Environmental Endocrine Disruptors and Thyroid Dysfunction: A Systematic Review of Mechanisms and Human Evidence

Introduction:
Endocrine-disrupting chemicals (EDCs) are environmental contaminants that interfere with hormone synthesis, metabolism, and receptor signaling, thereby disrupting endocrine homeostasis. The thyroid gland is particularly sensitive to these compounds, and increasing evidence suggests that EDC exposure is associated with thyroid dysfunction and adverse health outcomes.

Methods:
A systematic literature review was conducted using electronic databases, including Google Scholar, PubMed, and ScienceDirect. Studies published between 2015 and 2025 were identified using keywords such as “endocrine-disrupting chemicals,” “thyroid function,” “thyroid hormones,” “bisphenol A,” “phthalates,” “phenols,” “parabens,” and “flame retardants.” Additional filters were applied to identify relevant human, epidemiological, and experimental studies.

Results:
Evidence from epidemiological and experimental studies indicates that EDC exposure is associated with alterations in thyroid function. Human studies show that phthalates are linked to thyroid abnormalities, including nodules and disrupted hormone homeostasis. Population-based analyses demonstrate negative associations between exposure to phenols, parabens, and phthalate metabolites and circulating thyroxine (T4) levels, with modifying effects of iodine status and thyroid autoimmunity. Experimental studies further show that bisphenol A (BPA) alters thyroid hormone balance, increasing thyroid-stimulating hormone (TSH) levels and disrupting T3/T4 regulation. In addition, exposure to flame retardants has been associated with an increased risk of papillary thyroid cancer. Mechanistically, contaminants such as perchlorate, nitrate, and thiocyanate impair iodide uptake by inhibiting the sodium–iodide symporter (NIS), thereby reducing thyroid hormone synthesis.

Conclusions:
Current evidence suggests that EDC exposure is associated with thyroid dysfunction through multiple biological pathways. Although findings remain heterogeneous, the consistency of epidemiological and experimental data highlights the need for further longitudinal and mechanistic studies to clarify dose–response relationships and inform public health strategies.