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. We conducted a cross-sectional study among steelworkers. Participants underwent audiometric testing to assess hearing levels and were surveyed for tinnitus. Blood samples were genotyped for GSTM1 and GSTT1 deletion polymorphisms using polymerase chain reaction. Multivariable logistic regression was used to evaluate associations between tinnitus and pure-tone audiometry (PTA), distortion product otoacoustic emission (DPOAE), and GST genotypes while controlling for age and other covariates. Among 239 male steelworkers (mean age ± SD: 48.29 ± 7.6 years), 27% reported tinnitus. Cumulative noise exposure and thresholds at low- and high-frequency PTA were significantly associated with tinnitus (adjusted odds ratio (OR) = 1.03, 1.06, and 1.04, 95% confidence interval (CI) = 1.00,1.06, 1.02,1.11, and 1.02,1.06 , p = 0.045, 0.002, <0.001, respectively). Although neither DPOAE nor GSTM1 nor GSTT1 genotypes showed a significant effect on tinnitus, we observed a significant interaction between low-frequency PTA and GSTM1 genotype ( p = 0.03). Specifically, compared with workers with non-null GSTM1 genes, workers with the GSTM1 null genotype were significantly more susceptible to low-frequency PTA-associated tinnitus (OR = 1.02 and 1.13, 95% CI = 0.96,1.08 and 1.06,1.22, respectively). The interactive effect of auditory functional status and antioxidant gene polymorphisms suggests that hair cell damage and oxidative stress in the cochlea both contribute to tinnitus development .
Lin et al. (Sun,) studied this question.