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How PFAS Affect the Heart at a Cellular Level

By Dana Dolinoy posted 2 hours ago

  
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Thisblogis being shared under theSOT Secretarysname as part of their official duties and should not be interpreted as their personal or professional opinions.   

This blog was written by Talia Sager.

During the 2026 Poster Session “PFAS I,” I spoke with Norah Nguyen, a senior at the University of Massachusetts Amherst, about her poster, “Unveiling PFAS-Induced Cardiovascular Endothelial Toxicity: Differential DNA Damage and Oxidative Stress Responses, which shared research she completed during her internship with UL Research Institutes’ Chemical Insights.

The study explores how per- and polyfluoroalkyl substances (PFAS), also known as forever chemicals, affect human coronary artery endothelial cells (HCAEC), which supply oxygen and nutrients to the heart. While PFAS exposure has already been associated with hypertension and cardiovascular dysfunction, little research has examined how these chemicals may cause genetic damage in HCAEC.

The research team sought to fill this gap by testing several PFAS compounds, including PFPeA, PFHxA, PFHpA, PFOA, PFNA, PFDA, and a composite mixture, exposing HCAECs to low (10nM) and high (10uM) concentrations. After 24 hours, they assessed cell viability, production of reactive oxygen species (ROS), and activation of DNA damage pathways. Higher-dose exposures caused notable cytotoxicity and elevated ROS levels, indicating oxidative stress. At lower doses, PFAS activated the ATR-Chk1/Chk2, the first responder of the DNA damage cascade, causing cell proliferation to cease instead of cell death.

Key findings from this study also indicate a pattern of chain length-dependent toxicity where PFAS with longer chains, such as PFNA and PFDA, produced stronger oxidative stress and more pronounced DNA damage responses. This suggests that even low-level exposure to certain PFAS might impair vascular health in ways not previously understood.

This study highlights the urgent need to further examine PFAS impacts on the cardiovascular system, where new mechanistic insights could inform both regulatory policy and public health protection.

This blog reports on the Poster Session titled PFAS I that was held during the 2026 SOT Annual Meeting andToxExpo.

This blog was prepared by an SOT Reporter andrepresentsthe views of the author. SOT Reporters are SOT members who volunteer to write about sessions and events in which theyparticipateduring the SOT Annual Meeting andToxExpo. SOT does not propose or endorse any position by posting this article. If you are interested inparticipatingin the SOT Reporter program in the future, pleaseemail SOT Headquarters.


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