AIR pollution may raise tinnitus risk, especially in people with higher genetic susceptibility, a large cohort study suggests.
Air Pollution and Tinnitus Risk
Composite air pollution exposure was associated with higher odds of current tinnitus in a large UK Biobank analysis of 79,277 adults with available tinnitus, environmental exposure, and genetic data. The study assessed particulate matter and nitrogen-based pollutants, including PM2.5, PM2.5–10, PM10, nitrogen dioxide, and nitrogen oxides, alongside a polygenic risk score derived from six tinnitus associated genetic variants.
Overall, 10,501 participants, or 13.2%, reported current tinnitus. Each interquartile range increase in the composite air pollution score was associated with 6% higher odds of current tinnitus in the primary analysis. The association persisted after full adjustment for sociodemographic, lifestyle, health, workplace noise, hearing difficulty, speech recognition threshold, and hearing aid related factors, although the effect size was attenuated.
Individual pollutants showed weaker and less consistent associations after full covariate adjustment, suggesting that combined exposure may better capture the environmental burden relevant to auditory health than any single pollutant alone.
Genetic Susceptibility Strengthens Tinnitus Risk Signal
Genetic susceptibility was independently associated with tinnitus prevalence. Participants with both high air pollution exposure and high polygenic risk had substantially higher odds of current tinnitus compared with those with low pollution exposure and low genetic risk. This joint profile was associated with increased odds of current tinnitus, constant tinnitus, and transient tinnitus.
The strongest signal was observed for constant tinnitus, where high pollution exposure and high genetic risk were linked to 55% higher odds. Findings for tinnitus severity were less consistent, with no clear association for upsetting or non-upsetting tinnitus after adjustment.
What the Findings Mean for Auditory Health
The results support a potential role for integrated environmental and genetic assessment in tinnitus risk stratification. Proposed biological pathways include oxidative stress, inflammatory responses, cochlear vulnerability, and neuronal damage, although the study was not designed to establish causality.
Important limitations remain. The analysis was primarily cross sectional, tinnitus was self-reported, and air pollution exposure was modeled from residential estimates rather than directly measured. Longitudinal analyses did not clearly reproduce the cross-sectional findings, meaning the results should be interpreted as exploratory and hypothesis generating.
Still, the findings add to growing evidence that auditory health may be shaped by both environmental exposures and inherited susceptibility, highlighting the need for longer follow up and more diverse population studies.
Reference
Yang D et al. Effects of Composite Air Pollution and Genetic Susceptibility on Tinnitus Risk: A Large Population-Based Study. Journal of Otolaryngology – Head & Neck Surgery. 2026;55:1–12.
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