ArticleEpigenetics2018
Maternal levels of endocrine disrupting chemicals in the first trimester of pregnancy are associated with infant cord blood DNA methylation.
Article in Epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Prenatal phthalate exposure and cord blood DNA methylation.Scientific reports · 2023Pooled it
- Environmental Xenobiotics and Epigenetic Modifications: Implications for Human Health and Disease.Journal of xenobiotics · 2025Review
- Review
- Phthalates and epigenetics: An emerging public health concern.Current research in toxicology · 2025Review
- The ENDOMIX perspective: how everyday chemical mixtures impact human health and reproduction by targeting the immune system†.Biology of reproduction · 2024Review
- Environmental exposures influence multigenerational epigenetic transmission.Clinical epigenetics · 2024Review
- Sex-Specific Associations between Prenatal Exposure to Bisphenols and Phthalates and Infant Epigenetic Age Acceleration.Epigenomes · 2024Article
- Prenatal exposure to environmental phenols and phthalates and altered patterns of DNA methylation in childhood.Environment international · 2024Article
- Association between pre- and postnatal exposure to endocrine-disrupting chemicals and birth and neurodevelopmental outcomes: an extensive review.Clinical and experimental pediatrics · 2024Article
- Methylation profiles at birth linked to early childhood obesity.Journal of developmental origins of health and disease · 2024Article
- Chemical mixture that targets the epidermal growth factor pathway impairs human trophoblast cell functions.Toxicology and applied pharmacology · 2024Article
- Methylation profiles at birth linked to early childhood obesity.medRxiv : the preprint server for health sciences · 2024Article
- Prenatal exposures to endocrine disrupting chemicals: The role of multi-omics in understanding toxicity.Molecular and cellular endocrinology · 2023Review
- Imprinting and Reproductive Health: A Toxicological Perspective.International journal of molecular sciences · 2023Review
- Review
- Epidemiologic Advances Generated by the Human Health Exposure Analysis Resource Program.Current epidemiology reports · 2023Article
- Human-relevant exposure to di-n-butyl phthalate tampers with the ovarian insulin-like growth factor 1 system and disrupts folliculogenesis in young adult mice.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Phthalates cause a low-renin phenotype commonly found in premature infants with idiopathic neonatal hypertension.Pediatric nephrology (Berlin, Germany) · 2023Review
- The State of Research and Weight of Evidence on the Epigenetic Effects of Bisphenol A.International journal of molecular sciences · 2023Article
- Probing prenatal bisphenol exposures and tissue-specific DNA methylation responses in cord blood, cord tissue, and placenta.Reproductive toxicology (Elmsford, N.Y.) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Endocrine disrupting chemicals (EDCs) pose a public health risk through disruption of normal biological processes. Identifying toxicoepigenetic mechanisms of developmental exposure-induced effects for EDCs, such as phthalates or bisphenol A (BPA), is essential. Here, we investigate whether maternal exposure to EDCs is predictive of infant DNA methylation at candidate gene regions. In the Michigan Mother-Infant Pairs (MMIP) cohort, DNA was extracted from cord blood leukocytes for methylation analysis by pyrosequencing (n = 116) and methylation changes related to first trimester levels of 9 phthalate metabolites and BPA. Growth and metabolism-related genes selected for methylation analysis included imprinted (IGF2, H19) and non-imprinted (PPARA, ESR1) genes along with LINE-1 repetitive elements. Findings revealed decreases in methylation of LINE-1, IGF2, and PPARA with increasing phthalate concentrations. For example, a log unit increase in ΣDEHP corresponded to a 1.03 [95% confidence interval (CI): -1.83, -0.22] percentage point decrease in PPARA methylation. Changes in DNA methylation were also inversely correlated with PPARA gene expression determined by RT-qPCR (r = -0.34, P = 0.02), thereby providing evidence in support of functional relevance. A sex-stratified analysis of EDCs and DNA methylation showed that some relationships were female-specific. For example, urinary BPA exposure was associated with a 1.35 (95%CI: -2.69, -0.01) percentage point decrease in IGF2 methylation and a 1.22 (95%CI: -2.27, -0.16) percentage point decrease in PPARA methylation in females only. These findings add to a body of evidence suggesting epigenetically labile regions may provide a conduit linking early exposures with disease risk later in life and that toxicoepigenetic susceptibility may be sex specific.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.