Impulse noise: can hitting a softball harm your hearing?
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ABSTRACT:
SUBMITTER: Cook K
PROVIDER: S-EPMC3981188 | biostudies-other | 2014
REPOSITORIES: biostudies-other
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Project description: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.
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Project description:Noise-induced hearing loss (NIHL) is the most significant occupational health issue worldwide. We conducted a genome-wide association study to identify single-nucleotide polymorphisms (SNPs) associated with hearing threshold shift in young males undergoing their first encounter with occupational impulse noise. We report a significant association of SNP rs7598759 (p < 5 x 10(-7); p = 0.01 after permutation and correction; Odds Ratio = 12.75) in the gene coding for nucleolin, a multifunctional phosphoprotein involved in the control of senescence and protection against apoptosis. Interestingly, nucleolin has been shown to mediate the anti-apoptotic effect of HSP70, a protein found to prevent ototoxicity and whose polymorphisms have been associated with susceptibility to NIHL. Increase in nucleolin expression has also been associated with the prevention of apoptosis in cells undergoing oxidative stress, a well-known metabolic sequela of noise exposure. To assess the potential role of nucleolin in hearing loss, we tested down-regulation of nucleolin in cochlear sensory cells HEI-OC1 under oxidative stress conditions and report increased sensitivity to cisplatin, a chemotherapeutic drug with ototoxic side effects. Additional SNPs were found with suggestive association (p < 5 x 10(-4)), of which 7 SNPs were located in genes previously reported to be related to NIHL and 43 of them were observed in 36 other genes previously not reported to be associated with NIHL. Taken together, our GWAS data and in vitro studies reported herein suggest that nucleolin is a potential candidate associated with NIHL in this population.
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Project description:Noise-induced hidden hearing loss (HHL) is a new type of hearing loss that has been identified in recent years and leads to insidious damage to the cochlea, unlike the well-known noise-induced hearing loss (NIHL). However, the cellular and molecular basis for it remains to be elucidated. Here, we established a single-cell transcriptome profile of the C57BL/6J mouse cochlea, in which we describe the transcriptome changes of individual cell types within the cochlea with HHL and NIHL. Mice in the HHL group were exposed to 110 dB of noise for 2 hours, and those in the NIHL group were exposed to 115 dB of noise for 4 hours for 3 days. The cochlea was taken 6 hours after the last noise exposure. The control group was not exposed to noise, with other conditions being the same as those in the noise-exposed group. The results of sequencing at the single-cell level help us gain a deeper understanding of the mechanisms of the development of HHL and NIHL.
2024-06-24 | GSE252285 | GEO
Project description:ObjectiveDetermine effective preloading timepoints for D-methionine (D-met) otoprotection from steady state or impulse noise and impact on cochlear and serum antioxidant measures.DesignD-met started 2.0-, 2.5-, 3.0-, or 3.5- days before steady-state or impulse noise exposure with saline controls. Auditory brainstem response (ABRs) measured from 2 to 20 kHz at baseline and 21 days post-noise. Samples were then collected for serum (SOD, CAT, GR, GPx) and cochlear (GSH, GSSG) antioxidant levels.Study sampleTen Chinchillas per group.ResultsPreloading D-met significantly reduced ABR threshold shifts for both impulse and steady state noise exposures but with different optimal starting time points and with differences in antioxidant measures. For impulse noise exposure, the 2.0, 2.5, and 3.0 day preloading start provide significant threshold shift protection at all frequencies. Compared to the saline controls, serum GR for the 3.0 and 3.5 day preloading groups was significantly increased at 21 days with no significant increase in SOD, CAT or GPx for any impulse preloading time point. Cochlear GSH, GSSG, and GSH/GSSG ratio were not significantly different from saline controls at 21 days post noise exposure. For steady state noise exposure, significant threshold shift protection occurred at all frequencies for the 3.5, 3.0 and 2.5 day preloading start times but protection only occurred at 3 of the 6 test frequencies for the 2.0 day preloading start point. Compared to the saline controls, preloaded D-met steady-state noise groups demonstrated significantly higher serum SOD for the 2.5-3.5 day starting time points and GPx for the 2.5 day starting time but no significant increase in GR or CAT for any preloading time point. Compared to saline controls, D-met significantly increased cochlear GSH concentrations in the 2 and 2.5 day steady-state noise exposed groups but no significant differences in GSSG or the GSH/GSSG ratio were noted for any steady state noise-exposed group.ConclusionsThe optimal D-met preloading starting time window is earlier for steady state (3.5-2.5 days) than impulse noise (3.0-2.0). At 21 days post impulse noise, D-met increased serum GR for 2 preloading time points but not SOD, CAT, or GpX and not cochlear GSH, GSSG or the GSH/GSSG ratio. At 21 days post steady state noise D-met increased serum SOD and GPx at select preloading time points but not CAT or GR. However D-met did increase the cochlear GSH at select preloading time points but not GSSG or the GSH/GSSG ratio.
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Project description:Hearing in noise is a core problem in audition, and a challenge for hearing-impaired listeners, yet the underlying mechanisms are poorly understood. We explored whether harmonic frequency relations, a signature property of many communication sounds, aid hearing in noise for normal hearing listeners. We measured detection thresholds in noise for tones and speech synthesized to have harmonic or inharmonic spectra. Harmonic signals were consistently easier to detect than otherwise identical inharmonic signals. Harmonicity also improved discrimination of sounds in noise. The largest benefits were observed for two-note up-down "pitch" discrimination and melodic contour discrimination, both of which could be performed equally well with harmonic and inharmonic tones in quiet, but which showed large harmonic advantages in noise. The results show that harmonicity facilitates hearing in noise, plausibly by providing a noise-robust pitch cue that aids detection and discrimination.
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Project description:Our current knowledge on sound detection in fishes is mainly based on data acquired under quiet laboratory conditions. However, it is important to relate auditory thresholds to background noise in order to determine the signal-detecting abilities of animals in the natural environment. We investigated the influence of two noise levels within the naturally occurring range on the auditory sensitivity of two hearing specialists (otophysines) and a hearing generalist. Audiograms of the goldfish Carassius auratus, the lined Raphael catfish Platydoras costatus and the pumpkinseed sunfish Lepomis gibbosus (hearing generalist) were determined between 200 and 4000 Hz (100-800 Hz for L. gibbosus) under laboratory conditions and under continuous white noise by recording auditory evoked potentials (AEPs). Baseline thresholds showed greatest hearing sensitivity around 500 Hz in goldfish and catfish and at 100 Hz in the sunfish. Continuous white noise of 110 dB RMS elevated the thresholds by 15-20 dB in C. auratus and by 4-22 dB in P. costatus. White noise of 130 dB RMS elevated overall hearing thresholds significantly in the otophysines by 23-44 dB. In the goldfish, threshold did not shift at 4 kHz. In contrast, auditory thresholds in the sunfish declined only at the higher noise level by 7-11 dB. Our data show that the AEP recording technique is suitable for studying masking in fishes, and that the occurrence and degree of the threshold shift (masking) depend on the hearing sensitivity of fishes, the frequency, and noise levels tested. The results indicate that acoustic communication and orientation of fishes, in particular of hearing specialists, are limited by noise regimes in their environment.
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Project description:Hearing aid equivalent input noise (EIN) measures assume the primary source of internal noise to be located prior to amplification and to be constant regardless of input level. EIN will underestimate internal noise in the case that noise is generated following amplification. The present study investigated the internal noise levels of six hearing aids (HAs). Concurrent with HA processing of a speech-like stimulus with both adaptive features (acoustic feedback cancellation, digital noise reduction, microphone directionality) enabled and disabled, internal noise was quantified for various stimulus levels as the variance across repeated trials. Changes in noise level as a function of stimulus level demonstrated that (1) generation of internal noise is not isolated to the microphone, (2) noise may be dependent on input level, and (3) certain adaptive features may contribute to internal noise. Quantifying internal noise as the variance of the output measures allows for noise to be measured under real-world processing conditions, accounts for all sources of noise, and is predictive of internal noise audibility.
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Project description:Given the extraordinary ability of humans and animals to recognize communication signals over a background of noise, describing noise invariant neural responses is critical not only to pinpoint the brain regions that are mediating our robust perceptions but also to understand the neural computations that are performing these tasks and the underlying circuitry. Although invariant neural responses, such as rotation-invariant face cells, are well described in the visual system, high-level auditory neurons that can represent the same behaviorally relevant signal in a range of listening conditions have yet to be discovered. Here we found neurons in a secondary area of the avian auditory cortex that exhibit noise-invariant responses in the sense that they responded with similar spike patterns to song stimuli presented in silence and over a background of naturalistic noise. By characterizing the neurons' tuning in terms of their responses to modulations in the temporal and spectral envelope of the sound, we then show that noise invariance is partly achieved by selectively responding to long sounds with sharp spectral structure. Finally, to demonstrate that such computations could explain noise invariance, we designed a biologically inspired noise-filtering algorithm that can be used to separate song or speech from noise. This novel noise-filtering method performs as well as other state-of-the-art de-noising algorithms and could be used in clinical or consumer oriented applications. Our biologically inspired model also shows how high-level noise-invariant responses could be created from neural responses typically found in primary auditory cortex.
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Project description:INTRODUCTION:Noise-induced hearing loss (NIHL) due to industrial, military, and recreational noise exposure is a major, but also potentially preventable cause of acquired hearing loss. For the United States it is estimated that 26 million people (15% of the population) between the ages of 20 and 69 have a high-frequency NIHL at a detriment to the quality of life of the affected individuals and great economic cost to society. Areas covered: This review outlines the pathology and pathophysiology of hearing loss as seen in humans and animal models. Results from molecular studies are presented that have provided the basis for therapeutic strategies successfully applied to animals. Several compounds emerging from these studies (mostly antioxidants) are now being tested in field trials. Expert opinion: Although no clinically applicable intervention has been approved yet, recent trials are encouraging. In order to maximize protective therapies, future work needs to apply stringent criteria for noise exposure and outcome parameters. Attention needs to be paid not only to permanent NIHL due to death of sensory cells but also to temporary effects that may show delayed consequences. Existing results combined with the search for efficacious new therapies should establish a viable treatment within a decade.
| S-EPMC5527323 | biostudies-literature
Project description:PurposeTo give a systematic review of the development of noise-induced hearing loss (NIHL) in working life.MethodsA literature search in MEDLINE, Embase, Web of Science, Scopus, and Health and Safety Abstracts, with appropriate keywords on noise in the workplace and health, revealed 22,413 articles which were screened by six researchers. A total of 698 articles were reviewed in full text and scored with a checklist, and 187 articles were found to be relevant and of sufficient quality for further analysis.ResultsOccupational noise exposure causes between 7 and 21 % of the hearing loss among workers, lowest in the industrialized countries, where the incidence is going down, and highest in the developing countries. It is difficult to distinguish between NIHL and age-related hearing loss at an individual level. Most of the hearing loss is age related. Men lose hearing more than women do. Heredity also plays a part. Socioeconomic position, ethnicity and other factors, such as smoking, high blood pressure, diabetes, vibration and chemical substances, may also affect hearing. The use of firearms may be harmful to hearing, whereas most other sources of leisure-time noise seem to be less important. Impulse noise seems to be more deleterious to hearing than continuous noise. Occupational groups at high risk of NIHL are the military, construction workers, agriculture and others with high noise exposure.ConclusionThe prevalence of NIHL is declining in most industrialized countries, probably due to preventive measures. Hearing loss is mainly related to increasing age.
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