Related Experiment Video
Updated: Aug 13, 2025
A Modified QuEChERS-HPLC Method for Detection of Polycyclic Aromatic Hydrocarbons in Zebrafish Embryos Exposed to Fine Particulate Matter
Published on: June 13, 2025
Placental transcriptomic signatures of prenatal exposure to Hydroxy-Polycyclic aromatic hydrocarbons
Alison G Paquette1, Samantha Lapehn2, Sophie Freije3
1Seattle Children's Research Institute, Seattle, WA, USA; University of Washington, Seattle, WA, USA.
Insights
Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) alters placental gene expression, potentially impacting infant health. This study identified specific genes and pathways affected by these common pollutants.
Area of Science:
- Environmental Health
- Genomics
- Toxicology
Background:
- Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants.
- Prenatal exposure to PAHs can negatively affect infant and child development.
- PAHs are known to cross the placenta, posing risks during pregnancy.
Purpose of the Study:
- To conduct the first human transcriptomic analysis of PAHs in the placenta.
- To investigate the relationship between prenatal PAH exposure and placental gene expression.
- To understand how PAHs might disrupt placental function.
Main Methods:
- Quantified prenatal PAH exposure using urinary monohydroxy-PAH (OH-PAH) metabolites in 629 pregnant participants.
- Analyzed placental gene expression using RNA sequencing.
- Used linear models for association analysis and performed sex-stratified evaluations.
- Validated findings in cell cultures exposed to phenanthrene.
Main Results:
- Found associations between 6 OH-PAHs and the placental expression of 8 genes.
- Identified 3 biological pathways linked to 4 OH-PAHs.
- Observed increased placental expression of SGF29 and TRIP13, and the vitamin digestion and absorption pathway.
- Noted more associations in female fetuses compared to males.
Conclusions:
- Identified novel genes (e.g., TRIP13) in the placenta affected by OH-PAHs.
- Suggests TRIP13 upregulation may indicate a DNA damage response.
- Highlights potential alterations in vitamin metabolism pathways due to PAH exposure.
- Recommends further research on identified genes' roles in placental function and health outcomes.
Background:
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous pollutants originating from petrogenic and pyrogenic sources. PAH compounds can cross the placenta, and prenatal PAH exposure is linked to adverse infant and childhood health outcomes.
Objective:
In this first human transcriptomic assessment of PAHs in the placenta, we examined associations between prenatal PAH exposure and placental gene expression to gain insight into mechanisms by which PAHs may disrupt placental function.
Methods:
The ECHO PATHWAYS Consortium quantified prenatal PAH exposure and the placental transcriptome from 629 pregnant participants enrolled in the CANDLE study. Concentrations of 12 monohydroxy-PAH (OH-PAH) metabolites were measured in mid-pregnancy urine using high performance liquid chromatography tandem mass spectrometry. Placental transcriptomic data were obtained using paired-end RNA sequencing. Linear models were fitted to estimate covariate-adjusted associations between maternal urinary OH-PAHs and placental gene expression. We performed sex-stratified analyses to evaluate whether associations varied by fetal sex. Selected PAH/gene expression analyses were validated by treating HTR-8/SVneo cells with phenanthrene, and quantifying expression via qPCR.
Results:
Urinary concentrations of 6 OH-PAHs were associated with placental expression of 8 genes. Three biological pathways were associated with 4 OH-PAHs. Placental expression of SGF29 and TRIP13 as well as the vitamin digestion and absorption pathway were positively associated with multiple metabolites. HTR-8/SVneo cells treated with phenanthrene also exhibited 23 % increased TRIP13 expression compared to vehicle controls (p = 0.04). Fetal sex may modify the relationship between prenatal OH-PAHs and placental gene expression, as more associations were identified in females than males (45 vs 28 associations).
Discussion:
Our study highlights novel genes whose placental expression may be disrupted by OH-PAHs. Increased expression of DNA damage repair gene TRIP13 may represent a response to double-stranded DNA breaks. Increased expression of genes involved in vitamin digestion and metabolism may reflect dietary exposures or represent a compensatory mechanism to combat damage related to OH-PAH toxicity. Further work is needed to study the role of these genes in placental function and their links to perinatal outcomes and lifelong health.
More Related Videos
08:08Determination of the Transport Rate of Xenobiotics and Nanomaterials Across the Placenta using the ex vivo Human Placental Perfusion Model
Published on: June 18, 2013
12:02Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption
Published on: July 30, 2016
