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系統識別號 U0026-0108201016204100
論文名稱(中文) 噪音暴露勞工抗氧化能力與環境因子對噪音引起的聽覺影響
論文名稱(英文) Anti-oxidation Capability and Environmental Factors for Noise Induced Hearing Loss
校院名稱 成功大學
系所名稱(中) 環境醫學研究所
系所名稱(英) Institute of Environmental and Occupational Health
學年度 98
學期 2
出版年 99
研究生(中文) 林政佑
研究生(英文) Cheng-Yu Lin
電子信箱 yu621109@ms48.hinet.net
學號 s7893108
學位類別 博士
語文別 中文
論文頁數 101頁
口試委員 指導教授-蔡朋枝
共同指導教授-郭育良
召集委員-吳俊良
口試委員-石東生
口試委員-孫逸民
中文關鍵字 噪音性聽力損失;暫時性聽力損失;永久性聽力損失;穀胱甘肽硫轉移酶;基因多型性;工作暴露矩陣;N-乙醯基半胱氨酸;藥物臨床試驗 
英文關鍵字 noise-induced hearing loss  temporary threshold shift  permanent threshold shift  Glutathione S-transferase  genetic polymorphism  job-exposure matrix  N-Acetylcysteine  clinical trial 
學科別分類
中文摘要 噪音性聽力損失是一個複雜的疾病,可能同時由遺傳因子與環境因素交互作用所致。過去針對環境中化學物質對聽力損失的研究已有多位學者投入,近年來在動物實驗中也發現,大量噪音暴露會引起聽覺系統內部活性氧物質(reactive oxygen species, ROS)過度產生,進而破壞耳蝸內的聽覺細胞,因此氧化壓力的存在有可能與聽力損失有關聯。
本研究主題共分成三部分,第一部分是採橫斷式研究方法,利用標準化聽力檢測步驟,建立國內一般民眾的聽力資料庫,藉以作為相關流行學研究的參考依據。本研究是以大台南地區的民眾為母群體,針對七大行政區域作系統性分層隨機抽樣,以家庭為基本抽樣單位,凡是家庭成員大於20歲者皆邀請參與研究,受測個案在標準聽力檢測艙接受聽力檢查。研究結果顯示優耳聽閾值大於25分貝的聽損盛行率為21.4%,年齡、性別與中耳疾病是影響聽力損失嚴重度的重要因子,此外職業性噪音暴露的盛行率在男性、女性個案分別為18.3%與4.4%。因此噪音性聽力損失是不可忽視的重要研究主題。
第二部分是針對噪音性聽力損失的形成機轉,探討人體內負責保護性抗氧化系統的基因多型性與噪音性聽力損失的易感性高低是否有關聯,以及研究環境中哪些因子會影響噪音性聽力損失的易感性高低。本研究針對噪音暴露工人,分析他們體內涉及氧化壓力反應的穀胱甘肽硫轉移酶(Glutathione S-transferase, GST)基因多型性,包括GSTT1與GSTM1這兩個基因的缺損型(deletion)多型性,以及源自GSTP1基因的單一核苷酸多型性(Single nucleotide polymorphism, SNP)。本研究以南台灣某一製造業工廠工人為母群體,採隨機抽樣方式,收集工作年數大於5年的個案。先作問卷調查,詳細記錄噪音暴露史、耳鳴史、煙酒史、藥物習慣史與計算身體質量指數(Body Mass Index, BMI),並且收集個案的血液,由專業醫師作耳鏡局部檢查,測量上班前與下班後的聽損嚴重程度,包括在500, 1K, 2K, 3K, 4K, 6K, 8K 赫玆的純音聽力閾值,以及利用個人噪音劑量器測量當天工人噪音暴露總量,此外偵測各工作單位的背景噪音量,計算每位工人的噪音暴露總量(工作暴露矩陣)(Job-Exposure Matrix)。利用統計分析方法,控制各個可能干擾因子之後,比較不同GST基因多型性的噪音暴露族群,各自在高頻區域的聽力損失嚴重度是否有統計上顯著差異。經研究發現高頻區域的暫時性噪音性聽力損失與全天噪音暴露總量有明顯相關性,工作前的聽閾值與全天噪音暴露量是影響高頻暫時性噪音性聽力損失嚴重度的重要因子,此外,當勞工個體同時具有GSTT1與GSTM1這兩個基因的缺損型(Null)多型性,以及源自GSTP1基因的Ile105/Ile105多型性時,他們的高頻暫時性噪音性聽力損失嚴重度比較明顯。藉由工作暴露矩陣模式的評估,我們也發現高頻區域的永久性噪音性聽力損失與噪音暴露總量有明顯的劑量效應關係,而且當暴露於高噪音環境中(大於90分貝,40年),勞工個體同時具有GSTT1與GSTM1這兩個基因的缺損型(Null)多型性,以及源自GSTP1基因的Ile105/Ile105多型性者,他們的高頻永久性噪音性聽力損失嚴重度比較明顯。
第三部分是探討在噪音暴露之環境中,勞工有無服用抗氧化藥物N-乙醯基半胱氨酸(N-acetylcysteine),對噪音引起的暫時性噪音性聽力損失是否具有不同程度的保護作用,並且進一步探討不同抗氧化基因多型性個體是否會對N-乙醯基半胱氨酸呈現不同反應。結果發現,抗氧化藥物N-乙醯基半胱氨酸可以明顯減低高頻暫時性噪音性聽力損失嚴重度,而且若勞工個體同時具有GSTT1與GSTM1這兩個基因的缺損型(Null)多型性,該藥物保護作用比較明顯。
綜合上述成果,本研究發現在人類噪音性聽力損失形成機轉中,GST抗氧化酵素的基因多型性與環境因子所扮演的角色,亦證實抗氧化藥物N-乙醯基半胱氨酸(N-acetylcysteine)對於高頻暫時性噪音性聽損具有顯著保護效用。未來研究方向包括:增加研究個案數,增加不同的噪音類型(例如:穩定音、變動音、衝擊音) ,以及探討其他有關氧化壓力的基因多型性。此外也應進一步研究抗氧化藥物N-乙醯基半胱氨酸對於永久性噪音性聽損的保護效果,探討該藥物的最佳作用劑量,同時也可利用這些已建立的藥物臨床試驗模式、實驗技術,探討其他抗氧化劑(例如:維他命C、維他命E)是否也具有聽力保護作用。
英文摘要 Noise-induced hearing loss (NIHL) is a complex disease which might be caused by interactions between environmental and genetic factors. Noise is the best-known and one of the most studied environmental factors causing hearing loss. Genetic factors may modify the susceptibility to noise. The generation of reactive oxygen species (ROS) is thought to be part of the mechanism underlying NIHL. Glutathione is an important cellular antioxidant that limits cell damage by ROS.
This is a three-part study. The first part was a cross-sectional study. It was to create a reference database that can be used for epidemiological studies of hearing impairment (as determined by otological status assessment and standardized audiological tests) in the Taiwanese population. A systematic stratified sampling framework involving the seven administrative areas in Tainan City was used, with each family being the basic sampling unit. All family members >20 years old, who consented to undergo all the examinations, were included. The overall prevalence of hearing impairment (>25 dB) in the population in Taiwan was 21.4%. Middle ear disease was a significant risk factor for hearing impairment in addition to age and gender. The prevalence of occupational noise exposure for female subjects was 4.4%, and that for male subjects was 18.3%. Therefore, NIHL is an important issue for further research.
In the second part, we investigated whether Glutathione S-transferase (GST) genetic variants in the human antioxidant system were associated with the susceptibility to NIHL. The noise-exposed workers from steel industries in Southern Taiwan, who have worked for more than 5 years, were recruited. Firstly, questionnaires interview about noise exposure, smoking, alcohol drinking, drug habit history and calculation of Body Mass Index (BMI) were done. After detailed local examination with otoscope, these subjects received hearing tests by pure-tone audiometry (PTA) before and after their daily works. The amount of noise exposure was calculated by Job-Exposure Matrix (JEM) using average yearly site-specific noise monitoring data and individual workers’ job history, to yield life-time total noise exposure level. Blood samples were collected. Deletion polymorphisms in the GSTT1 and GSTM1 genes, and single nucleotide polymorphisms (SNPs) in GSTP1 were determined. Statistical analysis was performed to compare their respective genotype frequencies. We found that noise-induced temporary threshold shift (TTS) for high frequencies (HF) by PTA was related to the daily noise exposure. It suggested that pre-shift hearing impairment and daily noise exposure had impacts on TTS for HF by PTA. Based on combinatory analysis, we found that individuals carrying all genotypes with GSTM1 null, GSTT1 null, and GSTP1 Ile105/Ile105 were more susceptible to noise-induced TTS. In addition, the JEM model-based estimates provided a significant dose-response relationship between noise exposure and noise-induced permanent threshold shift (PTS). We found that workers carrying GSTM1 null, GSTT1 null and GSTP1 Ile105/Ile105 genotypes were susceptible to noise-induced PTS, when a corresponding 40-year noise exposure level was higher than 90 dBA.
In the third part of the study, we conducted a study to determine whether the antioxidant, N-Acetylcysteine (NAC), protected men against noise-induced TTS, and whether subgroups with genetic polymorphisms of GSTM1 and GSTT1 responded to NAC differently. Our results presented that NAC significantly reduced noise-induced TTS. When the participants were grouped by GST M1/T1 genotypes, the NAC effect was only significant among workers with null genotypes in both GSTM1 and GSTT1.
In conclusion, the results of this study might help elucidate the relative importance of antioxidant enzymes as risk factors for NIHL. We also proved that the use of NAC could significantly reduce noise-induced TTS. Further studies should include a greater number of participants and involve workers exposed to different patterns of noise (i.e., steady noise, fluctuating noise, and impulse noise). Moreover, investigations of other genotypic variants involved in oxidative stress response for elucidating the gene-environment interaction for NIHL are warranted. We would also like to examine whether noise-induced PTS could be significantly reduced by the prophylactic oral administration of NAC in a prospective, randomized double-blind cross-over trial.
論文目次 中文摘要……………………………………………………………………………I
Abstract…………………………………………………………………………………………………………………………………IV
誌謝………………………………………………………………………………VII
Contents…………………………………………………………………………………………………………………………………IX
List of Tables…………………………………………………………………………………………………………………XV
List of Figures……………………………………………………………………………………………………………XVI
Abbreviations………………………………………………………………………………………………………………XVII
Chapter 1 Introduction……………………………………………………………………………………………1
1.1 Epidemiology of hearing impairment…………………………………1
1.2 Prevalence of hearing impairment in Taiwan……………1
1.3 Noise-induced hearing impairment: A complex
disease…………………………………………………………………………………………………………2
1.4 Genetic basis for Noise-induced hearing
impairment…………………………………………………………………………………………………3
1.5 Mechanisms of noise-induced hearing impairment…4
1.6 Glutathione S-transferase and noise-induced
hearing impairment……………………………………………………………………………8
1.7 Quantitative noise exposure assessment: Job-
exposure matrix……………………………………………………………………………………9
1.8 Antioxidant medicine: N-acetyl-cysteine……………………9
1.9 Research background and objectives of this
study……………………………………………………………………………………………………………10
Chapter 2 Materials and Methods…………………………………………………………………12
2.1 Study framework…………………………………………………………………………………12
2.2 Part 1—Prevalence of hearing impairment in an
adult population in southern Taiwan……………………………13
2.2.1 Subjects……………………………………………………………………………………………………13
2.2.2 Battery of tests………………………………………………………………………………15
2.2.3 Statistical analysis……………………………………………………………………16
2.3 Part 2—Relationship between GST genetic
polymorphisms and NIHL………………………………………………………………17
2.3.1 Glutathione S-transferase M1, T1, and P1
polymorphisms as susceptibility factors for
noise-induced temporary threshold shift…………………17
2.3.1.1 Subjects……………………………………………………………………………………………………17
2.3.1.2 Questionnaire………………………………………………………………………………………18
2.3.1.3 Noise exposure measurement……………………………………………………18
2.3.1.4 Assessment of hearing status………………………………………………19
2.3.1.5 Genotyping of GST polymorphisms………………………………………20
2.3.1.6 Statistical analysis……………………………………………………………………22
2.3.2 Gene-environmental interaction in noise-induced
permanent threshold shift………………………………………………………23
2.3.2.1 Subjects……………………………………………………………………………………………………23
2.3.2.2 Questionnaire………………………………………………………………………………………23
2.3.2.3 Daily noise exposure measurement……………………………………23
2.3.2.4 Total noise exposure assessment over a worker’s
career…………………………………………………………………………………………………………24
2.3.2.5 Evaluation of hearing status………………………………………………25
2.3.2.6 Genotyping of GST polymorphisms………………………………………26
2.3.2.7 Statistical analysis……………………………………………………………………26
2.4 Part 3—N-acetyl-cysteine against noise-induced
temporary threshold shift in male workers……………27
2.4.1 Subjects……………………………………………………………………………………………………27
2.4.2 Study design…………………………………………………………………………………………28
2.4.3 Assessment measures………………………………………………………………………29
2.4.4 Questionnaire………………………………………………………………………………………30
2.4.5 Noise exposure measurement……………………………………………………30
2.4.6 Assessment of hearing status………………………………………………30
2.4.7 Genotyping of GST polymorphisms………………………………………31
2.4.8 Statistical analysis……………………………………………………………………31
Chapter 3 Results………………………………………………………………………………………………………33
3.1 Prevalence of hearing impairment in an adult
population in southern Taiwan……………………………………………33
3.1.1 Demographic data and prevalence of hearing
impairment………………………………………………………………………………………………33
3.1.2 Overall prevalence of hearing impairment in
female and male subjects…………………………………………………………34
3.1.3 Median hearing threshold levels for different
age groups………………………………………………………………………………………………35
3.1.4 Prevalence of occupational noise exposure for
female and male subjects…………………………………………………………36
3.1.5 Significant risk factors for the prevalence of
hearing impairment…………………………………………………………………………37
3.2 Glutathione S-transferase M1, T1, and P1
polymorphisms as susceptibility factors for
noise-induced temporary threshold shift…………………38
3.2.1 Demographic and personal characteristics………………38
3.2.2 Audiometry and temporary threshold shift………………40
3.2.3 Association between risk factors and daily pure-
tone threshold changes………………………………………………………………42
3.3 Gene-environmental interaction in noise-induced
permanent threshold shift ……………………………………………………44
3.3.1 Demographic and personal characteristics………………44
3.3.2 Noise exposure and hearing threshold levels………46
3.3.3 Association between risk factors and permanent
hearing threshold……………………………………………………………………………48
3.4 N-acetyl-cysteine against noise-induced
temporary threshold shift in male workers……………50
3.4.1 Demographic and personal characteristics………………50
3.4.2 Effects of N-acetyl-cysteine and placebo on
temporary hearing threshold shifts………………………………52
3.4.3 Association between GST genetic variants and
effects of N-acetyl-cysteine………………………………………………53
Chapter 4 Discussion………………………………………………………………………………………………54
4.1 Prevalence of hearing impairment in an adult
population in southern Taiwan……………………………………………54
4.1.1 Comparison of the prevalence of hearing
impairment in different countries…………………………………54
4.1.2 Association between gender and the severity of
hearing impairment…………………………………………………………………………56
4.1.3 Association between age and the deterioration of
hearing impairment…………………………………………………………………………56
4.1.4 Possible selection bias in the community-based
epidemiological investigation……………………………………………57
4.2 Glutathione S-transferase M1, T1, and P1
polymorphisms as susceptibility factors for
noise-induced temporary threshold shift…………………58
4.2.1 GST antioxidant ability and noise-induced
temporary threshold shift………………………………………………………58
4.2.2 GSTP1 polymorphic variants and the risk of noise-
induced temporary threshold shift…………………………………59
4.2.3 Combined effect of GSTM1, GSTT1 and GSTP1 on
noise-induced temporary threshold shift…………………59
4.2.4 Risk factors on noise-induced temporary
threshold shift…………………………………………………………………………………60
4.2.5 Limitation of GSTM1 and GSTT1 genotypes
categorization……………………………………………………………………………………61
4.2.6 Comparison of the frequency of GST genotypes in
different countries………………………………………………………………………62
4.2.7 Age-related hearing impairment and noise-induced
hearing impairment…………………………………………………………………………62
4.2.8 Limitation of the study……………………………………………………………63
4.3 Gene-environmental interaction in noise-induced
permanent threshold shift ……………………………………………………63
4.3.1 GST antioxidant ability and noise-induced
permanent threshold shift………………………………………………………63
4.3.2 Influence of hearing protectors on noise-induced
permanent threshold shift………………………………………………………64
4.3.3 Combined effect of GSTM1, GSTT1 and GSTP1 on
noise-induced permanent threshold shift…………………64
4.3.4 Risk factors on noise-induced permanent
threshold shift…………………………………………………………………………………65
4.3.5 A-weighted sound levels and the risks of noise-
induced permanent hearing impairment…………………………66
4.3.6 Gene-environmental interaction in the studies of
noise-induced hearing loss……………………………………………………67
4.3.7 Job-exposure matrix model to predict total noise
exposure……………………………………………………………………………………………………67
4.3.8 Limitation of the study……………………………………………………………68
4.4 N-acetyl-cysteine against noise-induced
temporary threshold shift in male workers……………68
4.4.1 Human clinical trials relating to efficacy of N-
acetyl-cysteine…………………………………………………………………………………68
4.4.2 Effects of N-acetyl-cysteine on noise-induced
temporary threshold shift………………………………………………………69
4.4.3 Compensatory mechanism in antioxidation for low
GST enzymes activities………………………………………………………………70
4.4.4 Randomized double-blind study design prevent
biased hearing assessment………………………………………………………71
4.4.5 Strengths and limitations of the study……………………71
4.4.6 Chemoprevention in occupational hearing
impairment………………………………………………………………………………………………72
Chapter 5 Conclusions and recommendations………………………………………73
References……………………………………………………………………………………………………………………………75
Appendixes……………………………………………………………………………………………………………………………94
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