Exploring the causal relationship between long-term exposure to particulate matter 2.5 and risk of thyroid disorders: a Mendelian randomization analysis.

Particulate matter 2.5 (PM2.5) has been increasingly linked to thyroid dysfunction, yet causal evidence remains limited. This study employs a two-sample Mendelian Randomization (MR) approach to assess the causal relationship between long-term PM2.5 exposure and thyroid disorders. Genetic instruments for PM2.5 exposure were sourced from the UK Biobank, while outcome data on thyroid dysfunction and its subtypes were obtained from the FinnGen consortium. The primary method was inverse-variance weighted (IVW), supplemented by MR-Egger, weighted median, simple mode and weighted mode analyses. Pleiotropy and heterogeneity were evaluated with MR-Egger intercept, MR-PRESSO, and Cochran's Q test. The IVW method revealed a significant 77% increased risk of thyroid disorders per standard deviation rise in PM2.5 exposure (OR = 1.77, 95% CI: 1.29-2.43, p = 3.93 × 10-4). Notably, a strong causal association was identified with autoimmune hypothyroidism (OR = 1.83, 95% CI: 1.26-2.64, p = 1.33 × 10-3), but not with autoimmune hyperthyroidism or other subtypes. Sensitivity analyses showed no pleiotropy or heterogeneity. These findings support a causal role of PM2.5 in , thyroid dysfunction and highlight the importance of reducing air pollution to protect thyroid health.