Abstract
Numerous compelling epidemiological studies have linked air pollution to Sudden Sensorineural Hearing Loss (SSNHL). However, the causal relationship behind this association has not yet been established. We employed a Two-Sample Mendelian Randomization (MR) approach to investigate the causal relationship between air pollution (nitrogen dioxide, nitrogen oxides, PM(2.5), PM(10), and PM(2.5-10)) and SSNHL.Independent genetic variants associated with air pollution and SSNHL were selected as instrumental variables (IVs) at a genome-wide significance level. All summary data were obtained from GWAS databases. The primary method used for MR analysis was the Inverse Variance Weighted (IVW) method, supplemented by various MR analyses method, including weighted median, simple mode, weighted mode, and MR-Egger, to ensure robustness. Cochran's Q test was employed for heterogeneity assessment. To identify potential pleiotropy, we utilized MR-Egger regression and the MR-PRESSO global test. Additionally, sensitivity analyses were performed using the leave-one-out approach. The MR analysis using the IVW method showed no substantial evidence supporting a direct causal relationship between air pollution and the risk of SSNHL (Nitrogen dioxide: P = 0.488, Nitrogen oxides: P = 0.572, PM(2.5): P = 0.480, PM(10): P = 0.225, and PM(2.5-10): P = 0.608). There was no evidence of heterogeneity or pleiotropy, and sensitivity analyses based on the leave-one-out approach indicated that individual single nucleotide polymorphisms (SNPs) did not affect the robustness of the results.This study found no substantial evidence to support a causal relationship between air pollution and the risk of SSNHL in the European population.