ENVIRONMENTAL
9, 48-54 (1975)
RESEARCH
Effects
of Intense Low Frequency Sound (Sonic Boom) on the Cochlea
RICHARD
P. BOBBIN AND MARIA
1. GONDRA
Kresge Hewing Research Luborutory of the South, Depurtment Louisiunu State UniLvrsity Medical Center. 1100 Florida Nell, Orleum, Louisiunu 70119
of Otorhinolaryngology, Avenue, Building 164,
Received May 30. 1974 The effect of sonic boom on hearing was studied by exposing guinea pigs to intense lowfrequency tones. Low frequencies were found to affect cochlear function and structure; however, it was concluded that the typical sonic boom does not contain low frequencies of sufficient intensity to damage the cochlea.
Sonic booms have been described as N-waves generated by supersonic aircraft (see discussions by Hubbard, 1966; Kryter, 1966). An N-wave contains a spectrum of frequencies with all odd and even harmonics being present. The intensity of the frequencies contained in an N-wave decrease with increasing frequencies at the rate of 6 dB/octave. Because of this decrease, high frequencies are not present at potentially damaging intensities (above 70 dB SPL) in a typical sonic boom (N-wave of 200 msecond duration and 134 dB SPL peak level). However, the low frequencies of 2-200 Hz may be present at damaging intensities. Several authors have suggested that sonic boom exposure presents no hazard to hearing (Rice and Coles, 1968; Gierke, 1966; Nixon et al., 1968). However, Majeau-Chargois et al. (1970) presented data obtained from guinea pigs which seemed to show that sonic booms produce an increase in the number of damaged hair cells in the cochlea of guinea pigs. The present study was carried out to examine further the question of whether the low frequencies present in sonic booms are of sufficient intensities to produce significant damage to the cochlea of guinea pigs. We chose to use pure-tone exposure as test stimuli instead of artificially generated N-waves, since pure tones were easier to generate and control. Detrimental effects on the cochlea were monitored as changes in cochlear electrical phenomena and changes in the number of damaged cochlear hair cells. METHODS Effect of Low-Frequency
Exposure on Cochlenr Electricul Activity
Pigmented guinea pigs were anesthetized with sodium pentobarbital (Nembutal, Abbott; 25 mg/kg, ip) and paralyzed with gallamine triethoidide (Flaxidil, Davis and Geck; 8 mg/kg, iv). The trachea was cannulated and the animal artificially respired. Animal body temperature was maintained at 36.5-38°C. 48 Copyrtght 0 1975 by Academic Printed in the Umted States.
Press. Inc. All rights of reproduction
in any form reserved.
SONIC
49
BOOM
Cochlear microphonic potentials evoked by a 6 kHz tone burst and obtained by the differential electrode technique were used to monitor the state of the basal turn hair cells (Tasaki et al., 1952). The state of the hair cells in the apex were monitored by cochlear microphonic potentials evoked by tone bursts of 125 Hz, 60 Hz, and of the frequency of exposure (28, 49, or 76 Hz). They were obtained by a single-ended recording from the apex. The tone bursts were generated by a TDH-39 earphone connected to the ear in a closed fashion. Frequencies of 28, 49, 76, and 125 Hz at 128 dB SPL intensity and of 30 minute duration were used as the high intensity, low-frequency exposure stimuli. A plane wave tube, 20 ft long and 1 ft in diameter, with a 30 in. electrovoice speaker mounted at one end of the tube was used to generate these tones. This was the same apparatus used by Majeau-Chargois et (11.(1970) to generate sonic booms. Polyethylene tubing, 50 ft long and $ in. in diameter, was used to conduct the tones to the ear being tested. One end of the polyethylene tubing was inserted through a port in the plane wave tube, one foot from the speaker, while the other end was inserted through a port in the sound-proof room and connected to a hollow bar inserted into the external auditory canal of the guinea pig’s right ear. All sound pressure measurements were made in a closed fashion by coupling the ear bar to a f in. B & K microphone. Eflects of Low Frequency
Exposure on Cochlear
Huir Cells
Pigmented guinea pigs were placed in a small box so that their heads protruded. The guinea pig and box were placed inside the above mentioned plane wave tube so that the guinea pig faced the 30 in. speaker and was one foot from it (125 Hz, 76 Hz), or in a resonator box at the end of the plane wave tube (73 Hz). The free-field sound pressure level was recorded at the level of the guinea Pk. In this case, exposures consisted of three different stimuli: 1. 125 Hz at 145 dB SPL for 4 hours. 2. 76 Hz at 145 dB SPL for 4 hours. 3. 73 Hz at 120 dB SPL for 4 hours one day and 4 hours the next day. Data from five pairs of control (nonexposed) and experimental (exposed) animals with good left and right ears were obtained for each of the three different stimuli. All animals were sacrificed 30 days after exposure. The bullae were removed and the cochleae fixed as described by Engstriim et al. (1966). Sections of organ of Corti corresponding to Engstrijm’s sections +, It, zg, and 36 and apex were removed from both ears and examined for damaged hair cells with a microscope (Engstrijm et al., 1966, pp. 21-176). An example of a damaged hair cell is shown in Fig. 1. The number of such damaged and missing hair cells were counted for each row and expressed as a fraction of the number of row 3 outer hair cells which would have normally been present in the section examined. This figure was then converted to percent and transformed by Arcsin for expression and Analysis of Variance. Duncan’s New Multiple Range Test was used to test for significance (p < 0.05) between means (Edwards, 1964).
50
BOBBIN
AND
GONDRA
preparation of a section of organ of Corti demonstrating intact inner FI IF. 1. Surface (IHc C). outer pillar cells (OP), inner pillar cells (IP). and intact rows 1 and 3 of outer (OH IC). Row 2 OHC has one missing. scarred hair cell (arrow).
hair cells hair cells
SONIC BASAL TURN
51
BOOM Al'fX
1' "
IO00 I 500
I 200 c 60
70
80
90
100
110
120
50
60
70
so
90
100
110
120
INTENSITY I" dB SPI
FIG. 2. Effect of exposing the cochlea to a tone of 125 Hz at 128 dB SPL for 30 minutes on the cochlear microphonic input -output function elicited by a 6 kHz tone burst and recorded at the basal turn and the cochlear microphonic input-output function elicited by a 125 Hz tone burst and recorded at the apex.
RESULTS
Exposure of the guinea pig cochlea to 125 (five animals), 76 (two animals), 59 (one animal), or 28 Hz (two animals) at an intensity of 128 dB SPL for a duration of 30 minutes did not alter the cochlear microphonic potentials evoked by the 6 kHz tone burst and recorded from the basal turn. In contrast, the cochlear microphonic potentials recorded from the apex did change after exposure to the four frequencies. Figure 2 illustrates the effect of the 125 Hz exposure on the basal and apical responses. The cochlear potential input-output curves were shifted both on the rising and maximum portions of the curves to approximately the same extent; thus, the data are summarized by measuring the dB shift at the 400 E.CVlevel only (Table 1). It was found that as the frequency of exposure was TABLE EFFECT
OF EXPOSING
FOR 30
MINUTES.
THE COCHLEAR
Intense CM
exposure
frequency
GUINEA THE
EFFECT
MICROPHONIC
frequency:
(Hz) 125 60 76 49 28
PIG COCHLEA
IS MEASURED
(CM)
(128 dB SPL)
AS THE dB
INPUT-OUTPUT AT THE APEX
125 Hz(dB)
29 27
I
TO INTENSE
SHIFT FUNCTION
76 Hz(dB)
27 27 27
Low
FREQUENCY
AT THE 400 CURVE
49 HztdB)
20 27
PV
LEVEL
SOUNDS OF
RECORDED
28 HztdB)
9 8
20 7
52
BOBBIN ,
AND
73Hz
GONDRA
76Hz
Apex
* I
31/2
I-
L-1,
I n
n-
-.100 L
r-dl=cL-? lki
-.-+b 2
3
IHCI
12
3
-, IHC
1
2
3
FIG. 3. Percent distribution of hair cell damage in the inner hair cell row (IHC) and three outer hair cell rows (1, 2, 3) for three of the cochlear sections examined (apex, 3&, 24). Exposures were: 125 Hz at 145 dB SPL for 4 hours, 76 Hz at 145 dB SPL for 4 hours, and 73 Hz at 120 dB SPL for 4 hours on two consecutive days. *Significant P i 0.05 1 experimental; 0 control.
decreased, less dB shift was observed in the cochlear microphonic (Table 1).
potentials
Effect on Hair Cells In control animals the number of damaged hair cells increased from the base to the apex. Little or no damage was found in sections S and 14. Damage began to appear in section 2& and continued to increase towards the apex (Fig. 3). In control animals, each turn’s damage increased from the inner hair cell to row 3 of the outer hair cells (Fig. 3). Exposure to 73 Hz at 120 dB SPL for 4 hours one day and 4 hours the next day did not produce a significant degree of damage when these animals were compared to their controls (Fig. 3). Exposure to the 76 and 125 Hz at 145 dB SPL for 4 hours produced similar patterns of damage (Fig. 3). The damage seems to be present only in section 3& at the outer hair cell rows 2 and 3 for 76 Hz and outer hair cell row 3 for 125 Hz. However, only the 125 Hz, section 3+, outer hair cell row 3 damage was significantly greater than its control. DISCUSSION
It has been demonstrated that pure tones of select intensity and duration will produce changes in cochlear potentials recorded at one turn of the cochlea that are greater than the changes recorded at another turn (Beagley, 1965; Suga et al., 1967). The data obtained in this study confirm the above and demonstrate that low frequencies of sufficient intensities can be found which induce shifts in the cochlear potentials recorded at the apex, while inducing no change in the potentials recorded at the basal turn. This reemphasizes the opinion that changes in
SONIC
BOOM
53
cochlear potentials after intense sound stimulation must be measured near the point of maximal stimulation on the basilar membrane by the test tone (Suga et al., 1967). Others have shown that less hearing loss and hair cell damage is produced by low frequencies than high frequencies of equal intensity (Stockwell ef ul., 1969). One of the contributing factors to this phenomena is that the frequency transfer characteristics of the middle ear decrease with low frequencies at the rate of 6 dB/octave for guinea pig and 12 dB/octave for man (Dallos, 1970). Our data concur by demonstrating that the amount of cochlear microphonic shift decreased- as the frequency of exposure was decreased from 125 to 28 Hz-despite stimulation at all frequencies with equal intensity. The N-wave data of Majeau-Chargois et uf. (1970) suggested that frequencies of 30 and 10 Hz were damaging at the 1 lo- 120 dB level when presented for 20 minutes (one N-wave/second for 1000 seconds). Our data show that frequencies of 125, 76, 59, and 28 Hz at the 128 dB SPL level when presented for 30 minutes produce only a 7-29 dB shift in the cochlear potentials with the amount of shift decreasing with frequency. Others have shown that cochlear potential shifts of at least 60 dB are necessary for the appearance of permanent destruction observed in the form of hair cell damage (Eldredge and Covell, 1958). That such low frequencies and intensities would not induce hair cell damage was confirmed in this study by exposing guinea pigs to 73 Hz for 4 hours on two consecutive days at an intensity of 120 dB SPL. However, significant hair cell damage was induced by the exposure of 125 Hz at 145 dB SPL for 4 hours. As mentioned above, less damage to the hair cells should be produced as the frequency of exposure is decreased. This was confirmed by the finding that the exposure of 76 Hz at 145 dB SPL for 4 hours did not induce significant hair-cell damage. Therefore, for frequencies lower than 125 Hz to produce the same degree of damage as 125 Hz in this study, the intensities would have to be above 145 dB. Of course, Kryter (1966) showed that for N-waves to contain 125 Hz at 128 dB SPL the peak pressures would have to be greatly above the pressures generated by a typical sonic boom, or the N-waves used by Majeau-Chargois et al. ( 1970). Therefore, our data appear to demonstrate that the low frequencies present in sonic booms are not of sufficient intensity to alter cochlear function permanently. This conclusion is different from that of Majeau-Chargois et ul. ( 1970) who found damage in the apex. The reason for this difference is presently unknown. However, in our study a large percent of damaged hair cells was found in the apex of control animals. Thus, it seems possible that in their study this damage may have been confused with that induced by sound exposure. ACKNOWLEDGMENT This research supported in part versity of New Orleans Computer facilities provided through a grant It is a pleasure to acknowledge C. Wiesendanger.
by funds obtained from The Deafness Research Foundation; Unisupport under NSF Grant No. GJ-I 3 1; and necessary laboratory from the Kresge Foundation. the assistance of C. 1. Berlin, L. F. Hughes, J. K. Cullen, Jr., and
54
BOBBIN
AND
GONDRA
REFERENCES BEAGLEY, H. A. (1965). Acoustic trauma in the guinea pig. 1. Electrophysiology Otohryn~d.
(Stockh.)
60, 437-45
DALLOS. P. (1970). Low-frequency Amer.
and histology. A[,trr
I.
auditory characteristics:
Species dependence. J. Acoust. Sot,.
48, 489-499.
EDWARDS, A. L. (1964). “Experimental Design in Psychological Research.” Holt, Rinehart and Winston, New York. ELDREDGE, D. H.. AND COVELL, W. P. (1958). A laboratory method for the study of acoustic trauma. Laryngoscope 68, 465-477. ENGSTR~M, H., ADES, H. W., AND ANDERSSON, A. (1966). “Structural Pattern of the Organ of Corti.” Almqvist and Wiksell, Stockholm, Sweden. GIERKE. H. E.. VON (1966). Effects of sonic boom on people: Review and outlook. J. AUXU~. SOC.. Amer.
39, S43-SSO.
HUBBARD, H. H. (1966). Nature of the sonic boom problem. J. Acorrst. SOC. Amer. 39, Sl-S6. KRYTER, K. D. ( 1966). Laboratory tests of physiological-psychological reactions to sonic booms. .I. Ac.oust.
Sot. Amer.
39, S65-S72.
MAJEAU-CHARGOIS, D. A.. BERLIN, C. I.. AND WHITEHOUSE, G. D. (1970). Sonic boom effects on the organ of corti. Luryngoxwpe 80, 620-630. NIXON, C. W.. HILLE, H. K., SOMMER, H. C., AND GUII.D, E. (1968). Sonic booms resulting from extremely low-altitude supersonic flight: Measurements and observations on houses, livestock, and people. Aerospace Medrwl Rrsrurc~h Lahorutop No. AMRL-TR-68-52. RICE, C. G., AND COLES, R. R. A. (1968). Auditory hazard from sonic booms. Int. Adid. 7, 211-217. STOCKWELL. C. Q., ADES, H. W., AND ENGSTR~M. H. (1969). Patterns of hair cell damage after intense auditory stimulation. Ann. 01ol. Rhino/. Laryngol. 78, 1 144-l 169. SUGA, F., SNOW, J. B., PRESTON, W. J., AND GLOMSET, J. L. (1967). Tonal patterns of cochlear impairment following intense stimulation with pure tones. Luryngoscope 77, 784-805. TASAKI, I., DAVIS, H., AND LEGOUIX, I. P. (1952). The space time pattern of the cochlear microphonics (guinea pigs) as recorded by differential electrodes. ./. Aumsf. Sot. Amer. 45, 502-5 19.
9, 48-54 (1975)
RESEARCH
Effects
of Intense Low Frequency Sound (Sonic Boom) on the Cochlea
RICHARD
P. BOBBIN AND MARIA
1. GONDRA
Kresge Hewing Research Luborutory of the South, Depurtment Louisiunu State UniLvrsity Medical Center. 1100 Florida Nell, Orleum, Louisiunu 70119
of Otorhinolaryngology, Avenue, Building 164,
Received May 30. 1974 The effect of sonic boom on hearing was studied by exposing guinea pigs to intense lowfrequency tones. Low frequencies were found to affect cochlear function and structure; however, it was concluded that the typical sonic boom does not contain low frequencies of sufficient intensity to damage the cochlea.
Sonic booms have been described as N-waves generated by supersonic aircraft (see discussions by Hubbard, 1966; Kryter, 1966). An N-wave contains a spectrum of frequencies with all odd and even harmonics being present. The intensity of the frequencies contained in an N-wave decrease with increasing frequencies at the rate of 6 dB/octave. Because of this decrease, high frequencies are not present at potentially damaging intensities (above 70 dB SPL) in a typical sonic boom (N-wave of 200 msecond duration and 134 dB SPL peak level). However, the low frequencies of 2-200 Hz may be present at damaging intensities. Several authors have suggested that sonic boom exposure presents no hazard to hearing (Rice and Coles, 1968; Gierke, 1966; Nixon et al., 1968). However, Majeau-Chargois et al. (1970) presented data obtained from guinea pigs which seemed to show that sonic booms produce an increase in the number of damaged hair cells in the cochlea of guinea pigs. The present study was carried out to examine further the question of whether the low frequencies present in sonic booms are of sufficient intensities to produce significant damage to the cochlea of guinea pigs. We chose to use pure-tone exposure as test stimuli instead of artificially generated N-waves, since pure tones were easier to generate and control. Detrimental effects on the cochlea were monitored as changes in cochlear electrical phenomena and changes in the number of damaged cochlear hair cells. METHODS Effect of Low-Frequency
Exposure on Cochlenr Electricul Activity
Pigmented guinea pigs were anesthetized with sodium pentobarbital (Nembutal, Abbott; 25 mg/kg, ip) and paralyzed with gallamine triethoidide (Flaxidil, Davis and Geck; 8 mg/kg, iv). The trachea was cannulated and the animal artificially respired. Animal body temperature was maintained at 36.5-38°C. 48 Copyrtght 0 1975 by Academic Printed in the Umted States.
Press. Inc. All rights of reproduction
in any form reserved.
SONIC
49
BOOM
Cochlear microphonic potentials evoked by a 6 kHz tone burst and obtained by the differential electrode technique were used to monitor the state of the basal turn hair cells (Tasaki et al., 1952). The state of the hair cells in the apex were monitored by cochlear microphonic potentials evoked by tone bursts of 125 Hz, 60 Hz, and of the frequency of exposure (28, 49, or 76 Hz). They were obtained by a single-ended recording from the apex. The tone bursts were generated by a TDH-39 earphone connected to the ear in a closed fashion. Frequencies of 28, 49, 76, and 125 Hz at 128 dB SPL intensity and of 30 minute duration were used as the high intensity, low-frequency exposure stimuli. A plane wave tube, 20 ft long and 1 ft in diameter, with a 30 in. electrovoice speaker mounted at one end of the tube was used to generate these tones. This was the same apparatus used by Majeau-Chargois et (11.(1970) to generate sonic booms. Polyethylene tubing, 50 ft long and $ in. in diameter, was used to conduct the tones to the ear being tested. One end of the polyethylene tubing was inserted through a port in the plane wave tube, one foot from the speaker, while the other end was inserted through a port in the sound-proof room and connected to a hollow bar inserted into the external auditory canal of the guinea pig’s right ear. All sound pressure measurements were made in a closed fashion by coupling the ear bar to a f in. B & K microphone. Eflects of Low Frequency
Exposure on Cochlear
Huir Cells
Pigmented guinea pigs were placed in a small box so that their heads protruded. The guinea pig and box were placed inside the above mentioned plane wave tube so that the guinea pig faced the 30 in. speaker and was one foot from it (125 Hz, 76 Hz), or in a resonator box at the end of the plane wave tube (73 Hz). The free-field sound pressure level was recorded at the level of the guinea Pk. In this case, exposures consisted of three different stimuli: 1. 125 Hz at 145 dB SPL for 4 hours. 2. 76 Hz at 145 dB SPL for 4 hours. 3. 73 Hz at 120 dB SPL for 4 hours one day and 4 hours the next day. Data from five pairs of control (nonexposed) and experimental (exposed) animals with good left and right ears were obtained for each of the three different stimuli. All animals were sacrificed 30 days after exposure. The bullae were removed and the cochleae fixed as described by Engstriim et al. (1966). Sections of organ of Corti corresponding to Engstrijm’s sections +, It, zg, and 36 and apex were removed from both ears and examined for damaged hair cells with a microscope (Engstrijm et al., 1966, pp. 21-176). An example of a damaged hair cell is shown in Fig. 1. The number of such damaged and missing hair cells were counted for each row and expressed as a fraction of the number of row 3 outer hair cells which would have normally been present in the section examined. This figure was then converted to percent and transformed by Arcsin for expression and Analysis of Variance. Duncan’s New Multiple Range Test was used to test for significance (p < 0.05) between means (Edwards, 1964).
50
BOBBIN
AND
GONDRA
preparation of a section of organ of Corti demonstrating intact inner FI IF. 1. Surface (IHc C). outer pillar cells (OP), inner pillar cells (IP). and intact rows 1 and 3 of outer (OH IC). Row 2 OHC has one missing. scarred hair cell (arrow).
hair cells hair cells
SONIC BASAL TURN
51
BOOM Al'fX
1' "
IO00 I 500
I 200 c 60
70
80
90
100
110
120
50
60
70
so
90
100
110
120
INTENSITY I" dB SPI
FIG. 2. Effect of exposing the cochlea to a tone of 125 Hz at 128 dB SPL for 30 minutes on the cochlear microphonic input -output function elicited by a 6 kHz tone burst and recorded at the basal turn and the cochlear microphonic input-output function elicited by a 125 Hz tone burst and recorded at the apex.
RESULTS
Exposure of the guinea pig cochlea to 125 (five animals), 76 (two animals), 59 (one animal), or 28 Hz (two animals) at an intensity of 128 dB SPL for a duration of 30 minutes did not alter the cochlear microphonic potentials evoked by the 6 kHz tone burst and recorded from the basal turn. In contrast, the cochlear microphonic potentials recorded from the apex did change after exposure to the four frequencies. Figure 2 illustrates the effect of the 125 Hz exposure on the basal and apical responses. The cochlear potential input-output curves were shifted both on the rising and maximum portions of the curves to approximately the same extent; thus, the data are summarized by measuring the dB shift at the 400 E.CVlevel only (Table 1). It was found that as the frequency of exposure was TABLE EFFECT
OF EXPOSING
FOR 30
MINUTES.
THE COCHLEAR
Intense CM
exposure
frequency
GUINEA THE
EFFECT
MICROPHONIC
frequency:
(Hz) 125 60 76 49 28
PIG COCHLEA
IS MEASURED
(CM)
(128 dB SPL)
AS THE dB
INPUT-OUTPUT AT THE APEX
125 Hz(dB)
29 27
I
TO INTENSE
SHIFT FUNCTION
76 Hz(dB)
27 27 27
Low
FREQUENCY
AT THE 400 CURVE
49 HztdB)
20 27
PV
LEVEL
SOUNDS OF
RECORDED
28 HztdB)
9 8
20 7
52
BOBBIN ,
AND
73Hz
GONDRA
76Hz
Apex
* I
31/2
I-
L-1,
I n
n-
-.100 L
r-dl=cL-? lki
-.-+b 2
3
IHCI
12
3
-, IHC
1
2
3
FIG. 3. Percent distribution of hair cell damage in the inner hair cell row (IHC) and three outer hair cell rows (1, 2, 3) for three of the cochlear sections examined (apex, 3&, 24). Exposures were: 125 Hz at 145 dB SPL for 4 hours, 76 Hz at 145 dB SPL for 4 hours, and 73 Hz at 120 dB SPL for 4 hours on two consecutive days. *Significant P i 0.05 1 experimental; 0 control.
decreased, less dB shift was observed in the cochlear microphonic (Table 1).
potentials
Effect on Hair Cells In control animals the number of damaged hair cells increased from the base to the apex. Little or no damage was found in sections S and 14. Damage began to appear in section 2& and continued to increase towards the apex (Fig. 3). In control animals, each turn’s damage increased from the inner hair cell to row 3 of the outer hair cells (Fig. 3). Exposure to 73 Hz at 120 dB SPL for 4 hours one day and 4 hours the next day did not produce a significant degree of damage when these animals were compared to their controls (Fig. 3). Exposure to the 76 and 125 Hz at 145 dB SPL for 4 hours produced similar patterns of damage (Fig. 3). The damage seems to be present only in section 3& at the outer hair cell rows 2 and 3 for 76 Hz and outer hair cell row 3 for 125 Hz. However, only the 125 Hz, section 3+, outer hair cell row 3 damage was significantly greater than its control. DISCUSSION
It has been demonstrated that pure tones of select intensity and duration will produce changes in cochlear potentials recorded at one turn of the cochlea that are greater than the changes recorded at another turn (Beagley, 1965; Suga et al., 1967). The data obtained in this study confirm the above and demonstrate that low frequencies of sufficient intensities can be found which induce shifts in the cochlear potentials recorded at the apex, while inducing no change in the potentials recorded at the basal turn. This reemphasizes the opinion that changes in
SONIC
BOOM
53
cochlear potentials after intense sound stimulation must be measured near the point of maximal stimulation on the basilar membrane by the test tone (Suga et al., 1967). Others have shown that less hearing loss and hair cell damage is produced by low frequencies than high frequencies of equal intensity (Stockwell ef ul., 1969). One of the contributing factors to this phenomena is that the frequency transfer characteristics of the middle ear decrease with low frequencies at the rate of 6 dB/octave for guinea pig and 12 dB/octave for man (Dallos, 1970). Our data concur by demonstrating that the amount of cochlear microphonic shift decreased- as the frequency of exposure was decreased from 125 to 28 Hz-despite stimulation at all frequencies with equal intensity. The N-wave data of Majeau-Chargois et uf. (1970) suggested that frequencies of 30 and 10 Hz were damaging at the 1 lo- 120 dB level when presented for 20 minutes (one N-wave/second for 1000 seconds). Our data show that frequencies of 125, 76, 59, and 28 Hz at the 128 dB SPL level when presented for 30 minutes produce only a 7-29 dB shift in the cochlear potentials with the amount of shift decreasing with frequency. Others have shown that cochlear potential shifts of at least 60 dB are necessary for the appearance of permanent destruction observed in the form of hair cell damage (Eldredge and Covell, 1958). That such low frequencies and intensities would not induce hair cell damage was confirmed in this study by exposing guinea pigs to 73 Hz for 4 hours on two consecutive days at an intensity of 120 dB SPL. However, significant hair cell damage was induced by the exposure of 125 Hz at 145 dB SPL for 4 hours. As mentioned above, less damage to the hair cells should be produced as the frequency of exposure is decreased. This was confirmed by the finding that the exposure of 76 Hz at 145 dB SPL for 4 hours did not induce significant hair-cell damage. Therefore, for frequencies lower than 125 Hz to produce the same degree of damage as 125 Hz in this study, the intensities would have to be above 145 dB. Of course, Kryter (1966) showed that for N-waves to contain 125 Hz at 128 dB SPL the peak pressures would have to be greatly above the pressures generated by a typical sonic boom, or the N-waves used by Majeau-Chargois et al. ( 1970). Therefore, our data appear to demonstrate that the low frequencies present in sonic booms are not of sufficient intensity to alter cochlear function permanently. This conclusion is different from that of Majeau-Chargois et ul. ( 1970) who found damage in the apex. The reason for this difference is presently unknown. However, in our study a large percent of damaged hair cells was found in the apex of control animals. Thus, it seems possible that in their study this damage may have been confused with that induced by sound exposure. ACKNOWLEDGMENT This research supported in part versity of New Orleans Computer facilities provided through a grant It is a pleasure to acknowledge C. Wiesendanger.
by funds obtained from The Deafness Research Foundation; Unisupport under NSF Grant No. GJ-I 3 1; and necessary laboratory from the Kresge Foundation. the assistance of C. 1. Berlin, L. F. Hughes, J. K. Cullen, Jr., and
54
BOBBIN
AND
GONDRA
REFERENCES BEAGLEY, H. A. (1965). Acoustic trauma in the guinea pig. 1. Electrophysiology Otohryn~d.
(Stockh.)
60, 437-45
DALLOS. P. (1970). Low-frequency Amer.
and histology. A[,trr
I.
auditory characteristics:
Species dependence. J. Acoust. Sot,.
48, 489-499.
EDWARDS, A. L. (1964). “Experimental Design in Psychological Research.” Holt, Rinehart and Winston, New York. ELDREDGE, D. H.. AND COVELL, W. P. (1958). A laboratory method for the study of acoustic trauma. Laryngoscope 68, 465-477. ENGSTR~M, H., ADES, H. W., AND ANDERSSON, A. (1966). “Structural Pattern of the Organ of Corti.” Almqvist and Wiksell, Stockholm, Sweden. GIERKE. H. E.. VON (1966). Effects of sonic boom on people: Review and outlook. J. AUXU~. SOC.. Amer.
39, S43-SSO.
HUBBARD, H. H. (1966). Nature of the sonic boom problem. J. Acorrst. SOC. Amer. 39, Sl-S6. KRYTER, K. D. ( 1966). Laboratory tests of physiological-psychological reactions to sonic booms. .I. Ac.oust.
Sot. Amer.
39, S65-S72.
MAJEAU-CHARGOIS, D. A.. BERLIN, C. I.. AND WHITEHOUSE, G. D. (1970). Sonic boom effects on the organ of corti. Luryngoxwpe 80, 620-630. NIXON, C. W.. HILLE, H. K., SOMMER, H. C., AND GUII.D, E. (1968). Sonic booms resulting from extremely low-altitude supersonic flight: Measurements and observations on houses, livestock, and people. Aerospace Medrwl Rrsrurc~h Lahorutop No. AMRL-TR-68-52. RICE, C. G., AND COLES, R. R. A. (1968). Auditory hazard from sonic booms. Int. Adid. 7, 211-217. STOCKWELL. C. Q., ADES, H. W., AND ENGSTR~M. H. (1969). Patterns of hair cell damage after intense auditory stimulation. Ann. 01ol. Rhino/. Laryngol. 78, 1 144-l 169. SUGA, F., SNOW, J. B., PRESTON, W. J., AND GLOMSET, J. L. (1967). Tonal patterns of cochlear impairment following intense stimulation with pure tones. Luryngoscope 77, 784-805. TASAKI, I., DAVIS, H., AND LEGOUIX, I. P. (1952). The space time pattern of the cochlear microphonics (guinea pigs) as recorded by differential electrodes. ./. Aumsf. Sot. Amer. 45, 502-5 19.
