ArticleEnvironment & health (Washington, D.C.)2025
Association of Per- and Polyfluoroalkyl Substance Exposure with Coronary Stenosis and Prognosis in Acute Coronary Syndrome.
Article in Environment & health (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed.
- Imaging and Molecular Biomarkers of PFAS-Related Vascular Aging: A Narrative Review.International journal of molecular sciences · 2026Review
- Per- and Polyfluoroalkyl Substances Exposure and Ischemic Heart Disease: Emerging Evidence from the Literature.Antioxidants (Basel, Switzerland) · 2026Review
- Mechanistic insights into PFAS derivatives-induced coronary heart disease and atherosclerotic renal artery stenosis via integrated network toxicology and molecular modeling.Toxicology research · 2026Article
- PFOS and Its Substitute OBS Cause Endothelial Dysfunction to Promote Atherogenesis in ApoEEnvironment & health (Washington, D.C.) · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Per- and polyfluoroalkyl substances (PFAS) have been associated with an increased risk of acute coronary syndromes (ACS), but the influence on the degree of coronary stenosis and prognosis is unclear. This study enrolled 571 newly diagnosed ACS cases and investigated the association of 12 PFAS with coronary stenosis severity and prognosis. Coronary stenosis was assessed via Gensini score (GS) and number of lesioned vessels (LVN). Prognosis was estimated by tracking major adverse cardiovascular events (MACE). Statistical analyses included ordered logistic regression, Cox regression, threshold effect models, Bayesian kernel machine regression, and quantile g-computation models. The adverse outcome pathway (AOP) framework was applied to reveal the underlying mechanism. The results showed positive association between perfluorooctanesulfonic acid (PFOS) and coronary stenosis, with an odds ratio (95% confidence interval, CI) of 1.33 (1.06, 1.67) for GS and 1.36 (1.08, 1.71) for LVN. PFOS significantly increased the incidence of poor prognosis, with hazard ratios (95% CI) of 1.96 (1.34, 2.89) for MACE. Threshold effects were observed for PFAS on coronary stenosis and prognosis, with PFOS thresholds of 4.65 ng/mL for GS, 4.54 ng/mL for LVN, and 5.14 ng/mL for MACE, and 5.03 ng/mL for nonfatal myocardial infarction. PFAS mixture exposure increased the occurrence of MACE and nonfatal myocardial infarction. The AOP framework shows that PFAS may impact protein binding, the cytoskeleton, multicellular biological processes, and heart function. In summary, our study revealed the adverse effects of PFAS on the degree of coronary stenosis and prognosis in ACS and identified potentially relevant molecular loci.
Identifiers
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Registered trials
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