scholarly journals Sensorineural Hearing Loss Due to Exposure of Noisy Trains on Populations Around Turirejo Train Railroad Cross

2020 ◽  
Vol 12 (1) ◽  
pp. 59
Author(s):  
Diana Kusuma Wardhani ◽  
Jojok Mukono Mukono

Introduction: As one of the preferred modes of land transportation, the frequency of train services was very high. One of the negative impacts arising from train activity was noise. The high noise intensity of the train causes hearing loss. Method: This study aims to analyze the differences in the incidence of hearing loss in 2 groups of residents in Turirejo Lawang Malang. This research used the observational method and the data were analyzed descriptive qualitative. A total of 20 people were selected as respondents by purposive sampling. Noise intensity was measured by Sound Level Meter and audiometric measurements were examined at SIMA Malang Laboratory. Result and Discussion: The prevalence of sensorineural hearing loss was more common in residents whose homes at 3-7 m away from the railroad tracks. In addition, residents who lived at least 15 years at a distance of 3-7 m also experienced more hearing loss. One cause of hearing loss is due to exposure to high noise and for a long time and will damage the hair cells in the cochlea, causing hearing loss. If noise exposure continues and for a long period of time damage to hair cells will be permanent and cannot return to normal. Conclusion: There needs to be a policy from the government in determining the minimum limit of the distance of the house to the railroad tracks. In addition, it is necessary to install a barrier near people’s homes to reduce noise.

2021 ◽  
Vol 15 ◽  
Author(s):  
Lingna Guo ◽  
Wei Cao ◽  
Yuguang Niu ◽  
Shuangba He ◽  
Renjie Chai ◽  
...  

Inner ear hair cells (HCs) and spiral ganglion neurons (SGNs) are the core components of the auditory system. However, they are vulnerable to genetic defects, noise exposure, ototoxic drugs and aging, and loss or damage of HCs and SGNs results in permanent hearing loss due to their limited capacity for spontaneous regeneration in mammals. Many efforts have been made to combat hearing loss including cochlear implants, HC regeneration, gene therapy, and antioxidant drugs. Here we review the role of autophagy in sensorineural hearing loss and the potential targets related to autophagy for the treatment of hearing loss.


2020 ◽  
pp. 775-785
Author(s):  
L HE ◽  
J-Y GUO ◽  
K LIU ◽  
G-P WANG ◽  
S-S GONG

Sensorineural hearing loss and vertigo, resulting from lesions in the sensory epithelium of the inner ear, have a high incidence worldwide. The sensory epithelium of the inner ear may exhibit extreme degeneration and is transformed to flat epithelium (FE) in humans and mice with profound sensorineural hearing loss and/or vertigo. Various factors, including ototoxic drugs, noise exposure, aging, and genetic defects, can induce FE. Both hair cells and supporting cells are severely damaged in FE, and the normal cytoarchitecture of the sensory epithelium is replaced by a monolayer of very thin, flat cells of irregular contour. The pathophysiologic mechanism of FE is unclear but involves robust cell division. The cellular origin of flat cells in FE is heterogeneous; they may be transformed from supporting cells that have lost some features of supporting cells (dedifferentiation) or may have migrated from the flanking region. The epithelial-mesenchymal transition may play an important role in this process. The treatment of FE is challenging given the severe degeneration and loss of both hair cells and supporting cells. Cochlear implant or vestibular prosthesis implantation, gene therapy, and stem cell therapy show promise for the treatment of FE, although many challenges remain to be overcome.


F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 927 ◽  
Author(s):  
M Charles Liberman

The classic view of sensorineural hearing loss has been that the primary damage targets are hair cells and that auditory nerve loss is typically secondary to hair cell degeneration. Recent work has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of the synaptic connections between hair cells and the auditory nerve. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained a “hidden hearing loss” for two reasons: 1) the neuronal cell bodies survive for years despite loss of synaptic connection with hair cells, and 2) the degeneration is selective for auditory nerve fibers with high thresholds. Although not required for threshold detection when quiet, these high-threshold fibers are critical for hearing in noisy environments. Research suggests that primary neural degeneration is an important contributor to the perceptual handicap in sensorineural hearing loss, and it may be key to the generation of tinnitus and other associated perceptual anomalies. In cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from surviving auditory neurons and re-establishment of their peripheral synapses; thus, treatments may be on the horizon.


Author(s):  
Melanie Holmgren ◽  
Lavinia Sheets

Hair cells are the mechanosensory receptors of the inner ear and can be damaged by noise, aging, and ototoxic drugs. This damage often results in permanent sensorineural hearing loss. Hair cells have high energy demands and rely on mitochondria to produce ATP as well as contribute to intracellular calcium homeostasis. In addition to generating ATP, mitochondria produce reactive oxygen species, which can lead to oxidative stress, and regulate cell death pathways. Zebrafish lateral-line hair cells are structurally and functionally analogous to cochlear hair cells but are optically and pharmacologically accessible within an intact specimen, making the zebrafish a good model in which to study hair-cell mitochondrial activity. Moreover, the ease of genetic manipulation of zebrafish embryos allows for the study of mutations implicated in human deafness, as well as the generation of transgenic models to visualize mitochondrial calcium transients and mitochondrial activity in live organisms. Studies of the zebrafish lateral line have shown that variations in mitochondrial activity can predict hair-cell susceptibility to damage by aminoglycosides or noise exposure. In addition, antioxidants have been shown to protect against noise trauma and ototoxic drug–induced hair-cell death. In this review, we discuss the tools and findings of recent investigations into zebrafish hair-cell mitochondria and their involvement in cellular processes, both under homeostatic conditions and in response to noise or ototoxic drugs. The zebrafish lateral line is a valuable model in which to study the roles of mitochondria in hair-cell pathologies and to develop therapeutic strategies to prevent sensorineural hearing loss in humans.


2015 ◽  
Vol 273 (5) ◽  
pp. 1099-1105 ◽  
Author(s):  
Lisa Aarhus ◽  
Kristian Tambs ◽  
Per Nafstad ◽  
Eskil Bjørgan ◽  
Bo Engdahl

2019 ◽  
Vol 6 (2) ◽  
pp. 107-111
Author(s):  
Rohmatullah Subekti ◽  
Muyassaroh Muyassaroh ◽  
Zulfikar Naftali

Latar belakang: Kebisingan di tempat kerja seringkali menjadi problem bagi tenaga kerja. Paparan bising dapat menyebabkan gangguan auditori yaitu noise-induced hearing loss (NIHL) dan gangguan non auditori berupa gangguan kejiwaan seperti depresi, kecemasan serta stress. Tujuan: Untuk mengetahui hubungan antara kebisingan terhadap kejadian gangguan pendengaran dan kejiwaan pada pekerja terpapar bising. Metode: Penelitian ini bersifat deskriptif analitik dengan design belah lintang. Tingkat kebisingan diukur dengan menggunakan alat sound level meter (SLM), gangguan pendengaran dinilai dari hasil audiometri, gangguan kejiwaan dinilai dari jawaban kuesioner Depression Anxiety Stress Scale 42 (DASS 42) dari WHO. Analisis data dengan uji chi square. Hasil : Data yang didapatkan dari 326 sampel menunjukkan bahwa 179 (54.9%) subjek mempunyai masa kerja lebih dari 10 tahun dan 147 (45.1%) subjek mempunyai masa kerja kurang dari 10 tahun. Sebanyak 51 (15.6%) pekerja mengalami NIHL dan 154 (47.2%) pekerja mengalami gangguan jiwa. Terdapat hubungan antara lama paparan bising (P= 0.000) dan intensitas kebisingan (P= 0.022) terhadap kejadian NIHL, dan intensitas kebisingan terhadap derajat keparahan depresi (P= 0.007) Kesimpulan: Lama paparan dan intensitas bising berhubungan dengan gangguan pendengaran sedangkan intensitas bising berhubungan dengan derajat keparahan depresi. Dibandingkan dengan intensitas bising, lama paparan bising mempunyai hubungan yang lebih besar terhadap kejadian NIHL. Kata kunci : Kebisingan, NIHL, depresi, ansietas, stres   Background: Noise can raise significant issues in the workplaces. It can affect either auditory disturbance called Noise Induce Hearing Loss (NIHL) or non-auditory disturbance involving psychiatric disorders such as depression, anxiety and stress. Objective: To examine the relationship between noise in the workplace and the incidence of hearing impairment and psychiatric disorders. Method: The study design is analitic desciptive with cross-sectional approach. The noise level was measured with sound-level-metre (SLM), hearing disorders was assessed with audiometric and psychiatric disorder was assessed with Depression Anxiety Stress Scale 42 (DASS 42). The data were analized with chi square. Results : A total of 326 workers were sampled during this study showing that  179 (54.9%) workers have worked over 10 years and 179 (54.9%) workers have worked less than 10 years. It was found that 51 (15.6%) workers suffered from NHIL and 154 (47.2%) workers suffered from mental disorders. A significant relationship was found between the incidence of NIHL and years of noise exposure (P= 0.000) and noise intensity (P= 0.022). A significant relationship was found between noise intensity and depression severity (P= 0.007) Conclusion: The years of noise exposure and noise intensity were related to haring disorders. The noise intensity were related to the depression severity. In comparison with noise intensity, a stronger relationship was found between years of noise exposure and the incidence of NIHL. Keywords : Noise, NIHL, depression, anxiety, stress


2018 ◽  
Vol 01 (02) ◽  
pp. 089-093
Author(s):  
Raghul Sekar ◽  
Arun Alexander ◽  
Nagarajan Krishnan

Abstract Background Sensorineural hearing loss is a condition with several etiologies and varies with the age of the individual. Carotid–cochlear interval is the minimum distance between basal turn of cochlea and the genu of petrous part of internal carotid artery. It is believed that constant pulsations from carotid can cause fluid pressure changes within the cochlea leading to damage to hair cells causing hearing loss. Objective To study the correlation between carotid–cochlear interval and degree of hearing loss at different frequencies in patients with sensorineural deafness and compare this interval with normal subjects. Methods Seventy cases with sensorineural hearing loss between 18 and 60 years undergoing HRCT temporal bone were grouped together and 70 cases with normal hearing undergoing CT nose and paranasal sinuses were grouped together. Carotid–cochlear interval measured in both the groups was correlated with the degree and frequency of hearing loss and compared with normal subjects. Results The mean carotid–cochlear interval in sensorineural hearing loss and in normal subjects was found to be 1.30 + 0.68 (SD) mm and 1.83 + 0.74 (SD) mm, respectively with p < 0.001. The coefficient of correlation between carotid–cochlear interval and pure tone average in patients with sensorineural deafness was r = −0.740 with p-value < 0.001. Conclusion Carotid–cochlear interval is significantly low in patients with sensorineural hearing loss and bears a strong negative correlation with the degree of hearing loss at mid- and high-frequency ranges. Thus we hypothesize that pulsations from carotid artery cause damage to hair cells in the organ of Corti producing audiological symptoms such as hearing loss.


CoDAS ◽  
2013 ◽  
Vol 25 (3) ◽  
pp. 224-228 ◽  
Author(s):  
Kelly Martins ◽  
Marília Fontenele ◽  
Silva Câmara ◽  
Edi Lúcia Sartorato

PURPOSE: This study aimed to correlate probable predisposing factors for sensorineural hearing loss in elderly by investigating the audiologic characteristics and frequency of mutations in genes considered responsible for non-syndromic hearing loss. METHODS: Sixty elderly patients were separated into two groups: the Case Group, composed of 30 individuals, 21 females and nine males, all 60 years old or older and presenting diagnoses of sensorineural hearing loss, and the Control Group, composed of 30 elderly individuals matched to the experimental group by age and gender, presenting normal hearing. The patients underwent anamnesis and pure tone audiometry in frequencies of 250, 500, 1000, 2000, 3000, 4000 and 6000 Hz. Blood samples were collected from each patient for analysis of mutations in nuclear and mitochondrial genes related to non-syndromic sensorineural hearing loss. RESULTS: It was observed a greater tendency to noise exposure and consumption of alcohol in the Case Group. The statistically significant symptoms between the groups were tinnitus and hearing difficulty in several situations as: silent environment, telephone, television, sound location and in church. All the individuals of Case Group presented sensorineural and bilateral hearing loss. The symmetry and progression of the hearing impairment were also statistically significant between the groups. No genetic mutations were identified. CONCLUSION: The most reported symptoms were communication difficulties and tinnitus. The predominant auditory characteristics included sensorineural, bilateral, progressive and symmetrical hearing loss. It was not evidenced a relationship between sensorineural hearing loss in elderly and genes considered responsible for non-syndromic hearing loss as no genetic mutation was found in this study.


Author(s):  
V. B. Pankova ◽  
M. F. Vilk ◽  
N. A. Daikhes

Modern, problematic issues of prevalence, structure and high rates of hearing loss from exposure to industrial noise in the form of clinical stages of chronic sensorineural hearing loss are reflected. The possibility of harmonization of the List of occupational diseases of the ICD 10th and 11th reviews in hearing impairment is discussed


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