Ann. occup. Hyg., Vol. 36, No. 2, pp. 199-209, 1992. Printed in Great Britain.
0003-4878/92 $5.00+0.00 Pergamon Press pic © 1992 British Occupational Hygiene Society.
REVIEW CONTROVERSIES IN NOISE-INDUCED HEARING LOSS (NIHL) JOSEPH B. TOUMA Huntington Ear Clinic Inc., Fairfield Professional Building, 1616 Thirteenth Avenue, Suite 100, Huntington, WV 25701-3840, U.S.A.
Abstract—When diagnosing and evaluating noise-induced hearing loss (NIHL) for purposes of compensation, the otolaryngologist often finds himself caught between industry and unions, between management and workers. In several controversial areas, conflicting evidence is available. The following extensive review of the literature was undertaken to provide an overview of research and clarify some of the issues in this ongoing debate. The author's aim is to rule out unreliable or biased information and direct the otolaryngologist toward credible studies that can help him make a sound decision.
INTRODUCTION
IN THE United States during the past few years, there has been an explosion in compensation claims for noise-induced hearing loss (NIHL), especially in heavily industrialized states or states experiencing economic hardship. Usually the claimant blames his hearing loss entirely on noise at work, while the employer shifts the blame to other causes. This review of the literature shows that hearing loss is probably influenced by various factors, including noise (which often exacerbates an existing condition): its aim is to help the otolaryngologist to identify factors which increase the vulnerability and susceptibility of the cochlea to industrial and other noise and so contribute to NIHL. In most cases, there is solid scientific evidence to help the otologist to judge the degree to which a given hearing loss is noise-induced: different regulations exist in different states in the U.S.A. and in various nations in the industrialized world.
ENVIRONMENTAL FACTORS
(1) Types of industrial noise (a) Impulse noise. There are two types of impulse noise (BOETTCHER et al., 1987): type A occurs most commonly in gunfire, and type B is produced by the concussion of two objects, usually metals, causing a ringing noise. Industrial type B impulses range from 100 to 140 dB peak SPL for 50-300 ms. Both types can cause direct damage to the organ of Corti. In their early studies, SATALOFF (1973) and SATALOFF et al. (1983) recognized that chipping and banging on metal causes a characteristic configuration of NIHL. More recently SATALOFF et al. (1983) concluded that exposure to intermittent loud noise causes severe high frequency sensorineural hearing loss but almost no hearing loss in the lower frequencies. 199
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(Received 8 January 1991 and in final form 2 July 1991)
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(b) Continuous noise. Continuous noise is more common than impulse noise, and the damage to hearing that it causes, which is related to length of exposure and loudness, is well known [see for example the FEDERAL REGISTER (1983)].
(3) The 4000 Hz notch The first frequency to be affected is usually 4000 Hz. The 4000 Hz notch is an important diagnostic sign of early NIHL. Fox (1953), SATALOFF (1957, 1980) and SATALOFF et al. (1980) found that if exposure to noise continues for a period of years, damage will spread both to higher and to lower frequencies, so that the notch will gradually flatten. In advanced cases of NIHL the audiogram begins to slope downwards at frequencies as low as 500 Hz (SATALOFF, 1980, 1957; SATALOFF et al., 1980). The degree of hearing loss is plotted against duration of noise exposure in Fig. 1, which is similar to the corresponding figure in the U.S. ARMY'S Manual of Prevention of Hearing Loss (1980).
Hz 250 500 1000 2000 3000 4000
10
6000
8000
Very ei rly
20 30
Early
40 50 60
\
N
M
MaximumX
Intermediate
Advanced***-
FIG. 1. Stages of noise-induced hearing loss.
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(2) Assessing the degree of noise exposure In most industrial situations it is nearly impossible to assess the degree of noise exposure because the conditions are complex and extremely difficult to evaluate. As KRYTER (1970) and MANNINEN and ARO (1979) suggest, damage due to noise exposure can be measured precisely only by monitoring hearing on annual audiograms: these would also show the type of N1HL, since constant loud noise causes a different type of NIHL from that of intermittent spikes. WARD (1980), SATALOFF (1973,1980) and SATALOFF et al. (1980,1983) demonstrated that impact noise (chipping and banging on metal) causes a unique, identifiable configuration of NIHL limited to frequencies over 1000 Hz. Retrospective quantitative assessment of the effect of noise on hearing is achieved only by comparing serial audiograms. Without serial audiograms it becomes virtually impossible to determine the rate of hearing deterioration, or the effect of various jobs on the hearing loss if the worker held more than one.
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(5) Hearing loss in hunters exposed to occupational noise Gunfire, which is characterized by rapid rise time and rarefaction, is a type A impulse noise (BOETTCHER et al., 1987). Type A exposures range from 120 to 175 dB peak SPL lasting from several hundred microseconds to as much as 4 ms. If this kind of impulse noise is generated in an enclosed space the reverberation adds to the initial wave, producing one similar to type B impulse noise. The direct mechanical action of either type can damage or even destroy the organ of Corti. CHUNG et al. (1981), who studied 29953 workers who had been exposed both to industrial noise and to gunfire, concluded that shooting may cause a greater hearing loss than occupational noise exposure alone, but that as long as compensable frequencies remained below 3000 kHz and exposure was less than 10 years with some protection, gunfire was not likely to affect compensation. PROSSER et al. (1988), in a study of 133 railway workers who also hunted, concluded that the additional loss caused by gunshot noise affected the high frequency range, especially in the ear on the opposite side from the shoulder supporting the firearm. Several factors influence the degree of additional hearing loss, i.e. the number of
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(4) Asymmetrical NIHL In 1988, RUDFN et al. (1988) found that in the general population of men born between 1913 and 1923 hearing acuity in the right ear was generally better than that in the left, which he suggested might be due to a biological difference between the two ears. Other studies have shown that, even in cases of general noise exposure, the right ear is less affected (by a few decibels) than the left. PFEIFFER and MAUE (1983) demonstrated a similar difference in a few cases. CHUNG et al. (1983a,b) studied 1461 audiometric records of claims for NIHL and found that 4.7% had a well defined pattern of hearing loss in which, at 2 kHz, there was an asymmetry of 20 dB or more; of these, 82% were worse on the left side. In a study of single sawyers a small percentage was found to have asymmetrical hearing. This asymmetry might be due not to a biological difference, but to asymmetrical exposure to noise, since in the words of a leading authority "if exposure to noise is asymmetrical, the resulting damage should also be asymmetrical" (D. WARD, personal communication). Asymmetrical exposure can result simply from the fact that a worker is right-handed or left-handed and adjusts his position accordingly. In fact noise exposure is almost always to some extent asymmetrical. DUFRESNE et al. (1988) documented lateralization of NIHL in truck drivers in the United States, who have a greater loss in the left ear because in left-hand drive vehicles the aerodynamic noise is on the left. NERBONNE and ACCARDI (1975) also found a greater hearing loss in the left ear in various groups they studied, which could be explained by environmental factors. In summary, asymmetrical NIHL is apparent in certain groups of workers. In these cases it is therefore important to take into account the type of noise exposure, the way the worker holds the power tool, the location of heavy equipment and other factors in the work environment. But, because asymmetrical NIHL is not universal, the otologist must carefully examine the patient's history to rule out diseases such as acoustic neuroma, otosclerosis and other otological disorders that might cause unilateral hearing loss. Certainly asymmetric left ear NIHL in right-handed people can be related to rifle shooting in the armed forces with most of the asymmetry being near 3000 Hz.
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shots; the calibre of the firearm; the type of ammunition; the use of ear protectors; and whether the shots were fired in an open or closed area. Up to 1000 Hz there was no difference between right and left ears, and the maximum difference occurred at 4 kHz. SEGAL et al. (1988) studied 841 individuals with acute acoustic trauma and concluded that hearing could continue to deteriorate for as long as 1 year after the last exposure to gunfire.
(7) Tinnitus in occupational hearing loss Tinnitus is strictly a subjective symptom, but it is known that it can result from high frequency sensorineural hearing loss from presbycusis or NIHL. ALBERTI (1987) found no apparent relationship between the incidence of tinnitus and the severity of hearing loss, and also concluded that the incidence of tinnitus is higher in workers exposed to impulse noise than in those exposed to steady-state noise. These findings were supported by AXELSSON and SANDH (1985), CAHANI et al. (1983) and MAN and NAGGAN (1981). Other factors such as systemic diseases (hypertension, hyperthyroidism, etc.), medications (Salicylate, Quinidine, etc.), exhaustion, stress, etc., can contribute to or aggravate tinnitus. In compensation cases involving NIHL it is impossible to validate tinnitus, though it is widely agreed that the condition is often associated with high frequency sensorineural hearing loss. METABOLIC AND CIRCULATORY FACTORS (1) Hyperlipoproteinaemia and NIHL SPENCER (1973, 1974, 1975) and some other workers believe that high cholesterol, high triglycerides and hyperlipoproteinaemia can cause sensorineural hearing loss that mimics NIHL. However, this has been disputed by LOWRY (1975), LOWRY and ISAACSON (1978), BOOTH (1977), AXELSSON and LINDGREN (1985), TAMI et al. (1985) and
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(6) Hearing loss resulting from steady industrial noise exposure combined with impulse noise The effect of the combination of continuous industrial noise and impulse noise depends on the intensity and type of each. In animal studies, HAMERNIK et al. (1974, 1987) examined their synergistic effect on chinchillas and observed that sensorineural loss and hair cell damage increased with impulse noise exposure. WALKER (1972), who studied 11 subjects exposed both to steady-state noise and to impulse noise, but who expressed his results in general rather than quantitative terms, found that the presence of noise pulses superimposed on a hazardous level of steady noise actually reduced the risk, but that when the impulse noise increased the risk also increased. Walker surmised that the stapedial reflex had a protective effect up to a certain level. COHEN et al. (1966) found that 90 and 100 dB steady-state and impact noises combined caused less threshold shift than when one or the other was presented alone, because the steadystate noise aroused and sustained the acoustic reflex with its attendant sound attenuation, but that when the steady-state noise was increased above 100 dB the protective effect disappeared. BOETTCHER et al.'s (1987) explanation for this phenomenon was that the combination of factors increases cochlear vulnerability. In summary, combined exposure to steady industrial and impact noise does not increase the risk of NIHL as long as neither component exceeds 100 dB. If either component (or both) is higher than this, the damage will be greater than that caused by either agent alone.
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(2) Hypertension, heart disease and NIHL It has been suggested that hypertension and heart disease are significant risk factors in the development of sensorineural hearing loss. BORG (1982a,b) found no difference between audiograms obtained from normotensive and hypertensive rats. He also pointed out that exposure to loud noise produced significantly greater hearing loss and loss of hair cells in hypertensive rats than in normotensive animals; and DRETTNER et al. (1975), who studied 1000 50-year-old men from the general population, found no significant differences between normotensive and hypertensive individuals with NIHL. In other studies, MALCHAIRE and MULLIER (1979), BORG and MOLLER (1978), MANNINEN and ARO (1979) and Wu et al. (1987) all concluded that industrial noise exposure did not cause hypertension. PAPARELLA et al. (1988) found no correlation between sensorineural hearing loss and cardiovascular disease. In a study of the Mabaans of southern Sudan, who live in a noise-free environment and have no coronary heart disease or hypertension, ROSEN et al. (1964) and ROSEN and OLIN (1965) found a much slower cochlear aging process than in people with hypertension who consume an atherogenic diet. He did not try to correlate these factors with industrial NIHL. SUSMANO and ROSENBUSH (1988) found that patients with hearing loss of unknown aetiology had eight times more ischaemic heart disease than those with normal hearing, but most researchers have found no correlation between hypertension, smoking, or obesity and hearing loss, unless there was also exposure to noise. In conclusion, coronary artery disease, arteriosclerotic vascular disease and hypertension do not cause appreciable hearing loss by themselves. They do, however, increase the susceptibility of the cochlea to noise, increasing the risk of NIHL. (3) Diabetes and NIHL In the past, there was much controversy concerning the relationship between diabetes mellitus and sensorineural hearing loss, and several studies (ROSEN et al., 1972;
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others. PILLSBURY (1986) conducted extensive research on 64 rats, half in a quiet environment, and half in a noisy one. Each group was divided into two subgroups, one fed a normal diet and the other an atherogenic diet. He concluded that in a quiet environment, hypertension and an atherogenic diet do not produce hearing loss at any frequency but that when chronic noise exposure was added the group on an atherogenic diet sustained significantly more hearing loss than that on a normal diet. These findings were supported by similar studies by MORIZONO et al. (1985), SIDMAN et al. (1988) and SIKORA et al. (1986). The former U.S. Surgeon General, Dr C. Everett Koop, reported in July 1988 that approximately 60 million Americans have high cholesterol, 54 million have high blood pressure and 36 million are overweight. Therefore, it is important that the working public be aware of the synergistic effect of an atherogenic diet and noise sensitivity. From these studies, it is clear that hyperlipoproteinaemia and atherogenic diet alone do not cause sensory neural hearing loss. However, they increase the susceptibility of the cochlea to loud noise, especially in the high frequencies, possibly because of metabolic exhaustion. This is very important in relation to compensation because all ears are equally exposed to industrial noise, whether or not they are especially susceptible.
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FRIEDMAN et al., 1975; KOSLOV, 1975; TAYLOR and IRWIN, 1978) have suggested that they were correlated. Recent studies, however, such as those by GIBBIN and DAVIS (1981), MILLER et al. (1983), AXELSSON and FAGERBERG (1968), PAPARELLA et al. (1988) and others, have shown no significant difference in hearing between diabetics and control groups. The effects of industrial noise on the hearing of diabetics were also studied by HODGSON et al. (1987), who found no evidence of higher hearing threshold shifts in diabetics than in controls, but despite the absence of positive proof, it makes sense that vascular changes caused by diabetes might increase the risk of damage to the cochlea from excessive noise.
OTHER FACTORS (I)
Age
The FEDERAL REGISTER (1983) contains detailed charts of expected hearing loss for various age-groups of males and females. These are based on population averages and provide statistical averages of predicted hearing loss at various frequencies for various age-groups and clearly show that most hearing loss is at frequencies above 3000 Hz; Fig. 2 shows the results for males, and demonstrates for example that for the average 70-year-old male the loss will be 35 dB at 3000 Hz.
Without the Effects of Occupational Noise (Age in Years) 10 20 30 40 50 60
10
70
••«.
20
N
=3
30
X
40
V \
50
60 70 FIG. 2. Hearing loss from aging.
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(4) Smoking and NIHL SIEGLAUB et al. (1974), BARONE et al. (1987), THOMAS et al. (1981) and others found that smokers are at a slightly higher risk for NIHL than non-smokers because of cardiovascular changes resulting from smoking.
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Recently, a controversy has arisen over the effect of noise on young vs old ears. et al. (1987) claim that older people are more susceptible to noise than are younger people, but other investigators dispute this, and the question remains open. PYYKKO
(2) Eye colour and susceptibility to NIHL THOMAS et al. (1981) and CARTER (1980) found that blue-eyed workers are slightly more susceptible to NIHL than brown-eyed workers. They offered no explanation for this phenomenon.
(4) Synergistic effect of noise and ototoxic drugs BOETTCHER et al. (1987) has published an excellent review of the literature concerning the synergistic interactions of noise and ototoxic drugs. Aminoglycosides. Animal studies by BROWN et al. (1978), DAYAL et al. (1971), and human studies by FINITZOis an increase in hearing loss and cochlear damage in people exposed to both noise and aminoglycoside antibiotics, the metabolic stress on the cochlea from the synergistic effect of noise and aminoglycosides damaging the hair cells. This is especially important for neonatal intensive care units, where the combination of incubator noise and ototoxic antibiotics increases the incidence and severity of hearing loss. GANNON et al. (1979) and RYAN and BONE (1982), HIEBER et al. (1979) and others concluded that there
Loop-inhibiting diuretics. Studies by VERNON et al. (1977), and by KISIEL and (1982), failed to demonstrate any synergistic effect from noise and loopinhibiting diuretics, because each affects a different area of the cochlea. If hearing loss in BOBBIN
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(3) Vestibular involvement in acoustic trauma YLIKOSKI et al. (1988) found evidence of subclinical vestibular pathology in patients with NIHL caused by intense impulse noise. On a stable platform these patients showed significantly more body sway than the control group. The more severe the NIHL, the more apparent the symptoms, which suggests a causal relationship between noise exposure and vestibular disturbance. YLIKOSKI (1988) also found that Meniere-type symptoms appear to be significantly higher among soldiers exposed to impulse noise than in the normal population, so corroborating the work of MCGABE and LAWRENCE (1958), who found extensive damage to the utricle, saccule and semi-circular canals consequent upon noise exposure in laboratory animals. KEMINK and GRAHAM (1985) and MAN et al. (1980) demonstrated vestibular involvement and a lowered threshold for vestibular irritation in cases of acoustic trauma. TULLIO (1929) [as reported by ROGGEVEEN and VAN DISHOECK (1956)], demonstrated abnormal vestibular stimulation secondary to noise exposure in pigeons, and KRYTER (1970) reported that 100 dB of sound can cause nystagmus in healthy individuals. COLLINS (1958) reported a large percentage of patients with acoustic trauma who exhibited vestibular symptoms in the form of directional preponderance of canal paresis.
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an individual receiving loop-inhibiting diuretics is aggravated by noise exposure this is usually temporary, and the individual soon recovers. Salicylates. Animal studies by MITCHELL et al. (1974) and EDDY et al. (1976), as well as human studies by MCFADDEN and PLATTSMTER (1983) and LINDGREN and AXELSSON (1987), suggest that the threshold shift caused by salicylate may be temporarily increased by noise exposure. However, MCCABE and DEY (1965) found no evidence that salicylates increase the risk of NIHL.
CONCLUSION
In cases of NIHL the otolaryngologist can consult a great number of scientific studies to help him assess the likelihood that any given hearing loss is noise induced. The information referred to in this article and the physician's own evaluation of the individual patient can enable him to form a fair, informed and defensible opinion in compensation cases.
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noise: effects on hearing. Ann. Otol. Rhinol. Laryng. 92, 623-628. SATALOFF, J., SATALOFF, R. T. and VASSALLO, L. A. (1980) Occupational deafness: legislation, compensation, conservation. In Hearing Loss (2nd Edn), pp. 383-412. J. B. Lippincott, Philadelphia. SEGAL, S., HARELL, M., SHAHAR, A. and ENGLENDER, M. (1988) Acute acoustic trauma: dynamics of hearing loss following cessation of exposure. Am. J. Olol. 9, 293-298. SIDMAN, J. D., PRAZMA,J., PULVER, S. H.and PILLSBURY, H. C , III (1988) Cochlea and heart as end-organs in small vessel disease. Ann. Olol. Rhinol. Laryng. 97, 9-13. SIEGLAUB, A. B., FRIEDMAN, G. D., ADOUR, K. and SELTZER, C. C. (1974) Hearing loss in adults: relation to age, sex, exposure to loud noise, and cigarette smoking. Archs Environ. Hlth 29, 107-109. SIKORA, M. A., MORIZONO, T., WARD, W. D., PAPARELLA, M. M. and LESLIE, K. (1986) Diet-induced
hyperlipidemia and auditory dysfunction. Ada Otolaryng. (Slockh.) 102, 372-381. SPENCER, J. T., JR (1973) Hyperlipoproteinemias in the etiology of inner ear disease. Laryngoscope 83, 639 678. SPENCER, J. T., JR (1974) Hyperlipoproteinemia and inner ear disease. West Virginia Med. J. 70, 215-221. SPENCER, J. T., JR (1975) Hyperlipoproteinemia and inner ear disease. Ololaryng. Clin. N. Am. 8,483-492. SPENCER, J. T., JR (1981) Hyperlipoproteinemia, hyperinsulinism, and Meniere's disease. Southern Med. J.
74, 1194-1197, 1200. SUSMANO, A. and ROSENBUSH, S. W. (1988) Hearing loss and ischemic heart disease. Am. J. Olol. 9,403-408. TAMI, T. A., FANKHAUSER, C. E. and MEHLUM, D. L. (1985) Effects of noise exposure and hypercholesterolemia on auditory function in the New Zealand white rabbit. Otolaryng. Head Neck Surg. 93, 235 239. TAYLOR, I. G. and IRWIN, J. (1978) Some audiological aspects of diabetes mellitus. / . Laryng. Otol. 92, 99 113. THOMAS, G. B., WILLIAMS, C. E. and HOGER, N. G. (1981) Some non-auditory correlates of the hearing threshold levels of an aviation noise-exposed population. Aviation, Space, Environ. Med. 52, 531-536. TULLIO, P. (1929) Reported by ROGGEVEEN, L. J. and VAN DISHOECK, H. A. E. (1956) Vestibular reactions as a result of acoustic stimulation. Practica Oto-Rhino-Laryng. 18, 205-213. U.S. ARMY (1980) Manuel of Prevention of Hearing Loss, pp. 1-12. VERNON, J., BRLMMETT, R. and BROWN, R. (1977) Noise trauma induced in the presence of loop-inhibiting diuretics. Trans. Am. Acad. Ophthal. Olol. 84, 407-413. WALKER, J. G. (1972) Temporary threshold shift caused by combined steady-state and impulse noises. J. Sound Vibr. 2A, 493-504. WARD, D. W. (1980) Noise-induced hearing damage. In Otolaryngology (2nd Edn) (Edited by PAPARELLA, M. M. et al.), pp. 1788-1803. W. B. Saunders, Philadelphia.
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NERBONNE, M. A. and ACCARDI, A. E. (1975) Noise-induced hearing loss in a truck driver population. J. Audit. Res. 15, 119-122. PAPARELLA, M. M., SCHACHERN, P. A. and GOYCOOLEA, M. V. (1988) Multiple otopathologic disorders. Ann. Olol. Rhinol. Laryng. 97, 14-18. PFEIFFER, B. H. and MAUE, J. H. (1983) Seitendifferente larmbelastung am arbeitsplatz? Arbeitsmed. Sozialmed. Pravemivmed. 18, 269-276. PILLSBURY, H. C. (1986) Hypertension, hyperlipoproteinemia, chronic noise exposure: is there synergism in cochlear pathology? Laryngoscope 96, 1112-1138. PROSSER, S., TARTARI, M. C. and ARSLAN, E. (1988) Hearing loss in sports hunters exposed to occupational noise. Br. J. Audiol. 22, 85-91. PYYKKO, I., PEKKARINEN, J. and STARCK,J. (1987) Sensory-neural hearing loss during combined noise and vibration exposure. An analysis of risk factors. Int. Archs occup. Environ. Hlth 59, 439-454. ROSEN, S. and OLIN, P. (1965) Hearing loss and coronary heart disease. Archs Otolaryng. 82, 236-243. ROSEN, S., PLESTER, D., EL-MOFTY, A. and ROSEN, H. V. (1964) Relation of hearing loss to cardiovascular disease. Trans. Am. Acad. Ophthal. Otolaryng. 68, 433-444. ROSEN, Z., YANKO, L. and COHEN, A. M. (1972) Diabetic labyrinthopathy and retinopathy. Isr. J. Med. Sci. 8, 781-782. RUDIN, R., ROSENHALL, U. and SVARDSUDD, K. (1988) Hearing capacity in samples of men from the general population. The study of men born in 1913 and 1923. Scand. Audiol. 17, 3-10. RYAN, A. F. and BONE, R. C. (1982) Non-simultaneous interaction of exposure to noise and kanamycin intoxication in the chinchilla. Am. J. Otolaryng. 3, 264—272. SATALOFF, J. (1957) Hearing testing and noise measurement. In Industrial Deafness, pp. 41-42. McGraw-Hill, New York. SATALOFF, J. (1973) Occupational hearing loss. J. occup. Med. 15, 360-363. SATALOFF, J. (1980) Noise induced hearing loss. In Hearing Conservation, pp. 70-84. Charles Thomas, Springfield, Illinois.
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Wu, T. N., CHOU, F. S. and CHANG, P. Y. (1987) A study of noise-induced hearing loss and blood pressure in steel mill workers. Int. Archs occup. Environ. Hlth 59, 529-536. YLIKOSKI, J. (1988) Delayed endolymphatic Hydrops syndrome after heavy exposure to impulse noise. Am.J. Otol. 9, 282-285. YLIKOSKI, J., JUNTUNEN, J., MATIKAINEN, E., YLIKOSKI, M. and OJALA, M. (1988) Subclinical vestibular
pathology in patients with noise-induced hearing loss from intense impulse noise. Ada Ololaryng. (Swckh.) 105, 558-563.
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0003-4878/92 $5.00+0.00 Pergamon Press pic © 1992 British Occupational Hygiene Society.
REVIEW CONTROVERSIES IN NOISE-INDUCED HEARING LOSS (NIHL) JOSEPH B. TOUMA Huntington Ear Clinic Inc., Fairfield Professional Building, 1616 Thirteenth Avenue, Suite 100, Huntington, WV 25701-3840, U.S.A.
Abstract—When diagnosing and evaluating noise-induced hearing loss (NIHL) for purposes of compensation, the otolaryngologist often finds himself caught between industry and unions, between management and workers. In several controversial areas, conflicting evidence is available. The following extensive review of the literature was undertaken to provide an overview of research and clarify some of the issues in this ongoing debate. The author's aim is to rule out unreliable or biased information and direct the otolaryngologist toward credible studies that can help him make a sound decision.
INTRODUCTION
IN THE United States during the past few years, there has been an explosion in compensation claims for noise-induced hearing loss (NIHL), especially in heavily industrialized states or states experiencing economic hardship. Usually the claimant blames his hearing loss entirely on noise at work, while the employer shifts the blame to other causes. This review of the literature shows that hearing loss is probably influenced by various factors, including noise (which often exacerbates an existing condition): its aim is to help the otolaryngologist to identify factors which increase the vulnerability and susceptibility of the cochlea to industrial and other noise and so contribute to NIHL. In most cases, there is solid scientific evidence to help the otologist to judge the degree to which a given hearing loss is noise-induced: different regulations exist in different states in the U.S.A. and in various nations in the industrialized world.
ENVIRONMENTAL FACTORS
(1) Types of industrial noise (a) Impulse noise. There are two types of impulse noise (BOETTCHER et al., 1987): type A occurs most commonly in gunfire, and type B is produced by the concussion of two objects, usually metals, causing a ringing noise. Industrial type B impulses range from 100 to 140 dB peak SPL for 50-300 ms. Both types can cause direct damage to the organ of Corti. In their early studies, SATALOFF (1973) and SATALOFF et al. (1983) recognized that chipping and banging on metal causes a characteristic configuration of NIHL. More recently SATALOFF et al. (1983) concluded that exposure to intermittent loud noise causes severe high frequency sensorineural hearing loss but almost no hearing loss in the lower frequencies. 199
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(Received 8 January 1991 and in final form 2 July 1991)
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(b) Continuous noise. Continuous noise is more common than impulse noise, and the damage to hearing that it causes, which is related to length of exposure and loudness, is well known [see for example the FEDERAL REGISTER (1983)].
(3) The 4000 Hz notch The first frequency to be affected is usually 4000 Hz. The 4000 Hz notch is an important diagnostic sign of early NIHL. Fox (1953), SATALOFF (1957, 1980) and SATALOFF et al. (1980) found that if exposure to noise continues for a period of years, damage will spread both to higher and to lower frequencies, so that the notch will gradually flatten. In advanced cases of NIHL the audiogram begins to slope downwards at frequencies as low as 500 Hz (SATALOFF, 1980, 1957; SATALOFF et al., 1980). The degree of hearing loss is plotted against duration of noise exposure in Fig. 1, which is similar to the corresponding figure in the U.S. ARMY'S Manual of Prevention of Hearing Loss (1980).
Hz 250 500 1000 2000 3000 4000
10
6000
8000
Very ei rly
20 30
Early
40 50 60
\
N
M
MaximumX
Intermediate
Advanced***-
FIG. 1. Stages of noise-induced hearing loss.
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(2) Assessing the degree of noise exposure In most industrial situations it is nearly impossible to assess the degree of noise exposure because the conditions are complex and extremely difficult to evaluate. As KRYTER (1970) and MANNINEN and ARO (1979) suggest, damage due to noise exposure can be measured precisely only by monitoring hearing on annual audiograms: these would also show the type of N1HL, since constant loud noise causes a different type of NIHL from that of intermittent spikes. WARD (1980), SATALOFF (1973,1980) and SATALOFF et al. (1980,1983) demonstrated that impact noise (chipping and banging on metal) causes a unique, identifiable configuration of NIHL limited to frequencies over 1000 Hz. Retrospective quantitative assessment of the effect of noise on hearing is achieved only by comparing serial audiograms. Without serial audiograms it becomes virtually impossible to determine the rate of hearing deterioration, or the effect of various jobs on the hearing loss if the worker held more than one.
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(5) Hearing loss in hunters exposed to occupational noise Gunfire, which is characterized by rapid rise time and rarefaction, is a type A impulse noise (BOETTCHER et al., 1987). Type A exposures range from 120 to 175 dB peak SPL lasting from several hundred microseconds to as much as 4 ms. If this kind of impulse noise is generated in an enclosed space the reverberation adds to the initial wave, producing one similar to type B impulse noise. The direct mechanical action of either type can damage or even destroy the organ of Corti. CHUNG et al. (1981), who studied 29953 workers who had been exposed both to industrial noise and to gunfire, concluded that shooting may cause a greater hearing loss than occupational noise exposure alone, but that as long as compensable frequencies remained below 3000 kHz and exposure was less than 10 years with some protection, gunfire was not likely to affect compensation. PROSSER et al. (1988), in a study of 133 railway workers who also hunted, concluded that the additional loss caused by gunshot noise affected the high frequency range, especially in the ear on the opposite side from the shoulder supporting the firearm. Several factors influence the degree of additional hearing loss, i.e. the number of
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(4) Asymmetrical NIHL In 1988, RUDFN et al. (1988) found that in the general population of men born between 1913 and 1923 hearing acuity in the right ear was generally better than that in the left, which he suggested might be due to a biological difference between the two ears. Other studies have shown that, even in cases of general noise exposure, the right ear is less affected (by a few decibels) than the left. PFEIFFER and MAUE (1983) demonstrated a similar difference in a few cases. CHUNG et al. (1983a,b) studied 1461 audiometric records of claims for NIHL and found that 4.7% had a well defined pattern of hearing loss in which, at 2 kHz, there was an asymmetry of 20 dB or more; of these, 82% were worse on the left side. In a study of single sawyers a small percentage was found to have asymmetrical hearing. This asymmetry might be due not to a biological difference, but to asymmetrical exposure to noise, since in the words of a leading authority "if exposure to noise is asymmetrical, the resulting damage should also be asymmetrical" (D. WARD, personal communication). Asymmetrical exposure can result simply from the fact that a worker is right-handed or left-handed and adjusts his position accordingly. In fact noise exposure is almost always to some extent asymmetrical. DUFRESNE et al. (1988) documented lateralization of NIHL in truck drivers in the United States, who have a greater loss in the left ear because in left-hand drive vehicles the aerodynamic noise is on the left. NERBONNE and ACCARDI (1975) also found a greater hearing loss in the left ear in various groups they studied, which could be explained by environmental factors. In summary, asymmetrical NIHL is apparent in certain groups of workers. In these cases it is therefore important to take into account the type of noise exposure, the way the worker holds the power tool, the location of heavy equipment and other factors in the work environment. But, because asymmetrical NIHL is not universal, the otologist must carefully examine the patient's history to rule out diseases such as acoustic neuroma, otosclerosis and other otological disorders that might cause unilateral hearing loss. Certainly asymmetric left ear NIHL in right-handed people can be related to rifle shooting in the armed forces with most of the asymmetry being near 3000 Hz.
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shots; the calibre of the firearm; the type of ammunition; the use of ear protectors; and whether the shots were fired in an open or closed area. Up to 1000 Hz there was no difference between right and left ears, and the maximum difference occurred at 4 kHz. SEGAL et al. (1988) studied 841 individuals with acute acoustic trauma and concluded that hearing could continue to deteriorate for as long as 1 year after the last exposure to gunfire.
(7) Tinnitus in occupational hearing loss Tinnitus is strictly a subjective symptom, but it is known that it can result from high frequency sensorineural hearing loss from presbycusis or NIHL. ALBERTI (1987) found no apparent relationship between the incidence of tinnitus and the severity of hearing loss, and also concluded that the incidence of tinnitus is higher in workers exposed to impulse noise than in those exposed to steady-state noise. These findings were supported by AXELSSON and SANDH (1985), CAHANI et al. (1983) and MAN and NAGGAN (1981). Other factors such as systemic diseases (hypertension, hyperthyroidism, etc.), medications (Salicylate, Quinidine, etc.), exhaustion, stress, etc., can contribute to or aggravate tinnitus. In compensation cases involving NIHL it is impossible to validate tinnitus, though it is widely agreed that the condition is often associated with high frequency sensorineural hearing loss. METABOLIC AND CIRCULATORY FACTORS (1) Hyperlipoproteinaemia and NIHL SPENCER (1973, 1974, 1975) and some other workers believe that high cholesterol, high triglycerides and hyperlipoproteinaemia can cause sensorineural hearing loss that mimics NIHL. However, this has been disputed by LOWRY (1975), LOWRY and ISAACSON (1978), BOOTH (1977), AXELSSON and LINDGREN (1985), TAMI et al. (1985) and
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(6) Hearing loss resulting from steady industrial noise exposure combined with impulse noise The effect of the combination of continuous industrial noise and impulse noise depends on the intensity and type of each. In animal studies, HAMERNIK et al. (1974, 1987) examined their synergistic effect on chinchillas and observed that sensorineural loss and hair cell damage increased with impulse noise exposure. WALKER (1972), who studied 11 subjects exposed both to steady-state noise and to impulse noise, but who expressed his results in general rather than quantitative terms, found that the presence of noise pulses superimposed on a hazardous level of steady noise actually reduced the risk, but that when the impulse noise increased the risk also increased. Walker surmised that the stapedial reflex had a protective effect up to a certain level. COHEN et al. (1966) found that 90 and 100 dB steady-state and impact noises combined caused less threshold shift than when one or the other was presented alone, because the steadystate noise aroused and sustained the acoustic reflex with its attendant sound attenuation, but that when the steady-state noise was increased above 100 dB the protective effect disappeared. BOETTCHER et al.'s (1987) explanation for this phenomenon was that the combination of factors increases cochlear vulnerability. In summary, combined exposure to steady industrial and impact noise does not increase the risk of NIHL as long as neither component exceeds 100 dB. If either component (or both) is higher than this, the damage will be greater than that caused by either agent alone.
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(2) Hypertension, heart disease and NIHL It has been suggested that hypertension and heart disease are significant risk factors in the development of sensorineural hearing loss. BORG (1982a,b) found no difference between audiograms obtained from normotensive and hypertensive rats. He also pointed out that exposure to loud noise produced significantly greater hearing loss and loss of hair cells in hypertensive rats than in normotensive animals; and DRETTNER et al. (1975), who studied 1000 50-year-old men from the general population, found no significant differences between normotensive and hypertensive individuals with NIHL. In other studies, MALCHAIRE and MULLIER (1979), BORG and MOLLER (1978), MANNINEN and ARO (1979) and Wu et al. (1987) all concluded that industrial noise exposure did not cause hypertension. PAPARELLA et al. (1988) found no correlation between sensorineural hearing loss and cardiovascular disease. In a study of the Mabaans of southern Sudan, who live in a noise-free environment and have no coronary heart disease or hypertension, ROSEN et al. (1964) and ROSEN and OLIN (1965) found a much slower cochlear aging process than in people with hypertension who consume an atherogenic diet. He did not try to correlate these factors with industrial NIHL. SUSMANO and ROSENBUSH (1988) found that patients with hearing loss of unknown aetiology had eight times more ischaemic heart disease than those with normal hearing, but most researchers have found no correlation between hypertension, smoking, or obesity and hearing loss, unless there was also exposure to noise. In conclusion, coronary artery disease, arteriosclerotic vascular disease and hypertension do not cause appreciable hearing loss by themselves. They do, however, increase the susceptibility of the cochlea to noise, increasing the risk of NIHL. (3) Diabetes and NIHL In the past, there was much controversy concerning the relationship between diabetes mellitus and sensorineural hearing loss, and several studies (ROSEN et al., 1972;
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others. PILLSBURY (1986) conducted extensive research on 64 rats, half in a quiet environment, and half in a noisy one. Each group was divided into two subgroups, one fed a normal diet and the other an atherogenic diet. He concluded that in a quiet environment, hypertension and an atherogenic diet do not produce hearing loss at any frequency but that when chronic noise exposure was added the group on an atherogenic diet sustained significantly more hearing loss than that on a normal diet. These findings were supported by similar studies by MORIZONO et al. (1985), SIDMAN et al. (1988) and SIKORA et al. (1986). The former U.S. Surgeon General, Dr C. Everett Koop, reported in July 1988 that approximately 60 million Americans have high cholesterol, 54 million have high blood pressure and 36 million are overweight. Therefore, it is important that the working public be aware of the synergistic effect of an atherogenic diet and noise sensitivity. From these studies, it is clear that hyperlipoproteinaemia and atherogenic diet alone do not cause sensory neural hearing loss. However, they increase the susceptibility of the cochlea to loud noise, especially in the high frequencies, possibly because of metabolic exhaustion. This is very important in relation to compensation because all ears are equally exposed to industrial noise, whether or not they are especially susceptible.
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FRIEDMAN et al., 1975; KOSLOV, 1975; TAYLOR and IRWIN, 1978) have suggested that they were correlated. Recent studies, however, such as those by GIBBIN and DAVIS (1981), MILLER et al. (1983), AXELSSON and FAGERBERG (1968), PAPARELLA et al. (1988) and others, have shown no significant difference in hearing between diabetics and control groups. The effects of industrial noise on the hearing of diabetics were also studied by HODGSON et al. (1987), who found no evidence of higher hearing threshold shifts in diabetics than in controls, but despite the absence of positive proof, it makes sense that vascular changes caused by diabetes might increase the risk of damage to the cochlea from excessive noise.
OTHER FACTORS (I)
Age
The FEDERAL REGISTER (1983) contains detailed charts of expected hearing loss for various age-groups of males and females. These are based on population averages and provide statistical averages of predicted hearing loss at various frequencies for various age-groups and clearly show that most hearing loss is at frequencies above 3000 Hz; Fig. 2 shows the results for males, and demonstrates for example that for the average 70-year-old male the loss will be 35 dB at 3000 Hz.
Without the Effects of Occupational Noise (Age in Years) 10 20 30 40 50 60
10
70
••«.
20
N
=3
30
X
40
V \
50
60 70 FIG. 2. Hearing loss from aging.
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(4) Smoking and NIHL SIEGLAUB et al. (1974), BARONE et al. (1987), THOMAS et al. (1981) and others found that smokers are at a slightly higher risk for NIHL than non-smokers because of cardiovascular changes resulting from smoking.
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Recently, a controversy has arisen over the effect of noise on young vs old ears. et al. (1987) claim that older people are more susceptible to noise than are younger people, but other investigators dispute this, and the question remains open. PYYKKO
(2) Eye colour and susceptibility to NIHL THOMAS et al. (1981) and CARTER (1980) found that blue-eyed workers are slightly more susceptible to NIHL than brown-eyed workers. They offered no explanation for this phenomenon.
(4) Synergistic effect of noise and ototoxic drugs BOETTCHER et al. (1987) has published an excellent review of the literature concerning the synergistic interactions of noise and ototoxic drugs. Aminoglycosides. Animal studies by BROWN et al. (1978), DAYAL et al. (1971), and human studies by FINITZOis an increase in hearing loss and cochlear damage in people exposed to both noise and aminoglycoside antibiotics, the metabolic stress on the cochlea from the synergistic effect of noise and aminoglycosides damaging the hair cells. This is especially important for neonatal intensive care units, where the combination of incubator noise and ototoxic antibiotics increases the incidence and severity of hearing loss. GANNON et al. (1979) and RYAN and BONE (1982), HIEBER et al. (1979) and others concluded that there
Loop-inhibiting diuretics. Studies by VERNON et al. (1977), and by KISIEL and (1982), failed to demonstrate any synergistic effect from noise and loopinhibiting diuretics, because each affects a different area of the cochlea. If hearing loss in BOBBIN
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(3) Vestibular involvement in acoustic trauma YLIKOSKI et al. (1988) found evidence of subclinical vestibular pathology in patients with NIHL caused by intense impulse noise. On a stable platform these patients showed significantly more body sway than the control group. The more severe the NIHL, the more apparent the symptoms, which suggests a causal relationship between noise exposure and vestibular disturbance. YLIKOSKI (1988) also found that Meniere-type symptoms appear to be significantly higher among soldiers exposed to impulse noise than in the normal population, so corroborating the work of MCGABE and LAWRENCE (1958), who found extensive damage to the utricle, saccule and semi-circular canals consequent upon noise exposure in laboratory animals. KEMINK and GRAHAM (1985) and MAN et al. (1980) demonstrated vestibular involvement and a lowered threshold for vestibular irritation in cases of acoustic trauma. TULLIO (1929) [as reported by ROGGEVEEN and VAN DISHOECK (1956)], demonstrated abnormal vestibular stimulation secondary to noise exposure in pigeons, and KRYTER (1970) reported that 100 dB of sound can cause nystagmus in healthy individuals. COLLINS (1958) reported a large percentage of patients with acoustic trauma who exhibited vestibular symptoms in the form of directional preponderance of canal paresis.
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an individual receiving loop-inhibiting diuretics is aggravated by noise exposure this is usually temporary, and the individual soon recovers. Salicylates. Animal studies by MITCHELL et al. (1974) and EDDY et al. (1976), as well as human studies by MCFADDEN and PLATTSMTER (1983) and LINDGREN and AXELSSON (1987), suggest that the threshold shift caused by salicylate may be temporarily increased by noise exposure. However, MCCABE and DEY (1965) found no evidence that salicylates increase the risk of NIHL.
CONCLUSION
In cases of NIHL the otolaryngologist can consult a great number of scientific studies to help him assess the likelihood that any given hearing loss is noise induced. The information referred to in this article and the physician's own evaluation of the individual patient can enable him to form a fair, informed and defensible opinion in compensation cases.
REFERENCES ALBERTI, P. W. (1987) Tinnitus in occupational hearing loss: nosological aspects. J. Otolaryng. 16, 34-35. AXELSSON, A. and FAGERBERG, S. E. (1968) Auditory function in diabetics. Ada Olo-Laryngologica 66, 49-64. AXELSSON, A. and LINDGREN, F. (1985) Is there a relationship between hypercholesterolaemia and noiseinduced hearing loss? Ada Otolaryng. (Stockh.) 100, 379-386. AXELSSON, A. and SANDH, A. (1985) Tinnitus in noise-induced hearing loss. Br. J. Audiol. 19, 271-276. BARONE,J. A., PETERS, J. M.,GARABRANT, D. H., BERNSTEIN, L. and KREBSBACH, R. (1987) Smoking as a risk
factor in noise-induced hearing loss. J. occup. Med. 29, 741-745. BOETTCHER, F. A., HENDERSON, D., GRATTON, M. A., DANIELSON, R. W. and BYRNE, C. D. (1987) Synergistic
interactions of noise and other ototraumatic agents. Ear Hearing 8, 192-212. BOOTH, J. B. (1977) Hyperlipidaemia and deafness: a preliminary survey. Proc. R. Soc. Med. 70, 642-646. BORG, E. (1982a) Noise-induced hearing loss in rats with renal hypertension. Hearing Res. 8, 93-99. BORG, E. (1982b) Noise-induced hearing loss in normotensive and spontaneously hypertensive rats. Hearing Res.S, 117-130. BORG, E. and MOLLER, A. R. (1978) Noise and blood pressure: effect of lifelong exposure in the rat. Ada Physiol. Scand. 103, 340-342. BROWN, J. J., BRUMMETT, R. E., MEIKLE, M. B. and VERNON, J. (1978) Combined Effects of noise and
neomycin: cochlear changes in the guinea pig. Ada Otolaryng. 86, 394-400. CAHANI, M., PAUL, G. and SHAHAR, A. (1983) Tinnitus pitch in acoustic trauma. Audiology 22, 357-362. CARTER, N . L. (1980) Eye colour and susceptibility to noise-induced permanent threshold shift. Audiology 19, 86-93. CHUNG, D. Y., GANNON, R. P.,WILLSON,G. N.and MASON, K. (1981) Shooting, sensorineural hearing loss, and workers' compensation. J. occup. Med. 23, 481-484. CHUNG, D. Y., MASON, K., WILLSON, G. N . and GANNON, R. (1983a) Asymmetrical noise exposure and
hearing loss among shingle sawyers. J. occup. Med. 25, 541-543. CHUNG, D. Y., WILLSON, G. N. and GANNON, R. P. (1983b) Lateral differences in susceptibility to noise damage. Audiology 22, 199-205.
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Cisplatinum. LAURELL and BORG (1986) postulated that a combination of noise exposure and cisplatinum chemotherapy increases the risk of permanent hearing loss because of increased vulnerability of the cochlea.
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COHEN, A., KYLIN, B. and LABENZ, P. (1966) Temporary threshold shifts in hearing from exposure to combined impact/steady-state noise conditions. J. Acoust. Soc. Am. 40, 1371-1380. COLLINS, E. G. (1958) Aural trauma caused by gunfire. J. Laryng. Otol. 62, 388-390. DAYAL, V. S., KOKSHANIAN, A. and MITCHELL, D. P. (1971) Combined effects of noise and kanamycin. Ann. Otol. Rhinol. Laryng. 80, 897-902. DRETTNER, B., HEDSTRAND, H., KLOCKHOFF, I. and SVEDBERG, A. (1975) Cardiovascular risk factors and
hearing loss. A study of 1000 fifty-year-old men. Ada Otolaryng. 79, 366-371. DUFRESNE, R. M., ALLEYNE, B. C. and REESAL, M. R. (1988) Asymmetric hearing loss in truck drivers. Ear Hearing 9, 41-42. EDDY, L. B., MORGAN, R. J. and CARNEY, H. C. (1976) Hearing loss due to combined effects of noise and sodium salicylate. ISA Trans. 15, 103-108. FEDERAL REGISTER (1983) Vol. 48, No. 46, 8 March. Rules and Regulations. FINITZO-HIEBER, T., MCCRACKEN, G. H., JR, ROESER, R. J., ALLEN, D. A., CHRANE, D. F. and MORROW, J.
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