Environmental Epigenetics最新文献

{"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":"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":"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}

{"title":"Longitudinal leucocyte DNA methylation changes in Mesoamerican nephropathy.","authors":"Amin Oomatia, Olga Chervova, Ali M Al-Rashed, Evangelia-Theano Smpokou, Simone Ecker, Neil Pearce, Brianna Heggeseth, Dorothea Nitsch, Andres Cardenas, Stephan Beck, Marvin Gonzalez-Quiroz, Ben Caplin","doi":"10.1093/eep/dvaf001","DOIUrl":"10.1093/eep/dvaf001","url":null,"abstract":"<p><p>Mesoamerican nephropathy (MeN) is a leading cause of morbidity and mortality in Central America, yet its aetiology remains unclear. Environmental exposures including heat stress, pesticides, and heavy metals have all been suggested as possible causes or exacerbating factors of the disease, but intermittent and cumulative exposures are difficult to capture using conventional biomonitoring. Locus-specific differential DNA-methylation (DNAm) which is known to occur in association with these environmental exposures can be readily measured in peripheral blood leucocytes, and therefore have the potential to be used as biomarkers of these exposures. In this study, we aimed first to perform a hypothesis-free epigenome-wide association study of MeN to identify disease-specific methylation signatures, and second to explore the association of DNAm changes associated with potentially relevant environmental exposures and MeN onset. Whole-blood epigenome-wide DNAm was analysed from a total of 312 blood samples: 53 incident cases (pre- and post-evidence of disease onset), 61 matched controls and 16 established cases, collected over a 5-year period. Mixed-effect models identified three unique differentially methylated regions that associated with incident kidney injury, two of which lie within the intron of genes (<i>Amphiphysin</i> on chromosome 7, and <i>SLC29A3</i> chromosome 10), none of which have been previously reported with any other kidney disease. Next, we conducted a hypothesis-driven analysis examining the coefficients of CpG sites reported to be associated with ambient temperature, pesticides, arsenic, cadmium, and chromium. However, none showed an association with MeN disease onset. Therefore, we did not observe previously reported patterns of DNA methylation that might support a role of pesticides, temperature, or the examined metals in causing MeN.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvaf001"},"PeriodicalIF":4.8,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11801219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364151","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":"Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis.","authors":"Daniel González, Alexis Infante, Liliana López, Danilo Ceschin, María José Fernández-Sanchez, Alejandra Cañas, Carlos Zafra-Mejía, Adriana Rojas","doi":"10.1093/eep/dvae026","DOIUrl":"10.1093/eep/dvae026","url":null,"abstract":"<p><p>Fine particulate matter (PM_2.5), an atmospheric pollutant that settles deep in the respiratory tract, is highly harmful to human health. Despite its well-known impact on lung function and its ability to exacerbate asthma, the molecular basis of this effect is not fully understood. This integrated transcriptomic and epigenomic data analysis from publicly available datasets aimed to determine the impact of PM_2.5 exposure and its association with asthma in human airway epithelial cells. Differential gene expression and binding analyses identified 349 common differentially expressed genes and genes associated with differentially enriched H3K27ac regions in both conditions. Co-expression network analysis revealed three preserved modules (Protein Folding, Cell Migration, and Hypoxia Response) significantly correlated with PM_2.5 exposure and preserved in asthma networks. Pathways dysregulated in both conditions included epithelial function, hypoxia response, interleukin-17 and TNF signaling, and immune/inflammatory processes. Hub genes like TGFB2, EFNA5, and PFKFB3 were implicated in airway remodeling, cell migration, and hypoxia-induced glycolysis. These findings elucidate common altered expression patterns and processes between PM_2.5 exposure and asthma, helping to understand their molecular connection. This provides guidance for future research to utilize them as potential biomarkers or therapeutic targets and generates evidence supporting the need for implementing effective air quality management strategies.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvae026"},"PeriodicalIF":4.8,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028231","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":"Air pollution exposure is associated with gene expression in children.","authors":"Siddhartha Das, Amanda Rundblad, Irene Fontes Marques, Ana Goncalves Soares, Vincent W Jaddoe, Martine Vrijheid, Mark Nieuwenhuijsen, Joost Verlouw, Jason Matthews, Kirsten B Holven, Magne Thoresen, Nicholas J Timpson, Janine F Felix, Stine M Ulven","doi":"10.1093/eep/dvae025","DOIUrl":"10.1093/eep/dvae025","url":null,"abstract":"<p><p>Environmental exposures, including air pollutants and lack of natural spaces, are associated with suboptimal health outcomes in children. We aimed to study the associations between environmental exposures and gene expression in children. Associations of exposure to particulate matter (PM) with diameter <2.5 (PM_2.5) and < 10 (PM₁₀) micrometers, nitrogen dioxide, green spaces, and blue space, with whole-blood gene expression were explored in children from the Dutch Generation R Study (<i>n</i> = 172). Analyses were adjusted for age, sex, batch, maternal education, and area socioeconomic status. Follow-up analysis was carried out using lymphoblastoid cell line gene expression in children from the ALSPAC Study (<i>n</i> = 946). Gene set enrichment analysis (GSEA) using hallmark and immune gene sets from the molecular signature database was carried out to identify significantly over-represented gene sets for insights into biological mechanisms Exposure to PM_2.5 was associated with expression of 86 genes in discovery analyses in the Generation R Study [false discovery rate (FDR)-adjusted <i>P</i>-value < .25]. Of these, PM_2.5 was also associated with <i>GNG11</i> expression in the same direction in follow-up analysis (FDR-adjusted <i>P</i>-value < .05). The remaining exposures showed much fewer associations in the discovery analyses. GSEA using PM_2.5 association results for both cohorts indicated suppression of gene sets related to interferon response and response to bacterial and viral exposure. In conclusion, gene expression analysis performed in two independent cohorts suggests that PM_2.5 exposure in children may be involved in interferon and microbial infection responses.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"10 1","pages":"dvae025"},"PeriodicalIF":4.8,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893039","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":"A systematic review of associations between the environment, DNA methylation, and cognition.","authors":"Sophie Glover, Jacob Illyuk, Claire Hill, Bernadette McGuinness, Amy Jayne McKnight, Ruth F Hunter","doi":"10.1093/eep/dvae027","DOIUrl":"10.1093/eep/dvae027","url":null,"abstract":"<p><p>The increasing prevalence of neurodegenerative diseases poses a significant public health challenge, prompting a growing focus on addressing modifiable risk factors of disease (e.g. physical inactivity, mental illness, and air pollution). The environment is a significant contributor of risk factors which are known to impact the brain and contribute to disease risk (e.g. air pollution, noise pollution, green and blue spaces). Epigenetics can offer insights into how various environmental exposures impact the body to contribute to cognitive outcomes. In this systematic review, we examined studies which have associated an environmental exposure to a type of epigenetic modification, DNA methylation, and a cognitive outcome. We searched four databases with keywords \"environmental exposures,\" \"epigenetics,\" and \"cognition.\" We yielded 6886 studies that we screened by title/abstract followed by full text. We included 14 studies which focused on four categories of environmental exposure: air pollution (<i>n</i> = 3), proximity to roads (<i>n</i> = 1), heavy metals (<i>n </i>= 6), and pesticides (<i>n</i> = 4). Overall, <i>n</i> = 10/14 studies provided evidence that DNA methylation is statistically significant in the association between the environment and a cognitive outcome. Furthermore, we identified that <i>n</i> = 5/14 studies performed a type of biological pathway analysis to determine the presence of biological pathways between their environmental exposure and cognitive outcome. Our findings underscore the need for methodological improvements and considerations in future studies, including investigation of other environmental exposures considering tissue-specificity of methylation profiles and stratifying analysis by sex, ethnicity and socioeconomic determinants of disease. This review demonstrates that further investigation is warranted, the findings of which may be of use in the development of preventative measures and risk management strategies for neurodegenerative disease.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"11 1","pages":"dvae027"},"PeriodicalIF":4.8,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064614","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}