Tinnitus is a known long-term health effect of noise exposure. Whether susceptible genotypes predispose noise-exposed workers to tinnitus remains unclear. This study investigated the interactive effects of noise exposure, auditory function, and glutathione S-transferase (GST) gene polymorphisms on tinnitus risk.
Audiologists working in occupational health settings should be aware that genetic susceptibility (GSTM1 null genotype) may amplify tinnitus risk in noise-exposed workers, though genetic screening is not yet standard of care and no protocol change is warranted now.
Identifying a gene–environment interaction in occupational tinnitus risk points toward future personalized prevention strategies for noise-exposed workers.
- 01Cross-sectional study of noise-exposed steelworkers examining tinnitus risk factors.
- 02GSTM1 null genotype (a variant affecting antioxidant defense) interacts with occupational hearing loss to raise tinnitus risk.
- 03Both genetic and environmental (noise exposure) factors independently and jointly influence tinnitus prevalence.
- 04Cross-sectional design limits causal inference; prospective studies are needed.
- 05Relevant to occupational audiology and industrial hearing conservation programs.
GSTM1 genotype interacts with occupational hearing loss to increase tinnitus risk in noise-exposed steelworkers.
studypartially supportedOccupational noise-induced hearing loss is independently associated with tinnitus in steelworkers.
studysupported- PMID
- 42382212
- DOI
- 10.1016/j.shaw.2026.03.002.
- Journal
- Safety and Health at Work
- Publication type
- research_article
- Evidence level
- 3
- Population
- Noise-exposed steelworkers
- Intervention
- Glutathione S-Transferase M1 (GSTM1) genotype and occupational hearing loss (combined exposure)
- Comparator
- Workers without GSTM1 null genotype and/or without occupational hearing loss
Primary outcomes
Tinnitus prevalence; Interactive effect of GSTM1 genotype and occupational hearing loss on tinnitus risk