Air pollution and thyroid function - narrative review.

Air pollution is recognised as one of the primary environmental health hazards. The gas molecules including NO₂, CO, SO₂, O₃, particulate matter (PM₁₀, PM_2.5), and volatile organic compounds are being identified as particularly harmful. Despite this, a significant portion of the global population resides in areas with unsatisfactory air quality. Research suggests that air pollutants may act as endocrine disruptors, potentially interfering with thyroid function and contributing thyroid cancer development through oxidative stress, inflammation, and hormonal dysregulation. This paper reviews current literature on the effects of air pollution on thyroid function and thyroid cancer risk, focusing on epidemiological studies and mechanisms of endocrine disruption. Air pollutants are suspected endocrine disruptors that may interfere with thyroid function through receptor binding, hormone displacement, and disruptions in hormone transport, metabolism, and gene expression. Exposure to these pollutants, particularly during fetal development, can impair neonatal thyroid homeostasis, increasing the risk of hypothyroidism and long-term cognitive complications. Prolonged exposure to PM_2.5 has been associated with an increased risk of papillary thyroid cancer (PTC), particularly at higher concentrations and with long-term exposure. Elevated levels of NO₂ and O₃, as well as urban exposure to CO, have also been linked to a heightened risk of thyroid cancer. In contrast, an inverse relationship has been observed for PM₁₀ and SO₂. Additionally, studies suggest a potential association between PM_2.5 exposure and both increased risk and mortality of thyroid cancer, although multiple confounding factors must be considered. Air pollution with PM_2.5, NO₂, CO has also been found to affect thyroid hormone (TH) levels, but findings remain inconsistent, with relationships varying based on age, sex, and internal factors such as obesity. While evidence suggests a link between air pollution and thyroid dysfunction, as well as thyroid cancer risk, inconsistencies in findings highlight the need for further research. A deeper understanding of the mechanisms underlying these associations is crucial to assessing health risks and developing effective public health interventions.