This review aims to provide a comprehensive overview to understand the role of pollution in the development of noncommunicable diseases (NCDs), with a focus on metabolic diseases.

In the context of NCDs, the incidence of metabolic diseases such as obesity and diabetes are increasing at an alarming rate. In addition to the well-known role of the so-called "obesogenic" environment, characterized by unhealthy diet and physical inactivity, great attention has been paid in recent years to the effects of pollution. Indeed, progressive urbanization has been associated with increased exposure to pollutants. The harmful effects of some pollutants on the endocrine system have been known for decades, but data on the metabolic impact of pollution are rather recent. Pollution in its various forms promotes a systemic inflammatory state, insulin resistance, and oxidative stress, which appear to be closely associated with increased risk of NCD, particularly obesity and diabetes.

In conclusion, urbanization has so far had a predominantly negative impact on collective health, but a better understanding of the mechanisms linking pollution to metabolic health is crucial to implement preventive strategies, including careful urban planning to improve community health, understood not only as the absence of disease but also as psychological and social well-being, overcoming the risks associated with urbanization.

Endocrine-disrupting chemicals (EDCs) are natural or synthetic compounds that are ubiquitous in the environment and in daily-usage products and interfere with the normal function of the endocrine system leading to adverse health effects in humans. Exposure to these chemicals might elevate the risk of metabolic disorders, developmental and reproductive defects, and endocrine-related cancers. Prostate cancer is the most common hormone-dependent cancer in men, and the fifth leading cause of cancer-related mortality, partly owing to a lack of knowledge about the mechanisms that lead to aggressive castration-resistant forms. In addition to the dependence of early-stage prostate cancer on androgen actions, the prostate is a target of oestrogenic regulation. This hormone dependence, along with the fact that exogenous influences are major risk factors for prostate cancer, make the prostate a likely target of harmful actions from EDCs. Various sources of EDCs and their different modes of action might explain their role in prostate carcinogenesis.

The pervasive presence of endocrine-disrupting chemicals (EDCs), particularly progesterone, in aquatic ecosystems poses significant ecological and human health risks, necessitating the development of sustainable and efficient removal strategies. This study introduces an innovative, eco-friendly approach utilizing non-edible reishi mushroom (Ganoderma lucidum) and its calcined form as natural adsorbents for progesterone removal while simultaneously exploring the potential of the formed composites as sustainable agricultural amendments. The adsorption efficiency of both reishi mushroom powder and its calcined form was systematically optimized under varying pH, adsorbent dose, temperature, and contact time conditions. The adsorption capacities of reishi mushroom and its calcined form for progesterone were assessed using nine non-linear isotherm models. Among these, the Langmuir and Freundlich models provided the best fit to the experimental data (R 2 ∼ 0.99), demonstrating high adsorption capacities of 90.52 mg g-1 for reishi mushroom and 118.10 mg g-1 for calcined reishi mushroom under optimal conditions (pH 3, 25 °C, 0.1 g and 0.075 g doses, respectively) following pseudo-second-order and mixed-order kinetic models. Both materials were fully characterized before and after the adsorption process using XRD, FTIR, and SEM techniques. Thermodynamic analysis revealed the process to be exothermic, spontaneous, and highly ordered, driven by hydrophobic interactions and van der Waals forces. Molecular docking analysis shows that ganoderic acid A and progesterone bind strongly to key plant hormone receptors (GID1, TIR1, BRI1), indicating their potential to enhance plant growth by influencing gibberellin, auxin, and brassinosteroid signaling pathways. Beyond environmental remediation, the formed composites exhibited exceptional potential in enhancing agricultural productivity. Composite treatments, particularly progesterone adsorbed on calcined reishi mushroom, significantly improved seed germination rates (95%), shoot-to-root elongation (2.5 : 1), and overall plant growth (39 cm height, 200 g fresh weight). Soil quality assessments revealed increased organic matter content and improved fertility, highlighting the dual benefit of these adsorbents in environmental remediation and sustainable agriculture. The greenness profile of the proposed method, evaluated using NEMI, AGP, and Modified GAPI metrics, further underscores its eco-sustainability, with an eco-scale score of 94 and a BAGI blueness score of 75, affirming its alignment with green analytical chemistry principles. This study introduces a novel, cost-effective, and eco-friendly method for progesterone removal while pioneering the use of waste-derived adsorbents in circular agriculture. By utilizing reishi mushroom and its calcined form, this research addresses both water contamination and sustainable farming, advancing eco-friendly technologies.

Glucocorticoids (GCs) are synthetic drugs widely used for treating several diseases with inflammatory pathophysiology. In general, 1-20% of the concentration of GCs initially administered is eliminated unchanged in the urine while still in its active form, and therefore, fractions of GCs are constantly released in effluents. Currently, water treatment plants do not have sufficiently effective technologies to remove these substances completely, favoring the presence of these emerging pollutants in the effluents of wastewater treatment plants. In this context, we conduct a systematic review to identify studies that found GCs in surface water. The general data of the included studies, the GCs found and their concentration, the water body where the GCs were found, and the place and date of sampling were summarized. GCs have already been found in the surface water of 24 countries, mainly China, Malaysia, and the United States. Countries with the highest concentrations of GCs found in surface water were Mexico, India, and Brazil. Betamethasone, budesonide, corticosterone, cortisol, cortisone, dexamethasone, fludrocortisone, fluticasone, hydrocortisone, methylprednisolone, prednisolone, prednisone, and triamcinolone were reported at concentrations ranging from 0.00098 to 24760 ng/L, including in water for human consumption. Revised data showed that the real presence of these substances worldwide is still underestimated, requiring further studies to determine their real distribution. Furthermore, we believe that some strategies can be adopted to mitigate surface water contamination by GCs, such as the intensification of public programs about educational activities related to the rational use of medicines, and the urgent need to improve and expand the water treatment methods.

Antepartum depression arises from hormonal, environmental, and genetic factors. Endocrine-disrupting compounds (EDCs) disrupt the endocrine system, increasing vulnerability to depressive symptoms. Genetic variations, particularly in estrogen receptor (ER) pathways, are linked to peripartum depression, with EDCs exposure exacerbating these effects by further disrupting estrogen pathways. Additionally, EDCs exposure in antepartum women is associated with adverse maternal and fetal outcomes. Hence, study aims to evaluate the relationship between EDCs and genetic polymorphisms with antepartum depressive symptoms and assess the impact of EDCs and antepartum depressive symptoms on maternal and fetal outcomes.

We conducted a prospective cohort study to evaluate depressive symptoms during pregnancy in 400 women between 28 and 40 weeks of gestation, utilizing the Edinburgh Postnatal Depression Scale (EPDS). Women with elevated EPDS scores and matched controls were assessed for urinary bisphenol A and methylparaben levels, along with ER1 gene polymorphism using Tetra-ARMS PCR. The cohort group was followed to document maternal-fetal outcomes, with statistical analyses performed using SPSS.

Twenty-three percent of antepartum women exhibited depressive symptoms. A linear regression analysis indicated that a one-unit increase in log bisphenol A levels corresponded to a 1.1-point increase in EPDS-measured depressive symptom scores. ER1 polymorphisms (A/A and T/A genotypes) and the frequency of the A allele correlate with an increased risk of experiencing antepartum depressive symptoms. Elevated EPDS scores correlated with pregnancy-induced hypertension, anemia, hypothyroidism, and fetal distress. Notably, bisphenol A and methylparaben levels were higher in homozygous genotypes, with bisphenol A linked to maternal anemia, hypothyroidism, and fetal distress, while methylparaben was associated with maternal anemia and fetal distress.

Nearly a quarter of antepartum women displayed depressive symptoms, correlating with elevated endocrine disruptor levels. Higher bisphenol A and methylparaben levels were observed in individuals with mutant genotypes, indicating gene-environment interactions with antepartum depressive symptoms. The observed association of EDCs with maternal anemia, hypothyroidism, and fetal distress highlights the possible effect of EDC on maternal and fetal health.

Iodine is a critical trace element in the human body. It is primarily obtained through dietary sources such as dairy products, seafood, fish, eggs and certain vegetables. Iodine plays an essential role in various bodily functions, most notably in producing the thyroid hormones, triiodothyronine and thyroxine. Additionally, it influences the immune, cardiovascular, reproductive and gastrointestinal systems. Historically, iodine deficiency has been a significant global health issue; however, over the past decade, there has been a rise in iodine excess. This surge has been primarily attributed to inadequate monitoring and over-iodization of salt. Despite the well-documented consequences of iodine deficiency, the ramifications of excessive iodine intake remain underexplored. In view of rising global infertility rates, excess iodine has been linked to significant reproductive health effects. These include decreased sperm count, motility and morphology in males, as well as adverse pregnancy outcomes in females, such as maternal thyroid dysfunction and congenital hypothyroidism. This mini-review aims to collate and analyze current literature pertaining to the effects of iodine excess on reproductive health and shed light on its increasing incidence worldwide. Further research on the biological and clinical effects of iodine excess is required to derive a better understanding of this issue. Given the rising prevalence of iodine excess, it is crucial to raise awareness and implement proactive measures to prevent it from escalating into a major public health crisis in the future.

Altrenogest is one of the most commonly used steroid hormones; however, there are currently no relevant reports on monospecific molecular recognition elements and immunoassay methods for altrenogest. Herein, a computer-aided precise hapten design strategy was proposed for monospecific monoclonal antibodies (mAb) preparation. Based on this strategy, a monospecific and sensitive mAb-D7 was prepared for the first time. The mAb-D7 has the 50 % inhibitory concentration (IC50) of 0.12 ng/mL for altrenogest and does not cross-react with other common steroid hormones. Additionally, a single-chain variable fragment (scFv) for altrenogest was constructed for the first time, which exhibits an IC50 of 1.7 ng/mL for altrenogest. The molecular recognition mechanism studies showed the monospecific mAb-D7 to altrenogest originated from the amino acids PHE-94 and LEU-237, demonstrating the reliability of this strategy. Finally, two monospecific, rapid, and sensitive immunoassays were established for altrenogest in pork and pork liver for the first time.

Endocrine disruptors (EDs) are environmental chemicals that interfere with hormone function, posing significant risks to human health, including the cardiovascular system. This review comprehensively examines the impact of EDs on cardiovascular health, with a specific focus on sex differences observed in various models. Utilizing in-vitro studies, in vivo animal models, and human clinical data, we delineate how sex-specific hormonal environments influence the cardiovascular effects of ED exposure. In vitro studies highlight cellular and molecular mechanisms that differ between male and female-derived cells. In vivo models reveal distinct physiological responses and susceptibilities to EDs, influenced by sex hormones. Human studies provide epidemiological evidence and clinical observations that underscore the variability in cardiovascular outcomes between men and women. This review underscores the necessity of considering sex as a critical factor in understanding the cardiovascular implications of ED exposure, advocating for gender-specific risk assessment and therapeutic strategies. The findings aim to enhance awareness and inform future research and policy-making to mitigate the adverse cardiovascular effects of EDs across different sexes.

Fetal exposure to endocrine-disrupting chemicals (EDCs) has been associated with reduced male fecundity, but with few studies considering chemical mixtures.

We assessed the association between fetal exposure to a mixture of EDCs and biomarkers of male fecundity in young adulthood.

The study population comprised 841 young adult males enrolled in the Fetal Programming of Semen Quality cohort, established as a male offspring sub-cohort within the Danish National Birth Cohort. Maternal blood samples were analyzed for concentrations of per- and polyfluoroalkyl substances (PFAS), phthalate metabolites, and triclosan. We used quantile g-computation to estimate the change in semen characteristics, testicular volume, and reproductive hormone levels with 95% confidence intervals (CI) per one-quartile increase in all chemicals within three chemical mixtures; an overall chemical mixture, a PFAS mixture, and a non-persistent chemical mixture.

Fetal exposure to a one-quartile increase in the overall chemical mixture was associated with 4.0 million/mL lower sperm concentration (95% CI: -9.1, 1.1), 16.1 million lower total sperm count (95% CI: -33.8, 1.6), 0.5 mL smaller testicular volume (95% CI: -1.2, 0.3), 5% higher proportion of non-progressive and immotile spermatozoa (95% CI: 0.99, 1.11), and 7% higher concentration of FSH (95% CI: 0.99, 1.16), but with limited precision. Effect sizes were greatest in magnitude for sperm concentration and total sperm count. We observed somewhat similar associations for the PFAS mixture and no associations for the non-persistent chemical mixture.

Results suggest that fetal exposure to an overall mixture of EDCs may be adversely associated with several biomarkers of male fecundity, but findings are also compatible with null associations. These associations, if true, appeared to be driven by PFAS, but misclassification due to a single measurement of the phthalate metabolites and triclosan may have attenuated the results.

4-Octylphenol, a major environmental degradation product of alkylphenols (Aps) used in industry, is an endocrine-disrupting chemical with significant estrogenic activity. It is one of the most toxic Aps, poorly biodegradable in the environment, and can accumulate in organisms through the food chain, thereby affecting the male reproductive system. In this study, the effect of 4-octylphenol on male reproductive health was analyzed. Male pubertal mice were exposed to 4-octylphenol at doses of 0, 1, 10, and 100 mg/kg once daily for 28 days. Our findings indicated that pubertal exposure to 4-octylphenol has significant negative effects on the male reproductive system. Pubertal mice exposed to 4-octylphenol exhibited dose-dependent reproductive toxicity. In the medium- and high-dose groups, a significant reduction in testicular mass, structural damage to the seminiferous tubules, increased oxidative stress and apoptosis within the testicular tissue, and a decline in sperm quality were observed. Additionally, autophagy processes in the testicular tissue, germ cell proliferation, and meiotic processes are inhibited. Serum testosterone and estradiol levels decreased, whereas oxidative stress levels in the testes and spermatozoa increased. In contrast, the low-dose group showed only a reduction in body weight, a decrease in motile sperm count, and mild oxidative stress in the testes without significant pathological changes in western blot experiments. These results indicate that 4-octylphenol exposure during puberty caused reproductive toxicity in male mice.

The presence of endocrine disrupting chemicals (EDCs) in water can impart detrimental effects on public health by mimicking the behaviors of natural hormones and their associated receptors in human body. Studies have demonstrated that ligninolytic enzymes such as laccase can degrade various phenolic compounds, including a broad range of EDCs. In this study, the technique of covalent immobilization of laccase through carbodiimide coupling chemistry on highly adsorptive reduced graphene oxide (rGO) sponges was utilized to effectively remove two representative EDCs; namely, bisphenol A (BPA) and triclosan (TCS) from water. The bio-functionalized adsorbent (rGO-LA) showed a significant improvement in removing BPA (87 % after 24 h) compared to pristine rGO sponge, (~40 % after 24 h). The removal efficiency of both adsorbents for TCS was as high as 84 %, with faster kinetics being observed for rGO-LA. Further investigation using gas-chromatography-mass spectroscopy revealed that the bio-functionalization not only improved the removal efficiency of the adsorbent, but also facilitated the adsorption of the metabolites generated during the biodegradation of BPA and TCS. When temperature was increased to 40 °C, the removal efficiency and kinetics of rGO-LA sponges were improved significantly for BPA (83 % removal in 4 h) and TCS (73 % removal after 4 h). The study highlights the synergy of enzymatic degradation and adsorption, with enhanced performance observed at elevated temperatures, offering a promising solution for effective EDCs mitigation in water treatment, while also ensuring comprehensive contaminant removal by adsorbing the generated metabolites.

Hexabromocyclododecane (HBCD) is a brominated flame retardant, that is added, but not chemically bonded, to consumer products. HBCD is sold as a commercial-grade HBCD mixture containing three major stereoisomers: alpha (α), beta (β), and gamma (γ), with relative amounts of 12% for α-HBCD, 6% for β-HBCD, and 82% for γ-HBCD. HBCDs are widely measured in the environment and in biological matrices. The toxicological effects of its exposure in humans are not clearly understood. A recent reassessment pointed out potential thyroid disruption as a primary effect. This current work aims to update a physiologically based pharmacokinetic (PBPK) model for γ-HBCD in C57BL/6 mice and incorporate equations and codes for α-HBCD and β-HBCD isomers and simulate them as a mixture. Physiological parameters were taken from the literature, calculated based on the log Kow or optimized with the dataset. The elimination of HBCDs in urine and feces was optimized to reflect the percent dose excreted, as published in the literature. Compared with data from the literature for α-HBCD, β-HBCD, and γ-HBCD in multiple tissues, the model simulations accurately described the pharmacokinetics of HBCDs in the mouse. The utility of the model was demonstrated by predicting blood concentrations from three studies in adult mice evaluating dopaminergic changes in the brain. Although this PBPK model for the mixture explicitly describes α-HBCD, β-HBCD, and γ-HBCD as individual exposures, but also as a mixture, more experimental data with commercial HBCD mixtures is still needed to improve the model.

Tributyltin is a biocide and bisphenol S is a plasticizer. The effects of the TBT + BPS mix on thyroid axis function are unknown. This study evaluated the effects of subacute exposure to TBT and BPS, both in mix and alone, in female young Wistar rats. Thyroid morphophysiology, gene expression, oxidative stress and collagen deposition were evaluated. TBT and BPS exposure resulted in a decrease in thyroid hormone levels, whereas TBT alone resulted in a decrease in TSH levels. The TBT + BPS group exhibited an increase in T4 levels, a decrease in T3 levels, a decrease in TPO activity, and an increase in TSHr mRNA expression. Deiodinase 1 (D1) and 2 (D2) were increased in the hypothalamus-pituitary-thyroid (HPT) axis (except for D2 in the pituitary gland) and in the liver of the TBT + BPS group, beside increases in the pituitary TRHr and thyroid ER mRNAs. The thyroid morphology of the TBT + BPS group revealed significant expansion of both the thyroid follicle and its surrounding tissue. In contrast, the TBT and BPS groups displayed numerous thyroid follicles undergoing fusion, a decrease in epithelial height and the epithelial/colloid ratio. The BPS group was the only group that exhibited increased collagen deposition. The TBT + BPS group demonstrated significant increases in the transcript levels of nrf2 and keap1. In all groups, the number of thiol groups decreased. There was an increase in SOD activity in the TBT + BPS group. Overall, subacute exposure to a mix deregulates the HPT axis, which correspondingly affects gene expression and causes enzymatic and morphological changes in the thyroid gland.

Obesity due to excessive fat accumulation, affects health and quality of life and increases the risk of diseases such as type 2 diabetes and cardiovascular conditions. Traditional causes, such as calorie excess and sedentary behavior, do not fully explain the obesity epidemic, leading to the hypothesis that endocrine-disrupting chemicals or obesogens contribute to obesity. The obesogenic mechanisms of representative obesogenic substances, such as bisphenols, have been discussed, mainly focusing on their interactions with estrogen receptors. Based on several studies showing that obesogens induce obesity by mimicking glucocorticoids, this review focused on the role of the glucocorticoid receptor pathway. In addition, the anti-obesogenic bioactive substances that have been studied to this date along with their inhibitory mechanisms were discussed.

This study examines the impact of estrogenic compounds like bisphenol A (BPA), estradiol (E2), and zearalenone (ZEA) on human ovarian cancer, focusing on constructing a risk model, conducting gene set variation analysis (GSVA), and evaluating immune infiltration. Differential gene expression analysis identified 980 shared differentially expressed genes (DEGs) in human ovarian cells exposed to BPA, E2, and ZEA, indicating disruptions in ribosome biogenesis and RNA processing. Using the cancer genome atlas ovarian cancer (TCGA-OV) dataset, a least absolute shrinkage and selection operator (LASSO)-based risk model was developed incorporating prognostic genes 4-hydroxyphenylpyruvate dioxygenase like (HPDL), Thy-1 cell surface antigen (THY1), and peptidase inhibitor 3 (PI3). This model effectively stratified ovarian cancer patients into high-risk and low-risk categories, showing significant differences in overall survival, disease-specific survival, and progression-free survival. GSVA analysis linked HPDL expression to pathways related to the cell cycle, DNA damage, and repair, while THY1 and PI3 were associated with apoptosis, hypoxia, and proliferation pathways. Immune infiltration analysis revealed distinct immune cell profiles for high and low-expression groups of HPDL, THY1, and PI3, indicating their influence on the tumor microenvironment. The findings demonstrate that estrogenic compounds significantly alter gene expression and oncogenic pathways in ovarian cancer. The risk model integrating HPDL, THY1, and PI3 offers a strong prognostic tool, with GSVA and immune infiltration analyses providing insights into the interplay between these genes and the tumor microenvironment, suggesting potential targets for personalized therapies.

The relationships between maternal exposure to endocrine-disrupting chemicals (EDCs) and congenital heart diseases (CHD) are not elucidated yet. The exposure levels of EDCs are generally estimated based on self-reported questionnaires or occupational exposure evaluations in the literature. Therefore, a study based on epidemiological data from human biospecimens is required to provide stronger evidence between maternal exposure to EDC and CHD. Embase, Pubmed, Scopus, and the Cochrane Library databases were searched for related research which provided risk estimates regarding the relationships between maternal EDC exposure and CHD in human offspring. Baseline characteristics and outcomes of CHD were extracted from each included study. Odds ratios (ORs) with 95% confidence intervals (CIs) were pooled to calculate the overall estimates of CHD. Subgroup and meta-regression analyses were performed to identify the sources of heterogeneity. Bootstrapping techniques were used in analyses where several studies originated from a similar population. A total of seventeen studies were involved in the meta-analyses. Maternal EDC exposure was significantly related to CHD in offspring (OR 2.15; 95%CI 1.64 to 2.83). EDC exposure was significantly associated with septal defects (OR 2.34; 95%CI 1.77 to 3.10), conotruncal defects (OR 2.54; 95%CI 1.89 to 3.43), right ventricular outflow tract obstruction (OR 2.65; 95%CI 1.73 to 4.07), left ventricular outflow tract obstruction (OR 3.58; 95%CI 2.67 to 4.79), anomalous pulmonary venous return (OR 2.31; 95%CI 1.34 to 4.00), and other heart defects (OR 2.49; 95%CI 1.75 to 3.54). In addition, maternal exposure to heavy metals, which included lead (OR 2.19; 95%CI 1.29 to 3.71), cadmium (OR 1.81; 95%CI 1.28 to 2.56), mercury (OR 2.23; 95%CI 1.13 to 4.44), and manganese (OR 2.65; 95%CI 1.48 to 4.74), increased risks for CHD significantly. In conclusion, based on the latest evidence, maternal EDC exposure may increase CHD risks in human offspring, especially in heavy metal exposure conditions.

The rising prevalence of depressive disorders has sparked concerns regarding environmental risk factors, particularly exposure to endocrine-disrupting chemicals (EDCs). However, the link between EDC exposure and depressive symptoms remains largely unexplored.

The Chang Gung Community Medicine Research Center carried out a cross-sectional study across four regions in northeastern Taiwan. Out of 887 participants, 120 subjects were chosen according to their EDC exposure scores. These participants underwent urinary EDC analysis and were evaluated for depressive symptoms through the standardized Hospital Anxiety and Depression Scale - Depression subscale (HADS-D) questionnaire.

Participants with HADS-D scores ≥ 8 exhibited significantly higher EDC exposure score compared to those with lower scores. The correlation analyses identified a notible positive association between urinary monobenzyl phthalate (MBzP) levels and HADS-D scores (r = 0.244, p = 0.007). Multiple regression analysis revealed that MBzP was independently linked to increased HADS-D scores in a positive manner (β ± SE: 0.139 ± 0.050, p = 0.006). Multivariable logistic regression indicated that higher MBzP (OR: 1.150, 95 % CI: 1.036-1.278, p = 0.009) and methylparaben (MP) levels (OR: 1.008, 95 % CI: 1.003-1.013, p < 0.001) showed a significant correlation with the likelihood of HADS-D scores ≥ 8. Receiver operating characteristic curve analysis demonstrated that elevated levels of MBzP, MP and the EDCs exposure score were associated with a greater likelihood of depressive symptoms.

Exposure to EDCs, particularly MBzP and MP, could be associated with a heightened risk of depressive symptoms.

Di-n-butyl phthalate (DBP) is a phthalate-based material used as a plasticizer to soften polyvinyl chloride, and classified as an endocrine disruptor with antiandrogen effects. Exposure to DBP induces oxidative stress in rat testes, resulting in testicular toxicity. Black ginseng (BG) exhibits a higher antioxidant activity than white or red ginseng following repeated heat treatment and processing. This study aimed to investigate whether the antioxidant activity of BG might protect against DBP-induced testicular toxicity in juvenile Sprague-Dawley rats. A significant decrease in testicular weight was observed in most groups treated with DBP alone or in combination with BG. However, a significant testicular weight increase was detected after exposure to BG (10 ml/kg) + DBP (500 mg/kg). The epididymal weight was significantly reduced with associated histological changes including irregular arrangement, atrophy of seminiferous tubules and Sertoli cells, and Leydig cell damage following exposure to DBP alone as well as BG (2.5 ml/kg) + DBP (500 mg/kg). However, no marked changes were observed in the shape of seminiferous tubules in control and BG + DBP groups. A significant decrease in serum testosterone levels was found after exposure to DBP, but no marked alterations in the BG + DBP groups. Protein expression levels of nuclear factor erythroid-derived 2-related factor (Nrf2), NAD(P)H dehydrogenase 1 (NQO1), and, heme oxygenase-1; (HO-1) were significantly higher following DBP treatment, but lowered in the BG + DBP groups. Evidence indicates that BG exerts a protective effect against DBP-induced testicular toxicity in rats.

Phthalate acid esters (PAEs) and bisphenol A (BPA) are recognized as common endocrine disruptors associated with various adverse effects on human health. However, limitations in existing systematic studies, particularly in air detection, have raised concerns about potential health risks from inhalation exposure. In this study, PM2.5 samples were collected in Dongying, a petrochemical city, from October 27 to December 6, 2021. The concentrations and compositions of PAEs and BPA in PM2.5 were analyzed, and health risks associated with inhalation exposure were assessed. The hazard index (HI) and cancer risk (CR) were calculated according to EPA standard methods for both adults and children. The mean concentrations of PAEs and BPA were determined to be 1152 and 3.7 ng/m3, respectively. BPA concentrations were found to increase during heating, whereas PAE concentrations were observed to decrease slightly. Diisobutyl phthalate (DiBP), a major PAE, was reduced by approximately 20% during heating. However, 1,4-dimethylphthalazine (DMP) and bis(2-ethylhexyl) phthalate (DEHP) were observed to increase from 4.2 to 14% and from 5.9 to 11%, respectively. It is hypothesized that variations in the concentrations and compositions of airborne PAEs and BPA were influenced by district heating. An increase in the percentage of DEHP in PM2.5 was noted on polluted days, likely influenced by saturated vapor pressure. The estimated daily intake (EDI) for children was calculated to be higher than that for adults, indicating that children were exposed to significantly greater potential risks, although overall risks were observed to be low. The results of this study provide essential baseline data, such as concentration, for the management and control of emerging pollutants like endocrine disruptors in the urban atmosphere.

The St. Lawrence Estuary (SLE) beluga (Delphinapterus leucas) population in Canada is Endangered, and endocrine disrupting contaminants, such as polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), and other halogenated flame retardants, have been identified as a threat to the recovery of this population. Here, potential impacts of these contaminants on SLE beluga were evaluated by comparing skin transcriptome profiles and biological pathways between this population and a population less exposed to contaminants (Eastern Beaufort Sea) used as a reference. Differential gene expression analysis indicated potential seasonal or geography-related (Arctic vs temperate regions) effects on the skin transcriptome. Among the gene transcripts that were associated with Σ31PCB (123 genes), Σ29PBDE (198 genes), HBB (347 genes), and PBEB (126 genes) blubber concentrations, several were related to immune response pathways. In addition, 18 toxicology-related gene transcripts selected from the literature were correlated with organohalogen concentrations and were used to derive new threshold values in beluga skin for potential biological effects of ΣPCB (1,500 ng/g lw), ΣPBDE (52 ng/g lw), and two other flame retardants, i.e., HBB (1.2 ng/g lw) and PBEB (0.04 ng/g lw). Results suggest that exposure to these organohalogens pose a risk to the immune system of SLE beluga.

A high prevalence of chronic diseases exposes diverse healthcare pain points due to the limited effectiveness of pharmaceutical drugs and biologics, sedentary lifestyles, insufficient health literacy, chronic stress, unsatisfactory patient experience, environmental pollution and competition with commercial determinants of health. To improve patient care and long-term outcomes, the impact of the home environment is overlooked and underutilized by healthcare. This cross-disciplinary work describes perspectives on (1) the home environment as a therapeutic target for the prevention and treatment of chronic diseases and (2) transforming health-centric household goods e-commerce platforms into digital health interventions. We provide a rationale for creating therapeutic home environments grounded in biophilic design (multisensory, environmental enrichment) and supporting physical activities, quality sleep, nutrition, music, stress reduction, self-efficacy, social support and health education, hence providing clinical benefits through the modulation of the autonomic nervous system, neuroplasticity and behavior change. These pleiotropic "active non-pharmacological ingredients" can be personalized for people living with depression, anxiety, migraine, chronic pain, cancer, cardiovascular and other conditions. We discuss prospects for integrating e-commerce with digital health platforms to create "therapeutic home environment" interventions delivered through digital therapeutics and their combinations with prescription drugs. This multimodal approach can enhance patient engagement while bridging consumer spending with healthcare outcomes.

Lactic acid bacteria are gaining global attention, especially due to their role as a probiotic. They are increasingly being used as a flavoring agent and food preservative. Besides their role in food processing, lactic acid bacteria also have a significant role in degrading insecticide residues in the environment. This review paper highlights the importance of lactic acid bacteria in degrading insecticide residues of various types, such as organochlorines, organophosphorus, synthetic pyrethroids, neonicotinoids, and diamides. The paper discusses the mechanisms employed by lactic acid bacteria to degrade these insecticides, as well as their potential applications in bioremediation. The key enzymes produced by lactic acid bacteria, such as phosphatase and esterase, play a vital role in breaking down insecticide molecules. Furthermore, the paper discusses the challenges and future directions in this field. However, more research is needed to optimize the utilization of lactic acid bacteria in insecticide residue degradation and to develop practical strategies for their implementation in real-world scenarios.

Previous studies have shown that nickel sulfate (NiSO4) increases autophagy in thyroid cells and tissues. As an important organ of the endocrine system, the pancreas not only contributes to the exocrine function of digestion but also has the endocrine function of regulating blood sugar. However, it remains unknown whether NiSO4 increases pancreatic autophagy. Bradykinin (BK) is an important component of the kallikrein-kinin system (KKS) and has many biological functions, such as reducing autophagy. The purpose of the present study was to explore the effects of BK on NiSO4-induced changes in pancreatic endocrine function. The present results demonstrate that NiSO4 increases fasting blood glucose (FBG) within a certain range and decreases insulin levels in mice. Moreover, NiSO4 triggers incomplete autophagy in MIN6 cells by upregulating microtubule-associated protein 1 light chain 3-II (LC3II) and Beclin 1 but downregulating p62. Mechanistically, NiSO4 leads to abnormal activation of autophagy by inhibiting the PI3K/AKT/mTOR signaling pathway. Moreover, BK decreases FBG and increases insulin secretion in mice exposed to NiSO4. Light microscopy and transmission electron microscopy (TEM) analyses revealed that BK pretreatment partially restores MIN6 cell viability and decreases the number of autophagic bodies. BK significantly upregulates the protein levels of LC3II and Beclin1 but downregulates p62 in NiSO4-induced MIN6 cells. In addition, BK increases the levels of phosphorylated phosphatidylinositol 3-kinase (P-PI3K), phosphorylated protein kinase B (P-AKT) and mammalian target of rapamycin (mTOR). Most of these effects of BK are reversed by treatment with the HOE140 B2R inhibitor. The present results suggested that BK ameliorates NiSO4-induced pancreatic β-cell dysfunction through B2R-mediated activation of the PI3K/AKT/mTOR signaling pathway and inhibition of autophagy.

The increasing prevalence of cancer has been linked to various environmental factors associated with modern industrial and societal advancements. Di-(2-ethylhexyl) phthalate (DEHP), a commonly used plasticizer, is one such environmental contaminant with potential carcinogenic effects. While epidemiological studies have suggested a positive association between DEHP exposure and cancer risk, the specific role of DEHP in cancer initiation and progression requires further clarification. This review systematically examines the relationship between DEHP exposure and cancer, highlighting key mechanisms involved in tumorigenesis. DEHP has been found to influence several critical aspects of cancer biology, including cell proliferation, apoptosis, metastasis, invasion, epithelial-mesenchymal transition, angiogenesis, drug resistance, immune regulation, and cancer stem cell maintenance. These carcinogenic effects are mediated through multiple pathways, such as the PI3K/AKT signaling pathway, estrogen receptor activation, epigenetic modifications, oxidative stress, and inflammation. By elucidating the molecular mechanisms underlying DEHP's role in cancer, this review aims to contribute to the development of targeted prevention and intervention strategies to mitigate the cancer risks associated with DEHP exposure.

50% of pharmaceuticals and 25% of herbicides used worldwide are chiral. Each enantiomer has a unique toxicity and biodegradation profile, affecting differently to organisms. Chirality plays a key role in the behavior of these emerging contaminants (ECs) in terms of their pharmacological or herbicidal activity, but this peculiarity is often overlooked in environmental research. The complexity of chiral ECs is underestimated, as the varying sensitivity of biological systems to enantiomers is rarely considered. Biofilters can promote the activity of specific microbial communities, facilitating the degradation of ECs, due to the greater interaction between water and microorganisms and their compact design. Here, we show that an electroactive biofilter can alter the chirality of drugs and herbicides in wastewater treatment, impacting their removal and toxicity. The electrochemical biofilter (BioeF) removed 80% of pharmaceuticals and 50-75% of herbicides, outperforming the conventional filter (ConF). BioeF also showed greater chiral alterations and lower ecotoxicity. This work provides the first evidence of a relationship between changes in contaminant chirality and detoxification capacity, enhanced by electroactive systems. The increased microbial activity observed in the BioeF suggests that bioelectrochemical systems offer a valuable advance for ECs removal and ecotoxicity reduction, addressing the environmental challenge posed by ECs.

This study investigated the relationship between exposure to endocrine-disrupting chemicals (EDCs), specifically phthalates, bisphenol A, bisphenol F, and bisphenol S, and the severity of attention-deficit/hyperactivity disorder (ADHD) symptoms using neuropsychological tests in children diagnosed with ADHD.

This study included 67 medication-naïve children with ADHD aged 6-16 years. The urinary concentrations of EDCs were measured, and ADHD symptom severity was evaluated using neuropsychological tests and clinical symptom scale measurements. The Jonckheere-Terpstra test, Pearson and Spearman correlation analyses, linear regression models, and multiple regression models were used to examine the relationship between EDC exposure and ADHD symptoms.

A significant correlation was observed between urinary phthalate metabolite concentrations and commission error T-scores in the visual Advanced Test of Attention test. No significant associations were found with other neuropsychological indicators or bisphenol levels.

Phthalate exposure affects impulsivity in children with ADHD, which is consistent with the results of previous studies that used parental surveys. However, bisphenols are not clearly associated with ADHD symptoms, which is consistent with the results of previous studies.

Dibutyl phthalate (DBP) is a low-molecular-weight phthalate commonly found in personal care products, such as perfumes, aftershaves, and nail care items, as well as in children's toys, pharmaceuticals, and food products. It is used to improve flexibility, make polymer products soft and malleable, and as solvents and stabilizers in personal care products. Pregnancy represents a critical period during which both the mother and the developing embryo can be significantly impacted by exposure to endocrine disruptors. This article aims to elucidate the effects of prenatal exposure to DBP on the health and development of offspring, particularly on the reproductive, neurological, metabolic, renal, and digestive systems. Extensive research has examined the effects of DBP on the male reproductive system, where exposure is linked to decreased testosterone levels, reduced anogenital distance, and male infertility. In terms of the female reproductive system, DBP has been shown to elevate serum estradiol and progesterone levels, potentially compromising egg quality. Furthermore, exposure to this phthalate adversely affects neurodevelopment and is associated with obesity, metabolic disorders, and conditions such as hypospadias. These findings highlight how urgently stronger laws prohibiting the use of phthalates during pregnancy are needed to lower the risks to the fetus's health and the child's development.

Endocrine-disrupting chemicals (EDCs), found in various cosmetic products, interfere with the normal functioning of the endocrine system, impacting hormone regulation and posing risks to human health. Common cosmetic EDCs, such as ultraviolet (UV) filters, parabens, and triclosan, can enter the human body through different routes, including skin absorption. Their presence has been linked to adverse effects on reproduction, immune function, and development. High-throughput in vitro assays, using various human cell lines, were employed to assess the effects of common cosmetic EDCs such as ethylhexyl methoxycinnamate (EHMC), benzophenone-3 (BP-3), homosalate, and parabens. Despite ongoing regulatory efforts, gaps persist in understanding their long-term impacts, particularly when they are present as mixtures or degradation products in the environment. This study focuses on recent in vitro research to investigate the mechanisms through which cosmetic-related EDCs disrupt the endocrine system and other physiological systems. The in vitro findings highlight the broader systemic impact of these chemicals, extending beyond the endocrine system to include immune, reproductive, and cardiovascular effects. This research underscores the importance of developing safer cosmetic formulations and enhancing public health protection, emphasizing the need for stricter regulations.

Over the last decades, the human species has seen an increase in the incidence of pathologies linked to the genitourinary tract. Observations in animals have allowed us to link these increases, at least in part, to changes in the environment and, in particular, to an increasing presence of endocrine disruptors. These can be physical agents, such as light or heat; natural products, such as phytoestrogens; or chemicals produced by humans. Endocrine disruptors may interfere with the signaling pathways mediated by the endocrine system, particularly those linked to sex hormones. These factors and their general effects are presented before focusing on the male and female genitourinary tracts by describing their anatomy, development, and pathologies, including bladder and prostate cancer.

This study was conducted to develop a scale for assessing the attitudes of adults regarding the determination of Bisphenol A exposure.

The study sample comprised of 370 individuals who volunteered to participate. According to the Explanatory Factor Analysis (EFA) results of the investigation, a scale structure consisting of a total of 3 sub-dimensions was obtained. In the Confirmatory Factor Analysis, the scale item factor loading values were acceptable.

The fit indices for the scale were CMIN/df = 1,618, RMSEA = 0.058, NFI = 0.914, CFI = 0.965, and IFI = 0.790, indicating a satisfactory level of agreement. The scale was determined to have a Cronbach value of 0.79 and a high degree of reliability. The item-total score correlation coefficients of the scale ranged from 0.327 to 0.534 and exhibited a high degree of discrimination, as determined.

Based on the analyses conducted, it was determined that the Adult Bisphenol A Exposure Scale is a valid and reliable instrument for determining the attitudes of adults toward contact with and use of Bisphenol A-containing products.

Background/Objectives: Endocrine disruptors are substances capable of altering the functions of the endocrine system. There is evidence that some pesticides can be endocrine disruptors and, among some of their effects, we find alterations in pubertal development and in the function of the thyroid gland, which could be related to a greater tendency of obesity. The aim was to evaluate the evidence from clinical and preclinical studies on the association between pesticides used in agriculture and found in plant-based foods with overweight/obesity. Methods: This is a systematic review of articles on the impact of the use of endocrine disrupting pesticides on obesity, conducted according to the PRISMA-2020 guidelines. Results: There was evidence that some pesticides, such as chlorpyrifos, pyrethroids, and neonicotinoids, may promote obesity and other anthropometric changes by altering lipid and glucose metabolism, modifying genes, or altering hormone levels such as leptin. Other studies suggest that perinatal exposure to chlorpyrifos or pesticides such as vinclozolin may alter lipid metabolism and promote weight gain in adulthood, whereas other pesticides such as boscalib, captan, thiacloprid, and ziram were not associated with changes in weight. Exposure to pesticides such as vinclozolin may be associated with a higher prevalence of overweight/obesity in later generations. Conclusions: The few studies that do not show these associations have methodological limitations in data collection with confounding variables. Further studies are needed to provide more and higher quality evidence to determine the true effect of these substances on obesity.

Endocrine-disrupting chemicals (EDCs) are a growing health hazard for humankind and respiratory health in particular. Such chemical compounds are present in the environment and food and may interfere with physiological processes through interference with functions of the endocrine system, making humans more susceptible to various types of diseases. This review aims to discuss the effects of EDCs on the respiratory system. Exposure to EDCs during fetal development and adulthood increases susceptibility to respiratory diseases such as asthma, COPD, and pulmonary fibrosis. EDCs are both multiple and complex in the ways they can act. Indeed, these chemicals may induce oxidative stress, modify cell proliferation and differentiation, interfere with tissue repair, and modulate the inflammatory response. Moreover, EDCs may also break the integrity of the blood-air barrier, allowing noxious substances to penetrate into the lung and thus enhancing the opportunity for infection. In conclusion, the scientific evidence available tends to indicate that EDCs exposure is strongly linked to the initiation of respiratory disease. Further research will be important in discovering the underlying molecular mechanisms and devising preventive and therapeutic measures.

Assessment of breast cancer (BC) risk generally relies on mammography, family history, reproductive history, and genotyping of major mutations. However, assessing the impact of environmental factors, such as lifestyle, health-related behavior, or external exposures, is still challenging. DNA methylation (DNAm), capturing both genetic and environmental effects, presents a promising opportunity. Previous studies have identified associations and predicted the risk of BC using DNAm in blood; however, these studies did not distinguish between genetic and environmental contributions to these DNAm sites. In this study, associations between DNAm and BC are assessed using paired twin models, which control for shared genetic and environmental effects, allowing testing for associations between DNAm and non-shared environmental exposures and behavior.

Pre-diagnosis blood samples of 32 monozygotic (MZ) and 76 dizygotic (DZ) female twin pairs discordant for BC were collected at the mean age of 56.0 years, with the mean age at diagnosis 66.8 years and censoring 75.2 years. We identified 212 CpGs (p < 6.4*10-8) and 15 DMRs associated with BC risk across all pairs using paired Cox proportional hazard models. All but one of the BC risks associated with CpGs were hypomethylated, and 198/212 CpGs had their DNAm associated with BC risk independent of genetic effects. According to previous literature, at least five of the top CpGs were related to estrogen signaling. Following a comprehensive two-sample Mendelian randomization analysis, we found evidence supporting a dual causal impact of DNAm at cg20145695 (gene body of NXN, rs480351) with increased risk for estrogen receptor positive BC and decreased risk for estrogen receptor negative BC.

While causal effects of DNAm on BC risk are rare, most of the identified CpGs associated with the risk of BC appear to be independent of genetic effects. This suggests that DNAm could serve as a valuable biomarker for environmental risk factors for BC, and may offer potential benefits as a complementary tool to current risk assessment procedures.

Micro- and nano-plastics (MNPs) and per- and polyfluoroalkyl substances (PFAS) are prevalent in ecosystems due to their exceptional properties and widespread use, profoundly affecting both human health and ecosystem. Upon entering the environment, MNPs and PFAS undergo various transformations, such as weathering, transport, and accumulation, potentially altering their characteristics and structural dynamics. Their interactions, governed by factors like hydrogen bonding, hydrophobic interactions, Van der Waals forces, electrostatic attractions, and environmental conditions, can amplify or mitigate their toxicity toward human health within ecological conditions. Several studies demonstrate the in vivo effects of PFAS and MNPs, encompassing growth and reproductive impairments, oxidative stress, neurotoxicity, apoptosis, DNA damage, genotoxicity, immunological responses, behavioral changes, modifications in gut microbiota, and histopathological alterations. Moreover, in vitro investigations highlight impacts on cellular uptake, affecting survival, proliferation, membrane integrity, reactive oxygen species (ROS) generation, and antioxidant responses. This review combines knowledge on the co-existence and adsorption of PFAS and MNPs in the environment, defining their combined in vivo and in vitro impacts. It provides evidence of potential human health implications. While significant research originates from China, Europe, and the USA, studies from other regions are limited. Only freshwater and marine organisms and their impacts are extensively studied in comparison to terrestrial organisms and humans. Nonetheless, detailed investigations are lacking regarding their fate, combined environmental exposure, mode of action, and implications in human health studies. Ongoing research is imperative to comprehensively understand environmental exposures and interaction mechanisms, addressing the need to elucidate these aspects thoroughly.

Nitrate is ubiquitously found in the environment and is one of the main components of nitrogen fertilizers. Previous studies have shown that nitrate disrupts the reproductive system in aquatic animals, but no study has evaluated the impact of nitrate exposure on the uterus in mammals. This study aimed to evaluate the impact of maternal exposure to nitrate during the prenatal period on uterine morphology and gene expression in adult female F1 rats.

Pregnant Wistar rats were either treated with sodium nitrate 20 mg/L or 50 mg/L dissolved in drinking water from the first day of pregnancy until the birth of the offspring or were left untreated. On postnatal day 90, the uteri of female offspring rats were collected for histological and gene expression analyses. Morphometric analyses of the uterine photomicrographs were performed to determine the thickness of the layers of the uterine wall (endometrium, myometrium, and perimetrium) and the number of endometrial glands.

The highest nitrate dose increased the myometrial thickness of the exposed female rats. Treatment with both nitrate doses reduced the number of endometrial glands compared with no treatment. Additionally, nitrate treatment significantly increased the expression of estrogen receptors and reduced the expression of progesterone receptors in the uterus.

Our results strongly suggest that prenatal exposure to nitrate programs gene expression and alters the uterine morphology in female F1 rats, potentially increasing their susceptibility to developing uterine diseases during adulthood.

Spermatogenesis starts with the onset of puberty within the seminiferous epithelium of the testes. It is a complex process under intricate control of the endocrine system. Physiological regulations by steroid hormones in general and by estrogens in particular are due to their chemical nature prone to be disrupted by exogenous factors acting as endocrine disruptors (EDs). 17α-Ethynylestradiol (EE2) is an environmental pollutant with a confirmed ED activity and a well-known effect on spermatogenesis and chromatin remodeling in haploid germ cells. The aim of our study was to assess possible effects of two doses (2.5ng/ml; 2.5 μg/ml) of EE2 on both histone-to-protamine exchange and epigenetic profiles during spermatogenesis performing a multi/transgenerational study in mice. Our results demonstrated an impaired histone-to-protamine exchange with a significantly higher histone retention in sperm nuclei of exposed animals, when this process was accompanied by the changes of histone post-translational modifications (PTMs) abundancies with a prominent effect on H3K9Ac and partial changes in protamine 1 promoter methylation status. Furthermore, individual changes in molecular phenotypes were partially transmitted to subsequent generations, when no direct trans-generational effect was observed. Finally, the uncovered specific localization of the histone retention in sperm nuclei and their specific PTMs profile after EE2 exposure may indicate an estrogenic effect on sperm motility and early embryonic development via epigenetic mechanisms.

The quest for a good life, urbanization, and industrialization have led to the widespread distribution of endocrine-disrupting chemicals (EDCs) in water bodies through anthropogenic activities. This poses an imminent threat to both human and environmental health. In recent years, the utilization of advance materials for the removal of EDCs from wastewater has attracted a lot of attention. Metal-oxide nanocatalysts have emerged as promising candidates due to their high surface area, reactivity, and tunable properties, as well as enhanced surface properties such as mesoporous structures and hierarchical morphologies that allow for increased adsorption capacity, improved photocatalytic activity, and enhanced selectivity towards specific EDCs. As a result, they have shown extraordinary efficacy in removing a wide range of EDCs from aqueous solutions, including pharmaceuticals, agrochemicals, personal care items, and industrial chemicals. This study give insight into the unique physicochemical characteristics of metal-oxide nanocatalysts to effectively and efficiently remove harmful EDCs from wastewater. It also discussed the advances in the synthesis, and properties of metal-oxide nanocatalysts, and insight into understanding the fundamental mechanisms underlying the adsorption and degradation of EDCs on metal-oxide nanocatalysts using advanced characterization techniques such as spectroscopic analysis and electron microscopy. The findings of the study present metal-oxide nanocatalysts as a good candidate for the spontaneous sequestration of EDCs from wastewater is an intriguing approach to mitigating water pollution and safeguarding public health and the environment.

With the rapid industrialization and urbanization in Asian countries, the challenge of rising emerging contaminants in the environment, including the water cycle, has become more pronounced. Consequently, the presence of CECs in drinking water systems is inevitable due to their ubiquitous nature in aquatic environments. This scoping review aims to identify epidemiological concerns regarding drinking water CECs in Asian countries over the past decade by describing the types of assessed CECs, their associated health effects, and identifying gaps and future research prospects through a summary of relevant studies. Searches were conducted on PubMed and Scopus up to February 29, 2024. Included were epidemiological studies from the past 10 years (since January 2014) in Asian countries that assessed emerging contaminants in drinking water through direct measurement or analysis as factors. From an initial pool of 3198 results, 15 relevant studies were selected. These studies assessed various types of CECs, including disinfection byproducts (n = 10), endocrine disruptors (n = 2), pesticides (n = 2), and a protozoan pathogen (n = 1). The meticulous assessment of CECs and associated health outcomes in Asian epidemiological studies over the past decade has been deemed inadequate to address the wide range of ubiquitous CECs in drinking water and their potential health effects that have not yet been addressed. While not the sole objective, the primary aim of epidemiological studies is to inform policy decisions and increase awareness among the public and policymakers. Therefore, researchers in Asian countries, particularly in environmental and public health fields, should prioritize the development of research in this area by exploring more CECs type and associated health outcomes.

Bisphenol A (BPA) raises concerns among the scientific community as it is one of the most widely used compounds in industrial processes and a component of polycarbonate plastics and epoxy resins. In this review, we discuss the mechanism of BPA toxicity in food-grade plastics. Owing to its proliferation in the aqueous environment, we delved into the performance of various biological, physical, and chemical techniques for its remediation. Detailed mechanistic insights into these removal processes are provided. The toxic effects of BPA unravel as changes at the cellular level in the brain, which can result in learning difficulties, increased aggressiveness, hyperactivity, endocrine disorders, reduced fertility, and increased risk of dependence on illicit substances. Bacterial decomposition of BPA leads to new intermediates and products with lower toxicity. Processes such as membrane filtration, adsorption, coagulation, ozonation, and photocatalysis have also been shown to be efficient in aqueous-phase degradation. The breakdown mechanism of these processes is also discussed. The review demonstrates that high removal efficiency is usually achieved at the expense of high throughput. For the scalable application of BPA degradation technologies, removal efficiency needs to remain high at high throughput. We propose the need for process intensification using an integrated combination of these processes, which can solve multiple associated performance challenges.

Bisphenol A (BPA), an endocrine-disrupting substance commonly found in plastics and receipts, is associated with adverse effects, including endocrine disorders, reduced fertility, and metabolic issues. To gain insights into its effects on biological systems, we observed the adverse effects of BPA in male Institute of Cancer Research (ICR) mice exposed to BPA at the lowest observed adverse effect level for 6 weeks, in comparison with the control groups. We constructed a comprehensive transcriptome profile using 20 different tissues to analyze the changes in the whole-body systems. This involved employing differential gene expression, tissue-specific gene, and gene co-expression network analyses. The study revealed that BPA exposure led to significant differences in the transcriptome in the thymus, suggesting activation of T-cell differentiation and maturation in response to BPA treatment. Furthermore, various tissues exhibited immune response activation, potentially due to the migration of immune cells from the thymus. BPA exposure also caused immune-related functional changes in the colon, liver, and kidney, as well as abnormal signaling responses in the sperm. The transcriptome analysis serves as a valuable resource for understanding the functional impact of BPA, providing profound insights into the effects of BPA exposure and emphasizing the need for further research on potential associated health risks.

Endocrine-disrupting chemicals (EDCs) are environmental and industrial agents that interfere with hormonal functions. EDC exposure is linked to various endocrine diseases, especially in reproduction, although the mechanisms remain unclear and effects vary among individuals. Neuroinflammation, particularly hypothalamic inflammation, is an emerging research area with implications for endocrine-related diseases like obesity. The hypothalamus plays a crucial role in regulating reproduction, and its inflammation can adversely affect reproductive health. EDCs can cross the blood-brain barrier, potentially causing hypothalamic inflammation and disrupting the reproductive axis. This review examines the existing literature on EDC-mediated hypothalamic inflammation. Our findings suggest that exposure to 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD), polychlorinated biphenyl (PCB), tributyltin (TBT), phthalates, bisphenol A (BPA), and chlorpyrifos (CPF) in animals is linked to hypothalamic inflammation, specifically affecting the hypothalamic centers of the gonadotropic axis. To our knowledge, this is the first comprehensive review on this topic, indicating hypothalamic inflammation as a possible mediator between EDC exposure and reproductive dysfunction. Further human studies are needed to develop effective prevention and treatment strategies against EDC exposure.

Breast cancer is highly susceptible to metastasis formation. During the time of disease progression, tumor pathophysiology can be impacted by endogenous factors, like hormonal status, as well as by environmental exposures, such as those related to diet and lifestyle. New lines of evidence point toward a potential role for foodborne endocrine disruptive chemicals in this respect; however, mechanistic understanding remains limited. At the molecular level, crucial steps toward metastasis formation include cell structural changes, alteration of adhesion, and reorganization of cytoskeletal proteins involved in motility. Hence, this study investigates the potential of dietary xenoestrogens to impact selected aspects of breast cancer cell mechanotransduction. Taking the onset of the metastatic cascade as a model, experiments focused on cell-matrix adhesion, single-cell migration, and adaptation of cell morphology. Dietary mycoestrogens alternariol (AOH, 1 μM) and α-zearalenol (α-ZEL, 10 nM), soy isoflavone genistein (GEN, 1 μM), and food packaging plasticizer bisphenol A (BPA, 10 nM) were applied as single compounds or in mixtures. Pursuing the hypothesis that endocrine active molecules could affect cell functions beyond the estrogen receptor-dependent cascade, experiments were performed comparing the MCF-7 cell line to the triple negative breast cancer cells MDA MB-231. Indeed, the four compounds functionally affected the motility and the adhesion of both cell types. These responses were coherent with rearrangements of the actin cytoskeleton and with the modulation of the expression of integrin β1 and cathepsin D. Mechanistically, molecular dynamics simulations confirmed a potential interaction with fragments of the α1 and β1 integrin subunits. In sum, dietary xenoestrogens proved effective in modifying the motility and adhesion of breast cancer cells, as predictive end points for metastatic behavior in vitro. These effects were measurable after short incubation times (1 or 8 h) and contribute to shed novel light on the activity of compounds with hormonal mimicry potential in breast cancer progression.