Permanent Hearing Threshold Shift Research Articles

Similar susceptibility to temporary hearing threshold shifts despite different audiograms in harbor porpoises and harbor seals.

When they are exposed to loud fatiguing sounds in the oceans, marine mammals are susceptible to hearing damage in the form of temporary hearing threshold shifts (TTSs) or permanent hearing threshold shifts. We compared the level-dependent and frequency-dependent susceptibility to TTSs in harbor seals and harbor porpoises, species with different hearing sensitivities in the low- and high-frequency regions. Both species were exposed to 100% duty cycle one-sixth-octave noise bands at frequencies that covered their entire hearing range. In the case of the 6.5 kHz exposure for the harbor seals, a pure tone (continuous wave) was used. TTS was quantified as a function of sound pressure level (SPL) half an octave above the center frequency of the fatiguing sound. The species have different audiograms, but their frequency-specific susceptibility to TTS was more similar. The hearing frequency range in which both species were most susceptible to TTS was 22.5-50 kHz. Furthermore, the frequency ranges were characterized by having similar critical levels (defined as the SPL of the fatiguing sound above which the magnitude of TTS induced as a function of SPL increases more strongly). This standardized between-species comparison indicates that the audiogram is not a good predictor of frequency-dependent susceptibility to TTS.

Alterations of auditory sensory gating in mice with noise-induced tinnitus treated with nicotine and cannabis extract.

Tinnitus is a phantom sound perception affecting both auditory and limbic structures. The mechanisms of tinnitus remain unclear and it is debatable whether tinnitus alters attention to sound and the ability to inhibit repetitive sounds, a phenomenon also known as auditory gating. Here we investigate if noise exposure interferes with auditory gating and whether natural extracts of cannabis or nicotine could improve auditory pre-attentional processing in noise-exposed mice. We used 22 male C57BL/6J mice divided into noise-exposed (exposed to a 9-11 kHz narrow band noise for 1 h) and sham (no sound during noise exposure) groups. Hearing thresholds were measured using auditory brainstem responses, and tinnitus-like behavior was assessed using Gap prepulse inhibition of acoustic startle. After noise exposure, mice were implanted with multi-electrodes in the dorsal hippocampus to assess auditory event-related potentials in response to paired clicks. The results showed that mice with tinnitus-like behavior displayed auditory gating of repetitive clicks, but with larger amplitudes and longer latencies of the N40 component of the aERP waveform. The combination of cannabis extract and nicotine improved the auditory gating ratio in noise-exposed mice without permanent hearing threshold shifts. Lastly, the longer latency of the N40 component appears due to an increased sensitivity to cannabis extract in noise-exposed mice compared to sham mice. The study suggests that the altered central plasticity in tinnitus is more sensitive to the combined actions on the cholinergic and the endocannabinoid systems. Overall, the findings contribute to a better understanding of pharmacological modulation of auditory sensory gating.

Cx26 heterozygous mutations cause hyperacusis-like hearing oversensitivity and increase susceptibility to noise.

Gap junction gene GJB2 (Cx26) mutations cause >50% of nonsyndromic hearing loss. Its recessive hetero-mutation carriers, who have no deafness, occupy ~10 to 20% of the general population. Here, we report an unexpected finding that these heterozygote carriers have hearing oversensitivity, and active cochlear amplification increased. Mouse models show that Cx26 hetero-deletion reduced endocochlear potential generation in the cochlear lateral wall and caused outer hair cell electromotor protein prestin compensatively up-regulated to increase active cochlear amplification and hearing sensitivity. The increase of active cochlear amplification also increased sensitivity to noise; exposure to daily-level noise could cause Cx26+/- mice permanent hearing threshold shift, leading to hearing loss. This study demonstrates that Cx26 recessive heterozygous mutations are not "harmless" for hearing as previously considered and can cause hyperacusis-like hearing oversensitivity. The data also indicate that GJB2 hetero-mutation carriers are vulnerable to noise and should avoid noise exposure in daily life.

Applying technical guidance from the USA for management of impacts of anthropogenic noise on wildlife in other countries: the Canadian context

Technical Guidance from the US National Marine Fisheries Service recommends Federal agencies use estimated thresholds for peak sound pressure levels and weighted cumulative sound exposure levels for the onset of permanent (and temporary) hearing threshold shifts in marine mammals. These dual metrics were developed to inform impact assessments within the US legal landscape. Despite its merits, the Technical Guidance contains uncertainties due to limited data on marine mammal hearing and auditory response to noise. The underlying assumptions about how representative existing data are for all marine mammal species also create limitations in the applicability of the Technical Guidance. These limitations warrant consideration before the Technical Guidance can be applied effectively in other jurisdictions with different legal standards. Using the Canadian legal framework as a working example, we found that many Canadian species are underrepresented in the dataset informing the Technical Guidance. The Technical Guidance also does not address all relevant noise impact types. Thus, the Technical Guidance alone cannot address all Canadian legal standards and, if the Technical Guidance is incorporated, some adjustments to the criteria within may be needed to meet the precautionary requirements of many Canadian legal standards.

Application of ISO 1999:2013 (E) model in risk assessment of hearing loss caused by industrial noise

To assess the risk of hearing loss caused by industrial noise exposure of welders and assemblers in a mechanical equipment manufacturing enterprise, and to explore the practical application and possible underestimation of ISO 1999∶2013(E) model. A total of 829 noise-exposed male workers from a mechanical equipment manufacturing enterprise were selected as study subjects. The questionnaire survey was administered, and individual noise exposure level(L_(Aeq.8 h)) and hearing loss level were measured. The risk assessment method of ISO 1999∶2013(E) was used to calculate the change of hearing threshold level and the risk of noise-induced hearing loss. By comparing the median of permanent hearing threshold shift caused by actual noise with the median of ISO1999 predicted value, the reason of the difference between the predicted value of ISO 1999∶2013(E) model and the actual value was analyzed. The L_(Aeq.8 h )was 89.5 dB(A), 77.4%(n=62)of the individual noise exposure levels exceeded 85 dB(A), and 24.6% of the participants(n=829) had different degrees of hearing loss. There was significant difference in hearing loss rate between welding and assembly positions(χ~2=10.07, P<0.01). The risk of noise-induced high-frequency hearing loss of 90% welders was 11.2% at the age of 50, and 14.0% at the age of 60. The risk of noise-induced deafness of 90% welders was 4.3% at the age of 60. The risk of high noise-induced frequency hearing loss of 90% assemblers was at the range of 4.0%-9.0% at the age of 40, 20.8% at the age of 50, and 22.5% at the age of 60. The risk of noise-induced deafness of 90% assemblers was at the range of 1.4%-6.4% at the age of 50, and 9.0% at the age of 60. Compared with actual median of permanent hearing threshold shift, ISO1999∶2013(E) predictions underestimated the median of permanent hearing threshold shift at 10.7 dB. The noise hazards of welding and assembly positions in mechanical equipment manufacturing enterprises are high relatively. ISO1999∶2013(E) can be used to predict the risk of noise-induced hearing loss in workers, but attention should be paid to the risk underestimation of this model.

Binaural brainstem and spatial hearing deficits in a guinea pig model of noise-Induced cochlear synaptopathy

Animal studies have revealed that moderate-level noise exposure can cause a permanent loss of ribbon synapses between inner hair cells and auditory-nerve fibers, but only temporary threshold shifts. Such noise-induced cochlear synaptopathy has been called ‘hidden hearing loss’ because while there is a significant degeneration of ribbon synapses, the resulting hearing dysfunction is effectively hidden from typical clinical assays. Here we used guinea pigs to study the mechanisms leading to hearing deficits resulting from a moderate noise. We measured distortion product otoacoustic emissions and auditory brainstem responses to assay peripheral hearing. We tested spatial hearing ability through the prepulse inhibition (PPI) of the acoustic startle reflex. PPI was used to measure hearing-in-noise ability, or spatial release from masking, as this task approximates the “cocktail party” effect. Finally, we performed immunohistochemistry to confirm synaptopathy. Results show that the noise exposure induces no permanent hearing threshold shift, but despite recovery of normal audibility, both behavioral and electrophysiological binaural hearing deficits persisted. Cochlear synaptopathy was objectively confirmed by visualizing the loss of ribbon synapses in the cochlea. The results demonstrate that cochlear synaptopathy causes deficits in brainstem circuits known to be critical for binaural and spatial hearing. [Work supported by Otolaryngology T32 DC012280.]

Acute High Level Noise Exposure Can Cause Physiological Dysfunction in Macaque Monkeys: Insight on the Medical Protection for Special Working Environmental Personnel.

The high level noise caused by intense acoustic weapons and blasting is a common source of acute acoustic trauma faced by some special environmental personnel. Studies have shown that high level noise can cause auditory and non-auditory effects. However, there are few reports on the biological effects, especially the non-auditory effects of acute high level noise exposure in simulated special working environments, and the great differences between experimental animals and human beings make it difficult to extrapolate from research conclusions. In this study, macaque monkeys were used to detect the effects of acute high level noise exposure on hearing, cognition, and cardiovascular function. Auditory brainstem response, auditory P300, and electrocardiogram (ECG) of macaque monkeys were measured. Results showed that acute high level noise exposure caused permanent hearing threshold shifts; partial hearing loss which couldn’t recover to normal levels in the detection period; pathological changes in T wave and QRS complexes; and large fluctuations in cognitive ability after exposure, which finally recovered to normal. These alterations may be a combination of effects caused by stress-induced neuroendocrine dysfunction and mechanical damage of auditory organs. To elaborate the exact mechanism, further studies are still needed. Meanwhile, positive measures should be taken to reduce the incidence of acute high level noise injury.

Research progress of hidden hearing loss in occupational health surveillance

According to the research on the pathogenesis of the hidden hearing loss in recent years, the occurrence of the hidden hearing loss is earlier than the permanent hearing threshold shift. This paper reviews the risk factors of hidden hearing loss, the pathogenesis of noise-induced hidden hearing loss, and the detection methods of hidden hearing loss. To explore the significance of hidden hearing loss in occupational health surveillance, and to provide reference for hearing protection of workers exposed to noise and hearing loss early in the future.

Anthropogenic Sound Exposure-Induced Stress in Captive Dolphins and Implications for Cetacean Health

Many cetaceans are exposed to increasing pressure caused by anthropogenic activities in their marine environment. Anthropogenic sound has been recognized as a possible stressor for cetaceans that may have impacts on health. However, the relationship between stress, hormones, and cytokines secretion in cetaceans is complex and not fully understood. Moreover, the effects of stress are often inconsistent because the character, intensity, and duration of the stressors are variable. For a better understanding of how anthropogenic sounds affect the psychophysiology of cetaceans, the present study compared the changes of cortisol concentration and cytokine gene transcriptions in blood samples and behaviors of captive bottlenose dolphins (Tursiops truncatus) after sound exposures. The sound stimuli were 800 Hz pure-tone multiple impulsive sound for 30 min at three different sound levels (estimated mean received SPL: 0, 120, and 140 dB re 1 μPa) that likely cause no permanent and temporary hearing threshold shift in dolphins. Six cytokine genes (IL-2Rα, IL-4, IL-10, IL-12, TNF-α, and IFN-γ) were selected for analysis. Cortisol levels and IL-10 gene transcription increased and IFNγ/IL-10 ratio was lower after a 30-min high-level sound exposure, indicating the sound stimuli used in this study could be a stressor for cetaceans, although only minor behavior changes were observed. This study may shed light on the potential impact of pile driving-like sounds on the endocrine and immune systems in cetaceans and provide imperative information regarding sound exposure for free-ranging cetaceans.

Social Noise Exposure in a Sample of Slovak University Students.

Purpose: Social noise exposure is currently an emerging problem in adolescents and young adults. Various leisure time activities may be responsible for hearing impairment (temporary or permanent hearing threshold shift or hearing loss). The study aimed to quantify environmental noise from various sources—voluntary (social) noise (personal music players (PMPs), high-intensity noise exposure events), and road traffic noise and to detect hearing disorders in relation to individual listening to PMPs in the sample of young adults living and studying in Bratislava, the capital city of Slovakia. Methods: The study included 1003 university students (306 men and 697 women, average age 23.1 ± 2) living in Bratislava for 4 or more years; 347 lived in the student housing facility exposed to road traffic noise (LAeq = 67.6 dB) and 656 in the control one (LAeq = 53.4 dB). Respondents completed a validated ICBEN 5-grade scale “noise annoyance questionnaire”. In the exposed group a significant source of annoyance was road traffic noise (p < 0.001), noise from entertainment facilities (p < 0.001), industrial noise (p < 0.001), and noise from neighboring flats (p = 0.003). The exposure to PMPs was objectified by the conversion of the subjective evaluation of the volume setting and duration. With the cooperation of the Ear, Nose and Throat (ENT)specialist, we arranged audiometric examinations on the pilot sample of 41 volunteers. Results: From the total sample of respondents, 79.2% reported the use of a PMP in the course of the last week, and the average time was 285 min. There was a significant difference in PMP use between the road traffic noise-exposed (85.6%) and the control group (75.8%) (p = 0.01). Among PMP users 30.7% exceeded the lower action value (LAV) for industry (LAeq,8h = 80 dB). On a pilot sample of volunteers (n = 41), audiometry testing was performed indicating a hearing threshold shift at higher frequencies in 22% of subjects. Conclusions: The results of the study on a sample of young healthy individuals showed the importance of exposure to social noise as well as to road traffic noise and the need for prevention and intervention.

Acoustic Trauma Modulates Cochlear Blood Flow and Vasoactive Factors in a Rodent Model of Noise-Induced Hearing Loss.

Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and spiral ligament fibrocytes in the lateral wall consist of a significant proportion of cells in the cochlea, relatively little is known regarding their functional significance. In this study, 6-week-old male C57BL/6 mice were exposed to noise trauma to induce transient hearing threshold shift (TTS) or permanent hearing threshold shift (PTS). Compared to mice with TTS, mice with PTS exhibited lower cochlear blood flow and lower vessel diameter in the stria vascularis, accompanied by reduced expression levels of genes involved in vasodilation and increased expression levels of genes related to vasoconstriction. Ultrastructural analyses by transmission electron microscopy revealed that the stria vascularis and spiral ligament fibrocytes were more damaged by PTS than by TTS. Moreover, mice with PTS expressed significantly higher levels of proinflammatory cytokines in the cochlea (e.g., IL-1β, IL-6, and TNF-α). Overall, our findings suggest that cochlear microcirculation and lateral wall pathologies are differentially modulated by the severity of acoustic trauma and are associated with changes in vasoactive factors and inflammatory responses in the cochlea.

Effects of shipping on marine acoustic habitats in Canadian Arctic estimated via probabilistic modeling and mapping

Canadian Arctic and Subarctic regions experience a rapid decrease of sea ice accompanied with increasing shipping traffic. The resulting time-space changes in shipping noise are studied for four key regions of this pristine environment, for 2013 traffic conditions and a hypothetical tenfold traffic increase. A probabilistic modeling and mapping framework, called Ramdam, which integrates the intrinsic variability and uncertainties of shipping noise and its effects on marine habitats, is developed and applied. A substantial transformation of soundscapes is observed in areas where shipping noise changes from present occasional-transient contributor to a dominant noise source. Examination of impacts on low-frequency mammals within ecologically and biologically significant areas reveals that shipping noise has the potential to trigger behavioral responses and masking in the future, although no risk of temporary or permanent hearing threshold shifts is noted. Such probabilistic modeling and mapping is strategic in marine spatial planning of this emerging noise issues.

Statistical tool to detect small hearing threshold shifts

Objective: The aim of this study is to present a new tool that can be used in the prevention of noise-induced hearing loss. Even in most countries where noise levels are well regulated, many workers are still exposed to high levels of noise and suffer from permanent threshold shifts. It is necessary to develop a new strategy to prevent such damage. Method: A statistical process control (SPC) scheme is presented that is able to detect both large and small hearing threshold shifts. Monte Carlo simulations were used to assess the performance of this hearing monitoring scheme. Different hearing threshold shifts were simulated to evaluate the performance of a variety of hearing development scenarios. Results: It is possible to detect hearing threshold shifts smaller than the standard deviation of the hearing tests performed. This means that permanent hearing threshold shifts smaller than 5 dB can be detected and acted on. Outliers can also be automatically detected and treated, increasing the robustness of the monitoring scheme. Conclusion: The proposed statistical framework can be used as an early warning indicator of noise-induced hearing loss with the aim of improving workers’ safety. Individual counteractions can be implemented, reducing the risk of further damage.

Development of the acoustic startle response in rats and its change after early acoustic trauma

Even brief acoustic trauma during the critical period of development that results in no permanent hearing threshold shift may lead to altered auditory processing in adulthood. By monitoring the acoustic startle response (ASR), we examined the development of auditory function in control rats and in rats exposed to intense noise at the 14th postnatal day (P14). First ASRs appeared on P10–P11 to intense low-frequency tones. By P14, the range of sound intensities and frequencies eliciting ASRs extended considerably, the ASR reactivity being similar at all frequencies (4–32kHz). During the subsequent two weeks, ASR amplitudes to low-frequency stimuli (4–8kHz) increased, whereas the ASRs to high-frequency tones were maintained (16kHz) or even decreased (32kHz). Compared to controls, noise exposure on P14 (125dB SPL for 8, 12, or 25min) produced transient hyper-reactivity to startle stimuli, manifested by a decrease of ASR thresholds and an increase of ASR amplitudes. ASR enhancement occurred regardless of permanent hearing loss and was more pronounced at high frequencies. The hyper-reactivity of ASRs declined by P30; the ASR amplitudes in adult exposed rats were lower than in controls. The histological control did not reveal loss of hair cells in adult exposed rats, however, the number of inner hair cell ribbon synapses was significantly decreased, especially in the high-frequency part of the cochlea. The results indicate that early acoustic trauma may result in complex changes of ASRs during development.

Mitochondrial DNA common deletion increases susceptibility to noise-induced hearing loss in a mimetic aging rat model

Noise-induced hearing loss (NIHL) is an important occupational health hazard. However, susceptibility to NIHL remains poorly understood. The present study was designed to investigate whether mitochondrial DNA common deletion (CD) increases the susceptibility of individuals to NIHL. A mimetic aging rat model harboring increased CD in the inner ear was established by chronic d-galactose administration, and the synergic effect of CD and noise on hearing sensitivity was assessed. We determined that although developed the same magnitude of temporary threshold shifts and hair cell loss, the d-galactose treated rats with increased CD in the inner ear exhibited a longer hearing recovery process and experienced higher permanent hearing threshold shifts at high frequencies than the saline-treated control rats. Greater supporting cell damage and stria vascularis ultrastructural changes were observed in d-galactose treated rats three weeks after recovery. The results suggested that the elevated CD in the inner ear could increase an individual’s susceptibility to NIHL, which likely through a reduction in the self-repairing capability within the cochlea after acoustic injury.

Therapeutic effects of orally administrated antioxidant drugs on acute noise-induced hearing loss

Objective. The objective of this study was to investigate the dose-dependent therapeutic effect of the orally administrated antioxidant drugs [4-hydroxy alpha-phenyl-tert-butylnitrone (4-OHPBN) and N-acetyl-L-cysteine (NAC)] on acute noise-induced hearing loss because oral administration is the most commonly used method of drug administration due to its convenience, safety, and economical efficiency. Methods. Thirty chinchilla were exposed to a 105 dB octave band noise centered at 4 kHz for 6 h and randomly assigned to a control group (saline only) and three experimental groups [4-OHPBN (10 mg/kg) plus NAC (20 mg/kg), 4-OHPBN (20 mg/kg) plus NAC (50 mg/kg), and 4-OHPBN (50 mg/kg) plus NAC (100 mg/kg)]. The drugs were orally administrated beginning 4 h after noise exposure and then administered twice daily for the next 2 days. Permanent auditory brainstem response threshold shifts, distortion product otoacoustic emission threshold shifts, and the percentage of missing outer hair cell were determined. Results. The oral administration significantly reduced permanent hearing threshold shift, distortion product otoacoustic emission threshold shift, and the percentage of missing outer hair cell in a dose-dependent manner. Discussion. This result demonstrates that orally administered drugs can treat acute noise-induced hearing loss in a dose-dependent manner. This suggests that oral administration was effective in treating acute noise-induced hearing loss as in intraperitoneal administration.

Prevalence of permanent hearing threshold shift among workers of Indian iron and steel small and medium enterprises: a study.

Occupational noise exposure and noise-induced hearing loss (NIHL) have been recognized as a problem among workers in Indian industries. The major industries in India are based on manufacturing. There are appreciable numbers of casting and forging units spread across the country. The objective of this study is to determine the prevalence of permanent hearing threshold shift among the workers engaged in Indian iron and steel small and medium enterprises (SMEs) and compared with control group subjects. As a part of hearing protection intervention, audiometric tests were conducted at low (250-1000 Hz), medium (1500-3000 Hz), and high (4000-8000 Hz) frequencies. The occurrence of hearing loss was determined based on hearing threshold levels with a low fence of 25 dB. Comparisons were made for hearing threshold at different frequencies between the exposed and control groups using Student's t test. ANOVA was used for the comparison of hearing threshold dB at different frequencies among occupation and year of experience. A P value <0.05 was considered as statistically significant. All data were presented as mean value (SD). Over 90% of workers engaged in various processes of casting and forging industry showed hearing loss in the noise-sensitive medium and higher frequencies. Occupation was significantly associated with NIHL, and hearing loss was particularly high among the workers of forging section. The analyses revealed a higher prevalence of significant hearing loss among the forging workers compared to the workers associated with other activities. The study shows alarming signals of NIHL, especially in forging workers. The occupational exposure to noise could be minimized by efficient control measures through engineering controls, administrative controls, and the use of personal protective devices. Applications of engineering and/or administrative controls are frequently not feasible in the developing countries for technical and financial reasons. A complete hearing conservation programme, including training, audiometry, job rotation, and the use of hearing protection devices, is the most feasible method for the protection of industrial workers from prevailing noise in workplace environments in the developing countries.

Ambient noise levels in the chemotherapy clinic

Many of the drugs used for chemotherapy treatments are known to be ototoxic, and can result in permanent hearing threshold shifts. The degree of ototoxic damage can be influenced by many factors including dosage, duration of exposure, genetics, and coadministration with other ototoxic agents. Cisplatin is known for its ototoxic effects on hearing thresholds, particularly in the high frequencies. Recent studies have indicated a synergistic relationship between Cisplatin administration and moderate to high noise level exposure starting between 70-85 dB SPL. This study measured the noise levels in the Portland Veteran's Affairs Medical Center's outpatient chemotherapy clinic. Average (LAeq) and peak (LCpeak) noise measures were recorded every minute from 7 am until 6 pm on the two busiest clinic days. Patients, visitors, and staff members filled out anonymous surveys regarding their reactions to noise levels. Cumulative noise levels were not at levels known to interact with Cisplatin for a significant period of time. Noise measurement analysis indicated that levels were at or above 70 dB SPL for less than ten minutes during the 11-hour recording window. The patient and visitor surveys indicated that both groups were unbothered by noise in the clinic. However, most staff members were bothered by or concerned about noise levels, and many felt that it caused stress and difficulty communicating on the phone.

Physiological and Morphological Assessment of the Saccule in Guinea Pigs After Noise Exposure

To investigate whether the saccule exhibits temporary or permanent functional loss resembling threshold shifts in auditory brainstem response (ABR) of guinea pigs following noise exposure. Randomly bred guinea pigs were divided into 3 groups: A (short-term noise exposure, 30 minutes, n = 15), B (long-term noise exposure, 40 hours, n = 9), and C (no noise exposure, n = 5). University hospital. All animals underwent vestibular-evoked myogenic potential (VEMP) and ABR tests. Chronological changes of VEMP and ABR responses following noise exposure were analyzed and compared. After audiovestibular function testing, animals were killed for morphological study with light and electron microscopy. In group A, temporary VEMP loss and ABR threshold shifts recovered 2 and 4 days, respectively, after short-term noise exposure, with an interval of 2 days earlier in the recovery of VEMPs than that of ABR thresholds. In contrast, in group B, 78% and 83% of the ears exhibited permanent VEMP loss and ABR threshold shifts, respectively, 10 days following long-term noise exposure. In group C, all animals showed normal VEMPs and ABRs throughout the study period. Light and electron microscopic studies confirmed that loss of VEMPs correlated with saccular lesion. The saccule can exhibit temporary or permanent functional loss resembling hearing threshold shifts in guinea pigs following noise exposure. Recovery of VEMP precedes restoration of hearing threshold after damage from short-term noise exposure. Conversely, permanent VEMP loss after long-term noise exposure may reflect permanent hearing threshold shifts.

Preventive effect of magnesium supplement on noise-induced hearing loss in the guinea pig.

The effect of magnesium (Mg) on noise-induced hearing loss was investigated in two groups of adult pigmented guinea pigs maintained either on optimal or suboptimal (physiologically high or low) Mg produced by different diets. The total Mg concentrations of the perilymph (PL), cerebrospinal fluid, blood plasma and red blood cells were measured by atomic absorption spectrometry and were found to differ significantly between the two groups (P < 0.01). One ear of each animal was exposed to either a single shooting impulse at a peak pressure level of 187 dB or two impulse noise series at a rate of 1/s and peak pressure levels of 150 dB (1,000 impulses) and 167 dB (2,280 impulses), respectively. Temporary (TTS) and permanent (PTS) hearing threshold shifts in anesthetized animals were measured 2 h and 1 week after the noise exposure, using auditory brain stem response (ABR) audiometry at a frequency range from 3.75 to 30 kHz. Exposure to the single noise impulse resulted in a mean TTS that was significantly lower in the high Mg group than that in the low Mg group (P < 0.05), although no substantial PTS was observed in either group. In the animals exposed to 150 dB noise, the TTS showed a tendency towards an Mg-related reduction at the higher frequencies. A small difference in PTS was found between the low Mg and high Mg groups, but was not significant. Exposure to the 167-dB noise series caused a considerable TTS, which was significantly lower in the high Mg group at 7.5 and 15 kHz than in the low Mg group (P < 0.05). The mean PTS showed a significant difference between the two Mg groups over the whole frequency range (P < 0.05) and was found to correlate negatively with the total Mg concentrations of both PL and plasma (P < 0.05). Moreover, the high Mg group showed a faster recovery from the hearing threshold shift than the low Mg group. The present findings show that preventive oral Mg supplements can significantly reduce the rate of acoustic trauma caused by high-level impulse noise exposure in the guinea pig.