Commentary on the regulatory implications of noise-induced cochlear neuropathy

Abstract

Objective: A discussion on whether recent research on noise-induced cochlear neuropathy in rodents justifies changes in current regulation of occupational noise exposure. Design: Informal literature review and commentary, relying on literature found in the authors’ files. No formal literature search was performed. Study sample: Published literature on temporary threshold shift (TTS) and cochlear pathology, in humans and experimental animals, as well as the regulations of the US Occupational Safety and Health Administration (OSHA). Results: Humans are less susceptible to TTS, and probably to cochlear neuropathy, than rodents. After correcting for inter-species audiometric differences (but not for differences in susceptibility), exposures that caused cochlear neuropathy in rodents already exceed OSHA limits. Those exposures also caused “pathological TTS” (requiring more than 24?h to recover), which does not appear to occur with human broadband noise exposure permissible under OSHA. Conclusion: It would be premature to conclude that noise exposures permissible under OSHA can cause cochlear neuropathy in humans.     

D-methionine pre-loading reduces both noise-induced permanent threshold shift and outer hair cell loss in the chinchilla

Abstract

Objective: This study tested multiple dosing epochs of pre-loaded D-methionine (D-met) for otoprotection from noise-induced hearing loss (NIHL). Design: Auditory brainstem response (ABR) thresholds were measured at baseline, 1 day, and 21 days following a 6-hour 105 dB sound pressure level (SPL) octave band noise (OBN) exposure. Outer hair cell (OHC) counts were measured after day 21 sacrifice. Study sample: Three groups of five Chinchillas laniger each were given a 2-day regimen comprising five doses of D-met (200 mg/kg/dose) intraperitoneally (IP) starting 2, 2.5, or 3 days prior to noise exposure. A control group (n = 5) received five doses of equivalent volume saline IP starting 2.5 days prior to noise exposure. Results: ABR threshold shifts from baseline to day-21 post-noise exposure were reduced in all D-met groups versus controls, reaching significance (p < 0.05) in the 3-day group. D-met groups showed reduced OHC loss relative to controls at day-21 post-noise exposure, reaching significance (p < 0.05) at all frequency regions in the 3-day group and at the 2, 4, and 8 kHz frequency regions in the 2.5-day group. Conclusions: D-met administration in advance of noise-exposure, without further administration, significantly protects from noise-induced ABR threshold shift and OHC loss.     

The possibility of cochlear synaptopathy in young people using a personal listening device

ObjectiveTo evaluate the association of listening to music loudly through personal listening devices with cochlear synaptopathy in young adults.MethodsFifty healthy young adults selected among 109 volunteers were included in the study. Participants of high risk (n=25) and low risk (n=25) groups estimated according to ETDNL (estimated total daily noise level) were evaluated using pure tone audiometry, tympanometry, matrix test, electrocochleography (EcochG) and auditory brainstem response (ABR) to evaluate the occurrence of cochlear synaptopathy.ResultsAudiometric thresholds between the groups were not significantly different (p>0.05). High risk group participants showed poorer performance than the low-risk group on the TurMatrix test, in non-adaptive noise with -5 SNR and -7.5 SNR, and at the 50% understanding SNR level with headphones (p<0.01). There was no difference in the adaptive free field in noise test at which 50% understanding was achieved (p>0.05). The AP amplitudes on EcochG and wave V amplitudes on ABR were significantly smaller in the high-risk group (p<0.05). There was no association between ETDNL and I/V ratio on ABR.ConclusionPoorer performance in TurMatrix and other electrophysiologic tests revealed the negative effect of personal listening devices on the auditory system. Our findings support the hypothesis that personal listening devices could cause cochlear synaptopathy. Long-term studies are needed to determine the effects of binaural hearing and duration of noise exposure on the auditory system.     

Unitary ototoxic gentamicin exposure may not disrupt the function of cochlear outer hair cells in mice

Background: Previous study showed that mild ototoxic exposure could induce a reversible hearing impairment, and the loss and secondary incomplete recovery of cochlear ribbon synapses could be responsible for the hearing loss. However, it remains unclear whether cochlear outer hair cells’ (OHCs) functions are affected.

Objective: To verify whether the function of OHCs are also affected significantly after the ototoxic exposure.

Methods: Mice were injected intraperitoneally with 100?mg/kg concentration of gentamicin daily for 14 days. Distortion Product of Oto-acoustic Emission (DPOAE) was detected at control (pre-treatment), Day 0, day 4, day 7, day 14 and day 28 after the ototoxic exposure, respectively. In addition, the morphology of OHCs was observed by electron microscopy, OHCs has been counted by light microscopy, and the hearing thresholds were detected by auditory brain response (ABR).

Results: No significant changes have been found in OHC and OHC stereocilia among the experimental groups (p?>?.05). Further, no significant changes or loss was found in the morphology of OHCs either. However, we found ABR threshold elevations occurred after ototoxic exposure.

Conclusions: Unitary ototoxic gentamicin exposure may not disrupt the function of cochlear OHCs in mice, regardless of hearing loss identified in this ototoxic exposure.     

Potentiation of noise-induced hearing loss by amikacin in guinea pigs.

Noise and aminoglycosides initially attack cochlear outer hair cells (OHCs). Distortion product otoacoustic emissions (DPOAEs) are used for the early diagnosis of damage to OHCs. The effects of sub-damaging doses of amikacin, an aminoglycoside antibiotic agent, on noise-induced hearing loss (NIHL) were examined in guinea pigs. Animals were grouped by gender and exposed to broadband noise at 105 dB SPL for 12 h and/or injected i.m. with either amikacin (100 mg/kg/day) or saline for 10 days. Auditory brainstem response (ABR) thresholds, along with DPOAE amplitudes, were measured serially before and after noise exposure. DPOAE amplitudes decreased and ABR thresholds elevated immediately after noise exposure and then gradually recovered. At all frequencies, the emission amplitudes recovered completely to pre-exposure baseline values by 4 days after noise exposure. There was no effect of amikacin on either the ABR threshold or DPOAE amplitudes, in animals treated with amikacin only. However, amikacin significantly prolonged the effect of noise exposure on DPOAE amplitude but not on the noise-induced temporary threshold shift (TTS) of the ABR. In animals treated with a combination of noise and amikacin, significant changes in DPOAE amplitudes were still observed at 4 weeks after cessation of noise exposure. No gender difference in the responses to noise and/or amikacin could be demonstrated. The present findings indicate that even sub-damaging dosages of amikacin might impair recovery from NIHL in guinea pigs.     

Estimation of the status of spiral ganglion neurons and Schwann cells in the auditory neural degeneration mouse using the auditory brainstem response

Conclusion: The auditory brainstem response (ABR) wave I threshold, latency and amplitude are insensitive to spiral ganglion neurons (SGNs) degeneration, but are sensitive to the degeneration of Schwann cells and can estimate the status of Schwann cells in a neural degeneration mouse model. The thorough pre-operative ABR assessment would be helpful in predicting cochlear implant performance.

Objectives: This study aimed in finding a non-invasive electrophysiological method to evaluate the status of the auditory nerve and the Schwann cells in sensorineural hearing loss (SNHL) and auditory neuropathy (AN) ears, and providing useful information for candidates screening and outcome prediction in cochlear implantation.

Methods: The frequency-specific acoustic ABR was recorded in mice. The immunohistochemical staining was performed to detect the SGNs and Schwann cells in mice cochlea. The correlations between ABR wave I metrics and SGNs, Schwann cells were investigated.

Results: In SNHL and AN mice cochlea, statistically significant correlations between ABR wave I thresholds, latencies and amplitudes at 8, 16, and 32?kHz and their corresponding SGNs densities were found only in wave I amplitude at 8?kHz. While the ABR wave I metrics at all three frequencies showed strong significant correlations with their corresponding Schwann cells densities.     

Noise induced reversible changes of cochlear ribbon synapses contribute to temporary hearing loss in mice

Conclusion: Noise exposure can cause a decline in cochlear ribbon synapses and result in consequent hearing loss. The reduction of synaptic puncta appears reversible and may contribute to hearing restoration in mice after noise exposure. Objective: To detect whether noise induced reversible changes of cochlear ribbon synapses contribute to temporary hearing loss in C57BL/6J mice. Methods: The mice were assigned randomly to five groups and exposed to white noise at 110 dB SPL for 2 h except the control group. ABR thresholds were acquired before noise exposure (control), immediately following exposure (Day 0), or on Days 4, 7, or 14 after noise exposure. Light microscopy, scanning emission microscopy, and whole mounts examination was utilized to study whether there is morphology change of outer hair cells (OHC), inner hair cells (IHC), or spiral ganglion cells (SGN) due to the 110 dB white noise. Moreover, experimental approaches, including immunostaining and confocal microcopy, were used to detect whether ribbon synapses were the primary targets of noise-induced temporary hearing loss. Result: Exposure to 110 dB white noise for 2 h induced TTS in mice, with the maximal ABR threshold elevations seen on the 4^th day after noise exposure. There were no significant morphological changes in the cochlea. Paralleled changes of pre-synaptic ribbons in both the number and post-synaptic density (PSDs) during this noise exposure were detected. The number of pre-synaptic ribbon, post-synaptic density (PSDs), and co-localized puncta correlated with the shifts of ABR thresholds. Moreover, a complete recovery of ABR thresholds and synaptic puncta was seen on the 14^th day after the noise stimulations.     

Molecular mechanisms underlying the protective effects of hydrogen-saturated saline on noise-induced hearing loss

Objectives: This study aimed to explore the molecular mechanism of the protective effects of hydrogen-saturated saline on NIHL.

Methods: Guinea pigs were divided into three groups: hydrogen-saturated saline; normal saline; and control. For saline administration, the guinea pigs were given daily abdominal injections 3 d before and 1?h before noise exposure. ABR were tested to examine cochlear physiology changes. The changes of 8-hydroxy-desoxyguanosine (8-HOdG), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), intercellular cell adhesion molecule-1 (ICAM-1) and high mobility group box-1 protein (HMGB1) in the cochlea were also examined.

Results: The results showed that pre-treatment with hydrogen-saturated saline could significantly attenuate noise-induced hearing loss. The concentration of 8-HOdG was also significantly decreased in the hydrogen-saturated saline group compared with the normal saline group. After noise exposure, the concentrations of IL-1, IL-6, TNF-α, and ICAM-1 in the cochlea of guinea pigs in the hydrogen-saturated saline group were dramatically reduced compared to those in the normal saline group. The concentrations of HMGB-1 and IL-10 in the hydrogen-saturated saline group were significantly higher than in those in the normal saline group immediately and at 7 d after noise exposure.

Conclusions: This study revealed for the first time the protective effects of hydrogen-saturated saline on noise-induced hearing loss (NIHL) are related to both the anti-oxidative activity and anti-inflammatory activity.     

Protective effect of a purified polyphenolic extract from Ecklonia cava against noise-induced hearing loss: Prevention of temporary threshold shift

ObjectiveNoise is one of the most common causes of hearing loss. Approximately 16% of American teenagers (12–19 years) have hearing loss caused by loud noise. The implication of noise-induced hearing loss (NIHL) in teenagers has received increasing attention. Although temporary threshold shift (TTS), a type of NIHL, is a transient hearing loss, it can accelerate age-related hearing loss. Reactive oxygen species are a primary cause of TTS. As the polyphenols from Ecklonia cava are known to have potent antioxidant effects, we investigated the protective effects of a purified polyphenolic extract of Ecklonia cava (PPEE) against TTS in mice.MethodsThe radical-scavenging activity of PPEE was evaluated using the 1,1-diphenyl-2-picrylhydrazyl assay. The PPEE + Noise and Saline + Noise groups were administered intraperitoneal PPEE (100 mg/kg) and saline, respectively, for 5 days before exposure to noise at 100 dB SPL for 60 min. Hearing ability was assessed following noise exposure using auditory brainstem responses and distortion product otoacoustic emissions.ResultsPPEE exhibited significant radical scavenging activity. The ABR threshold shifts 1 day after exposure to noise at 16 kHz and 1, 7, and 14 days after exposure to noise at 32 kHz, were significantly less in the PPEE + Noise than in the Saline + Noise group. One day after noise exposure, mice in the PPEE + Noise group showed a significant degree of protection in relation to their DPOAE level at f2, 17, and 28 kHz.ConclusionsThese findings suggest that PPEE may be a potential preventive agent against TTS. In addition, as a food ingredient approved by the United States Food and Drug Administration, PPEE may be administered to those who are exposed to noise inevitably with little likelihood of adverse effects, thereby contributing to the prevention of TTS.     

Speech-in-noise screening tests by internet,Part 2: Improving test sensitivity for noise-induced hearing loss

Abstract

Objective: An easily accessible screening test can be valuable in the prevention of noise-induced hearing loss (NIHL). The Dutch National Hearing Foundation developed ‘Earcheck’, an internet-based speech-in-noise test, presenting CVC-words in stationary broadband noise. However, its sensitivity to detect NIHL appeared to be low, 51% (, part 1). The aim of the current study is to examine ways to improve Earcheck's sensitivity for (early) NIHL using different forms of noise filtering. Design: The test's stationary broadband masking noise is replaced by six alternatives, including noises that have been temporally modulated, spectrally filtered by high-pass or low-pass filters, and combinations of temporal modulation and spectral filtering. Study sample: In this multi-centre study, 49 normal-hearing and 49 subjects with different degrees of NIHL participated. Results: Hearing-impaired subjects deviated more clearly from normal performance when executing the test with alternative masking noises, except for the high-pass filtered conditions. Earcheck with low-pass filtered noise made the best distinction between normal hearing and NIHL, without reducing test reliability. The use of this noise condition improved the sensitivity of Earcheck to 95%. Conclusion: The use of low-pass filtered masking noise makes speech-in-noise tests more sensitive to detect NIHL in an early stage.

Sumario

Objetivo: Una prueba de tamiz accessible podría tener valor en la prevención de hipoacusia inducida por ruido (NIHL). La Fundación Nacional Holandesa para la Audición desarrolló la prueba “Earcheck”; una prueba de lenguaje en ruido por internet que presenta palabras CVC en ruido de banda ancha estacionario. Sin embargo, al parecer su sensibilidad para detectar la hipoacusia inducida por ruido es baja, 51% (Leensen et al, parte 1, 2011). El objetivo de este estudio es examinar las formas para mejorar la sensibilidad de Earcheck en la detección de NIHL (incipiente), utilizando diferentes formas de filtración del ruido. Diseño: el ruido estacionario enmascarante de banda ancha de la prueba, es sustituído por seis diferentes alternativas, incluyendo ruidos que han sido temporalmente modulados, espectralmente filtrados por filtros pasa bajo o pasa alto y combinaciones de modulación temporal y filtración espectral. Muestra: en este estudio multicéntrico participaron 49 normoyentes y 49 sujetos con diferentes grados de NIHL. Resultados: Los sujetos con hipoacusia se desviaron más claramente del desempe o normal cuando ejecutaron la prueba con ruido enmascarante alternativo, excepto en las condiciones de filtro pasa alto. La mayor distinción entre normoyentes y sujetos con NIHL en la prueba Earcheck fue con el ruido con filtro pasa-bajo. El uso de este tipo de ruido mejor la sensibilidad de la prueba Earcheck hasta llegar a un 95%. Conclusiones: El uso de ruido enmascarante con filtro pasa-bajo hace que la prueba de lenguaje en ruido sea más sensible para detectar NIHL en una fase inicial.     

一氧化氮合酶抑制剂和神经营养因子3对噪声暴露下豚鼠耳蜗的保护作用

目的观察一氧化氮合酶抑制剂——N-硝基左旋精氨酸甲酯（N^G-nitro-L-arginine methyl ester，L-NAME）和神经营养因子3（neurotrophin 3，NT3）对噪声性听力损失的保护作用。方法80只雄性杂色豚鼠按区组随机分为非噪声组（n=20）和噪声暴露组（n=60），噪声暴露组又分为生理盐水组（n=20）、L-NAME组（n=20）、L-NAME＋NT3组（n=20）。L-NAME组和L-NAME＋NT3组动物在噪声暴露（4kHz倍频程、声压级115dB，5h）之前2d和噪声暴露前30min给予L-NAME 10mg／kg（腹腔注射），生理盐水组动物给予等体积的生理盐水。NT3（10μg／ml）在噪声暴露前4d经微量渗透泵（200μl，0．5μl／h）输入到L-NAME＋NT3组动物的右侧耳蜗鼓阶，持续到噪声暴露后10d。噪声暴露前和暴露后10d测试听性脑干反应（auditory brainstem response，ABR），暴露后3d测试耳蜗组织一氧化氮（nitric oxide，NO）水平，最后一次ABR测试后计数耳蜗毛细胞的存活率。结果无噪声暴露组动物无明显的听力改变和毛细胞缺失；生理盐水组动物的ABR阈移、毛细胞缺失率及耳蜗组织NO水平均高于L-NAME组和L-NAME＋NT3组，差异有统计学意义（P值均〈0．01）；与L-NAME组相比，L-NAME＋NT3组豚鼠的ABR阈移减小，差异有统计学意义（P〈0．01），而耳蜗组织NO水平和毛细胞缺失率差异则没有统计学意义（P=0．197及P=0．095）。结论与单独给予L-NAME相比，联合使用NT3可以更大程度减轻噪声对豚鼠耳蜗的损伤。     

Noise-induced hearing loss in young adults: The role of personal listening devices and other sources of leisure noise

Concept: No consensus exists regarding the magnitude of the risk of noise-induced hearing loss (NIHL) associated with leisure noise, in particular, personal listening devices in young adults. Objective: Examine the magnitude of hearing loss associated with personal listening devices and other sources of leisure noise in causing NIHL in young adults. Study Design: Prospective auditory testing of college student volunteers with retrospective history exposure to home stereos, personal listening devices, firearms, and other sources of recreational noise. Methods: Subjects underwent audiologic examination consisting of estimation of pure-tone thresholds, speech reception thresholds, and word recognition at 45 dB HL. Results: Fifty subjects aged 18 to 30 years were tested. All hearing thresholds of all subjects (save one—a unilateral 30 dB HL threshold at 6 kHz) were normal, (i.e., 25 dB HL or better). A 10 dB threshold elevation (notch) in either ear at 3 to 6 kHz as compared with neighboring frequencies was noted in 11 (22%) subjects and an unequivocal notch (15 dB or greater) in either ear was noted in 14 (28%) of subjects. The presence or absence of any notch (small or large) did not correlate with any single or cumulative source of noise exposure. No difference in pure-tone threshold, speech reception threshold, or speech discrimination was found among subjects when segregated by noise exposure level. Conclusion: The majority of young users of personal listening devices are at low risk for substantive NIHL. Interpretation of the significance of these findings in relation to noise exposure must be made with caution. NIHL is an additive process and even subtle deficits may contribute to unequivocal hearing loss with continued exposure. The low prevalence of measurable deficits in this study group may not exclude more substantive deficits in other popu lations with greater exposures. Continued education of young people about the risk to hearing from recreational noise exposure is warranted.     

Effects of kynurenic acid as a glutamate receptor antagonist in the guinea pig

Glutamate excitotoxicity is implicated in both the genesis of neural injury and noise-induced hearing loss (NIHL). Acoustic overstimulation may result in excessive synaptic glutamate, resulting in excessive binding to post-synaptic receptors and the initiation of a destructive cascade of cellular events, thus leading to neuronal degeneration and NIHL. The purpose of this study was to determine whether this apparent excitotoxicity can be attenuated by kynurenic acid (KYNA), a broad-spectrum glutamate receptor antagonist, and protect against noise-induced temporary threshold shifts (TTS). Guinea pigs were randomly assigned to three separate groups. Baseline compound action potentials (CAP) thresholds and cochlear microphonics (CM) were recorded. Group I was treated with physiologic saline as a vehicle control applied to the round window membrane that was followed by 110 dB SPL wide-band noise for 90 min. Group II received 5 mM KYNA followed by noise exposure, and group III received 5 mM KYNA alone without noise exposure. Post-drug and noise levels of CAP thresholds and CM were then obtained. Noise exposure in the control group caused a significant temporary threshold shift (TTS) of 30–40 dB across the frequencies tested (from 3 kHz to18 kHz). Animals that received 5 mM KYNA prior to noise exposure (group II) showed statistically significant protection against noise-induced damage and demonstrated a minimal TTS ranging between 5 and 10 dB at the same frequencies. Animals in group III receiving KYNA without noise exposure showed no change in thresholds. Additionally, cochlear microphonics showed no considerable difference in threshold shifts when controls were compared to KYNA-treated animals. These results show that antagonizing glutamate receptors can attenuate noise-induced TTS, suggesting that glutamate excitotoxicity may play a role in acoustic trauma. Received: 2 March 1998 / Accepted: 23 February 1999     

Candidate's thesis: enhancing intrinsic cochlear stress defenses to reduce noise-induced hearing loss

OBJECTIVES/HYPOTHESIS: Oxidative stress plays a substantial role in the genesis of noise-induced cochlear injury that causes permanent hearing loss. We present the results of three different approaches to enhance intrinsic cochlear defense mechanisms against oxidative stress. This article explores, through the following set of hypotheses, some of the postulated causes of noise-induced cochlear oxidative stress (NICOS) and how noise-induced cochlear damage may be reduced pharmacologically. 1) NICOS is in part related to defects in mitochondrial bioenergetics and biogenesis. Therefore, NICOS can be reduced by acetyl-L carnitine (ALCAR), an endogenous mitochondrial membrane compound that helps maintain mitochondrial bioenergetics and biogenesis in the face of oxidative stress. 2) A contributing factor in NICOS injury is glutamate excitotoxicity, which can be reduced by antagonizing the action of cochlear -methyl-D-aspartate (NMDA) receptors using carbamathione, which acts as a glutamate antagonist. 3) Noise-induced hearing loss (NIHL) may be characterized as a cochlear-reduced glutathione (GSH) deficiency state; therefore, strategies to enhance cochlear GSH levels may reduce noise-induced cochlear injury. The objective of this study was to document the reduction in noise-induced hearing and hair cell loss, following application of ALCAR, carbamathione, and a GSH repletion drug D-methionine (MET), to a model of noise-induced hearing loss. STUDY DESIGN: This was a prospective, blinded observer study using the above-listed agents as modulators of the noise-induced cochlear injury response in the species chinchilla langier. METHODS: Adult chinchilla langier had baseline-hearing thresholds determined by auditory brainstem response (ABR) recording. The animals then received injections of saline or saline plus active experimental compound starting before and continuing after a 6-hour 105 dB SPL continuous 4-kHz octave band noise exposure. ABRs were obtained immediately after noise exposure and weekly for 3 weeks. After euthanization, cochlear hair cell counts were obtained and analyzed. RESULTS ALCAR administration reduced noise-induced threshold shifts. Three weeks after noise exposure, no threshold shift at 2 to 4 kHz and <10 dB threshold shifts were seen at 6 to 8 kHz in ALCAR-treated animals compared with 30 to 35 dB in control animals. ALCAR treatment reduced both inner and outer hair cell loss. OHC loss averaged <10% for the 4- to 10-kHz region in ALCAR-treated animals and 60% in saline-injected-noise-exposed control animals. Noise-induced threshold shifts were also reduced in carbamathione-treated animals. At 3 weeks, threshold shifts averaged 15 dB or less at all frequencies in treated animals and 30 to 35 dB in control animals. Averaged OHC losses were 30% to 40% in carbamathione-treated animals and 60% in control animals. IHC losses were 5% in the 4- to 10-kHz region in treated animals and 10% to 20% in control animals. MET administration reduced noise-induced threshold shifts. ANOVA revealed a significant difference (P <.001). Mean OHC and IHC losses were also significantly reduced (P <.001). CONCLUSIONS: These data lend further support to the growing body of evidence that oxidative stress, generated in part by glutamate excitotoxicity, impaired mitochondrial function and GSH depletion causes cochlear injury induced by noise. Enhancing the cellular oxidative stress defense pathways in the cochlea eliminates noise-induced cochlear injury. The data also suggest strategies for therapeutic intervention to reduce NIHL clinically.     

氢气对噪声性聋的有效防护时间及机制研究

目的 近年研究表明氢气对噪声性聋具有良好的预防作用,但其对噪声性聋预防作用持续时间尚不明确,本实验通过建立豚鼠噪声性聋模型探索氢气预防作用持续时间及防护机制.方法 选用听力正常的豚鼠30只,随机等分为氢气组和噪声组,氢气组在首次脉冲噪声暴露前给予1h氢气吸入,两组动物随后每隔两小时重复施加脉冲噪声(峰值声强为163dB...     

Protection from noise-induced temporary threshold shift by D-methionine is associated with preservation of ATPase activities

OBJECTIVE: The present study was designed to test whether noise-induced temporary threshold shift (TTS) could be attenuated by D-methionine and its possible relation to the biochemical changes of cochlear lateral walls such as ATPase activities and oxidative stress in guinea pigs. DESIGN: Thirty-two normal-hearing male guinea pigs were randomly divided into saline-treated and D-methionine-treated (300 mg/kg) experimental groups. One hour after treatment, they were exposed to a continuous broadband white noise at 105 +/- 2 dB sound pressure level for 10 min, causing TTS. Each group was then divided into four subgroups based on the number of survival days after noise exposure (0, 1, 2, and 7 days). Each subgroup had four animals and eight ears included. By means of click-evoked auditory brain stem responses (ABR), auditory thresholds of guinea pigs were measured before noise exposure, immediately after noise exposure, and before killing. After animals were killed, cochlear lateral walls were immediately harvested and assayed for enzyme-specific activities of Na+, K+-ATPase and Ca2+-ATPase, lipid peroxidation, and nitric oxide. RESULTS: A 15.31 +/- 3.80 dB threshold shift was found immediately after noise exposure in saline-pretreated guinea pigs. In contrast, ABR threshold shift was significantly attenuated to 4.06 +/- 2.35 dB in D-methionine-treated animals. Furthermore, D-methionine enhanced the restoration of ABR threshold to baseline level by 1 day. In addition, noise significantly decreased Na+, K+-ATPase, and Ca2+-ATPase activities and increased lipid peroxidation and nitric oxide levels of the cochlear lateral walls. D-methionine significantly protected against all of these changes. CONCLUSIONS: Noise not only induced TTS but also inhibited ATPase activities as well as increased oxidative stress in guinea-pig cochlear lateral walls; all of these changes could be attenuated by d-methionine through its antioxidative property. These results suggest the potential usefulness of d-methionine in protecting from noise-induced ototoxicity.     

Speech-in-noise screening tests by internet,Part 3: Test sensitivity for uncontrolled parameters in domestic usage

Abstract

Objective: The online speech-in-noise test ‘Earcheck’ is sensitive for noise-induced hearing loss (NIHL). This study investigates effects of uncontrollable parameters in domestic self-screening, such as presentation level and transducer type, on speech reception thresholds (SRTs) obtained with Earcheck. Design: Subjects performed 26 Earchecks that differed regarding presentation level (65, 71, and 77 dBA), presentation mode (monotic or diotic), and masking noise (two different low-pass filtered noises) in the lab. To investigate effects of test environment, participants conducted eight additional Earchecks at home using different transducer types (headphones or loudspeakers). Study sample: Thirty noise-exposed workers, either normal-hearing (n = 10), or with different degrees of NIHL (n = 20), participated. Results: There was a minor effect of presentation levels exceeding 65 dBA in severely impaired listeners. Diotic presentation mode yielded lower SRTs compared to monotic presentation mode. Normal-hearing test results at home were poorer than in the laboratory, whereas hearing-impaired subjects performed better in domestic testing. Using loudspeakers deteriorated SRTs significantly in comparison to headphones, but only in hearing-impaired subjects. Conclusions: A monotic presentation mode using headphones is recommended for domestic screening. Since domestic testing affects SRT results, a follow up study using a large study population should assess Earcheck's validity when performed at home.     

Influence of well-known risk factors for hearing loss in a longitudinal twin study

Abstract

Objective: The aim was to investigate the influence of environmental exposures on hearing loss in a twin cohort. Study sample: Male twins born 1914–1958, representing an unscreened population, were tested for hearing loss at two occasions, 18 years apart. Design: Clinical audiometry and a questionnaire were performed at both time points in this longitudinal study. Noise and solvent exposure were assessed using occupational work codes and a job exposure matrix. Hearing impairment was investigated using two different pure tone averages: PTA4 (0.5, 1, 2, and 4?kHz) and HPTA4 (3, 4, 6, and 8?kHz). Results: Age affected all outcome measures. Noise exposure between time point one and two affected the threshold shifts of PTA4 and HPTA4 more in participants with a pre-existing hearing loss at time point one. Lifetime occupational noise exposure was a risk factor especially for the low-frequency hearing threshold PTA4. Firearm use was a statistically significant risk factor for all outcome measures. Conclusions: Pre-existing hearing loss can increase the risk of hearing impairment due to occupational noise exposure. An increased risk for NIHL was also seen in the group with exposures below 85?dB(A), a result that indicates awareness of NIHL should be raised even for those working in environments where sound levels are below 85?dB(A).     

模拟失重条件下飞船内噪声对豚鼠耳蜗形态与功能的影响

目的探讨模拟失重条件下,飞船内稳态噪声对豚鼠耳蜗形态与功能的影响。方法32只豚鼠随机分为单纯失重组16只、失重＋稳态噪声组16只。后肢悬吊法模拟失重,暴露于模拟飞船内在天飞行段的噪声环境,共5天。实验前、实验结束后即刻和实验结束后3天测试脑干诱发电位（ABR）阈值,取耳蜗标本行扫描电镜和透射电镜观察。结果实验组实验结束后即刻ABR阈值较实验前及实验结束后3天均增高（P〈0.01）;实验结束后3天ABR阈值较实验前高（P〈0.05）;实验结束后即刻及实验结束后3天失重＋稳态噪声组ABR阈值均较单纯失重组高（P〈0.01）。扫描电镜观察实验组实验结束后即刻耳蜗内、外毛细胞均受损。实验结束后3天,单纯失重组少数耳蜗各回内、外毛细胞的损伤程度比实验结束即刻加重;失重＋稳态噪声组耳蜗各回内毛细胞损伤较实验结束即刻重,外毛细胞损伤较实验结束即刻轻。实验组各时间段内毛细胞的损伤均重于外毛细胞,自第一回至第四回毛细胞损伤逐渐加重。透射电镜观察实验组耳蜗毛细胞及神经节细胞均可见空泡样改变,线粒体分布减少,细胞核固缩,可见细胞凋亡和细胞坏死两种细胞死亡现象。结论失重及失重＋稳态噪声均可造成豚鼠耳蜗形态和功能损伤,后者造成的损伤更重。失重对耳蜗毛细胞损伤以内毛细胞为重,损伤从底回至顶回逐渐加重。实验结束后3天较实验后即刻的听功能有所恢复但内毛细胞损伤加重。     

A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift

Objective: A non-synonymous single nucleotide polymorphism (rs61742642; C to T, P386S) in the ligand-binding domain of human estrogen-related receptor beta (ESRRβ) showed possible association to noise-induced hearing loss (NIHL) in our previous study. Design: This study was conducted to examine the effect of the ESRRβ rs61742642 T variant on temporary threshold shift (TTS). TTS was induced by 10?minutes of exposure to audiometric narrow-band noise centered at 2000?Hz. Hearing thresholds and distortion product otoacoustic emissions input output function (DP IO) at 2000, 3000, and 4000?Hz were measured before and after the noise exposure. Study sample: Nineteen participants with rs61742642 CT genotype and 40 participants with rs61742642?CC genotype were recruited for the study. Results: Participants with the CT genotype acquired a significantly greater TTS without convincing evidence of greater DP IO temporary level shift (DPTLS) compared to participants with the CC genotype. Conclusion: The results indicated that the ESRRβ polymorphism is associated with TTS. Future studies were recommended to explore molecular pathways leading to increased susceptibility to NIHL.