INTRODUÇÃO: Em consequência da modernização tecnológica e industrial, surgiram novos fatores que originaram estudos específicos e direcionados sobre os possíveis efeitos nocivos desta evolução no trabalhador. Dentre estes, está o ruído, agente físico que pode causar danos ao organismo humano com efeitos de curto e médio prazo. O ruído, ao atuar sobre o trabalhador pode alterar processos internos do organismo, com consequências fisiológicas e emocionais. A diminuição gradual da acuidade auditiva decorrente da exposição continuada a níveis elevados de pressão sonora é denominada perda auditiva induzida pelo ruído (PAIR), segundo o Comitê Nacional de Ruído e Conservação Auditiva. A PAIR é caracterizada por perda neurossensorial, irreversível, quase sempre bilateral e simétrica, não ultrapassando 40dB(NA) nas frequências graves e 75dB(NA) nas frequências agudas; manifesta-se, primeiramente, em 6kHz, 4kHz e/ou 3kHz, progredindo lentamente às frequências de 8kHz, 2kHz, 1kHz, 500Hz e 250Hz. (MTE, Portaria 19, 1998). Entre os fatores que influenciam no desencadeamento da PAIR, destacam-se as características físicas do ruído (tipo, espectro e intensidade da pressão sonora), o tempo de exposição e a suscetibilidade individual. A PAIR está entre as doenças do trabalho de maior prevalência, com agravante de tratar-se de uma doença irreversível. Acomete com mais frequência o setor industrial. Este estudo avalia a incidência de perda auditiva por ruído e a existência de uma associação positiva entre estes diagnósticos e a exposição a diferentes níveis de pressão sonora em trabalhadores de duas unidades de uma mineradora e pelotizadora de minério de ferro. MÉTODOS: Estudo de coorte histórica com 1.069 trabalhadores divididos em dois grupos, tendo como referência os níveis de pressão sonora aos quais estavam expostos (menor ou igual a 88 dB e acima de 88 dB). A avaliação da audição foi realizada por análise dos resultados das audiometrias realizadas nos exames admissionais e periódicos constantes dos prontuários médicos. Foram calculadas as incidências de perda auditiva de acordo com os grupos de exposição e o tempo médio de início das alterações auditivas em cada grupo. Foram realizadas análises descritivas das variáveis, comparação de médias (teste U de Mann-Whitney), teste de associação de qui-quadrado e, para estimar fatores de risco, modelos de regressão logística univariada e múltipla. RESULTADOS: Entre os participantes do estudo foram identificados 128 casos (11,97%) de perda auditiva. No grupo composto pelos trabalhadores que ficaram expostos aos níveis mais altos de pressão sonora encontra-se uma incidência de 11,84% em alterações de exames audiométricos, enquanto no grupo menos exposto obteve-se uma incidência de 12,4%. O tempo médio para o desencadeamento de alterações audiométricas foi de 3,07 anos (desvio padrão = 1,21) no grupo mais exposto e de 2,88 anos (desvio padrão = 1,53) no grupo menos exposto. Estar na faixa etária acima de 28 anos e 8 meses (RC = 3,33; IC 95%: 2,01 - 5,49) e trabalhar na Unidade 1 (RC = 1,64; IC 95%: 1,09 - 2,46) se mostraram fatores de risco robustos para perda auditiva induzida por ruído. CONCLUSÃO: A perda auditiva ocorre de maneira precoce, prioritariamente até o terceiro ano de exposição e faixa etária, e unidade de trabalho se mostraram os fatores de risco mais relevantes para a perda auditiva induzida por ruído. O estudo mostra a necessidade de uma integração maior entre as áreas de saúde ocupacional e segurança do trabalho na busca de ações preventivas e corretivas, que possam minimizar o surgimento de novos casos ou o agravamento dos já identificados. Este é um estudo preliminar que servirá de apoio a pesquisas futuras sobre o assunto / INTRODUCTION: As a result of technological and industrial modernization new factors have arisen which led to specific studies have focused on the possible harmful effects of this evolution on the worker. Among these factors is noise, a physical agent which can harm the human body with short and medium term effects. Noise can alter internal body processes, with physiological and emotional consequences. The gradual reduction of hearing acuity resulting from a continued exposure to high levels of noise pressure is called noise-induced hearing loss (NIHL), according to the National Committee of Noise and Hearing Conservation. NIHL is characterized by a permanent sensorioneural impairment, almost always bilateral and symmetrical, not exceeding 40dB (NA) at lower frequencies and 75dB (NA) at higher frequencies. It first manifests at 6kHz, 4kHz and/or 3kHz, slowly progressing to the frequencies of 8kHz, 2kHz, 1kHz, 500Hz and 250Hz. (MTE, Ruling 19, 1998). Among the factors which trigger NIHL are the physical characteristics of the noise (type, spectrum and intensity of sound pressure), duration of exposure, and individual susceptibility. NIHL is among the most common occupational diseases, with the aggravating aspect of being irreversible. It is most often found in the industrial sector. This study will evaluate the incidence of noise-induced hearing loss and the existence of a positive association between these diagnoses and the exposure to different levels of sound pressure in workers at two operational units of a iron ore mining and pelletizing organization. METHODS: historical cohort study with 1069 workers, divided in two groups, using as baseline the sound pressure levels to which they were exposed (less than or equal to 88 dB and above 88 dB). The hearing assessment was carried out by means of an analysis of the results of the audiometry exam upon induction and at regular intervals, as recorded in the medical history of the individual. A calculation was made of the degree of hearing loss according to the groups of exposure, and the average time it took for hearing changes to be observed in each group. RESULTS: Among the participants in the study, 128 (11.97%) cases of hearing loss were identified. In the group formed by workers who had been exposed to the highest levels of sound pressures, we found an incidence of 11.84% of changes in the audiometry exams, while in the group subject to lesser exposure we observed an incidence of 12.4%. The average time for the development of hearing impairment was 3.07 years (standard deviation = 1.21) in the group with greater exposure, and 2.88 years (standard deviation = 1.53) in the group with lesser exposure. Robust risk factors for noise-induced hearing loss included being aged over 28 years and 8 months (RC = 3,33; IC 95%: 2,01 - 5,49) and working at Unit 1 (RC = 1,64 ; IC 95%: 1,09 - 2,46). CONCLUSION: Early hearing impairment occurs mainly before the end of the third year of exposure, and age bracket and work location proved to be the most relevant risk factors for noise-induced hearing loss. The study showed the need for a greater integration among the occupational health and safety areas to seek the design and implementation of preventive and corrective actions to minimize the development of new cases or the aggravation of those already identified. This is a preliminary study which will serve as a basis for a more detailed subsequent data analysis

Millions of people across the world are suffering from noise induced hearing loss (NIHL), especially under working conditions of either continuous Gaussian or non-Gaussian noise that might affect human's hearing function. Impulse noise is a typical non-Gaussian noise exposure in military and industry, and generates severe hearing loss problem. This study mainly focuses on characterization of impulse noise using digital signal analysis method and prediction of the auditory hazard of impulse noise induced hearing loss by the Auditory Hazard Assessment Algorithm for Humans (AHAAH) modeling. A digital noise exposure system has been developed to produce impulse noises with peak sound pressure level (SPL) up to 160 dB. The characterization of impulse noise generated by the system has been investigated and analyzed in both time and frequency domains. Furthermore, the effects of key parameters of impulse noise on auditory risk unit (ARU) are investigated using both simulated and experimental measured impulse noise signals in the AHAAH model. The results showed that the ARUs increased monotonically with the peak pressure (both P+ and P-) increasing. With increasing of the time duration, the ARUs increased first and then decreased, and the peak of ARUs appeared at about t = 0.2 ms (for both t+ and t-). In addition, the auditory hazard of experimental measured impulse noises signals demonstrated a monotonically increasing relationship between ARUs and system voltages.

<p>  </p> <p>Noise-induced hearing loss (NIHL) is a significant occupational health concern in the construction industry, necessitating effective hearing protection for workers. This project explores the detrimental consequences of environmental pollutants, specifically noise pollution common in construction settings. The research incorporates user interviews with construction workers and managers to identify challenges and motivations surrounding the use of hearing protection devices.</p> <p>My findings underscore the necessity of addressing pollution in the construction industry to safeguard the well-being of workers. Noise pollution emerges as a primary concern, leading to hearing loss, stress, decreased productivity, and safety hazards. The research revealed that workers grapple with obstacles, including discomfort, lack of awareness, and cost barriers, while also recognizing driving forces, including fear of hearing loss and the encouragement of supervisors. The design process involved thorough research, including a literature review, competitive analysis, and semi-structured user interviews, resulting in an advanced hearing protection device that prioritizes effective communication, cleanliness, and user comfort. The final product incorporates innovative features such as lighting indicators, a compact charging case, strategically positioned buttons, secure fit with magnets, and a range of color options. Furthermore, the accompanying application features customizable ambient sounds, performance feedback, and gamification elements.</p>

No description available.

A exposição contínua ao ruído de alta intensidade é o fator ambiental mais importante como causa de problemas auditivos em adultos. Esses tipos de perdas crônicas e irreversíveis causadas pelo ruído são chamados de Perdas Auditivas Induzidas por Ruído (PAIR). O objetivo desse estudo foi estudar a influência de fatores genéticos na susceptibilidade à PAIR. Para atingir esse objetivo comparamos uma amostra de indivíduos com PAIR e de indivíduos sem PAIR que trabalharam expostos ao ruído em relação à etnia, à história familial de perda auditiva, idade, tempo de exposição ao ruído, tabagismo e alcoolismo social. Para verificar a possível contribuição de fatores genéticos, testamos a presença de mutações conhecidas como causas freqüentes de surdez. As mutações testadas foram 35delG e 167delT no gene GJB2, as deleções &#916;(GJB6-D13S1830) e &#916;(GJB6-D13S1854) no gene GJB6 e A1555G (RFLP) no gene MT-RNR1. Determinamos as freqüências alélicas e genotípicas de um polimorfismo no gene GJB2 (SNP RS877098) e dos polimorfismos do tipo presença/deleção dos genes GSTM1 e GSTT1. Também verificamos a ocorrência e a freqüência de variações nas seqüências dos genes mitocondriais MT-RNR1 e MT-TS1, dois genes mitocondriais importantes como causa de surdez de herança materna. Nossa amostra constituiu-se de 107 indivíduos que apresentavam audiometrias sugestivas de PAIR (grupo PAIR), 44 indivíduos afetados por perdas de audição com curvas audiométricas que não eram sugestivas de PAIR (grupo PANO) e 104 indivíduos com audição normal (grupo NORMAL). Nossos resultados apontaram aumento significativo no número de parentes afetados por problemas de audição no grupo PAIR. O tabagismo, a idade e o tempo de exposição ao ruído também influenciaram significativamente na manifestação da PAIR. Aparentemente, não houve contribuição das mutações associadas à manifestação de surdez, 35delG e 167delT no gene GJB2, &#916;(GJB6-D13S1830) e &#916;(GJB6-D13S1854) no gene GJB6 e A1555G no gene MT-RNR1. Não houve diferença significativa nas freqüências dos alelos do SNP RS87098 (gene GJB2) entre os afetados e os não afetados. Observamos um aumento significativo do genótipo que corresponde a presença dos dois genes das enzimas GSTM1 e GSTT1 entre os indivíduos do grupo PAIR, sugerindo possível papel dessas enzimas relacionadas a proteção contra espécies reativas de oxigênio na etiologia da PAIR. Não observamos associação significativa entre nenhuma das 54 variantes de seqüências do DNA mitocondrial averiguadas nos genes MT-RNR1 e MT-TS1 (32 já previamente descritas e 22 detectadas nesse estudo) e a ocorrência de PAIR. Não observamos associação significativa da PAIR com o número total de variantes de seqüência do DNA mitocondrial observado em cada indivíduo. Não foi detectada associação significativa com os haplótipos constituídos por pares de variantes de seqüência do DNA mitocondrial. A comparação entre a concentração de peróxidos e de grupos sulfidril no soro de 15 indivíduos com PAIR com amostras de 15 indivíduos sem PAIR não revelou diferenças significativas. Em resumo, nosso estudo evidenciou a influência da história familial de perda auditiva na probabilidade de manifestação da PAIR e o possível papel das enzimas GSTT1 e GSTM1 na susceptibilidade a essa condição. Nossos achados reforçam a idéia de que a susceptibilidade à PAIR possa ser determinada por fatores genéticos. / Chronic exposure to loud noise is the most important environmental cause of hearing impairment among adults. Chronic and irreversible hearing loss due to exposure to noise is named Noise Induced Hearing Loss (NIHL). The aim of this study was to investigate the influence of genetic factors in the susceptibility to NIHL. We compared individuals with and without NIHL regarding ethnic origin, familial history of hearing loss, age, noise exposure time, alcohol consumption and smoking habits. In order to investigate genetic factors associated to NIHL we screened frequent deafness causative mutations. The investigated mutations were 35delG and 167delT in the GJB2 gene, &#916;(GJB6- D13S1830) and &#916;(GJB6- D13S1854) in the GJB6 gene and A1555G in the MT-RNR1 gene. Allelic and genotypic frequencies were determined for the SNP RS877098 in the GJB2 gene, and for the polymorphic deletions of GSTM1 and GSTT1 genes. We also investigated the frequency of variants in the mitochondrial genes MT-RNR1 and MT-TS1, which are known to harbor many hearing loss causative mutations. Our sample comprised 107 individuals with suggestive NIHL audiograms, 44 individuals with hearing impairment and non-suggestive NIHL audiograms, and 104 normal hearing individuals. A significant increase in the number of relatives affected by hearing impairment was detected in the NIHL group, when compared to the normal hearing group. Smoking habits, age and noise exposure time significantly affected the probability of NIHL. We did not detected any effect of the deafness-causing mutations 35delG and 167delT in the GJB2 gene, &#916; (GJB6- D13S1830) and &#916; (GJB6- D13S1854) in the GJB6 gene, and A1555G in the MT-RNR1 gene. There was no significant difference in allelic and genotypic frequencies of SNP RS87098 (gene GJB2), but the presence of the two genes encoding GSTM1 and GSTT1 enzymes was increased in the NIHL group. We did not detect any significant association of any of the 54 sequence variants in the mitochondrial genes MT-RNR1 and MT-TS1 (32 previously described and 22 novel) with the occurrence of NIHL. No significant associations were observed between NIHL and either the total number of sequence variants detected in each individual or haplotypes (combinations of two variants). The comparison of peroxides and sulfhydryl groups concentrations in serum from 15 individuals with NIHL and 15 individuals without NIHL did not show significant differences. In conclusion, our study demonstrated a significant effect of family history of hearing loss on the probability of presenting NIHL and pointed to a possible role of GSTT1 and GSTM1 enzymes on the susceptibility to this condition. These findings reinforce the idea that susceptibility to NIHL has a genetic basis.

This study focused on designing a training programme for audiometricians, using the principles of instructional design. Instructional design is the continuing, systematic development of instructional specifications, utilizing researched strategies and principles to create detailed outcomes for the development, implementation, evaluation and maintenance of training programmes. An audiometrician is defined by SANS (10083:2004), as a person registered with the Health Professions Council of South Africa as an audiometrician, hearing aid acoustician or someone trained in audiometry. Audiometricians are adult learners. Therefore, in addition to instructional design principles, the principles of adult learning were also incorporated in the training programme. The successful training of audiometricians may ensure that noise induced hearing loss is significantly reduced when audiometric monitoring is appropriately implemented as part of a hearing conservation programme. Training for audiometricians is critical in this process as incorrect audiometric monitoring may negatively influence the outcomes of a hearing conservation programme. This study followed a descriptive research design where the results were described in a quantitative manner. Data was collected by means of electronically mailed questionnaires. All participants were practicing audiometricians at the time of the study and were registered with the South African Society for Occupational Health Nursing. All participants had an audiometric certificate as qualification. For the analysis of data, 181 completed questionnaires were used. The results were analyzed and described in terms of the respondents’ own experience regarding audiometry; their opinions regarding the topics they have been taught in audiometry; the duration of their own training programmes and their opinions regarding a future training programme for audiometricians. Based on the results of the above analysis, the instructional design programme for audiometricians was developed. The obtained results were used to determine what the topics, content, duration, learning outcomes and learner evaluation methods should be in the development of a training programme for audiometricians. This research study developed a training programme for audiometricians in order to ensure that all future audiometricians have the necessary knowledge to perform comprehensive hearing evaluations, interpret audiometric findings and thereby assist in reducing noise induced hearing loss in the industrial sector through hearing conservation programmes. AFRIKAANS : Hierdie studie is toegespits op die ontwerp van ‘n onderrigprogram vir oudiometriste waarin die beginsels van onderrigontwerp toegepas is. Onderrigontwerp behels die deurlopende en stelselmatige ontwikkeling van onderrigspesifikasies deur gebruik te maak van nagevorsde strategieë en beginsels om gedetailleerde uitkomste vir die ontwikkeing, evaluering en onderhoud van opleidingsprogramme daar te stel. ‘n Oudiometris word gedefinieer deur wetgewing (SANS 10083:2004) as ‘n person wat geregistreer is by die Health Professions Council of South Africa as ‘n oudiometris, gehoorapparaat akoestikus of iemand wat opgelei is in oudiometrie. Oudiometriste is volwasse leerders. Om hierdie rede is nie net die beginsels van onderrigontwerp nie, maar ook die beginsels van volwasse leer in die onderrigprogram geïnkorporeer. Suksesvolle onderrig van oudiometriste kan verseker dat die voorkoms van geraas-geïnduseerde gehoorverlies verminder, mits oudiometriese monitering toepaslik as deel van ‘n program vir gehoorkonservering geïntegreer word. Opleiding vir oudiometriste is krities belangrik in hierdie proses want indien oudiometriese monitering verkeerd gedoen word, kan dit die gehoorkonserveringsprogram in totaliteit negatief beïnvloed. ‘n Beskrywende navorsingsontwerp is in hierdie studie gebruik en die resultate is kwantitatief beskryf. Data is deur middel van vraelyste wat elektronies versend is, versamel. Al die deelnemers was ten tye van die studie praktiserende oudiometriste wat by die South African Society for Occupational Health Nursing geregistreer was. Elkeen was in besit van ‘n oudiometriese sertifikaat as kwalfikasie. Vir data-ontleding is 181 voltooide vraelyste gebruik. Die data was geanaliseer en beskryf in terme van die respondente se eie ervaring ten opsigte van oudiometrie; hul mening omtrent die temas wat by hul opleiding ingesluit was; die duur van hul opleidingsprogramme en hul idees omtrent ‘n toekomstige opleidingsprogram vir oudiometriste. Die onderrigontwerp-program is op grond van die resultate van bognoemde analise ontwikkel. Die resultate wat verkry is, is gebruik om die temas, inhoud, duur, leeruitkomste en evalueringsmetodes in die ontwikkeling van ‘n opleidingsprogram vir oudiometriste te bepaal. Hierdie studie is gerig op die ontwikkeling van ‘n opleidingsprogram vir oudiometriste met die doel om te verseker dat hulle oor die nodige kennis beskik om omvattende gehoorevaluerings uit te voer, om oudiometriese bevindinge te interpreteer en daardeur, in gesondheidssorgprogramme, by te dra tot die vermindering van geraas-geïnduseerde gehoorverlies in die industriële sektor Copyright / Dissertation (MCommunication Pathology)--University of Pretoria, 2012. / Speech-Language Pathology and Audiology / unrestricted

A exposição contínua ao ruído de alta intensidade é o fator ambiental mais importante como causa de problemas auditivos em adultos. Esses tipos de perdas crônicas e irreversíveis causadas pelo ruído são chamados de Perdas Auditivas Induzidas por Ruído (PAIR). O objetivo desse estudo foi estudar a influência de fatores genéticos na susceptibilidade à PAIR. Para atingir esse objetivo comparamos uma amostra de indivíduos com PAIR e de indivíduos sem PAIR que trabalharam expostos ao ruído em relação à etnia, à história familial de perda auditiva, idade, tempo de exposição ao ruído, tabagismo e alcoolismo social. Para verificar a possível contribuição de fatores genéticos, testamos a presença de mutações conhecidas como causas freqüentes de surdez. As mutações testadas foram 35delG e 167delT no gene GJB2, as deleções &#916;(GJB6-D13S1830) e &#916;(GJB6-D13S1854) no gene GJB6 e A1555G (RFLP) no gene MT-RNR1. Determinamos as freqüências alélicas e genotípicas de um polimorfismo no gene GJB2 (SNP RS877098) e dos polimorfismos do tipo presença/deleção dos genes GSTM1 e GSTT1. Também verificamos a ocorrência e a freqüência de variações nas seqüências dos genes mitocondriais MT-RNR1 e MT-TS1, dois genes mitocondriais importantes como causa de surdez de herança materna. Nossa amostra constituiu-se de 107 indivíduos que apresentavam audiometrias sugestivas de PAIR (grupo PAIR), 44 indivíduos afetados por perdas de audição com curvas audiométricas que não eram sugestivas de PAIR (grupo PANO) e 104 indivíduos com audição normal (grupo NORMAL). Nossos resultados apontaram aumento significativo no número de parentes afetados por problemas de audição no grupo PAIR. O tabagismo, a idade e o tempo de exposição ao ruído também influenciaram significativamente na manifestação da PAIR. Aparentemente, não houve contribuição das mutações associadas à manifestação de surdez, 35delG e 167delT no gene GJB2, &#916;(GJB6-D13S1830) e &#916;(GJB6-D13S1854) no gene GJB6 e A1555G no gene MT-RNR1. Não houve diferença significativa nas freqüências dos alelos do SNP RS87098 (gene GJB2) entre os afetados e os não afetados. Observamos um aumento significativo do genótipo que corresponde a presença dos dois genes das enzimas GSTM1 e GSTT1 entre os indivíduos do grupo PAIR, sugerindo possível papel dessas enzimas relacionadas a proteção contra espécies reativas de oxigênio na etiologia da PAIR. Não observamos associação significativa entre nenhuma das 54 variantes de seqüências do DNA mitocondrial averiguadas nos genes MT-RNR1 e MT-TS1 (32 já previamente descritas e 22 detectadas nesse estudo) e a ocorrência de PAIR. Não observamos associação significativa da PAIR com o número total de variantes de seqüência do DNA mitocondrial observado em cada indivíduo. Não foi detectada associação significativa com os haplótipos constituídos por pares de variantes de seqüência do DNA mitocondrial. A comparação entre a concentração de peróxidos e de grupos sulfidril no soro de 15 indivíduos com PAIR com amostras de 15 indivíduos sem PAIR não revelou diferenças significativas. Em resumo, nosso estudo evidenciou a influência da história familial de perda auditiva na probabilidade de manifestação da PAIR e o possível papel das enzimas GSTT1 e GSTM1 na susceptibilidade a essa condição. Nossos achados reforçam a idéia de que a susceptibilidade à PAIR possa ser determinada por fatores genéticos. / Chronic exposure to loud noise is the most important environmental cause of hearing impairment among adults. Chronic and irreversible hearing loss due to exposure to noise is named Noise Induced Hearing Loss (NIHL). The aim of this study was to investigate the influence of genetic factors in the susceptibility to NIHL. We compared individuals with and without NIHL regarding ethnic origin, familial history of hearing loss, age, noise exposure time, alcohol consumption and smoking habits. In order to investigate genetic factors associated to NIHL we screened frequent deafness causative mutations. The investigated mutations were 35delG and 167delT in the GJB2 gene, &#916;(GJB6- D13S1830) and &#916;(GJB6- D13S1854) in the GJB6 gene and A1555G in the MT-RNR1 gene. Allelic and genotypic frequencies were determined for the SNP RS877098 in the GJB2 gene, and for the polymorphic deletions of GSTM1 and GSTT1 genes. We also investigated the frequency of variants in the mitochondrial genes MT-RNR1 and MT-TS1, which are known to harbor many hearing loss causative mutations. Our sample comprised 107 individuals with suggestive NIHL audiograms, 44 individuals with hearing impairment and non-suggestive NIHL audiograms, and 104 normal hearing individuals. A significant increase in the number of relatives affected by hearing impairment was detected in the NIHL group, when compared to the normal hearing group. Smoking habits, age and noise exposure time significantly affected the probability of NIHL. We did not detected any effect of the deafness-causing mutations 35delG and 167delT in the GJB2 gene, &#916; (GJB6- D13S1830) and &#916; (GJB6- D13S1854) in the GJB6 gene, and A1555G in the MT-RNR1 gene. There was no significant difference in allelic and genotypic frequencies of SNP RS87098 (gene GJB2), but the presence of the two genes encoding GSTM1 and GSTT1 enzymes was increased in the NIHL group. We did not detect any significant association of any of the 54 sequence variants in the mitochondrial genes MT-RNR1 and MT-TS1 (32 previously described and 22 novel) with the occurrence of NIHL. No significant associations were observed between NIHL and either the total number of sequence variants detected in each individual or haplotypes (combinations of two variants). The comparison of peroxides and sulfhydryl groups concentrations in serum from 15 individuals with NIHL and 15 individuals without NIHL did not show significant differences. In conclusion, our study demonstrated a significant effect of family history of hearing loss on the probability of presenting NIHL and pointed to a possible role of GSTT1 and GSTM1 enzymes on the susceptibility to this condition. These findings reinforce the idea that susceptibility to NIHL has a genetic basis.

<div>Hearing loss hinders the communication ability of many individuals despite state-of-the-art interventions. Animal models of different hearing-loss etiologies can help improve the clinical outcomes of these interventions; however, several gaps exist. First, translational aspects of animal models are currently limited because anatomically and physiologically specific data obtained from animals are analyzed differently compared to noninvasive evoked responses that can be recorded from humans. Second, we lack a comprehensive understanding of the neural representation of everyday sounds (e.g., naturally spoken speech) in real-life settings (e.g., in background noise). This is even true at the level of the auditory nerve, which is the first bottleneck of auditory information flow to the brain and the first neural site to exhibit crucial effects of hearing-loss. </div><div><br></div><div>To address these gaps, we developed a unifying framework that allows direct comparison of invasive spike-train data and noninvasive far-field data in response to stationary and nonstationary sounds. We applied this framework to recordings from single auditory-nerve fibers and frequency-following responses from the scalp of anesthetized chinchillas with either normal hearing or noise-induced mild-moderate hearing loss in response to a speech sentence in noise. Key results for speech coding following hearing loss include: (1) coding deficits for voiced speech manifest as tonotopic distortions without a significant change in driven rate or spike-time precision, (2) linear amplification aimed at countering audiometric threshold shift is insufficient to restore neural activity for low-intensity consonants, (3) susceptibility to background noise increases as a direct result of distorted tonotopic mapping following acoustic trauma, and (4) temporal-place representation of pitch is also degraded. Finally, we developed a noninvasive metric to potentially diagnose distorted tonotopy in humans. These findings help explain the neural origins of common perceptual difficulties that listeners with hearing impairment experience, offer several insights to make hearing-aids more individualized, and highlight the importance of better clinical diagnostics and noise-reduction algorithms. </div>