Abstract
Fine particulate matter (PM(2.5)) refers to particulate matter with an aerodynamic diameter of 2.5 μm or less. As a major air pollutant, PM(2.5) not only damages the respiratory and cardiovascular systems but is also closely associated with thyroid diseases. To gain a deeper understanding of the link between PM(2.5) exposure and adverse thyroid outcomes, we analyzed published epidemiological studies, summarizing the effects of PM(2.5) exposure on thyroid function, structure, and related diseases, as well as its potential mechanisms. Studies have shown that PM(2.5) exposure can lead to abnormal thyroid hormone levels, increasing the risk of various thyroid diseases, including thyroid dysfunction, thyroid autoimmune diseases, thyroid nodules, and thyroid cancer. Further analysis revealed that the mechanisms involve a multi-system interaction network, including oxidative stress, inflammatory response, hypothalamic-pituitary-thyroid (HPT) axis dysfunction, direct disruption of thyroid follicular structure and function, and the emerging intestinal-thyroid axis regulatory pathways. These mechanisms collectively lead to thyroid hormone imbalance and tissue damage. Despite ongoing research, our understanding of the effects of PM(2.5) on the thyroid remains limited. Therefore, this article summarizes the effects of PM(2.5) on the thyroid gland and its potential toxic mechanisms, outlines future research directions, and provides a scientific basis for developing precise protection strategies and air quality standards.