Noise-induced Hearing Impairment Research Articles

Hearing Loss and Oxidative Stress: A Comprehensive Review.

Hearing loss is a prevalent condition affecting millions of people worldwide. Hearing loss has been linked to oxidative stress as a major factor in its onset and progression. The goal of this thorough analysis is to investigate the connection between oxidative stress and hearing loss, with an emphasis on the underlying mechanisms and possible treatments. The review addressed the many forms of hearing loss, the role of reactive oxygen species (ROS) in causing damage to the cochlea, and the auditory system's antioxidant defensive mechanisms. The review also goes over the available data that support the use of antioxidants and other methods to lessen hearing loss brought on by oxidative stress. We found that oxidative stress is implicated in multiple types of hearing loss, including age-related, noise-induced, and ototoxic hearing impairment. The cochlea's unique anatomical and physiological characteristics, such as high metabolic activity and limited blood supply, make it particularly susceptible to oxidative damage. Antioxidant therapies have shown promising results in both animal models and clinical studies for preventing and mitigating hearing loss. Emerging therapeutic approaches, including targeted drug delivery systems and gene therapy, offer new possibilities for addressing oxidative stress in the auditory system. The significance of this review lies in its comprehensive analysis of the intricate relationship between oxidative stress and hearing loss. By synthesizing current knowledge and identifying gaps in understanding, this review provides valuable insights for both researchers and clinicians. It highlights the potential of antioxidant-based interventions and emphasizes the need for further research into personalized treatment strategies. Our findings on oxidative stress mechanisms may also affect clinical practice and future research directions. This review serves as a foundation for developing novel therapeutic approaches and may inform evidence-based strategies for the prevention and treatment of hearing loss, ultimately contributing to improved quality of life for millions affected by this condition worldwide.

To the revision of the ISO 1999:2013 standard "Acoustics. Assessment of hearing loss due to noise exposure": an excessive correction for the "impulsiveness" of noise

Introduction. In connection with the development of measuring and computer technology, new opportunities and approaches are opening up to solve the problem of measurement, hygienic assessment, normalization and prediction of hearing impairment from exposure to unstable, in particular, pulse noise.
 The study aims to analyze the applicability of a model for assessing hearing loss based on the use of an excessive correction to the exposure of impacting noise, according to the draft ISO 1999:2023 standard.
 Materials and methods. The scientists have conducted an expert and analytical comparative analysis of ISO 1999 standards, which define the basis for assessing hearing loss due to noise exposure. The experts have carried out a literary review of domestic and foreign sources on the problem of using the index of the distribution of instantaneous values of sound pressure — excess to assess constant and non-constant noise, as well as its role in the formation of hearing loss under the action of non-Gaussian pulse noise, the applicability of the prediction model of the ISO 1999 standard to various types of noise exposure.
 Results. The scientists presented the results of the analysis of: indicators for assessing the adverse effects of non-constant, including pulse noise; the relationship between the effects of non-Gaussian noise and the constant shift in the hearing thresholds of workers; statistical indicator of excess — an indirect indicator of the temporal structure of noise, a significant risk factor in combination with noise exposure in the assessment of hearing loss.
 Conclusion. Revision of the ISO 1999:2013 standard with the introduction of a new indicator of the temporal structure of noise — kurtosis, will improve the accuracy of the method of predicting hearing loss when exposed to constant, non-constant noise, including impulsive.
 Ethics. In preparing the article, the authors were guided by the ethical principles of medical research set out in the Helsinki Declaration of the World Medical Association of the last revision.
 Limitation. Features of ISO 1999 standards dedicated to the assessment of the impact of industrial noise and the assessment of noise-induced hearing impairment.

The summating potential polarity encodes the ear health condition

The summating potential (SP), the DC potential which, along with the AC response, is produced when the hair cells convert the vibrational mechanical energy of sound into electrical signals, is the most enigmatic of the cochlear potentials because its polarity and function have remained elusive for more than seven decades. Despite the tremendous socioeconomic consequences of noise-induced hearing loss and the profound physiological importance of understanding how loud noise exposure impairs the hair cell receptor activation, the relationship between the SP and noise-induced hearing impairment remains poorly characterized. Here, I show that in normally hearing ears, the SP polarity is positive and its amplitude relative to the AC response grows exponentially across frequencies, and becomes negative and decreases exponentially across frequencies following noise-induced hearing injury. Since the SP is thought to be generated by K+ outflow down the gradient through the hair cell basolateral K+ channels, the SP polarity switch to negative values is consistent with a noise-induced shift in the operating point of the hair cells.

Spatial architecture of the cochlear immune microenvironment in noise-induced and age-related sensorineural hearing loss.

The cochlea encodes sound stimuli and transmits them to the central nervous system, and damage to sensory cells and synapses in the cochlea leads to hearing loss. The inner ear was previously considered to be an immune privileged organ to protect the auditory organ from reactions with the immune system. However, recent studies have revealed the presence of resident macrophages in the cochlea, especially in the spiral ligament, spiral ganglion, and stria vascularis. The tissue-resident macrophages are responsible for the detection, phagocytosis, and clearance of cellular debris and pathogens from the tissues, and they initiate inflammation and influence tissue repair by producing inflammatory cytokines and chemokines. Insult to the cochlea can activate the cochlear macrophages to initiate immune responses. In this review, we describe the distribution and functions of cochlear macrophages in noise-induced hearing impairment and age-related hearing disabilities. We also focus on potential therapeutic interventions concerning hearing loss by modulating local immune responses.

English

BACKGROUND Dentists are liable to loss of hearing during dental treatment due to noise exposure. A study was carried out to determine whether or not dental professionals from the Department of Periodontics, Conservative Dentistry and Endodontics and Prosthodontics ought to cause hearing decrement with the aid of using continual excessive frequency sounds created by dental equipments. METHODS This study involved 38 dentists from the specialities of Periodontics, Conservative Dentistry and Endodontics, and Prosthodontics who were subjected to noise during operating for 6 hours per day and 38 medical professionals who were matched served as a control group. Three audiometric examinations included an otoscopic exam; tympanometry and pure tone audiometry were performed by the participants. RESULTS According to the data, 15.8 % of dentists and 2.6 % of the control group suffered from loss of hearing. In the pure tone audiometry test, there was no substantial difference between the two groups; however, the qualitative analysis showed that the dentists' group had a greater percentage of hearing loss than their control counterparts. In the pure tone audiometry test, there was a statistically significant difference between the specialists from periodontics, conservative dentistry and endodontics, and prosthodontics (P = 0.005). CONCLUSIONS Noise from dental clinics has been shown to cause hearing problems, with the left ear being affected when compared to that of the right; again, these problems aren't serious. Dentists were common among noise-induced hearing impairment and periodontic specialists than conservative dentistry and endodontics, and prosthodontic specialists than the control group. KEY WORDS Dental Professionals, Long Term Exposure, Noise-Induced Hearing Loss, Pure Tone Audiometry.

Analysis of Early Biomarkers Associated With Noise-Induced Hearing Loss Among Shipyard Workers

It is important to determine what frequencies and auditory perceptual measures are the most sensitive early indicators of noise-induced hearing impairment. To examine whether hearing loss among shipyard workers increases more rapidly at extended high frequencies than at clinical frequencies and whether subtle auditory processing deficits are present in those with extensive noise exposure but little or no hearing loss. This cross-sectional study collected audiometric data (0.25-16 kHz), survey questionnaires, and noise exposure levels from 7890 shipyard workers in a Shanghai shipyard from 2015 to 2019. Worsening hearing loss was evaluated in the group with hearing loss. Speech processing and temporal processing were evaluated in 610 participants with noise exposure and clinically normal hearing to identify early biomarkers of noise-induced hearing impairment. Data analysis was conducted from November to December 2020. Linear regression was performed to model the increase in hearing loss as function of cumulative noise exposure and compared with a group who were monitored longitudinally for 4 years. Auditory processing tests included speech-in-noise tests, competing sentence tests, dichotic listening tests, and gap detection threshold tests and were compared with a control group without history of noise exposure. Of the 5539 participants (median [interquartile range (IQR)] age, 41.0 [34.0-47.0] years; 3861 [86.6%] men) included in the cross-sectional analysis, 4459 (80.5%) were hearing loss positive and 1080 (19.5%) were hearing loss negative. In younger participants (ie, ≤40 years), the maximum rate of increase in hearing loss was 0.40 (95% CI, 0.39-0.42) dB per A-weighted dB-year (dB/dBA-year) at 12.5 kHz, higher than the growth rates of 0.36 (95% CI, 0.35-0.36) dB/dBA-year at 4 kHz, 0.32 (95% CI, 0.31-0.33) dB/dBA-year at 10 kHz, 0.31 (95% CI, 0.30-0.31) dB/dBA-year at 6 kHz, 0.27 (95% CI, 0.26-0.27) dB/dBA-year at 3 kHz, and 0.27 (95% CI, 0.27-0.28) dB/dBA-year at 8 kHz. In the 4-year longitudinal analysis of hearing loss among 403 participants, the mean (SD) annual deterioration in hearing was 2.70 (2.98) dB/y at 12.5 kHz, almost twice as that observed at lower frequencies (eg, at 3kHz: 1.18 [2.15] dB/y). The auditory processing scores of participants with clinically normal hearing and a history of noise exposure were significantly lower than those of control participants (eg, median [IQR] score on speech-in-noise test, noise-exposed group 1 vs control group: 0.63 [0.55-0.66] vs 0.78 [0.76-0.80]; P < .001). These findings suggest that the increase in hearing loss among shipyard workers was more rapid at 12.5 kHz than at other frequencies; workers with clinically normal hearing but high cumulative noise exposure are likely to exhibit deficits in speech and temporal processing.

Cochlear protection against noise exposure requires serotonin type 3A receptor via the medial olivocochlear system.

The cochlear efferent feedback system plays important roles in auditory processing, including regulation of the dynamic range of hearing, and provides protection against acoustic trauma. These functions are performed through medial olivocochlear (MOC) neurons. However, the underlying cellular and molecular mechanisms are not fully understood. The serotonin type 3A (5-HT3A) receptor is widely expressed throughout the nervous system, which suggests important roles in various neural functions. However, involvement of the 5-HT3A receptor in the MOC system remains unclear. We used mice in this study and found that the 5-HT3A receptor was expressed in MOC neurons that innervated outer hair cells in the cochlea and was involved in the activation of MOC neurons by noise exposure. 5-HT3A receptor knockout impaired MOC functions, potentiated noise-induced hearing loss, and increased loss of ribbon synapses following noise exposure. Furthermore, 5-HT3 receptor agonist treatment alleviated the noise-induced hearing loss and loss of ribbon synapses, which enhanced cochlear protection provided by the MOC system. Our findings demonstrate that the 5-HT3A receptor plays fundamental roles in the MOC system and critically contributes to protection from noise-induced hearing impairment.

Noise and hearing disorders

Hearing is one of the most important human senses. It is highly sensitive to any acoustic stimuli – some of them may be harmful. Hearing damage caused by noise is becoming more common these days. It affects not only adults, but also adolescents and children. It is often irreversible and may arise as a result of a single exposure to noise or during long-term occupational exposure. Noise has a strong impact on the hearing organ. It is a dangerous stimulus that damages external hair cells. Its effect may be caused by both long-term and short-term exposure. To prevent noise-induced hearing impairment, it is necessary to avoid loud acoustic stimuli. Noise is ubiquitous and sometimes we do not realize how harmful it is to our hearing. People of all ages are exposed to hearing loss caused by noise. In order to avoid or reduce the effects of noise, one should follow preventive recommendations. Noise has a huge impact on the quality of our hearing.

Novel oral multifunctional antioxidant prevents noise-induced hearing loss and hair cell loss

Oxidative stress is a major contributor to noise-induced hearing loss, the most common cause of hearing loss among military personnel and young adults. HK-2 is a potent, orally-active, multifunctional, redox-modulating drug that has been shown to protect against a wide range of neurological disorders with no observed side effects. HK-2 protected cochlear HEI-OC1 cells against various forms of experimentally-induced oxidative stressors similar to those observed during and after intense noise exposure. The mechanisms by which HK-2 protects cells is twofold, first by its ability to reduce oxidative stress generated by free radicals, and second, by its ability to complex biologically active transition metals such as Fe+2, thus reducing their availability to participate in the Fenton reaction where highly toxic hydroxyl radicals are generated. For the rat in vivo studies, HK-2 provided significant protection against noise-induced hearing loss and hair cell loss. Noise-induced hearing loss was induced by an 8–16 kHz octave band noises presented for 8 h/d for 21 days at an intensity of 95 dB SPL. In the Prevention study, HK-2 was administered orally beginning 5 days before the start of the noise and ending 10 days after the noise. Treatment with HK-2 dose-dependently reduced the amount of noise-induced hearing impairment, reflected in the cochlear compound action potential, and noise-induced hair cell loss. In a subsequent Rescue experiment in which HK-2 was administered for 10 days starting after the noise was turned off, HK-2 also significantly reduced the amount of hearing impairment, but the effect size was substantially less than in the Prevention studies. HK-2 alone did not adversely affect HEI-OC1 cell viability, nor did it cause any adverse changes in rat body weight, behavior, cochlear function or hair cell integrity. Thus, HK-2 is a novel, safe, orally-deliverable and highly effective otoprotective compound with considerable potential for preventing hearing loss from noise and other hearing disorders linked to excessive oxidative stress.

ISO estimates of noise-induced hearing impairment.

The revision of International Organization for Standardization (ISO) standard ISO 1999 [(1971). International Organization of Standardization, Geneva, Switzerland)] in 1990 was based on two noise and hearing study databases, one presented by Burns and Robinson [(1970). Hearing and Noise in Industry (Her Majesty's Stationary Office, London)] and the other by Passchier-Vermeer [(1968). Report No. 35 and Supplement to Report No. 35 (Institute for Public Health Engineering, the Netherlands)]. However, the mathematical expression of these data in ISO 1999 neither closely predicts the distribution of hearing threshold levels in these two databases nor those in the National Institute for Occupational Safety and Health database. As a result, lower estimates of the risk of noise-induced hearing impairment are found using ISO 1999. An explanation of the revision is needed to justify these lower risk values.

Machine Learning Models for the Hearing Impairment Prediction in Workers Exposed to Complex Industrial Noise: A Pilot Study.

Objectives:To demonstrate the feasibility of developing machine learning models for the prediction of hearing impairment in humans exposed to complex non-Gaussian industrial noise.Design:Audiometric and noise exposure data were collected on a population of screened workers (N = 1,113) from 17 factories located in Zhejiang province, China. All the subjects were exposed to complex noise. Each subject was given an otologic examination to determine their pure-tone hearing threshold levels and had their personal full-shift noise recorded. For each subject, the hearing loss was evaluated according to the hearing impairment definition of the National Institute for Occupational Safety and Health. Age, exposure duration, equivalent A-weighted SPL (LAeq), and median kurtosis were used as the input for four machine learning algorithms, that is, support vector machine, neural network multilayer perceptron, random forest, and adaptive boosting. Both classification and regression models were developed to predict noise-induced hearing loss applying these four machine learning algorithms. Two indexes, area under the curve and prediction accuracy, were used to assess the performances of the classification models for predicting hearing impairment of workers. Root mean square error was used to quantify the prediction performance of the regression models.Results:A prediction accuracy between 78.6 and 80.1% indicated that the four classification models could be useful tools to assess noise-induced hearing impairment of workers exposed to various complex occupational noises. A comprehensive evaluation using both the area under the curve and prediction accuracy showed that the support vector machine model achieved the best score and thus should be selected as the tool with the highest potential for predicting hearing impairment from the occupational noise exposures in this study. The root mean square error performance indicated that the four regression models could be used to predict noise-induced hearing loss quantitatively and the multilayer perceptron regression model had the best performance.Conclusions:This pilot study demonstrated that machine learning algorithms are potential tools for the evaluation and prediction of noise-induced hearing impairment in workers exposed to diverse complex industrial noises.

Urban noise levels are high enough to damage auditory sensorineural health

ABSTRACT This commentary outlines the preventable auditory sensorineural health risk of cumulative episodic high-level indoor and outdoor non-occupational urban noise. Irreversible auditory sensorineural damage includes hidden hearing loss (cochlear synaptopathy), tinnitus, signal-to-noise ratio loss, noise-induced hearing impairment, and accelerated age-related hearing loss (presbycusis). There is evidence of ubiquitous high-level urban noise exceeding public health limits, and increased prevalence of sensorineural auditory damage in all age groups internationally. Sensorineural components differ greatly between late-onset sensory presbycusis in people with no hazardous exposure and early-onset neural presbycusis in people with a history of high noise exposure. Public health auditory safe listening limits are more stringent than occupational limits in order to fully protect the general population from permanent sensorineural noise damage. Speech interference noise limits prevent social isolation of individuals with noise-induced auditory system damage or hearing impairment from any cause. Quieter urban noise levels meeting public health limits are urgently needed to protect auditory sensorineural health, lower healthcare costs, and permit communication access in public spaces for people with auditory disabilities.

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss

Acquired hearing loss is caused by complex interactions of multiple environmental risk factors, such as elevated levels of lead and noise, which are prevalent in urban communities. This study delineates the mechanism underlying lead-induced auditory dysfunction and its potential interaction with noise exposure. Young-adult C57BL/6 mice were exposed to: 1) control conditions; 2) 2 mM lead acetate in drinking water for 28 days; 3) 90 dB broadband noise 2 h/day for two weeks; and 4) both lead and noise. Blood lead levels were measured by inductively coupled plasma mass spectrometry analysis (ICP-MS) lead-induced cochlear oxidative stress signaling was assessed using targeted gene arrays, and the hearing thresholds were assessed by recording auditory brainstem responses. Chronic lead exposure downregulated cochlear Sod1, Gpx1, and Gstk1, which encode critical antioxidant enzymes, and upregulated ApoE, Hspa1a, Ercc2, Prnp, Ccl5, and Sqstm1, which are indicative of cellular apoptosis. Isolated exposure to lead or noise induced 8–12 dB and 11–25 dB shifts in hearing thresholds, respectively. Combined exposure induced 18–30 dB shifts, which was significantly higher than that observed with isolated exposures. This study suggests that chronic exposure to lead induces cochlear oxidative stress and potentiates noise-induced hearing impairment, possibly through parallel pathways.

Molecular Understanding of Hearing - How Does This Matter to the Hearing Impaired?

This review addresses the advances of our molecular understanding of hearing and how this benefits the hearing impaired. Classical biochemical methods usually fall short in contributing to the analysis of the molecular mechanisms of hearing e. g. in the cochlea, the auditory part of the inner ear, due to the scarcity of the cells of interest. Genetics, molecular cell biology, and physiology, on the other hand, have elucidated the intricate molecular and cellular mechanisms that bring about the outstanding performance of the auditory system. Many of those mechanisms are quite unique and specialized to serve the specific needs of hearing. Hence, their defects often spare other organs and lead to specific non-syndromic deafness. High throughput sequencing can reveal causes of sporadic deafness when combined with careful bioinformatics. Molecular approaches are also helpful for understanding more common forms of hearing impairment such as noise-induced hearing impairment. While molecular therapies are not yet clinically available, careful molecular genetic analysis helps to counsel the hearing impaired subjects.

Are Bullet Riders at Risk of Noise Induced Hearing Impairment?

Are Bullet Riders at Risk of Noise Induced Hearing Impairment?

A Review of Occupational Disease Certification Criteria for Noise-Induced Hearing Impairment

소음성 난청은 전형적으로 양측성 난청으로, 초기에는 3, 4, 6 kHz의 청력역치에서 노치(notch), 즉 청력이 급격히 나빠져 V자형 순음청력도로 나타나며 8 kHz 청력은 상대적으로 양호 하다. 반면, 노인성 난청은 전형적인 노치가 없다. 노인성 난청이 없는 소음성 난청은 저주파역에서는 40 dB HL 이하의 경도 난 청을 보이며, 고주파역에서 심한 난청 소견을 보인다. 기간 경과 에 따라 소음성 난청의 진행은 느려지고 노인성 난청의 진행은 가속화된다. 매일 85 dB (A) 이상의 소음에 노출될 경우 노출 강 도가 클수록 소음성 난청의 위험도가 증가한다. 영구적인 청력 역치 변화에 앞서 일시적인 역치 변화가 선행한다(ACOEM, 2012). 소음성 난청으로 생각하기 어려운 순음청력도의 유형으 로는 주파수와 관계없이 편평한 형태의 난청, 고주파보다 저주파 청력이 더 나쁜 경우, 특히 50세 미만의 근로자가 70 dB HL 이상 의 고도 난청 혹은 농일 경우, 청력역치 변화가 매우 심할 때, 좌· 우측 난청의 정도 차이가 매우 클 때를 제시하고 있다(National Hearing Conservation Association, 2011).

A study on morbidity profile of lignite miners in western India

Background: Mining is a hazardous occupation in which workers are exposed to adverse conditions. In India, there are nine working lignite mines, producing about 30 million tons annually. The mines are located in the states of Tamilnadu, Rajasthan and Gujrat. Objective: The present study was carried out in a lignite mine in India to determine the health status of the miners. Methods: 143 workers engaged actively in mining activities were included. The health status of the employees was evaluated by well defined medical questionnaire along with pulmonary function test (PFT) and Audiometry. Result: Findings of the study showed poor literacy rate amongst the miners. Pulmonary impairment was present in 11.88% and noise induced hearing impairment in about 12.15% of the miners. Conclusion: The study findings indicate the need for regular health checkups, health education, personal protective devices and engineering control.

Higway traffic noise effects on annoyance

Noise pollution has been a major issue in the last decade. Noise was shown to cause adverse health effects including noise-induced hearing impairment, annoyance, sleep disturbance, and cardiovascular diseases. Transportation noise has been the most common one among all noise sources in urban areas. A study has been initiated in Istanbul, Turkey in order to evaluate the effects of highway noise on annoyance and myocardial infarction. A total of 2000 surveys will be conducted in 6 hospitals in Istanbul. The highway noise levels are obtained from the noise maps prepared by Environmental Protection Department of Istanbul Metropolitan Municipality. This manuscript presents the highway noise exposure levels in Istanbul and early findings regarding the annoyance effects of highway traffic noise.

Central Nervous Activity upon Systemic Salicylate Application in Animals with Kanamycin-Induced Hearing Loss--A Manganese-Enhanced MRI (MEMRI) Study.

This study investigated the effect of systemic salicylate on central auditory and non-auditory structures in mice. Since cochlear hair cells are known to be one major target of salicylate, cochlear effects were reduced by using kanamycin to remove or impair hair cells. Neuronal brain activity was measured using the non-invasive manganese-enhanced magnetic resonance imaging technique. For all brain structures investigated, calcium-related neuronal activity was increased following systemic application of a sodium salicylate solution: probably due to neuronal hyperactivity. In addition, it was shown that the central effect of salicylate was not limited to the auditory system. A general alteration of calcium-related activity was indicated by an increase in manganese accumulation in the preoptic area of the anterior hypothalamus, as well as in the amygdala. The present data suggest that salicylate-induced activity changes in the auditory system differ from those shown in studies of noise trauma. Since salicylate action is reversible, central pharmacological effects of salicylate compared to those of (permanent) noise-induced hearing impairment and tinnitus might induce different pathophysiologies. These should therefore, be treated as different causes with the same symptoms.

Olfactory epithelium neural stem cell implantation restores noise-induced hearing loss in rats

ObjectiveIn this study, we aimed to elucidate the restorative effects of olfactory epithelium neural stem cells (oe-NSCs) implantation on noise-induced hearing loss and establish their mechanism of action. MethodsTo model hearing loss, rats were subjected to consecutive seven-day noise exposure. Then, oe-NSCs were implanted into cochlear tissue by retroauricular approach. Auditory brainstem response (ABR) method was used to evaluate the hearing function. Immunohistochemical staining was utilized to determine cell survival and migration of oe-NSCs. After IL-1β stimulation, nerve growth factor (NGF), neurotrophin-3 (NT-3), and NT-4 levels were evaluated in oe-NSCs. The protective action of oe-NSCs against hydrogen peroxide-induced cell injury was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Resultsoe-NSCs implantation into cochlear tissues ameliorated the noise-induced hearing impairment (p<0.05). After implantation, green fluorescent cells were observed in an even suspension in the lymph fluid of the cochlea, and 65% of the GFP+ cells reached the cochlear duct wall three days after implantation, but did not expand to the Corti-organ. After IL-1β stimulation, olfactory epithelial stem cell increased their secretion of NGF and NT-3 (p<0.05), but not that of NT-4. TUNEL assay results revealed that oe-NSCs co-culturing with injured neurons reduced the apoptotic cell death induced by hydrogen peroxide. ConclusionAfter transplantation into the inner ear, oe-NSCs not only survived, but also migrated around the spiral ganglion neurons (SGNs) in Rosenthal's canal (RC). Hearing loss induced by noise exposure was restored after oe-NSCs implantation. Mechanically, oe-NSCs secreted NGF and NT-3, which likely contributed to the prevention of neuronal injury. This study provides novel data in support of the effective action of implanted oe-NSCs in the restoration of noise-induced hearing loss in a rat model.