Search Results (195)

Background/Objectives: Microbial resistance to antibiotics has become a major global public health problem, threatening the effectiveness of current therapeutic strategies. The present study seeks to investigate natural compounds originating from fungal sources for their ability to interfere with efflux pump-mediated resistance in multidrug-resistant (MDR) bacteria, with the overarching goal of uncovering new candidates for antimicrobial therapeutic development. A chemical investigation of the ethanol extract of Termitomyces clypeatus was carried out to isolate and identify its constituents. Methods: Structural elucidation of the isolated metabolites was achieved through 1D and 2D NMR spectroscopy supported by mass spectrometric data. The crude extract and the purified compounds were then evaluated for their antibacterial activities individually, in the presence of an efflux pump inhibitor, and in combination with three antibiotics, using standardized microdilution assays. Results: Chromatographic separation of the extract yielded eleven known compounds, including three sphingolipids: (9Z,12Z)-N-(1,3,4-trihydroxyoctadecan-2-yl)octadeca-9,12-dienamide (1), 2-hydroxy-N-(1,3,4-trihydroxyoctadecan-2-yl)hexadecanamide (2), and cerebroside B (3); four steroids: ergosterol (4), cerevisterol (5), ergosterol peroxide (6), and 5α,6α-epoxy-(22E,24R)-ergosta-8(14),22-diene-3β,7α-diol (7); one alkaloid: piperine (8); one carbohydrate: D-mannitol (9); and two phthalates: dimethyl phthalate (10) and bis(2-ethylhexyl) terephthalate (11). GC–MS analysis led to the identification of eight fatty acid derivatives (12–19). Sub-fraction A, along with compounds 3, 4, and 8, exhibited moderate antibacterial activity against some tested strains, with MIC values of 64 μg/mL. These compounds were identified as substrates of bacterial efflux pumps, and their presence enhanced the antibacterial effects of ciprofloxacin, doxycycline, and amikacin. Conclusions: The findings of the present work indicate that Termitomyces clypeatus contains compounds with potential therapeutic value, as adjuvants that enhance the activity of conventional antibiotics. Full article

Introduction: Intermittent fasting (IF) is becoming increasingly popular as a method of weight management, but it is unknown whether it affects plasticiser intake with resultant changes in glycaemic control in diabetes and vitamin D (VitD) levels; therefore, this study was undertaken in a cohort of control and type-2 diabetic (T2D) subjects during Ramadan time-restricted feeding (TRF). Methods: In T2D subjects (n = 19) and controls (n = 31) undertaking TRF, 24 h urinary levels of phthalate metabolites, bisphenols and serum VitD were determined pre- and post-TRF by liquid chromatography–tandem mass spectrometry (LC-MS/MS). Anthropometric data and glycosylated haemoglobin (HbA1c) were measured. Results: T2D subjects were older (52 versus 36.73 years, p < 0.001), and had higher BMI (36.54 versus 27.67 kg/m², p < 0.001), body weight (101.77 versus 80.36 kg, p < 0.001), and HbA1c (8.38 versus 5.46%, p < 0.001) compared to controls, while VitD levels did not differ (60.43 versus 63.95 nmol/L, p > 0.05). Post-TRF, HbA1c was unchanged in T2D subjects and there was no difference in weight, BMI or VitD. Increased mono-iso-butyl phthalate (MiBP) in T2D subjects (10 versus 6.1 ng/mL, p = 0.001) and mono-n-butyl phthalate (MnBP) in T2D subjects (37 versus 13 ng/mL, p = 0.018) and controls (8.3 versus 5.4 ng/mL, p = 0.007) were observed post-TRF; however, significance was lost after adjusting for baseline differences in age, BMI, and HbA1c using a general linear model (GLM) repeated-measures ANOVA. Despite having no median differences in DEHP (di-2-ethylhexyl phthalate) metabolites pre- and post-TRF, analyses revealed a significant time × HbA1c interaction for [mono(2-ethyl-5-carboxypentyl) phthalate, MECPP: F(1,42) = 4.79, p = 0.03, mono(2-ethyl-5-hydroxyhexyl) phthalate, MEHHP: F(1,42) = 8.56, p = 0.006, mono(2-ethylhexyl) phthalate, MEHP: F(1,42) = 4.64, p = 0.03 and mono(2-ethyl-5-oxohexyl) phthalate, MEOHP: F(1,42) = 8.19, p = 0.007] and time × group interactions [MEHHP: F(1,42) = 14.27, p < 0.001, MEHP: F(1,42) = 6.35, p = 0.01 and MEOHP: F(1,42) = 10.30, p = 0.003]. Estimated marginal means (adjusted for age, BMI, HbA1c, and VitD) further confirmed higher concentrations of DEHP metabolites [MECPP, MEHHP, MEHP, and MEOHP] in T2D participants over time compared with controls. Additionally, monomethyl phthalate (MMP) trajectories were significantly influenced by the time × group interaction (F(1,42) = 4.28, p = 0.04), with post-TRF elevations observed in T2D subjects. Vitamin D status was observed to modify MCPP and MEP trajectories over time. Conclusion: Ramadan TRF is associated with changes in plasticiser metabolite levels, with estimated increased levels in T2D subjects versus healthy controls. Metabolite levels were influenced by HbA1c and vitamin D, though BMI was not observed to be a contributing factor. Full article

The degradation of plastic waste leads to the release of numerous chemical additives, including phthalate plasticizers, which have been implicated in the pathogenesis of metabolic disorders. Di (2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer whose primary metabolite, mono (2-ethyl-5-carboxypentyl) phthalate (MECPP), has been associated with multiple metabolic diseases. In this study, we applied an integrated approach combining network toxicology and molecular docking to systematically investigate the potential mechanistic role of MECPP in metabolic dysregulation. Our strategy included multi-platform target prediction, disease gene association analysis, functional enrichment, protein–protein interaction network construction, and molecular docking analysis. The results suggested that MECPP may be associated with six common core targets, including BCL2, BCL2L1, MAPK14, MMP2, MMP9, and TNFRSF1A, which are mainly involved in apoptosis, inflammatory regulation, and extracellular matrix remodeling. Pathway enrichment analysis further indicated the potential involvement of several disease-overlapping pathways, including insulin resistance, neuroactive ligand–receptor interaction, efferocytosis, advanced glycation end product–receptor for advanced glycation end product (AGE–RAGE) signaling, phospholipase D signaling, and renin secretion. Overall, these findings suggest that MECPP may contribute to metabolic dysregulation through overlapping molecular mechanisms across multiple diseases. This study provides a computational basis for future experimental validation and environmental risk assessment. Full article

Phthalates (PAEs) are ubiquitous endocrine-disrupting chemicals (EDCs), but their association with early pregnancy loss (gestational age ≤ 12 weeks) remains controversial. This study enrolled pregnant women aged 20–45 years in Zunyi City, China, and included 107 cases and 349 controls following propensity score matching. Logistic regression, restricted cubic spline (RCS) analysis, Bayesian kernel machine regression (BKMR), and weighted quantile sum (WQS) regression were employed to investigate associations between urinary phthalate metabolites and early pregnancy loss. We found that monoethyl phthalate (MEP), mono(2-ethylhexyl) phthalate (MEHP), monooctyl phthalate (MOP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) were associated with spontaneous abortion in early pregnancy, with corresponding odds ratios (ORs; 95% confidence intervals [CIs]) of 1.62 (1.26–2.09), 1.49 (1.07–2.09), 1.64 (1.26–2.12), 1.78 (1.27–2.50), 2.63 (1.90–3.64), 1.41 (1.11–1.79), and 5.39 (3.53–8.25). Non-linear dose–response relationships were observed between exposure to MMP, MEP, MEHP, MOP, monobenzyl phthalate (MBZP), MEOHP, MEHHP, and mono-(3-carboxypropyl) phthalate (MECPP) and early pregnancy loss (non-linear p < 0.05; overall p < 0.05). Co-exposure to multiple phthalate metabolites was also linked to a significantly non-linear elevation in the risk of early pregnancy loss (OR; 95% confidence interval [CI]) of 1.92 (1.76–2.15). Among these metabolites, MMP, MOP, MEOHP, and MECPP make the largest contribution to the correlation. In summary, our findings indicate that exposure to phthalate esters during early pregnancy is associated with early pregnancy loss, with MMP, MOP, MEOHP, and MECPP as the primary contributors. However, these results are based on a single urine sample, and caution is warranted when interpreting the findings. Full article

Background/Objective: Di-2-ethylhexyl phthalate and its bioactive metabolite mono-2-ethylhexyl phthalate (MEHP) are ubiquitous endocrine-disrupting chemicals implicated in carcinogenesis. However, the molecular mechanisms linking MEHP exposure, host genetic susceptibility, and prostate cancer progression remain incompletely defined. Methods: We integrated transcriptomic profiling of MEHP-exposed human prostate epithelial cells with a genetic association study of 630 patients with prostate cancer receiving androgen deprivation therapy. MEHP-responsive genes were identified from public microarray datasets and subjected to pathway enrichment analyses. Germline single-nucleotide polymorphisms (SNPs) in MEHP-regulated genes were evaluated for their association with progression-free survival, overall survival, and cancer-specific survival. The clinical and functional relevance of the key genes was further assessed using large-scale public prostate cancer expression datasets. Results: MEHP exposure induced widespread transcriptional reprogramming, prominently suppressing focal adhesion and cell–matrix interaction pathways. Genetic analyses identified multiple prognostically relevant SNPs within MEHP-responsive genes, with anoctamin 4 (ANO4) variants showing consistent associations across all clinical endpoints. The minor allele of rs17485225 in ANO4 was significantly associated with reduced all-cause and prostate cancer-specific mortality. Pooled analyses revealed reduced ANO4 expression levels in prostate cancer tissues and improved survival in patients with high ANO4 expression levels. Pathway analyses linked low ANO4 expression levels with enhanced cell cycle activity and compromised cell adhesion. Conclusions: Our findings suggest that ANO4 may act as a mediator of MEHP-associated prostate cancer progression and support a gene–environment interaction model in which environmental toxicant exposure and germline variation converge on focal adhesion dysregulation to potentially contribute to aggressive disease. Full article

Background/Objectives: Phthalates are encountered in everyday consumer and indoor environments, and their metabolites are commonly detected in urine. Although phthalate exposure has been linked to diabetes mellitus (DM), associations may vary by life stage. Therefore, we evaluated age-specific association between urinary phthalate metabolites and DM using nationally representative Korean data. Methods: We conducted a cross-sectional analysis of the Korean National Environmental Health Survey Cycle 4 (2018–2020). Adults aged ≥19 years with complete data were included. Eight urinary metabolites were evaluated. Metabolites were log-transformed, and those showing interaction were analyzed by tertiles. Complex survey-weighted logistic regression estimated odds ratios (95% confidence intervals) for DM, adjusting for demographic, socioeconomic, and health behavior factors. Analyses were stratified by age group. Results: Geometric mean (GM) concentrations among participants with DM varied significantly by age groups for several metabolites. Interaction analyses identified statistically significant effects for selected phthalate metabolites, including MnBP, MCPP, and MEP. In the age-stratified adjusted models, MnBP and MCPP were more strongly associated with DM in young adults, whereas the pattern for MEP appeared more evident in older adults, suggesting potential life-course differences in metabolic vulnerability. Conclusions: Associations between urinary phthalate metabolites and DM vary substantially by age, indicating life-course differences in exposure pathways and metabolic vulnerability. Age-specific prevention and surveillance strategies may improve environmental health interventions for DM. Full article

Plastic pollutants, including phthalates, bisphenol A (BPA), per- and polyfluoroalkyl substances (PFAS), and microplastics (MPs), are increasingly recognized as emerging environmental cofactors that intersect with infectious disease dynamics. These compounds, once considered inert, can alter immune function, reshape host–pathogen interactions, and directly influence viral survival and transmission. In this review, we compile current evidence on the chemistry, environmental occurrence, and biological activity of major plastic-associated pollutants with emphasis on their role in viral infections. Phthalates such as di(2-ethylhexyl) phthalate (DEHP) and its metabolite MEHP modulate innate immune signaling and have been shown to exacerbate infections, including Dengue and Coxsackievirus B3. Other DEHP-like phthalates, such as dibutyl phthalate (DBP), exhibit consistent infection-enhancing effects, while high molecular weight or cyclical phthalates such as polyvinyl acetate phthalate (PVAP) display conflicting results in their modulation of viral infections. BPA, widely detected in human tissues, acts through endocrine and immune disruption, worsening viral myocarditis, and altering influenza outcomes. PFAS, persistent “forever chemicals,” reshape adaptive immune responses and are associated with increased susceptibility, viral persistence, or severity of infection of herpesvirus (HCMV, EBV, HSV-1), hepatitis virus, and influenza infection. Microplastics represent a distinct risk by acting as physical carriers for viruses and bacteria, stabilizing viral RNA, enhancing host cell uptake, and skewing immune responses. Together, these pollutants extend beyond toxicology into virology, providing novel insights into how environmental exposures converge with viral pathogenesis. We highlight mechanistic advances and critical knowledge gaps and propose future directions for integrating environmental health and infectious disease research. Full article

Continuous monocropping of cassava (Manihot esculenta Crantz) often leads to soil degradation and yield decline, commonly referred to as continuous cropping obstacles (CCOs), which are closely linked to changes in soil physicochemical properties and microbial communities. Biochar has been widely used as a soil amendment to improve soil quality and microbial activity and is considered a potential strategy for alleviating CCOs. Understanding the effects of biochar on soil bacteria and metabolites under field conditions is essential, as it provides insights into its practical effectiveness in reducing CCOs and improving soil health in cassava cultivation systems. In this study, a field experiment was conducted in a continuous cassava system to investigate the effects of a single biochar application rate on soil bacterial diversity, community composition, and metabolite profiles in both rhizosphere and bulk soils. High-throughput 16S rRNA gene sequencing and UHPLC–MS/MS-based non-targeted metabolomics were employed to analyze soil bacterial and metabolic patterns. Biochar was associated with increased α-diversity in rhizosphere soil and distinct shifts in β-diversity. Biochar increased the relative abundance of Chloroflexi and Actinobacteriota in the bulk soil, while Cyanobacteria and Nitrospirota were more abundant in the rhizosphere. Network analysis revealed the compartment-specific differences after biochar application, with higher network complexity in the rhizosphere and lower complexity in the bulk soil relative to the control. Metabolomic profiling identified 402 metabolites in positive ion mode and 357 in negative ion mode. In the rhizosphere, biochar-treated soil exhibited higher relative abundances of alkaloids (e.g., trigonelline, berberine, vincristine) and flavonoids (e.g., catechin, naringin, rutin, and taxifolin), which are commonly linked to plant stress responses. In the bulk soil, biochar application resulted in lower levels of several anthropogenic organic compounds (e.g., monobutyl phthalate, terephthalic acid, and p–toluenesulfonic acid). These findings provide preliminary field evidence that biochar application can lead to compartment-specific changes in soil bacterial communities and metabolite profiles. Such changes are closely related to soil quality and nutrient cycling, pointing to a possible role of biochar in mitigating soil degradation under continuous cassava cultivation. Full article

Depression is a major public health concern, and evidence continues to show that environmental toxicants may contribute to its development. This study evaluated the association between depressive symptoms and per- and polyfluoroalkyl substances (PFAS), heavy metals, phthalates, and organophosphate metabolites using data from NHANES 2017–2018. Depressive symptoms were measured with the Patient Health Questionnaire-9 (PHQ-9). Environmental exposure variables were analyzed using multivariable linear regression and Bayesian Kernel Machine Regression (BKMR). All models adjusted for demographic, socioeconomic, behavioral, and clinical covariates. In multivariable linear regression models adjusted for demographic, socioeconomic, behavioral, and clinical covariates, higher urinary dimethylphosphate concentrations were significantly associated with increased depressive symptom scores (β = 0.15; 95% CI: 0.04, 0.27; p = 0.0098). Mono-(2-ethylhexyl) phthalate (MEHP) was also positively associated with PHQ-9 scores (β = 0.001; 95% CI: 0.0003, 0.0019; p = 0.0043). Because environmental mixtures tend to follow non-linear patterns, BKMR analysis was run. BKMR analyses indicated that organophosphate metabolites exhibited the greatest overall contribution to depressive symptoms (group posterior inclusion probability = 0.7875), with diethylphosphate emerging as the most influential individual exposure within the group (conditional PIP = 0.7211). Exposure–response functions suggested non-linear and threshold relationships for several metabolites. These findings identify specific organophosphate and phthalate metabolites as potential contributors to depressive symptoms and support the importance of evaluating chemical mixtures rather than single exposures. Additional longitudinal studies are needed to clarify temporal relationships and to inform public health efforts aimed at reducing exposure to organophosphate pesticides and endocrine-disrupting chemicals. Full article

Background: Exposure to environmental pollutants, especially endocrine-disrupting chemicals, disproportionately affects vulnerable populations like pregnant women, lactating mothers, and preterm infants. This study aimed to assess the detection patterns of DiNP-, DEP-, and DEHP-related metabolites in maternal urine and breast milk, examine agreement between matrices, and explore maternal factors associated with phthalate exposure. Methods: Fifty-five mothers who delivered at ≤32 gestational weeks and whose infants were hospitalized in the Neonatal Intensive Care Unit (NICU) were enrolled. Breast milk and urine samples were analyzed using a validated isotope-dilution LC–MS/MS method. Urinary phthalate metabolite concentrations were adjusted for specific gravity. Linear mixed-effects models with a random intercept for mother were used to examine associations between urinary and breast milk phthalate metabolite concentrations, assess temporal changes, and evaluate the influence of breast milk lipid content. Results: DEHP and DiNP metabolites were detected in nearly all maternal urine samples. Breast milk contained predominantly primary metabolites (MEHP and MiNP), while secondary oxidative metabolites were rarely detected. Urine concentrations consistently exceeded breast milk concentrations. Urinary and breast milk phthalate concentrations were not correlated across sampling periods, indicating limited matrix concordance. Conclusions: Mothers of very preterm infants experience sustained phthalate exposure in the postpartum period; however, limited metabolite transfer to breast milk indicates that maternal urine remains the preferred biomonitoring matrix for assessing systemic phthalate exposure. Breast milk phthalate profiles exhibit compound-specific temporal changes and appear largely independent of concurrent urinary exposure biomarkers. Full article

Background: Plasticisers with endocrine-disrupting potential are ubiquitous and associate with obesity and type-2 diabetes (T2D), with higher levels reported in the Middle East. However, no data exist on plasticiser exposure in Bahrain where T2D affects 15% of the national population. Methods: An observational exploratory study in T2D (n = 60) and controls (n = 96), analysed for 24 h urinary plasticiser levels (liquid chromatography tandem mass spectrometry (LC-MS/MS)). Correlation and generalised linear model (GLM) analyses were employed to examine associations. Results: T2D were older (p < 0.001), had higher body mass index (BMI) (p < 0.001), body weight (p < 0.001) and glycosylated haemoglobin A1c (HbA1c) (p < 0.001). Correlation analysis revealed differences in inter-plasticiser, and plasticiser and biomarker relationships, with loss or reversal in T2D compared to controls. Mono-n-butyl phthalate (MnBP) levels were higher in T2D (p = 0.04); however, regression analysis revealed significant association with age. The GLM analyses demonstrated marked differences in the levels of mono(3-carboxypropyl) phthalate (MCPP), mono(2-ethyl-5-carboxypentyl) phthalate (MECPP), monoethyl phthalate (MEP) and bisphenol S (BPS), with lower levels in T2D versus controls (B = −3.41, p = 0.01; B = −5.28, p < 0.001; B = −8.94, p < 0.001; B = −6.09, p = 0.006, respectively); however, these contrasts appeared to be substantially confounded by BMI and/or age. Positive influence of age and negative influence of BMI when observed across the full dataset were generally reversed in T2D. Levels were complementary to those previously reported for the Middle East. Conclusions: The study indicates the phthalate levels in Bahrain are elevated though complementary to studies of phthalates in the Middle East; within those levels, the study indicates differential exposure–response relationships with plasticisers, influenced by age and BMI, in those with T2D compared to healthy controls. Full article

Endocrine-disrupting chemicals (EDCs), widespread in aquatic environments, interfere with endocrine function in organisms and threaten ecosystem stability. Rotifers, critical live feed for marine fish, shrimp, and crab larvae, link EDC-induced reproductive impairment to marine ecosystem stability and aquaculture sustainability. This PRISMA-compliant review synthesizes key findings, consequences, and gaps in EDC–rotifer reproductive toxicity research. Traditional EDCs (heavy metals, per- and polyfluoroalkyl substances (PFASs), phenols, phthalate esters, polybrominated diphenyl ethers (PBDEs), and steroid hormones) and emerging EDCs (disinfection byproducts, microplastics, pharmaceutical metabolites) induce distinct reproductive harm—e.g., Hg²⁺ shows extreme toxicity (24 h LC₅₀ = 4.51 μg L⁻¹ in Brachionus plicatilis), BDE-47 damages ovaries, and microplastics cause transgenerational delays. Rotifer species and exposure duration affect sensitivity (e.g., BDE-47: 96 h LC₅₀ = 0.163 mg L⁻¹ vs. 24 h LC₅₀ > 22 mg L⁻¹ in B. plicatilis). Oxidative stress is a universal mechanism, and combined EDC exposure produces context-dependent synergistic/antagonistic effects. EDC-induced impairment reduces rotifer population density, alters structure, and propagates through food webs, threatening aquaculture and biodiversity; transgenerational toxicity (e.g., 4-nonylphenol: F₁ inhibition 28% vs. 12% in F₀) weakens resilience. This review supports EDC risk assessment, with gaps including long-term low-concentration data, transgenerational mechanisms, EDC–microbiome interactions, and emerging PFAS toxicity—priorities for future research. Full article

Associations between prenatal exposure to phthalates, bisphenols and their mixtures and early childhood allergic conditions and asthma were examined. Five hundred and fifty-six mother–child pairs from the Alberta Pregnancy Outcomes and Nutrition (APrON) cohort participated. Urine samples collected from mothers during the second trimester of pregnancy were analyzed for phthalates and bisphenols. A child health questionnaire, completed by mothers when children were 12, 24, and 36 months, asked whether children had experienced allergic conditions (i.e., food allergies, eczema, rash) or asthma. In single-chemical models, associations varied with child age. Higher prenatal concentrations of mono-benzyl phthalate (MBzP) were associated with lower odds of eczema at 12 months. At 36 months, higher mono-methyl phthalate (MMP) was associated with increased odds of eczema, whereas higher mono-carboxy-octyl phthalate (MCOP) was associated with reduced odds. Higher prenatal MCOP was also associated with higher odds of rash at 12 months, and higher MMP was associated with higher odds of rash at 36 months. Higher bisphenol S (BPS) was associated with increased odds of asthma at 12 months but decreased odds of eczema and rash at 36 months. Sex-specific effects were also noted. In multi-chemical exposure least absolute shrinkage and selection operator (LASSO) models, several phthalate metabolites and BPS were selected as the best predictors of eczema and rash at 36 months of age. Bayesian kernel machine regression (BKMR) mixture models suggested that BPS was the most important chemical in predicting eczema in children at 36 months, while MMP and BPS were the most important chemicals in predicting rash at 36 months. Prenatal exposure to certain phthalate metabolites and BPS predicted allergic conditions and asthma in young children, with patterns varying by age and sex. Prenatal exposure to these chemicals may differentially influence immune development and contribute to the development of early-life allergic conditions, with potentially sex-specific susceptibility. Full article

Di(2-ethylhexyl) phthalate (DEHP) is known to adversely affect reproduction. Our previous study demonstrated that DEHP exposure during embryogenesis impaired fertility in adult female zebrafish. The objective of this study was to investigate developmental events underlying this effect. Embryos were exposed to DEHP 5 h post-fertilization (hpf), and the distribution of primordial germ cells (PGCs), along with the expression of genes involved in PGC migration, maintenance, and neuroendocrine regulation, was assessed. Molecular docking simulations were performed to evaluate whether DEHP’s main metabolite, mono(2-ethylhexyl) phthalate (MEHP), is able to bind to zebrafish estrogen receptors (Esr). Our results show that DEHP reduced the expression of cxcr4b, cxcr7b, esr1, and esr2a at 24 hpf. Using vasa:egfp transgenic embryos, we found that DEHP altered the distribution of PGCs. In addition, DEHP inhibited the expression of PGC-specific dazl. DEHP also induced the expression of lhb and cyp19a1 and reduced the expression of esr2a in 120 hpf larvae, consistent with disruption of the neuroendocrine reproductive axis. Molecular docking indicates that MEHP can bind to the ligand-binding domains of Esr1, Esr2a, and Esr2b. Collectively, the results show that DEHP disrupts both PGC distribution and early neuroendocrine signaling pathways, providing mechanistic insight into reduced fertility in adult female zebrafish following embryonic DEHP exposure. Full article

Endocrine-disrupting chemicals (EDCs) are widespread organic compounds that interfere with hormone signaling and are linked to reproductive, developmental, cardiovascular, and cancer-related health effects. Key EDCs include bisphenol-A and its analogs, phthalates, parabens, triclosan, and per-and polyfluoroalkyl substances (PFAS), which are commonly present in personal care products and plastics. Human exposure occurs via environmental exposure through ingestion, inhalation, and dermal contact, with persistent compounds such as PFAS accumulating in blood, while others are excreted in urine as free or conjugated metabolites. Accurate assessment of EDC exposure, particularly during pregnancy and early childhood, requires robust analytical methods. Liquid and gas chromatography coupled with mass spectrometry (LC-MS and GC-MS) are the most widely used techniques to date. LC-MS is favored for its sensitivity, specificity, and minimal sample preparation, whereas GC-MS provides adequate performance but often requires time-consuming derivatization. This review summarizes current LC-MS and GC-MS methodologies for multi-class EDC biomonitoring, emphasizing sample preparation, analyte coverage, and methodological strengths and limitations, providing a practical reference for human exposure studies using common biological matrices such as urine and blood. Full article