scholarly journals Threshold shift produced by continuous noise exposure in the parakeet (Melopsittacus undulatus)

1974 ◽  
Vol 55 (S1) ◽  
pp. S77-S77 ◽  
Author(s):  
Robert J. Dooling ◽  
James C. Saunders
1977 ◽  
Vol 86 (6) ◽  
pp. 821-826 ◽  
Author(s):  
William Melnick

Nine men were exposed to 24 hours of continuous noise in a sound field. The noise was an octave band centered at 4 kHz at levels 80 and 85 dB. Hearing thresholds were measured monaurally at 11 test frequencies ranging from 250 to 10000 Hz before, during, and after exposure. Temporary threshold shift (TTS) reached maximum levels at 8 to 12 hours of exposure. Maximum TTS occurred at 4 and 6 kHz. Mean asymptomtic threshold shifts (ATS) resulting from the 80 dB exposure level were 9.3 dB for 4 kHz and 7.2 dB for 6 kHz. For the 85 dB noise level, these threshold shifts were 17.8 dB and 14.6 dB respectively. The increase in ATS with increase of noise level for these two frequencies could be fitted with a straight line having a slope of 1.6.


2013 ◽  
Vol 24 (06) ◽  
pp. 461-473 ◽  
Author(s):  
Eric C. Bielefeld

Background: Toxic levels of reactive oxygen species are key contributors to the lesion of dead outer hair cells (OHCs) seen in the cochlea after noise exposure. The current study follows previous work in which paraquat was used to demonstrate that NADPH oxidase is active in the cochlea and can contribute to cochlear reactive oxygen species formation and hair cell loss. Purpose: The current study was undertaken to test whether pharmacological blockade of NADPH oxidase in the cochlea would lead to reduced noise-induced hearing loss and OHC death. Study Sample: A total of 18 chinchillas (36 ears) were assessed in the study. Intervention: AEBSF (4-[2-aminoethyl]benzenesulfonyl fluoride), an inhibitor of NADPH oxidase activation, was dissolved in distilled water and delivered into the cochlea via diffusion across the round window membrane. The contralateral ears received distilled water as a vehicle control. Following treatment, chinchillas were exposed to one of two noises: a 4 kHz octave band noise at 106 dB SPL for 6 hr or an impulse noise that consisted of 75 pairs of 155 dB pSPL impulses. Data Collection and Analysis: Pre– and post–noise exposure, thresholds of the auditory brainstem response at 2–8 kHz were measured. Postmortem OHC counts were conducted at the conclusion of the study. Two- and three-factor ANOVAs were used for statistical analysis of the OHC losses and ABR threshold shifts induced by the noise exposures. Results: Permanent threshold shift from the impulse noise was reduced in the ears treated with the NADPH oxidase inhibitor, but no differences were found in the groups exposed to the continuous noise. OHC losses were not statistically different between the treated and untreated ears for either noise exposure. Conclusions: The results suggest that NADPH oxidase-mediated superoxide has a role in cochlear damage from impulse noise, and pharmacologic inhibition of NADPH oxidase can reduce cochlear susceptibility to noise damage. The lack of protection from the longer-duration continuous noise can be attributed to a number of possibilities related to dose level and delivery schedule.


1976 ◽  
Vol 19 (2) ◽  
pp. 216-224 ◽  
Author(s):  
James T. Yates ◽  
Jerry D. Ramsey ◽  
Jay W. Holland

The purpose of this study was to compare the damage risk of 85 and 90 dBA of white noise for equivalent full-day exposures. The damage risk of the two noise levels was determined by comparing the temporary threshold shift (TTS) of 12 subjects exposed to either 85 or 90 dBA of white noise for equivalent half- and full-day exposures. TTS was determined by comparing the pre- and postexposure binaural audiograms of each subject at 1, 2, 3, 4, 6, and 8 kHz. It was concluded that the potential damage risk, that is, hazardous effect, of 90 dBA is greater than 85 dBA of noise for equivalent full-day exposures. The statistical difference between the overall effects of equivalent exposures to 85 dBA as compared to 90 dBA of noise could not be traced to any one frequency. The damage risk of a full-day exposure to 85 dBA is equivalent to that of a half-day exposure to 90 dBA of noise. Within the limits of this study, TTS t was as effective as TTS 2 for estimating the damage risk of noise exposure.


Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 443
Author(s):  
Hyunjun Woo ◽  
Min-Kyung Kim ◽  
Sohyeon Park ◽  
Seung-Hee Han ◽  
Hyeon-Cheol Shin ◽  
...  

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.


1958 ◽  
Vol 67 (3) ◽  
pp. 824-837 ◽  
Author(s):  
Aram Glorig ◽  
Anne Summerfield ◽  
W. Dixon Ward

2017 ◽  
Vol 19 (91) ◽  
pp. 263 ◽  
Author(s):  
Veronika Weilnhammer ◽  
Wenjia Wei ◽  
Stefanie Heinze ◽  
DorisG Gerstner ◽  
SandraM Walser ◽  
...  

1995 ◽  
Vol 24 (2) ◽  
pp. 137-141 ◽  
Author(s):  
Kari J. Kvœrner ◽  
Bo Engdahl ◽  
Atle R. Arnesen ◽  
Iain W. S. Mair

Author(s):  
Kathleen C. M. Campbell ◽  
Nicole Cosenza ◽  
Robert Meech ◽  
Michael Buhnerkempe ◽  
Jun Qin ◽  
...  

2020 ◽  
pp. 1671-1673
Author(s):  
David Koh ◽  
Tar-Ching Aw

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.


1974 ◽  
Vol 39 (2) ◽  
pp. 163-168 ◽  
Author(s):  
Lynne Marshall ◽  
John F. Brandt

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.


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