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Oxytetracycline (OTC) is listed as an emerging contaminant due to the adverse effects that it has on human health and the environment. Being a broad spectrum antibiotic, OTC is widely used and is found in large concentrations in wastewater. Advanced wastewater treatment is an effective method for the removal of this pollutant; however, these tertiary treatments are expensive and generally not applied in nondeveloped countries. In this work, the removal of OTC by adsorption using sustainable materials synthesized from hydroxyapatite (HA) and aluminosilicates by chemical precipitation method was performed. Four different adsorbent materials were obtained: mixing hydroxyapatite and kaolin (HA-K), hydroxyapatite with natural clay (HA-NC), hydroxyapatite with synthetic zeolite (HA-SZ), and hydroxyapatite with natural aluminosilicates (HA-NA). The adsorbent materials were characterized by FT-IR, pHpzc, cation exchange capacity (CEC), SEM/EDX, TEM (particle size), and XRD. Kinetic tests and adsorption isotherms of OTC were carried out by varying conditions of the aqueous media as pH value, temperature, and the presence of ionic strength. Different kinetic and isothermal models were applied to the obtained data. All the synthesized materials showed an acceptable sorption capacity for OTC removal. The elimination of this antibiotic was greater than 50% in the four synthesized materials. Experimental data showed a better fit to the Elovich kinetic model, indicative of a heterogeneous chemical sorption process. Kinetic and thermodynamic parameters showed that the synthetized materials from HA and aluminosilicates are potential and alternative adsorbent materials for OTC removal from water.

Brain-derived neurotrophic factor (BDNF), a neurotrophic growth factor mainly expressed in the brain, has been proposed as a potential effect biomarker; that is, as a measurable biomarker whose values could be associated with several diseases, including neurological impairments. The European Human Biomonitoring Initiative (HBM4EU) has also recognized effect biomarkers as a useful tool for establishing link between exposure to environmental pollutants and human health. Despite the well-establish protocol for measuring serum BDNF, there is a need to validate its assessment in urine, a non-invasive sample that can be easily repeated over time. The aim of this study was to develop, standardize and validate a methodology to quantify BDNF protein levels in urine samples before its implementation in biomonitoring studies. Different experimental conditions and non-competitive commercial enzyme-linked immunosorbent assay (ELISA) kits were tested to determine the optimal analytical procedure, trying to minimize the shortcomings of ELISA kits. The fine-tune protocol was validated in a pilot study using both upon awakening (  = 150) and prior to sleeping (  = 106) urine samples from the same Spanish adolescent males in a well-characterized study population (the Spanish INMA-Granada cohort). The best results were obtained in 0.6 ml of urine after the acidification and extraction (pre-concentration) of samples. The highest reproducibility was obtained with the ELISA kit from Raybiotech. Urinary BDNF concentrations of adolescent males were within the previously reported range (morning = 0.047-6.801 ng/ml and night = 0.047-7.404 ng/ml). Urinary BDNF levels in the awakening and pre-sleep samples did not follow a normal distribution and were not correlated. The developed methodology offers good sensitivity and reproducibility. Having reliable markers in urine may facilitate both diagnosis and monitoring possible diseases (and treatment). Further studies are needed to implement urinary BDNF in biomonitoring studies to further elucidate its usefulness and biological significance for neurological impairments.

Brain-derived neurotrophic factor (BDNF) and its isoforms (pro- and mBDNF) are promising neurobiomarkers. While total serum BDNF levels have been previously validated, the newer isoforms have not. We aimed to identify the most common serum pro- and mBDNF assays through a literature search (MEDLINE/PubMed, until March 2024), and to compare their methodological performance in 23 human serum samples [total BDNF: R&D Systems, #DBNT00; both isoforms: R&DSystems (#DY3175, #DBD00); Aviscera-Bioscience (#SK00752-09, #SK00752-01); FineTest (#EH4255, #EH0043)]. Western-blot and cross-reactivity assays were used to confirm whether the kits tested for the declared isoforms. The total BDNF (#DBNT00) and pro-BDNF (#DY3175) ELISA kits from R&D Systems, and the pro-BDNF ELISA kits from FineTest (#EH4255) and Aviscera-Bioscience (#SK00752-01) showed high specificity, sensitivity, accuracy, and reproducibility. None of the commercial brands tested for mBDNF quantification showed optimal specificity, although R&D Systems (#DBD00) showed an acceptable result. Additionally, comparison of serum mBDNF levels by direct measurement and estimation (total minus pro-BDNF) using the three R&D Systems kits in the 23 serum samples showed acceptable variation (± 15%). This work indicated that there is a need to continue improving the specificity of some ELISA kits, mainly those measuring mBDNF. Total, pro- and m-BDNF serum levels can be quantified using the R&D Systems kits, whereas pro-BDNF serum levels could, in principle, be measured using any of the three brands evaluated.

Bisphenol A (BPA) and its substitutes, bisphenol F (BPF) and S (BPS), have previously shown in vitro obesogenic activity. This study was designed to investigate their combined effect on the adipogenic differentiation of human adipose-derived stem cells (hASCs). Cells were exposed for 14 days to an equimolar mixture of bisphenols (MIX) (range 10 nM–10 µM). Oil Red staining was used to measure intracellular lipid accumulation, quantitative real-time polymerase chain reaction (qRT-PCR) to study gene expression of adipogenic markers (PPARγ, C/EBPα, LPL, and FABP4), and Western Blot to determine their corresponding proteins. The MIX promoted intracellular lipid accumulation in a dose-dependent manner with a maximal response at 10 µM. Co-incubation with pure antiestrogen (ICI 182,780) inhibited lipid accumulation, suggesting that the effect was mediated by the estrogen receptor. The MIX also significantly altered the expression of PPARγ, C/EBPα, LPL, and FABP4 markers, observing a non-monotonic (U-shaped) dose-response, with maximal gene expression at 10 nM and 10 µM and lesser expression at 1 µM. This pattern was not observed when bisphenols were tested individually. Exposure to MIX (1–10 µM) also increased all encoded proteins except for FABP4, which showed no changes. Evaluation of the combined effect of relevant chemical mixtures is needed rather than single chemical testing.

We aimed to explore the relationship of adipose tissue concentrations of some persistent organic pollutants (POPs) with the risk of endometriosis and the endometriotic tissue expression profile of genes related to the endometriosis-related epithelial–mesenchymal transition (EMT) process. This case–control study enrolled 109 women (34 cases and 75 controls) between January 2018 and March 2020. Adipose tissue samples and endometriotic tissues were intraoperatively collected to determine concentrations of nine POPs and the gene expression profiles of 36 EMT-related genes, respectively. Associations of POPs with endometriosis risk were explored with multivariate logistic regression, while the relationship between exposure and gene expression profiles was assessed through Spearman correlation or Mann–Whitney U tests. After adjustment, increased endometriosis risk was associated with p,p’-DDT, PCB-180, and ΣPCBs. POP exposure was also associated with reduced gene expression levels of the CLDN7 epithelial marker and increased levels of the ITGB2 mesenchymal marker and a variety of EMT promoters (HMGA1, HOXA10, FOXM1, DKK1, CCR1, TNFRSF1B, RRM2, ANG, ANGPT1, and ESR1). Our findings indicate that exposure to POPs may increase the risk of endometriosis and might have a role in the endometriosis-related EMT development, contributing to the disease onset and progression. Further studies are warranted to corroborate these findings.

Increasing evidence has been published over recent years on the implication of endocrine-disrupting chemicals (EDCs), including parabens and benzophenones in the pathogenesis and pathophysiology of endometriosis. However, to the best of our knowledge, no study has been published on the ways in which exposure to EDCs might affect cell-signaling pathways related to endometriosis. We aimed to describe the endometriotic tissue expression profile of a panel of 23 genes related to crucial cell-signaling pathways for the development and progression of endometriosis (cell adhesion, invasion/migration, inflammation, angiogenesis, and cell proliferation/hormone stimulation) and explore its relationship with the exposure of patients to parabens (PBs) and benzophenones (BPs). This cross-sectional study included a subsample of 33 women with endometriosis from the EndEA study, measuring their endometriotic tissue expressions of 23 genes, while urinary concentrations of methyl-, ethyl-, propyl-, butyl-paraben, benzophenone-1, benzophenone-3, and 4-hydroxybenzophenone were determined in 22 women. Spearman’s correlations test and linear and logistic regression analyses were performed. The expression of 52.2% of studied genes was observed in >75% of endometriotic tissue samples and the expression of 17.4% (n = 4) of them in 50–75%. Exposure to certain PB and BP congeners was positively associated with the expression of key genes for the development and proliferation of endometriosis. Genes related to the development and progression of endometriosis were expressed in most endometriotic tissue samples studied, suggesting that exposure of women to PBs and BPs may be associated with the altered expression profile of genes related to cellular pathways involved in the development of endometriosis.

Objective To assess the genetic and epigenetic effects promoted by Bisphenol A (BPA) exposure in adolescent males from the Spanish INMA-Granada birth cohort, and in human cells. Methods DNA methylation was analysed using MEDIP. Repeat number variation in genomic DNA was evaluated, along with the analysis of H3K4me3 by using chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Analyses were performed with material extracted from whole blood of the adolescents, complemented by in vitro assessments of human (HeLa) cells exposed to 10 nM BPA, specifically, immunofluorescence evaluation of protein levels, gene expression analysis and ChIP‒qPCR analysis. Results Adolescents in the high urinary BPA levels group presented a higher level of Satellite A (SATA) repetitive region copy numbers compared to those in the low BPA group and a tendency towards increase in telomere length. We also observed decreased DNA methylation at the promoters of the imprinted genes H19, KCNQ1, and IGF2 ; at LINE1 retroelements; and at the ARID2, EGFR and ESRRA and TERT genes. Genome-wide sequencing revealed increased H3K4me3 occupancy at the promoters of genes encoding histone acetyltransferases, telomeric DNA binding factors and DNA repair genes. Results were supported in HeLa cells exposed to 10 nM BPA in vitro. In accordance with the data obtained in blood samples, we observed higher H3K4me3 occupancy and lower DNA methylation at some specific targets in HeLa cells. In exposed cells, changes in the expression of genes encoding DNA repair factors ( ATM, ARID2, TRP53 ) were observed, and increased expression of several genes encoding telomeric DNA binding factors ( SMG7, TERT, TEN1, UPF1, ZBTB48 ) were also found. Furthermore, an increase in ESR1/ERa was observed in the nuclei of HeLa cells along with increased binding of ESR1 to KAT5, KMT2E and TERF2IP promoters and decreased ESR1 binding at the RARA promoter. The DNA damage marker p53/TP53 was also increased. Conclusion In this pilot study, genome-wide analysis of histone trimethylation in adolescent males exposed to BPA revealed a global impact on the expression of genes encoding telomeric binding proteins and histone acetyltransferase factors with similar results in HeLa cells. Nevertheless, larger studies should confirm our findings.

Based on toxicological evidence, children’s exposure to phthalates may contribute to altered neurodevelopment and abnormal regulation of brain-derived neurotrophic factor (BDNF). We analyzed data from five aligned studies of the Human Biomonitoring for Europe (HBM4EU) project. Ten phthalate metabolites and protein BDNF levels were measured in the urine samples of 1148 children aged 6–12 years from Italy (NACII-IT cohort), Slovakia (PCB-SK cohort), Hungary (InAirQ-HU cohort) and Norway (NEBII-NO). Serum BDNF was also available in 124 Slovenian children (CRP-SLO cohort). Children’s total, externalizing and internalizing behavioral problems were assessed using the Child Behavior Checklist at 7 years of age (only available in the NACII-IT cohort). Adjusted linear and negative binomial regression models were fitted, together with weighted quantile sum (WQS) regression models to assess phthalate mixture associations. Results showed that, in boys but not girls of the NACII-IT cohort, each natural-log-unit increase in mono-n-butyl phthalate (MnBP) and Mono(2-ethyl-5-oxohexyl) phthalate (MEOHP) was cross-sectionally associated with higher externalizing problems [incidence rate ratio (IRR): 1.20; 95% CI: 1.02, 1.42 and 1.26; 95% CI: 1.03, 1.55, respectively]. A suggestive mixture association with externalizing problems was also observed per each tertile mixture increase in the whole population (WQS—IRR = 1.15; 95% CI: 0.97, 1.36) and boys (IRR = 1.20; 95% CI: 0.96, 1.49). In NACII-IT, PCB-SK, InAirQ-HU and NEBII-NO cohorts together, urinary phthalate metabolites were strongly associated with higher urinary BDNF levels, with WQS regression confirming a mixture association in the whole population (percent change (PC) = 25.9%; 95% CI: 17.6, 34.7), in girls (PC = 18.6%; 95% CI: 7.92, 30.5) and mainly among boys (PC = 36.0%; 95% CI: 24.3, 48.9). Among CRP-SLO boys, each natural-log-unit increase in ∑DINCH concentration was associated with lower serum BDNF levels (PC: −8.8%; 95% CI: −16.7, −0.3). In the NACII-IT cohort, each natural-log-unit increase in urinary BDNF levels predicted worse internalizing scores among all children (IRR: 1.15; 95% CI: 1.00, 1.32). Results suggest that (1) children’s exposure to di-n-butyl phthalate (DnBP) and di(2-ethylhexyl) phthalate (DEHP) metabolites is associated with more externalizing problems in boys, (2) higher exposure to DINCH may associate with lower systemic BDNF levels in boys, (3) higher phthalate exposure is associated with higher urinary BDNF concentrations (although caution is needed since the possibility of a “urine concentration bias” that could also explain these associations in noncausal terms was identified) and (4) higher urinary BDNF concentrations may predict internalizing problems. Given this is the first study to examine the relationship between phthalate metabolite exposure and BDNF biomarkers, future studies are needed to validate the observed associations.

Intercellular communication is mediated by extracellular vesicles (EVs), particles released by all cell types that transfer bioactive cargo (proteins, lipids, nucleic acids) to recipient cells, influencing their function. Furthermore, the human population is simultaneously exposed to mixtures of endocrine-disrupting chemicals (EDCs), capable of altering hormonal homeostasis. Epidemiological and experimental evidence, in animal and cellular models, show that EDCs can contribute to the initiation, development, and progression of carcinogenesis. This review analyzes the EDC–EV–Cancer axis, connecting the biology of EVs to environmental toxicology and the processes that lead to tumor development. It has been examined how specific pollutants—arsenic, polycyclic aromatic hydrocarbons, bisphenol A, phthalates, particulate matter 2.5, and cigarette smoke—modify the secretion and content of EVs. These altered EVs may subsequently trigger critical oncogenic mechanisms in recipient cells, including proliferation, angiogenesis, migration, immunosuppression, and metastasis. Specific mechanisms, pathways, miRNAs, and proteins have been identified, following exposure to various EDCs that are capable of modulating cells and the tumor microenvironment to induce carcinogenesis and tumor progression. Therefore, EVs represent a promising platform for investigating the role of exposome in tumor development, serving as a real-time monitoring system that would allow tracking of combined and dynamic human environmental exposure and help in cancer prevention.

Progressive disseminated histoplasmosis (PDH) is a leading cause of morbidity and mortality among persons with HIV (PWH) in the Americas. Clinical presentation often overlaps with other opportunistic infections -especially tuberculosis (TB)- and sensitive diagnostics are frequently unavailable. In Mexico, epidemiological data on histoplasmosis in PWH are scarce. This study aims to describe the clinical and demographic characteristics along with final diagnosis of hospitalized PWH who had clinical suspicion of progressive disseminated histoplasmosis. We conducted a multicenter, prospective, cross-sectional study involving 415 hospitalized PWH and clinical suspicion of PDH across ten tertiary care hospitals in Mexico. Participants underwent comprehensive evaluation for Histoplasmosis infection, including cultures, histopathology, and urine antigen testing. Of the total cohort, 108 patients (26%) had proven PDH, 162 (39%) received an alternative diagnosis, and 145 (35%) had no definitive diagnosis. In univariate analyses, proven PDH was more frequently associated with skin lesions, thrombocytopenia, elevated AST and LDH levels (>2x ULN), and micronodular infiltrates on chest imaging. In contrast, lymphadenopathy, tree-in-bud patterns, pleural effusion, hepatomegaly, and splenomegaly in imaging were more commonly observed in patients without proven PDH. Among patients without proven PDH, 41 met the criteria for probable PDH. Compared with proven PDH, probable cases exhibited higher rates of lymphadenopathy (73% vs 50%). Conversely, elevated AST (61% vs 39%) and LDH (74% vs 35%) levels were more frequent in proven PDH cases. While radiographic lung involvement was common in both groups, mediastinal lymphadenopathy (29% vs 12%), pleural effusion (17% vs 3.7%), and hepatomegaly (56% vs 37%) were significantly more frequent in probable PDH cases. Clinical response to antifungal therapy was higher in proven PDH (38% vs 24%), although this difference was not statistically significant. Compared to patients with tuberculosis (TB) alone, those with proven PDH alone showed more profound immunosuppression, with a greater proportion presenting CD4 + counts <50 cells/mm3. Skin lesions, LDH elevation, and micronodular pulmonary infiltrates were also more frequent in the proven PDH group, underscoring their diagnostic relevance. In contrast, lymphadenopathy, tree-in-bud opacities, hepatomegaly, and splenomegaly were more common in TB. Importantly, TB coinfection was present in 13 patients with proven PDH (12%) and in 12 with probable PDH (29%). In an exploratory analysis of predictors for proven PDH, elevated LDH level was the strongest predictor (adjusted prevalence odds ratio [aPOR] of 6.82, 95% CI 3.56 - 13.4, p < 0.001), followed by the presence of micronodular infiltrates on chest imaging (aPOR 1.94, 95% CI 1.06 - 3.62, p = 0.33). In contrast, pleural effusion on imaging was the strongest negative predictor for proven PDH (aPOR 0.28, 95% CI 0.07 - 0.92, p = 0.0498). Histoplasmosis represents a substantial diagnostic burden among PWH in Mexico, particularly in those with advanced disease. Our findings highlight the urgent need to expand access to rapid and sensitive diagnostic tools, improve clinical awareness, and promote routine screening for PDH in PWH presenting with febrile illness, especially in TB-endemic regions. Elevated LDH levels, skin lesions, and micronodular infiltrates on chest imaging were the most useful features to differentiate proven histoplasmosis from tuberculosis and probable histoplasmosis.