Department of Psychology, The University of Western Ontario, London, Ontario, Canada N6A 5C2
Received 9 September 1998; in revised form 13 January 1999; accepted 10 March 1999
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ABSTRACT |
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INTRODUCTION |
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The purpose of the present study was to assess whether or not alcohol causes behaviourally demonstrable effects on auditory sensitivity and to explore possible reasons for the equivocal nature of previous behavioural studies. In reviewing the literature, we noted three possible sources for the discrepant findings. The first is that each study used a very limited range of frequencies, often only a single frequency, that differed across studies. It may be that the choice of frequency influenced the outcome. A second potential source of variability arises from the differences in blood-alcohol concentrations (BAC) and the stages of alcohol absorption when measurements were obtained (Goldberg, 1943; Goldstein, 1983
). Based on the finding that behavioural consequences of alcohol consumption may be greater during the absorption of alcohol than during the elimination of alcohol (Goldberg, 1943
), it would be desirable to measure effects during both the rising and falling portions of the BAC curve. The absorption or rising phase of the alcohol curve is more rapid than the elimination of alcohol. Thus, in order to study the effects of alcohol on auditory sensitivity to a range of frequencies, a relatively fast method of assessing thresholds (<15 min) would be necessary. Finally, the earlier studies differed with respect to stimulus presentation. Presentation of signals in a free-field or over headphones, and monaurally or binaurally, may also have contributed to the differential findings.
The present study had two goals: first, to establish whether alcohol does influence auditory sensitivity, and second, to explore possible explanations for any observed changes. In the initial experiment we measured the effects of alcohol on monaural and binaural thresholds for six pure tones of different frequencies. We compared thresholds obtained in a placebo condition with those obtained at BACs of ~60 mg/dl during both the absorption and elimination phases of the BAC function. This methodology allowed us to provide a more complete description of the effects of alcohol on auditory thresholds than is presently available and helped us to account for the equivocal reports in the literature.
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EXPERIMENT 1 |
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Apparatus and stimuli. Stimuli were generated in real time with 16-bit precision by a Kyma Sound Design Workstation (Symbolic Sound Corporation) equipped with a Capybara-66, running at a sample rate of 44.1 kHz. The output of this system was low-pass filtered with a cut-off frequency of 8 kHz. Tones were presented over a pair of TDH-39 earphones within a sound attenuation chamber. The system was controlled by a computer that also recorded participants' responses to stimuli. Subjects responded by clicking a mouse key on the appropriate button of a virtual control panel displayed on a monitor.
All auditory stimuli were calibrated using a Simpson Model 886 Type 2 Sound Level Meter and a Type 4152 Artificial Ear. Detection thresholds were measured for six frequencies (100, 200, 400, 800, 1600 and 3200 Hz). Tones were 500 ms in duration, including a 10 ms onset and offset ramp.
Procedure. Each volunteer participated in the alcohol and placebo conditions on separate days. Half completed the alcohol condition prior to the placebo conditions, whereas the remaining half participated in the placebo session first. All testing began at 10.00 and subjects were asked to consume a light low-fat breakfast ~2 h before testing to avoid adverse effects from consuming alcohol on an empty stomach.
In the alcohol condition, the participant was served an amount of alcohol (40% grain alcohol) mixed with juice in a 1:4 ratio. Drinks were served in cups with lids, and consumed through a straw. Upon arrival in the laboratory, the participant was asked to consume a number of drinks estimated to raise his or her BAC to 80 mg/dl. A breath measuring device (Alcometer 7410, Draeger, Inc., Lübeck, Germany) was employed to estimate BAC every 15 min for the duration of the experiment in both the placebo and alcohol conditions. Participants reached an average peak BAC of 72 mg/dl, although sensitivity was measured when BAC reached 60 mg/dl on both the rising and falling portions of the BAC curve or, in the placebo condition, 15 and 45 min after consumption of the juice.
To obtain rapid assessments of thresholds during the absorption phase of the BAC curve, all of the data were gathered using a transformed random dual staircase procedure (Cornsweet, 1962; Levitt, 1971
). Stimulus presentation and data tabulation were under computer control. The stimulus intensity was varied from trial to trial according to the rule: one yes response to move the intensity down by 1 dB SPL (sound pressure level) and one no to move it up by the same amount. Two randomly interleaved staircases were run for each frequency, with the final six reversals (intensity values at which the response changed) for each being averaged to calculate the threshold. Ascending staircases had an initial intensity value 10 dB below the expected threshold, whereas descending staircases had an initial intensity 10 dB above that value. All frequencies were tested in a single experimental run. Two blocks of trials were used: one in which the tones were presented monaurally and another in which the presentations were binaural. Because the measurement of the monaural and binaural thresholds was accomplished twice for each of the two drinking conditions (alcohol and placebo), the order of the listening conditions (monaural and binaural) was counterbalanced within subjects. Each participant accomplished the measurement of the monaural and binaural thresholds in the same order under the placebo and alcohol conditions. The threshold measurements took ~15 min to complete. Participants could leave the laboratory once their BAC had dropped below 0.05% (50 mg/dl).
Results
For each subject, a total of 48 threshold estimates were obtained. These represented thresholds determined in 2 sessions (alcohol, placebo) x2 BAC estimates (on the rising and falling curves) x2 listening conditions (monaural, binaural) x6 frequencies (100, 200, 400, 800, 1600 and 3200 Hz). Due to the small sample size used in this investigation, an alpha level of 0.1 was adopted for all statistical comparisons, though the actual levels obtained are reported for each comparison. We attempted to measure performance when BAC was 60 mg/dl on both the rising and falling portions of the BAC curve, however the differences in the speed of absorption and elimination of alcohol resulted in more variable BAC (mg/dl; mean ± SD) during the absorption phase (Mstart = 60 ± 3; Mend = 68 ± 10) than during the elimination phase (Mstart = 62 ± 6; Mend = 61 ± 13). Although BAC varied more during the rising phase, an initial F-test on the thresholds obtained under the alcohol conditions showed no evidence of a significant difference between the threshold measurements obtained during rising and falling phases (F(1, 5) = 1.35, P > 0.1). Because no significant differences were obtained between the measurements obtained during the rising and falling BAC phases, these thresholds were pooled and the averaged values were used in all subsequent analyses. Because the effects of alcohol were greater than anticipated, the value of post-alcohol thresholds at 100 Hz exceeded the calibrated maximum output of the system (60 dB SPL) for most participants. For this reason, the results for this tone have been excluded from all analyses.
The thresholds obtained under the placebo and alcohol conditions are plotted as a function of frequency for monaural and binaural listening in Fig. 1. Detection thresholds were generally higher for lower frequencies. In addition, a greater effect of alcohol appears to exist for lower frequencies and for monaural signals.
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Although the overall shape of the detection function for both experimental conditions showed the typical decline as a function of frequency, alcohol significantly increased thresholds for low frequency tones, but did not affect higher frequencies. Alcohol also affected monaural thresholds to a greater degree than binaural ones. This frequency selective effect of alcohol may go some way towards explaining why some studies have reported that alcohol impaired auditory thresholds (Hansen, 1925, as cited in Schneider and Carpenter, 1969; Moody et al., 1980
; Hienz et al., 1989
, 1992
), whereas others did not (Schwab and Ey, 1955 and Bablik, 1968, as cited in Wallgren and Barry, 1970
; also Specht, 1907, as cited in Schneider and Carpenter, 1969
). It seems reasonable to suggest that the absence of effects of alcohol on audition in some of these studies was a consequence of the choice of stimuli. Our own results are consistent with those previous studies which indicated that alcohol does impair hearing (Hansen, 1925, as cited in Schneider and Carpenter, 1969
; Moody et al., 1980
; Hienz et al., 1989
, 1992
). Most of these (Moody et al., 1980
; Hienz et al., 1989
, 1992
) used non-human primates and tested frequencies that were much higher than those used in the present investigation. Further work is necessary to establish whether alcohol also impairs human performance at these higher frequencies.
Previous studies have focused on the empirical question of whether alcohol affects auditory thresholds. Although the primary purpose of this investigation was to explore the behaviourally based effects of alcohol on audition, the inclusion of a larger range of stimuli than had been used in previous studies permitted inferences regarding the physiological mechanisms through which alcohol may be acting.
Alcohol is generally considered to be a central nervous system depressant. Hence, one hypothesis is that alcohol will change the overall arousal state or attentional processes (Wallgren and Barry, 1970; Moskowitz et al., 1972
; Moskowitz, 1974
). In the present study, all the frequencies were presented in random order and a staircase procedure was used to obtain the threshold estimates. This method was chosen because it permits the rapid estimation of thresholds necessary to obtain measurements over a small range of BAC during the rapidly rising phase of the curve. Because the staircases were randomly interleaved, it is impossible for the participant to anticipate the intensity or frequency of the signal on each trial. A generalized change in attention or arousal would be expected to yield changes in performance for all frequencies, rather than at particular frequencies. A further argument against changes in arousal or attentional processes is the consistency of the individual results. The individual results revealed a very similar pattern of losses for all subjects. If the results were a consequence of attending to one range of frequencies rather than another, it would be necessary that all subjects selected the higher frequencies to attend to.
A second possibility is that alcohol affects signal detection performance by shifting the individuals' response criterion. Again, this argument does not provide a parsimonious account for the frequency-selective effects of alcohol on monaural and binaural signals. A change in response criterion would be expected to result in a change in the thresholds obtained for all frequencies rather than at particular frequencies.
An alternative explanation for the findings relies on previous physiological observations and the known properties underlying the minimum audibility function. Whereas physiological studies have shown that even small amounts of alcohol reduce the amplitude of auditory cortical responses (Grenell, 1959; Nakai et al., 1966
; Hari et al., 1978
; Chu and Squires, 1980
; Teo and Ferguson, 1986
), studies on subcortical neural responses have generally failed to show changes in amplitude or latency following acute or chronic exposure to alcohol (Squires et al., 1978
; Begleiter et al., 1981
). This evidence for a central locus of alcohol's actions is further supported by the finding that large doses of alcohol are necessary to cause even a minimal change in potentials recorded from the organ of Corti (Gieldanowski, 1965
). In addition, Wolff and Gross (1968), in a study of the auditory systems of chronic alcoholics, found no damage to sensory end organs. The physiological findings suggest that alcohol may affect the central auditory system while the more peripheral mechanisms are spared. Given the physiological data, one might expect alcohol to affect audibility thresholds only to the extent that central mechanisms contribute to the detection of pure tones.
Audibility curves are primarily determined by the transmission properties of the outer and middle ears. For frequencies >3 kHz, thresholds can be fully accounted for on the basis of these transmission properties. However, for frequencies <3 kHz, measured thresholds are higher than expected on the basis of the transmission properties of the peripheral auditory apparatus. The function describing auditory thresholds for frequencies <3 kHz, exclusive of the transmission properties of the outer and middle ear, reveals a monotonic relationship between log frequency and audibility. Although the slope of this function is the same for all frequencies, a high frequency sound will result in neural signals that are temporally closer together than those of a low frequency tone. A model proposed by Zwislocki (1960) has shown that the elevated thresholds for low frequencies can be accounted for by assuming that the neural signals are summated in the auditory system for a fixed duration. Since fewer neural signals will occur for low frequency stimuli within this temporal summation period, a low frequency tone must produce neural signals of greater amplitude for the threshold to be reached. Thus, the stimuli must be more intense for a low frequency stimulus relative to a higher frequency one (Zwislocki, 1960). Several lines of evidence support the view that this decrease in audibility for low frequencies is a consequence of temporal summation processes in the central auditory nervous system (Kiang, 1968
; Lynch et al., 1982
; Moore et al., 1988
; Plack and Moore, 1990
).
Our results also revealed a trend toward a greater effect of alcohol on monaural thresholds compared to binaural ones. Binaural listening has a well-documented advantage over monaural listening, a phenomenon known as binaural summation. It is generally considered to be the result of the neural combination of signals from each ear (Gulick et al., 1989). Given that the neural signals from the two ears are not combined prior to the superior olive, binaural summation is also a reflection of central processes of the auditory system.
Several lines of evidence suggest that the decline in audibility of low frequency and the increase in binaural summation may be mediated by a common mechanism. First, the temporal summation model of Zwislocki (1960) that accounts for the reduced audibility for low frequency tones has been extended to explain binaural summation in the auditory system (Hellman and Zwislocki, 1963). Assuming similar mechanisms for binaural and temporal summation, one might expect alcohol to have a more pronounced effect on monaural signals, since they, like low frequency tones, are dependent upon higher amplitude neural responses for detection.
In summary, the results of this experiment suggest that a central auditory mechanism involved in the temporal and binaural summation of auditory signals may be significantly affected by alcohol. To further explore this possibility, Experiment 2 examined the effects of alcohol on another task thought to involve temporal processing of signals in the central auditory system the ability to discriminate frequency.
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EXPERIMENT 2 |
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While the available evidence on the effects of alcohol on auditory thresholds is mixed, several reviews have concluded that discrimination may be more susceptible than detection to the effects of alcohol (Jellinek and McFarland, 1940; Wallgren and Barry, 1970
). This conclusion, however, is largely based upon a small number of studies that investigated the effects of alcohol consumption on auditory intensity discrimination (Hansen, 1925 and Specht, 1907, as cited in Schneider and Carpenter, 1969
; Schwab and Ey, 1955, as cited in Wallgren and Barry, 1970
). All of these studies showed increases in differential intensity thresholds as a consequence of alcohol consumption.
To date, only one study has explored the consequences of alcohol for auditory frequency discrimination (Pihkanen and Kauko, 1962). In this study, three blind piano tuners were tested on a number of auditory measures, including frequency discrimination. The results of the frequency discrimination measure showed ceiling effects with these highly experienced listeners. However, two of the three participants showed a significant decrease in their ability to discriminate frequencies after alcohol consumption. No information about the effects of alcohol as a function of frequency, if any, was reported. As recognized by the authors, the small specialized sample used in this investigation, which resulted also in an inability to counterbalance the alcohol and no-alcohol conditions, calls into question the generality of these results.
More recently, a study of the perception of auditory Mach bands in alcoholics suggested that chronic use of alcohol does affect auditory mechanisms involved in the processing of frequency (Alpert and Bogorad, 1975). Carterette et al. (1969) showed that, in the presence of bandpass noise, thresholds are most elevated for frequencies near the lower edge of the noise band. They referred to this phenomenon as auditory Mach bands, because the effect of masking was greatest near the noise boundary. Alpert and Bogorad (1975) measured the thresholds for ten frequencies in the presence of bandpass noise and the masking effect of the noise was compared across frequencies for controls and alcoholics. Relative to the control group, alcoholics showed a reduction of their auditory Mach bands.
The previous study on auditory thresholds obtained results that were consistent with a change in the operation of a centrally located temporal process. Assuming that the temporal coding of frequency also relies on a combination of neural signals at a central location, and given that this process is particularly important for the encoding of frequencies that exceed the maximal firing rate of individual neurons, one might expect that alcohol would cause differential impairments across frequencies. Specifically, while no impairment would be expected for frequencies of <1000 Hz, alcohol would be expected to show effects for frequencies between 1000 and 5000 Hz.
Subjects and methods
Participants.
Six paid volunteers (three males, three females, age range 2139 years, mean ± SD 28 ± 6.7 years) from the student population at the University of Western Ontario participated. Three of these volunteers had also participated in the previous study on a separate occasion. Exclusion criteria were as described in Experiment 1.
Stimuli and apparatus. The stimuli and apparatus were identical to those described in Experiment 1, with the exceptions that all of the stimuli were set to a level of ~70 dB SPL. Frequency discrimination thresholds were measured for six carrier frequencies (100, 200, 400, 800, 1600 and 3200 Hz). Each trial was 4 s in duration. On each trial, one of the six carrier frequencies was presented for the first second, followed by a glide up to the test frequency over the subsequent 0.5 s. The frequency remained at this level for 1 s, followed by a 0.5 s glide back down to the carrier frequency, which remained on for one additional second.
Procedure. The procedure was essentially the same as that described for Experiment 1. Data for the placebo and alcohol conditions were gathered on two separate days and the order of testing was counterbalanced across subjects. On both occasions, participants expected that alcohol would be served. Participants reached an average peak BAC of 74 mg/dl in the alcohol condition. As in Experiment 1, sensitivity was measured when BAC reached 60 mg/dl on both the rising the falling portions of the BAC curve or, in the placebo condition, 15 and 45 min after consumption of the juice.
A transformed random dual staircase procedure (Cornsweet, 1962; Levitt, 1971
), similar to that described for Experiment 1, was employed. Instead of varying intensity as was done in the first experiment, the test frequency was varied by 1 Hz from trial to trial according to the subject's response. Due to the time constraints imposed by the rapid rate at which BAC increases, only the discrimination thresholds for an increase in frequency were measured. Two randomly interleaved staircases were run for each frequency, with the final six reversals for each being used to calculate the threshold. Ascending staircases had an initial test frequency value 5 Hz above the carrier frequencies, whereas descending staircases had an initial frequency value 15 Hz above the carrier frequencies. All frequencies were tested in a single experimental run. The threshold measurement took ~20 min to complete.
Results
The differences in the speed of absorption and elimination of alcohol resulted in more variable BAC (mg/dl; mean ± SD) during the absorption phase (Mstart = 67 ± 4; Mend = 73 ± 12) than during the elimination phase (Mstart = 65 ± 6; Mend = 63 ± 3). Although BAC varied more during the rising phase, no significant differences between the discrimination thresholds were found for rising and falling phases, so the data were pooled. Figure 3 shows the frequency discrimination thresholds as a function of frequency for both the alcohol and no alcohol conditions. Inspection of the graph reveals that discrimination thresholds increased as a function of frequency in both the alcohol and placebo conditions. It is also evident that the effects of alcohol are frequency-dependent.
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Discussion
The results of the frequency discrimination task revealed that alcohol significantly affected the ability to discriminate higher frequencies. The increase in the discrimination threshold was <1 Hz at frequencies of <1000 Hz. At frequencies of >1000 Hz, increases in discrimination thresholds were at least 3-fold greater than those found with lower frequencies.
The frequency discrimination thresholds were greater than those obtained in other investigations (Wier et al., 1977; Fastl and Hesse, 1984
). There are several plausible reasons for these differences. Previous investigations have tested frequency discrimination monaurally, and with participants who either had extensive experience in psychoacoustic experiments (Fastl and Hesse, 1984
) or who had at least 20 h of training on the experimental task (Wier et al., 1977
). In addition, the present study interleaved frequencies randomly, whereas other studies have estimated discrimination thresholds for specific frequencies in block presentations.
The results of our Experiment 1 and a number of physiological studies (Grenell, 1959; Nakai et al., 1966
; Hari et al., 1978
; Chu and Squires, 1980
; Teo and Ferguson, 1986
) suggest that alcohol may act on audition via central auditory mechanisms. The data of Experiment 2 are consistent with the hypothesis that alcohol may influence central mechanisms involved in the summation of signals across time and between the ears. For frequency discrimination, we postulated that frequency discrimination performance would show greater effects for higher frequencies than for low ones. This hypothesis was based on the fact that temporal models of frequency encoding require the combination of signals across time and separate neurons for frequencies of >1000 Hz. This combination of temporal signals occurs at a central locus in the auditory system. The present results revealed that frequency discrimination performance for frequencies of <1000 Hz showed little or no effect of alcohol, whereas performance for higher frequencies was significantly affected.
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GENERAL CONCLUSIONS AND COMMENTS |
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ACKNOWLEDGEMENTS |
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FOOTNOTES |
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2 Present address: School of Graduate and Professional Studies, Cameron University, Lawton, Oklahoma 73505-6377, USA.
* Author to whom correspondence should be addressed at: Dean's Office, Social Science Centre, University of Western Ontario, London, ON, Canada N6A 5C2.
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