Prenatal airborne polycyclic aromatic hydrocarbon exposure, altered regulation of peroxisome proliferator-activated receptor gamma (Ppar)γ, and links with mammary cancer

Lichtiger, Lydia; Jezioro, Jacqueline; Rivera, Janelle; McDonald, Jacob D.; Terry, Mary Beth; Sahay, Debashish; Miller, Rachel L.

doi:10.1016/j.envres.2023.116213

Cited by 1 publication

(1 citation statement)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar results have been presented in the literature, suggesting associations between PAH metabolites and metabolic syndrome, cardiovascular conditions, and systemic inflammation [ 62 , 63 ]. Additionally, a mice-based study suggested prenatal exposure to PAHs and their associated multi-generational (offspring and grand-offspring) epigenetic effects [ 64 ]. Furthermore, Jednak et al identified associations between maternal MCPP exposures and placenta methylation, identifying differential methylation regions of the fibroblast growth factor 12 ( FGF12) (chr3:192445514–192445539), and the ADP-ribosyltransferase 5 ( ART5) (chr11:3663491–3663843) genes, suggesting potential alterations in protein function [ 65 ].…”

Section: Discussionmentioning

confidence: 99%

Gestational exposure to environmental chemicals and epigenetic alterations in the placenta and cord blood mononuclear cells

Puvvula,

Braun,

DeFranco

et al. 2024

Epigenetics Commun.

View full text Add to dashboard Cite

Background Exposure to environmental chemicals such as phthalates, phenols, and polycyclic aromatic hydrocarbons (PAHs) during pregnancy can increase the risk of adverse newborn outcomes. We explored the associations between maternal exposure to select environmental chemicals and DNA methylation in cord blood mononuclear cells (CBMC) and placental tissue (maternal and fetal sides) to identify potential mechanisms underlying these associations. Method This study included 75 pregnant individuals who planned to give birth at the University of Cincinnati Hospital between 2014 and 2017. Maternal urine samples during the delivery visit were collected and analyzed for 37 biomarkers of phenols (12), phthalates (13), phthalate replacements (4), and PAHs (8). Cord blood and placenta tissue (maternal and fetal sides) were also collected to measure the DNA methylation intensities using the Infinium HumanMethylation450K BeadChip. We used linear regression, adjusting for potential confounders, to assess CpG-specific methylation changes in CBMC (n = 54) and placenta [fetal (n = 67) and maternal (n = 68) sides] associated with gestational chemical exposures (29 of 37 biomarkers measured in this study). To account for multiple testing, we used a false discovery rate q-values < 0.05 and presented results by limiting results with a genomic inflation factor of 1±0.5. Additionally, gene set enrichment analysis was conducted using the Kyoto Encyclopedia of Genes and Genomics pathways. Results Among the 29 chemical biomarkers assessed for differential methylation, maternal concentrations of PAH metabolites (1-hydroxynaphthalene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 1-hydroxypyrene), monocarboxyisononyl phthalate, mono-3-carboxypropyl phthalate, and bisphenol A were associated with altered methylation in placenta (maternal or fetal side). Among exposure biomarkers associated with epigenetic changes, 1-hydroxynaphthalene, and mono-3-carboxypropyl phthalate were consistently associated with differential CpG methylation in the placenta. Gene enrichment analysis indicated that maternal 1-hydroxynaphthalene was associated with lipid metabolism and cellular processes of the placenta. Additionally, mono-3-carboxypropyl phthalate was associated with organismal systems and genetic information processing of the placenta. Conclusion Among the 29 chemical biomarkers assessed during delivery, 1-hydroxynaphthalene and mono-3-carboxypropyl phthalate were associated with DNA methylation in the placenta.

show abstract