Noise-induced Temporary Threshold Shift Research Articles

The Role of Connexin26 and Connexin30 in the Mouse Cochlea of Noise-Induced Hearing Loss.

We aimed to explore the role of connexin26 (Cx26) and connexin30 (Cx30) in the cochlea in noise-induced permanent threshold shifts (PTS) and temporary threshold shift (TTS). Prospective, controlled. Laboratory. A mouse model of noise-induced PTS and TTS was constructed. Western blots were used to detect the expression of Cx26 and Cx30 in the cochlea. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to assess the potential biological pathways. Both the expression of Cx26 and Cx30 showed a trend of first rising and then falling in noise-induced PTS. The expression of Cx26 increased greatly in the 24 hours noise exposure (P < .05) and reached the highest level in the 4 hours after noise exposure (P < .05), then decreased gradually and returned to the control level on the seventh day after the noise exposure, when compared with the control group. The expression of Cx30 showed a similar trend in noise-induced PTS. However, both the expression of Cx26 and Cx30 showed a trend of first falling and then rising in noise induced TTS. The expression of Cx26/Cx30 reached its lowest level in the 4 hours after noise exposure (P < .05), and then increased to the control level on the second day after noise exposure (P > .05), compared with the control group. The first KEGG and GO pathway may be related with oxidative phosphorylation. Cx26 and Cx30 may have an effect in noise induced PTS and TTS. Future studies are needed to confirm the results.

Examining the utility of near infrared light as pre-exposure therapy to mitigate temporary noise-induced hearing loss in humans.

This study sought to determine the effect of Occupational Safety and Health Administration (OSHA) compliant noise on auditory health and assess whether pre-noise near infrared (NIR) light therapy can mitigate the effects of noise exposure. Over four visits, participants (n = 30, NCT#: 03834714) with normal hearing completed baseline hearing health assessments followed by exposure to open ear, continuous pink noise at 94 dBA for 15 min. Immediately thereafter, post-noise hearing tests at 3000, 4000, and 6000 Hz and distortion product otoacoustic emissions (DPOAEs) were conducted along with the Modified Rhyme Test (MRT), Masking Level Difference Test (MLD), and Fixed Level Frequency Tests (FLFT) [collectively referred to as the Central and Peripheral Auditory Test Battery (CPATB)] to acquire baseline noise sensitivity profiles. Participants were then randomized to either Active or Sham NIR light therapy for 30 min binaurally to conclude Visit 1. Visit 2 (≥24 and ≤ 48 h from Visit 1) began with an additional 30-min session of Active NIR light therapy or Sham followed by repeat CPATB testing and noise exposure. Post-noise testing was again conducted immediately after noise exposure to assess the effect of NIR light therapy. The remaining visits were conducted following ≥2 weeks of noise rest in a cross-over design (i.e., those who had received Active NIR light therapy in Visits 1 and 2 received Sham therapy in Visits 3 and 4). Recovery hearing tests and DPOAEs were completed at the end of each visit. Participants experienced temporary threshold shifts (TTS) immediately following noise exposure, with a mean shift of 6.79 dB HL (±6.25), 10.61 dB HL (±6.89), and 7.30 dB HL (±7.25) at 3000, 4000, and 6000 Hz, respectively, though all thresholds returned to baseline at 3000, 4000, and 6000 Hz within 75 min of noise exposure. Paradoxically, Active NIR light therapy threshold shifts were statistically higher than Sham therapy at 3000 Hz (p = 0.04), but no other differences were observed at the other frequencies tested. An age sub-analysis demonstrated that TTS among younger adults were generally larger in the Sham therapy group versus Active therapy, though this was not statistically different. There were no differences in CPATB test results across Active or Sham groups. Finally, we observed no changes in auditory function or central processing following noise exposure, suggestive of healthy and resilient inner ears. In this study, locally administered NIR prior to noise exposure did not induce a significant protective effect in mitigating noise-induced TTS. Further exploration is needed to implement effective dosage and administration for this promising otoprotective therapy.

Temporary Hearing Threshold Shift in California Sea Lions (Zalophus californianus) Due to a Noise Band Centered at 32 kHz

To determine their frequency-dependent susceptibility to noise-induced temporary hearing threshold shift (TTS), two California sea lions (Zalophus californianus) were exposed for 60 min to a continuous one-sixth-octave noise band (NB) centered at 32 kHz as the fatiguing sound, at sound pressure levels of 132 to 156 dB re 1 µPa (sound exposure levels [SELs] of 168 to 192 dB re 1 µPa2s). Using a psychoacoustic technique, TTSs were quantified at the center frequency of the fatiguing sound and at half an octave and one octave above the center frequency (at 32, 44.8, and 63 kHz). When significant TTS occurred, higher SELs resulted in greater TTSs. TTSs and hearing recovery patterns were similar in both sea lions. The mean onset of TTS1-4 min (defined as 6 dB TTS) in sea lion F01 is estimated to occur after exposure to an SEL of 179 dB re 1 µPa2s (at hearing test frequency 44.8 kHz). After exposure to an SEL of 180 dB re 1 µPa2s, a mean TTS1-4 min of 6.7 dB was measured at hearing test frequency 44.8 kHz. In California sea lions, TTS onset levels are not as closely related (especially at the lower and higher frequencies) to the unmasked hearing thresholds (audiograms) as was previously assumed.

Experimental study on the effect of sound stimulation on hearing and behavior of juvenile black rockfish (Sebastes schlegelii)

Assessing the potential impacts of wind farm noise on fish is a crucial aspect of Environmental Impact Assessment (EIA) studies. There is increasing evidence of disturbances and effects on hearing and behavior in animals. The black rockfish (Sebastes schlegelii) is a commercially valuable rocky reef fish native to East Asia. However, empirical studies that measure the actual consequences are lacking. In this study, we used auditory evoked potentials (AEP) to assess the effects of dominant frequency noise emitted by offshore wind farms on the auditory sensitivity, hearing threshold, swimming, and feeding behavior of juvenile black rockfish. The experimental findings revealed that the most sensitive sound frequency was 200 Hz, with the lowest hearing threshold recorded at 86.4 ± 3.4 dB re 1 μPa. Following 3 and 7 days of exposure to 200 Hz noise at 110 dB, threshold shifts in black rockfish reached 19.0 dB and 13.3 dB, respectively. During the subsequent recovery phase, these shifts decreased to approximately 9.8 dB after 3 days, respectively. The noise-exposed group exhibited higher swimming duration, moving distance, and caudal fin swing frequency compared to the control group without noise exposure. Furthermore, noise prolonged the feeding rate of black rockfish. Our findings provide the first evidence of noise-induced temporary threshold shift and behavioral disturbances in juvenile black rockfish, implying potential fitness consequences associated with noise pollutant.

Temporary threshold shifts in Boris the bottlenose dolphin (Tursiops truncatus), varying noise duration and intensity

There is much concern regarding increasing noise levels in the ocean and how it may affect marine mammals. Early on, there was little information regarding how sound affects marine mammals and no empirical data on the relationship between noise intensity and exposure duration. Working with Boris the bottlenose dolphin, Tursiops truncatus, we explored the effects of octave-band noise, and sonar signals on odontocete hearing and noise-induced temporary hearing threshold shifts (TTS). Sound pressure levels (SPLs) and exposure durations were varied to measure the effects of exposure duration and amplitude. Hearing thresholds were initially measured behaviorally, and later using auditory evoked potentials before and after sound exposure to track TTS and recovery. These efforts showed that threshold shifts were not linear but rather shorter sounds required greater sound exposure levels to induce TTS; a contrast to some early published literature. Further, sound exposure levels of sonar signals required to induce TTS were high, supporting the notion that relatively short sounds must be of relatively high intensity to induce threshold shifts. From these data and this remarkable animal, a novel algorithm was written that predicts the physiological effects of anthropogenic noise if the intensity and duration of exposure are known.

The adaptation of noise-induced temporary hearing threshold shift predictive models for modelling the public health policy.

It has been shown that monitoring temporary threshold shift (TTS) after exposure to noise may have a predictive value for susceptibility of developing permanent noise-induced hearing loss. The aim of this study is to present the assumptions of the TTS predictive model after its verification in normal hearing subjects along with demonstrating the usage of this model for the purposes of public health policy. The existing computational predictive TTS models were adapted and validated in a group of 18 bartenders exposed to noise at the workplace. The performance of adapted TTS predictive model was assessed by receiver operating characteristic (ROC) analysis. The demonstration example of the usage of this model for estimating the risk of TTS in general unscreened population after exposure to loud music in discotheque bars or music clubs is provided. The adapted TTS predictive model shows a satisfactory agreement in distributions of actual and predicted TTS values and good correlations between these values in examined bartenders measured at 4 kHz, and as a mean at speech frequencies (0.5-4 kHz). An optimal cut-off level for recognizing the TTS events, ca. 75% of young people (aged ca. 35 years) may experience TTS >5 dB, while <10% may exhibit TTS of 15-18 dB. The final TTS predictive model proposed in this study needs to be validated in larger groups of subjects exposed to noise. Actual prediction of TTS episodes in general populations may become a helpful tool in creating the hearing protection public health policy. Int J Occup Med Environ Health. 2023;36(1):125-38.

Local Long-Term Inner Ear Drug Delivery in Normal Hearing Guinea Pig-An Animal Model to Develop Preventive Treatment for Noise-Induced Hearing Loss.

Noise-induced hearing loss (NIHL) is one of the leading causes of sensorineural hearing loss with global importance. The current treatment of choice for patients with hearing problems is a hearing aid or a cochlear implant. However, there is currently no treatment to restore physiological hearing. The development of preventive drugs is currently the focus of hearing research. In order to test the efficacy of a drug, the active ingredient has to be applied at reliable concentrations over a period of time. Osmotic minipumps can provide local drug delivery into the perilymph. Combined with a cochlear implant or a tube, the implantation of the pumps may lead to increased hearing thresholds. Such surgery-related threshold shifts complicate the examination of other factors, such as noise. The aim of the present study was to develop an animal model for the examination of substances that potentially prevent NIHL. For this purpose, six male guinea pigs were unilaterally implanted with a silicon catheter with a hook-shaped microcannula at its tip, attached to an artificial perilymph containing osmotic minipump. One week after surgery, the animals were exposed to four hours of a musical piece, presented at 120 dB SPL, to induce a threshold shift. The implantation of the hook-delivery device caused a moderate threshold shift that allows to detect an additional noise-induced temporary threshold shift. This method enables to investigate drug effects delivered prior to the noise insult in order to establish a preventive strategy against noise-induced temporary threshold shifts. The established drug delivery approach allows the release of drugs into the inner ear in a known concentration and for a known duration. This provides a scientific tool for basic research on drug effects in normal hearing animals.

What is the safe noise level to prevent noise-induced hearing loss?

Noise causes short-term mechanical and chemical changes in the cochlea, transduced into electrical signals transmitted to the brain. Excessive noise exposure overwhelms the cochlea’s ability to reverse these changes, causing noise-induced hearing loss (NIHL). The Centers for Disease Control and Prevention state that NIHL is the only completely preventable type of hearing loss. What is the evidence-based safe noise exposure level to prevent NIHL? The National Institute for Occupational Safety and Health (NIOSH) recommended exposure level (REL), 85 dBA, does not prevent NIHL. Occupational exposures are calculated for 8 hours/day, 240 days/year, for 40 years. To calculate the noise exposure level to prevent NIHL in the public, 70 dB for 24 hours (Leq(24) = 70), the Environmental Protection Agency (EPA) adjusted the REL for 24 hours/day, 365 days/year exposure. The actual safe noise exposure must be lower than 70 dB because 1) the EPA did not adjust for lifetime noise exposure, 2) NIOSH based its REL on limited-frequency pure tone audiometry, an insensitive measure of auditory damage, and 3) non-occupational noise exposure has increased. The safe noise level may be as low as 55 dBA, the effective quiet level required for humans to recover from noise-induced temporary threshold shift.

Temporary Hearing Threshold Shift in California Sea Lions (Zalophus californianus) Due to One-Sixth-Octave Noise Bands Centered at 0.6 and 1 kHz

To determine the frequency-dependent susceptibility of California sea lions (Zalophus californianus) to noise-induced temporary hearing threshold shift (TTS), one of two subjects were exposed for 60 minutes to two continuous one-sixth-octave noise bands (NBs) as fatiguing sounds: one centered at 0.6 kHz, at sound pressure levels (SPLs) of 168 to 174 dB re 1 µPa (sound exposure levels [SELs] of 204 to 210 dB re 1 µPa2s), or one centered at 1 kHz, at SPLs of 144 to 159 dB re 1 µPa (SELs of 180 to 195 dB re 1 µPa2s). Using a psychoacoustic technique, TTSs were quantified at 0.6, 0.85, 1, 1.2, 1.4, and 2 kHz (at the center frequency of each NB, half an octave higher, and one octave higher). When significant TTS occurred, higher SELs resulted in greater TTSs. In the sea lion that was tested 1 to 4 minutes after exposure to the fatiguing sounds, the largest TTSs occurred when the hearing test frequency was half an octave higher than the center frequency of the two fatiguing sounds. The highest TTS levels elicited were 8.7 dB at 0.85 kHz and 9.6 dB at 1.4 kHz. When their hearing was tested at the same time after the fatiguing sounds stopped, initial TTSs and hearing recovery patterns were similar in both sea lions. These findings will contribute to the protection of hearing of species in the Otariidae family from anthropogenic noise by facilitating the development of an evidence-based underwater sound weighting function.

Temporary Hearing Threshold Shift in California Sea Lions (Zalophus californianus) Due to One-Sixth-Octave Noise Bands Centered at 8 and 16 kHz: Effect of Duty Cycle and Testing the Equal-Energy Hypothesis

To determine the frequency-dependent susceptibility of California sea lions (Zalophus californianus) to noise-induced temporary hearing threshold shift (TTS), two subjects were exposed for 60 min to two fatiguing sounds: continuous one-sixth-octave noise bands (NBs) centered at 8 kHz (at sound exposure levels [SELs] of 166 to 190 dB re 1 µPa2s) and at 16 kHz (at SELs of 183 to 207 dB re 1 µPa2s). Using a psychoacoustic technique, TTSs were quantified at 8, 11.3, 16, 22.4, and 32 kHz (at the center frequency of each NB, half an octave higher, and one octave higher). For both NBs, higher SELs resulted in greater TTSs. In the SEL ranges that were tested, the largest TTSs occurred when the hearing test frequency was half an octave higher than the frequency of the fatiguing sound. When their hearing was tested at the same time after the fatiguing sounds stopped, initial TTSs and hearing recovery patterns were similar in both sea lions. The effect of fatiguing sound duty cycle on TTS was investigated with the 8 kHz NB, using 1,600 ms signals at a mean sound pressure level (SPL) of 154 dB re 1 µPa. Duty cycle reduction from 100 to 90% resulted in a large decrease in TTS; no TTS was observed at duty cycles ≤ 30%. The equal-energy hypothesis was tested with the 8 kHz NB and found to hold true: five combinations of SPL and exposure duration all resulting in a 182 dB SEL produced similar initial TTSs in both sea lions. These findings will contribute to the protection of otariid hearing from anthropogenic noise by facilitating the development of evidence-based underwater sound weighting functions. Our results also show that the introduction of short inter-pulse intervals to underwater sounds aids in the protection of otariid hearing by allowing recovery to take place.

Temporary hearing threshold shift in harbor seals (Phoca vitulina) due to one-sixth-octave noise bands centered at 0.5, 1, and 2 kHz.

This study concludes a larger project on the frequency-dependent susceptibility to noise-induced temporary hearing threshold shift (TTS) in harbor seals (Phoca vitulina). Here, two seals were exposed to one-sixth-octave noise bands (NBs) centered at 0.5, 1, and 2 kHz at several sound exposure levels (SELs, in dB re 1 μPa2s). TTSs were quantified at the center frequency of each NB, half an octave above, and one octave above, at the earliest within 1-4 min after exposure. Generally, elicited TTSs were low, and the highest TTS1-4 occurred at half an octave above the center frequency of the fatiguing sound: after exposure to the 0.5-kHz NB at 210 dB SEL, the TTS1-4 at 0.71 kHz was 2.3 dB; after exposure to the 1-kHz NB at 207 dB SEL, the TTS1-4 at 1.4 kHz was 6.1 dB; and after exposure to the 2-kHz NB at 215 dB SEL, TTS1-4 at 2.8 kHz was 7.9 dB. Hearing always recovered within 60 min, and susceptibility to TTS was similar in both seals. The results show that, for the studied frequency range, the lower the center frequency of the fatiguing sound, the higher the SEL required to cause the same TTS.

Lack of reproducibility of temporary hearing threshold shifts in a harbor porpoise after exposure to repeated airgun sounds.

Noise-induced temporary hearing threshold shift (TTS) was studied in a harbor porpoise exposed to impulsive sounds of scaled-down airguns while both stationary and free-swimming for up to 90 min. In a previous study, ∼4 dB TTS was elicited in this porpoise, but despite 8 dB higher single-shot and cumulative exposure levels (up to 199 dB re 1 μPa2s) in the present study, the porpoise showed no significant TTS at hearing frequencies 2, 4, or 8 kHz. There were no changes in the study animal's audiogram between the studies or significant differences in the fatiguing sound that could explain the difference, but audible and visual cues in the present study may have allowed the porpoise to predict when the fatiguing sounds would be produced. The discrepancy between the studies may have resulted from self-mitigation by the porpoise. Self-mitigation, resulting in reduced hearing sensitivity, can be achieved via changes in the orientation of the head, or via alteration of the hearing threshold by processes in the ear or central nervous system.

Safety and efficacy of ebselen for the prevention of noise-induced hearing loss: a randomised, double-blind, placebo-controlled, phase 2 trial

Noise-induced hearing loss is a leading cause of occupational and recreational injury and disease, and a major determinant of age-related hearing loss. No therapeutic agent has been approved for the prevention or treatment of this disorder. In animal models, glutathione peroxidase 1 (GPx1) activity is reduced after acute noise exposure. Ebselen, a novel GPx1 mimic, has been shown to reduce both temporary and permanent noise-induced hearing loss in preclinical studies. We assessed the safety and efficacy of ebselen for the prevention of noise-induced hearing loss in young adults in a phase 2 clinical trial. In this single-centre, randomised, double-blind, placebo-controlled phase 2 trial, healthy adults aged 18-31 years were randomly assigned (1:1:1:1) at the University of Florida (Gainsville, FL, USA) to receive ebselen 200 mg, 400 mg, or 600 mg, or placebo orally twice daily for 4 days, beginning 2 days before a calibrated sound challenge (4 h of pre-recorded music delivered by insert earphones). Randomisation was done with an allocation sequence generated by an independent third party. The primary outcome was mean temporary threshold shift (TTS) at 4 kHz measured 15 min after the calibrated sound challenge by pure tone audiometry; a reduction of 50% in an ebselen dose group compared with the placebo group was judged to be clinically relevant. All participants who received the calibrated sound challenge and at least one dose of study drug were included in the efficacy analysis. All randomly assigned patients were included in the safety analysis. This trial is registered with ClinicalTrials.gov, number NCT01444846. Between Jan 11, 2013, and March 24, 2014, 83 participants were enrolled and randomly assigned to receive ebselen 200 mg (n=22), 400 mg (n=20), or 600 mg (n=21), or placebo (n=20). Two participants in the 200 mg ebselen group were discontinued from the study before the calibrated sound challenge because they no longer met the inclusion criteria; these participants were excluded from the efficacy analysis. Mean TTS at 4 kHz was 1·32 dB (SE 0·91) in the 400 mg ebselen group compared with 4·07 dB (0·90) in the placebo group, representing a significant reduction of 68% (difference -2·75 dB, 95% CI -4·54 to -0·97; p=0·0025). Compared with placebo, TTS at 4 kHz was non-significantly reduced by 21% in the 200 mg ebselen group (3·23 dB [SE 0·91] vs 4·07 dB [0·90] in the placebo group; difference -0·84 dB, 95% CI -2·63 to 0·94; p=0·3542) and by 7% in the 600 mg ebselen group (3·81 dB [0·90] vs 4·07 dB [0·90] in the placebo group; difference -0·27, 95% CI -2·03 to 1·50; p=0·7659). Ebselen treatment was well tolerated across all doses and no significant differences were seen in any haematological, serum chemistry, or radiological assessments between the ebselen groups and the placebo group. Treatment with ebselen was safe and effective at a dose of 400 mg twice daily in preventing a noise-induced TTS. These data lend support to a role of GPx1 activity in acute noise-induced hearing loss. Sound Pharmaceuticals.

Autophagy attenuates noise-induced hearing loss by reducing oxidative stress.

Reactive oxygen species play a dual role in mediating both cell stress and defense pathways. Here, we used pharmacological manipulations and siRNA silencing to investigate the relationship between autophagy and oxidative stress under conditions of noise-induced temporary, permanent, and severe permanent auditory threshold shifts (temporary threshold shift [TTS], permanent threshold shift [PTS], and severe PTS [sPTS], respectively) in adult CBA/J mice. Levels of oxidative stress markers (4-hydroxynonenal [4-HNE] and 3-nitrotyrosine [3-NT]) increased in outer hair cells (OHCs) in a noise-dose-dependent manner, whereas levels of the autophagy marker microtubule-associated protein light chain 3 B (LC3B) were sharply elevated after TTS but rose only slightly in response to PTS and were unaltered by sPTS noise. Furthermore, green fluorescent protein (GFP) intensity increased in GFP-LC3 mice after TTS-noise exposure. Treatment with rapamycin, an autophagy activator, significantly increased LC3B expression, while diminishing 4-HNE and 3-NT levels, reducing noise-induced hair cell loss, and, subsequently, noise-induced hearing loss (NIHL). In contrast, treatment with either the autophagy inhibitor 3-methyladenine (3MA) or LC3B siRNA reduced LC3B expression, increased 3-NT and 4-HNE levels, and exacerbated TTS to PTS. This study demonstrates a relationship between oxidative stress and autophagy in OHCs and reveals that autophagy is an intrinsic cellular process that protects against NIHL by attenuating oxidative stress. The results suggest that the lower levels of oxidative stress incurred by TTS-noise exposure induce autophagy, which promotes OHC survival. However, excessive oxidative stress under sPTS-noise conditions overwhelms the beneficial potential of autophagy in OHCs and leads to OHC death and NIHL.

Noise-induced cochlear F-actin depolymerization is mediated via ROCK2/p-ERM signaling.

Our previous work has suggested that traumatic noise activates Rho-GTPase pathways in cochlear outer hair cells (OHCs), resulting in cell death and noise-induced hearing loss (NIHL). In this study, we investigated Rho effectors, Rho-associated kinases (ROCKs), and the targets of ROCKs, the ezrin-radixin-moesin (ERM) proteins, in the regulation of the cochlear actin cytoskeleton using adult CBA/J mice under conditions of noise-induced temporary threshold shift (TTS) and permanent threshold shift (PTS) hearing loss, which result in changes to the F/G-actin ratio. The levels of cochlear ROCK2 and p-ERM decreased 1h after either TTS- or PTS-noise exposure. In contrast, ROCK2 and p-ERM in OHCs decreased only after PTS-, not after TTS-noise exposure. Treatment with lysophosphatidic acid, an activator of the Rho pathway, resulted in significant reversal of the F/G-actin ratio changes caused by noise exposure and attenuated OHC death and NIHL. Conversely, the down-regulation of ROCK2 by pretreatment with ROCK2 siRNA reduced the expression of ROCK2 and p-ERM in OHCs, exacerbated TTS to PTS, and worsened OHC loss. Additionally, pretreatment with siRNA against radixin, an ERM protein, aggravated TTS to PTS. Our results indicate that a ROCK2-mediated ERM-phosphorylation signaling cascade modulates noise-induced hair cell loss and NIHL by targeting the cytoskeleton. We propose the following cascade following noise trauma leading to alteration of the F-actin arrangement in the outer hair cell cytoskeleton: Noise exposure reduces the levels of GTP-RhoA and subsequently diminishes levels of RhoA effector ROCK2 (Rho-associated kinase 2). Phosphorylation of ezrin-radixin-moesin (ERM) by ROCK2 normally allows ERM to cross-link actin filaments with the plasma membrane. Noise-decreased levels of ROCK results in reduction of phosphorylation of ERM that leads to depolymerization of actin filaments. Lysophosphatidic acid (LPA), an agonist of RhoA, binds to the G-protein-coupled receptor (GPCR) leading to activation of RhoA through Gα12/13 and RhoGEF. Administration of LPA rescues the noise-diminished F/G-actin ratio.

The dissimilar time course of temporary threshold shifts and reduction of inhibition in the inferior colliculus following intense sound exposure

Excessive noise exposure is known to produce an auditory threshold shift, which can be permanent or transient in nature. Recent studies showed that noise-induced temporary threshold shifts are associated with loss of synaptic connections to the inner hair cells and with cochlear nerve degeneration, which is reflected in a decreased amplitude of wave I of the auditory brainstem response (ABR). This suggests that, despite normal auditory thresholds, central auditory processing may be abnormal.We recorded changes in central auditory processing following a sound-induced temporary threshold shift. Anesthetized guinea pigs were exposed for 1 h to a pure tone of 11 kHz (124 dB sound pressure level). Hearing thresholds, amplitudes of ABR waves I and IV, and spontaneous and tone-evoked firing rates in the inferior colliculus (IC) were assessed immediately, one week, two weeks, and four weeks post exposure.Hearing thresholds were elevated immediately following overexposure, but recovered within one week. The amplitude of the ABR wave I was decreased in all sound-exposed animals for all test periods. In contrast, the ABR wave IV amplitude was only decreased immediately after overexposure and recovered within a week. The proportion of IC units that show inhibitory responses to pure tones decreased substantially up to two weeks after overexposure, especially when stimulated with high frequencies. The proportion of excitatory responses to low frequencies was increased. Spontaneous activity was unaffected by the overexposure.Despite rapid normalization of auditory thresholds, our results suggest an increased central gain following sound exposure and an abnormal balance between excitatory and inhibitory responses in the midbrain up to two weeks after overexposure. These findings may be associated with hyperacusis after a sound-induced temporary threshold shift.

Comparison of the effects of N-acetyl-cysteine and ginseng in prevention of noise induced hearing loss in male textile workers.

Previous studies revealed the role of antioxidant agents in prevention of noise induced hearing loss (NIHL). The aim of this study was to compare the protective effect of N-acetyl-cysteine (NAC) and ginseng on protection of NIHL in textile workers exposed to continuous noise in daily working. In this study, 48 participants were randomly allocated to three groups; Group I received NAC 1200 mg/day, Group II received ginseng 200 mg/day, and Group III (control group) received no supplement. Pure tone audiometry and high frequency audiometry were performed preshift before and after 14 days (on day 15). Linear regression analysis results showed reduced noise-induced temporary threshold shift (TTS) for NAC and ginseng groups at 4, 6 and 16 kHz (P < 0.001) in both ears. Furthermore, the protective effects were more prominent in NAC than ginseng. Our results show that NAC and ginseng can reduce noise induced TTS in workers exposed to occupational noise. Further studies are needed to prove antioxidants benefits in hearing conservation programs.

Involvement of retinoic acid-induced peroxiredoxin 6 expression in recovery of noise-induced temporary hearing threshold shifts

All-trans retinoic acid (ATRA) is reported to reduce hair cell loss and hearing deterioration caused by noise-induced hearing loss (NIHL). The present study investigates the involvement of peroxiredoxin 6 (Prdx 6) in ATRA-mediated protection of temporary threshold shift of hearing. Mice fed with ATRA before or after exposure to white noise showed a faster recovery than untreated controls within 1 week, with a concomitant increase of cochlear Prdx 6 expression. Treatment of mouse auditory cells with ATRA induced Prdx 6 expression. A putative retinoic acid (RA)-response element (RARE) was identified in a murine Prdx 6 promoter region. Prdx 6 promoter activities were elevated in wild-type reporter plasmid-transfected cells, whereas no significant change in activity was in those with RARE-disrupted mutant reporter. RA receptor α (RARα) functions as a transactivator of Prdx 6 gene expression. These findings suggest that ATRA-induced Prdx 6 expression may be associated with rapid recovery from temporary NIHL.

The Effect ofGingko Bilobaon Hearing in Mice with Noise-Induced Temporary Threshold Shift

Background and ObjectivesGingko biloba extract is known for enhancing blood circulation, scavenging free radicals, and antagonizing against platelet-activating factor. This study evaluated the effect of Gingko biloba on the noise-induced temporary threshold shift of hearing.Materials and MethodsTemporary threshold shift was induced by exposing mice to 110 dB SPL sound for 1 hour. The experimental group consisted of mice fed Gingko biloba [3 mg/kg, 6 mg/kg, and 12 mg/kg in 0.5% carboxymethyl cellulose (CMC)] for 7 days before noise exposure. CMC solution without Gingko biloba was fed to control mice. Hearing threshold was measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE).ResultsThe hearing threshold increased after noise exposure and recovered to normal within 5 days in all groups. Compared to control mice (fed CMC solution only), mice fed Gingko biloba showed more rapid recovery of ABR threshold at 16 kHz in all three experimental groups. At the other frequencies, there was no significant change in hearing recovery in the Gingko biloba groups. There was no difference in DPOAE between groups.ConclusionsTemporary threshold shift of hearing after noise exposure was partly affected by oral Gingko biloba.

Effects of Cigarette Smoking on Hearing Recovery From Noise-Induced Temporary Hearing Threshold Shifts in Mice

Cigarette smoking may potentiate noise-induced hearing loss. Many epidemiological studies have shown that cigarette smoking is a major risk factor for noise-induced hearing loss. BALB/c mice were exposed to passive smoking for 2 h/d for 2 weeks before exposure to 110-dB sound pressure level white noise for 3 hours once. Hearing was assessed via the auditory brainstem response with tone-burst stimulation and distortion product otoacoustic emissions before and at 1, 3, 5, 7, 14, 21, and 28 days after noise exposure. Oxidative stress and hypoxia were assessed by immunostaining with 8-oxoG and hypoxia-inducible factor 1α, respectively. Control mice unexposed to both smoking and noise and mice exposed to smoking only showed no shift in hearing threshold. In contrast, mice exposed to noise only or smoking plus noise showed abrupt increases in hearing threshold. In mice exposed to noise only, hearing threshold returned to prenoise levels after 2 weeks. However, in mice exposed to smoking plus noise, the loss of hearing was significantly higher, and hearing threshold did not return to the pre-exposure levels until 4 weeks later. Positive staining with 8-oxoG and hypoxia-inducible factor 1α were observed in the inner ear of the smoking-only and smoking-plus-noise group similar to noise-only mice, whereas no positive staining was observed in control group. These results indicate that cigarette smoking may potentiate the harmful effects of noise on hearing and disturb the recovery mechanism in the cochlea.