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Application of a kurtosis correction to frequency-weighted sound exposure level (SEL) improved predictions of risk of hearing damage in humans and terrestrial mammals for sound exposures with different degrees of impulsiveness. To assess whether kurtosis corrections may lead to improved predictions for marine mammals, corrections were applied to temporary threshold shift (TTS) growth measurements for harbor porpoises ( Phocoena phocoena) exposed to different sounds. Kurtosis-corrected frequency-weighted SEL predicted accurately the growth of low levels of TTS (TTS1-4 < 10 dB) for intermittent sounds with short (1–13 s) silence intervals but was not consistent with frequency-weighted SEL data for continuous sound exposures.

Introduction Noise-induced hearing loss is one of the most common forms of sensorineural hearing loss. Nevertheless, the mechanisms of noise-induced hearing loss are still not fully understood. Objective To investigate the dynamics of inflammatory responses in the mammalian cochlea following noise trauma at two different times, once during the light cycle and once during the dark. Methods We challenged C57BL/6J mice with moderate, continuous noise trauma at either 9 a.m. or 9 p.m. Auditory function, histological changes in hair cells, and modifications in gene expression levels of inflammatory mediators were assessed at specific time points. Shifts in auditory brainstem response thresholds were measured at 1, 3, 7 and 14 days after noise exposure to measure potential noise-induced hearing loss. Cochlear basilar-membrane immunofluorescent staining was performed at 3 and 14 days after noise exposure. The mRNA levels of several inflammatory mediators were measured via quantitative real-time polymerase chain reaction before (pre) and after (0, 3, 12, 24 and 72 h) noise exposure. Results We found that all noise-exposed mice developed a temporary threshold shift and that there were no significant differences between daytime and nighttime noise exposures in terms of inducing hearing-threshold shifts. Similarly, we did not detect significant histological changes in hair cells between these two groups. However, we discovered an interesting phenomenon in that the peak mRNA levels of IL-1β, IL-6, CCL2 and TNF-α were higher in day noise-exposed mice compared to those in night noise-exposed mice, and these mRNA levels subsided more slowly in day noise-exposed mice. Conclusion Overall, these observations suggest that the circadian timing of noise exposure has a significant effect on noise-induced inflammatory responses in the mouse cochlea and that a greater inflammatory response might occur after daytime exposure.

Music is for many people an integral part of their lives. In recent years, loud music, whether recorded or played live, has been a significant source of noise. The aim of the study was to assess the relationship between exposure to high sound levels and temporary threshold shift (TTS) in people working as fitness instructors.The study included a total of 29 people (26 women and 3 men, age: 33±6 years) employed in 8 fitness clubs. The sound levels and the frequency characteristics of noise were assessed using individual dosimetry. Hearing threshold was evaluated by pre- and post-exposure pure tone audiometry (PTA), yielding a total of 116 audiograms.Occupational exposure of fitness instructors to noise lasted 60-120 min and the A-weighted sound pressure level (LFitness instructors may be a risk of hearing impairment related to their work. Med Pr. 2021;72(4):391-7.Muzyka jest dla wielu osób nieodłącznym elementem życia. W ostatnich latach głośna muzyka, zarówno grana na żywo, jak i odtwarzana, stanowi istotne źródło hałasu. Celem niniejszej pracy była ocena związku między ekspozycją na wysokie poziomy dźwięku a czasowym przesunięciem progu słuchu (Badaniem objęto 29 osób (26 kobiet i 3 mężczyzn, średnia wieku: 33±6 lat) zatrudnionych w 8 klubach fitness. Poziomy dźwięków i charakterystykę częstotliwościową hałasu zmierzono z zastosowaniem dozymetrii indywidualnej. Progi słuchu oceniano za pomocą audiometrii tonalnej przeprowadzanej przed rozpoczęciem zajęć fitness oraz bezpośrednio po ich zakończeniu, otrzymując łącznie 116 audiogramów przed- i poekspozycyjnych.Zawodowe narażenie instruktorów fitness na hałas trwało 60–120 min, a równoważny poziom ciśnienia akustycznego A (LPraca instruktorów w klubach fitness może stwarzać ryzyko uszkodzenia słuchu związanego z pracą zawodową. Med. Pr. 2021;72(4):391–397.

It is widely accepted that even a single acute noise exposure at moderate intensity that induces temporary threshold shift (TTS) can result in permanent loss of ribbon synapses between inner hair cells and afferents. However, effects of repeated or chronic noise exposures on the cochlear synapses especially medial olivocochlear (MOC) efferent synapses remain elusive. Based on a weeklong repeated exposure model of bandwidth noise over 2-20 kHz for 2 hours at seven intensities (88 to 106 dB SPL with 3 dB increment per gradient) on C57BL/6J mice, we attempted to explore the dose-response mechanism of prolonged noise-induced audiological dysfunction and cochlear synaptic degeneration. In our results, mice repeatedly exposed to relatively low-intensity noise (88, 91, and 94 dB SPL) showed few changes on auditory brainstem response (ABR), ribbon synapses, or MOC efferent synapses. Notably, repeated moderate-intensity noise exposures (97 and 100 dB SPL) not only caused hearing threshold shifts and the inner hair cell ribbon synaptopathy but also impaired MOC efferent synapses, which might contribute to complex patterns of damages on cochlear function and morphology. However, repeated high-intensity (103 and 106 dB SPL) noise exposures induced PTSs mainly accompanied by damages on cochlear amplifier function of outer hair cells and the inner hair cell ribbon synaptopathy, rather than the MOC efferent synaptic degeneration. Moreover, we observed a frequency-dependent vulnerability of the repeated acoustic trauma-induced cochlear synaptic degeneration. This study provides a sight into the hypothesis that noise-induced cochlear synaptic degeneration involves both afferent (ribbon synapses) and efferent (MOC terminals) pathology. The pattern of dose-dependent pathological changes induced by repeated noise exposure at various intensities provides a possible explanation for the complicated cochlear synaptic degeneration in humans. The underlying mechanisms remain to be studied in the future.

Intense sound sources, such as pile driving, airguns, and military sonars, have the potential to inflict hearing loss in marine mammals and are, therefore, regulated in many countries. The most recent criteria for noise induced hearing loss are based on empirical data collected until 2015 and recommend frequency-weighted and species group-specific thresholds to predict the onset of temporary threshold shift (TTS). Here, evidence made available after 2015 in light of the current criteria for two functional hearing groups is reviewed. For impulsive sounds (from pile driving and air guns), there is strong support for the current threshold for very high frequency cetaceans, including harbor porpoises ( Phocoena phocoena). Less strong support also exists for the threshold for phocid seals in water, including harbor seals ( Phoca vitulina). For non-impulsive sounds, there is good correspondence between exposure functions and empirical thresholds below 10 kHz for porpoises (applicable to assessment and regulation of military sonars) and between 3 and 16 kHz for seals. Above 10 kHz for porpoises and outside of the range 3–16 kHz for seals, there are substantial differences (up to 35 dB) between the predicted thresholds for TTS and empirical results. These discrepancies call for further studies.

The present study involved performing an experiment to clarify whether vibration measurement values on the tool handle, in accordance with ISO 5349-1, can assess risk from workplace environments. The study investigated the relationship between the vibration magnitude of a hand-held electric drill with different operating postures. The experiment included the determination of the participant’s temporary threshold shift (TTS) of vibrotactile perception threshold (VPT) at the tip of the index finger. The experimental hypothesis was that the vibration measurement values on the tool handle, in accordance with the ISO 5349-1 standard, include the effect of posture on the vibration measurements obtained despite the variation in posture and test participants. The hand-transmitted vibration (HTV) was applied using a hand-held electric drill applied to a pre-cast concrete paving slab substrate (600 × 600 × 50 mm, 55 MPa) using a 10 mm diameter masonry drill bit (without hammer action). The tool was operated using the right hand on twelve male subjects with three working postures (n = 36). Vibration was measured in three orthogonal directions according to the international standard ISO 5349-1 procedure. Vibration magnitudes were expressed as root-mean-square (r.m.s.) acceleration, frequency-weighted using the Wh frequency weighting. Clause 4.3 states that the characterisation of the vibration exposure is assessed from the acceleration of the surface in contact with the hand as the primary quantity. The experimental results indicate that the TTS following vibration exposure is not related to the measured vibration magnitude on the tool handle. Therefore, the automatic inclusion of posture and test participant variation is not proven. The results suggest that the vibration measurement values on the tool handle do not predict the TTS after hand-transmitted vibration in varying posture across the test participants. The research concludes that tool handle vibration measurement, in accordance with ISO 5349-1, does not properly assess the potential hazard from authentic workplace tool usage conditions of varying postures.

Background Intraoperative auditory brainstem response (ioABR) testing under general anesthesia is commonly performed on children when sleep-deprived ABR and behavioral testing are not reliable or feasible. Several studies have reported potential confounding results when tube insertion is combined with ABR testing. Purpose This article evaluates whether a temporary threshold shift (TTS) occurs following placement of tympanostomy tubes (TTs) in children who undergo ioABR testing. Research Design A case–control prospective study. Patients scheduled for combined TT and ioABR procedures were enrolled into this study. Study Sample Twenty children (38 ears), ranging in age from 6 months to 10.5 years, were enrolled. Data Collection and Analysis ABR thresholds for tone bursts with center frequencies of 2 and 4 kHz were compared before and after tube insertion. The indication for surgery, comorbidities, and status of the middle ear were also recorded. A paired t-test was used to determine statistical significance. Results Data collection did not necessarily indicate suctioning and tube placement were causing a TTS; however, fluid present in the middle ear space prior to TT placement appeared to influence results. Although a paired t-test did not show statistically significant differences in ABR thresholds between groups of individuals with and without fluid and before and after tube placement, 50% of patients with mucoid fluid (two out of four patients) were noted to have 10 dB or greater worsening in ABR thresholds in two out of six ears. Twenty-nine percent of patients with serous fluid (two out of seven patients) were noted to have at least a 10 dB worsening in ABR threshold in 2 out of 10 ears. Further testing is needed to confirm these trends. Conclusion This pilot study indicates that children with mucoid or serous fluid may experience worse ABR thresholds following TT insertion. ioABR testing immediately after TT tube placement and in the presence of middle ear fluid should be interpreted with caution. Additional studies with a larger sample size are needed to confirm these results.

Noise exposure during lifespan is one of the main causes of hearing loss. The highest risk of noise-induced hearing loss (NIHL) is related to exposures in the workplace, and affects about 7% of the population. Occupational NIHL is irreversible, thus its prevention must be considered a priority. Although current hearing conservation programs (HCPs) have proved to be very beneficial, the incidence of occupational NIHL is still high, reaching about 18% of overexposed workers. This paper reviews recent research on the effects of noise on hearing in pursuit of more effective methods for the prevention of occupational NIHL. The paper discusses the translational significance of noise-induced cochlear neuropathy, as recently shown in animals, and the concept of hidden hearing loss in relation to current NIHL damage risk criteria. The anticipated advantages of monitoring the incidents of the temporary threshold shift (TTS) in workers exposed to high levels of noise have been analyzed in regard to the preclinical diagnostics of NIHL, i.e., at the stage when hearing loss is still reversible. The challenges, such as introducing speech-in-noise audiometry and TTS computational predictive models into HCPs, have been discussed. Finally, the paper underscores the need to develop personalized medical guidelines for the prevention of NIHL and to account for several NIHL risk factors other than these included in the ISO 1999:2013 model. Implementing the steps mentioned above would presumably further reduce the incidence of occupational NIHL, as well as associated social costs. Int J Occup Med Environ Health. 2020;33(6):841-8.

Cochlear damage is often thought to result in hearing thresholds shift, whether permanent or temporary. The report of tinnitus in the absence of any clear deficit in cochlear function was believed to indicate that hearing loss and tinnitus, while comorbid, could arise independently from each other. In all likelihood, tinnitus that is not of central nervous system origin is associated with hearing loss. As a correlate, although a treatment of most forms of tinnitus will likely emerge in the years to come, curing tinnitus will first require curing hearing loss.

Funding: Data collection was funded as part of the Department of Energy and Climate Change’s (now Department of Business, Energy and Industrial Strategy) Offshore Energy Strategic Environmental Assessment programme, with additional resources from National Capability funding from the Natural Environment Research Council to the Sea Mammal Research Unit (Grant No. SMRU1001). Sound propagation modelling and subsequent analyses were funded by RaceBank Wind Farm Ltd. KFW was funded by University of St Andrews and the Department of Business, Energy and Industrial Strategy, as part of a PhD studentship. Understanding the potential effects of pile driving sounds on marine wildlife is essential for regulating offshore wind developments. Here, tracking data from 24 harbour seals were used to quantify effects and investigate sensitivity to the methods used to predict these. The Aquarius pile driving model was used to model source characteristics and acoustic propagation loss (16 Hz–20 kHz). Predicted cumulative sound exposure levels (SELcums) experienced by each seal were compared to different auditory weighting functions and damage thresholds to estimate temporary (TTS) and permanent (PTS) threshold shift occurrence. Each approach produced markedly different results; however, the most recent criteria established by Southall et al. [(2019) Aquat. Mamm. 45, 125–232] suggests that TTS occurrence was low (17% of seals). Predictions of seal density during pile driving made by Russell et al. [(2016) J. Appl. Ecol. 53, 1642–1652] were compared to distance from the wind farm and predicted single-strike sound exposure levels (SELss) by multiple approaches. Predicted seal density significantly decreased within 25 km or above SELss (averaged across depths and pile installations) of 145 dB re 1 μPa²·s. However, there was substantial variation in SELss with depth and installation, and thus in the predicted relationship with seal density. These results highlight uncertainty in estimated effects, which should be considered in future assessments. Publisher PDF

Objectives: To investigate a temporary threshold shift (TTS) of hearing and pain/discomfort caused by the microsuction procedure. Hearing loss induced by impacted cerumen was also investigated.Desi...

Regulations designed to mitigate the effects of man-made sounds on marine mammal hearing specify maximum daily sound exposure levels. The limits are lower for impulsive than non-impulsive sounds. The regulations do not indicate how to quantify impulsiveness; instead sounds are grouped by properties at the source. To address this gap, three metrics of impulsiveness (kurtosis, crest factor, and the Harris impulse factor) were compared using values from random noise and real-world ocean sounds. Kurtosis is recommended for quantifying impulsiveness. Kurtosis greater than 40 indicates a sound is fully impulsive. Only sounds above the effective quiet threshold (EQT) are considered intense enough to accumulate over time and cause hearing injury. A functional definition for EQT is proposed: the auditory frequency-weighted sound pressure level (SPL) that could accumulate to cause temporary threshold shift from non-impulsive sound as described in Southall, Finneran, Reichmuth, Nachtigall, Ketten, Bowles, Ellison, Nowacek, and Tyack [(2019). Aquat. Mamm. 45, 125-232]. It is known that impulsive sounds change to non-impulsive as these sounds propagate. This paper shows that this is not relevant for assessing hearing injury because sounds retain impulsive character when SPLs are above EQT. Sounds from vessels are normally considered non-impulsive; however, 66% of vessels analyzed were impulsive when weighted for very-high frequency mammal hearing.

Two female harbor seals were exposed for 60 min to a continuous one-sixth-octave noise band centered at 32 kHz at sound pressure levels of 92 to 152 dB re 1 mu Pa, resulting in sound exposure levels (SELs) of 128 to 188 dB re 1 mu Pa(2)s. This was part of a larger project determining frequency-dependent susceptibility to temporary threshold shift (TTS) in harbor seals over their entire hearing range. After exposure, TTSs were quantified at 32, 45, and 63 kHz with a psychoacoustic technique. At 32 kHz, only small TTSs (up to 5.9 dB) were measured 1-4 min (TTS1-4) after exposure, and recovery was within 1 h. The higher the SEL, the higher the TTS induced at 45 kHz. Below similar to 176 dB re 1 mu Pa(2)s, the maximum TTS1-4 was at 32 kHz; above similar to 176 dB re 1 mu Pa(2)s, the maximum TTS1-4 (up to 33.8 dB) was at 45 kHz. During one particular session, a seal was inadvertently exposed to an SEL of similar to 191 dB re 1 mu Pa(2)s and at 45 kHz, her TTS1-4 was >45 dB; her hearing recovered over 4 days. Harbor seals appear to be equally susceptible to TTS caused by sounds in the 2.5-32 kHz range.

Noise is pervasive in everyday life and can cause both auditory and nonauditory health effects. Noise-induced hearing loss remains highly prevalent in occupational settings. Nonauditory effects of noise can cause tinnitus, headache, auricular plenitude, dizziness, and gastric, visual, sleep, and mood disorders, endocrine imbalance, and cardiovascular disorders. A cross-sectional study among resident above the age of 18 years of the selected urban slum near railway track of Raipur City with a sample size of 400 was conducted. 23.0% of the study subjects responded of facing auditory fatigue, followed by 11.5% of the study subjects reported of hearing loss, 6% of the study participants perceived that the surrounding noise led to an increase in their blood pressure. Loss of sleep/insomnia was reported by 6% of resident in our study. Health effects of environmental noise are manifold, serious and, because of the widespread exposure, very prevalent. These factors stress the need to regulate and reduce environmental noise exposure.

Recent studies have identified sex-differences in auditory physiology and in the susceptibility to noise-induced hearing loss (NIHL). We hypothesize that 17β-estradiol (E2), a known modulator of auditory physiology, may underpin sex-differences in the response to noise trauma. Here, we gonadectomized B6CBAF1/J mice and used a combination of electrophysiological and histological techniques to study the effects of estrogen replacement on peripheral auditory physiology in the absence of noise exposure and on protection from NIHL. Functional analysis of auditory physiology in gonadectomized female mice revealed that E2-treatment modulated the peripheral response to sound in the absence of changes to the endocochlear potential compared to vehicle-treatment. E2-replacement in gonadectomized female mice protected against hearing loss following permanent threshold shift (PTS)- and temporary threshold shift (TTS)-inducing noise exposures. Histological analysis of the cochlear tissue revealed that E2-replacement mitigated outer hair cell loss and cochlear synaptopathy following noise exposure compared to vehicle-treatment. Lastly, using fluorescent in situ hybridization, we demonstrate co-localization of estrogen receptor-2 with type-1C, high threshold spiral ganglion neurons, suggesting that the observed protection from cochlear synaptopathy may occur through E2-mediated preservation of these neurons. Taken together, these data indicate the estrogen signaling pathways may be harnessed for the prevention and treatment of NIHL.

International audience; Recent studies demonstrated that reversible continuous noise exposure may induce a temporary threshold shift (TTS) with a permanent degeneration of auditory nerve fibers, although hair cells remain intact. To probe the impact of TTS-inducing impulse noise exposure on hearing, CBA/J Mice were exposed to noise impulses with peak pressures of 145 dB SPL. We found that 30 min after exposure, the noise caused a mean elevation of ABR thresholds of ~30 dB and a reduction in DPOAE amplitude. Four weeks later, ABR thresholds and DPOAE amplitude were back to normal in the higher frequency region (8–32 kHz). At lower frequencies, a small degree of PTS remained. Morphological evaluations revealed a disturbance of the stereociliary bundle of outer hair cells, mainly located in the apical regions. On the other hand, the reduced suprathreshold ABR amplitudes remained until 4 weeks later. A loss of synapse numbers was observed 24 h after exposure, with full recovery two weeks later. Transmission electron microscopy revealed morphological changes at the ribbon synapses by two weeks post exposure. In addition, increased levels of oxidative stress were observed immediately after exposure, and maintained for a further 2 weeks. These results clarify the pathology underlying impulse noise-induced sensory dysfunction, and suggest possible links between impulse-noise injury, cochlear cell morphology, metabolic changes, and hidden hearing loss.

Exposure to 120 dB sound pressure level (SPL) band-limited noise results in delayed onset latency and reduced vestibular short-latency evoked potential (VsEP) responses. These changes are still present 4 wk after noise overstimulation. Noise-induced hearing loss (NIHL) has been shown to vary in extent and duration based on the noise intensity. This study investigated whether noise-induced peripheral vestibular hypofunction (NPVH) would also decrease in extent and/or duration with less intense noise exposure. In the present study, rats were exposed to a less intense noise (110 dB SPL) but for the same duration (6 h) and frequency range (500-4,000 Hz) as used in previous studies. The VsEP was assessed 1, 3, 7, 14, 21, and 28 days after noise exposure. In contrast to 120 dB SPL noise exposure, the 110 dB SPL noise exposures produced smaller deficits in VsEP responses that fully recovered in 62% (13/21) of animals within 1 wk. These findings suggest that NPVH, a loss or attenuation of VsEP responses with a requirement for elevated stimulus intensity to elicit measurable responses, is similar to NIHL, that is, lower sound levels produce a smaller or transient deficit. These results show that it will be important to determine the extent and duration of vestibular hypofunction for different noise exposure conditions and their impact on balance.

Introduction Noise or noise pollution is a phenomenon that causes an auditory sensation considered unpleasant, undesirable, and annoying, which may present a danger to health in general and the auditory system in particular. The objective of this study was to evaluate the impact of noise pollution among workers in a brewery in the city of Conakry. Patient and methods This is a prospective descriptive study, of two months' duration (November 11, 2019, to January 10, 2020) carried out in the industrial unit of the Limited Company of Breweries of Guinea (SOBRAGUI). We included all the workers of the company exposed to noise pollution in their workplaces, after their informed consent. Results The age of the workers varied between 22 and 70 years, with a mean age of 44.14 ± 8.07 years. We noted a male predominance of 99.22% (n=128) cases. The average duration of exposure was 14.28 ± 6.78 years, with variations ranging from one year to 35 years. Among the auditory disorders, we noted tinnitus in 63.8% (n=74), hypoacusis in 56.9% (n=66), and auditory fatigue in 52.6% (n=61) of cases. These signs were often associated with each other and with other extra-auditory symptoms in the same worker. Audiometry revealed a moderate to severe hearing loss in 13.8% (n=16) and profound deafness in 0.9% (n=1) of cases. The impact of noise pollution on workers' performance was reflected in concentration difficulties in 57.7% (n=67) of cases. Conclusion Noise pollution is present in the SOBRAGUI bottling line. It has a negative impact on the health of workers and alters their work performance.

Objective Determine if D-methionine (D-met) rescue prevents temporary threshold shift (TTS) from steady-state or impulse noise and determine D-met's impact on serum and cochlear antioxidant levels. Design D-met at 50, 100 or 200 mg/kg/doses were administered 0, 6 and 18 hours-post noise. ABRs at baseline and 24 hours post-noise measured TTS. Serum (SOD, CAT, GR, GPx) and cochlear (GSH, GSSG) antioxidant levels measured physiological influence. Three control groups, with impulse or steady-state or without noise, were saline-injected. Study sample Ten Chinchillas/group. Results D-met rescue did not significantly reduce TTS or impact serum CAT, SOD, GPx or GR levels vs. noise-exposed control groups, but TTS was greater in all groups relative to no-noise controls. D-met significantly elevated CAT at 50 mg/kg vs. steady-state controls and SOD at 200 mg/kg vs. impulse noise controls. D-met significantly reduced cochlear GSH/GSSG ratios in the 100 mg/kg D-met group vs. impulse noise controls. Conclusions While D-met rescue has reduced permanent threshold shift in previous studies, it did not reduce TTS in this study. However, D-met rescue did alter selective serum and cochlear oxidative state changes 24 hours post-noise relative to controls. Results demonstrate TTS studies do not always predict PTS protection in otoprotectant experimental designs.

High-intensity noise can cause permanent hearing loss; however, short-duration medium-intensity noise only induces a temporary threshold shift (TTS) and damages synapses formed by inner hair cells (IHCs) and spiral ganglion nerves. Synaptopathy is generally thought to be caused by glutamate excitotoxicity. In this study, we investigated the expression levels of vesicle transporter protein 3 (Vglut3), responsible for the release of glutamate; glutamate/aspartate transporter protein (GLAST), responsible for the uptake of glutamate; and Na+/K+-ATPase α1 coupled with GLAST, in the process of synaptopathy in the cochlea. The results of the auditory brainstem response (ABR) and CtBP2 immunofluorescence revealed that synaptopathy was induced on day 30 after 100 dB SPL noise exposure in C57BL/6J mice. We found that GLAST and Na+/K+-ATPase α1 were co-localized in the cochlea, mainly in the stria vascularis, spiral ligament, and spiral ganglion cells. Furthermore, Vglut3, GLAST, and Na+/K+-ATPase α1 expression were disrupted after noise exposure. These results indicate that disruption of glutamate release and uptake-related protein expression may exacerbate the occurrence of synaptopathy.

Evidence for synaptopathy, the acute loss of afferent auditory nerve terminals, and degeneration of spiral ganglion cells associated with temporary threshold shift (TTS) in traditional laboratory animal models (e.g., mice, guinea pigs) has brought into question whether TTS should be considered a non-injurious form of noise impact in marine mammals. Laboratory animal studies also demonstrate that both neuropathic and non-neuropathic forms of TTS exist, with synaptopathy and neural degeneration beginning over a narrow range of noise exposures differing by ~6–9 dB, all of which result in significant TTS. Most TTS studies in marine mammals characterize TTS within minutes of noise exposure cessation, and TTS generally does not achieve the levels measured in neuropathic laboratory animals, which have had initial TTS measurements made 6–24 h post-exposure. Given the recovery of the ear following the cessation of noise exposure, it seems unlikely that the magnitude of nearly all shifts studied in marine mammals to date would be sufficient to induce neuropathy. Although no empirical evidence in marine mammals exists to support this proposition, the regulatory application of impact thresholds based on the onset of TTS (6 dB) is certain to capture the onset of recoverable fatigue without tissue destruction.

Previous study reported that either selective GSK-3β inhibitor or up-regulating autophagy can alleviate cisplatin-induced ototoxicity. Other studies indicate that the activity of GSK-3β is closely associated with the autophagy level. The purpose of this study is to primarily explore the role of autophagy in the alleviation effect of GSK-3β inhibition on cisplatin-induced ototoxicity in vivo and in vitro. We observed the autophagy changes induced by GSK-3β inhibitor in outer hair cells (OHCs) in a cisplatin-induced ototoxicity rat model. In addition, autophagy inhibitor 3-MA was used in vitro experiments to observe the influence of autophagy inhibition on the cell protection effect due to GSK-3β inactivation. The relationship among autophagy, GSK-3β and cell damage were inferred. Negative regulation of GSK-3β significantly enhanced autophagy and alleviated cisplatin-induced hearing loss, OHC death in vivo and apoptosis in vitro. The autophagy inhibitor 3-MA inverted the protective effect of negative regulation of GSK-3β. These results indicated that enhancing autophagy may be a key downstream effect of GSK-3β inhibition in the alleviation of cisplatin-induced ototoxicity both in vivo and in vitro.

In psychophysical studies of noise-induced hearing loss with marine mammals, exposure conditions are often titrated from levels of no effect to those that induce significant but recoverable loss of auditory sensitivity [temporary threshold shift (TTS)]. To examine TTS from mid-frequency noise, a harbor seal was exposed to a 4.1-kHz underwater tone that was incrementally increased in sound pressure level (SPL) and duration. The seal's hearing was evaluated at the exposure frequency and one-half octave higher (5.8 kHz) to identify the noise parameters associated with TTS onset. No reliable TTS was measured with increasing sound exposure level until the second exposure to a 60-s fatiguing tone of 181 dB re 1 μPa SPL (sound exposure level 199 dB re 1 μPa2s), after which an unexpectedly large threshold shift (>47 dB) was observed. While hearing at 4.1 kHz recovered within 48 h, there was a permanent threshold shift of at least 8 dB at 5.8 kHz. This hearing loss was evident for more than ten years. Furthermore, a residual threshold shift of 11 dB was detected one octave above the tonal exposure, at 8.2 kHz. This hearing loss persisted for more than two years prior to full recovery.

A major component of slowly reversible hearing loss which develops with sustained exposure to noise has been attributed to release of ATP in the cochlea activating P2X(2) receptor (P2X(2)R) type ATP-gated ion channels. This purinergic humoral adaptation is thought to enable the highly sensitive hearing organ to maintain function with loud sound, protecting the ear from acoustic overstimulation. In the study that established this hearing adaptation mechanism as reported by Housley et al. (Proc Natl Acad Sci U S A 110:7494–7499, 2013), the activation kinetics were determined in mice from auditory brainstem response (ABR) threshold shifts with sustained noise presentation at time points beyond 10 min. The present study was designed to achieve finer resolution of the onset kinetics of purinergic hearing adaptation, and included the use of cubic (2f(1)–f(2)) distortion product otoacoustic emissions (DPOAEs) to probe whether the active mechanical outer hair cell ‘cochlear amplifier’ contributed to this process. We show that the ABR and DPOAE threshold shifts were largely complete within the first 7.5 min of moderate broadband noise (85 dB SPL) in wildtype C57Bl/6J mice. The ABR and DPOAE adaptation rates were both best fitted by a single exponential function with ~ 3 min time constants. ABR and DPOAE threshold shifts with this noise were minimal in mice null for the P2rx2 gene encoding the P2X(2)R. The findings demonstrate a considerably faster purinergic hearing adaptation to noise than previously appreciated. Moreover, they strongly implicate the outer hair cell as the site of action, as the DPOAEs stem from active cochlear electromotility. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s11302-019-09648-3) contains supplementary material, which is available to authorized users.

Background Personnel assigned to aircraft carriers work and live in environments where hazardous noise areas and hearing recovery spaces such as sleeping areas are in close proximity to one another. Hazardous noise exposure occurring during on-duty time periods and elevated noise levels during off-duty periods in sleeping areas may be prohibiting adequate hearing recovery, thus potentially leading to hearing loss and may lead to adverse effects on sleep, leading to crew-member fatigue. This investigation characterizes Equivalent sound level (Leq) and standardized octave band center frequency noise levels according to berthing (sleeping) area location during flight operation and nonflight operation time periods on a US Navy aircraft carrier. In addition, the investigation compares noise measurements in sleeping areas to noise levels associated with auditory rest and poor sleep quality and quantity. Methods Noise levels were measured in berthing areas aboard a US Navy Nimitz-class aircraft carrier during a routine at-sea period. Sixty noise measurements were taken in eight sleeping locations. Leq in decibels ‘A’ weighted (dBA) and noise levels from 16 to 16 000 Hz in (dB) were measured during flight operations [Leq (flt ops)] and nonflight operations [Leq (nonflt ops)]. Leq was also measured according to sleep area shipboard locations of forward (FWD) Leq (FWD), middle (MID) Leq (MID), and rear (AFT) Leq (AFT). These data were compared to the 70 dBA American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value (TLV) for effective quiet areas. In addition, these data were compared to noise levels associated with hearing loss and sleep parameters. Statistical analysis was conducted with R version 3.5.2 using an alpha level of 0.05. Results Leq (flt ops) in sleeping areas was a statistically significant (P < 0.05) 6.4 dBA higher than the Leq (nonflt ops). Leq (FWD) and Leq (MID) in sleeping areas was a statistically significant (P < 0.05) 15.2 and 15.0 dBA higher, respectively, than the Leq (AFT) noise levels. Mean noise levels at standardized center (1/1) octave bands were highest between 500 and 4000 Hz, ranging from 65.2 to 69.8 dB. A total of 72% of all area Leq measurements exceeded the 70 dBA ACGIH TLV classified as effective quiet to allow for temporary threshold shift recovery. All noise measurements exceeded the World Health Organization’s noise threshold where adverse effects on sleep begin. Discussion/Conclusions Results suggest that sleeping area location in close proximity to relatively high noise sources and activities occurring on an aircraft carrier (i.e. flight operations) increase noise levels in sleeping areas. These findings raise serious concerns since high noise exposures both on duty and during off-duty/sleeping periods may inhibit auditory recovery from hazardous noise exposures. In addition, results suggest noise levels in sleeping areas are high enough to evoke negative sleep effects.

Purpose To assess whether working in preschools increases the risk of hearing-related symptoms and whether age, occupational noise, and stressful working conditions affect the risk. Methods Questionnaire data on hearing-related symptoms were analysed in women aged 24–65 (4718 preschool teachers, and 4122 randomly selected general population controls). Prevalence and risk ratio (RR) of self-reported hearing loss, tinnitus, difficulty perceiving speech, hyperacusis and sound-induced auditory fatigue were assessed by comparing the cohorts in relation to age and self-reported occupational noise and stressful working conditions (effort–reward imbalance and emotional demands). RR was calculated using log-binomial regression models adjusted for age, education, income, smoking, hearing protection, and leisure noise. Incidence rates and incidence rate ratios (IRR) were calculated for retrospectively reported onset of all symptoms except sound-induced auditory fatigue. Results Compared to the controls, preschool teachers had overall more than twofold RR of sound-induced auditory fatigue (RR 2.4, 95% confidence interval 2.2–2.5) and hyperacusis (RR 2.3, 2.1–2.5) and almost twofold for difficulty perceiving speech (RR 1.9, 1.7–2.0). Preschool teachers had a threefold IRR of hyperacusis (IRR 3.1, 2.8–3.4) and twofold for difficulty perceiving speech (IRR 2.4, 2.2–2.6). Significantly although slightly less increased RR and IRR were observed for hearing loss and tinnitus. RR and IRR were generally still increased for preschool teachers when stratified by age and occupational exposure to noise and stress. Conclusions This large cohort study showed that working as preschool teacher increases the risk of self-reported hearing-related symptoms, indicating a need of preventative measures. Electronic supplementary material The online version of this article (10.1007/s00420-019-01453-0) contains supplementary material, which is available to authorized users.

Objective: To assess the validity of a questionnaire (consisting of 10 items/questions) to identify hearing loss (HL) among three-wheeler tempo and noncommercial car drivers. Materials and Methods: This was a cross-sectional study conducted in an urban area of Lucknow city. Three-wheeler tempo drivers and noncommercial car drivers were assessed for HL by audiometry. A total of 300 subjects, who fulfilled the study criteria, were selected for the interview and health assessment. The pure tone audiometry was conducted after >12 hours of the last noise exposure to avoid temporary threshold shift. Results: The percentage of respondents aged between 31 and 40 years was 36%. The highest affirmative response item was “Do you have trouble hearing in noisy background?” constituting 68% and the lowest affirmative response item was “Do you have trouble understanding the speech of women and children?” constituting 33.7%. Kappa values showed that there was significantly (

Genetics and environmental factors frequently influence individual’s susceptibility to hearing loss. It is postulated that melanin in the inner ear is related to individual’s susceptibility to noise induced hearing loss (NIHL). General pigmentation in turn, suspected to be related to the amount of pigmentation in the inner ear. The amount of melanin in the inner ear is said to modulate the endocochlear potential and provide an otoprotective effect. Aim: The study aimed to determine the relationship between the contralateral suppression of otoacoustic emissions (CSOAE) in individuals with brown eyes and hair, and blue eyes and blond hair, and temporary emission shift (TES) after short-term noise exposure. Setting and Design: The research was conducted using a quantitative research design with a quasi-experimental repeated within the subject design to compare the CSOAE in subjects with different hair and eyes colour with TES after short-term noise exposure. Quantitative research was used to determine the relationship between the measurable variables to predict occurrence. Material and Method: The hearing sensitivity of young adults was determined by using pure tone audiometry followed by CSOAE’s and distortion product otoacoustic emissions (DPOAE) before listening to music for one hour individually. Pure tone audiometry and DPOAE’s were repeated after music exposure to determine the amount of TES and temporary threshold shift (TTS). Statistical Analysis used: One-way ANOVA was used during the analysis of the data obtained during this research study, in addition to, two-tailed Wilcoxon Sign Rank test and Friedman’s test. In all analyses, a 95% level of significance (P

Background Nurses can be exposed to hundreds of alarms during their shift, contributing to alarm fatigue. Purpose The purposes were to explore similarities and differences in perceptions of clinical alarms by labor nurses caring for generally healthy women compared with perceptions of adult intensive care unit (ICU) and neonatal ICU nurses caring for critically ill patients and to seek nurses' suggestions for potential improvements. Methods Nurses were asked via focus groups about the utility of clinical alarms from medical devices. Results There was consensus that false alarms and too many devices generating alarms contributed to alarm fatigue, and most alarms lacked clinical relevance. Nurses identified certain types of alarms that they responded to immediately, but the vast majority of the alarms did not contribute to their clinical assessment or planned nursing care. Conclusions Monitoring only those patients who need it and only those physiologic values that are warranted, based on patient condition, may decrease alarm burden.

Cisplatin is a potent chemotherapeutic compound for which ototoxicity is a significant side effect. Cisplatin has shown sensitivity to circadian time, in that cisplatin is most effective as an anti-tumor compound, and least nephrotoxic, when given in the active (dark) period of the light-dark cycle in rodents. The objective of the study was to determine the sensitivity of cisplatin ototoxicity to circadian time. Fifty-seven Fischer 344/NHsd rats were exposed to 12 mg/kg cisplatin by intra-peritoneal injection at one of six time points on a 12 h light-12 h dark cycle: 2, 6, or 10 h after light onset or 2, 6, or 10 h after light offset. Cochlear injury was evaluated using auditory brainstem response threshold shifts and postmortem outer hair cell counts. All animals experienced threshold shift in the highest frequencies tested (30 and 40 kHz). The animals exposed to cisplatin at 6 h after light onset (the inactive period) had significantly higher mid-frequency threshold shifts and outer hair cell losses than the groups exposed during the dark hours. The results indicate that cisplatin is less likely to cause ototoxicity in the Fischer 344/NHsd rat when given during the active period. This finding is consistent with the lower nephrotoxicity that has been detected in cisplatin-exposed animals treated during the dark hours, and the magnitude of differences in threshold shifts between the light and dark exposure indicates that circadian timing has a significant impact on susceptibility to cisplatin ototoxicity.

Acoustic hearing implants, such as direct acoustic cochlear implants (DACIs), can be used to treat profound mixed hearing loss. Electrophysiological responses in DACI subjects are of interest to confirm auditory processing intra-operatively, and to assist DACI fitting postoperatively. We present two related studies, focusing on DACI artifacts and electrophysiological measurements in DACI subjects, respectively. In the first study we aimed to characterize DACI artifacts, to study the feasibility of measuring frequency-specific electrophysiological responses in DACI subjects. Measurements of DACI artifacts were collected in a cadaveric head to disentangle possible DACI artifact sources and compared to a constructed DACI artifact template. It is shown that for moderate stimulation levels, DACI artifacts are mainly dominated by the artifact from the radio frequency (RF) communication signal, that can be modeled if the RF encoding protocol is known. In a second study, the feasibility of measuring intra-operative responses, without applying the RF artifact models, in DACI subjects is investigated. Auditory steady-state and brainstem responses were measured intra-operatively in three DACI subjects, immediately after implantation, to confirm proper DACI functioning and coupling to the inner ear. Intra-operative responses could be measured in two of the three tested subjects. Absence of intra-operative responses in the third subject can possibly be explained by the hearing loss, attenuation of intra-operative responses, the difference between electrophysiological and behavioral threshold, and a temporary threshold shift due to the DACI surgery. In conclusion, RF artifacts can be modeled, such that electrophysiological responses to frequency-specific stimuli could possibly be measured in DACI subjects, and intra-operative responses in DACI subjects can be obtained. ispartof: HEARING RESEARCH vol:370 pages:217-231 ispartof: location:Netherlands status: published

Introduction Ultrasonic bone removal devices (UBD) are capable of cutting through bony tissue without injury to adjacent soft tissue. The feasibility and safety of using this technology for removal of bone from an intact ossicular chain (as might be required for otosclerosis or congenital fixation) was investigated in an animal model. Methods This was a prospective animal study conducted on seven anesthetised adult chinchillas. An UBD was used to remove bone from the malleus head in situ. Pre and post-operative distortion product otoacoustic emission (DPOAE) levels and auditory brainstem response (ABR) thresholds were recorded. Scanning electron microscopy (SEM) was used to assess cochlear haircell integrity. Results Precise removal of a small quantity of bone from the malleus head was achieved by a 30s application of UBD without disruption of the ossicular chain or tympanic membrane. DPOAEs became undetectable after the intervention with signal-to-noise ratios (SNR) 85 dB SPL in 13 ears. SEM showed significant disruption of structural integrity of the organ of Corti, specifically loss and damage of outer haircells. Conclusions Although UBD can be used to reshape an ossicle without middle ear injury, prolonged contact with the ossicular chain can cause structural and functional injury to the cochlea. Extensive cochlea pathology was found, but we did not investigate for recovery from any temporary threshold shift. In the authors’ opinion, further study should be undertaken before consideration is given to use of the device for release of ossicular fixation. Graphical abstract

The auditory effects of single- and multiple-shot impulsive noise exposures were evaluated in a bearded seal (Erignathus barbatus). This study replicated and expanded upon recent work with related species [Reichmuth, Ghoul, Sills, Rouse, and Southall (2016). J. Acoust. Soc. Am. 140, 2646–2658]. Behavioral methods were used to measure hearing sensitivity before and immediately following exposure to underwater noise from a seismic air gun. Hearing was evaluated at 100 Hz—close to the maximum energy in the received pulse, and 400 Hz—the frequency with the highest sensation level. When no evidence of a temporary threshold shift (TTS) was found following single shots at 185 dB re 1 μPa2 s unweighted sound exposure level (SEL) and 207 dB re 1 μPa peak-to-peak sound pressure, the number of exposures was gradually increased from one to ten. Transient shifts in hearing thresholds at 400 Hz were apparent following exposure to four to ten consecutive pulses (cumulative SEL 191–195 dB re 1 μPa2 s; 167–171 dB re 1 μPa2 s with frequency weighting for phocid carnivores in water). Along with these auditory data, the effects of seismic exposures on response time, response bias, and behavior were investigated. This study has implications for predicting TTS onset following impulsive noise exposure in seals.