scholarly journals Effects of Recreational Noise on Threshold and Suprathreshold Measures of Auditory Function

2017 ◽  
Vol 38 (04) ◽  
pp. 298-318 ◽  
Author(s):  
Colleen Le Prell ◽  
Scott Griffiths ◽  
Edward Lobarinas ◽  
Angela Fulbright
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Nerve Fibers ◽  
Broadband Noise ◽  
Threshold Shift ◽  
Distortion Product Otoacoustic Emission ◽  
Hearing Tests ◽  
Indirect Measure ◽  
Brainstem Response ◽  
Exposure History

AbstractNoise exposure that causes a temporary threshold shift but no permanent threshold shift can cause degeneration of synaptic ribbons and afferent nerve fibers, with a corresponding reduction in wave I amplitude of the auditory brainstem response (ABR) in animals. This form of underlying damage, hypothesized to also occur in humans, has been termed synaptopathy, and it has been hypothesized that there will be a hidden hearing loss consisting of functional deficits at suprathreshold stimulus levels. This study assessed whether recreational noise exposure history was associated with smaller ABR wave I amplitude and poorer performance on suprathreshold auditory test measures. Noise exposure histories were collected from 26 men and 34 women with hearing thresholds ≤ 25 dB hearing loss (HL; 250 Hz to 8 kHz), and a variety of functional suprathreshold hearing tests were performed. Wave I amplitudes of click-evoked ABR were obtained at 70, 80, 90, and 99 dB (nHL) and tone-burst evoked ABR were obtained at 90 dB nHL. Speech recognition performance was measured in quiet and in competing noise, using the Words in Noise test, and the NU-6 word list in broadband noise (BBN). In addition, temporal summation to tonal stimuli was assessed in quiet and in competing BBN. To control for the effects of subclinical conventional hearing loss, distortion product otoacoustic emission amplitude, an indirect measure of outer hair cell integrity, was measured. There was no statistically significant relationship between noise exposure history scores and ABR wave I amplitude in either men or women for any of the ABR conditions. ABR wave I amplitude and noise exposure history were not reliably correlated with suprathreshold functional hearing tests. Taken together, this study found no evidence of noise-induced decreases in ABR wave I amplitude or signal processing in noise in a cohort of subjects with a history of recreational noise exposure.

scholarly journals Effect of Phlorofucofuroeckol A and Dieckol Extracted from Ecklonia cava on Noise-induced Hearing Loss in a Mouse Model

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 443
Author(s):  
Hyunjun Woo ◽  
Min-Kyung Kim ◽  
Sohyeon Park ◽  
Seung-Hee Han ◽  
Hyeon-Cheol Shin ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Noise Exposure ◽  
Radical Scavenging ◽  
Threshold Shift ◽  
Ecklonia Cava ◽  
Control Group ◽  
Noise Induced Hearing Loss ◽  
Antioxidant Agents ◽  
Brainstem Response

One of the well-known causes of hearing loss is noise. Approximately 31.1% of Americans between the ages of 20 and 69 years (61.1 million people) have high-frequency hearing loss associated with noise exposure. In addition, recurrent noise exposure can accelerate age-related hearing loss. Phlorofucofuroeckol A (PFF-A) and dieckol, polyphenols extracted from the brown alga Ecklonia cava, are potent antioxidant agents. In this study, we investigated the effect of PFF-A and dieckol on the consequences of noise exposure in mice. In 1,1-diphenyl-2-picrylhydrazyl assay, dieckol and PFF-A both showed significant radical-scavenging activity. The mice were exposed to 115 dB SPL of noise one single time for 2 h. Auditory brainstem response(ABR) threshold shifts 4 h after 4 kHz noise exposure in mice that received dieckol were significantly lower than those in the saline with noise group. The high-PFF-A group showed a lower threshold shift at click and 16 kHz 1 day after noise exposure than the control group. The high-PFF-A group also showed higher hair cell survival than in the control at 3 days after exposure in the apical turn. These results suggest that noise-induced hair cell damage in cochlear and the ABR threshold shift can be alleviated by dieckol and PFF-A in the mouse. Derivatives of these compounds may be applied to individuals who are inevitably exposed to noise, contributing to the prevention of noise-induced hearing loss with a low probability of adverse effects.

scholarly journals Inhalation of Molecular Hydrogen, a Rescue Treatment for Noise-Induced Hearing Loss

2021 ◽  
Vol 15 ◽  
Author(s):  
Anette Elisabeth Fransson ◽  
Pernilla Videhult Pierre ◽  
Mårten Risling ◽  
Göran Frans Emanuel Laurell
Keyword(s):  
Hearing Loss ◽  
Molecular Hydrogen ◽  
Noise Exposure ◽  
Real Life ◽  
Outer Hair Cells ◽  
Broadband Noise ◽  
Hydrogen Gas ◽  
Rescue Treatment ◽  
Brainstem Response ◽  
Antioxidant Effects

Noise exposure is the most important external factor causing acquired hearing loss in humans, and it is strongly associated with the production of reactive oxygen species (ROS) in the cochlea. Several studies reported that the administration of various compounds with antioxidant effects can treat oxidative stress-induced hearing loss. However, traditional systemic drug administration to the human inner ear is problematic and has not been successful in a clinical setting. Thus, there is an urgent need to develop rescue treatment for patients with acute acoustic injuries. Hydrogen gas has antioxidant effects, rapid distribution, and distributes systemically after inhalation.The purpose of this study was to determine the protective efficacy of a single dose of molecular hydrogen (H2) on cochlear structures. Guinea pigs were divided into six groups and sacrificed immediately after or at 1 or 2 weeks. The animals were exposed to broadband noise for 2 h directly followed by 1-h inhalation of 2% H2 or room air. Electrophysiological hearing thresholds using frequency-specific auditory brainstem response (ABR) were measured prior to noise exposure and before sacrifice. ABR thresholds were significantly lower in H2-treated animals at 2 weeks after exposure, with significant preservation of outer hair cells in the entire cochlea. Quantification of synaptophysin immunoreactivity revealed that H2 inhalation protected the cochlear inner hair cell synaptic structures containing synaptophysin. The inflammatory response was greater in the stria vascularis, showing increased Iba1 due to H2 inhalation.Repeated administration of H2 inhalation may further improve the therapeutic effect. This animal model does not reproduce conditions in humans, highlighting the need for additional real-life studies in humans.

scholarly journals The Physiological Bases of Hidden Noise-Induced Hearing Loss: Protocol for a Functional Neuroimaging Study (Preprint)

2017 ◽  
Author(s):  
Rebecca Susan Dewey ◽  
Deborah A Hall ◽  
Hannah Guest ◽  
Garreth Prendergast ◽  
Christopher J Plack ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Functional Neuroimaging ◽  
Nerve Fibers ◽  
High Threshold ◽  
Hearing Level ◽  
Noise Induced Hearing Loss ◽  
Brainstem Response ◽  
Neuroimaging Study ◽  
Hidden Hearing Loss

BACKGROUND Rodent studies indicate that noise exposure can cause permanent damage to synapses between inner hair cells and high-threshold auditory nerve fibers, without permanently altering threshold sensitivity. These demonstrations of what is commonly known as hidden hearing loss have been confirmed in several rodent species, but the implications for human hearing are unclear. OBJECTIVE Our Medical Research Council–funded program aims to address this unanswered question, by investigating functional consequences of the damage to the human peripheral and central auditory nervous system that results from cumulative lifetime noise exposure. Behavioral and neuroimaging techniques are being used in a series of parallel studies aimed at detecting hidden hearing loss in humans. The planned neuroimaging study aims to (1) identify central auditory biomarkers associated with hidden hearing loss; (2) investigate whether there are any additive contributions from tinnitus or diminished sound tolerance, which are often comorbid with hearing problems; and (3) explore the relation between subcortical functional magnetic resonance imaging (fMRI) measures and the auditory brainstem response (ABR). METHODS Individuals aged 25 to 40 years with pure tone hearing thresholds ≤20 dB hearing level over the range 500 Hz to 8 kHz and no contraindications for MRI or signs of ear disease will be recruited into the study. Lifetime noise exposure will be estimated using an in-depth structured interview. Auditory responses throughout the central auditory system will be recorded using ABR and fMRI. Analyses will focus predominantly on correlations between lifetime noise exposure and auditory response characteristics. RESULTS This paper reports the study protocol. The funding was awarded in July 2013. Enrollment for the study described in this protocol commenced in February 2017 and was completed in December 2017. Results are expected in 2018. CONCLUSIONS This challenging and comprehensive study will have the potential to impact diagnostic procedures for hidden hearing loss, enabling early identification of noise-induced auditory damage via the detection of changes in central auditory processing. Consequently, this will generate the opportunity to give personalized advice regarding provision of ear defense and monitoring of further damage, thus reducing the incidence of noise-induced hearing loss.

scholarly journals Deletion of C1ql1 Causes Hearing Loss and Abnormal Auditory Nerve Fibers in the Mouse Cochlea

2021 ◽  
Vol 15 ◽  
Author(s):  
Yue Qi ◽  
Wei Xiong ◽  
Shukui Yu ◽  
Zhengde Du ◽  
Tengfei Qu ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Confocal Microscopy ◽  
Auditory Brainstem ◽  
Nerve Fibers ◽  
Outer Hair Cells ◽  
Synaptic Proteins ◽  
Distortion Product Otoacoustic Emission ◽  
Distortion Product ◽  
Brainstem Response ◽  
Ganglion Neurons

Complement C1q Like 1 (C1QL1), a secreted component of C1Q-related protein, is known to play an important role in synaptic maturation, regulation, and maintenance in the central nervous system. C1ql1 is expressed in adult cochlear inner and outer hair cells (IHCs and OHCs) with preferential expression in OHCs. We generated C1ql1 null mice to examine the role of C1QL1 in the auditory periphery. C1ql1-null mice exhibited progressive hearing loss with elevated thresholds of auditory brainstem response and distortion product otoacoustic emission. Confocal microscopy showed that the number of nerve fibers innervating both IHCs and OHCs was significantly reduced. However, spiral ganglion neurons appeared to be normal under electron microscopy. IHC development and survival were not affected by deletion of C1ql1. Voltage-clamp recording and immunocytochmistry combined with confocal microscopy showed C1ql1-null IHCs showed no significant reduction of pre-synaptic proteins and synaptic vesicle release. This is in contrast to significant OHC loss in the KO mice. Our study suggests that C1ql1 is essential for development of hair cell innervation and OHC survival. But maturation of presynaptic machinery in IHCs does not depend on C1QL1.

Methionine Sulfoxide Reductase A Knockout Mice Show Progressive Hearing Loss and Sensitivity to Acoustic Trauma

2018 ◽  
Vol 23 (1) ◽  
pp. 20-31 ◽  
Author(s):  
Safa Alqudah ◽  
Mark Chertoff ◽  
Dianne Durham ◽  
Jackob Moskovitz ◽  
Hinrich Staecker ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Knockout Mice ◽  
Noise Exposure ◽  
Methionine Sulfoxide ◽  
Auditory Brainstem ◽  
Acoustic Trauma ◽  
Methionine Sulfoxide Reductase ◽  
Distortion Product Otoacoustic Emission ◽  
Distortion Product ◽  
Brainstem Response

Methionine sulfoxide reductases (MsrA and MsrB) protect the biological activity of proteins from oxidative modifications to methionine residues and are important for protecting against the pathological effects of neurodegenerative diseases. In the current study, we characterized the auditory phenotype of the MsrA knockout mouse. Young MsrA knockout mice showed small high-frequency threshold elevations for auditory brainstem response and distortion product otoacoustic emission compared to those of wild-type mice, which progressively worsened in older MsrA knockout mice. MsrA knockout mice showed an increased sensitivity to noise at young and older ages, suggesting that MsrA is part of a mechanism that protects the cochlea from acoustic damage. MsrA mRNA in the cochlea was increased following acoustic stimulation. Finally, expression of mRNA MsrB1 was compromised at 6 months old, but not in younger MsrA knockout mice (compared to controls). The identification of MsrA in the cochlea as a protective mediator from both early onset hearing loss and acoustic trauma expands our understanding of the pathways that may induce protection from acoustic trauma and foster further studies on how to prevent the damaging effect of noise exposure through Msr-based therapy.

scholarly journals Partial Hearing Restoration after ERBB2 Induction in Deafened Adult Mice

2019 ◽  
Author(s):  
Jingyuan Zhang ◽  
Daxiang Na ◽  
Miriam Dilts ◽  
Kenneth S. Henry ◽  
Patricia M. White
Keyword(s):  
Cell Proliferation ◽  
Hearing Loss ◽  
Noise Exposure ◽  
Supporting Cell ◽  
Supporting Cells ◽  
Adult Mice ◽  
Hearing Thresholds ◽  
Brainstem Response ◽  
Noise Damage ◽  
Cochlear Supporting Cells

AbstractNoise induced hearing loss (NIHL) affects over ten million adults in the United States, and there is no biological treatment to restore endogenous function after damage. We hypothesized that activation of signaling from ERBB2 receptors in cochlear supporting cells could mitigate NIHL damage. We used the Tet-On genetic expression system to drive a constitutively active variant of ERBB2 (CA-ERBB2) in cochlear supporting cells three days after permanent noise damage in young adult mice. Hearing thresholds were assessed with auditory brainstem response tests prior to noise damage, and hearing recovery was assessed over a three month period. We evaluated supporting cell proliferation, inner and outer hair cell (IHC and OHC) survival, synaptic preservation, and IHC cytoskeletal alterations with histological techniques. Mice harboring CA-ERBB2 capability had similar hearing thresholds to control littermates prior to and immediately after noise exposure, and incurred similar levels of permanent hearing loss. Two and three months after noise exposure, CA-ERBB2+ mice demonstrated a partial but significant reversal of NIHL threshold shifts at the lowest frequency tested, out of five frequencies (n=19 total mice, p=0.0015, ANOVA). We also observed improved IHC and OHC survival (n=7 total cochleae, p=5 × 10−5, Kruskal-Wallis rank sum test). There was no evidence for sustained supporting cell proliferation. Some mortality was associated with doxycycline and furosemide treatments to induce the Tet-ON system. These data suggest that ERBB2 signaling in supporting cells promotes HC repair and some functional recovery. Funded by NIH R01 DC014261, and grants from the Schmitt Foundation and UR Ventures.

Pure-Tone Hearing Asymmetry: A Logistic Approach Modeling Age, Sex, and Noise Exposure History

2012 ◽  
Vol 23 (07) ◽  
pp. 553-570 ◽  
Author(s):  
David A. Zapala ◽  
Robin E. Criter ◽  
Jamie M. Bogle ◽  
Larry B. Lundy ◽  
Michael J. Cevette ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Logistic Regression ◽  
Regression Model ◽  
Pure Tone ◽  
Logistic Regression Model ◽  
Noise Exposure ◽  
Clinical Decision Making ◽  
Clinical Impression ◽  
Patient History ◽  
Exposure History

Background: Asymmetric hearing loss (AHL) can be an early sign of vestibular schwannoma (VS). However, recognizing VS-induced AHL is challenging. There is no universally accepted definition of a “medically significant pure-tone hearing asymmetry,” in part because AHL is a common feature of medically benign forms of hearing loss (e.g., age- or firearm-related hearing loss). In most cases, the determination that an observed AHL does not come from a benign cause involves subjective clinical judgment. Purpose: Our purpose was threefold: (1) to quantify hearing asymmetry distributions in a large group of patients with medically benign forms of hearing loss, stratifying for age, sex, and noise exposure history; (2) to assess how previously proposed hearing asymmetry calculations segregate tumor from nontumor cases; and (3) to present the results of a logistic regression method for defining hearing asymmetry that incorporates age, sex, and noise information. Research Design: Retrospective chart review. Study Sample: Five thousand six hundred and sixty-one patients with idiopathic, age- or noise exposure-related hearing loss and 85 untreated VS patients. Data Collection and Analysis: Audiometric, patient history, and clinical impression data were collected from 22,785 consecutive patient visits to the audiology section at Mayo Clinic in Florida from 2006 to 2009 to screen for eligibility. Those eligible were then stratified by VS presence, age, sex, and self-reported noise exposure history. Pure-tone asymmetry distributions were analyzed. Audiometric data from VS diagnoses were used to create four additional audiograms per patient to model the hypothetical development of AHL prior to the actual hearing test. The ability of 11 previously defined hearing asymmetry calculations to distinguish between VS and non-VS cases was described. A logistic regression model was developed that integrated age, sex, and noise exposure history with pure-tone asymmetry data. Regression model performance was then compared to existing asymmetry calculation methods. Results: The 11 existing pure-tone asymmetry calculations varied in tumor detection performance. Age, sex, and noise exposure history helped to predict benign forms of hearing asymmetry. The logistic regression model outperformed existing asymmetry calculations and better accounted for normal age-, sex-, and noise exposure-related asymmetry variability. Conclusions: Our logistic regression asymmetry method improves the clinician's ability to estimate risk of VS, in part by integrating categorical patient history and numeric test data. This form of modeling can enhance clinical decision making in audiology and otology.

Noise

2020 ◽  
pp. 1671-1673
Author(s):  
David Koh ◽  
Tar-Ching Aw
Keyword(s):  
Cardiovascular Disease ◽  
Hearing Loss ◽  
Sleep Disturbance ◽  
Cognitive Performance ◽  
Noise Exposure ◽  
Threshold Shift ◽  
Temporary Threshold Shift ◽  
Noise Induced Hearing Loss ◽  
Occupational Setting ◽  
Human Ear

Noise can affect hearing in the occupational setting but can have other effects where exposures are non-occupational. For clinical purposes, noise is measured in decibels weighted according to the sensitivity of the human ear (dB(A)). Regardless of source, the effects of overexposure to noise are similar. Initially there is a temporary threshold shift, where reversibility of hearing loss is possible with removal away from further noise. Noise-induced hearing loss occurs following prolonged or intense exposure, with poor prospects for improvement of hearing. The classical audiogram for noise-induced hearing loss shows a 4 kHz dip. Non-auditory effects of prolonged noise exposure include annoyance, sleep disturbance, hypertension, and cardiovascular disease, stress, and impaired cognitive performance. Prevention of noise-induced hearing loss is by reducing exposure to noise at source minimizing exposure time, using hearing protection, and participating in surveillance.

Temporary Threshold Shift from a Toy Cap Gun

1974 ◽  
Vol 39 (2) ◽  
pp. 163-168 ◽  
Author(s):  
Lynne Marshall ◽  
John F. Brandt
Keyword(s):  
Hearing Loss ◽  
Sound Pressure Level ◽  
Sound Pressure ◽  
Noise Exposure ◽  
Pressure Level ◽  
Threshold Shift ◽  
Temporary Threshold Shift ◽  
Fixed Frequency ◽  
Before And After ◽  
The Subject

Temporary threshold shift resulting from exposure to one and five toy cap gun pistol shots was investigated using 11 normal-hearing adult subjects and one subject with a noise-induced hearing loss. The subjects fired the cap gun at arm’s length, and absolute thresholds at 4000 Hz were obtained before and after noise exposure by a fixed-frequency Bekesy technique. After exposure to one gunshot, five subjects showed a small TTS, five demonstrated no TTS, and two (including the subject with the hearing loss) exhibited negative TTS. No TTS occurred in any of the subjects after exposure to five shots. It was postulated that the small amount of TTS was due to the unexpectedly low sound pressure level produced by the cap gun and to the contraction of the middle ear muscles in some subjects prior to firing.

scholarly journals miR-153/KCNQ4 axis contributes to noise-induced hearing loss in a mouse model

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Qin Wang ◽  
Wei Li ◽  
Cuiyun Cai ◽  
Peng Hu ◽  
Ruosha Lai
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Sensory Epithelium ◽  
Outer Hair Cells ◽  
Broadband Noise ◽  
Hek293 Cells ◽  
Auditory Brainstem Responses ◽  
Luciferase Reporter

AbstractDamage to the cochlear sensory epithelium is a key contributor to noise-induced sensorineural hearing loss (SNHL). KCNQ4 plays an important role in the cochlear potassium circulation and outer hair cells survival. As miR-153 can target and regulate KCNQ4, we sought to study the role of miR-153 in SNHL. 12-week-old male CBA/J mice were exposed to 2–20 kHz broadband noise at 96 dB SPL to induce temporary threshold shifts and 101 dB SPL to induce permanent threshold shifts. Hearing loss was determined by auditory brainstem responses (ABR). Relative expression of miR-153 and KCNQ4 in mice cochlea were determined by Real-Time quantitative PCR. miR-153 mimics were co-transfected with wild type or mutated KCNQ4 into HEK293 cells. Luciferase reporter assay was used to validate the binding between miR-153 and KCNQ4. AAV-sp-153 was constructed and administrated intra-peritoneally 24- and 2-h prior and immediately after noise exposure to knockdown miR-153. The KCNQ4 is mainly expressed in outer hair cells (OHCs). We showed that the expression of KCNQ4 in mice cochlea was reduced and miR-153 expression was significantly increased after noise exposure compared to control. miR-153 bound to 3′UTR of KNCQ4, and the knockdown of miR-153 with the AAV-sp-153 administration restored KCNQ4 mRNA and protein expression. In addition, the knockdown of miR-153 reduced ABR threshold shifts at 8, 16, and 32 kHz after permanent threshold shifts (PTS) noise exposure. Correspondingly, OHC losses were attenuated with inhibition of miR-153. This study demonstrates that miR-153 inhibition significantly restores KNCQ4 in cochlea after noise exposure, which attenuates SNHL. Our study provides a new potential therapeutic target in the prevention and treatment of SNHL.

Sign in / Sign up

Export Citation Format

Share Document