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Acta Otolaryngol 2003; 123: 936-940
Acute Effects of Alcohol on Auditory Thresholds and Distortion Product
Otoacoustic Emissions in Humans
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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.
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.l-H. Hwang et al.
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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]