Parameters influencing auditory fatigue among professionals working in the amplified music sector: noise exposure and individual factors.

OBJECTIVE: Hearing disorders are common among music professionals, as they are frequently exposed to sound levels exceeding 100 dB(A). By assessing auditory fatigue, situations that are deleterious for hearing could be identified, allowing the deployment of preventive measures before permanent impairment occurs. However, little is known about the factors contributing to auditory fatigue. The objective is to determine the exposure parameters most influencing auditory fatigue during occupational exposure to amplified music. DESIGN: Auditory fatigue was defined as variations of both pure tone auditory (ΔPTA) and efferent reflex thresholds (ΔER) during the workday. Noise exposure was monitored and information on the volunteers was gathered using a questionnaire. STUDY SAMPLE: The population consisted of 43 adult volunteers exposed to amplified music (sound, light or stage technicians, security agents, barmen) and 24 unexposed administrative agents. RESULTS: ΔPTA and ΔER were positively correlated with the energy of noise exposure and its stability over time, i.e a steady noise tends to create more auditory fatigue. CONCLUSION: In addition to a global decrease of music levels and a systematic use of hearing protection, our results advocate for the provision of quiet periods within noise exposures as they reduce auditory fatigue accumulation and long-term risks for hearing.

Temporary and Permanent Auditory Effects Associated with Occupational Coexposure to Low Levels of Noise and Solvents.

This study aimed to assess temporary and permanent auditory effects associated with occupational coexposure to low levels of noise and solvents. Cross-sectional study with 25 printing industry workers simultaneously exposed to low noise (<80 dBA TWA) and low levels of solvents. The control group consisted of 29 industry workers without the selected exposures. Participants answered a questionnaire and underwent auditory tests. Auditory fatigue was measured by comparing the acoustic reflex threshold before and after the workday. Workers coexposed to solvents and noise showed significantly worse results in auditory tests in comparison with the participants in the control group. Auditory brainstem response results showed differences in III−V interpeak intervals (p = 0.046 in right ear; p = 0.039 in left ear). Mean dichotic digits scores (exposed = 89.5 ± 13.33; controls = 96.40 ± 4.46) were only different in the left ear (p = 0.054). The comparison of pre and postacoustic reflex testing indicated mean differences (p = 0.032) between the exposed (4.58 ± 6.8) and controls (0 ± 4.62) groups. This study provides evidence of a possible temporary effect (hearing fatigue) at the level of the acoustic reflex of the stapedius muscle. The permanent effects were identified mainly at the level of the high brainstem and in the auditory ability of binaural integration.

Effects of co-exposure to CS2 and noise on hearing and balance in rats: continuous versus intermittent CS2 exposures.

BACKGROUND: Carbon disulfide (CS2) exacerbates the effect of noise on hearing, and disrupts the vestibular system. The goal of this study was to determine whether these effects are also observed with intermittent CS2 exposure. METHODS: Rats were exposed for 4 weeks (5 days/week, 6 h/day) to a band noise at 106 dB SPL either alone or combined with continuous (63 ppm or 250 ppm) or intermittent (15 min/h or 2 × 15 min/h at 250 ppm) CS2. Hearing function was assessed by measuring distortion product otoacoustic emissions (DPOAEs); balance was monitored based on the vestibulo-ocular reflex (VOR). Functional measurements were performed before, at the end of exposure and 4 weeks later. Histological analyses of the inner ear were also performed following exposure and after the 4-week recovery period. RESULTS: The results obtained here confirmed that CS2 exposure exerts two differential temporary effects on hearing: (1) it attenuates the noise-induced DPOAE decrease below 6 kHz probably through action on the middle ear reflex when exposure lasts 15 min per hour, and (2) continuous exposure to 250 ppm for 6 h extends the frequency range affected by noise up to 9.6 kHz (instead of 6 kHz with noise alone). With regard to balance, the VOR was reversibly disrupted at the two highest doses of CS2 (2 × 15 min/h and continuous 250 ppm). No morphological alterations to the inner ear were observed. CONCLUSION: These results reveal that short periods of CS2 exposure can alter the sensitivity of the cochlea to noise at a dose equivalent to only 10 times the short-term occupational limit value, and intermittent exposure to CS2 (2 × 15 min/h) can alter the function of the vestibular system.

Measuring the middle-ear reflex: A quantitative method to assess effects of industrial solvents on central auditory pathways.

Volatile organic solvents are frequently present in industrial atmospheres. Their lipophilic properties mean they quickly reach the brain following inhalation. Acute exposure to some solvents perturbs the middle ear reflex, which could jeopardize cochlear protection against loud noises. As the physiological mechanisms involved in this protective reflex are highly complex, in vivo rodent models are required to allow rapid and reliable identification of any adverse effects of solvents on the middle ear reflex (MER). In this study, MER amplitude was measured in anesthetized Brown-Norway rats by monitoring the decrease in distortion product otoacoustic emissions (DPOAEs) caused by a contralateral stimulation. Our screening test consisted in measuring the impact of inhalation of solvent vapors at 3000 ppm for 15 min on the MER amplitude. We had previously studied a selection of aromatic solvents with this model; here, we extended the analysis to volatile compounds from other chemical families. The results obtained shed light on the mechanisms involved in the interactions between solvents and their neuronal targets. Thus, benzene and chlorobenzene had the greatest effect on MER (≥ + 1.8 dB), followed by a group composed of toluene, styrene, p-xylene, m-xylene, tetrachloroethylene and cyclohexane, which had a moderate effect on the MER (between + 0.3 and + 0.7 dB). Finally, trichloroethylene, n-hexane, methyl-ethyl-ketone, acetone, o-xylene, and ethylbenzene had no effect on the MER. Thus, the effect of solvents on the MER is not simply linked to their lipophilicity, rather it depends on specific interactions with neuronal targets. These interactions appear to be governed by the compound's chemical structure, e.g. the presence of an aromatic ring and its steric hindrance. In addition, perturbation of the MER by a solvent is independent of its toxic effects on cochlear cells. As the MER plays a protective role against exposure to high-intensity noises, these findings could have a significant impact in terms of prevention for subjects exposed to both noise and solvents.

Combined exposure to carbon disulfide and low-frequency noise reversibly affects vestibular function.

Chronic occupational exposure to carbon disulfide (CS2) has debilitating motor and sensory effects in humans, which can increase the risk of falls. Although no mention of vestibulotoxic effects is contained in the literature, epidemiological and experimental data suggest that CS2 could cause low-frequency hearing loss when associated with noise exposure. Low-frequency noise might also perturb the peripheral balance receptor through an as-yet unclear mechanism. Here, we studied how exposure to a low-frequency noise combined with 250-ppm CS2 affected balance in rats. Vestibular function was tested based on post-rotary nystagmus recorded by a video-oculography system. These measurements were completed by behavioral tests and analysis of the cerebellum to measure expression levels for gene expression associated with neurotoxicity. Assays were performed prior to and following a 4-week exposure, and again after a 4-week recovery period. Functional measurements were completed by histological analyses of the peripheral organs.Nystagmus was unaltered by exposure to noise alone, while CS2 alone caused a moderate 19% decrease of the saccade number. In contrast, coexposure to 250-ppm CS2 and low-frequency noise decreased both saccade number and duration by 33% and 34%, respectively. After four weeks, recovery was only partial but measures were not significantly different from pre-exposure values. Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of cerebellar tissue revealed a slight but significant modification in expression levels for two genes linked to neurotoxicity in CS2-exposed animals. However, neither histopathological changes to the peripheral receptor nor behavioral differences were observed. Based on all these results, we propose that the effects of CS2 were due to reversible neurochemical disturbance of the efferent pathways managing post-rotatory nystagmus. Because the nervous structures involving the vestibular function appear particularly sensitive to CS2, post-rotary nystagmus could be used as an early, non-invasive measurement to diagnose CS2 intoxication as part of an occupational conservation program.

Auditory fatigue among call dispatchers working with headsets.

OBJECTIVES: To determine whether call center dispatchers wearing headsets are subject to auditory fatigue at the end of a work shift. MATERIAL AND METHODS: Data was gathered at times when call centers were busiest. All call operators wore a headset for up to 12 h. Acoustic environment and noise exposure under the headset were continuously recorded during the entire work shift. Variations in auditory parameters were assessed using pure-tone air-conduction audiometry and an objective test based on distortion product otoacoustic emissions - contralateral suppression of distortion product otoacoustic emission (DPOAE) amplitudes (EchoScan test). Thirty-nine operators and 16 controls, all volunteers, were selected from 3 call centers (sales, assistance, and emergency) where all cognitive tasks were accomplished by phone and on computers. RESULTS: No acoustic shock was detected during the investigation. The highest normalized noise exposure (daily noise exposure level - LEX,8 h) measured was 75.5 dBA. No significant variation in auditory performances was detected with either pure-tone air-conduction audiometry or the EchoScan test. Nevertheless, dispatchers expressed a feeling of tiredness. CONCLUSIONS: For an equivalent diffuse field noise exposure, the use of a headset does not seem to worsen auditory fatigue for call center operators. The dispatcher's fatigue was probably due to the duration of the work shift or to the tasks they performed rather than to the noise exposure under a headset. Int J Occup Med Environ Health 2018;31(2):217-226.

Continuous exposure to low-frequency noise and carbon disulfide: Combined effects on hearing.

Carbon disulfide (CS2) is used in industry; it has been shown to have neurotoxic effects, causing central and distal axonopathies.However, it is not considered cochleotoxic as it does not affect hair cells in the organ of Corti, and the only auditory effects reported in the literature were confined to the low-frequency region. No reports on the effects of combined exposure to low-frequency noise and CS2 have been published to date. This article focuses on the effects on rat hearing of combined exposure to noise with increasing concentrations of CS2 (0, 63,250, and 500ppm, 6h per day, 5 days per week, for 4 weeks). The noise used was a low-frequency noise ranging from 0.5 to 2kHz at an intensity of 106dB SPL. Auditory function was tested using distortion product oto-acoustic emissions, which mainly reflects the cochlear performances. Exposure to noise alone caused an auditory deficit in a frequency area ranging from 3.6 to 6 kHz. The damaged area was approximately one octave (6kHz) above the highest frequency of the exposure noise (2.8kHz); it was a little wider than expected based on the noise spectrum.Consequently, since maximum hearing sensitivity is located around 8kHz in rats, low-frequency noise exposure can affect the cochlear regions detecting mid-range frequencies. Co-exposure to CS2 (250-ppm and over) and noise increased the extent of the damaged frequency window since a significant auditory deficit was measured at 9.6kHz in these conditions.Moreover, the significance at 9.6kHz increased with the solvent concentrations. Histological data showed that neither hair cells nor ganglion cells were damaged by CS2. This discrepancy between functional and histological data is discussed. Like most aromatic solvents, carbon disulfide should be considered as a key parameter in hearing conservation régulations.

Carbon disulfide potentiates the effects of impulse noise on the organ of Corti.

Occupational noise can damage workers' hearing, and the phenomenon is even more dangerous when noise is associated with an ototoxic solvent. Aromatic solvents are known to provoke chemical-induced hearing loss, but little is known about the effects on hearing of carbon disulfide (CS2) when combined with noise. Co-exposure to CS2 and noise may have a harmful effect on hearing, but the mechanisms involved are not well understood. For instance, CS2 is not thought to have a cochleotoxic effect, but rather it is thought to cause retrocochlear hearing impairment. In other words, CS2 could have a distal neuropathic effect on the auditory pathway. However, a possible pharmacological effect of CS2 on the central nervous system (CNS) has never been mentioned in the literature. The aim of this study was to assess, in rats, the effects of a noise (continuous vs. impulse), associated with a low concentration of CS2 [(short-term threshold limit value) x 10 as a safety factor] on the peripheral auditory receptor. The noise, whatever its nature, was an octave band noise centered at 8kHz, and the 250-ppm CS2 exposure lasted 15min per hour, 6h per day, for 5 consecutive days. The impact of the different experimental conditions on hearing loss was assessed using distortion product oto-acoustic emissions and histological analyses. Although the LEX,8h (8-h time-weighted average exposure) for the impulse noise was lower (84dB SPL) than that for the continuous noise (89dB SPL), it appeared more damaging to the organ of Corti, in particular to the outer hair cells. CS2 exposure alone did not have any effect on the organ of Corti, but co-exposure to continuous noise with CS2 was less damaging than exposure to continuous noise alone. In contrast, the cochleo-traumatic effects of impulse noise were significantly enhanced by co-exposure to CS2. Therefore, CS2 can clearly modulate the middle-ear reflex function. In fact, CS2 may have two distinct effects: firstly, it has a pharmacological effect on the CNS, modifying the trigger of the acoustic reflex; and secondly, it can make the organ of Corti more susceptible to impulse noise. The pharmacological effects on the CNS and the effects of CS2 on the organ of Corti are discussed to try to explain the overall effect of the solvent on hearing. Once again, the results reported in this article show that the temporal structure (continuous vs. impulse) of noise should be taken into consideration as a key parameter when establishing hearing conservation regulations.

Membrane fluidity does not explain how solvents act on the middle-ear reflex.

Some volatile aromatic solvents have similar or opposite effects to anesthetics in the central nervous system. Like for anesthetics, the mechanisms of action involved are currently the subject of debate. This paper presents an in vivo study to determine whether direct binding or effects on membrane fluidity best explain how solvents counterbalance anesthesia's depression of the middle-ear reflex (MER). Rats were anesthetized with a mixture of ketamine and xylazine while also exposed to solvent vapors (toluene, ethylbenzene, or one of the three xylene isomers) and the amplitude of their MER was monitored. The depth of anesthesia was standardized based on the magnitude of the contraction of the muscles involved in the MER, determined by measuring cubic distortion product oto-acoustic emissions (DPOAEs) while triggering the bilateral reflex with contralateral acoustic stimulation. The effects of the aromatic solvents were quantified based on variations in the amplitude of the DPOAEs. The amplitude of the alteration to the MER measured in anesthetized rats did not correlate with solvent lipophilocity (as indicated by logKow values). Results obtained with the three xylene isomers indicated that the positions of two methyl groups around the benzene ring played a determinant role in solvent/neuronal cell interaction. Additionally, Solid-state Nuclear Magnetic Resonance (NMR) spectra for brain microsomes confirmed that brain lipid fluidity was unaffected by solvent exposure, even after three days (6h/day) at an extremely high concentration (3000ppm). Therefore, aromatic solvents appear to act directly on the neuroreceptors involved in the acoustic reflex circuit, rather than on membrane fluidity. The affinity of this interaction is determined by stereospecific parameters rather than lipophilocity.

The tonotopicity of styrene-induced hearing loss depends on the associated noise spectrum.

The neuropharmacological and cochleotoxic effects of styrene can exacerbate the impact of noise on the peripheral auditory receptor. The mechanisms through which co-exposure to noise and styrene impairs hearing are complex as the slowly developing cochleotoxic process can be masked in the short-term by the rapid pharmacological effect on the central nervous system. The current investigation was therefore designed to delineate the auditory frequency range sensitive to noise, to styrene, and to noise and styrene combined. In case of different frequency ranges targeted by noise and styrene, it would be possible to point out the main factor responsible for cases of deafness by looking at the location of the audiometric deficits. Male Brown-Norway rats were exposed to 600-ppm styrene, to an octave band noise centered at 8 kHz, or to both noise and styrene. The noise exposure was of two different types: impulse noise with a LEX,8h (equivalent continuous noise level averaged over 8 h) of 80 dB and continuous noise with a LEX,8 h of 85 dB SPL. Hearing was tested using a non-invasive technique based on distortion product otoacoustic emissions. Hearing data were completed with histological analysis of cochleae. The results showed that exposure to styrene alone caused outer hair cell losses in the apical cochlear region, which discriminates low frequencies. In contrast, noise-induced hearing loss was located at half an octave above the central frequency of the spectrum, around 10-12 kHz. Damage due to impulse noise was significantly exacerbated by styrene, and the noise spectrum defined the location of the cochlear trauma. Combined exposure caused greater cell losses than the sum of losses measured with the impulse noise and styrene alone. The fact that the tonotopicity of the styrene-induced damage depends on the associated noise spectrum complicates the diagnosis of styrene-related hearing loss with a tone-frequency audiometric approach. In conclusion, there is not really a frequency specificity of impairments due to styrene.

Neuropharmacological and cochleotoxic effects of styrene. Consequences on noise exposures.

Occupational noise exposure can damage workers' hearing, particularly when combined with exposure to cochleotoxic chemicals such as styrene. Although styrene-induced cochlear impairments only become apparent after a long incubation period, the pharmacological impact of styrene on the central nervous system (CNS) can be rapidly measured by determining the threshold of the middle-ear acoustic reflex (MER) trigger. The aim of the study was to evaluate the effects of a noise (both continuous and impulse), and a low concentration of styrene [300ppm<(threshold limit value×10) safety factor] on the peripheral auditory receptor, and on the CNS in rats. The impact of the different conditions on hearing loss was assessed using distortion product oto-acoustic emissions, and histological analysis of cochleae. Although the LEX,8h (8-hour time-weighted average exposure) of the impulse noise was lower (80dB SPL sound pressure level) than that of the continuous noise (85dB SPL), it appeared more detrimental to the peripheral auditory receptors. A co-exposure to styrene and continuous noise was less damaging than exposure to continuous noise alone. In contrast, the traumatic effects of impulse noise on the organ of Corti were enhanced by co-exposure to styrene. The pharmacological effects of the solvent on the CNS were discussed to put forward a plausible explanation of these surprising results. We hypothesize that CNS effects of styrene may account for this apparent paradox. Based on the present results, the temporal structure of the noise should be reintroduced as a key parameter in hearing conservation regulations.

One-day measurement to assess the auditory risks encountered by noise-exposed workers.

UNLABELLED: Noise is one of the most pervasive hazards in the workplace. Despite regulations and preventive measures, noise-induced hearing loss is common. The current reference test is pure-tone air-conduction audiometry (PTA), but this test cannot be used to detect early hearing loss. OBJECTIVE: In this study, we assess one-day auditory fatigue using both PTA and efferent reflexes (ER) measured using DPOAEs associated with contralateral acoustic stimulation (CAS DPOAEs). DESIGN: The noise exposure history, PTA, and ER detection were performed in seven different companies where the L(EX,8h) was 85 dB(A). Hearing was tested before and at the end of the working day. STUDY SAMPLE: Forty-six volunteers were selected to carry out this study. RESULTS: After a single working day, a greater impact of noise was measured using ER thresholds than PTA or DPOAEs. ER measurements are objective, easy to perform, and do not require a sound-attenuated booth. CONCLUSION: Screening workers by periodically measuring ER thresholds using CAS DPOAEs helps detect early changes in hearing status, before the onset of noise-induced hearing loss. These tests can be readily applied as part of a hearing conservation program.

Inhaled toluene can modulate the effects of anesthetics on the middle-ear acoustic reflex.

Toluene (Tol) is an organic solvent widely used in the industry. It is also abused as an inhaled solvent, and can have deleterious effects on hearing. Recently, it was demonstrated that Tol has both anticholinergic and antiglutamatergic effects, and that it also inhibits voltage-dependent Ca(2+) channels. This paper describes a study of the effects of inhaled Tol on rats anesthetized with isoflurane, pentobarbital, or a mixture of ketamine/xylazine. Hearing was tested using distortion product oto-acoustic emissions (DPOAEs) associated with a contralateral noise to evaluate contraction of the middle-ear muscles. This allowed us to assess the interactions between the effects of Tol and anesthesia on the central nervous system (CNS). Although both anesthetics and Tol are known to inhibit the middle-ear acoustic reflex, our data indicated that inhaled Tol counterbalances the effects of anesthetic in a dose-dependent manner. In other terms, Tol can increase the amplitude of the middle-ear reflex in anesthetized rats, whatever the nature of the anesthetic used. This indicates that inhaling Tol (a Ca(2+)-channel-blocking drug) modifies the potency of anesthesia, and thereby the amplitude of the middle-ear reflex.

EchoScan: a new system to objectively assess peripheral hearing disorders.

Pure-tone air-conduction audiometry (PTA) is the reference clinical test used in Europe and the United States to measure the extent of hearing loss. It is a subjective, behavioral test, which measures thresholds of hearing sensations and perceptions based on patient responses to frequency-specific pure-tone stimuli. PTA can detect hearing problems due to cochlear or retro-cochlear impairment, without identifying the source of the problem. In contrast, cubic distortion product otoacoustic emissions (DPOAEs) detect inner-ear dysfunctions, particularly those involving the outer hair cells sensitive to noise and ototoxicants. Recently, ototoxicants were shown to have an action on the central nuclei driving the middle-ear acoustic reflex. Therefore, a new device, called EchoScan, was conceived to collect and measure performance both in the middle- and inner-ear. Its originality: the use of a battery of DPOAE measurements associated with contra-lateral acoustic stimulation. Changes in DPOAE amplitude due to ageing and gender were incidentally detected and EchoScan was more sensitive than impedancemetry to detect the stapedial reflex. EchoScan can be used both in clinical investigations and in occupational medicine, especially for the auditory follow-up of people exposed to noise or ototoxic agents. EchoScan could be promising to assess early detection in programs to prevent hearing loss.

Impact of noise or styrene exposure on the kinetics of presbycusis.

Presbycusis, or age-related hearing loss is a growing problem as the general population ages. In this longitudinal study, the influence of noise or styrene exposure on presbycusis was investigated in Brown Norway rats. Animals were exposed at 6 months of age, either to a band noise centered at 8 kHz at a Lex,8h = 85 dB (86.2 dB SPL for 6 h), or to 300 ppm of styrene for 6 h per day, five days per week, for four weeks. Cubic distortion product otoacoustic emissions (2f1-f2 DPOAEs) were used to test the capacity of the auditory receptor over the lifespan of the animals. 2f1-f2DPOAE measurements are easy to implement and efficiently track the age-related deterioration of mid- and high-frequencies. They are good indicators of temporary auditory threshold shift, especially with a level of primaries close to 60 dB SPL. Post-exposure hearing defects are best identified using moderate, rather than high, levels of primaries. Like many aging humans, aging rats lose sensitivity to high-frequencies faster than to medium-frequencies. Although the results obtained with the styrene exposure were not entirely conclusive, histopathological data showed the presbycusis process to be enhanced. Noise-exposed rats exhibit a loss of spiral ganglion cells from 12 months and a 7 dB drop in 2f1-f2DPOAEs at 24 months, indicating that even moderate-intensity noise can accelerate the presbycusis process. Even though the results obtained with the styrene exposure are less conclusive, the histopathological data show an enhancement of the presbycusis process.

Toluene effect on the olivocochlear reflex.

Animal studies have shown that toluene can cause hearing loss and can exacerbate the effects of noise by inhibiting the middle ear acoustic reflex. In this investigation, carried out in Long-Evans rats, the tensor tympani tendon was cutoff and the stapedius muscle was electrocoagulated in one or both middle ears. Rat hearing was evaluated by measuring cubic distortion otoacoustic emissions (2f1-f2; f1 = 8000 Hz; f2 = 9600 Hz; f1/f2 = 1.2) prior to, during, and after activation of the olivocochlear (OC) reflex. A band noise centered at 4 kHz was used as suppressor noise. It was delivered contralaterally to decrease 2f1-f2 amplitude. The strength of the inner ear acoustic reflex was tested by increasing contralateral noise intensity, and toluene injected into the carotid artery was used to study physiological efficacy. Results showed that the protective effect of the OC reflex is intensity dependent. In addition, the OC reflex was found to be less sensitive to toluene than the middle ear acoustic reflex. This may be because the efferent neurons involved in inner ear and middle ear reflexes are located differently. In conclusion, the synergistic effects on hearing of co-exposure to noise and aromatic solvents are because of solvents depressing the central nuclei, which mainly drive the middle ear acoustic reflex.

Neuronal circuits involved in the middle-ear acoustic reflex.

Human and animal studies have shown that certain aromatic solvents such as toluene can cause hearing loss and can exacerbate the effects of noise. The latter effects might be due to a modification of responses of motoneurons controlling the middle-ear acoustic reflex. In the present investigation, the audition of Long-Evans rats was evaluated by measuring cubic (2f1 - f2) distortion otoacoustic emissions (f1 = 8000 Hz; f2 = 9600 Hz; f1/f2 = 1.2) prior to, during, and after activation of the middle-ear acoustic reflex. A noise suppressor was used to modify the amplitude of the 2f1 - f2 distortion otoacoustic emissions. It was delivered either contralaterally (band noise centered at 4 kHz), or ipsilaterally (3.5 kHz sine wave) to test the role played by the central auditory nuclei. This audiometric approach was used to study the physiological efficiency of the middle-ear acoustic reflex during an injection of a bolus of Intralipid (as a vehicle) containing 58.4, 87.4, or 116.2mM toluene via the carotid artery. The results showed that toluene could either increase or decrease middle-ear acoustic reflex efficiency, depending on the toluene concentration and the ear receiving noise suppressor. A new neuronal circuit of the middle-ear acoustic reflex has been proposed to explain findings obtained in this investigation. Finally, the depressing action of toluene on the central auditory nuclei driving the middle-ear acoustic reflex might explain the synergistic effects of a co-exposure to noise and aromatic solvents.

Toluene-induced hearing loss in the guinea pig.

Toluene is a high-production industrial solvent, which can disrupt the auditory system in rats. However, toluene-induced hearing loss is species dependent. For instance, despite long-lasting exposures to high concentrations of aromatic solvent, no study has yet succeeded in causing convincing hearing loss in the guinea pig. This latter species can be characterized by two metabolic particularities: a high amount of hepatic cytochrome P-450s (P-450s) and a high concentration of glutathione in the cochlea. It is therefore likely that the efficiency of both the hepatic and cochlear metabolisms plays a key role in the innocuousness of the hearing of guinea pigs to exposure to solvent. The present study was carried out to test the auditory resistance to toluene in glutathione-depleted guinea pigs whose the P-450 activity was partly inhibited. To this end, animals on a low-protein diet received a general P-450 inhibitor, namely SKF525-A. Meanwhile, they were exposed to 1750 ppm toluene for 4 weeks, 5 days/week, 6 h/day. Auditory function was tested by electrocochleography and completed by histological analyses. For the first time, a significant toluene-induced hearing loss was provoked in the P-450-inhibited guinea pigs. However, the ototoxic process caused by the solvent exposure was different from that observed in the rat. Only the stria vascularis and the spiral fibers were disrupted in the apical coil of the cochlea. The protective mechanisms developed by guinea pigs are discussed in the present publication.