Association Between Air Pollution and Sudden Sensorineural Hearing Loss: A Nine-Year Retrospective Study

Background: Sudden sensorineural hearing loss (SSHL) is an acute auditory disorder with multifactorial causes. This study aimed to investigate the association between regional air pollution levels and SSHL case occurrence in our cohort. Methods: A total of 223 individuals diagnosed with sudden sensorineural hearing loss (SSHL) between 2016 and 2025 were included in the study at the Ear, Nose and Throat Clinic of Sivas Cumhuriyet University. An internal medicine specialist excluded metabolic causes based on concurrent laboratory tests and medical history records. The monthly averages of the following air pollution parameters were obtained from the central monitoring stations of the Ministry of Environment, Urbanisation and Climate Change in Sivas: PM₁₀, SO₂, PM_2.5, NOx, NO, CO and NO₂. The cumulative risk was then calculated by a public health specialist. The data were analyzed with a significance level set at 0.05. Results: A total of 223 patients with SSHL (mean age: 52.71 ± 7.38 years; 52.5% male) were analyzed, of whom 55.2% had left-ear involvement. Hearing thresholds differed significantly in both ears after treatment at all frequencies (250-6000 Hz) (p = 0.001), with the greatest mean change observed at 2000 Hz. Post-treatment hearing scores also showed statistically significant differences in both ears, and strong positive correlations were observed between pre- and post-treatment hearing levels (p < 0.001). Although there was no statistically significant seasonal variation in SSHL case distribution (p > 0.05), a significant association was identified between annual variations in air pollution levels and SSHL case occurrence. Conclusions: In this single-centre retrospective study, an association was identified between region-al air pollution levels and SSHL case occurrence. Given the retrospective single-centre design, ecological exposure assessment, and potential residual confounding, these findings should be interpreted as hypothesis-generating rather than as evidence of in-dividual-level causation or preventability. Larger multicentre studies incorporating individual exposure assessment are needed to further clarify this association.