Long-term effects of simulated sonic booms on hearing in rhesus monkeys

Journal of Sound and Vibration (1987) 113(2), 355-363

LONG-TERM EFFECTS OF SIMULATED SONIC BOOMS O N HEARING IN RHESUS MONKEYS S. REuNns, D. S. WEnSS, J. W. FEATIIERSTONE AND C. TSAROS

Department of Psychology, University of Waterloo, Waterloo, Ontario, Canada N2L 3GI and Institute for Aerospace Studies, University Toronto, Downsview, Ontario, Canada M3H 5T6 (Received 19 Januao, 1986, and in revisedform 22 April 1986) Two monkeys of the species Macaca mulatta were exposed at 1 min intervals to five simulated sonic booms lasting 200 ms at 200 Pa overpressure with a 10 ms rise time. Another group of five monkeys of the same species were exposed to 100 booms. Their hearing thresholds were tested 24 hours, two weeks, one month, two months, four months and six months later. In one animal exposed to five booms, changes of the hearing thresholds were observed 24 hours following the exposure, but not later. All five animals exposed to 100 sonic booms had threshold shifts in the high-frequency range 24 hours following the exposure. Of the three animals followed for the full period of six months, one recovered completely. In the two others, threshold shifts were still observed in the high frequency range. Histological examination revealed destruction of the organ of Corti in the basal turn of the cochlea. These data indicate that there is individual variability in the extent of the damage to the inner ear by the sonic boom (and, perhaps, by other types of impulsive noise). These data also indicate that there is a possibility of similar damage to human inner ears exposed either to sonic booms or to other types of impulsive noise, and that it may go undetected for a long time because the high-frequency hearing defect, over 8 kHz, may be overlooked when routine audiometric methods are used. I. INTRODUCTION Sonic booms are a special form of impulsive noise produced by aircraft flying faster than the speed of sound. The build-up of compressed air in front of the aircraft forms a cone-shaped shock which spreads out, eventually reaches the ground and is perceived as a.loud explosion-like noise. Sonic booms from Concorde aircraft at Mach 2 flying at 52 000 feet altitude were found to be of 250 ms duration, and their overpressure was 90 Pa. Low level military flights at less than 100 feet have been found to produce overpressures of up to 6700 Pa. When the speed of the aircraft changes, or when it makes turns, it is possible to generate more intensive booms, called superbooms. These superbooms have a shorter rise time and a larger overpressure than the "ordinary" booms [1]. In our previous papers we have shown that simulated sonic booms may cause bleeding into the basal turn of the cochlea of C57 BL mice, guinea pigs and chinchillas [2-4]. In the present study, we investigated the effect of sonic booms on another animal species, Rhesus monkeys (Macaca mulatta). We explored the long-term changes of the hearing thresholds induced by exposure to repeated simulated sonic booms. Although guinea pigs and chinchillas will continue to have their place in auditory research, the monkey, as next o f k i n to humans, appears to be the animal of choice for the evaluation of traumatic effects from different kinds of noise, including impulsive noise and sonic booms [5]. 355 o022-460x/87/050355 + 09 $03.00/0

Q 1987 Academic Press Inc. (London) Limited

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2. METHODS 2.1. SUBJECTS Nine Macaca mulatta monkeys of age between 7 and 12 years, weighing between 6 and 11.5 kg, were used. Subjects were housed in the Primate Housing Facility of the Department of Psychology, University of Waterloo. The monkeys had water available ad libitum but food consisted of a standard, premeasured issue o f Purina monkey chow and a daily fruit supplement. 2.2. A U D I O M E T R I C P R O C E D U R E The hearing of the animals was tested in a shielded cage in a sound-proof quiet quasi-anechoic room. A "low frequency" speaker for frequencies below 16 kHz and a special electrostatic ("high frequency") transmitter [6] were used to present the test tones to the subjects. The electrostatic ultrasonic transmitter was constructed at the University of Toronto Institute for Aerospace Studies (UTIAS) and is able to produce undistorted pure tones from 15 kHz to 130kHz. The "high frequency" transmitter was polarized by a positive direct current o f 130 V from a high voltage supply unit. Pure frequencies from an Interstate Electronics Corpora t i o n F 3 4 Function Generator were gated and a signal with a total duration of 100ms and rise and fall times of 10 ms was produced. One EEG surface electrode (Beckman Instruments) was placed on the shaven monkey forehead, and another on the temporal area. The ground electrode was clipped to the subject's ear. The evoked potentials were preamplified by routine methods, and digitized by the analog/digital input of the PDP 11/40 computer. The PDP 11/40 computer and its Laboratory Peripheral System was used for the sampling and summation of the cortical evoked potentials. During the recording of auditory evoked potentials, the subjects were anaesthetized with a combination of Ketamine (20mg/kg body weight) and Sodium Amobarbital (60 mg/kg body weight). A total of 400 evoked potentials (one per second) were averaged by the computer and then displayed on the video screen. A subject was first presented by a relatively high intensity sound about 50 dB above the expected threshold at each specific frequency and the subject's averaged Auditory Evoked Response (AER) was recorded. The intensity of the tone was then decreased and the new auditory evoked response (AER) was recorded. The stimulus intensity was decreased first in 20 dB steps, and then, closer to the threshold, in 10, 5 and 3 dB steps. The first, recorded AER was compared visually with the new evoked potential. When the evoked response (at least two positive and two negative waves) was still present, the intensity was further decreased. In the case of uncertainty, the recording was repeated and evaluated again. Also, it was summed with the previous recording and evaluated for the third time. The lowest intensity that produced an evoked potential was labelled the threshold at that frequency. Thresholds were determined for the following frequencies: 500 Hz, 1, 2, 4, 8, 16, 24, 30, 35 and 40 kHz, and if possible 45 kHz. 2.3. S O N I C BOOM E X P O S U R E After the audiogram for each subject was determined at least twice, the subject was transported to UTIAS in Toronto, anaesthetized with Ketamine (20 mg/kg) and placed one meter in front of the reflection eliminator of the Travelling Wave Horn Sonic-Boom Simulator. A detailed description of the sonic boom simulator can be found in the paper by Glass et al. [7]. Two subjects (El and E2) received at 1 min intervals five sonic booms. Five subjects (E3, E4, E5, E6, E7) received 100 sonic booms each. Two subjects were control animals (CI, C2) which were only placed in the boom simulator for 100 minutes while under anaesthetic, but were not exposed to simulated sonic booms.

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In two control and three experimental animals, the auditory threshold shifts were tested over a period after the exposure. 2.4. IIISTOLOGY Following the last auditory testing, the animals were sacrificed with an overdose of Euthanal and their temporal bones dissected. The middle ear ossicles were tested for mobility and the middle ear cavity was checked for infection. The cochleae considered healthy were then examined histologically by the surface specimen technique as described by Engstrom et al. [8]. The round window membrane was carefully punctured by an ophthalmological scalpel, the stapes with its footplate was extracted from the oval window, 9and the cochlea perfused with the fixative, a 2% veronal-buitered solution of osmic acid. The bones were thoroughly washed in water and dehydrated in up to 70% alcohol in the refrigerator. The cochlear wall of scala vestibuli was thinned by using a fine dental drill and finally detached. The stria vascularis was carefully picked away to expose the organ of Corti. Both Reissner's membrane and the tectorial membrane were removed. Half turns of the basilar membrane were then removed and mounted in glycerin on a glass slide and cover slipped. The specimens were examined with a Leitz phase-contrast microscope. The criterion for hair-cell loss estimation was presence or absence of the outer a n d / o r inner hair cells. 3. RESULTS The average pre-exposure hearing thresholds of all nine Rhesus monkeys used in the experiment are presented in Figure 1. Our data were quite similar to the hearing thresholds of this species obtained by behavioral methods and published by other authors [9-13]. I

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The variability in hearing thresholds of the control animals during repeated retesting over the six month period was minimal. In two animals, the 45 Hz hearing thresholds could not be determined. Therefore, the average hearing thresholds at 45 kHz was calculated from the data obtained from seven animals only. In animals exposed to five simulated sonic booms, we observed only a temporary increase of the hearing thresholds. Twenty-four hours after the exposure, monkey E 1 had threshold shift at 4, 24 and 30 kHz, with shifts of 50.2 dB, 9.6 dB and 14.9 dB respectively. The hearing thresholds returned to the normal values one week after the exposure. Monkey E2 showed no significant threshold shift. These two animals were then followed at monthly periods for six months, but their hearing thresholds did not deviate from the control values. Histological examination of the inner ears did not reveal any defects of the organ of Corti. The average hearing curve of five animals prior to exposure to 100 simulated sonic booms did not differ substantially from the hearing curves of the two control animals. Within the first 24 hours after exposure, there was a threshold shift in all monkeys, mainly between the frequencies of 8 and 35 kHz. in one of the animals, the experiments had to be terminated due to circumstances beyond our control two months after the exposure. At that time, there were still considerably increased hearing thresholds to the sound frequencies from 24 to 35 kHz. Over the whole period of observation, most threshold shifts were found in the range of 16-35 kHz. The threshold shifts are summarized in Table 1. Because ofseveral individual differences, each monkey is described separately. TABLE

1

The hearing shifts following exposure office monkeys to a series of 100 sonic booms (numerator of the fraction is a number of shifts aboice 5 dB, nominator is a number of tested animals). Frequency (kHz)

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0/4 0/4 0/4 0/4 0/4 0/4 2/4

0/4 0/4 0/4 0/4 0/4 0/4 2/4

Monkey E3. Twenty-four hours after exposure to 100 simulated sonic booms, this animal showed a threshold shift of 5"0 dB(SPL) above the SD at 0.5 kHz, 25.6 dB(SPL) at 8 kHz, 42.0 dB(SPL) at 24 kHz, 50.2 dB(SPL) at 30 kHz and 14.8 dB(SPL) at 35 kHz. After two weeks and one month, there was a shift of 43.6 dB(SPL) at 24 kHz, 51-2 dB(SPL) at 30 kHz and 14.8 dB(SPL) at 35 kHz. After two months, the threshold shift at 24 kHz was 44.9 dB(SPL), at 30 kHz it was 51.2 dB(SPL), and at 35 kHz it was 20.3 dB(SPL) (see Figure 2). The experiment was terminated two months after the exposure. Histological examination revealed a 3 mm long defect of the outer and inner hair cells of the organ of Corti in the basal turn of the cochlea.

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Monkey E4 showed a dramatic increase of hearing thresholds 24 hours after exposure to 100 booms. At 8 kHz there was a threshold shift of 21.2 dB(SPL), at 16 kHz a threshold shift of 49-3 dB(SPL), at 2 4 k H z a 58.6dB(SPL) shift occurred, and at 3 0 k H z a 40.8 dB(SPL) shift. An extreme threshold shift which could not be measured by our equipment occurred at 35 kHz. After two weeks, the hearing thresholds had dropped, but there was still a 47-4 db(SPL) shift at 16 kHz and a 28.8 dB(SPL) shift at 35 kHz. After one month, all the hearing thresholds returned to the normal threshold range and the pre-boom audiogram curve was found again at four months and at six months. Histological examination did not reveal any defect of the organ of Cord. Monkey E5, 24 hours after exposure to 100 sonic booms, had a small threshold shift at 24 kHz of 1.7 dB(SPL) and a 26.4 dB(SPL) shift at 30 kHz. This did not change after 2 weeks. After one month, at 24 kHz a 41.4 dB(SPL) shift was found, while at 30 kHz there was a shift of 39-8 dB(SPL). Similar results were found after two and four months, but at six months the threshold shift at 24 kHz had decreased to 17.5 dB(SPL) while at 30 kHz, the shift stayed at 39.8 dB(SPL) (Figure 3). An extensive defect of both the outer and inner hair cells of the organ of Corti, at least 6 mm long, along the basal turn was found during the histological evaluation. In this area, all hair cells had degenerated and the defect was covered by the epithelium. Monkey E6. After an exposure to 100 booms, this subject showed a threshold shift of 27-7 dB(SPL) above the SD at 1 kHz, 8.8 dB(SPL) at 2 kHz, 41-7 dB(SPL) at 4 k H z , 30.2 dB(SPL) at 16 kHz, and 48 dB(SPL) at 24 kHz, after 24 hours post-exposure. After two weeks, some thresholds decreased to the normal range, except at 1 kltz, where there was a positive 27.7 dB(SPL) shift still present, at 4 kHz, where there was a 44.2 dB(SPL) shift, and at 40 kHz where 13.8(SPL) shift was found. After one month, there was a shift

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Figure 3. Monkey E5, changes of the hearing thresholds six months after exposure to 100 simulated sonic booms. 9 ==, Values before exposure; F-I-- -9, values after exposure. of only 26 dB(SPL) at 4 kHz and a 13.8 dB(SPL) shift at 40 kHz. After two months, the shift at 4 kHz decreased to 12.3 dB(SPL) and at 40 kHz it stayed at 13.8 dB(SPL). After four months, there was even an improvement in hearing found at 1 kHz ( - 6 . 7 dB(SPL)), 2 kHz ( - 1 7 dB(SPL)), and 8 kHz ( - 1 3 dB(SPL)). At 16 kHz, a shift of 30.2 dB(SPL) was found, and a 15 dB(SPL) threshold shift was observed at 40 kHz. The negative threshold shifts were still observed after six months and there was still a positive 30.2 dB(SPL) shift at 16 kHz. No histological changes of the organ of Corti were noticed. Monkey E7 was only tested 24 hours after exposure to 100 sonic booms. A significant threshold shift of 21-2 dB(SPL) was found at 8 kHz, while at 16 kHz a 69.6 dB(SPL) was present. At 24 kHz, there was a 53-2 dB(SPL) shift, 30 kHz had a 30.5 dB(SPL) shift and at 35 kHz there was a 48-8 dB(SPL) shift. This experiment was terminated after 24 hours for reasons unrelated to the health of the animal or to our experiment (Figure 4). No histological evaluation was performed. 4. DISCUSSION The exposure to a series of 100 simulated sonic booms caused auditory threshold shifts in Rhesus monkeys. The extent of the threshold shifts as well as their duration was rather variable. These shifts, which were found in the high frequency range of the audiometric hearing curve, were still present in two out of three observed subjects after a six-month post-exposure period. Our previous data [2] showed that the effects o f repeated sonic booms may be cumulative. When, in our previous study, the experimental animals were exposed to one sonic boom per day for several days, the final damage was as extensive as that following the exposure to the same number of sonic booms administered in one-minute intervals. For

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Figure 4. Monkey E7 changes of the hearing thresholds 24 hours after exposure to 100 simulated sonic booms. II-------II, Values before exposure; I-1_ _ -F-I, values after exposure.

this reason, the exposure of our experimental animals to one hundred b o o m s within a short time interval is not unrealistic. To expand the exposure into long time series mimicking the life-tong exposure to one or two booms per day cannot be done within a reasonable time. Also, the intensity of the sonic booms which we used is not too far from the intensity of the sonic booms occurring in our environment. In some situations--during landing or turns of the a i r c r a f t - - m u c h higher intensities of the booms have been detected. In these conditions, the cumulation of the effect would proceed at a much faster rate. Certain persons and professions would certainly be exposed to these extreme conditions. Exposure to five simulated sonic b o o m s did not, however, cause any significant threshold shift in one subject, and only minor and temporary shift in another. Therefore, exposure to a small number of sonic b o o m s did not cause significant damage. An immediate general threshold shift after exposure to impulse noise had been reported by others [14, 15]. These threshold shifts tend to decrease over time. The results of the sonic b o o m exposure on hearing and structure of the inner ear are still controversial. In spite of a high public interest in the past decade, not too many research papers have been published in this field. Populations of whole regions have been exposed to repeated series of unexpected sonic b o o m s over long periods of time, although no extensive experimental tests had been performed beforehand. For this reason, our experimental data are still highly timely and relevant. Some investigators have reported that sonic b o o m does not damage the inner ear, nor does it cause changes in the hearing thresholds. Rice and Coles [16] measured audiometric curves up to 8 kHz after exposure to sonic b o o m s in humans and concluded that there was no effect, even though their results indicate some increase in all groups at 8 kHz.

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Bobbin and Gondra [17] concluded that sonic b o o m does not contain low frequencies of sufficient intensity to damage the cochlea, even though their study does point to greater hair cell damage in experimental subjects than controls. In their study, they did not use simulated sonic booms, but rather, low frequency sound (28 Hz, 49 Hz, 76 Hz and 125 Hz) presented as pure tones. The frequency components of a sonic b o o m of 350 ms duration with a rise time of 8 ms range from 0.1 Hz to 1 000 Hz [18-20]. About 90% of the energy of a b o o m lies in the first couple of low frequency cycles of the Fourier-resolved N-wave [21], but the damaging effect of the sonic b o o m depends, among other things, on its rise time [2]. Also, it is possible that sensitivity of the mechanism of the inner ear to the high-frequency components of the sonic b o o m is the cause of most of the damage. Bobbin and Gondra [17] left out these important components. Our data [2-4 and the present paper] indicate that the inner ears have been damaged by sonic booms in four animal species (mouse, guinea pig, chinchilla and monkey). In other animal species, we found a blood clot in the basal turn of the cochlea. In the monkey subjects ofthis paper, we did not expect to find blood clots because a considerable amount of time elapsed between the exposure to the sonic b o o m and the time of the animals' death. A necessary conclusion from these experiments is that extensive exposure of humans to numerous or intense sonic b o o m s should be avoided, even before more audiometric and pathological data are obtained. Future research on humans should be concentrated on the changes in high-frequency hearing, which is usually not determined in a routine audiometric examination where only frequencies below 8 kHz are tested. Thus, the testing of the high-frequency hearing in persons exposed to simulated sonic booms or any other types of impulsive noise may reveal early, inconspicuous changes. In such a way persons sensitive to the impulse noise damage may be recognized at an early stage and any further damage to the inner ear may be prevented. Our experimental study actually has an analogy in the p a p e r by Fausti et al. [22] who found, in young military veterans previously exposed to impulse noise from weapons, an extensive threshold shift in frequencies between 8 and 20 kHz.

ACKNOWLEDGMENTS We Wish to thank Professor I. I. Glass for reading the manuscript and for his constructive comments. The financial support received from ttie Canadian Ministry of Transport (Transportation Development Centre) is acknowledged with thanks. We are also grateful to Mr Reinhard Gnoyke for the construction of the electrostatic high-frequency transmitters, to Mr R. Ewart and C. Wingelaar for the construction o f the electronic equipment and its maintenance, and to C. Holdenmeyer and the staff of the Animal Research Facility of the Department of Psychology for the care o f the m o n k e y s .

REFERENCES I. S. HALL and L. F. HENDERSON 1974 Search 5, 96-103. Sonic-boom--recent Australian, British, American and European experience. 2. S. REINIS 1976 Journal of lhe Acoustical Society of America 60, 133-138. Acute changes in animal inner ears due to simulated sonic booms. 3. S. REINIS 1976 Journal of Sound and Vibration 59, 611-614. Bleeding into inner ears of chinchillas caused by simulated sonic boom. 4. S.REINIS, J. W. FEATHERSTONE and D. S. WEISS 1980 Scandinaz.,ian Audiology Supplement 12, 163-369. The effects of sonic booms in hearing and inner ear structure. 5. V. JORDON, M. PINttEIRO, K. CttlBA and A. JIMENEZ 1973 Acta Otolaryngologica Supplement (Stockhohn) 312, 16-30. Cochlear pathology in monkeys exposed to impulse noise.

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6. H. MACHMERTH, D. THEISS and H. D. SCHNITZLER 1975 Acustica 34, 81-85. Konstruktion eines Luftultraschallgebers mitkonstantem Frequenzgang im Bereich von 15 kHz bis 130 kHz. 7. 1. I. GLASS, H. S. RIBNER and J. J. GOTTLIEB 1972 Canadian Aeronautics and Space Journal 18, 235-246. Canadian sonic boom facilities. 8. H. ENGSTROM, H. W. ADES and A. ANDERSSON 1966 Structural Pattern of the Organ Corti. AImqvisst and Wiksell, Stockholm, Sweden. 9. S. FUJITA and D. N. ELLIOTT 1965 Journal of the Acoustical Socie O, of America 37, 139-144. Thresholds of audition for three species of monkey. 10. B. E. PFINGST, J. LAYCOCK, F. FLAMMINO, L. LONSBURY-MARTIN and G. MARTIN 1979 Hearing Research 1, 43-47. Pure tone thresholds for the Rhesus monkey. 11. J. D. HARRIS 1943 Journal of Comparatire Psychology 35, 255-265. The auditory acuity of pre-adolescent monkeys. 12. W. A. SEMENOFF and F. A. YOUNG 1964 Journal ofComparatit, e Physiology and Psychology 57, 89-93. Comparison of the auditory acuity of man and monkey. 13. I. BEilAR, J. N. CRONIlOLM and M. LOEB 1965 Journal of Comparatit'e Physiology and Psychology 59, 426-428. Auditory sensitivity of the Rhesus monkey. 14. G.A. LtJz and D. M. LIPSCOMB 1973 Journal of the AcousticaI Society of America 54, 1750-1754. Susceptibility to damage from impulse noise: Chinchilla versus man or monkey. 15. R. P. HAMERNIK, D. ItENDERSON and R. J. SALVI 1980 Scandinavian Audiology Supplement 12, 128-146. Contribution of animal studies to our understanding of impulse noise induced hearing loss. 16. C. G. RICE and R. R. A. COLES 1968 International Audiology 7, 85-93. Auditory hazards from sonic booms? 17. R. P. BOBBIN and M. !. GONDRA 1975 Environmental Research 9, 48-54. Effects of intense low frequency sound (sonic boom) on the cochlea. 18. A. NIEDZWlECKI and H. S. RIBNER 1978 Journal of the Acoustical Society of America 64, 1617-1621. Subjective loudness of N wave sonic booms. 19. A. NIEDZWlECKI and H. S. RIBNER 1978 Journal of the Acoustical Society of America 64, 1622-1626. Subjective loudness of "minimized" sonic boom waveforms. 20. A. NIEDZWIECKI and H. S. RIBNER 1979 Journal of the Acoustical Society of America 65, 705-707. Subjective loudness and annoyance of filtered N-wave sonic booms. 21. N. N. WAIIBA, I. I. GLASS and R. C. TENNYSON 1980 Journal of Sozmd and Vibration 68, 259-279. Pressures inside a room subjected to simulated sonic booms. 22. S. A. FAUSTI, D. A. ERICKSON, R. tt. FREY and B. Z. RAPPAPORT 1981 Scandinat;ian Audiology 10, 21-29. The effects of impulsive noise upon human hearing sensitivity (8 to 20 kHz).