Effects of industrial noise exposure on distortion product otoacoustic emissions (DPOAEs) and hair cell loss of the cochlea--long term experiments in awake guinea pigs

Distortion product otoacoustic emissions (DPOAEs), a sensitive detector of outer hair cell (OHC) function, cochlear microphonics (CM), and hair cell loss have been monitored in 12 awake guinea pigs before and after 2 h exposure to specific, played-back industrial noise (105 dB SPL maximal intensity). All animals had stable DPOAE levels before noise exposure. In the first hours after noise exposure DPOAE levels were reduced significantly. In about 70% a partial recovery of the DPOAEs was found within 4 months after noise exposure. In 16% of the investigated ears no recovery of DPOAEs was observed. However, in a few ears increased DPOAEs were observed after noise exposure. Exposure to industrial noise caused both morphological changes in the middle turns of the cochlea and electrophysiological changes in the middle frequency range. A close correlation existed between reduced DPOAE levels, loss in CM potentials, and area of damaged or lost OHCs, but not with the numbers of damaged or lost OHCs in the cochlea. It can be concluded that continuous industrial noise causes a damage to OHCs which differs form the damage caused by impulse noise.     

Is there a close relationship between changes in amplitudes of distortion product otoacoustic emissions and hair cell damage after exposure to realistic industrial noise in guinea pigs?

In long-term experiments in awake guinea pigs (n=12), distortion product otoacoustic emissions (DPOAEs) at various frequencies were measured repeatedly over 6–8 months. About 9 weeks after the first measurement, the animals were exposed to industrial noise (car industry, maximal intensity about 110 dB SPL) for 2 h. The amplitudes of DPOAE were measured prior to noise exposure and 10 min, 70 min, 1 day and 2 days after the noise exposure and then once every week. Three to four months after noise exposure, the animals were killed, and the cochleae were prepared for scanning electron microscopy. The row of inner hair cells (IHCs) was complete in all animals, while the rows of outer hair cells (OHCs) showed a considerable hair cell loss in some of the animals without a correlation to the change in amplitudes of DPOAE. However, a closer relationship between the decline of amplitudes of DPOAE and the number of missing and changed OHCs (fused stereocilia bundles, missing tip links) could be established. The number of lost OHC does not reflect the decline in DPOAE in all cases. This discrepancy must be considered when the degree of hearing loss needs to be established from changed DPOAE.     

The effect of impulse noise on distortion product otoacoustic emissions

The aim of this study was the evaluation of distortion product otoacoustic emissions (DPOAEs) before and after noise exposure from shooting, and the comparison of DPOAEs with pure-tone audiometry. Thirteen young male police officers were exposed to impulse noise from shooting, without using earplugs. Standard pure-tone audiometry, tympanometry, and DPOAEs were performed before exposure and at one hour post- and 24 hour post-exposure. In the one hour post-exposure testing mean pure-tone thresholds were elevated in the 1–8 kHz frequency zone and DPOAE levels were reduced at several frequencies. DPOAEs were more affected at 3 kHz or lower, whereas pure-tone thresholds were more affected at higher frequencies. After the final examination, non-significant partial shifts at high frequencies on both tests remained. Pure-tone audiometry was overall more sensitive, but DPOAEs provided additional information about the cochlear status of certain ears. These data suggest that besides behavioral testing, DPOAEs may play a role as a fast, objective, and easy to perform test for monitoring subjects exposed to impulse noise.     

The effect of impulse noise on distortion product otoacoustic emissions

The aim of this study was the evaluation of distortion product otoacoustic emissions (DPOAEs) before and after noise exposure from shooting, and the comparison of DPOAEs with pure-tone audiometry. Thirteen young male police officers were exposed to impulse noise from shooting, without using earplugs. Standard pure-tone audiometry, tympanometry, and DPOAEs were performed before exposure and at one hour post- and 24 hour post-exposure. In the one hour post-exposure testing mean pure-tone thresholds were elevated in the 1-8 kHz frequency zone and DPOAE levels were reduced at several frequencies. DPOAEs were more affected at 3 kHz or lower, whereas pure-tone thresholds were more affected at higher frequencies. After the final examination, non-significant partial shifts at high frequencies on both tests remained. Pure-tone audiometry was overall more sensitive, but DPOAEs provided additional information about the cochlear status of certain ears. These data suggest that besides behavioral testing, DPOAEs may play a role as a fast, objective, and easy to perform test for monitoring subjects exposed to impulse noise.     

Influence of contralateral stimulation by two-tone complexes,narrow-band and broad-band noise signals on the 2f1-f2 distortion product otoacoustic emission levels in humans

In order to test the frequency specificity of the efferent suppressive effect on otoacoustic emissions, changes in the 2f1-f2 distortion product otoacoustic emission (DPOAE) levels induced by contralateral stimuli of different spectra were measured in 10 normally hearing adults. Three types of contralateral stimuli were used: (i) a set of 6 pairs of pure tones with the same frequencies as used for DPOAE stimulation; (ii) 6 narrow-band noise signals with cut-off frequencies equal to the frequencies of the primary tones used for DPOAE stimulation; and (iii) broad-band noise with a bandwidth of 840-6,000 Hz. A small suppressive effect was observed mainly in the mid-frequency region. Broad-band noise was more effective at suppressing DPOAEs than narrow-band noises and two-tone complexes. Occasionally, small enhancements in DPOAE amplitudes were observed. Based on the results of this study, it is concluded that DPOAE changes induced by contralateral stimuli are not frequency-specific, and are too small to have routine clinical value.     

Influence of Contralateral Stimulation by Two-tone Complexes,Narrow-band and Broad-band Noise Signals on the 2f 1 -f 2 Distortion Product Otoacoustic Emission Levels in Humans

In order to test the frequency specificity of the efferent suppressive effect on otoacoustic emissions, changes in the 2f 1 -f 2 distortion product otoacoustic emission (DPOAE) levels induced by contralateral stimuli of different spectra were measured in 10 normally hearing adults. Three types of contralateral stimuli were used: ( i ) a set of 6 pairs of pure tones with the same frequencies as used for DPOAE stimulation; ( ii ) 6 narrow-band noise signals with cut-off frequencies equal to the frequencies of the primary tones used for DPOAE stimulation; and ( iii ) broad-band noise with a bandwidth of 840-6,000 Hz. A small suppressive effect was observed mainly in the mid-frequency region. Broad-band noise was more effective at suppressing DPOAEs than narrow-band noises and two-tone complexes. Occasionally, small enhancements in DPOAE amplitudes were observed. Based on the results of this study, it is concluded that DPOAE changes induced by contralateral stimuli are not frequency-specific, and are too small to have routine clinical value.     

Distortion-product otoacoustic emission (DPOAE) following pure tone and wide-band noise exposures

The aim of our investigations was to determine how the intensity of distortion-product otoacoustic emission (DPOAE) changes following different sound and noise exposures. We performed examinations on 20 healthy people with normal hearing. DPOAEs were recorded scanning the 0.5-6 kHz frequency interval before and after the exposures. We exposed the subjects to 0.5, 1, 2, 4 and 6 kHz pure tones and wide-band noise (intensity: 80 dB HL, duration: 3 minutes). We conclude that the amplitudes of DPOAEs changed immediately after exposures at most frequencies. DPOAE intensities decreased at some frequencies in the middle frequency range (1-2 kHz), and increased at low and particularly at high frequencies.     

Potentiation of noise-induced hearing loss by amikacin in guinea pigs.

Noise and aminoglycosides initially attack cochlear outer hair cells (OHCs). Distortion product otoacoustic emissions (DPOAEs) are used for the early diagnosis of damage to OHCs. The effects of sub-damaging doses of amikacin, an aminoglycoside antibiotic agent, on noise-induced hearing loss (NIHL) were examined in guinea pigs. Animals were grouped by gender and exposed to broadband noise at 105 dB SPL for 12 h and/or injected i.m. with either amikacin (100 mg/kg/day) or saline for 10 days. Auditory brainstem response (ABR) thresholds, along with DPOAE amplitudes, were measured serially before and after noise exposure. DPOAE amplitudes decreased and ABR thresholds elevated immediately after noise exposure and then gradually recovered. At all frequencies, the emission amplitudes recovered completely to pre-exposure baseline values by 4 days after noise exposure. There was no effect of amikacin on either the ABR threshold or DPOAE amplitudes, in animals treated with amikacin only. However, amikacin significantly prolonged the effect of noise exposure on DPOAE amplitude but not on the noise-induced temporary threshold shift (TTS) of the ABR. In animals treated with a combination of noise and amikacin, significant changes in DPOAE amplitudes were still observed at 4 weeks after cessation of noise exposure. No gender difference in the responses to noise and/or amikacin could be demonstrated. The present findings indicate that even sub-damaging dosages of amikacin might impair recovery from NIHL in guinea pigs.     

Effects of hyperbaric oxygen treatment on auditory hair cells after acute noise damage

Acute acoustic trauma (AAT) is a sudden sensorineural hearing loss caused by exposure of the hearing organ to acoustic overstimulation, typically an intense sound impulse, hyperbaric oxygen therapy (HOT), which favors repair of the microcirculation, can be potentially used to treat it. Hence, this study aimed to assess the effects of HOT on guinea pigs exposed to acoustic trauma. Fifteen guinea pigs were exposed to noise in the 4-kHz range with intensity of 110 dB sound level pressure for 72 h. They were assessed by brainstem auditory evoked potential (BAEP) and by distortion product otoacoustic emission (DPOAE) before and after exposure and after HOT at 2.0 absolute atmospheres for 1 h. The cochleae were then analyzed using scanning electron microscopy (SEM). There was a statistically significant difference in the signal-to-noise ratio of the DPOAE amplitudes for the 1- to 4-kHz frequencies and the SEM findings revealed damaged outer hair cells (OHC) after exposure to noise, with recovery after HOT (p = 0.0159), which did not occur on thresholds and amplitudes to BAEP (p = 0.1593). The electrophysiological BAEP data did not demonstrate effectiveness of HOT against AAT damage. However, there was improvement of the anatomical pattern of damage detected by SEM, with a significant reduction of the number of injured cochlear OHC and their functionality detected by DPOAE.     

Effects of contralateral white noise stimulation on distortion product otoacoustic emissions in myasthenic patients.

Myasthenia gravis (MG) induces a reduction of transient evoked otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs) that reverses partially after administration of an acetylcholinesterase (AChE) inhibitor. In normal subjects a contralateral acoustic stimulation (CAS) produces an amplitude reduction of TEOAEs and DPOAEs. This effect, called contralateral suppression (CS), is mediated by the efferent auditory system. Twenty subjects affected by MG underwent DPOAE recording with and without contralateral white noise in a drug-free baseline period ('basal') and 1 h ('post') after administration of a reversible AChE inhibitor. In 'basal' condition CAS did not induce significant DPOAE amplitude changes but a paradoxical slight increase was observed. After drug administration, CAS produced a significant decrease of DPOAE amplitudes for middle frequencies (f(2) between 1306 and 2600 Hz). In normal controls CAS caused a significant decrease (P<0.001) for all frequencies. The amount of CS in controls and in the MG 'post' condition was not significantly different. The increased acetylcholine (ACh) availability following drug consumption seems to partially restore outer hair cell function and enhances their electromotility; a further influx of ACh due to CAS yields to restoration of the CS. These findings also suggest that DPOAEs may be useful in the diagnosis of MG and for monitoring the effectiveness of treatment.     

The effect of various durations of noise exposure on auditory brainstem response, distortion product otoacoustic emissions and transient evoked otoacoustic emissions in rats

This study was designed to investigate the effect of various durations of noise exposure in animals on physiological responses from the cochlea which are also used clinically in humans: auditory brainstem response (ABR), transient evoked otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs). Rats were exposed to 113 dB SPL broad-band noise (12 h on/12 h off) for durations of 3, 6, 9, 12, 15 and 21 days, and tested 24 h after cessation of the noise and again after a period of 6 weeks. ABR threshold to click stimuli and to a 2-kHz tone burst (TB), TEOAE energy content and DPOAE amplitude in the exposed rats were compared to those in a group of control rats not exposed to noise. ABR thresholds (click and TB) were significantly elevated in all exposure duration groups compared to control rats. DPOAE amplitudes and TEOAE energy content were significantly reduced. The mean ABR thresholds following 21 days exposure were significantly greater (click = 100 dB pe SPL; TB = 115 dB pe SPL) than those following 3 days exposure (click = 86 dB pe SPL; TB = 91 dB pe SPL). Linear regression analysis between recorded responses and duration of noise exposure (days) showed a significant increase in ABR thresholds of approximately 0.8-- 1.4 dB/day. TEOAE and DPOAE responses showed no such dependence on noise duration and were already maximally reduced after only 3 days of exposure. This can be explained by the possibility that short noise exposures may cause damage to the early, more active stages of cochlear transduction (as shown by TEOAEs and DPOAEs). As the noise exposure continues, further damage may be induced at additional, later stages of the cochlear transduction cascade (as shown by ABR). Thus, ABR seems more sensitive to noise duration than OAE measures.     

The effect of impulse noise exposure on distortion product otoacoustic emissions in the awake guinea pig

Distortion product otoacoustic emissions (DPOAE) are a sensitive detector of outer hair cell (OHC) function and were monitored in awake guinea pigs before and after impulse noise damaging the cochlea (peak intensity 153 dB SPL, rise time < 0.1 ms). Animals had stable DPOAE levels before noise exposure. In the first hours after noise exposure DPOAE levels were reduced significantly. Three different patterns of recovery of DPOAE were seen in the post-exposure period: restitution exceeding controls, partial recovery and no recovery. In general, DPOAE levels declined and types of recovery closely corresponded to changes in amplitudes of cochlear microphonics after noise exposure. These data suggest that the monitoring of DPOAE is a suitable method for diagnosing impaired OHC function. Received: 25 February 1999 / Accepted: 1 July 1999     

DPOAE level shifts and ABR threshold shifts compared to detailed analysis of histopathological damage from noise

A detailed comparison of 2f(1)-f(2) distortion product otoacoustic emission (DPOAE) level shifts (LS) and auditory brainstem response (ABR) threshold shifts with noise-induced histopathology was conducted in chinchillas. DPOAE levels (i.e., L(1) and L(2)) at f(1) and f(2), respectively, ranged from 55-75 dB sound pressure level (SPL), with f(2)/f(1)=1.23, 6 points/octave, f(2)=0.41-20 kHz, and ABR thresholds at 0.5-20 kHz, 2 points/octave, were determined pre-exposure. The exposure was a 108 dB SPL octave band of noise centered at 4 kHz (1-1.75 h, n=6) or 80-86 dB SPL (24 h, n=5). DPOAE LSs (magnitude pre- minus post-exposure) and ABR threshold shifts (TS) were determined at 0 days and up to 28 days post-exposure. The cochleae were fixed, embedded in plastic and dissected into flat preparations. The length of the organ of Corti (OC) was measured; missing inner (IHC) and outer (OHC) hair cells counted; stereocilia damage rated; and regions of OC and nerve-fiber loss determined. Cytocochleograms were made showing functional loss and structural damage with the LS and TS overlaid. Some unexpected results were obtained. First, the best correlation of LS with histopathology required plotting the DPOAE data at f(1) with respect to the chinchilla-place map. The best correlation of TS was with IHC and nerve-fiber loss. Second, wide regions of up to 10% scattered OHC loss in the apical half of the OC showed little or no LS. Third, with the 108 dB SPL noise, there was 20-40 dB of recovery for DPOAEs at mid-high frequencies (3-10 kHz) in eight of 12 cochleae where there was 70-100% OHC loss in the basal half of the OC. The largest recovery at mid-high frequencies occurred in regions where the OC was entirely missing. Fourth, with the 80-86 dB SPL noise, there was no LS at small focal lesions (100% loss of OHCs over 0.4 mm) when the frequency place of either f(1) or f(2) was within the lesion but not both. There was no correlation of LS with OHC stereocilia loss, fusion or disarray. These results suggest that, after noise exposure, DPOAEs at mid-high frequencies can originate from or be augmented by generators located at someplace other than the frequency place of f(2), possibly the basal 20% of the OC when this region is intact. Also, noise-induced DPOAE LSs seemed to reflect differing mechanisms for temporary and permanent hearing loss.     

畸变产物耳声发射与瞬态诱发耳声发射的相关性观察

目的：探讨畸变产物耳声发射（DPOAE)和瞬态诱发耳声发射(TEOAE)的特点和相关性。方法：以20例（40耳）耳科正常青年人观察噪声暴露前后在无对侧抑制（NCS)状态下和有对侧抑制（CS)状态下TEOAE的频带信噪比、频带反应幅值，与DPOAE的2f1-f2幅值、信噪比相互间的相关性。结果：DPOAE与TEOAE虽由不同的刺激声所引出，有各自的图形特征，但在绝大多数相近频率点上，其测量值有较好的相关性，形成一定的数量关系。结论：TEOAE测试较为快捷并有中频优势，而DPOAE则有很好的频率特异性和高频优势。二者幅值及信噪比间有良好的相关性，可得出有统计意义的线性回归方程参数，听觉损害，噪声性。     

Correlation of transiently evoked to distortion-product otoacoustic emission measures in healthy children

OBJECTIVE: Transiently evoked (TEOAEs) and distortion-product otoacoustic emissions at the 2f1-f2 frequency (DPOAEs) are being used as a clinical tool for diagnosis of peripheral auditory pathology. Because both tests are fast and non-invasive, they may be an excellent method for hearing screening in infants and children. The purpose of this study was to compare the TEOAE and DPOAE measures obtained in a group of healthy children. METHODS: Sixty-six school-aged children with normal hearing were included in the study. Subjects with recent otologic disease or abnormal tympanograms were excluded. TEOAEs and DPOAEs were performed using a DP Echoport ILO 292 Otodynamics analyzer connected to a portable personal computer. Correlation between TEOAE amplitudes and DPOAE levels was estimated. RESULTS: Correlation between TEOAE amplitudes and DPOAE levels was highly significant across all measured frequencies. Correlation was more significant at the middle frequencies than at the low and high frequencies. CONCLUSIONS: Although frequency specific information may be obtained by both tests, most reliable results were obtained at the middle frequencies. TEOAE values were more prominent at low frequencies, whereas DPOAEs were more effective at high frequencies. Both methods are reliable, objective, fast and useful tests of the cochlear status and should be included in the standard audiological diagnostic work-up of children.     

Susceptibility of young adult and old rats to noise-induced hearing loss

This study was designed to test whether old rats show signs of presbyacusis and whether they would be either similarly or more or less susceptible to noise-induced hearing loss than young adult rats. Old (24 months) and young adult (3-4 months) Wistar rats were exposed to a broad-band noise of 113 dB SPL for a duration of 1 h (producing temporary threshold shifts) or 3 days (12 h noise/12 h quiet; permanent shifts). Auditory brainstem response (ABR), distortion product otoacoustic emissions (DPOAEs) and transient evoked otoacoustic emissions (TEOAEs) were measured before and after exposure. At the initial recording (before exposure), old rats demonstrated a small mean ABR threshold elevation, a reduction in amplitude of wave I (WI), a shortening of WI latency and a prolongation of the interpeak interval between WI and WIV, as compared to the young rats. The old rats also demonstrated a small DPOAE amplitude reduction and a reduction of peak-to-peak amplitude in the TEOAE response 2 ms after stimulus, but no reduction in TEOAE energy content between 2 and 4 kHz. These are signs of presbyacusis in the old rats. The noise exposures caused elevations in ABR threshold and reductions in DPOAE amplitude and TEOAE energy content that were similar in both the old and young rats. Their recovery from the noise-induced loss was also similar. Thus, the results of this study show that old and young adult rats, at least when considering clinically relevant intensities and durations of noise exposure, are equally susceptible to the effects of the exposure.     

Evaluating cochlear function and the effects of noise exposure in the B6.CAST+Ahl mouse with distortion product otoacoustic emissions

Cochlear function and susceptibility to noise over-exposure were examined in the congenic mouse strain B6.CAST+Ahl (B6.CAST) and compared to these same features in the CAST/Ei (CAST) and C57BL/6J (C57) parental strains. For both types of comparisons, the primary measure was the distortion-product otoacoustic emissions (DPOAE) at 2f1-2f2. Our assumption was that the B6.CAST mouse was corrected for the early onset age-related hearing loss (AHL) exhibited by one of its parental strains (C57) by the age-resistant properties of its other parental strain (CAST), and thus would exhibit neither AHL nor susceptibility to noise overstimulation effects. With respect to cochlear function, for 2.5-month mice, there was a tendency for DPOAEs to be slightly lower for mid-frequency primary tones for both C57 and B6.CAST mice, while the former mice showed clear AHL effects at the highest test frequency. However, by 5 months of age, the B6.CAST mice, like the CAST mice, displayed robust DPOAE levels that were significantly larger than DPOAE levels for the C57 mice, which were essentially absent for frequencies above about 30 kHz. To investigate the role of the Ahl gene in the susceptibility of the cochlea to the effects of noise over-exposure, two distinct paradigms consisting of temporary (TTS: 1-min, 105-dB SPL, 10-kHz pure tone) and permanent (PTS: 1-h, 105-dB SPL, 10-kHz octave band noise) threshold-shift protocols were used. The brief TTS exposure produced reversible reductions in DPOAEs that for both the B6.CAST and CAST mice recovered to within a few dB of their baseline levels by 3 min post-exposure. In contrast, the C57 mice recovered somewhat slower and, by 5 min post-exposure, emission levels were still 5 dB or more below their corresponding pre-exposure values. At 3 months of age, the TTS mice along with another group of na?ve subjects representing the same three mouse strains were exposed to the PTS paradigm. By 4 days post-exposure, for B6.CAST and CAST mice, DPOAE levels had recovered to their pre-exposure control levels. However, DPOAEs for the C57 mice at most of the measurable frequencies were at least 10-30 dB lower than their counterpart baseline levels. Together these data suggest that the Ahl allele in the C57 strain contributes to both the early onset AHL exhibited by these mice as well as their susceptibility to both TTS and PTS over-exposures.     

Recognition of speech in noise and relations with suppression of otoacoustic emissions and the acoustic reflex

Subjects presenting difficulties in understanding speech with competing sounds may have absence of otoacoustic emission suppression and the acoustic reflex.Aim: To study the performance of the efferent auditory system in normal hearing subjects complaining of difficulties to understand speech in noise.Material and methods: A prospective study comprising 50 normal-hearing subjects aged from 19 to 32 years, reporting difficulties with speech recognition in noise (with complaints - WC) or not (with no complaints - WNC). Distortion product evoked otoacoustic emissions (DPOAEs) were tested at frequencies from 1500 to 6000 Hz.The contralateral acoustic reflex (CAR) was investigated from 500 to 4000 Hz.Results: Groups differed statistically as to the occurrence of CAR in the left ear at 4000 Hz. At 1500 Hz, there was a statistically significant effect - absence of DPOAEs in the WC group in the right ear. In left ears, absence of DPOAE suppression was higher in the WC at 1500 Hz and 2000 Hz.Conclusion: An association between self-reported difficulties in discriminating speech in noise and the absence of contralateral acoustic reflex at 4000 Hz in the left ear was observed; there was also absence of the suppression effect of DPOAEs, especially at middle frequencies in both ears.     

Outer and middle ear status and distortion product otoacoustic emissions in children with sickle cell disease

The purpose of this study was to investigate distortion product otoacoustic emissions (DPOAEs) and outer/middle ear status in 12 African American children with normal hearing and homozygous sickle cell disease (SCD) and age-, gender-, and ear-matched African American controls. C. R. Downs, A. Stuart, & D. Holbert (2000) reported that DPOAE amplitudes were significantly larger for children with SCD. Because the integrity of the middle ear system directly influences OAE characteristics, it was felt that concurrent investigation of DPOAE amplitudes and outer/middle ear function in children with SCD was warranted. DPOAEs were evoked by 13 primary-tone pairs with f2 frequencies ranging from 1000 to 4500 Hz. Outer/middle ear status was assessed with tympanometry through indices of peak compensated static acoustic admittance, tympanometric width, tympanometric peak pressure, ear canal volume, and middle ear resonance frequency. Tympanograms were recorded with probe-tone frequencies of 226 and 678 Hz. DPOAE amplitudes were significantly larger for children with SCD (p < .05). There were no group differences in any of the middle ear indices (p > .05). These findings suggest that increased DPOAE amplitudes for children with SCD cannot be attributed to differences in outer/middle ear function as assessed with tympanometry.     

Assessment of outer hair cell function and blood antioxidant status of rabbits exposed to noise and metal welding fumes

OBJECTIVES: To investigate the interaction between welding fumes and noise in causation of hearing impairment. METHODS: Groups of rabbits (n=6) were exposed to noise, welding fumes or combination of both prior to Distortion Product Otoacoustic-Emissions (DPOAEs) analysis. The function of outer hair cells (OHCs) was examined by DPOAE assessment over a broad range of frequencies. Variations in DPOAE amplitude were compared between control (n=6) and exposed (n=18) groups. RESULTS: The DPOAEs levels measured at different frequencies (1379-6299 Hz) were found to decrease significantly (P<0.05) in rabbits exposed to 110 dB sound pressure level (SPL) broadband noise (8h/day, 12 days). In rabbits, exposed to carbon-steel welding fumes alone (157 mg/m(3)), the threshold shift was limited to the high frequencies (2759-6299 Hz), whereas, mixed exposure to noise and fumes resulted in reduction of DPOAEs at all the frequencies. Changes in DPOAEs were associated with increased susceptibility of erythrocytes to oxidation (P<0.05). Exposure to noise or fumes alone or simultaneously, suppressed total antioxidant ability of plasma as measured by ferric reducing ability of plasma (FRAP). Noise alone or in combination with fumes resulted in depletion of blood glutathione (GSH). Despite suppression of FRAP in the exposed groups, GSH was found to remain unchanged due to welding fumes suggesting that antioxidants other than GSH are affected by toxicants present in metal welding fumes. CONCLUSION: Exposure to very high levels of welding fumes can increase noise-related effects on OHC function by extending hearing threshold shift to wide band frequencies.