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PubMed2005

Noise-induced cell death in the mouse medial geniculate body and primary auditory cortex.

Noise-induced effects within the inner ear have been well investigated for several years. However, this peripheral damage cannot fully explain the audiological symptoms in noise-induced hearing loss (NIHL), e.g. tinnitus, recruitment, reduced speech intelligibility, hyperacusis. There are few reports on central noise effects. Noise can induce an apoptosis of neuronal tissue within the lower auditory pathway. Higher auditory structures (e.g. medial geniculate body, auditory cortex) are characterized by metabolic changes after noise exposure. However, little is known about the microstructural changes of the higher auditory pathway after noise exposure. The present paper was therefore aimed at investigating the cell density in the medial geniculate body (MGB) and the primary auditory cortex (AI) after noise exposure. Normal hearing mice were exposed to noise (10 kHz center frequency at 115 dB SPL for 3 h) at the age of 21 days under anesthesia (Ketamin/Rompun, 10:1). After 1 week, auditory brainstem response recordings (ABR) were performed in noise exposed and normal hearing animals. After fixation, the brain was microdissected and stained (Kluever-Barrera). The cell density in the MGB subdivisions and the AI were determined by counting the cells within a grid. Noise-exposed animals showed a significant ABR threshold shift over the whole frequency range. Cell density was significantly reduced in all subdivisions of the MGB and in layers IV-VI of AI. The present findings demonstrate a significant noise-induced change of the neuronal cytoarchitecture in central key areas of auditory processing. These changes could contribute to the complex psychoacoustic symptoms after NIHL.

Acoustic Stimulation↗
PubMed1979

Pattern A personality and noise-induced vasoconstriction.

A perplexing question about noise-induced hearing loss is why some persons seem to be more affected by high intensity noise than others. Hawkins (1971) has shown noise-induced vasoconstriction to be implicated in noise-induced hearing loss in animals as evidenced by vascular changes within the inner ear and he asks the question: Are these changes caused by the noise itself or mediated by the autonomic nervous system (ANS)? Our research employed a plethysmograph to measure ANS mediated vasoconstriction during noise exposure. The subjects were stress prone males and females (Pattern A) whose behavior in noise was compared to non-stress prone males and females (Pattern B). The results indicated Pattern A males showed marked vasoconstriction in the presence of noise whereas Pattern B males did not. Pattern A females performed very much like Pattern A males with no statistical difference between these two groups. However, Pattern B females demonstrated a significant increase in vasoconstriction in the presence of noise and in this respect Pattern B females are different from Pattern B males. This difference possibly resulted from the use of a test to assess personality type which was intended for use with male subjects. The authors conclude there is strong evidence to suggest that being prone to stress in the presence of noise is a contributing factor to noise-induced hearing loss.

Adolescent↗
PubMed2005

Noise burden and the risk of myocardial infarction.

AIMS: Chronic noise exposure is associated with adverse pathophysiological effects and may contribute to the progression of cardiovascular disease. We, therefore, determined the risk of noise for the incidence of myocardial infarction. METHODS AND RESULTS: In a case-control study, 4115 patients (3054 men, 56+/-9 years; 1061 women, 58+/-9 years) consecutively admitted to all 32 major hospitals in Berlin with confirmed diagnosis of acute myocardial infarction were enrolled from 1998 to 2001 in the Noise and Risk of Myocardial Infarction (NaRoMI) study. Controls were matched for gender, age, and hospital. In standardized interviews, information was obtained on environmental and work noise annoyance. The sound levels of environmental and work noise were assessed using traffic noise maps as proxy and international standards for workplaces, respectively. In multivariate logistic regression models, the adjusted odds ratios of noise variables were determined. There was a marginally increased risk of myocardial infarction associated with annoyance by environmental noise in women (adjusted odds ratio 1.47, 95% confidence interval 0.95-2.25, P=0.081) but not in men, and not associated with annoyance by work noise. Environmental sound levels were associated with increased risk in men and women (odds ratios 1.46, 1.02-2.09, P=0.040 and 3.36, 1.40-8.06, P=0.007) and work sound levels in men only (1.31, 1.01-1.70, P=0.045). CONCLUSION: Chronic noise burden is associated with the risk of myocardial infarction. The risk increase appears more closely associated with sound levels than with subjective annoyance. Further investigation of the gender-related risk of noise exposure may aid in improving prevention.

Case-Control Studies↗
PubMed2002

Potentiation of noise-induced hearing loss by low concentrations of hydrogen cyanide in rats.

Noise-induced hearing loss is the most prevalent occupational injury in the United States despite the adoption of clear permissible exposure limits and protocols for hearing conservation. This study identifies low-level chemical asphyxiant exposure as a risk factor capable of potentiating noise-induced hearing loss. Rats were exposed to 10, 30, and 50 ppm hydrogen cyanide (HCN) alone for 3.5 h (n = 28) or in combination with 2 h octave band noise exposure (100 dB(lin); n = 28). Additional groups received noise exposure alone (n = 16) and no treatment other than placement in an inhalation chamber with clean air and quiet (n = 16). Pure tone compound action potential (CAP) thresholds were determined 4 weeks following the exposure in order to assess pure tone auditory sensitivity and permanent threshold impairment. Cochleae from an additional 13 subjects were processed for light microscopy to permit assessment of hair cell loss. The results demonstrate that the noise exposure alone impaired CAP threshold by about 10 dB, averaged between 12-40 kHz, and produced a 5% loss of outer hair cells at the base of the cochlea, but no inner hair cell loss. The combined exposure to noise and HCN caused a cyanide dose-dependent CAP threshold impairment that exceeds the noise exposure alone. This effect reached statistical significance at a HCN level of 30 ppm. Combined exposure also produced more outer hair cell loss than noise alone. HCN alone did not cause significant hearing loss or hair cell loss. A risk assessment analysis was conducted for the auditory threshold data using benchmark dose software published by the U. S. EPA (BMDS version 1.3). A continuous model showed that the data could be described by a linear function. For a benchmark response corresponding to a 5 dB increase in auditory threshold above the effect of noise alone, the lower bound on the 95% confidence interval for the benchmark dose was 9 ppm. The benchmark dose that impaired auditory threshold 10% above the effect of noise alone had a lower bound of 2 ppm. The lower bound to the HCN dose that produced a 1 SD elevation in noise-induced hearing loss was 16 ppm. These exposure levels provide a range of concentrations below to slightly above the short-term exposure limit for HCN. However, if these levels are adjusted for an 8 h time-weighted average (TWA), the resulting levels are below the permissible exposure level (PEL) for HCN.

Animals↗
PubMed2002

Distribution of risk factors for hearing loss: implications for evaluating risk of occupational noise-induced hearing loss.

This paper presents an analysis of hearing threshold levels among 2066 white male workers employed in various U.S. industries studied in the 1968-72 NIOSH Occupational Noise and Hearing Survey (ONHS). The distribution of hearing threshold levels (HTL) is examined in relation to various risk factors (age, prior occupational noise, medical conditions) for hearing loss among a population of noise exposed and control (low noise-exposed) industrial workers. Previous analyses of a subset of these data from the ONHS focused on 1172 highly "screened" workers. An additional 894 male workers (609 noise-exposed and 285 controls), who were excluded for various reasons (i.e., nonoccupational noise exposure, otologic or medical conditions affecting hearing, prior occupational noise exposure) have been added to examine hearing loss in an unscreened population. Data are analyzed by age, duration of exposure, and sound level (8-h TWA) by individual test frequency. Results indicate that hearing threshold levels are higher among unscreened noise-exposed and control workers relative to screened workers. Analysis of risk factors such as nonoccupational noise exposure, medical conditions, and type of industry among unscreened controls indicated that these factors were not significantly associated with increased mean HTLs or risk of material impairment over and above what is expected due to age. Age-specific mean hearing threshold levels (and percentiles of the distribution) among the unscreened ONHS control population may be used as a comparison population of low-noise exposed white male industrial workers for evaluating the effectiveness of hearing conservation programs for workers less than 55 years of age. To make valid inferences regarding occupational noise-induced hearing loss, it is important to use hearing data from reference (control) populations that are similar with respect to the degree of subject screening, type of work force (blue vs white collar), and the distribution of other risk factors for hearing loss.

Adult↗
PubMed2004

External and internal noise surveys of London primary schools.

Internal and external noise surveys have been carried out around schools in London, UK, to provide information on typical levels and sources to which children are exposed while at school. Noise levels were measured outside 142 schools, in areas away from flight paths into major airports. Here 86% of the schools surveyed were exposed to noise from road traffic, the average external noise level outside a school being 57 dB L(Aeq). Detailed internal noise surveys have been carried out in 140 classrooms in 16 schools, together with classroom observations. It was found that noise levels inside classrooms depend upon the activities in which the children are engaged, with a difference of 20 dB L(Aeq) between the "quietest" and "noisiest" activities. The average background noise level in classrooms exceeds the level recommended in current standards. The number of children in the classroom was found to affect noise levels. External noise influenced internal noise levels only when children were engaged in the quietest classroom activities. The effects of the age of the school buildings and types of window upon internal noise were examined but results were inconclusive.

Child↗
PubMed1998

Effectiveness of intermittent and continuous acoustic stimulation in preventing noise-induced hearing and hair cell loss.

Resistance to noise-induced hearing loss (NIHL) was studied in gerbils exposed either to intermittent or continuous low-level noise prior to an intense noise. Auditory-evoked brainstem response (ABR) thresholds, distortion product otoacoustic emissions (DPOAEs), Q10dB values from compound action potential (CAP) tuning curves, and outer hair cell (OHC) loss were measured for each group. Subjects were exposed to A-weighted noise (octave band noise centered at 2 kHz) on an intermittent (80 dB, 6 h/day) or continuous schedule (74 dB, 24 h/day) for 10 days, allowed to rest in quiet for 2 days, then exposed to intense A-weighted noise (107 dB, 24 h/day) for 2 days. A "noise-only" group was exposed only to the intense noise. Gerbils exposed in both the "intermittent" and "continuous" groups had less (15-30 dB) temporary threshold shift (TTS) than those in the noise-only group. In addition, the continuous group had less (10-15 dB) permanent threshold shift (PTS) than the other groups. These data suggest that resistance to NIHL is evident in both the intermittent and continuous groups when TTS is measured, but resistance to PTS is afforded only by the continuous paradigm. Both paradigms decreased OHC loss as compared to the noise-only group, with the continuous paradigm being most effective. However, neither paradigm conserved DPOAE amplitudes or tuning curve Q10dB values relative to the noise-only group.

Acoustic Stimulation↗
PubMedDate not supplied

Variables affecting the drill-generated noise levels in ear surgery.

The manner in which the variables rotation speed, type of burr, burr size and site of drilling influence bone-conducted, drill-generated noise levels in ear surgery, has been investigated. From the results obtained, the following conclusions can be drawn. 1. The noise levels were primarily influenced by the size of the burr. The 6 mm cutting burrs gave a noise level of 88-108 dB, the use of a 4 mm one resulted in a reduction of 1-6 dB and the use of a 2 mm one, 5-16 dB. The mean noise levels of the diamond burrs were 5-11 dB lower than the mean noise levels of the cutting ones. 2. Variations in rotation speed had only a slight influence on the noise levels produced (0-5 dB). 3. Three different types of cutting burr were tested. All gave noise levels of about the same order of magnitude. 4. The noise levels around the cochlea were only slightly influenced by the localization of the drilling within the ear (less than 1.8 dB). 5. Drill-induced noise levels in ear surgery cannot be reduced to any great extent. Possible noise traumas to the inner ear can only be avoided by minimizing the duration of drilling and thus, the duration of harmful noise exposure to the cochlea.

Ear↗
PubMed1992

Apportionment of noise-induced hearing disability and its prognosis in a medicolegal context: a modelling study.

Apportionment of liability for noise-induced hearing loss is required in medicolegal work when two or more separate instances of noise exposure have occurred. In general there are insufficient audiometric records to determine how much hearing loss was caused by each noise exposure, and hence there is insufficient information on which to base apportionment of liability. Apportionment must then be based on a theoretical understanding of the way in which hearing loss is related to patterns of noise exposure and how the increased hearing threshold levels lead to greater disability. A model is developed which combines existing models of the relationship of hearing impairment to noise exposure and age, and the relationship of hearing disability to impairment. The model is evaluated for a wide range of notional patterns of noise exposure, leading to a simple equation which predicts the relative attribution of disability to previous noise exposures sufficiently accurately for the purposes of apportionment. The model also shows that disability due to noise exposure generally increases slightly with increasing age even after noise exposure has ceased. Thus the difference in disability between a person exposed to noise and a noise-free control of the same age and sex can be expected to increase somewhat as the subject and control grow older. However, the magnitude of this effect, often termed prognosis, is shown to be small and can be assumed to be zero in practice.

Age Factors↗
PubMed2000

Intense noise-induced apoptosis in hair cells of guinea pig cochleae.

Cells can die by two distinct pathways: apoptosis and necrosis. To explore whether intense noise can induce hair cell (HC) death via the apoptotic pathway, we systematically examined morphological changes in guinea pig cochlear HC nuclei stained with Hoechst 33342, a fluorescent dye specifically labelling the nuclear DNA. A narrow band noise centred at 4 kHz with levels at 110 dB, 115 dB or 120 dB (SPL) was applied for 4 h and the exposed cochleae were collected at various intervals (3 h, 3 or 14 days) after the noise exposure. Auditory function was monitored by measuring thresholds of auditory brain stem responses. In the noise-damaged cochleae, there were two major types of nuclear changes, nuclear condensation appeared as karyorrhexis or karyopyknosis and nuclear swelling. Karyorrhexis and karyopyknosis predominately appeared in the severely damaged cochlear region in the animals exposed to 120 dB noise and examined 3 h after the noise exposure. In contrast, swelling of nuclei occurred in all of the noise-exposed cochleae, and was the feature change in the animals exposed to 110 and 115 dB noise. This pathological change persisted at least for 14 days after the noise exposure. The typical changes of karyorrhexis and karyopyknosis noted in the animals exposed to 120 dB noise were morphologically similar to those nuclear changes described in previous studies for apoptosis, suggesting that the apoptotic process may be involved in intense noise-induced HC death.

Animals↗
PubMed2000

Degeneration in the cochlea after noise damage: primary versus secondary events.

PURPOSE: To determine if noise damage in the organ of Corti is different in the low- and high-frequency regions of the cochlea. MATERIALS AND METHODS: Chinchillas were exposed for 2 to 432 days to a 0.5 (low-frequency) or 4 kHz (high-frequency) octave band of noise at 47 to 95 dB sound pressure level. Auditory thresholds were determined before, during, and after the noise exposure. The cochleas were examined microscopically as plastic-embedded flat preparations. Missing cells were counted, and the sequence of degeneration was determined as a function of recovery time (0-30 days). RESULTS: With high-frequency noise, primary damage began as small focal losses of outer hair cells in the 4-8 kHz region. With continued exposure, damage progressed to involve loss of an entire segment of the organ of Corti, along with adjacent myelinated nerve fibers. Much of the latter loss is secondary to the intermixing of cochlear fluids through the damaged reticular lamina. With low-frequency noise, primary damage appeared as outer hair cell loss scattered over a broad area in the apex. With continued exposure, additional apical outer hair cells degenerated, while supporting cells, inner hair cells, and nerve fibers remained intact. Continued exposure to low-frequency noise also resulted in focal lesions in the basal cochlea that were indistinguishable from those resulting from exposure to high-frequency noise. CONCLUSIONS: The patterns of cochlear damage and their relation to functional measures of hearing in noise-exposed chinchillas are similar to those seen in noise-exposed humans. Thus, the chinchilla is an excellent model for studying noise effects, with the long-term goal of identifying ways to limit noise-induced hearing loss in humans.

Animals↗
PubMedDate not supplied

[Interaction between continuous and impulse noise: anatomic and functional evaluation in relation to the intensity of the exposure].

Interaction between continuous and impulse noise was studied. One group of chinchillas was exposed to octave band of noise of 0.5 kHz 95 dB SPL intensity. Three groups were exposed to impulse noises of 113, 119 and 125 prak SPL emitted at 1 imp/sec, 1 imp/4 sec and 1 imp/16 sec respectively. Three groups were exposed to noise created by a combination of above continuous and impulse noises. All exposures lasted for 5 days. Hearing thresholds were measured in 35 animals using auditory evoked potentials. The combined continuous and impulse noises showed equal energy contents, but the groups exposed to 119 and 125 dB impulse noise intensities developed an exacerbation of PTS and cell hair loss. Therefore, the critical level, under which the damage associated with noise exposure is related to the total noise energy (Equal Energy Hypothesis) was reduced when impulse noise was added to continuous noise.

Animals↗
PubMed1983

[Measurement of industrial noise].

n this paper a comprehensive method for description and measurement of industrial noise is presented keeping the following aspects into account: 1) evaluation by data collection questionnaire of work environment, working variables, noise sources, noise exposure, etc.; 2) noise measurement with particular regards to noise characteristics (steady noise, intermittent, fluctuating, irregular, impulsive), to sampling methods (position, duration, etc.) also in wiew to drawing up "noise maps"; 3) noise data processing ( LAEQ , LEX); on this aspect many applying examples are specified; 4) noise data representation and recording, also using computer aids. The AA draw the attention to adopt, also in anticipation of the European noise standards, a standardized method for industrial noise evaluation.

Environmental Exposure↗
PubMed1991

Cardiovascular responses and electroencephalogram disturbances to intermittent noises: effects of nocturnal heat and daytime exposure.

During sleep, in thermoneutral conditions, the noise of a passing vehicle induces a biphasic cardiac response, a transient peripheral vasoconstriction and sleep disturbances. The present study was performed to determine whether or not the physiological responses were modified in a hot environment or after daytime exposure to both heat and noise. Eight young men were exposed to a nocturnal thermoneutral (20 degrees C) or hot (35 degrees C) environment disturbed by traffic noise. During the night, the peak intensities were of 71 dB(A) for trucks, 67 dB(A) for motorbikes and 64 dB(A) for cars. The background noise level (pink noise) was set at 30 dB(A). The noises were randomly distributed at a rate of 9.h-1. Nights were equally preceded by daytime exposure to combined heat and noise or to no disturbance. During the day, the noises as well as the background noise levels were increased by 15 dB(A) and the rate was 48.h-1. Electroencephalogram (EEG) measures of sleep, electrocardiograms and finger pulse amplitudes were continuously recorded. Regardless of the day condition, when compared with undisturbed nights, the nocturnal increase in the level of heart rate induced by heat exposure disappeared when noise was added. Percentages, delays, magnitudes and costs of cardiac and vascular responses as well as EEG events such as transient activation phases (TAP) due to noise were not affected by nocturnal thermal load or by the preceding daytime exposure to disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

A chamber-experiment investigation of the interaction between perceptions of noise and odor in humans.

OBJECTIVES: This study was designed to investigate human comfort and health effects following exposure to noise and odor and to explore the interaction between perceptions of noise and odor in humans. MATERIALS AND METHODS: Nine healthy subjects were randomly exposed to noise, odor, and their combination, in a 3 x 3 Latin square design for 80 min in an exposure chamber. Continuous noise was broadcast at an average level of 75 dBA by a loudspeaker, and odor was provided by furfurylmercaptan (a coffee-aroma constituent). A standardized 28-item questionnaire, together with mood-scale ratings, nasal dimensions by acoustic rhinometry, addition tests for distraction, and skin humidity, were performed before and at the end of exposure. RESULTS: In the questionnaire investigation, the perceived "sound level" was significantly affected by noise and the combined exposures, while "odor intensity", "air quality", and "need more ventilation" was significantly affected by odor and the combined exposures. Perceptions of symptoms became worse with increasing exposure time, such as perceived "dry nose" and "sleepiness" by odor and combined exposures, "headache" by noise, "concentration difficulty", "general well being", and "stressed by being in the chamber" by noise, odor and combined exposures. In addition, the occurrence of interactions was analyzed by comparison of the ratings of perceived "sound level", "odor intensity", "air quality", and "need more ventilation" during the combined exposure with two single exposures. Insignificant interaction was found but it indicated a decreased tendency to perceptions of discomfort from "odor intensity", "air quality", and "need for more ventilation" when noise was added to odor exposure. CONCLUSION: It may be concluded that noise and odor cause discomfort in humans. Moreover, the study might indicate that additions of noise reduce (mask) the perception of discomfort from odor, and additions of odor have no or little affect on the perception of noise.

Adult↗
PubMed1997

Combined effects of hand-arm vibration and noise on temporary threshold shifts of hearing in healthy subjects.

OBJECT: To investigate whether hand-arm vibration and noise have a combined effect on temporary threshold shift (TTS) of hearing among healthy subjects. METHOD AND DESIGN: Nineteen healthy subjects with an average age of 25.7 (SD 7.7) years were exposed to vibration (30 m/s2, 60 Hz), noise [90 dB(A)] and both, respectively. The subject's right hand was placed on the plate of a vibrator and the right ear exposed to noise via headphones. Subjects were exposed to vibration and/or noise for 3 min and after a 1-min pause the exposure was repeated five times. Hearing thresholds at 1, 4 and 6 kHz were measured during the time periods before, between (during pauses) and after exposure. RESULTS: Exposure to vibration alone caused almost no hearing threshold changes at every frequency tested. But exposure to noise or a combination of vibration and noise caused a significant increase in TTSs at 4 and 6 kHz. Moreover, exposure to a combination of vibration and noise caused significantly higher TTSs than exposure to noise at 4 and 6 kHz. CONCLUSION: The present results demonstrate the combined effects of hand-arm vibration and noise can enhance exposure to hand-arm vibration and noise can enhance the TTS of hearing more than noise exposure, though hand-arm vibration alone may hardly affect TTS.

Adult↗
PubMed2005

Noise susceptibility of cochlear implant users: the role of spectral resolution and smearing.

The latest-generation cochlear implant devices provide many deaf patients with good speech recognition in quiet listening conditions. However, speech recognition deteriorates rapidly as the level of background noise increases. Previous studies have shown that, for cochlear implant users, the absence of fine spectro-temporal cues may contribute to poorer performance in noise, especially when the noise is dynamic (e.g., competing speaker or modulated noise). Here we report on sentence recognition by cochlear implant users and by normal-hearing subjects listening to an acoustic simulation of a cochlear implant, in the presence of steady or square-wave modulated speech-shaped noise. Implant users were tested using their everyday, clinically assigned speech processors. In the acoustic simulation, normal-hearing listeners were tested for different degrees of spectral resolution (16, eight, or four channels) and spectral smearing (carrier filter slopes of -24 or -6 dB/octave). For modulated noise, normal-hearing listeners experienced significant release from masking when the original, unprocessed speech was presented (which preserved the spectro-temporal fine structure), while cochlear implant users experienced no release from masking. As the spectral resolution was reduced, normal-hearing listeners' release from masking gradually diminished. Release from masking was further reduced as the degree of spectral smearing increased. Interestingly, the mean speech recognition thresholds of implant users were very close to those of normal-hearing subjects listening to four-channel spectrally smeared noise-band speech. Also, the best cochlear implant listeners performed like normal-hearing subjects listening to eight- to 16-channel spectrally smeared noise-band speech. These findings suggest that implant users' susceptibility to noise may be caused by the reduced spectral resolution and the high degree of spectral smearing associated with channel interaction. Efforts to improve the effective number of spectral channels as well as reduce channel interactions may improve implant performance in noise, especially for temporally modulated noise.

Acoustic Stimulation↗
PubMed1986

Differential susceptibility to noise-induced permanent threshold shift between albino and pigmented guinea pigs.

Evidence that reduced levels of cochlear melanin are associated with increased auditory sensitivity, increased levels of auditory fatigue and an increased susceptibility to noise-induced hearing loss led us to investigate the effects of noise exposure on the cochlear microphonic (CM) in albino and pigmented English shorthair guinea pigs. CMs were recorded from the round window prior to and at 90 min and 7 days after exposure to 45 min of 126 dB noise. Thresholds for the first detectable elicitation of the CM for four pure tones were determined and the output voltage of each cochlea was measured in 10 dB steps through intensity levels which produced a maximum voltage amplitude in the CM and voltage rollover. This analysis demonstrated that: albino guinea pigs displayed significantly lower auditory thresholds than did pigmented animals before exposure to noise; thresholds were elevated to comparable levels in both groups 90 min after noise exposure; pigmented guinea pigs showed a reliable recovery in CM thresholds 7 days after exposure to noise while thresholds in the albinos remained elevated to the same degree at both 90 min and 7 days after noise; 90 min after noise exposure, the maximum voltage output of albino cochleas was significantly less than that recorded from the cochleas of the pigmented guinea pigs. These results demonstrate that albino guinea pigs are more susceptible to the ototoxic effects of high intensity noise than pigmented guinea pigs. Converging evidence indicates that some aspects of cochlear function involve melanin pigment and that its absence may produce auditory abnormalities. Reduced melanin pigmentation may also contribute to such phenomena as noise-induced threshold shifts and individual differences in noise-induced hearing loss.

Albinism↗