This review examines the growing body of evidence connecting exposure to air pollution with thyroid dysfunction across various populations and life stages. Recent epidemiological, clinical, and mechanistic investigations increasingly identify air pollution – both particulate matter and gaseous pollutants – as a potential endocrine disruptor affecting thyroid function. Evidence suggests that airborne contaminants, especially fine particulate matter (PM₂.₅; particles with an aerodynamic diameter of ≤2.5 μm), may disrupt thyroid hormone balance, contribute to autoimmune thyroid conditions, and potentially increase thyroid cancer risk. Key biological mechanisms underlying these associations include oxidative stress, inflammation, direct endocrine disruption, neuroendocrine system disruption, and epigenetic alterations. Particularly susceptible populations include pregnant women, developing fetuses, children, older adults, and individuals with preexisting thyroid conditions or compromised thyroid function. This review identifies significant research gaps, including the need for enhanced exposure assessment methodologies, longitudinal studies, and investigation of component-specific effects within air pollution mixtures, particularly heavy metals. Given the essential role of thyroid hormones in metabolism, development, and numerous physiological processes, these findings carry noteworthy inferences for clinical practice and public health policy. The development of targeted interventions, improved screening protocols, and stronger air quality standards are necessary to address this emerging public health concern. Comprehensive air quality management represents a promising approach to minimize the global burden of thyroid disorders.