Demonstrates links between PFAS and metal exposures and cardiovascular risk markers, indicating that dietary inflammation may partially mediate these harmful effects.
Background: Cardiovascular disease (CVD) is a major global health burden influenced by genetic, behavioral, and environmental factors. Among these, exposure to per- and poly-fluoroalkyl substances (PFASs) and toxic metals has been increasingly implicated in adverse cardiovascular outcomes. However, the mediating role of dietary inflammation in these associations remains unclear. Objective: This study investigates the relationship between PFAS and metal exposures and CVD risk, focusing on the potential mediating role of diet, operationalized through the Dietary Inflammatory Index (DII). Additionally, this study examines age as an effect modifier in these associations. Methods: = 660), we assessed environmental exposures (lead, cadmium, mercury, perfluorooctanoic acid-PFOA, perfluorooctane sulfonate-PFOS), dietary inflammatory potential (DII), and cardiovascular markers (blood pressure, lipid profile, C-reactive protein). Statistical analyses included linear regression and Bayesian Kernel Machine Regression-Causal Mediation Analysis (BKMR-CMA) to estimate the direct, indirect (through DII), and total effects of exposure on CVD risk biomarkers. Mediation analysis suggested dietary inflammation may play a role, though estimates were imprecise. Conclusions: PFAS and metals may influence CVD risk through inflammatory pathways, with potential age-related differences. Future longitudinal studies are needed to clarify these complex interactions, reduce measurement error, and guide age-specific exposure regulations.
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Odediran et al. (2025) studied this question.
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