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|Year : 2022
: 24 | Issue : 114 | Page
|Effects of Noise and Chemical Exposure on Peripheral and Central Auditory Pathways in Normal-hearing Workers
Júlio CS Trabanco1, Bruno Morita1, Carla Gentile Matas1, Karina Mary de Paiva2, Renata R Moreira3, Seisse GG Sanches1, Alessandra G Samelli1
1 Department of Physical Therapy, Speech-language Pathology and Audiology, and Occupational Therapy, Faculty of Medicine (FMUSP), University of São Paulo, Brazil
2 Department of Speech-language Pathology and Audiology, Federal University of Santa Catarina (UFSC), Florianópolis, Brazil
3 Audiological Service, University Hospital, University of São Paulo, Brazil
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|Date of Submission||15-Feb-2022|
|Date of Decision||18-May-2022|
|Date of Acceptance||02-Jun-2022|
|Date of Web Publication||16-Sep-2022|
Objectives: To assess the effects of noise and chemical exposure on peripheral and central auditory pathways in normal-hearing workers exposed to chemicals or high noise levels and compare the groups with each other and with workers not exposed to either of these agents. Methods: A total of 54 normal-hearing workers were divided into three groups (chemical, noise, control) and submitted to the following assessments: conventional and extended high-frequency pure-tone audiometry; transient and distortion-product otoacoustic emissions, the inhibitory effect of the efferent auditory pathway; and Staggered Spondaic Word (SSW) and Pitch Pattern Sequence (PPS) test. Results: There were no significant differences between the groups in extended high-frequency hearing thresholds. Significantly lower amplitudes were observed in the noise group for otoacoustic emissions. There were significantly more absences of the inhibitory effect of the efferent system in the noise group. There was no difference between the groups in the SSW test, while in PPS, the noise group performed worse than the control group. Conclusion: These findings suggest that noise exposure produced deleterious effects on the workers’ peripheral and central auditory systems, despite their normal hearing thresholds. The chemical group did not have significantly different results from those of the control group. It is important that individuals exposed to noise or chemicals have their auditory pathways monitored with complementary assessments.
Keywords: Auditory pathways, chemicals, noise, noise-induced hearing loss
|How to cite this article:|
Trabanco JC, Morita B, Matas CG, de Paiva KM, Moreira RR, Sanches SG, Samelli AG. Effects of Noise and Chemical Exposure on Peripheral and Central Auditory Pathways in Normal-hearing Workers. Noise Health 2022;24:182-90
|How to cite this URL:|
Trabanco JC, Morita B, Matas CG, de Paiva KM, Moreira RR, Sanches SG, Samelli AG. Effects of Noise and Chemical Exposure on Peripheral and Central Auditory Pathways in Normal-hearing Workers. Noise Health [serial online] 2022 [cited 2023 Mar 27];24:182-90. Available from: https://www.noiseandhealth.org/text.asp?2022/24/114/182/356126
| Introduction|| |
Exposure to high noise levels can damage the auditory system, especially the outer hair cells, which are vulnerable to various deleterious stimuli. Such damage may permanently impair hearing thresholds and speech intelligibility, and cause tinnitus and changes in central auditory function.,
Studies have assessed the effects of occupational noise as a predominant risk for hearing. Moreover, there is evidence that various chemical products potentially affect hearing, aggravating the harmful effects of noise and even triggering neurotoxic effects.
Any chemical substance causing functional damage to the inner ear can be defined as an ototoxic agent. The action mechanism of these substances can have specificities according to the affected region, specific cells, and biochemical pathways, possibly causing damage to the peripheral and central auditory systems.,,
In occupational practice, hearing is assessed with pure-tone audiometry to determine hearing thresholds. This examination is adequate to subjectively assess hearing thresholds, but it has a limited frequency range, from 250 to 8000 Hz. Cochlear damage resulting from ototoxicity or exposure to high noise levels can reduce high-frequency hearing thresholds not initially identified with conventional pure-tone audiometry. Hence, studies point out the importance of using other auditory assessment methods in individuals exposed to chemical products or noise, such as extended high-frequency audiometry and otoacoustic emission assessment, which detect changes earlier than conventional pure-tone audiometry.,
As previously mentioned, ear-damaging agents can affect hearing function through different mechanisms. However, physical (noise) and chemical agents (ototoxic) have some characteristics in common. The most common finding is usually sensorineural hearing loss resulting from cochlear hair cell damage. In studies with animals, both agents have proved to cause hair cell loss, which may be related to the formation of free radicals or reactive oxygen species.,
Also, studies in both animals and humans have already demonstrated the deleterious effects of ear-damaging agents on the central auditory system. Noise as a physical threat mainly causes mechanical and metabolic damage to the peripheral auditory receptor (the cochlea) and, more rarely, to the central auditory pathways. On the other hand, chemicals that reach the bloodstream can more easily access not only the cochlea but also the central nervous system. Despite the characteristics inherent to each element, some studies indicate that prolonged exposure to noise can also facilitate changes in auditory processing.
Recent studies observed animals whose cortical activity was affected by both noise and noise/chemical interaction. The authors highlight the importance of conducting such research in humans to determine the relevance of dysfunctions similar to the ones verified in animal samples. Other studies applied behavioral tests and identified deficits in the central auditory processing of individuals exposed to chemical products,; these studies emphasized the need for incorporating tools to assess the central auditory function since recent findings demonstrate that both peripheral and central auditory systems can be affected by these agents.
Although much is known about the effects of these ear-damaging agents on the cochlea, there are still many questions on the subject, especially concerning the central auditory nervous system (the afferent and efferent systems) of individuals exposed to noise or chemicals. Given the importance of the topic and the knowledge gaps related to it, a study comparing individuals exposed and not exposed to chemicals or noise can help understand the damages resulting from the exposure to these agents in the peripheral and central auditory pathways, as well as indicate assessments that provide diagnoses earlier than those commonly used in clinical practice.
It should be highlighted that most studies in the literature examining the effects of noise and/or chemicals assess only the peripheral auditory system. No studies were found in the literature simultaneously assessing the peripheral and central auditory pathways in individuals exposed to noise or chemicals, as proposed in this study.
The hypothesis is that individuals exposed to chemical agents or high noise levels present more evident changes in otoacoustic emissions and extended high-frequency audiometry (even with normal hearing thresholds in conventional pure-tone audiometry) than individuals without such exposure, thus indicating an impairment in the peripheral auditory system. In addition, the inhibitory effect of the efferent auditory pathway and some auditory processing skills are expected to be different between individuals exposed and not exposed to these ear-damaging agents, suggesting changes in the central auditory system.
Therefore, this study aimed to evaluate the effects of exposure to noise or chemicals on the peripheral and central auditory systems of workers exposed to chemical agents or high noise levels, comparing one group with the other and with workers not exposed to either of these agents.
| Methods|| |
The project was approved by the institution’s Research Ethics Committee. The procedures were also in accordance with the Declaration of Helsinki.
The study was carried out with workers from University of São Paulo, who were divided into three groups:
- Chemicals group: Individuals who work in the university laboratory. They are exposed to organic solvents (n-hexane, toluene, styrene, trichloroethylene, and xylene) and metals (mercury, lead, tin, and manganese), intermittently, during the 8-hour workday. Mean time of 12.6 years (SD: 6.3 years) in the position (exposure).
- Noise group: Individuals who work in maintenance at the university. They are exposed to intermittent noise (Lavg 86 dBA, minimum 65 dBA of sound pressure level, maximum 111 dBA of sound pressure level; 69% of the daily dose), during the 8-hour workday. Mean time of 13.6 years (SD: 6.4 years) in the position (exposure).
- Control group: The control group worked in administrative areas of the university. Mean time of 9.5 years (7.6 years) in the position (exposure).
The workers were selected based on the university’s Environmental Risks Prevention Program, which describes the risks to which each worker is exposed in their workday. The groups were matched for age to avoid the influence of this variable.
Inclusion and exclusion criteria
Participants who met the following criteria were included in the research: being 18 to 55 years old; having been exposed to chemical agents for >1 year, but not to noise (chemicals group); having been exposed to noise for >1 year, but not to chemicals (noise group); having been exposed to neither chemical agents nor noise (control group); not having excessive cerumen or middle ear changes − which was verified with acoustic immittance (tympanometric curve and ipsilateral acoustic reflex; AT235, Interacoustics, Middelfart, Denmark); and having normal thresholds − that is, <25 dB HL on average at 500, 1000, 2000, and 4000 Hz, assessed in a sound booth with conventional air-conduction pure-tone audiometry, which assesses hearing thresholds (in dB HL) at 250 to 8000 Hz (audiometers AC40, Interacoustics (Interacoustic, Middelfart, Denmark); and Itera II, Madsen/Otometrics, Otometrics - Newington, Australia).
All selected participants went through the following procedures:
- Extended high-frequency audiometry to assess hearing thresholds (in dB HL) at 9 to 16 kHz (9, 10, 11.2, 12.5, 14, and 16 kHz) (audiometers: AC-40 and Itera II), in a sound booth.
- Transient evoked otoacoustic emissions (TEOAE), with nonlinear click stimuli at 80 dB peak eq. Responses were considered present when the signal-to-noise ratio (SNR) was higher than 3 dB SPL (DPEchoport ILO292 (Otodynamics, Hatfield, UK), Otodynamics; connected to a notebook).
- Distortion-product otoacoustic emissions (DPOAE): two different frequencies were simultaneously presented (f1 and f2), in which f1/f2 = 1.22, at 65 dB SPL for f1 and 55 dB SPL for f2. Responses were considered present when SNR was higher than 3 dB SPL in relation to the second background noise standard deviation in the f2 frequencies 1001, 1501, 2002, 3003, 4004, 5005, and 6006 Hz (DPEchoport ILO292; connected to a notebook).
- Inhibitory effect of the efferent auditory pathway (for TEOAE): for individuals presenting TEOAE, the inhibitory effect of the efferent auditory pathway was assessed through the ILO292 protocol: linear click stimuli at 60 dB peak eq, with or without contralateral white noise at 60 dB SPL, alternately. The percentage of the inhibitory effect was calculated, considering both TEOAE results: in the presence and absence of contralateral white noise. To calculate the inhibitory effect, the TEOAE results in the absence and presence of noise were transformed into micropascals (μPa), obtaining the difference between both results. Differences that resulted in positive values indicated the presence of the inhibitory effect of the efferent auditory pathway. Then, the percentage of the inhibitory effect was calculated. Since the right ear has an advantage over the left ear regarding the inhibitory effect of the efferent pathway, only the results from the right ear were considered for this analysis.
- Staggered Spondaic Word (SSW − Brazilian Portuguese version) test: SSW is a binaural integration test that assesses dichotic listening abilities. The test has 40 sequences with four disyllable words each, presented in the noncompeting right ear, competing right ear (CR), competing left ear (CL), and noncompeting left ear. The intensity used was 50 dB SL. The results were analyzed with the percentage of correct responses in CR and CL. The normal value was set at 90% of correct responses.
- Pitch Pattern Sequence (PPS) test, version proposed by Musiek, which assesses temporal ordering ability. A set of 60 sequences of three tone bursts with different pitches (1122 Hz and 880 Hz) was presented binaurally at 50 dB SL. The subject was asked to describe the sequences presented. The percentage of correct answers was calculated. The normal value was set at 75% of correct responses.
Also, information on occupational history and use of protective equipment during exposure to risks were obtained through interviews.
Descriptive data analyses were conducted (mean, median, and standard deviation), as well as hypothesis testing. For analyses with categorical variables, the groups were compared with the homogeneity chi-square test. The groups’ mean ages were compared with ANOVA with a fixed factor (group). For the other variables, a normal mixed model was adjusted, in which the subjects’ effect was random and the groups’ and ears’ effects were fixed. Since these variables did not have a normal distribution, their means were compared with the nonparametric Kruskal–Wallis test between the three groups. When necessary, the chi-square test was used. The 5% significance level was used.
| Results|| |
We analyzed 54 workers, carefully divided into three groups according to the type of exposure:
- chemicals group: 18 workers (11 females and seven males), mean age 40 years (minimum 30; maximum 53);
- noise group: 18 workers (seven females and 11 males), mean age 42 years (minimum 32; maximum 54);
- control group: 18 workers (10 females and eight males), mean age 39.5 years (minimum 30; maximum 54).
There was no difference between the three groups in the proportion of the sexes (P-value = 0.381) and ages (P-value = 0.659).
A total of 55% of the professionals in the chemicals group, 25% in the noise group, and 32% in the control group had a higher education degree (P-value = 0.122).
Concerning safety, 100% of the individuals in the chemicals group used both personal (e.g., gloves, goggles, respirators, gauntlets, and padded sleeves) and collective protective equipment. Most individuals (61.1%) in the noise group reported inconsistently wearing hearing protection devices (plugs or earmuffs) during the workday.
An increase in hearing thresholds in both ears was observed in the extended high-frequency audiometry at 11200 Hz. However, there was no between-group difference (P-values ≥ 0.088) [Table 1].
|Table 1 Descriptive analysis regarding hearing thresholds (in dB HL), and comparative analysis between the groups|
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There were between-group differences in DPOAE responses in both ears at 4004 and 5042 Hz [Table 2]. At 4004 Hz, the chemicals group had higher responses than the noise group in both ears. At 5042 Hz, there was no difference between the chemicals and control groups, but their responses were significantly higher than those of the noise group.
|Table 2 Descriptive analysis regarding response of the distortion product evoked otoacoustic emissions (dB SPL), and comparative analysis between the groups|
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There was no difference between the groups for the global TEOAE response in the right ear [Table 3]. However, in the left ear [Table 3], there was a significantly higher response in the chemicals group than in the noise group.
|Table 3 Descriptive analysis regarding global response of the transient otoacoustic emissions (dB SPL), and comparative analysis between the groups|
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In the qualitative analysis, a group effect was noted for the presence/absence of TEOAE [Table 4], in which the noise group presented a higher proportion of TEOAE absences, with a statistically significant difference. Regarding the presence/absence of the inhibitory effect, 100% of the individuals in the control group presented an inhibitory effect versus 80% of individuals in the chemicals group and 61.5% of individuals in the noise group, with a significant difference between the noise and control groups [Table 4].
|Table 4 Descriptive analysis regarding presence/absence of the transient evoked otoacoustic emissions and of the inhibitory effect of the efferent pathway, and comparative analysis between the groups|
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In the quantitative analysis of the percentage of reduced efferent responses, no significant difference was found between the groups [Table 5].
|Table 5 Descriptive analysis regarding percentage of the inhibitory effect of the efferent auditory pathway in the right ear, and comparative analysis between the groups|
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In the SSW test, there was no difference between the groups [Table 6] and [Table 7]. However, in the PPS test, the noise and chemicals groups performed worse than the control group, with a significant difference between the control and noise groups in the qualitative analysis [Table 6] and between the control/chemical groups and noise group in the quantitative analysis [Table 7].
|Table 6 Descriptive analysis regarding normal/abnormal results in SSW and PPS and comparative analysis between the groups|
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|Table 7 Descriptive analysis regarding results to SSW (%) and PPS (%) and comparative analysis between the groups|
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| Discussion|| |
No differences in extended high-frequency hearing thresholds, otoacoustic emissions, inhibitory effect of the efferent pathway, SSW, or PPS were found between the control and chemicals groups. On the other hand, significant differences were observed in many of these variables in the noise group, although all individuals had normal hearing thresholds. In addition, despite the absence of significant differences, the chemicals group performed slightly worse than the control group in tests that assess central auditory function (inhibitory effect of the efferent pathway, SSW, and PPS), suggesting that both groups present risks to hearing health caused by noise (more evident) or chemicals. Hence, they must be monitored to avoid hearing loss and further compromising the auditory system.
Despite the upper age limit of almost 55 years, all individuals in the study presented normal hearing thresholds in conventional audiometry in the three groups. Also, even with a large age variation between the lower and upper limits, the three groups showed the same variability, since the individuals were matched for age, seeking to minimize the influence of this variable between the groups.
Studies have suggested that extended high-frequency audiometry can be used as an earlier indicator of cochlear damage caused by noise or chemicals, in contrast with conventional audiometry. Although no significant differences between the groups were observed, as verified in other studies,, at frequencies above 11,200 Hz, the hearing thresholds of the chemicals and noise groups tended to be higher than in the control group.
Individuals concomitantly exposed to high noise levels and solvents tend to present higher hearing thresholds in extended high-frequency audiometry than individuals not exposed to noise and chemicals,, indicating that noise and chemicals can damage hearing. In comparison with our findings, we can suggest that each ear-damaging agent alone is also capable of impairing extended high-frequency hearing thresholds.
It is important to highlight that in addition to exposure to noise or chemical agents, countless factors can interfere with hearing thresholds, especially at higher frequencies. In the chemicals group, 100% of the individuals used both personal and collective protective equipment, which can mitigate their contact with such products and thus have fewer consequences to the auditory system. Moreover, research participants had different amounts and times of exposure to each component, and their daily time of exposure varied. The noise group, on the other hand, was more exposed to the ear-damaging agent, since most individuals reported not wearing hearing protection devices constantly.
The evoked otoacoustic emissions are also an important tool in the early diagnosis of noise-induced cochlear damage. We verified significantly lower TEOAE and DPOAE amplitudes (at 4004 and 5042 Hz) in the noise group than in the other two groups. This suggests cochlear dysfunctions in this group, despite normal hearing thresholds.,,
Studies conducted in normal-hearing adults and those exposed and not exposed to noise (or music) showed the absence or reduction of otoacoustic emissions for both types of evoked emissions,,, providing the first indications of cochlear damage. This finding was also observed in this study, as the noise group presented a significantly higher number of absences of TEOAE than the other groups.
Concerning the chemicals, most studies using otoacoustic emissions assessed individuals concomitantly exposed to both chemicals and noise. They verified a greater prevalence of hearing loss and diminished otoacoustic emissions in the noise-exposed group (consistent with the findings in this study) or in the noise plus chemicals group.
In one study, workers (divided into three groups: low, medium, and high levels of exposure to styrene) were assessed with pure-tone audiometry and TEOAE. No differences regarding hearing thresholds or TEOAE results were found between the three groups. However, worse hearing thresholds at some frequencies were found in the group exposed to high levels of styrene.
Another study with gasoline station workers verified significantly lower DPOAE amplitudes than nonexposed control participants in most evaluated frequencies. This suggests that peripheral auditory dysfunctions may be related to exposure to solvents.
In this study, the chemicals group did not differ significantly from the control group regarding otoacoustic emissions (OAE), unlike previous studies., Nevertheless, monitoring them with otoacoustic emissions over time is an important tool in the early detection of cochlear changes.
The inhibitory effect of the efferent auditory pathway, also known as suppression of otoacoustic emissions, is characterized by a decrease in otoacoustic emission amplitude in the presence of contra or ipsilateral noise, which is more evident in the right ear. Until recently, it was believed that the olivocochlear efferent system had the role of protecting hair cells from noise exposure. However, after the vulnerability of the synapses between hair cells and auditory nerves resulting from noise exposure was discovered, some studies emphasized the protective role of the efferent system against synaptopathy., This assessment measures the functioning of part of the central auditory nervous system and may be an early indicator of whether ear-damaging agents have compromised the function of this portion of the efferent system, even before peripheral changes are identified., Two studies in animals (mice exposed to both noise and age effect), verified that the section of the efferent bundle exacerbated the synaptopathy.
In our study, the inhibitory effect of the efferent auditory pathway was not absent in any individual in the control group, in contrast with >38% of those in the noise group (significantly different from the other groups) and 20% of the individuals in the chemicals group (not significantly different from the other groups).
These results might suggest that individuals (noise and chemicals groups) had auditory impairments not restricted to the cochlea, since this dysfunction already affects the efferent central nervous system. It is noteworthy that the investigation of the inhibitory effect of the efferent auditory pathway can only be performed in individuals who present with otoacoustic emissions, that is, who do not have a cochlear dysfunction, suggesting that some individuals in the noise and chemical groups who have normal hearing thresholds and the presence of otoacoustic emissions present with changes in the central auditory pathways.
Similar findings were observed in a previous study that verified that workers exposed to occupational noise presented a significant decrease in the inhibitory effect of the efferent auditory system in relation to not exposed individuals. However, Hope et al. found no differences in the inhibitory effect of the efferent system comparing individuals exposed and unexposed to noise who presented similar results in pure-tone audiometry. Peng et al. observed that young adults using personal music devices presented a reduced inhibitory effect of the efferent system, though not significantly different from nonusers.
The effect of emission suppression in normal-hearing workers exposed to pesticides and noise and a control group was analyzed; less suppression was observed in the group exposed to noise and pesticides. Our study did not evaluate workers simultaneously exposed to chemical agents and noise, which may justify the different results from the previous study The different findings can also be explained in part by the wide variety of methodologies and protocols employed, as well as the different populations assessed and the ear-damaging products the individuals have been exposed to (types, amounts, cumulative doses, and combinations thereof).
Traditionally, pure-tone hearing thresholds are used to determine the extension of noise-induced hearing loss, which can be associated with decreased speech recognition scores, even with normal thresholds in the audiogram. This might be related to changes in the synaptic mechanisms and decreased auditory processing skills, which can be affected by oxidative stress., Similar mechanisms can be involved in the hearing losses related to ototoxicity and age.
For this reason, we included tests to assess central auditory processing skills. No statistically significant difference was verified between the groups regarding SSW, which is consistent with a previous study. Nevertheless, despite being an easy test for adults, the noise and chemicals groups had two individuals each with abnormal results in this test, while the control group had none.
In qualitative analysis, the noise and chemicals groups performed worse in the PPS, with a significant difference between the noise and control groups. In quantitative analysis, the noise group performed worse than the control and chemicals groups.
These findings suggest that the temporal auditory processing ability of the noise and chemical groups may have been compromised by these ear-damaging agents, especially by noise. Hence, the central auditory functioning would be affected, even without evidence of peripheral changes since hearing thresholds were normal.
Similar findings were observed in previous studies., Using the same type of test (PPS), Fuente et al. found a significant difference between normal-hearing individuals with and without exposure to chemicals. Kumar et al. evaluated normal-hearing adults exposed and not exposed to occupational noise and verified the noise-exposed group performed worse in the gap and modulation detection, duration pattern test, and speech intelligibility test. This suggests that noise affects speech and temporal processing skills in individuals exposed to occupational noise even with normal hearing thresholds.
It is important to emphasize that the educational level, which can influence the results, particularly of the auditory processing tests, did not present a significant difference between the groups. Therefore, it probably did not interfere with the results in the present study.
Hence, future studies should use other protocols to assess other auditory skills involved in speech perception in noise when investigating the effects of noise and chemicals on central auditory skills.
This study had some limitations. Its type is subject to selection bias since it uses a convenience sample. Regarding the chemicals group, as it is a university laboratory, the amounts and doses of exposure are low and therefore the effects of chemicals on the auditory system are limited. Nevertheless, it is worth noting that this type of population made it possible to isolate these risk factors, despite the low doses of exposure. Furthermore, no group of workers exposed concomitantly to noise and chemicals was used to assess the synergistic effect of these two ear-damaging elements. Data from a review showed that exposure to chemicals, including solvents, and other risk factors (occupational and personal), stand out for exacerbating the effects of noise exposure.
Another limitation refers to differences between the sexes, especially regarding noise exposure. However, due to study population characteristics, especially in the chemicals group, it was necessary to include both sexes. Care was taken to balance them between the groups and the proportions of both sexes were not statistically different between the three groups. Therefore, this variable probably did not affect the results.
| Conclusion|| |
Based on the results obtained in this study, it can be suggested that noise exposure produced deleterious effects on the peripheral and central auditory systems of workers exposed to high noise levels, despite conventional audiometry results indicating normal hearing thresholds. The chemicals group did not present results significantly different from those of the control group. It is important that individuals exposed to noise or chemicals have their auditory pathways monitored with complementary assessments.
Financial support and sponsorship
This study was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior − Brazil (CAPES) with the Finance Code 001.
Conflicts of interest
There are no conflicts of interest.
| References|| |
Campo P, Venet T, Thomas A, Cour C, Brochard C, Cosnier F. Neuropharmacological and cochleotoxic effects of styrene. Consequences on noise exposures. Neurotoxicol Teratol 2014;44:113-20.
Irgens-Hansen K, Baste V, Bratveit M, Lind O, Koefoed VF, Moen BE. Hearing loss in the Royal Norwegian Navy: a longitudinal study. Noise Health 2016;18:157-65.
] [Full text]
Fuente A, McPherson B. Central auditory damage induced by solvent exposure. Int J Occupat Safety Ergonom 2007;13:391-7.
Johnson AC, Morata TC. Occupational exposure to chemicals and hearing impairment. The Nordic Expert Group for Criteria Documentation of Health Risks from Chemicals. Nordic Expert Group. Gothenburg: Arbete och Hälsa. 2010;44:177. http://hdl.handle.net/2077/23240
Frota S, Iório MC. Distortion-product otoacoustic emissions and pure tone audiometry: a study of temporary threshold shifts. Rev Bras Otorrinolaringol 2002;68:15-20.
Lopes AC, Otubo KA, Basso TC, Marinelli EJ, Lauris JR. Occupational hearing loss: tonal audiometry x high frequencies audiometry. Int Arch Otorhinolaryngol 2009;13:293-9.
Choi SH, Choi CH. Noise-induced neural degeneration and therapeutic effect of antioxidant drugs. J Audiol Otol 2015;19:111-9.
Fuente A, McPherson B, Muñoz V, Pablo Espina J. Assessment of central auditory processing in a group of workers exposed to solvents. Acta Otolaryngol 2006;126:1188-94.
Massa CG, Rabelo CM, Moreira RR, Matas CG, Schochat E, Samelli AG. P300 in workers exposed to occupational noise. Braz J Otorhinolaryngol 2012;78:107-12.
Guthrie OW, Wong BA, Mcinturf SM, Reboulet JE, Ortiz PA, Mattie DR. Background noise contributes to organic solvent induced brain dysfunction. Neural Plast 2016;2016:8742725.
Ryan S, Kemp DT. The influence of evoking stimulus level on the neural suppression of transient evoked otoacoustic emissions. Hear Res 1996;94:140-7.
Bidelman G, Bhagat S. Right-ear advantage drives the link between olivocochlear efferent ‘antimasking’ and speech-in-noise listening benefits. Neuroreport 2015;26:483-7.
Pereira LD, Schochat E. [Behavioral Hearing Tests to Assess Central Auditory Processing]. 1st ed. São Paulo: Pro Fono; 2011.
Musiek FE. Frequency (pitch) and duration pattern tests. J Am Acad Audiol 1994;5:265-8.
Mehrparvar AH, Mirmohammadi SJ, Ghoreyshi A, Mollasadeghi A, Loukzadeh Z. High-frequency audiometry: a means for early diagnosis of noise-induced hearing loss. Noise Health 2011;13:402-6.
] [Full text]
Sena TR, Dourado SS, Lima LV, Antoniolli AR. The hearing of rural workers exposed to noise and pesticides. Noise Health 2018;20:23-6.
] [Full text]
Morata TC, Dunn DE, Kretschmer LW, Lemasters GK, Keith RW. Effects of occupational exposure to organic solvents and noise on hearing. Scand J Work Environ Health 1993;19:245-54.
Alcarás PA, Lacerda AB, Marques JM. Study of evoked otoacoustic emissions and suppression effect on workers exposed to pesticides and noise. CoDAS 2013;25:527-33.
Boger ME, Sampaio AL, De Oliveira CA. Analysis of hearing and tinnitus in workers exposed to occupational noise. Int Tinnitus J 2016;20:88-92.
Henning RL, Bobholz K. Distortion product otoacoustic emissions in college music majors and nonmusic majors. Noise Health 2016;18:10-20.
] [Full text]
Sliwinska-Kowalska M, Kotylo P, Hendler B. Comparing changes in transient-evoked otoacoustic emission and pure-tone audiometry following short exposure to industrial noise. Noise Health 1999;1:50-7.
] [Full text]
Prasher D, Al-Hajjaj H, Aylott S, Aksentijevic A. Effect of exposure to a mixture of solvents and noise on hearing and balance in aircraft maintenance workers. Noise Health 2005;7:31-9.
] [Full text]
Johnson AC, Morata TC, Lindblad AC et al.
Audiological findings in workers exposed to styrene alone or in concert with noise. Noise Health 2006;8:45-57.
] [Full text]
Triebig G, Bruckner T, Seeber A. Occupational styrene exposure and hearing loss: a cohort study with repeated measurements. Int Arch Occup Environ Health 2009;82:463-80.
Roggia SM, França AG, Morata TC, Krieg E, Earl B. Auditory system dysfunction in Brazilian gasoline station workers. Inter J Audiol 2019;58:484-96.
Khalfa S, Collet L. Functional asymmetry of medial olivocochlear system in humans. Towards a peripheral auditory lateralization. Neuroreport 1996;7:993-6.
Maison SF, Usubuchi H, Liberman MC. Efferent feedback minimizes cochlear neuropathy from moderate noise exposure. J Neurosci 2013;33:5542-52.
Yin Y, Liberman LD, Maison SF, Liberman MC. Olivocochlear innervation maintains the normal modiolar-pillar and habenular-cuticular gradients in cochlear synaptic morphology. J Assoc Res Otolaryngol 2014;15:571-83.
Kujawa SC, Liberman MC. Synaptopathy in the noise-exposed and aging cochlea: primary neural degeneration in acquired sensorineural hearing loss. Hear Res 2015(Pt B);330:191-9.
Sliwinska-Kowalska M, Kotylo P. Occupational exposure to noise decreases otoacoustic emission efferent suppression. Int J Audiol 2000;41:113-9.
Hope AJ, Luxon LM, Bamiou DE. Effects of chronic noise exposure on speech-in-noise perception in the presence of normal audiometry. J Laryngol Otol 2013;127:233-8.
Peng JH, Wang JB, Chen JH. Recreational noise exposure decreases olivocochlear efferent reflex strength in young adults. J Otolaryngol Head Neck Surg 2010;39:426-32.
Le TN, Straatman LV, Lea J, Westerberg B. Current insights in noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options. J Otolaryngol Head Neck Surg 2017;46:41.
Wong AC, Ryan AF. Mechanisms of sensorineural cell damage, death and survival in the cochlea. Front Aging Neurosci 2015;7:58.
Santos CS, Juchem LS, Rossi AG. Auditory processing of servicemen exposed to occupational noise. Rev CEFAC 2008;10:92-103.
Kumar UA, Ameenudin S, Sangamanatha AV. Temporal and speech processing skills in normal hearing individuals exposed to occupational noise. Noise Health 2012;14:100-5. [Full text]
Golmohammadi R, Darvishi E. The combined effects of occupational exposure to noise and other risk factors − a systematic review. Noise Health 2019;21:125-41.
] [Full text]
Alessandra G Samelli
Rua Cipotânea, 51, Cidade Universitária, São Paulo 05360-160
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]