Comparing the electrophysiological effects of traumatic noise exposure between rodents

Noise-induced hearing deficits are important health problems in the industrialized world. As the underlying physiological dysfunctions are not well understood, research in suitable animal models is urgently needed. Three rodent species (Mongolian gerbil, rat and mouse) were studied to compare the temporal dynamics of noise-induced hearing loss after identical procedures of noise exposure. Auditory brainstem responses (ABRs) were measured before, during and up to eight weeks after noise exposure for threshold determination and ABR waveform analysis. Trauma induction with stepwise increasing sound pressure level was interrupted by five interspersed ABR measurements. Comparing short- and long-term dynamics underlying the following noise-induced hearing loss revealed diverging time courses between the three species. Hearing loss occurred early on during noise exposure in all three rodent species at or above trauma frequency. Initial noise level (105 dB SPL) was most effective in rats while the delayed level-increase to 115 dB SPL affected mice much stronger. Induced temporary threshold shifts in rats and mice were larger in animals with lower pre-trauma ABR thresholds. The increase in activity (gain) along the auditory pathway was derived by comparing the amplitudes of short- and long-latency ABR waveform components. Directly after trauma, significant effects were found for rats (decreasing gain) and mice (increasing gain) while gerbils revealed high individual variability in gain changes. Taken together, our comparative study revealed pronounced species-specific differences in the development of noise-induced hearing loss and the related processing along the auditory pathway.

Screening for Noise-Induced Hearing Loss among Palm Oil Mill Workers in Peninsular Malaysia: A Comparison across Noise Exposure Levels

Background: Palm oil mill workers in Malaysia are exposed to hazardous levels of noise in the workplace, and thus are at risk of developing noise-induced hearing loss (NIHL). In 2019, Malaysia introduced a new noise regulation, which reduced the level of permissible noise exposure. Objectives: This study aims to determine the prevalence of NIHL among palm oil mill workers based on screening data and assess the effects of different noise exposure levels on NIHL. Methods: A cross-sectional study was conducted by analyzing data from noise risk assessment reports of selected mills and screening audiometric data from workers. NIHL was defined as bilateral high-frequency hearing loss. Results: The overall NIHL prevalence was 50.8%. Noise exposure level and age were significant predictors of NIHL among the workers. The risk of developing NIHL was high even for workers who were not categorized in the high-risk group. Conclusions: In view of the findings, a precautionary approach is needed when evaluating the risk of NIHL in the study population. Vulnerable groups of workers must be protected from occupational noise hazards through the implementation of effective hearing conservation programs in the workplace.

TMT-Based Quantitative Proteomics Reveals Cochlear Protein Profile Alterations in Mice with Noise-Induced Hearing Loss

Noise-induced hearing loss (NIHL) is a global occupational disease affecting health. To date, genetic polymorphism studies on NIHL have been performed extensively. However, the proteomic profiles in the cochleae of mice suffering noise damage remain unclear. The goal of this current study was to perform a comprehensive investigation on characterizing protein expression changes in the cochlea based on a mouse model of NIHL using tandem mass tag (TMT)-labeling quantitative proteomics, and to reveal the potential biomarkers and pathogenesis of NIHL. Male C57BL/6J mice were exposed to noise at 120 dB SPL for 4 h to construct the NIHL mouse model. The levels of MDA and SOD, and the production of proinflammatory cytokines including TNF-α and IL-6 in the mice cochleae, were determined using chemical colorimetrical and ELISA kits. Moreover, differentially expressed proteins (DEPs) were validated using Western blotting. The mouse model showed that the ABR thresholds at frequencies of 4, 8, 12, 16, 24 and 32 kHz were significantly increased, and outer hair cells (HCs) showed a distinct loss in the noise-exposed mice. Proteomics analysis revealed that 221 DEPs were associated with NIHL. Bioinformatics analysis showed that a set of key inflammation and autophagy-related DEPs (ITGA1, KNG1, CFI, FGF1, AKT2 and ATG5) were enriched in PI3K/AKT, ECM-receptor interaction, and focal adhesion pathways. The results revealed that the MDA level was significantly increased, but the activity of SOD decreased in noise-exposed mice compared to the control mice. Moreover, TNF-α and IL-6 were significantly increased in the noise-exposed mice. Western blotting revealed that the expression levels of ITGA1, KNG1, and CFI were upregulated, but FGF1, AKT2, and ATG5 were significantly downregulated in noise-exposed mice. This study provides new scientific clues about the future biomarkers and pathogenesis studies underlying NIHL. Furthermore, the findings suggest that the validated DEPs may be valuable biomarkers of NIHL, and inflammation and autophagy may be pivotal mechanisms that underlie NIHL.

OCCUPATIONAL NOISE INDUCED HEARING LOSS: IT’S FREQUENCY & RISK FACTORS

Objective: To determine the frequency and risk factors of occupational noise induced hearing loss. Study Design: Cross sectional study. Place and Duration of Study: Dispensary Unit of Jaith Bhuta Sugar Mill near Rahim Yar Khan, Southern Punjab.from Aug 2017 to Jan 2018. Methodology: This study was conducted using nonprobability consecutive sampling. n=300 workers of bothgenders aged 18-40 years were assessed. Basic demographic parameters, otoscopic examination and Pure Tone Audiometry were used for data collection. The Data was analyzed by using SPSS version 21. Results: Study included 215 (71.7%) males and 85 (28.3%) females with male to female ratio of 2.53: 1 and meanage of 28.34 ± 4.61 years. The frequency rate of hearing impairment (HI) was 90 (30%) out of 300 respondents inthis study. Out of 70 (100%) of respondents were affected with duration of job of 6-10 years. There was significant association between gender, age, education, duration of noise exposure with occupational noise induced hearing loss with p-value <0.001. Conclusion: There was high frequency of occupational noise induced hearing loss (ONIHL) with significantrisk factors being level and duration of exposure to noise (ETN), age, gender, education and hearing protectivedevices (HPD)’s.

Development of a Training Software to Improve Speech- in-Noise Perception in the Elderly with Noise-Induced Hearing Loss

Background and Aim: The incidence of noise-induced hearing loss (NIHL) is increasing rapidly worldwide. It has been shown that the long-term exposure to noise leads to permanent hearing loss. There is currently no treatment for NIHL and it is mainly managed by preventive measures. This study aimed to develop a training software to improve speech-in-noise (SIN) perception in the elderly suffering from mild-to-moderate NIHL due to temporal fine structure (TFS) damage. Methods: This is a non-randomized clinical trial conducted on 8 older men aged 60-75 years (Mean age = 68 ± 4.5 years) with mild-to-moderate NIHL at high frequencies (43.75±6.0 dBHL) with at least for five years of work in noisy environment. They received rehabilitation using a researcher-developed training software targeted TFS for five weeks. To assess the efficiency of the training software, the signal-to-noise ratio for 50% correct scores (SNR-50%) was calculated using the word-in-noise test before and after the trial. Results: The SNR-50% improved significantly in all participants from 13±2.63 dB to 6.10±2.85 dB (p<0.001). In the multiple linear regression model, the rehabilitation by the training software predicted 68% of improvement in SNR-50% (coefficient of determination=0.676). Conclusion: Rehabilitation by the training software developed based on TFS can improve SIN. perception in the elderly with NIHL.

Changes in the spatiotemporal pattern of spontaneous activity across a cortical column after noise trauma

In the auditory modality, noise trauma has often been used to investigate cortical plasticity as it causes cochlear hearing loss. One limitation of these past studies, however, is that the effects of noise trauma have been mostly documented at the granular layer, which is the main cortical recipient of thalamic inputs. Importantly, the cortex is composed of six different layers each having its own pattern of connectivity and specific role in sensory processing. The present study aims at investigating the effects of acute and chronic noise trauma on the laminar pattern of spontaneous activity in primary auditory cortex of the anesthetized guinea pig. We show that spontaneous activity is dramatically altered across cortical layers after acute and chronic noise-induced hearing loss. First, spontaneous activity was globally enhanced across cortical layers, both in terms of firing rate and amplitude of spike-triggered average of local field potentials. Second, current source density on (spontaneous) spike-triggered average of local field potentials indicates that current sinks develop in the supra- and infragranular layers. These latter results suggest that supragranular layers become a major input recipient and that the propagation of spontaneous activity over a cortical column is greatly enhanced after acute and chronic noise-induced hearing loss. We discuss the possible mechanisms and functional implications of these changes.