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Purpose: Exposure to noise can cause damage to both auditory and vestibular systems. The objective of this study is to evaluate how noise exposure affects the hearing and vestibular systems in individuals with noise-induced hearing loss (NIHL). Methods: This study included 80 subjects (40 subjects with NIHL, and 40 controls), between 26 and 59 years old. For hearing assessment, pure-tone audiometry, extended high-frequency audiometry, tympanometry, acoustic reflex threshold, and distortion product otoacoustic emission tests were used; for vestibular assessment, the cervical and ocular vestibular evoked myogenic potentials tests were used. Results: Statistically significant differences were found between the two groups in 3 to 6 kHz frequency thresholds; in extended high-frequency audiometry tests, there were also significant differences between groups at all frequencies from 9.5 to 16 kHz. The cervical and ocular vestibular evoked myogenic potentials thresholds were significantly higher and N1-P1 amplitudes were significantly lower in the NIHL group. Conclusion: Noise can lead to damage to both auditory and vestibular functions. Therefore, audiological assessments and vestibular evoked myogenic potentials could be clinically useful for examining patients with NIHL.
Keywords: audiometry, hearing, noise-induced hearing loss, vestibular evoked myogenic potentials
How to cite this article:
Noise is defined as an undesirable and disturbing sound. Noise-induced hearing loss (NIHL) has been a well-known health problem for many years,[1],[2] and is one of the most common causes of hearing loss in adults.[3]
Exposure to excessive noise is one of the most potent causes of cochlear damage that can lead to permanent hearing loss.[4],[5],[6] The loss of auditory sensory cells in the cochlea, mostly the outer hair cells, is the defining pathogenic feature of NIHL.[7] Moreover, the synaptic excitotoxicity and oxidative stress are the potential reasons for morphological changes in the cochlea.[8],[9] Therefore, noise exposure is likely to cause damage to the hearing function. Considering this, our study assessed the effect of noise exposure on hearing function in participants with NIHL.
Noise exposure can also cause damage to the vestibular system,[2],[10],[11],[12] particularly to the otolith organs (both the saccule and utricle), which are more susceptible to noise-induced deterioration.[2],[13] The possibility of vestibular damage due to noise exposure is predominantly related to the anatomical proximity of the hearing and vestibular sensory organs, and the co-arterial vascularization between these sensory organs.[2],[13],[14] However, there is much less information in the literature about the impact of noise on the vestibular system. Previous studies have reported prolonged latencies, increased thresholds, and decreased amplitudes in cervical vestibular evoked myogenic potentials (c-VEMPs), by assessing the sacculo-collic reflex in individuals with NIHL.[15],[16],[17],[18] In addition, the effects of noise exposure on the utricular macula have not yet been entirely identified using ocular vestibular evoked myogenic potentials (o-VEMPs). As a result, the primary aim of this study is to examine the impact of noise exposure on the vestibular function in participants with NIHL.
Materials and methodsParticipants
The study included 40 adults (2F/38M) with NIHL and 40 controls (12F/28M) with normal hearing. The age range was from 26 to 59 years old (mean age = 41.73 y, SD = 1.31). The mean age of the NIHL group was 43.48 ± 1.18 (28 to 58) years and for the control group it was 39.98 ± 1.45 (26 to 59) years. There were no age differences between the groups computed by the independent sample t test (p = 0.06).
This study is a case-control study. The case group (NIHL group) included participants with sensorineural hearing loss, which was bilateral (symmetrical) at high frequencies (mostly at 4 kHz), and who had a history of working in noisy environments. The participants with NIHL had hearing thresholds of 30 dB HL and above at 4 kHz on pure-tone audiometry (PTA). They also had notches that were observed at one or more of the frequencies, 3, 4 or 6 kHz.[19] In line with the characteristics of NIHL,[19] the notches improved at 8 kHz; thus, NIHL usually appears as a “V” shape in the audiogram in the NIHL group in our study.
The control group consisted of healthy participants with normal hearing and no history of working in a noisy environment. Anyone who had ear malformations/disorders, neurological or systemic disease, or history of ototoxic/vestibulotoxic drug use were excluded from the study.
As the population of this study included people who had worked in noisy environments, most of the participants with NIHL were male (2F/38M). Thus, there is an unbalanced distribution of the sexes between the two groups. Such a distribution of sexes is a commonly seen disadvantage in existing studies related to NIHL[14],[16],[17] because participants have included workers with noisy jobs, such as in factories, and who are thus more likely to be male.
Ethics Committee Approval:
Ethical approval was obtained from Dokuz Eylul University Non-interventional Research Ethics Committee; the decision number is 2018/16-35, dated 28.06.2018 and numbered 4080–GOA. The study was conducted in accordance with the Declaration of Helsinki (2013)[20] and all participants provided informed written consent. The results of audiological and vestibular assessments were collected from the Hearing-Speech-Balance Unit, Dokuz Eylul University.
Materials
XXXX1) Hearing Screening:
An Otometrics Madsen Zodiac tympanometer was used to assess middle ear function and acoustic reflex thresholds (ARTs) according to the Jerger classification.[21] Participants who had a Type A tympanogram and who had ipsilateral and contralateral reflexes were recruited for this study (-100 to +50 daPa).
PTA, speech audiometry, and extended high-frequency audiometry (EHFA) tests were performed using Otometrics Madsen Astera.[2]. Air conduction (AC) thresholds were measured with TDH-39 headphones (from 125 to 8000 Hz), and for EHFA (9500 to 16000 Hz) Sennheiser HDA 300 headphones were used. Bone conduction (BC) thresholds were obtained (from 500 to 4000 Hz) using a B-71 bone vibrator. Hearing loss was determined using the Goodman classification.[22] Distortion product otoacoustic emissions (DPOAEs) were measured using an Otometrics Madsen Capella[2] at 500 to 8000 Hz, with a 65/55 dB stimulus to compare signal-to-noise ratios (SNRs) (f1/f2 = 1.22, octave = 2 pts/oct).[23]
XXX2) Cervical and Ocular Vestibular Evoked Myogenic Potentials (c-VEMPs and o-VEMPs):
The c-VEMPs and o-VEMPs were recorded in a sitting position, using ICS Chartr EP 200 (GN Otometrics, Schaumburg, IL) with (ER 3A/5A, 300 ohms) insert earphones. Latencies and P1-N1 amplitude were calculated based on the 95 dBnHL stimulus level.[24],[25]
c-VEMPs
Electrode placement
Two active electrodes were placed at the upper third of the right and left sternocleidomastoid (SCM) muscles. The negative electrode was placed on the sternoclavicular junction as a reference electrode, and the ground electrode was placed at the midpoint of the forehead. The two electrodes used for electromyography (EMG) monitoring were placed at the midpoints of the right and left SCM muscles, just below the active electrodes.[26] EMG muscle activity was defined in μV and a response was accepted within 50–100 μV.
Recording
The first positive wave observed during recording was marked as P13 (approximately at 13–15 milliseconds), whereas the following negative wave was marked as N23 (approximately at 20–23 milliseconds). The c-VEMPs response was obtained from the ipsilateral SCM muscle. The c-VEMPs EMG hand monitor, which is used to display EMG responses, was given to the participants. They were then instructed to turn their head toward the side opposite to the stimuli as soon as the stimuli were heard and to maintain their head position until the stimuli ended.
o-VEMPs
Electrode placement
The active electrodes were placed 3 to 4 mm below both infraorbital rims, and the reference electrodes were placed 1 to 2 cm below the active electrodes. The ground electrode was placed in the middle of the forehead.[26]
Recording
The first observed negative wave recorded was marked as N1 (approximately at 9–12 milliseconds), whereas the following positive wave was marked as P1 (approximately at 14–16 milliseconds). As the amplitudes of the ipsilateral o-VEMP responses are generally lower and the latencies are later, the recording was obtained from the contralateral eye muscle.[24] Participants were instructed to identify a point on the ceiling and look at this point when the stimuli came, and to remain in a fixed position until the stimuli stopped.
The stimulus and recording parameters for the c-VEMPs and o-VEMPs tests are detailed in [Table 1].]
Statistical Methods
The SPSS 23.0 program was used for the data analysis. The thresholds for EHFA and both c-VEMPs and o-VEMPs amplitudes and latencies were evaluated with independent sample t tests to investigate differences between the NIHL group and the control group. A Mann–Whitney U test or Wilcoxon Signed-rank test was conducted when the data did not comply with a normal distribution. All analyses were conducted at a 95% confidence interval with a significance level of 0.05. Pearson correlation analyses were performed to define exploratory analyses.
ResultsAuditory Findings
All participants in the NIHL group were exposed to occupational noise. The mean duration of exposure to noise was 157.77 ± 20.07 months in the NIHL group. The duration of exposure ranged from 5 months to 420 months.
The mean value of audiometric thresholds in both groups for the PTA and EHFA is demonstrated in [Figure 1]. Significantly higher PTA thresholds were found at 3, 4 and 6 kHz (p < 0.01), whereas significantly higher EHFA thresholds from 9500 to 16000 Hz (p < 0.05) were found in the NIHL group than in the control group.
Figure 1 The mean value of the audiometric thresholds (dB HL) at each frequency for PTA and EHFA in both groups.For DPOAEs, in the NIHL group, 20 (50%) participants had a DPOAE response, whereas 20 (50%) had no response. In the control group, 35 (87.5%) participants had a DPOAE response, whereas five (12.5%) had no response. Analyses were performed on the present DPOAE responses for both groups. There were significantly higher SNRs for the NIHL group compared to the control group from 2000 Hz to 8000 Hz (p < 0.01).
Vestibular Findings
c-VEMPs:
According to [Table 2], the c-VEMPs thresholds were significantly higher (p < 0.01) and c-VEMPs P1-N1 amplitudes were significantly smaller in the NIHL group than in the control group (p < 0.01). There were no significant differences in the c-VEMPs latencies (p > 0.05).
o-VEMPs:
As can be seen in [Table 3], o-VEMPs thresholds were significantly higher in the NIHL group than in the control group (p < 0.01), whereas o-VEMPs N1-P1 amplitudes were significantly smaller in the NIHL group than in the control group (p < 0.01). Moreover, o-VEMPs P1 latencies were significantly longer in the NIHL group than in the control group (p < 0.05). There were no significant differences in the o-VEMPs N1 latencies and N1-P1 latencies in both groups.
As an exploratory analysis, the relationship between the duration of the noise exposure and VEMPs responses were investigated. There was no significant correlation between the duration of noise exposure and any of the responses obtained from the c-VEMPs and o-VEMPs tests (p > 0.05). Additionally, the correlation between DPOAE SNRs at each frequency (from 500 to 8000 Hz) and VEMPs responses were done. There was a negative, moderate correlation between the both c-VEMPs and o-VEMPs thresholds and DPOAE SNRs measured at 2000 Hz (r = -0.37, p = 0.01), 3000 Hz (r = -0.37, p = 0.01), and 4000 Hz (r = -0.47, p < 0.01).
DiscussionIn this study, we mainly focused on the assessment of the vestibular function, on which the effect of noise exposure still remains unclear in the current literature. For both c-VEMPs and o-VEMPs tests, we found significantly higher thresholds, lower amplitudes, and delayed latencies in the NIHL group compared to the control group. Additionally, this study investigated to what extent the hearing function might be affected by NIHL. The study also provides new insights into the literature by presenting the c-VEMPs and o-VEMPs tests and audiological assessments together, and revealing the effect of noise on both hearing and vestibular functions.
Consistent with the existing studies, our study confirms that the highest hearing threshold in the NIHL group was found at 4 kHz, supporting the theory that high-frequency (especially 4 kHz) regions in the cochlea are likely to be more sensitive to noise-induced damage.[16],[28] We also showed significantly higher EHFA thresholds at all frequencies in the NIHL group, indicating similarities with previous studies.[29],[30] The reason for the high-frequency regions of the cochlea (above 4 kHz) being the most affected is the degeneration that occurs predominantly in the 9 to 13 mm region of the cochlea, which is specific to 4 kHz.[14]
As mentioned previously, VEMPs studies of participants with NIHL are limited in the literature. The c-VEMPs test assesses the saccule and inferior vestibular nerve, whereas the o-VEMPs test assesses the utricle and superior vestibular nerve.[31] Previous research has indicated that c-VEMPs responses are reduced or absent with increasing hearing thresholds, suggesting the saccule is likely to be affected by noise exposure.[15],[17] Subsequently, Tseng and Young (2013) demonstrated more delayed or absent c-VEMPs responses compared with o-VEMPs responses in the NIHL group. Similarly, our findings showed that participants in the NIHL group had more absent c-VEMPs responses than o-VEMPs responses, implying that o-VEMPs could be affected less than c-VEMPs.[16] Collectively, more abnormal responses in the c-VEMPs test suggest that the pars inferior (cochlea and saccule) may be more impacted by exposure to noise compared to the pars superior (utricular and semicircular canals).[9],[16]
The presented study is crucial due to the assessment of both c-VEMPs and o-VEMPs because previous studies are limited in terms of o-VEMPs in participants with NIHL. More recently, Ismail et al. (2021) performed c-VEMPs and o-VEMPs tests on individuals with NIHL and a control group. They reported similar findings to our study, showing lower amplitudes and delayed latencies in both c-VEMPs and o-VEMPs tests for the NIHL group.[2]. As for the underlying mechanisms, these abnormal results in both c-VEMPs and o-VEMPs could stem from mechanical and metabolic damage, such as toxic-free radicals, ischemia, and metabolic overload.[2],[14]
Extending the findings of Ismail and colleagues (2021), our study also provides further knowledge on how amplitudes and latencies in both c-VEMPs and o-VEMPs tests can be used separately for the quantifying of c-VEMPs and o-VEMPs. More information obtained via both c-VEMPs and o-VEMPs would help establish a greater degree of accuracy in relation to the effect of noise on the vestibular function. Hence, the presented results suggest that the saccule and inferior vestibular nerve, as evaluated by c-VEMPs, and the utricle and superior vestibular nerve, as evaluated by o-VEMPs, are likely to be affected by noise exposure.
Nevertheless, the current research was not specifically designed to evaluate factors related to the spectrum of noise exposure, and the exact amount of hearing protection device usage in the NIHL group. Further work is required to observe the potential effects of these factors on both hearing and vestibular functions in participants with NIHL.
ConclusionOur findings lead us to conclude that noise can cause damage to the vestibular function as well as to the auditory system. In particular, c-VEMPs and o-VEMPs tests are influential for observation of the effect of noise on the vestibular function. As a result, it can be recommended that hearing assessment including EHFAs, and both cervical and ocular VEMPs tests should to be used when assessing individuals with NIHL.
Financial support and sponsorship
Nil.
Conflicts of interest
No conflict of interest.
References
Correspondence Address:
Gunay Kirkim
İnciraltı mahallesi, Mithatpaşa caddesi, Dokuz Eylül Üniversitesi Araştırma Uygulama Hastanesi, İşitme Konuşma Denge Ünitesi, No:1606 Balçova/İZMİR/TÜRKİYE
Türkiye
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/nah.nah_74_22
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