Emerging Links Between PFAS Exposure and Autoimmune Thyroid Disease: A Narrative Review of Epidemiologic Evidence, Mechanistic Insights, and Research Gaps

Per‐ and polyfluoroalkyl substances (PFAS) are persistent synthetic chemicals widely distributed in the environment and human tissues. Known as endocrine‐disrupting chemicals, PFAS are increasingly investigated for their potential role in the rising global prevalence of autoimmune thyroid diseases (AITDs), such as Hashimoto's thyroiditis and Graves' disease. This narrative review synthesizes epidemiologic evidence and mechanistic insights to clarify this relationship. Epidemiologic findings remain heterogeneous; while some studies link PFOA and PFOS exposure to altered circulating thyroid hormones (e.g., increased FT3 and FT4), others report reduced T4 levels, particularly in vulnerable pregnant and neonatal populations. Mechanistically, PFAS interfere with thyroid homeostasis by disrupting iodide uptake via the sodium/iodide symporter (NIS), competing for transport proteins like transthyretin, and activating nuclear receptors like PPARα. Furthermore, PFAS promote immune dysregulation by modulating cytokine production and inducing oxidative stress, creating a microenvironment conducive to autoimmunity. Despite these biological plausibilities, many studies are limited by cross‐sectional designs and a lack of direct clinical AITD correlation. Future longitudinal research is essential to establish causality and guide public health interventions regarding environmental PFAS contamination.