scholarly journals Intensity of Noise Exposure and the Time‐Course of Recovery from Temporary Hearing Loss

1957 ◽  
Vol 29 (11) ◽  
pp. 1248-1248
Author(s):  
William J. Trittipoe ◽  
Walter Spieth
1991 ◽  
Vol 34 (2) ◽  
pp. 403-414 ◽  
Author(s):  
John H. Macrae

Humes and Jesteadt have proposed that the Modified Power Law (MPL) provides a means of predicting permanent threshold shift (PTS) due to noise exposure in subjects with preexisting sensorineural hearing loss. Data concerning PTS attributed to overamplification by hearing aids in 8 children with severe sensorineural hearing loss were used to evaluate the MPL hypothesis. The excessive amplification was partly due to use by the children of very high volume-control settings instead of mid-range volume-control settings. The PTS tended to be flat across frequency. Its course in time was a miniature version of the time course of PTS that would be induced by a similar noise exposure in a person with normal hearing. It began to occur soon after the start of hearing aid use and its rate of development was slower than that which would occur in a person with normal hearing. The growth of PTS could be predicted from the estimated real ear output levels of the children’s hearing aids by means of the MPL combined with the logarithmic equation proposed by Kraak for predicting the effect of noise exposure on hearing.


2021 ◽  
Vol 15 ◽  
Author(s):  
Qian Li ◽  
Hong Li ◽  
Xiuting Yao ◽  
Conghui Wang ◽  
Haiqing Liu ◽  
...  

Noise-induced hearing loss (NIHL) is one of the most prevalent forms of acquired hearing loss, and it is associated with aberrant microglial status and reduced hippocampal neurogenesis; however, the nature of these associations is far from being elucidated. Beyond its direct effects on the auditory system, exposure to intense noise has previously been shown to acutely activate the stress response, which has increasingly been linked to both microglial activity and adult hippocampal neurogenesis in recent years. Given the pervasiveness of noise pollution in modern society and the important implications of either microglial activity or hippocampal neurogenesis for cognitive and emotional function, this study was designed to investigate how microglial status and hippocampal neurogenesis change over time following acoustic exposure and to analyze the possible roles of the noise exposure-induced stress response and hearing loss in these changes. To accomplish this, adult male C57BL/6J mice were randomly assigned to either a control or noise exposure (NE) group. Auditory function was assessed by measuring ABR thresholds at 20 days post noise exposure. The time-course profile of serum corticosterone levels, microglial status, and hippocampal neurogenesis during the 28 days following noise exposure were quantified by ELISA or immunofluorescence staining. Our results illustrated a permanent moderate-to-severe degree of hearing loss, an early but transient increase in serum corticosterone levels, and time-dependent dynamic alterations in microglial activation status and hippocampal neurogenesis, which both present an early but transient change and a late but enduring change. These findings provide evidence that both the stress response and hearing loss contribute to the dynamic alterations of microglia and hippocampal neurogenesis following noise exposure; moreover, noise-induced permanent hearing loss rather than noise-induced transient stress is more likely to be responsible for perpetuating the neurodegenerative process associated with many neurological diseases.


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Fabiola Paciello ◽  
Marco Rinaudo ◽  
Valentina Longo ◽  
Sara Cocco ◽  
Giulia Conforto ◽  
...  

Although association between hearing impairment and dementia has been widely documented by epidemiological studies, the role of auditory sensory deprivation in cognitive decline remains to be fully understood. To address this issue we investigated the impact of hearing loss on the onset and time-course of cognitive decline in an animal model of Alzheimer’s disease (AD), that is the 3×Tg-AD mice and the underlying mechanisms. We found that hearing loss induced by noise exposure in the 3×Tg-AD mice before the phenotype is manifested caused persistent synaptic and morphological alterations in the auditory cortex. This was associated with earlier hippocampal dysfunction, increased tau phosphorylation, neuroinflammation, and redox imbalance, along with anticipated memory deficits compared to the expected time-course of the neurodegenerative phenotype. Our data suggest that a mouse model of AD is more vulnerable to central damage induced by hearing loss and shows reduced ability to counteract noise-induced detrimental effects, which accelerates the neurodegenerative disease onset.


2015 ◽  
Vol 16 (1) ◽  
pp. 15-24
Author(s):  
Vance Gunnell ◽  
Jeff Larsen

Hearing thresholds and distortion product otoacoustic emissions were measured for teachers of vocal performance who were gathered for a national conference. Results showed mean audiometric thresholds to be consistent with noise induced hearing loss, more than what would be expected with normal aging. Years of instruction and age were considered as factors in the hearing loss observed. It was concluded that hearing conservation should be initiated with this group to help raise awareness and protect them from hearing loss due to occupational noise exposure.


1978 ◽  
Vol 11 (3) ◽  
pp. 723-740 ◽  
Author(s):  
Allan J. Heffler
Keyword(s):  

2020 ◽  
Vol 21 (12) ◽  
pp. 1216-1224
Author(s):  
Fatemeh Forouzanfar ◽  
Samira Asgharzade

Noise exposure (NE) has been recognized as one of the causes of sensorineural hearing loss (SNHL), which can bring about irreversible damage to sensory hair cells in the cochlea, through the launch of oxidative stress pathways and inflammation. Accordingly, determining the molecular mechanism involved in regulating hair cell apoptosis via NE is essential to prevent hair cell damage. However, the role of microRNAs (miRNAs) in the degeneration of sensory cells of the cochlea during NE has not been so far uncovered. Thus, the main purpose of this study was to demonstrate the regulatory role of miRNAs in the oxidative stress pathway and inflammation induced by NE. In this respect, articles related to noise-induced hearing loss (NIHL), oxidative stress, inflammation, and miRNA from various databases of Directory of Open Access Journals (DOAJ), Google Scholar, PubMed; Library, Information Science & Technology Abstracts (LISTA), and Web of Science were searched and retrieved. The findings revealed that several studies had suggested that up-regulation of miR-1229-5p, miR-451a, 185-5p, 186 and down-regulation of miRNA-96/182/183 and miR-30b were involved in oxidative stress and inflammation which could be used as biomarkers for NIHL. There was also a close relationship between NIHL and miRNAs, but further research is required to prove a causal association between miRNA alterations and NE, and also to determine miRNAs as biomarkers indicating responses to NE.


Author(s):  
David C. Byrne ◽  
Thais C. Morata

Exposure to industrial noise and the resulting effect of occupational hearing loss is a common problem in nearly all industries. This chapter describes industrial noise exposure, its assessment, and hearing disorders that result from overexposure to noise. Beginning with the properties of sound, noise-induced hearing loss and other effects of noise exposure are discussed. The impact of hearing disorders and the influence of other factors on hearing loss are described. Typically, noise-induced hearing loss develops slowly, and usually goes unnoticed until a significant impairment has occurred. Fortunately, occupational hearing loss is nearly always preventable. Therefore, this chapter gives particular attention to recommendations for measures to prevent occupational hearing loss such as engineering noise controls and hearing protection devices.


Author(s):  
Feifan Chen ◽  
Zuwei Cao ◽  
Emad M. Grais ◽  
Fei Zhao

Abstract Purpose Noise-induced hearing loss (NIHL) is a global issue that impacts people’s life and health. The current review aims to clarify the contributions and limitations of applying machine learning (ML) to predict NIHL by analyzing the performance of different ML techniques and the procedure of model construction. Methods The authors searched PubMed, EMBASE and Scopus on November 26, 2020. Results Eight studies were recruited in the current review following defined inclusion and exclusion criteria. Sample size in the selected studies ranged between 150 and 10,567. The most popular models were artificial neural networks (n = 4), random forests (n = 3) and support vector machines (n = 3). Features mostly correlated with NIHL and used in the models were: age (n = 6), duration of noise exposure (n = 5) and noise exposure level (n = 4). Five included studies used either split-sample validation (n = 3) or ten-fold cross-validation (n = 2). Assessment of accuracy ranged in value from 75.3% to 99% with a low prediction error/root-mean-square error in 3 studies. Only 2 studies measured discrimination risk using the receiver operating characteristic (ROC) curve and/or the area under ROC curve. Conclusion In spite of high accuracy and low prediction error of machine learning models, some improvement can be expected from larger sample sizes, multiple algorithm use, completed reports of model construction and the sufficient evaluation of calibration and discrimination risk.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1686
Author(s):  
Adelaida M. Celaya ◽  
Lourdes Rodríguez-de la Rosa ◽  
Jose M. Bermúdez-Muñoz ◽  
José M. Zubeldia ◽  
Carlos Romá-Mateo ◽  
...  

Insulin-like growth factor 1 (IGF-1) deficiency is an ultrarare syndromic human sensorineural deafness. Accordingly, IGF-1 is essential for the postnatal maturation of the cochlea and the correct wiring of hearing in mice. Less severe decreases in human IGF-1 levels have been associated with other hearing loss rare genetic syndromes, as well as with age-related hearing loss (ARHL). However, the underlying mechanisms linking IGF-1 haploinsufficiency with auditory pathology and ARHL have not been studied. Igf1-heterozygous mice express less Igf1 transcription and have 40% lower IGF-1 serum levels than wild-type mice. Along with ageing, IGF-1 levels decreased concomitantly with the increased expression of inflammatory cytokines, Tgfb1 and Il1b, but there was no associated hearing loss. However, noise exposure of these mice caused increased injury to sensory hair cells and irreversible hearing loss. Concomitantly, there was a significant alteration in the expression ratio of pro- and anti-inflammatory cytokines in Igf1+/− mice. Unbalanced inflammation led to the activation of the stress kinase JNK and the failure to activate AKT. Our data show that IGF-1 haploinsufficiency causes a chronic subclinical proinflammatory age-associated state and, consequently, greater susceptibility to stressors. This work provides the molecular bases to further understand hearing disorders linked to IGF-1 deficiency.


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