy (SEM). Compared with free fungus cells, the PAN@H2 NFM displayed a high BPA removal efficiency (above 85%) at an initial concentration of 5 ppm, suggesting synergistic removal by simultaneous adsorption and biotransformation. Moreover, the biotransformation pathway was investigated, and the chemical structures of fungal metabolites of BPA were identified by ultra-high performance liquid chromatography - high-resolution mass (UHPLC-HRMS) analysis. In general, our results suggest that by combining the advantages of enzymatic activity and nanofibrous structure, the novel platform has the potential to be applied in the bioremediation of varied EDCs or even other pollutants found in water resources.

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Amongst the many treatments available for the removal of emerging contaminants in wastewater, microalgal cultures have been shown to be effective. However, the effectiveness of exposure of a native microalgal consortium to emerging contaminants such as bisphenol-A (BPA) and triclosan (TCS) to determine the half-maximum effective concentrations (EC50) has not yet been determined. The effect on growth and nutrient removal of such a treatment as well as on the production of biomolecules such as carbohydrates, lipids, and proteins are, at present, unknown. In this study, the EC50 of BPA and TCS (96-hour experiments) was determined using a consortium of native microalgae (Scenedesmus obliquus and Desmodesmus sp.) to define the maximum tolerance to these contaminants. The effect of BPA and TCS in synthetic wastewater (SWW) was investigated in terms of microalgal growth, chlorophyll a (Chl-a), carbohydrate, lipid, and protein content, as well as nutrient removal. Assays were performed in heterotrophic conditions (12/12 light/dark cycles). EC50-96 h values of 17 mg/L and 325 µg/L for BPA and TCS, respectively, were found at 72 h. For an initial microalgal inoculum of ≈ 300 mg TSS/L (total suspended solids per litre), growth increased by 16.1% when exposed to BPA and 17.78% for TCS. At ≈ 500 mg TSS/L, growth increased by 8.25% with BPA and 9.92% with TCS, respectively. At the EC50-96 h concentrations determined in the study, BPA and TCS did not limit the growth of microalgae in wastewater. Moreover, they were found to stimulate the content of Chl-a, carbohydrates, lipids, proteins, and enhance nutrient removal. AVAILABILITY OF DATA AND MATERIAL: Data sharing not applicable to this article as no datasets were generated or analysed during the present study.

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Bisphenol A (BPA) is a xenobiotic with endocrine disruptor properties which interacts with various receptors, eliciting a cellular response. In the plastic industry, BPA is widely used in the production of polycarbonate and epoxy-phenolic resins to provide elastic properties. It can be found in the lining of canned foods, certain plastic containers, thermal printing papers, composite dental fillings, and medical devices, among other things. Therefore, it is a compound that, directly or indirectly, is in daily contact with the human organism. BPA is postulated to be a factor responsible for the global epidemic of obesity and non-communicable chronic diseases, belonging to the obesogenic and diabetogenic group of compounds. Hence, this endocrine disruptor may be responsible for the development of metabolic disorders, promoting in fat cells an increase in proinflammatory pathways and upregulating the expression and release of certain cytokines, such as IL6, IL1ß, and TNFα. These, in turn, at a systemic and local level, are associated with a chronic low-grade inflammatory state, which allows the perpetuation of the typical physiological complications of obesity.

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With the growing population, access to clean water is one of the 21st-century world's challenges. For this reason, different strategies to reduce pollutants in water using renewable energy sources should be exploited. Photocatalysts with extended visible light harvesting are an interesting route to degrade harmful molecules utilized in plastics, as is the case of Bisphenol A (BPA). This work uses a microwave-assisted route for the synthesis of two photocatalysts (BiOI and Bi2MoO6). Then, BiOI/Bi2MoO6 heterostructures of varied ratios were produced using the same synthetic routes. The BiOI/Bi2MoO6 with a flower-like shape exhibited high photocatalytic activity for BPA degradation compared to the individual BiOI and Bi2MoO6. The high photocatalytic activity was attributed to the matching electronic band structures and the interfacial contact between BiOI and Bi2MoO6, which could enhance the separation of photo-generated charges. Electrochemical, optical, structural, and chemical characterization demonstrated that it forms a BiOI/Bi2MoO6 p-n heterojunction. The free radical scavenging studies showed that superoxide radicals (O2•-) and holes (h+) were the main reactive species, while hydroxyl radical (•OH) generation was negligible during the photocatalytic degradation of BPA. The results can potentiate the application of the microwave synthesis of photocatalytic materials.

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The female prostate is associated with the urogenital system and presents homology in morphological terms with the male prostate. Due to its responsiveness to endogenous hormones, this gland is under a constant risk of developing prostatic pathologies and neoplasia when exposed to certain exogenous compounds. Bisphenol A (BPA) is an endocrine disruptor found in different plastic and resin products. Studies have emphasized the effects of perinatal exposure to this compound on different hormone-responsive organs. However, there have been few studies highlighting the influence on female prostate morphology of perinatal exposure to BPA. The objective of this study was to describe the histopathological alterations caused by perinatal exposure to BPA (50 µg/kg) and 17-ß estradiol (E2) (35 µg/kg) in the prostate of adult female gerbils. The results showed that E2 and BPA induced proliferative lesions in the female prostate and acted along similar pathways by modulating steroid receptors in the epithelium. BPA was also found to be a pro-inflammatory and pro-angiogenic agent. The impacts of both agents were marked in the prostatic stroma. An increase in the thickness of the smooth muscle layer and a decrease in AR expression were observed, but no alterations in the expression of ERα and ERß, leading to estrogenic sensitivity of the prostate. However, a peculiar response of the female prostate was to diminish the collagen frequency under BPA exposure correlated to smooth muscle layer. These data therefore indicate the development of features related to estrogenic and non-estrogenic tissue repercussions by BPA perinatally exposure in gerbil female prostate.

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Inflammation in the established tumor microenvironment (TME) is often associated with a poor prognosis of breast cancer. Bisphenol A (BPA) is an endocrine-disrupting chemical that acts as inflammatory promoter and tumoral facilitator in mammary tissue. Previous studies demonstrated the onset of mammary carcinogenesis at aging when BPA exposure occurred in windows of development/susceptibility. We aim to investigate the inflammatory repercussions of BPA in TME in mammary gland (MG) during neoplastic development in aging. Female Mongolian gerbils were exposed to low (50 µg/kg) or high BPA (5000 µg/kg) doses during pregnancy and lactation. They were euthanized at 18 months of age (aging) and the MG were collected for inflammatory markers and histopathological analysis. Contrarily to control MG, BPA induced carcinogenic development mediated by COX-2 and p-STAT3 expression. BPA was also able to promote macrophage and mast cell (MC) polarization in tumoral phenotype, evidenced by pathways for recruitment and activation of these inflammatory cells and tissue invasiveness triggered by tumor necrosis factor-alpha and transforming growth factor-beta 1 (TGF-ß1). Increase of tumor-associated macrophages, M1 (CD68 + iNOS+) and M2 (CD163+) expressing pro-tumoral mediators and metalloproteases was observed; this aspect greatly contributed to stromal remodeling and invasion of neoplastic cells. In addition, the MC population drastically increased in BPA-exposed MG. Tryptase-positive MCs increased in disrupted MG and expressed TGF-ß1, contributing to EMT process during carcinogenesis mediated by BPA. BPA exposure interfered in inflammatory response by releasing and enhancing the expression of mediators that contribute to tumor growth and recruitment of inflammatory cells that promote a malignant profile.

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Bisphenol A (BPA) promotes colon cancer by altering the physiological functions of hormones. Quercetin (Q) can regulate signaling pathways through hormone receptors, inhibiting cancer cells. The antiproliferative effects of Q and its fermented extract (FEQ, obtained by Q gastrointestinal digestion and in vitro colonic fermentation) were analyzed in HT-29 cells exposed to BPA. Polyphenols were quantified in FEQ by HPLC and their antioxidant capacity by DPPH and ORAC. Q and 3,4-dihydroxyphenylacetic acid (DOPAC) were quantified in FEQ. Q and FEQ exhibited antioxidant capacity. Cell viability with Q+BPA and FEQ+BPA was 60% and 50%, respectively; less than 20% of dead cells were associated with the necrosis process (LDH). Treatments with Q and Q+BPA induced cell cycle arrest in the G0/G1 phase, and FEQ and FEQ+BPA in the S phase. Compared with other treatments, Q positively modulated ESR2 and GPR30 genes. Using a gene microarray of the p53 pathway, Q, Q+BPA, FEQ and FEQ+BPA positively modulated genes involved in apoptosis and cell cycle arrest; bisphenol inhibited the expression of pro-apoptotic and cell cycle repressor genes. In silico analyses demonstrated the binding affinity of Q > BPA > DOPAC molecules for ERα and ERß. Further studies are needed to understand the role of disruptors in colon cancer.

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In this work, analytical strategies were developed based on the technique of hollow fiber liquid-phase microextraction and chromatographic methods (LC-UV and GC/MS). These methods allowed the identification of the main Bisphenol-A by-products applying heterogeneous photocatalysis in water samples. BPA degradation in this study was in the order of 90%, and the conditions used in the HF-LPME were optimized through 23 factorial design (6 cm fiber length, stirring speed of 750 rpm, and an extraction time of 30 min). Using a HF-LPME/GC-MS analytical strategy, it was possible to identify six by-products of BPA photodegradation, two of which have not been reported in the literature so far. This knowledge was quite important since the degradation can lead to the formation of more toxic and persistent by-products than the BPA. With the Toxtree software, three degradation products were found to be persistent to the environment, in addition to BPA; however, in 360 minutes of reaction, chromatographic peaks of the precursors were not identified, suggesting that there may have been a total degradation of these compounds. The results showed a great application potential of a miniaturized extraction technique to extract and pre-concentrate the degradation products of emerging contaminants.

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This systematic review explored the literature pertaining to patient exposure to bisphenol A (BPA) through medical-hospital devices. The acronym PICO: Patient (Medical-hospital devices), Intervention/Exposure (Bisphenol A), Comparison (Different grades of exposure) and Outcome (Assessment of exposure levels) was used. The databases used were LILACS, IBECS, MEDLINE, Capes Journal Portal, Food Science Source, FSTA and CINAHL with Full Text from EBSCO, Embase and Scopus by Elsevier, Web of Science and SCIELO. A total of 9747 references were found. After removing duplicate records, 7129 studies remained. After applying exclusion criteria and qualitative analysis, 12 articles remained. Studies have shown associations between the use of medical-hospital devices and patients' exposure to BPA. For chronic renal patients, there was an association between plasma BPA and disease severity. This review identifies that exposure to BPA is increased after the use of medical-hospital devices. More studies that address the clinical outcome of patients exposed to medical-hospital materials containing BPA are needed.

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