Environmental Epigenetics最新文献

{"title":"Molecular responses of chicken embryos to maternal heat stress through DNA methylation and gene expression: a pilot study.","authors":"Keyvan Karami, Jules Sabban, Chloé Cerutti, Guillaume Devailly, Sylvain Foissac, David Gourichon, Alexandre Hubert, Jean-Noël Hubert, Sophie Leroux, Tatiana Zerjal, Sandrine Lagarrigue, Frédérique Pitel","doi":"10.1093/eep/dvaf009","DOIUrl":"10.1093/eep/dvaf009","url":null,"abstract":"<p><p>Climate change, with its repercussions on agriculture, is one of the most important adaptation challenges for livestock production. Poultry production is a major source of proteins for human consumption all over the world. With a growing human population, improving poultry's adaptation to environmental constraints becomes critical. Extensive evidence highlights the influence of environmental variations on epigenetic modifications. The aim of this paper is therefore to explore chickens' molecular response to maternal heat stress. We employed Reduced Representation Bisulfite Sequencing to generate genome-wide single-base resolution DNA methylation profiling and RNA sequencing to profile the transcriptome of the brains of embryos hatched from dams reared under either heat stress (32°C) or thermoneutrality (22°C). We detected 289 significant differentially methylated CpG sites (DMCs) and one differentially methylated region (DMR) between heat stressed and control groups. These DMCs were associated with 357 genes involved in processes such as cellular response to stimulus, developmental processes, and immune function. In addition, we identified 11 genes differentially expressed between the two groups of embryos, and identified ATP9A as a target gene of maternal heat stress on offspring. This study provides a body of fundamental knowledge on adaptive mechanisms concerning heat tolerance in chickens.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf009"},"PeriodicalIF":4.8,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12159801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal ambient air pollution associations with DNA methylation in asthma- and allergy-relevant genes: findings from ECHO.","authors":"Meredith Palmore, Emma E Thompson, Fang Fang, Theresa M Bastain, Carrie Breton, Scott Collingwood, Frank D Gilliland, Diane R Gold, Rima Habre, Tina Hartert, Gurjit K Khurana Hershey, Daniel J Jackson, Rachel Miller, Patrick Ryan, Lyndsey Shorey-Kendrick, Eliot R Spindel, Joseph Stanford, James Gern, Chris McKennan, Carole Ober, Christine Ladd-Acosta","doi":"10.1093/eep/dvaf013","DOIUrl":"10.1093/eep/dvaf013","url":null,"abstract":"<p><p>Prenatal exposure to air pollution is an important risk factor for child health outcomes, including asthma. Identification of DNA methylation changes associated with air pollutant exposure can provide new intervention targets to improve children's health. The aim of this study is to test the association between prenatal air pollutant exposure and DNA methylation in developmental and asthma-/allergy-relevant biospecimens (placenta, buccal, cord blood, nasal mucosa, and lavage). A subset of 2294 biospecimens collected from 1906 child participants enrolled in the Environmental Influences on Child Health Outcomes program with prenatal air pollutant and high-quality Illumina Asthma&Allergy DNA methylation array measures (<i>n</i> = 37 197 probes) were included. Prenatal ozone, nitrogen dioxide, and fine particulate matter were derived using residential history during pregnancy and spatiotemporal models. For each pollutant, biospecimen type, and prenatal exposure window, we estimated the effects of air pollution on gene DNA methylation levels. We compared results across pollutants, biospecimen types, and trimesters and tested for critical months of exposure using distributed lag models. DNA methylation levels at 154 out of 4746 tested genes were associated with air pollution; over 95% were exposure window, pollutant, and biospecimen-type specific. The fewest gene associations were detected in trimester 2, relative to other exposure windows. A variety of trends in methylation patterns were observed in response to lagged monthly pollution levels. Child DNA methylation changes at specific respiratory- and immune-relevant genes are associated with prenatal air pollutant exposures. Future studies should examine the relationship between these pollution-sensitive genes and child health.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf013"},"PeriodicalIF":4.8,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal per- and polyfluoroalkyl substance exposures and DNA methylation among newborns in the Environmental influences on Child Health Outcomes program.","authors":"Rose Schrott, Christine Ladd-Acosta, Vasantha Padmanabhan, Dana Boyd Barr, Carrie V Breton, Andres Cardenas, Courtney C Carignan, Dana Dabelea, Anne L Dunlop, Danielle M Fallin, Marie-France Hivert, Ellen M Howerton, Anna K Knight, Emily Oken, Alicia K Peterson, Michael C Petriello, Douglas Ruden, Rebecca J Schmidt, Alicia K Smith, Anne P Starling, Ivana V Yang, Yeyi Zhu, Jaclyn M Goodrich","doi":"10.1093/eep/dvaf010","DOIUrl":"10.1093/eep/dvaf010","url":null,"abstract":"<p><p>Gestation is a vulnerable window when exposure to per- and polyfluoroalkyl substances (PFAS) may impact child development and health. Epigenetic modification, including DNA methylation (DNAm), may be one mechanism linking prenatal PFAS exposure to offspring outcomes. We tested associations between prenatal PFAS and newborn DNAm in 1017 participants from 6 cohorts in the US Environmental influences on Child Health Outcomes consortium. Concentrations of PFAS [perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorohexanesulfonic acid (PFHxS), perfluorononanoic acid (PFNA), and perfluorodecanoic acid] were measured in maternal serum or plasma. DNAm was quantified in newborn dried blood spot or umbilical cord blood leukocytes using the Infinium HumanMethylation450 (450K) or MethylationEPIC (EPIC) arrays. We tested associations between prenatal PFAS and neonatal blood DNAm on the 450K (<i>n</i> = 772) and EPIC (<i>n</i> = 245) arrays; results were meta-analysed across the platforms. Regional changes in DNAm were investigated, and findings were checked for replication in the Michigan Mother-Infant Pairs (MMIP) cohort (<i>n</i> = 140). Following correction for false discovery rate (<i>q</i> = 0.1 for meta-analyses), we identified an association between PFHxS and one cytosine-guanine (CpG) mapped to <i>CASC3</i> (<i>q</i> = 0.065) that replicated in MMIP (<i>P</i> = .006). PFOS was associated with six CpG sites, of which five were mapped to the genes <i>KIAA1841, ABR, LEP, SERPINA1</i>, and <i>LOXL1</i>. One differentially methylated region (DMR) was associated with prenatal PFOA exposure, and one DMR was associated with PFOS exposure. In this multicohort analysis including a diverse group from the USA, PFOA, PFOS, PFHxS, and PFNA exposures in pregnancy were associated with offspring DNAm, and the implications for children's health merit further exploration.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf010"},"PeriodicalIF":4.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interaction of mercury exposure and DNA methylation with sustained attention in children in a novel analysis of epigenetic susceptibility.","authors":"Jessa V Ehlinger, Jaclyn M Goodrich, Dana C Dolinoy, Deborah J Watkins, Alejandra Cantoral, Adriana Mercado-García, Niladri Basu, Martha M Téllez-Rojo, Karen E Peterson","doi":"10.1093/eep/dvaf011","DOIUrl":"10.1093/eep/dvaf011","url":null,"abstract":"<p><p>The etiology of attention-deficit/hyperactivity disorder (ADHD) remains poorly understood, despite it being one of the most common neurodevelopmental disorders worldwide. Past research suggests methylmercury exposure and DNA methylation (DNAm) levels are each associated with ADHD in children, yet whether they interact to affect ADHD is unknown. Leveraging data from a longitudinal cohort of children in Mexico, this novel epigenetic-environment interaction study identified significant interactions between childhood mercury exposure (measured at 6-12 years of age) and adolescent blood leukocyte DNAm in their association with sustained attention [quantified via the Conners continuous performance test, 3rd edition (CPT3)] measured on average 5.6 ± 0.99 years later. Using adjusted linear regression, we assessed associations between hair and urine mercury concentrations and CPT3 scores reflecting inattention, impulsivity, vigilance, and sustained attention (<i>N</i> = 399). We then tested the interaction between mercury and DNAm at loci previously associated with the CPT3 outcomes (<i>N</i> = 374). Significant associations between mercury and CPT3 differed in magnitude and direction depending on the mercury biomarker and CPT3 variable. These associations often differed by gender. For example, urine mercury was positively associated with vigilance scores in males [β = 1.31(SE = 0.65), <i>P</i> = .045] but not in females [β = -0.20 (SE = 0.81), <i>P</i> = .80). In all children, three significant mercury-DNAm interactions were identified for either inattention or vigilance outcomes. Among females, 155 significant interaction terms were identified for the inattention models. In males, three significant interactions were identified for the impulsivity model. Overall, results suggest in some cases DNAm can influence the association between mercury exposure and ADHD-like symptoms.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf011"},"PeriodicalIF":4.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to fine particulate matter in adults is associated with immune cell gene expression related to inflammation, the electron transport chain, and cell cycle regulation.","authors":"Amanda Rundblad, Siddhartha Das, Bigina N R Ginos, Jason Matthews, Kirsten B Holven, Trudy Voortman, Stine M Ulven","doi":"10.1093/eep/dvaf008","DOIUrl":"10.1093/eep/dvaf008","url":null,"abstract":"<p><p>Exposure to air pollution and an unhealthy built environment increase disease risk by impacting metabolic risk factors and inflammation, potentially via epigenetic modifications and effects on gene expression. We aimed to explore associations between fine particulate matter (PM_2.5), black carbon, ozone, nitrogen dioxide, distance to nearest water body, normalized difference vegetation index, and impervious surface and gene expression profiles in adults. This study is a part of the LongITools project and includes cross-sectional data from the Rotterdam Study, a population-based cohort study, and NoMa, a randomized controlled trial. Environmental exposures were assigned using land-use regression (LUR) models and satellite data. Gene expression was assessed with whole blood RNA sequencing (Rotterdam Study, <i>n</i> = 758) and microarray analyses in peripheral blood mononuclear cells (NoMa, <i>n</i> = 100). We analysed transcriptomic profiles and enriched pathways associated with each of the environmental exposures. PM_2.5 had the strongest gene expression associations, while only a few significant associations were observed for the other environmental exposures. In both populations, exposure to PM_2.5 was associated with genes and pathways related to inflammation, oxidative stress, DNA metabolism, cell cycle regulation, histones, electron transport chain, oxidative phosphorylation, and neural signalling. This study is limited by different methods for RNA quantification, a cross-sectional design, and a small sample size. However, in both populations, exposure to PM_2.5 resulted in the maximum number of associations with gene expression. In conclusion, PM_2.5 is strongly associated with various gene expression profiles, which provide information about the underlying mechanisms of the detrimental health effects of exposure to PM_2.5.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf008"},"PeriodicalIF":4.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12159804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extended abstinence from morphine alters sperm smRNA expression and prevents transmission of intergenerational phenotypes.","authors":"Dana Zeid, Andre B Toussaint, Carmen Dressler, Angela Harbeck, Reza Karbalaei, Yandrés Cintrón, Andrew Pan, Mathieu Wimmer","doi":"10.1093/eep/dvaf006","DOIUrl":"10.1093/eep/dvaf006","url":null,"abstract":"<p><p>Paternal exposure to drugs of abuse can impact addiction-related behaviours in progeny via germline epigenome remodelling. Previously, we found that offspring of morphine-exposed male rats showed increased morphine-taking, diminished adolescent social play, and increased sensitivity to morphine-derived analgesia. Here, we first tested the impact of a 90-day paternal abstinence period following morphine self-administration on the transmission of the aforementioned phenotypes. The previously observed changes in morphine-related behaviours were no longer present in offspring of morphine-abstinent sires. We next compared small RNA (smRNA) content in sperm collected from four sire intravenous self-administration groups: morphine, saline, abstinent morphine, and abstinent saline. Two smRNAs (rno-miR-150-5p and an snoRNA annotated to <i>Snora42</i>/<i>Noc3l</i>) were differentially expressed specifically between morphine- and saline-treated sperm. No differential expression between abstinent morphine and saline sperm was observed. These data begin to delineate the temporal limits of heritable germline modifications associated with morphine exposure, in addition to identifying F0 germline factors coinciding with the manifestation of F1 multigenerational phenotypes. Furthermore, these data suggest that paternal abstinence at conception can prevent inheritance of germline factors that may alter offspring susceptibility to addiction-related endophenotypes.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf006"},"PeriodicalIF":4.8,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing <i>TET1</i> expression alters the epigenomic landscape and amplifies transcriptomic responses to allergen in airway epithelial cells.","authors":"Anthony P Brown, Sreeja Parameswaran, Lucy Cai, Sweeney Elston, Chi Pham, Artem Barski, Matthew T Weirauch, Hong Ji","doi":"10.1093/eep/dvaf007","DOIUrl":"10.1093/eep/dvaf007","url":null,"abstract":"<p><p>Previous studies have demonstrated that ten-eleven translocation methylcytosine dioxygenase 1 (TET1) plays a protective role against house dust mite (HDM)-induced allergic airway inflammation. TET1 transcriptionally responded to HDM extract and regulated the expression of genes involved in asthma in human bronchial epithelial cells (HBECs). How TET1 regulates the expression of these genes, however, is unknown. To this end, we measured mRNA expression, DNA methylation, chromatin accessibility, and histone modifications in control and <i>TET1</i> knockdown HBECs treated or untreated with HDM extract. Throughout our analyses of multiomics data, we detected significant similarities between the effects of <i>TET1</i> knockdown alone and the effects of HDM treatment alone, all enriched for asthma-related genes and pathways. One especially striking pattern was that both <i>TET1</i> knockdown and HDM treatment generally led to decreased chromatin accessibility at many of the same genomic loci. Transcription factor enrichment analyses indicated that altered chromatin accessibility following the loss of TET1 may affect, or be affected by, CCCTC-binding factor and CCAAT-enhancer-binding protein binding. Analysis of H3K27ac levels and comparison with existing datasets suggested a potential impact of TET1 on enhancer activity. <i>TET1</i> loss also led to changes in DNA methylation, but these changes were generally in regions where accessibility was not changing. Lastly, more significant transcriptomic changes were observed in HBEC cells with <i>TET1</i> knockdown compared to control cells following HDM challenges. Collectively, our data suggest that TET1 regulates gene expression through distinct mechanisms across various genomic regions in airway epithelial cells, restricting transcriptomic responses to allergen and potentially protecting against the development of asthma.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf007"},"PeriodicalIF":4.8,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal miR-34b-3p upregulated in response to hypoxia preconditioning modulates circadian rhythms through the targeting of Clock.","authors":"Yiquan Yan, Fengzhou Liu, Tongmei Zhang, Lu Zhao, Yateng Tie, Rui Wang, Qi Yang, Jin Ma, Xingcheng Zhao","doi":"10.1093/eep/dvaf002","DOIUrl":"10.1093/eep/dvaf002","url":null,"abstract":"<p><p>The relationship between circadian rhythm disorders and the development of various diseases appears to be significant, with limited current interventions available. Research literature suggests that hypoxia may influence the expression of clock genes and the shifting of rhythm phases. However, the precise mechanisms underlying the modulation of circadian rhythm through circulating exosomes by hypoxia preconditioning remain unclear. In this study, the mice were exposed to hypobaric conditions, simulating an altitude of 5000 m, for 1 h daily over the course of 1 week in order to achieve hypoxia preconditioning. Compared to the control group, no significant alteration was observed in the concentration, modal size, and mean size of circulating exosomes in hypoxia preconditioning mice. Exosomes derived from hypoxia preconditioning effectively suppressed the expression of <i>Per1, Clock</i>, and <i>Bmal1</i> in NIH 3T3 cells. The miRNA sequencing analysis revealed miR-34b-3p as a potential regulator of the <i>Clock</i>, resulting in the downregulation of clock gene expression and subsequent promotion of proliferation and migration in NIH 3T3 cells. This study elucidated a novel mechanism of hypoxia preconditioning in the regulation of circadian rhythm, proposing that exosomal miR-34b-3p functions as an unrecognized molecule entity involved in the modulation of circadian rhythm. These findings offer a new avenue for developing protective strategies and therapeutic targets for circadian rhythm disorders.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf002"},"PeriodicalIF":4.8,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-genotoxic carcinogens (TPA and mezerein) activate tumourous transformation through miR let-7-mediated Hmga2 expression in Bhas42 cells.","authors":"Moon Yi Ko, Euijun Min, Minjeong Kim, Heejin Park, Sumi Jang, Younhee Kim, Byoung-Seok Lee, Sung-Ae Hyun, Minhan Ka","doi":"10.1093/eep/dvaf005","DOIUrl":"10.1093/eep/dvaf005","url":null,"abstract":"<p><p>A Bhas42 cell transformation assay is a method used to detect the tumour-promoting activities of chemicals. However, the mechanisms underlying tumour transformations mediated by non-genotoxic carcinogens (NGCs) are poorly understood. This study aimed to examine the correlation between 12-<i>O</i>-tetradecanoylphorbol 13-acetate (TPA) or mezerein and the initiation of tumourous transformations by epigenetic regulation in Bhas42 cells. We found that TPA and mezerein prompted tumourous transformations by stimulating cell proliferation and migration in Bhas42 cells. Furthermore, we observed alterations in the expression levels of 134 genes, with 87 genes being upregulated and 47 genes being downregulated, following exposure to either TPA or mezerein. Among the differentially regulated genes, we identified 17 upregulated genes and 8 downregulated genes corresponding to differentially expressed genes in TNM [primary tumour (T), regional nodes (N), and metastasis (M)]. Importantly, we found that TPA and mezerein triggered the expression of Hmga2 and Ezh2 by loss of miRNA let-7 (miR let-7) in Bhas42 cells. Finally, the microRNA (miRNA) mimic of let-7 prevented the TPA- and mezerein-induced activation of Hmga2 and Ezh2 in Bhas42 cells. Our findings reveal a connection between tumourous transformations and the epigenetic regulator miR let-7 in NGCs, such as TPA and mezerein in Bhas42 cells. This highlights miR let-7 as a promising therapeutic target for mitigating tumourous transformations induced by NGCs.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf005"},"PeriodicalIF":4.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11967402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143778989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental Epigenetics 2025 update.","authors":"Michael K Skinner","doi":"10.1093/eep/dvaf004","DOIUrl":"https://doi.org/10.1093/eep/dvaf004","url":null,"abstract":"","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf004"},"PeriodicalIF":4.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}