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<p>This study utilized National Health and Nutrition Examination Survey (NHANES) data to examine associations between perfluoroalkyl substances (PFAS) exposure and cardiovascular disease (CVD) risk, addressing controversial evidence on their mixed effects. Serum concentrations of PFNA, PFOA, and PFOS were analyzed using an integrated multi-model approach combining restricted cubic splines (RCS), weighted quantile sum regression (WQS), and Bayesian kernel machine regression (BKMR). While individual analysis replicated the debated pattern showing PFOS negatively correlated with CVD risk (PFNA/PFOA nonsignificant), mixture analyses revealed novel insights: both WQS and BKMR demonstrated significantly negative associations between combined PFAS exposure and CVD risk score, with PFOS identified as the primary driver. Age was a key confounder, likely reflecting cumulative exposure. Molecular docking/dynamics simulations confirmed angiotensin II receptor type 1 (AGTR1) as a specific cardiovascular target of PFOS, suggesting potential disruption of angiotensin II signaling. The critical discrepancy—null effects of individual PFNA/PFOA versus significant negative mixture effects predominantly driven by PFOS—resolves the initial controversy and underscores the complexity of co-exposure interactions. These findings highlight that traditional single-substance assessments mask mixture-driven health effects, necessitating focused epidemiological and toxicological research on PFAS mixtures.</p>

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Single versus mixed perfluorinated compound exposures and cardiovascular disease risk: mechanistic insights from cross-sectional data and molecular interactions

  • 期刊论文

  • 发表日期：

    2026年2月7日

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  • Xiong-Bo Liu,
  • Jing-Xuan Zhou,
  • Zi-Yi Zheng,
  • Hong-Gang Ni

摘要

This study utilized National Health and Nutrition Examination Survey (NHANES) data to examine associations between perfluoroalkyl substances (PFAS) exposure and cardiovascular disease (CVD) risk, addressing controversial evidence on their mixed effects. Serum concentrations of PFNA, PFOA, and PFOS were analyzed using an integrated multi-model approach combining restricted cubic splines (RCS), weighted quantile sum regression (WQS), and Bayesian kernel machine regression (BKMR). While individual analysis replicated the debated pattern showing PFOS negatively correlated with CVD risk (PFNA/PFOA nonsignificant), mixture analyses revealed novel insights: both WQS and BKMR demonstrated significantly negative associations between combined PFAS exposure and CVD risk score, with PFOS identified as the primary driver. Age was a key confounder, likely reflecting cumulative exposure. Molecular docking/dynamics simulations confirmed angiotensin II receptor type 1 (AGTR1) as a specific cardiovascular target of PFOS, suggesting potential disruption of angiotensin II signaling. The critical discrepancy—null effects of individual PFNA/PFOA versus significant negative mixture effects predominantly driven by PFOS—resolves the initial controversy and underscores the complexity of co-exposure interactions. These findings highlight that traditional single-substance assessments mask mixture-driven health effects, necessitating focused epidemiological and toxicological research on PFAS mixtures.