Single Noise Exposure Research Articles

Complete Restoration of Hearing Loss and Cochlear Synaptopathy via Minimally Invasive, Single-Dose, and Controllable Middle Ear Delivery of Brain-Derived Neurotrophic Factor-Poly(dl-lactic acid-co-glycolic acid)-Loaded Hydrogel.

Noise-induced hearing loss (NIHL) often accompanies cochlear synaptopathy, which can be potentially reversed to restore hearing. However, there has been little success in achieving complete recovery of sensorineural deafness using nearly noninvasive middle ear drug delivery before. Here, we present a study demonstrating the efficacy of a middle ear delivery system employing brain-derived neurotrophic factor (BDNF)-poly-(dl-lactic acid-co-glycolic acid) (PLGA)-loaded hydrogel in reversing synaptopathy and restoring hearing function in a mouse model with NIHL. The mouse model achieved using the single noise exposure (NE, 115 dBL, 4 h) exhibited an average 20 dBL elevation of hearing thresholds with intact cochlear hair cells but a loss of ribbon synapses as the primary cause of hearing impairment. We developed a BDNF-PLGA-loaded thermosensitive hydrogel, which was administered via a single controllable injection into the tympanic cavity of noise-exposed mice, allowing its presence in the middle ear for a duration of 2 weeks. This intervention resulted in complete restoration of NIHL at frequencies of click, 4, 8, 16, and 32 kHz. Moreover, the cochlear ribbon synapses exhibited significant recovery, whereas other cochlear components (hair cells and auditory nerves) remained unchanged. Additionally, the cochlea of NE treated mice revealed activation of tropomyosin receptor kinase B (TRKB) signaling upon exposure to BDNF. These findings demonstrate a controllable and minimally invasive therapeutic approach that utilizes a BDNF-PLGA-loaded hydrogel to restore NIHL by specifically repairing cochlear synaptopathy. This tailored middle ear delivery system holds great promise for achieving ideal clinical outcomes in the treatment of NIHL and cochlear synaptopathy.

Effects of coexposure to noise and mixture of toluene, ethylbenzene, xylene, and styrene (TEXS) on hearing loss in petrochemical workers of southern China.

Many harmful factors existing simultaneously with noise are reported to induce hearing impairment, such as organic solvents. However, the existing hearing safety limits and current risk assessment for hearing loss rely on single noise exposure. It is urgent to clarify the combined effect of noise and other harmful factors on hearing loss. Petrochemical workers are always exposed to noise and organic solvents, mainly benzene, toluene, ethylbenzene, xylene, and styrene (BTEXS), while the combined effect of their coexposure on hearing remains unclear. Herein we conducted a cross-sectional survey, measuring pure-tone audiometry of 1496 petrochemical workers in southern China. Participants exposed to BTEXS were 569, 524, 156, 452, and 177 respectively. Individual cumulative noise exposure (CNE) levels and BTEXS exposure were assessed. The average CNE was 93.27 ± 4.92dB(A)·years, and the concentrations of BTEXS were far below the occupational exposure limits of China. Logistic regression analyses showed that CNE was consistently positively associated with hearing loss (HL) and high-frequency hearing loss (HFHL) but not related to speech-frequency hearing loss (SFHL). Compared with participants in the lowest quartile of CNE, those in the highest quartile showed an OR of 5.229 (95% CI: 3.179, 8.598) for HFHL. Two-pollutant model analysis indicated that TEXS exposure was positively associated with HL (OR 1.679, 95%CI 1.086, 2.597), SFHL (OR 2.440, 95%CI 1.255, 4.744), and HFHL (OR 1.475, 95%CI 1.077, 2.020). However, no interactions were observed between CNE and TEXS coexposure on hearing loss. In our study, covariates including smoking and drinking status, body mass index (BMI), ear protection and personal protective equipment, and use of earphone/headphone were adjusted. In conclusion, coexposure to noise and low-level TEXS could induce more severe damage on hearing function than exposure to each alone, especially SFHL. Therefore, petrochemical workers simultaneously exposed to noise and TEXS, even at low-level, should be included in hearing protection programs.

NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss.

The reactive oxygen species (ROS)-generating NADPH oxidase NOX3 isoform is highly and specifically expressed in the inner ear. NOX3 is needed for normal vestibular development but NOX-derived ROS have also been implicated in the pathophysiology of sensorineural hearing loss. The role of NOX-derived ROS in noise-induced hearing loss, however, remains unclear and was addressed with the present study. Two different mouse strains, deficient in NOX3 or its critical subunit p22phox, were subjected to a single noise exposure of 2 h using an 8–16 kHz band noise at an intensity of 116–120 decibel sound pressure level. In the hours following noise exposure, there was a significant increase in cochlear mRNA expression of NOX3 in wild type animals. By using RNAscope in situ hybridization, NOX3 expression was primarily found in the Rosenthal canal area, colocalizing with auditory neurons. One day after the noise trauma, we observed a high frequency hearing loss in both knock-out mice, as well as their wild type littermates. At day seven after noise trauma however, NOX3 and p22phox knockout mice showed a significantly improved hearing recovery and a marked preservation of neurosensory cochlear structures compared to their wild type littermates. Based on these findings, an active role of NOX3 in the pathophysiology of noise-induced hearing loss can be demonstrated, in line with recent evidence obtained in other forms of acquired hearing loss. The present data demonstrates that the absence of functional NOX3 enhances the hearing recovery phase following noise trauma. This opens an interesting clinical window for pharmacological or molecular intervention aiming at post prevention of noise-induced hearing loss.

Marine Mammal Noise Exposure Criteria: Assessing the Severity of Marine Mammal Behavioral Responses to Human Noise

Major progress has been made since the publication of noise exposure criteria by Southall et al. (2007) in addressing the probability and severity of marine mammal behavioral responses to measured noise exposures. New methodological developments for studying behavioral responses have broadened the spatial, temporal, and population scales of potential disturbance studies and expanded scientific data on responses of marine mammals (or lack thereof) to various human noise exposure scenarios. Experimental and observational studies have substantially expanded the resolution, parameters, and contexts for understanding individual and group responses to discrete noise events. The combined data strongly suggest that efforts to derive simple all-or-nothing thresholds for single noise exposure parameters (e.g., received noise level) and behavioral responses across broad taxonomic and sound categories can lead to significant errors in predicting effects that are fundamentally inconsistent with the probabilistic nature of responses. Differences between species, among individuals, across situational contexts, and with the temporal and spatial scales over which exposures occur lead to variability in the probability and severity of behavioral responses. Studies that account for such factors and the variability they cause can provide far more accurate probability functions for predicting effects and can reduce variabilities related to exposure level and response. To that end, several new approaches are developed here for evaluating response severity in laboratory and field conditions in terms of effects on vital rates. These are applied to selected studies of marine mammal behavioral response to demonstrate their application in more consistently addressing acute exposure contexts for individuals or discrete groups. Needs for new approaches and transparent processes are identified for addressing sustained and/or repeated noise exposures on population scales.

Combined road traffic, railway and aircraft noise sources: Total noise annoyance model appraisal from field data

Appraisal of environmental noise effects on health considers single noise exposure. In large cities, noise exposure is frequently due to multiple sources. Their combination, interaction or successive presence is known to affect people’s health. The prediction of their effects has been little studied and needs more investigation to address the problem. Studies dealing with annoyance due to combined noise sources proposed different total annoyance models. They were very rarely assessed using field annoyance data. The current work aims to assess them using data of annoyance due to different urban situations of two, and even three, combined transportation noise sources. The considered noises were from road, railway and aircraft traffic. Assessment of ten classical total annoyance models highlighted relevant existing models to account for combined transportation noise annoyance in cities. Perceptual total annoyance models, based on annoyance due to each transportation noise source, better performed total annoyance calculation than psychophysical total annoyance models based on the Lden index. As the dominant source effect mainly explained total annoyance responses from the residents, the strongest component model led to a good calculation of mean total annoyance ratings. But perceptual models with an interaction term, such as the vector summation and mixed models, better explained total annoyance judgments from residents as they account for the contribution of each combined noise source and their interaction. The perceptual linear regression model was also interesting as it accounted for the contribution of each combined noise source, and might be used for more than two combined noise sources. Those perceptual models accounted well for the resident feeling towards the different combined noise sources. These results might contribute to the endeavor aiming at filling the lack of consensus among the scientific community and the corresponding lack of regulations.

The influence of combined exposure to noise and whole-body vibration on hearing loss under simulated heavy equipment driving conditions

Noise-induced hearing loss (NIHL) is a serious problem in occupational environments; however, there is little information about hearing loss due to combined exposure to noise and vibration. This study aimed to investigate the combined effects of exposure to noise and whole-body vibration (WBV) on hearing responses under simulated heavy equipment driving conditions. A repeated measures study was designed to evaluate the changes in distortion product otoacoustic emissions (DPOAE) amplitudes as hearing responses to 40 min of noise and/or WBV exposure. Thirty healthy males with an average age of 30.17 (±3.94) years, exposed to noise level of 85 dB(A) and two WBV levels (0.87 and 1.3 m/s2) in six experimental scenarios. The findings revealed that there was a significant change in DPOAE amplitudes after single noise exposure and combined noise and WBV exposure (p < 0.05); however, there was no significant difference in WBV exposure alone (p > 0.05). The changes in DPOAE amplitudes were greater in combined exposure to noise and WBV (1.3 m/s2) in all sessions. The statistical analysis showed the effect sizes of the combined exposure to noise and WBV were more than the sum of the exposure to each one alone. It can be concluded that some synergic effects can occur in DPOAE amplitudes in the combined noise and WBV exposure under heavy equipment driving conditions. These findings can help the occupational health experts adapt the existing physical agents' exposure limits to the realistic conditions of the occupational settings.

Acoustic trauma from continuous noise: Minimum exposures, issues in clinical trial design, and comments on magnetic resonance imaging exposures.

Acoustic trauma (AT) is permanent hearing loss after a single noise exposure. A few human cases resulting from continuous, i.e., nonimpulsive noise, have been reported as reviewed by Ward [(1991). "Hearing loss from noise and music," presented at Audio Engineering Society, New York, October 4-8]. This paper updates that review by examining 11 cases in nine reports, from 1950 to 2006, with the intention of determining minimum exposures that may cause AT, including the potential risk of exposure to noise from magnetic resonance imaging machines. Diffuse-field related levels above 120 dBA for 10 s or more, or above 130 dBA for 2-3 s (values well above OSHA's unprotected exposure limits), can lead to AT. These cases appear to represent a susceptible fraction of the population, because much more intense exposures (e.g., 130 dBA for 32 min) have been tolerated by groups of volunteers who suffered only temporary threshold shifts. AT from continuous noise is unlikely to occur in OSHA-compliant hearing conservation programs, and probably rare enough in the general civilian population that clinical trials of drugs aimed at treating it are unlikely to be practical. AT from impulse noise, such as gunfire, which is specifically not the topic of the current work, is more amenable to clinical trials, especially in military settings.

Repeated temporary threshold shift and changes in cochlear and neural function

A robust temporary threshold shift (TTS) can create significant primary damage to the auditory synapse, termed cochlear synaptopathy (CS). The common model applied to examination of this pathology is a single noise exposure or extended duration exposures at relatively high noise dosages. It is unclear if a single noise exposure that does not produce physiological changes consistent with CS (such as suppressed suprathreshold responses) can create evidence consistent with the pathology induced by repeated exposures. Here, we exposed 16-week (wk) old Sprague-Dawley rats to repeated noise exposures (4 consecutive days, 8–16 kHz octave-band of noise, 97 dB SPL for 2 h) and examined measures of cochlear function (distortion product otoacoustic emissions) and auditory neural integrity (auditory brainstem response, wave 1 amplitude). Our results demonstrated a mean maximal threshold shift of 16 dB at 24 h post the initial noise exposure. Subsequent daily repeated exposures (4 consecutive days) resulted in diminished threshold shift at 24 h post repeated TTS. In addition to recovered thresholds, no sustained reduction in suprathreshold responses was observed. The findings are consistent with conditioning literature suggesting diminished TTS with repeated exposures. Repeated TTS that was not individually synaptopathic did not produce physiological evidence consistent with acute CS.

Effect of impact pile driving noise on marine mammals: A comparison of different noise exposure criteria.

Regulators in Europe and in the United States have developed sound exposure criteria. Criteria range from broadband levels to frequency weighted received sound levels. The associated differences in impact assessment results are, however, not yet understood. This uncertainty makes environmental management of transboundary anthropogenic noise challenging and causes confusion for regulators who need to choose appropriate exposure criteria. In the present study, three established exposure criteria frameworks from Germany, Denmark, and the US were used to analyse the effect of impact pile driving at a location in the Baltic Sea on harbor porpoise and harbor seal hearing. The acoustic modeling using MIKE showed that an unmitigated scenario would lead to auditory injury for all three criteria. Despite readily apparent variances in impact ranges among the applied approaches, it was also evident that noise mitigation measures could reduce underwater sound to levels where auditory injuries would be unlikely in most cases. It was concluded that each of the frameworks has its own advantages and disadvantages. Single noise exposure criteria follow the precautionary principle and can be enforced relatively easily, whereas criteria that consider hearing capabilities and animal response movement can improve the accuracy of the assessment if data are available.

Coding-in-Noise Deficits are Not Seen in Responses to Amplitude Modulation in Subjects with cochlear Synaptopathy Induced by a Single Noise Exposure

Since the first report of noise-induced synaptic damage in animals without permanent threshold shifts (PTSs), the concept of noise-induced hidden hearing loss (NIHHL) has been proposed to cover the functional deficits in hearing associated with noise-induced synaptopathy. Moreover, the potential functional deficit associated with the noise-induced synaptopathy has been largely attributed to the loss of auditory nerve fibers (ANFs) with a low spontaneous spike rate (SSR). As this group of ANFs is critical for coding at suprathreshold levels and in noisy background, coding-in-noise deficit (CIND) has been considered to be main consequence of the synaptopathy. However, such deficits have not been verified after a single, brief exposure to noise without PTS. In the present study, synaptopathy was generated by such noise exposure in both mice and guinea pigs. Responses to amplitude modulation (AM) were recorded at a high sound level in combination with masking to evaluate the existence of CINDs that might be associated with loss of low-SSR ANFs. An overall reduction in response amplitude was seen in AM-evoked compound action potential (CAP). However, no such reduction was seen in the scalp-recorded envelope following response (EFR), suggesting a compensation due to increased central gain. Moreover, there was no significant difference in masking effect between the control and noise groups. The results suggest that either there is no significant CIND after the synaptopathy we created, or the AM response tested with our protocol was not sufficiently sensitive to detect such a deficit; far-field EFR is not sensitive to cochlear pathology.

Apoptosis in the cochlear nucleus and inferior colliculus upon repeated noise exposure.

The time course of apoptosis and the corresponding neuronal loss was previously shown in central auditory pathway of mice after a single noise exposure. However, repeated acoustic exposure is a major risk factor for noise-induced hearing loss. The present study investigated apoptosis by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) assay after a second noise trauma in the ventral and dorsal cochlear nucleus and central nucleus of the inferior colliculus. Mice [Naval Medical Research Institute (NMRI) strain] were noise exposed [115 dB sound pressure level, 5–20 kHz, 3 h) at day 0. A double group received the identical noise exposure a second time at day 7 post-exposure and apoptosis was either analyzed immediately (7-day group-double) or 1 week later (14-day group-double). Corresponding single exposure groups were chosen as controls.No differences in TUNEL were seen between 7-day or 14-day single and double-trauma groups. Interestingly, independent of the second noise exposure, apoptosis increased significantly in the 14-day groups compared to the 7-day groups in all investigated areas.It seems that the first noise trauma has a long-lasting effect on apoptotic mechanisms in the central auditory pathway that were not largely influenced by a second trauma. Homeostatic mechanisms induced by the first trauma might protect the central auditory pathway from further damage during a specific time slot. These results might help to understand the underlying mechanisms of different psychoacoustic phenomena in noise-induced hearing loss.

Apoptotic mechanisms after repeated noise trauma in the mouse medial geniculate body and primary auditory cortex.

A correlation between noise-induced apoptosis and cell loss has previously been shown after a single noise exposure in the cochlear nucleus, inferior colliculus, medial geniculate body (MGB) and primary auditory cortex (AI). However, repeated noise exposure is the most common situation in humans and a major risk factor for the induction of noise-induced hearing loss (NIHL). The present investigation measured cell death pathways using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) in the dorsal, medial and ventral MGB (dMGB, mMGB and vMGB) and six layers of the AI (AI-1 to AI-6) in mice (NMRI strain) after a second noise exposure (double-exposure group). Therefore, a single noise exposure group has been investigated 7 (7-day-group-single) or 14days (14-day-group-single) after noise exposure (3h, 5-20kHz, 115dB SPL peak-to-peak). The double-exposure group received the same noise trauma for a second time 7days after the initial exposure and was either TUNEL-stained immediately (7-day-group-double) or 1week later (14-day-group-double) and data were compared to the corresponding single-trauma group as well as to an unexposed control group. It was shown that TUNEL increased immediately after the second noise exposure in AI-3 and stayed upregulated in the 14-day-group-double. A significant increase in TUNEL was also seen in the 14-day-group-double in vMGB, mMGB and AI-1. The present results show for the first time the influence of a repeated noise trauma on cell death mechanisms in thalamic and cortical structures and might contribute to the understanding of pathophysiological findings and psychoacoustic phenomena accompanying NIHL.

Assessment of annoyance due to urban road traffic noise combined with tramway noise.

Due to the expansion of urban areas, an increasing number of residents are exposed to combined community noise sources. Studies show that the exposure to transportation noise significantly affects health and well-being. Noise annoyance is one of these adverse health effects. Up to now, annoyance due to transportation noise is mostly assessed considering single noise exposure situations neglecting the effects of potential interactions between noise sources. In this study, perceptual phenomena involved in noise annoyance due to combined urban road traffic and tramway noises are assessed in laboratory conditions with imaginary and simulated contexts. The urban road traffic was composed of light vehicles, heavy vehicles, buses, and powered-two-wheelers in different driving conditions. The tramway traffic corresponded to tramways in in-curve operating configurations. It could be shown that the road traffic and tramway traffic partial annoyance responses were influenced by each other. Throughout the experiments the strongest component effect prevailed but secondary phenomena could also be observed. Considering the perceptual phenomena highlighted in the analysis, it is shown that total noise annoyance due to the combined noises can be most adequately predicted by the strongest component model. This result was obtained by calculating partial annoyance responses due to urban road and tramway traffic.

Applying Neurotrophins to the Round Window Rescues Auditory Function and Reduces Inner Hair Cell Synaptopathy After Noise-induced Hearing Loss.

Applying neurotrophins to the round window immediately after a single noise exposure will prevent noise-induced hidden hearing loss. Loud noise can eliminate neural connections between inner hair cells and their afferent neurons (thereby diminishing sound perception) without causing a detectable change on audiogram. This phenomenon is termed hidden hearing loss. Guinea pigs were exposed for 2 hours to 4 to 8 kHz noise at either 95 or 105 dB SPL. Immediately afterward a 4 μl bolus of neurotrophins (brain-derived neurotrophic factor 1 μg/μl, and neurotrophin-3 1 μg/μl) was delivered to the round window of one ear, and saline to the other. Auditory brainstem responses to pure-tone pips were acquired preoperatively, and at 1 and 2 weeks' postexposure. Cochleae were removed and whole mounted for immunohistochemical analysis, with presynaptic ribbons of inner hair cells and associated postsynaptic glutamatergic AMPA receptors identified using CtBP2 and GluA2 antibodies respectively. After exposure to 105 dB noise, threshold did not change, but the amplitude growth of the auditory brainstem response was significantly reduced in control ears in response to 16 and 32 kHz tones. The amplitude growth was also reduced neurotrophin ears, but to a lesser degree and the reduction was not significant. Similar results were obtained from control ears exposed to 95 dB, but amplitude growth recovered in neurotrophin-treated ears, this reaching statistical significance in response to 16 kHz tones. There were significantly more presynaptic ribbons, postsynaptic glutamate receptors, and colocalized ribbons after neurotrophin treatment. A single dose of neurotrophins delivered to the round window reduced synaptopathy and recovered high-frequency hearing in ears exposed to 95 dB noise. These findings suggest that hidden hearing loss may be reduced by providing trophic support to the cochlea after injury.

Size-dependent physiological responses of shore crabs to single and repeated playback of ship noise

Anthropogenic noise has fundamentally changed the acoustics of terrestrial and aquatic environments, and there is growing empirical evidence that even a single noise exposure can affect behaviour in a variety of vertebrate organisms. Here, we use controlled experiments to investigate how the physiology of a marine invertebrate, the shore crab (Carcinus maenas), is affected by both single and repeated exposure to ship-noise playback. Crabs experiencing ship-noise playback consumed more oxygen, indicating a higher metabolic rate and potentially greater stress, than those exposed to ambient-noise playback. The response to single ship-noise playback was size-dependent, with heavier crabs showing a stronger response than lighter individuals. Repeated exposure to ambient-noise playback led to increased oxygen consumption (probably due to handling stress), whereas repeated exposure to ship-noise playback produced no change in physiological response; explanations include the possibility that crabs exhibited a maximal response on first exposure to ship-noise playback, or that they habituated or become tolerant to it. These results highlight that invertebrates, like vertebrates, may also be susceptible to the detrimental impacts of anthropogenic noise and demonstrate the tractability for more detailed investigations into the effects of this pervasive global pollutant.

Differential Impact of Temporary and Permanent Noise-Induced Hearing Loss on Neuronal Cell Density in the Mouse Central Auditory Pathway

Although acoustic overstimulation has a major pathophysiological influence on the inner ear, central components of the auditory pathway can also be affected by noise-induced hearing loss (NIHL). The present study investigates the influence of a noise-induced temporary threshold shift (TTS) and/or permanent threshold shift (PTS) on neuronal cell densities in key structures of the central auditory pathway. Mice were noise-exposed (3 h, 5-20 kHz) at 115 dB sound pressure level (SPL) under anesthesia, and were investigated immediately (TTS group, n = 5) after the exposure, or 1 week later (PTS group, n = 6). Unexposed animals were used as controls (n = 7). Frequency-specific auditory brainstem responses (ABR) were recorded to examine auditory thresholds. Cell density was determined within the dorsal (DCN) and ventral (VCN) cochlear nucleus; the central nucleus of the inferior colliculus (ICC); the dorsal, ventral, and medial subdivisions of the medial geniculate body (MGBd, MGBv, and MGBm); and layer I to VI of the primary auditory cortex (AI I-VI). ABR thresholds were significantly elevated in the TTS group (52-69 dB SPL) and in the PTS group (33-42 dB SPL) compared to controls. There was a significant decrease in cell density only in the VCN of the TTS group (-10%), most likely induced by the acute overstimulation of neurons. Cell density was significantly reduced in all investigated auditory structures at 1 week post-exposure (PTS group), except in layer II of the AI (VCN: -30% and DCN: -30% (high-frequency); -39% (low-frequency); ICC: -31%; MGBd: -31%; MGBm: -28%; MGBv: -31%; AI: -10 to 14%). Thus there were dramatic changes within the neuronal cytoarchitecture of the central auditory pathway following a single noise exposure. The present findings should help clinicians to better understand the complex psychoacoustic phenomena of NIHL.

A major effect QTL on chromosome 18 for noise injury to the mouse cochlear lateral wall

We recently demonstrated a striking difference among inbred mouse strains in the effects of a single noise exposure, whereby CBA/J and CBA/CaJ (CBA) mice show moderate reversible reduction in the endocochlear potential (EP) while C57BL/6J (B6) mice do not (Ohlemiller, K.K., Gagnon, P.M., 2007. Genetic dependence of cochlear cells and structures injured by noise. Hear. Res. 224, 34–50). Acute EP reduction in CBA was reliably associated with characteristic pathology of the spiral ligament and stria vascularis, both immediately after noise and 8 weeks later. Analysis of B6 × CBA F1 hybrid mice indicated that EP reduction and its anatomic correlates are co-inherited in an autosomal dominant manner. Further analysis of N2 mice resulting from the backcross of F1 hybrids to B6 mice led us to suggest that the EP reduction phenotype principally reflects the influence of a small number of quantitative trait loci (QTLs). Here we report the results of QTL mapping of the EP reduction phenotype in CBA/J using 106 N2 mice from a (CBA × B6) × B6 backcross. Correlation of acute post-noise EP with 135 markers distributed throughout the genome revealed a single major effect QTL on chromosome 18 (12.5 cM, LOD 3.57) ( Nirep, for noise-induced reduction in EP QTL), and two marginally significant QTLs on chromosomes 5 and 16 (LOD 1.43 and 1.73, respectively). Our results underscore that fact that different cochlear structures may possess different susceptibilities to noise through the influence of non-overlapping genes. While Nirep and similar-acting QTLs do not appear to influence the extent of permanent hearing loss from a single noise exposure, they could reduce the homeostatic ‘reserve’ of the lateral wall in protracted or continual exposures, and thereby influence long term threshold stability.

Long-term assessment of auditory changes resulting from a single noise exposure associated with non-occupational activities

We examined the long-term sequelae in both ears of 42 patients who reported the occurrence of auditory changes resulting from a single exposure to intense sound levels during non-occupational activities. We divided these patients into two groups, based upon noise exposures of either continuous duration or single high-energy impulse. Audiometric data were available for each of these subjects shortly after their noise-exposure events and follow-up examinations took place more than one year after the noise occurrence (range: 1–16 years). The initial median hearing loss for the continuous-type noise exposure group at 3–8 kHz was found to be 9 dB, relative to the age-appropriate norms, in the more affected ears, and hearing function was found to have returned to normal levels at follow-up. The same initial hearing loss was measured for the impulse-type noise group, but a residual hearing loss of 4 dB was measured at follow-up. Furthermore, the majority of the subjects from both groups reported tinnitus and hypersensitivity to sound at follow-up, but with minimal impact on their lives.SumarioExaminamos en ambos oídos las secuelas a largo plazo en 42 pacientes que reportaban cambios auditivos como resultado de una exposición única a ruido intenso durante actividades no laborales. Dividimos a los pacientes en dos grupos, dependiendo de la exposición a ruido, ya fuera de duración continua o debida a un impulso de gran energía. Los datos audiométricos estuvieron disponibles para cada uno de estos sujetos poco después de su evento de exposición sonora y el seguimiento se llevó a cabo durante más de un año después de la exposición a ruido (rango de 1 a 16 años). El promedio de hipoacusia inicial entre 3 y 8 kHz para el grupo de exposición continua fue de 9dB, con relación a las normas adecuadas por edad en el oído más afectado, y la función auditiva había regresado a los niveles normales en el seguimiento. La misma pérdida auditiva fue medida en el grupo de ruido tipo impulso, pero en el seguimiento se detectó una pérdida de 4dB. Incluso la mayoría de los sujetos de ambos grupos reportaron acúfeno e hipersensibilidad al sonido en el seguimiento, pero con un impacto mínimo en sus vidas.

Synaptophysin in the Cochlear Nucleus Following Acoustic Trauma

Chinchillas are notable for a low-frequency hearing range similar to that of humans and a marked sensitivity to loud noise. A single noise exposure that produces cochlear damage may lead to progressive loss of synaptic endings in the cochlear nucleus, followed by new axonal growth. As an index of synaptic regulation during such changes, we have examined the expression of a synaptic vesicle protein, synaptophysin, in the cochlear nucleus following a damaging acoustic stimulus in adult chinchillas. With one ear protected by a plug, following a 3-h exposure to an octave-band noise of 108 dB sound pressure level, centered at 4 kHz, the unprotected cochlea and the cochlear nuclei exhibited degeneration of hair cells and axons over periods of 7, 14, 30, 90, and 150 days. Axonal degeneration, as revealed by a silver degeneration method, was heavy ipsilateral to the cochlear damage, but sparse degeneration also appeared on the contralateral, unexposed side. Synaptophysin immunostaining underwent a major, bilateral decline in the anteroventral and posteroventral cochlear nuclei, interrupted at intervening periods by transient increases in the numbers of stained structures. A distinction in staining between large perisomatic structures and smaller puncta in the neuropil and between the dorsal and the ventral zones of the ventral cochlear nuclei revealed some variations in the response and degree of recovery of synaptophysin staining. These findings could best be explained by degeneration of synaptic endings followed by new growth of terminals and by regulatory changes in the levels of synaptophysin expression and synaptic vesicle accumulation over time.

Acute noise stress, ACTH administration, and blood pressure alteration

Two groups of male Wistar rats were submitted to a single noise exposure (2640 Hz, 30 W, 102 dB, 15 min) (St group) or to a single dose of ACTH (1.5 IU/100 g b.wt.) (Ac group), respectively. A control group of nontreated rats (Co group) was used. Blood pressure (BP) was measured using an indirect tail cuff method and corticosterone (B) levels were measured by specific RIA. Haematocrit (Hc) and blood pH values were also evaluated. Acute treatments of both noise exposure and ACTH administration produced corticosterone hypersecretion and blood pressure elevation, with lower haematocrit and higher blood pH values than those found in the Co group. No differences were found between St and Ac treatments.