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Taylor &Francis healthsciences Acta Otolaryngol 2003; 123: 936-940 Acute Effects of Alcohol on Auditory Thresholds and Distortion Product Otoacoustic Emissions in Humans - 34x32 TAN^, CHING-WEN CHIANG' and s o m the Departments of Otolaryngology, ' ~ o h -Horpital, ~i I-- and 2~ationolTaiwan University Hospital, Taipei, TCU'HYUI Hwang J-H,Tan C-T, Cbiang C-W,Lm T-C. Acute eflects of alcohol on auditory thresholcls and dktwtwn product otoacoustic emissions in humans. Acta Otolaryngol 2003; 123: 936-940. Objective-To investigate the acute effects of alcohol consumpticm on pure-tone thmholds (PTs) and distortion product otoacoustic emissions (DPOAEs) in humans Material Plad Methotts-Eight healthy adults were asked to drink alcohol to the clinical intoxication level. PTs and DPOAEs were determined serially before and after alcohol ingestion. Results-Alcohol had no effect on PTs. DPOAE amplitudes above 5500 Hz dropped 30 min and 1 h after alcohol ingestion, returning to the pretest level 2 h after ingestion. Condrrdon-In humans, acute alcohol consumption to the intoxidon level may cause a temporary reduction in DPOAE amplitudes at high frequencies without affecting auditory thresholds Key wort&: alcohol, h w m q otoacowlk emissions, pure-tone audiometry. INTRODUCTION Acute alcohol (ethanol) challenge is known to induce various cognitive disturbances. Alcohol can also affect hearing by acting on the human central nervous reductions in the amplitude of system. Si&cant auditory cortical potentials have been reported after alcohol ingestion (1). Subcortical alterations of audibility under the influence of alcohol in humans have also been studied. Several investigators showed that acute and chronic ethanol hgestion could alter auditory brainstem potentials and middle latency responses (2, 3). Studies of the effects of alcohol on human auditory thresholds yielded varying results Murata et al. (4) reported that drinking even very small amounts of alcohol induces a temporary reduction in auditory threshold. It was also reported that moderate alcohol consumption ( r.140 glweek) could protect against hearing loss in older adults (5). A few animal studies have been carried out to investigate the effects of acute and chronic alcohol consumption on peripheral and antral auditory systems. In an animal modd of fetal alcohol syndrome, alcohol-exposed animals were found to have central auditory processing disorders characterized by prolonged transmission of neural potentials along the brainstem portion of the auditory pathway. Other animds also had peripheral auditory disorder in the form of congenital senmineural hearing loss (6). In 1981, Morizono and Sikora (7) reported that topical application of ethanol induced a reduction in all bioelectric functions of the inner ear, including cochlear microphonics, endocochlear potentials and whole nerve action potentials, in the guinea pig. However, in another experiment, exposure to ethanol Taylor & Francis 2003. ISSN 0001-6489 alone was found to have no effects on auditory sensitivity and did not cause any toxicity to outer hair cells (OHCs) (8). These conflicting results may be due to differences in the dosage, method or duration of alcohol exposure. In this study, we employed distortion product otoacoustic emissions (DmAEs) as a tool for investigating the acute effects of alcohol ingestion on the fvnction of human OHCs. MATERIAL AND METHODS Eight young adults (3 males, 5 females; mean age 25.6 years; range 22-29 years) volunteered to participate in this study. None of them had any history of ear disease or alcohol abuse. AU subjects initially underwent puretone audiometry (tested frequency range 250-8000 Hz) and DPOAE recordings. They were then asked to drink various amounts of whisky ( W !alcohol) based on their weight (3 &g) together with their breakfast over a 30-min period. After ingestion of alcohol, all subjects reached the stage of clinical intoxication, as distinguished by slight slurring of speech,, dizziness and slight ataxia. B i d alcohol levels were estimated based on a recent study by the Police Department of Taiwan (9). According to that study, the blood alcohol concentration incmwd quickly within 45 min after alcohol ingestion and declined greatly after 120 min Fig. 1. Pure-tone thresholds (PTs) and DPOAEs were recorded serially at 30 min and 1, 2 and 3 h after alcohol consumption. DPOAEs were recorded wing a GSI 60 D m A E system (GSI Inc., USA). Emissions were elicited by means of two continuous, pure primary tones at frequencies fi and fi (fi:fl was fixed at 1:2) generated by two separate transducers, which also contained a Effects of alcohol on DPOAEs Acta Oto~aryngol123 937 at any frequency for any subject after alcohol ingestion. DPOAEs Changes in DPOAE amplitudes at different tested frequencies in all subjects before and after alcohol ingestion are shown in Table I and the trends are depicted in Fig. 2. At frequencies of < 4375 Hz,there were no obvious amplitude changes in all subjects during the test period. At frequencies of > 5500 Hz, a tendency for the DPOAE amplitude to decrease was observed at 30 min and 1 h after alcohol ingestion. At 5500 Hz, the mean change in amplitude was -2.3 2.43dB at 30 min (paired t-test: p < 0.05) and -2.4 f 1.85 dB at 1 h (paired t-test: p < 0.05). At 6562 Hz, the mean change in amplitude was -3.5 f1.60 dB at 30 min (paired t-test: p ~ 0 . 0 5and ) 3.0+2.00 dB at 1 h (paired t-test: p <0.05). However, the DPOAE amplitude returned to the normal baseline at 2 and 3 h after ingestion. There was no si-cant change in noise level during the entire course of DPOAE measurements. The DPOAE amplitudes varied from person to person even when no alcohol was consumed. The mean DPOAE amplitudes at various times before and after alcohol intake did not differ significantly at each frequency (Table 11; one-way ANOVA: p > 0.05). This clearly shows the individual variations in DPOAE amplitudes + 0.5 1.0 2.0 (hour) 3.0 4.0 Fig. I. Blood alcohol concentration (mean +SD) at various times after alcohol ingestion (male: 1.0 g/kg; female: 0.8 g/ kg). miniature low-noise microphone for emission detection. The two primaries, L1 and Lt were both set to 70 dB SPL. The test-retest reliability of DPOAEs ( < 1 dB SPL) has been documented (10). The tested frequency range of f2 was 750-7187 Hz and 3 frequencies were sampled per octave. DPOAE amplitudes were measured at selected frequencies. Statistical analysis of DPOAE amplitudes was performed using a paired t-test and ANOVA. p < 0.05 was considered ~ i ~ c a n t . 4 RESULTS PTs All subjects had PTs within 15 dB SPL 'at all tested frequencies. There was no change in PT DISCUSSION A variety of factors, including amounts of food and alcohol consumed, speed of intake and individual absorption and metabolic rates, have been found to affkct blood alcohol concentration in different individuals. This may part~allyexplain the large individual Table I. Changes in DPOAE amplitude after alcohol intake . Geometric mean of ; fi and fi (Hz) 6562 5500 4375 3500 2750 2187 1687 1375 1062 812 687 * * p < 0.05 (paired t -test). Mean (+SD) change in DPOAE arnplitu.de (dB) Nmin 1h 2h -3.5 (1.60)* -2.3 (2.43)* -0.9 (3.00) -1.1 (2.03) -0.5 (1.60) -1.1 (1.73) 0.8 (1.04) -0.1 (1.25) 0.4 (1.60) -0.5 (1.93) -0.5 (1.77) -3.0 (2.00)* -2.4 (1.85)* -0.8 (2.31) - 1 .O (2.07) -0.5 (2.14) -0.9 (2.23) 0.3 (1.28) 0.0 (0.76) 0.1 (1.64) -0.6 (1.51) -0.6 (1.41) -0.9 (2.10) -0.9 (1.81) -0.3 (0.71) -0.8 (1.67) -0.4 (1 .M) -0.5 (1.77) 0.6 (1.06) -0.5 (1.07) 0.0 (1.69) -0.6 (2.07) 0.4 (1.69) 3h - 1.1 (2.42) - 1.3 (138) 0.3 (1.39) 0.4 (2.13) 1.1 (0.99) -0.4 (1.30) 0.3 (1.28) -0.6 (0.74) 0.5 (1.69) -0.1 (1.73) -0.5 (1.60) 938 1-H. Hwang er a/. I Acta Otolaryngol 123 Fig.2. Changes in DPOAE amplitude at various times after alcohol ingestion at each geometric mean frequency. differences in DPOAE amplitude changes after alcohol consumption. However, our results demonstrate a * sigmfica.nt decrease in the DPOAE amplitudes at high frequencies after moderate alcohol consumption (1.2 g k g ) , The time course of the changes in DPOAEs closely matches the changes in blood alcohol levels of Taiwanese subjects described in the report of Tsai (9). This strongly suggests that the changes in DPOAEs are caused by alcohol and are amcentration-dependent. In our study there was no change in the auditory threshold, which is in accordance with the results obtained by Loquet et al. (8). Therefore, we have demonstrated that changes in DPOAEs precede changes in the auditory threshold. In other words, DPOAE measurements are more sensitive for detecting early and minor changes in the OHCs than conventional audiometry. The reductions in DPOAE amplitudes at higher frequencies reflect impairment in OHC functions in the basal turn of the cochlea. The exact mechanisms by which alcohol a@ects the OHCs remain unknown. However, there are several possibilities First, the f .- . . -. - - - - - "-- .-A L&- .- .. Effeco of alcohol on DPOAEs Acts Otolaryngol 123 939 Table 11. Mean DPOAE amplitudes before and after alcohol intake Geometric mean of f~ and f, (Hz) Mean (fSD) DPOAE amplitudes (dB) Pre-alcohol 30 min alcohol itself may be ototoxic to the OHCs. In general, the OHCs in the basal turn are most vulnerable to ototoxic injuries. Morizono and Sikora (7) reported ototoxicity after local application of alcohol to the inner ear of guinea pigs. In their experiment, a reduction in cochlear microphonics was observed, indicating that the OHCs were damaged. A disturbance in the endocochlear environment by alcohol and its metabolites may also result in abnormal outer cell motility. Second, alcohol may influence neurotransmission in the inner ear. It has been suggested that alcohol suppresses the central nervous system by inhibiting excitatory transmission via N-methyl-Daspartate receptors and enhancing inhibitory transmission via y-aminobutyric acid subtype A (GABAA) receptors (1 I). A number of studies have confirmed the presence of cholinergic and GABAnergic efferents on OHCs in animals (12) and so alcohol may suppress the OHCs via these efferent pathways. Third, middle ear impedance m y be affected by alcohol. DPOAEs arc generated in the cochlea by non-linear interaction of two primary tones introduced externally through the middle ear. They also have to pass through the middle ear before being detected by a microphone in the ear canal. Therefore, the middle ear transfer function may play an important role in determining the frequency characteristics of DPOAEs. It has been reported that alcohol can & a t the acoustic reflex thresholds in humans by aecting the middle ear muscles (137. Therefore the changes in middle ear pressure or muscle tonic activity after alcohol ingestion may explain the decreased DPOAE amplitudes. In summary, we have demonstrated that consumption of moderate amounts of alcohol induces d u c tions in DPOAE amplitudes at hgh frequencies in humans. These amplitude changes are completely reversible. This suggests that alcohol not only affects hearing via the central nervous system, but also 1h 2h 3h influences the function of OHCs. However, the effects of chronic alcohol consumption on the central and peripheral auditory systems are still unclear and require further investigation. REFERENCES 1. Gross MM, Begleitcr H, Tobin M, Kissin B. Changes in auditory evoked response induced by alcohol. J Nerv Ment Dis 1966; 143: 152. 2. Squires KC, Chu NS, Starr A. Acute effects of alcohol on auditory brainstem potentials in humans. Science 1978; 201: 174-6. 3. Katbamma B, Metz DA, Adelman CL, Thodi C. Auditory-evoked responses in chronic alcohol and drug abuser. Biol Psychiatry 1993; 33: 750-2. 4. Murata K, Kawashima M, Inaba R. Auditory threshold reduction on alcohol ingestion. Psychopharmacology (Berl) 2001; 157: 188-92. 5. Popelka MM, Cruickshanks KJ, Wiley TL, et al. Moderate alcohol consumption and hearing loss: a protective effect. J Am Gcriatr Soc 2000; 48: 1273-8. 6. Church MW, Abel EL, Kaltenbach JA, Overbeck GW. Effects of prenatal alcohol exposure and aging on auditory function in the rat: preliminary results Alcohol Clin EXPRCS 1996; 20: 172-9. 7. Morizono T, Silcora MA. Ototoxicity of ethanol in the tympanic cleft in animals Acta Otolaryngol (Stockh) 1981; 92: 33-40. 8. Loquet G, Campo P, Lataye R, Cossec B, Bonnet F? Combined e f f ' of exposure to styrene and ethanol on the auditory function in the rat. Hear Rcs 2000; 148: 173-80. 9. Tsai CC. The effects of alcohol blood concentration and metabolism on behavior in Taiwanese. Police Torch 2001; 538: 56-7. 10. Hung CH, Hsu CJ, Lin KN. Effect of the sound pressure level of the stimulus to distortion product otoacoustic emissions in normal young adults J Taiwan Otolaryngol Head Neck Surg Sa: 1997; 32: 1-5. 11. Korpi ER. Role of GABA receptors in the actions of alcohol and in alcoholism: recent advances. Alcohol Alcohol 1994; 29: 115-29. 940 .l-H. Hwang et al. 12. Eybalin M. Neurotransmitters and neuz~modulatorsof the mammatian cochlea. Physiol Rev 1993; 73: 309-73. 13. Bauch CD, Robinette MS. Alcohol and the acoustic reflex: effects of stimulus spatrum, subject variability, and sex. J Am Auditory Soc 1978; 4: 104-12. Submitted October 31, 2002; accepted June I2, 2003 Acta Otolaryngol 123 Address for compondcncc: Tien-Chen Liu, MD, PhD Department of Otolaryngology National Taiwan UniveRiw Hospital No. 7, Chung-Shan S. Road Taipei 100 ~aiwim Tel.: +886 2 23123456, ext. 5221 Fax: +886 2 23410905 E-mail: [email protected]