Open AccessEffect of Glutathione S‐transferase Polymorphisms to Music‐Induced Hearing Loss
Author(s) -
Chang YuTuan,
Chao ChunChih,
Lin ChengYu,
Wu JiummLiang
Publication year - 2011
Publication title -
otolaryngology–head and neck surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.232
H-Index - 121
eISSN - 1097-6817
pISSN - 0194-5998
DOI - 10.1177/0194599811415823a242
Subject(s) - gstp1 , audiology , glutathione s transferase , hearing loss , noise induced hearing loss , absolute threshold of hearing , genotype , genetic predisposition , glutathione , medicine , genetics , biology , gene , noise exposure , biochemistry , enzyme
Objective Both genetic and environmental factors contribute to noise‐induced hearing loss (NIHL). The objective of this study is to investigate the hypothesis that Glutathione S‐transferase (GST) genetic polymorphisms is related to susceptibility to developing NIHL caused by music exposure. Method This cross‐sectional study recruited high school students who habitually listen to music with portable players. PTA, distortion product otoacoustic emission (DPOAE), and questionnaire were obtained. Cumulative noise exposure (CNE) was calculated by listening time and volume of using portable players. Effects of GST1, GSTM1, and GSTP1‐105 on NIHL were analyzed. Results A total of 312 subjects were analyzed. Mean of PTA at high frequency (average of 3000, 4000, and 6000 Hz) was 8.07 dB HL (SD = 5.98). DPOAE amplitude level at high frequency was 20.28 dB SPL (SD = 5.10). Mean of CNE was 84.57 dB‐year (SD = 11.42). With the regression analysis model, there was a good dose‐response relationship between CNE and DPOAE amplitude levels at high frequency ( P <. 05). Furthermore, those subjects, with GSTT1‐null, GSTM1‐null, and GSTP1‐105 Ile/Ile genotypes, had higher susceptibility for developing hearing threshold elevation at high frequency ( P <. 05). Conclusion This study identified that GST genetic polymorphisms might modify the susceptibility of hearing threshold elevation at high frequency caused by music exposure. Moreover, investigations of other genotypic variants involved in oxidative stress response for elucidating the gene‐environment interaction for NIHL are warranted.