Environmental toxicology and pharmacology最新文献

{"title":"Evaluation of hsa-miR-29a-3p expression and diazepam biotransformation via CYP2C19 in alcohol withdrawal syndrome","authors":"Tuğba Tezcan ,&nbsp;Selin Özkan-Kotiloğlu ,&nbsp;Mukaddes Asena Yıldırım ,&nbsp;Mustafa Danışman ,&nbsp;H. Ceren Bozmaoğlu ,&nbsp;Kenan Can Tok ,&nbsp;İrem Kar ,&nbsp;Mehmet Gümüştaş ,&nbsp;İnci Özgür-İlhan ,&nbsp;Halit Sinan Süzen ,&nbsp;Dilek Kaya-Akyüzlü","doi":"10.1016/j.etap.2025.104861","DOIUrl":"10.1016/j.etap.2025.104861","url":null,"abstract":"<div><div>This study investigated whether <em>hsa-miR-29a-3p</em> expression affects diazepam (DZP) metabolism by modulating <em>CYP2C19</em> gene expression in patients with alcohol withdrawal syndrome (AWS). Blood samples were obtained from 75 male AWS patients. <em>hsa-miR-29a-3p</em> expression was quantified using qRT-PCR, and plasma DZP and its active metabolite nordiazepam (NDZP) levels were measured via HPLC. No significant correlations were found between <em>hsa-miR-29a-3p</em> expression and DZP dose, plasma DZP/NDZP levels, dose-adjusted or weight-adjusted concentrations, or the metabolite-to-parent drug ratio. However, <em>hsa-miR-29a-3p</em> expression levels were significantly higher in patients exhibiting confusion (p = 0.016) and excessive fatigue (p = 0.039). Although <em>hsa-miR-29a-3p</em> did not appear to influence diazepam biotransformation directly, this study is the first to report a potential link between elevated <em>hsa-miR-29a-3p</em> expression and neuropsychiatric symptoms in AWS, suggesting a possible role of this microRNA in the clinical presentation of alcohol withdrawal.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"120 ","pages":"Article 104861"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145405035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Effect of hesperidin and neohesperidin from bittersweet orange (Citrus aurantium var. bigaradia) peel on indomethacin-induced peptic ulcers in rats” [Environ. Toxicol. Pharmacol. 37 (2014) 907–915]","authors":"Dalia I. Hamdan ,&nbsp;Mona F. Mahmoud ,&nbsp;Michael Wink ,&nbsp;Assem M. El-Shazly","doi":"10.1016/j.etap.2025.104851","DOIUrl":"10.1016/j.etap.2025.104851","url":null,"abstract":"","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"120 ","pages":"Article 104851"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular responses of human bronchial epithelial cells following short-term exposure to oxidative particulate matter","authors":"Alessandro Giammona ,&nbsp;Clarissa Gervasoni ,&nbsp;Gianluca Di Iulio ,&nbsp;Carmina Sirignano ,&nbsp;Stefano Listrani ,&nbsp;Matteo Rinaldi ,&nbsp;Silvia Canepari ,&nbsp;Alessia Lo Dico ,&nbsp;Francesca Costabile ,&nbsp;Gloria Bertoli","doi":"10.1016/j.etap.2025.104853","DOIUrl":"10.1016/j.etap.2025.104853","url":null,"abstract":"<div><div>Adverse health effects associated with fine particulate matter (PM_2.5) in urban areas can occur even at PM_2.5 concentrations below current regulatory limits — a situation increasingly observed in high-income countries. However, the underlying biological mechanisms remain poorly understood. In this study, we investigated the molecular and cellular responses in human bronchial epithelial cells exposed to low PM_2.5 using a novel methodology. We first identified specific meteorological conditions that favor low PM_2.5 mass concentrations (<span><math><mo>&lt;</mo></math></span>10 <span><math><mi>μ</mi></math></span>g m⁻³) combined with high traffic-related aerosol emissions, which we found to correspond to a highly oxidant atmosphere. Under these conditions, PM_2.5 samples were collected in the urban background of Rome. The cells were exposed <em>in vitro</em> using a novel methodological approach based on a direct filter-contact model. Our focus was on associating measurable aerosol properties with gene expression pathways related to oxidative stress, inflammation, and their epigenetic modulation through microRNAs. Our findings indicate that exposure to fresh traffic-related aerosols under low PM_2.5 concentrations elicited a biphasic gene expression response. The initial response involved the activation of genes such as <em>NRF2</em>, <em>NF-</em><span><math><mi>κ</mi></math></span><em>B</em>, <em>CAT1</em>, <em>SOD1</em>, <em>HIF-1</em><span><math><mi>α</mi></math></span>, and <em>HMOX1</em>; while a secondary response involved <em>TNF-</em><span><math><mi>α</mi></math></span> and <em>GPX4</em>. A strong association was observed between these biological effects and black carbon metrics related to fossil fuel, implicating fresh traffic emissions as key contributors. Additionally, a significant modulation of air pollution-associated microRNAs was observed, even at early times of exposure, suggesting an epigenetic dimension to the cellular stress response. These findings have important implications for future air quality regulations. We provide mechanistic insights into oxidative and epigenetic responses underlying PM_2.5 induced biological effects at low PM_2.5 levels, emphasizing that neither PM_2.5 mass concentration nor its oxidative potential — two metrics currently considered by legislation — are sufficient on their own to explain the observed effects.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"120 ","pages":"Article 104853"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145485027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dose-dependent toxicokinetics of permethrin in rats: A comparative analysis of four exposure levels","authors":"Zeineb Lakehal,&nbsp;Jonathan Côté,&nbsp;Sami Haddad,&nbsp;Michèle Bouchard","doi":"10.1016/j.etap.2025.104876","DOIUrl":"10.1016/j.etap.2025.104876","url":null,"abstract":"<div><div>Pyrethroid metabolites are used as biomarkers of human exposure but the influence of exposure levels on their toxicokinetics remains unclear. We examined the effect of administered dose on the toxicokinetics of permethrin metabolites. Sprague–Dawley rats were administered single gavage doses of permethrin (<em>trans</em>/<em>cis</em> 60:40) at 0.004, 0.04, 0.4 and 4 mg/kg bw. Serial blood, urine and fecal samples were collected. <em>Trans</em>- and <em>cis</em>-3-(2,2-dichlorovinyl)-2,2-dimethyl-cyclopropane-1-carboxylic acids (<em>trans</em>/<em>cis</em>-DCCA), 3-phenoxybenzoic acid (3-PBA), and 4-hydroxy-3-phenoxybenzoic acid (4-OH3PBA) were quantified. A clear effect of dose on metabolite profiles in blood was observed: appearance rate increased with doses, while terminal elimination half-life and mean residence time decreased. In urine, the predominant elimination route, fraction of metabolites recovered declined significantly at 0.4 and 4 mg/kg bw, whereas minor fecal excretion pathway was unaffected by dose. These findings show that permethrin dose governs both rates and extent of metabolite disposition, with key implications for exposure reconstruction from biomonitoring data.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"120 ","pages":"Article 104876"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145593131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterizing urinary metabolites by non-targeted analysis and their associations with endogenous metabolism in children from South Florida","authors":"Luciana Teresa Dias Cappelini ,&nbsp;Vinícius Guimarães Ferreira ,&nbsp;Olutobi Daniel Ogunbiyi ,&nbsp;Carolina Cuchimaque Lugo ,&nbsp;Monica Beatriz Perez ,&nbsp;Lisandra Menendez ,&nbsp;Maria Guerra de Navarro ,&nbsp;Mymuna Monem ,&nbsp;Florence George ,&nbsp;Piero Gardinali ,&nbsp;Daniel M. Bagner ,&nbsp;Natalia Quinete","doi":"10.1016/j.etap.2025.104877","DOIUrl":"10.1016/j.etap.2025.104877","url":null,"abstract":"<div><div>Children are vulnerable to environmental contaminants due to physiological immaturity and behaviors that increase contact with exogenous compounds. These exposures can disrupt central metabolic pathways, potentially affecting development and long-term health. A non-targeted analysis approach and advanced chemical annotation tools was used to characterize environmental compounds and urinary metabolites in South Florida children, exploring possible interactions through correlation analyses. Urine samples from children aged 9 months to 6 years were processed by online solid-phase extraction (Online SPE) and analyzed by liquid chromatography high-resolution mass spectrometry (LC-HRMS), followed by molecular annotation using the Compound Discoverer software. Correlation analyses identified statistical associations between detected environmental compounds and endogenous metabolites. The results showed co-variation patterns suggesting possible metabolic changes involving amino acid metabolism, fatty acid oxidation, and neurotransmitter-related processes. Although no specific associations were found with compounds linked to ingestion, the data indicated broader biological disruptions, possibly from combined environmental and dietary exposures.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"120 ","pages":"Article 104877"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145593521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contribution of ambient airborne particles on the susceptibility to respiratory viral infections","authors":"Chloé Chivé ,&nbsp;Lydie Martín-Faivre ,&nbsp;Vincent Michoud ,&nbsp;Armelle Baeza-Squiban ,&nbsp;Ignacio Garcia-Verdugo","doi":"10.1016/j.etap.2025.104797","DOIUrl":"10.1016/j.etap.2025.104797","url":null,"abstract":"<div><div>The respiratory tract is the primary entry point for inhaled particles from anthropogenic or biological origin such as respiratory viruses. Ambient particulate matter (PM) has adverse effects on the respiratory tract through mechanisms eliciting inflammatory responses, oxidative stress, and other pathophysiological effects. At the same time, respiratory viruses cause a range of infections. By compromising the integrity of the respiratory barrier and by modulating the host immune response, PM may facilitate viral entry and replication, thereby enhancing the pathogenicity of respiratory viruses. While epidemiological studies suggest that PM exposure may influence susceptibility to and severity of viral infection, the underlying mechanisms are not fully understood. This review aims to synthesise experimental studies that investigate how PM exposure may modulate virus infection and antiviral defence. These findings will be contextualised by an overview of the characteristics and effects of PM, the major respiratory viruses, and innate lung immunity.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104797"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship of fractalkine with arsenic exposure and the risk of cardiovascular diseases","authors":"Nesar Uddin ,&nbsp;Rajoana Karim Rimi ,&nbsp;Osman Goni ,&nbsp;Nayan Chandra Mohanto ,&nbsp;Kamrun Nahar Rossi ,&nbsp;Faysal Abedin ,&nbsp;Sharmin Akter Beauty ,&nbsp;Biplob Ahmed ,&nbsp;Sobuj Mia ,&nbsp;Sharon Jahan Sarder ,&nbsp;Sajib Hossain ,&nbsp;Mainul Islam ,&nbsp;Abu Shadat M. Noman ,&nbsp;Md Ashraful Hoque ,&nbsp;Daigo Sumi ,&nbsp;Koren K. Mann ,&nbsp;Zahangir Alam Saud ,&nbsp;Seiichiro Himeno ,&nbsp;Khaled Hossain","doi":"10.1016/j.etap.2025.104824","DOIUrl":"10.1016/j.etap.2025.104824","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs), the leading cause of arsenic-related morbidity and mortality, are a major public health concern in many countries, including Bangladesh. Understanding the mediators of increased CVD risk associated with arsenic exposure is decisive. Fractalkine (CX3CL1), a CX3C chemokine with both chemotactic and adhesive functions, acts by interacting with its specific receptor, CX3CR1. Fractalkine is implicated in atherosclerosis, leading to CVDs. However, the association between chronic arsenic exposure and serum fractalkine levels and its implication in CVDs have not yet been documented. The present study aimed to investigate the relationship between arsenic exposure and serum fractalkine levels, especially regarding the risk of CVDs. The study included 413 participants from low- and high-arsenic exposure rural areas in Bangladesh. Fractalkine levels in serum were measured by immunoassay, and the risk of CVDs was assessed by measuring the serum high-density lipoprotein cholesterol (HDL-C) and hypertension. We found that participants from high-exposure areas had nearly twice the serum fractalkine levels compared to those in low-exposure area (<em>p</em> &lt; 0.001). A one-unit increase of log₂-transformed water, hair, and nail arsenic showed significantly higher propensity score adjusted odd ratios (aORs) in the second and third tertiles of serum fractalkine in comparison to the first tertile. Serum fractalkine levels were inversely associated with HDL-C levels and positively linked to blood pressure and ORs of hypertension. Finally, the associations between arsenic exposure and hypertension were found to be mediated by serum fractalkine. These results suggest that arsenic-exposure-related increases in fractalkine levels may be implicated in the pathogenesis of CVDs.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104824"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145180854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benzophenone-3 (BP3), bisphenol A (BPA), and their combination impair ovarian response to gonadotropin stimulation in a multi-exposure multiparity model.","authors":"Valentina Galliani ,&nbsp;Joana Fessia ,&nbsp;Clarisa Guillermina Santamaría ,&nbsp;Julián Elías Abud ,&nbsp;Horacio Adolfo Rodríguez","doi":"10.1016/j.etap.2025.104821","DOIUrl":"10.1016/j.etap.2025.104821","url":null,"abstract":"<div><div>Despite prevailing evidence that endocrine-disrupting chemicals (EDCs) may exert effects across multiple pregnancies, most studies focus on the first pregnancy Using a multiparity murine model, we evaluated the effects of benzophenone-3 (BP3), bisphenol-A (BPA) or the combination (BP3 +BPA) exposure over two gestational periods (P1 and P2) on pregnancy outcomes and the gonadal function in female offspring from each pregnancy. While maternal weight, litter size, and sex ratio were unaffected, gestation length was altered in BPA and BP3 +BPA groups both in P1 and P2. Ovulation was affected in P2 offspring in all EDC exposed groups. Notably, antral follicle numbers were reduced in all exposed groups, while BPA and BP3 +BPA exposure diminished the primordial follicle reserve in P2 offspring. Estradiol levels were elevated in P2 offspring in the BP3 +BPA group with hCG stimulation. These findings highlight the importance of considering cumulative exposure and exposure to combinations of BP3 and BPA when assessing the long-term reproductive effects of EDCs.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104821"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145082986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory limits of aluminium content of vaccines have not been set based on toxicological studies","authors":"Loïc Angrand ,&nbsp;Romain K. Gherardi ,&nbsp;Guillemette Crépeaux","doi":"10.1016/j.etap.2025.104812","DOIUrl":"10.1016/j.etap.2025.104812","url":null,"abstract":"<div><div>Aluminium-Based Adjuvants (ABAs) have been used in vaccines since the 1920s to boost immune responses. Despite their widespread use, their mechanisms of action remain only partially understood, and growing concerns exist about their long-term safety, particularly in vulnerable populations. This study examines the regulatory history of the aluminium content limit in vaccines and identifies major gaps in toxicological and epidemiological evaluation.</div><div>Through a detailed review of regulatory records, historical archives, Freedom of Information Act (FOIA) requests and responses, and scientific literature, we found that the current aluminium threshold of 0.85 mg per dose was set in the mid-20th century based on immunological efficacy - not on toxicological data- and remains in place despite changes in vaccination schedules and cumulative exposure. The key documents supporting this limit, which date back to 1947 and 1952, do not evaluate the potential toxicity of ABAs and are, in any case, no longer relevant to the current vaccination schedule.</div><div>There is an urgent need for independent pharmacokinetic and toxicological studies, transparent access to proprietary adjuvant compound, and a comeback to safer alternatives such as biocompatible calcium phosphate. Updating these standards is crucial for strengthening public confidence in vaccination policies.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104812"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144917909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early-effect biomarkers and hazard index approaches to assessing risks from multiple exposure to metals among battery recyclers in France","authors":"Ogier Hanser,&nbsp;Aurélie Martin Remy,&nbsp;Mathieu Melczer,&nbsp;Nathalie Grova,&nbsp;Sophie Ndaw","doi":"10.1016/j.etap.2025.104819","DOIUrl":"10.1016/j.etap.2025.104819","url":null,"abstract":"<div><div>Battery-recycling can expose workers to several metals. This study aims to investigate this multiple exposure, by exploring the potential of effect biomarkers to improve risk assessment for workers, and by calculating a hazard index (HI) to assess the risk of cumulative exposure. Urine samples from 86 workers in three French recycling plants were analysed for metal biomarkers (Cd, Co, Cr, Li, Mn, Ni), kidney-injury biomarkers (α1-microglubulin, retinol binding protein, kidney injury molecule-1, N-acetyl-β-D-gluocosaminidase, albumin, total proteins), and oxidative-stress biomarkers (8-hydroxydeoxyguanosine, malondialdehyde). Kidney-injury biomarker levels successfully differentiated exposed recyclers from administrative workers, while oxidative-stress biomarker levels did not allow this differentiation. The calculation of a HI proved effective in detecting the risk associated with multiple metal exposure, offering a better risk assessment than when considering metals individually. This dual approach, combining HI calculation and analyzing kidney-injury biomarkers, should be strongly considered in the risk assessment of workers exposed to multiple metals.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104819"},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145070787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}