NOISE-INDUCED HEARING LOSS

Barbara A. Bohne, Ph.D.
Gary W. Harding, M.S.E.
Dept. of Otolaryngology, Washington University School of Medicine, St. Louis, MO

MAGNITUDE OF THE NOISE PROBLEM

At least 30 million working Americans (about 11% of the population) are subjected to excessive noise on a daily basis (NIDCD,1999). Other individuals who may be periodically exposed to excess noise include retirees, children and teens. About 10 million Americans have already sustained hearing impairments due to repeated exposure to hazardous levels of noise at work or at play. It doesn't matter whether the sound is pleasant or unpleasant, if a person's exposure is sufficiently loud or long hearing will be permanently damaged.

PARAMETERS OF NOISE WHICH AFFECT ITS DAMAGE POTENTIAL

The parameters of the noise to which an individual is exposed affect the pattern and magnitude of his/her inner-ear damage. For example, the frequency of the exposure determines the apex-to-base location of damage in the organ of Corti. The intensity in decibels (dB sound pressure level (SPL)) of the noise determines the rapidity with which the ear is damaged and the extent of the initial anatomical lesion. It also determines whether the associated hearing loss will be temporary (i.e., temporary threshold shift (TTS)) or permanent (i.e., permanent threshold shift (PTS)).

The duration of the exposure has a reciprocal relationship to intensity. The higher the intensity, the shorter the exposure can be and still cause permanent damage. Conversely, lower-intensity noise may be safe, even when the ear is exposed for long durations. For exposures which are equal in total energy, the scheduling of the exposure (i.e., continuous vs intermittent) affects the magnitude of damage that the ear sustains but does not affect the pattern of damage. Rest or quiet periods between successive exposures afford some protection for the ear, as long as the periods are not too brief.

DAMAGING EFFECTS OF NOISE ON INNER-EAR STRUCTURE

Shortly after a damaging exposure, the cells and tissues of the inner ear are in a dynamic state of injury, degeneration and/or repair. This has been termed the acute phase of noise damage. With intense exposures (>/= 140 dB SPL), a portion of the organ of Corti is displaced from its position on the basilar membrane and is often found floating within scala media (Lurie, 1942). Swollen hair cells are found at the edges of the lesion and signs of damage are apparent in the nonmyelinated nerve fibers of the organ of Corti both within and adjacent to the displaced portion (Bohne, 1976a).

With moderate-level exposures for long durations such as those found in noisy industries (i.e., </= 90 dB SPL), a few scattered sensory (i.e., hair) cells probably degenerate within the organ of Corti during each day of work. In general, the noise-induced loss of hair cells is very gradual. The amount of structural damage which is present in a given ear depends on its auditory history. The longer the exposure, the greater the number of missing sensory cells (Bredberg, 1968; Bohne and Clark, 1990).

Permanent noise damage initially consists of degeneration of hair cells. Although both types of hair cells may degenerate, outer hair cells (OHCs) are more sensitive to noise than inner hair cells (IHCs). With longer exposures or a more intense noise, there is further loss OHCs, IHCs, and supporting cells such as the outer and inner pillars. If the cell loss is confined to a narrow region of the organ of Corti, a 'focal' hair-cell lesion develops. Bohne and Clark define a focal lesion as a region in which 50% or more of the OHCs and/or IHCs are missing over a distance of at least 0.03 mm or three IHCs. Other scientists have termed focal hair-cell lesions 'cookie-bite' defects (e.g., Johnsson and Hawkins, 1976). Once IHC reaches moderate proportions, there is a beginning loss of myelinated nerve fibers within the osseous spiral lamina (Bohne et al., 1987). These myelinated fibers are the peripheral processes of the spiral ganglion cells. Hair cell and supporting cell losses within a focal lesion can gradually progress to involve 100% of the cells over a variable length of the organ of Corti. A lesion in which no recognizable cells of the organ of Corti remain on the basilar membrane is termed an 'OC wipeout' by Bohne and Clark. Eventually, the spiral ganglion cells which originally innervated the degenerated portion of the organ of Corti are progressively lost, including their central processes which form the auditory portion of the eighth nerve (Nadol and Xu, 1992).

There is evidence to suggest that once degeneration of the spiral ganglion cells has begun, there is a corresponding degeneration within the central nervous system including the cochlear nuclei, superior olive and inferior colliculus (Kim et al., 1997; Morest et al., 1998).

It has been shown that with interrupted exposures, the pattern of sensory-cell loss is the same as that with continuous noise while the magnitude of damage is generally less (Bohne et al., 1985; 1987). The amount of protection afforded by intermittency depends on the amount of rest between successive exposures. Too short a rest (quiet) period results in no protection. With longer quiet periods, some injured sensory cells may recover and the amount of damage will be proportionally less.

After a recovery period of a few days to one month, the histological appearance of the ear is considerably different from that seen acutely. The recovery period allows irreversibly damaged cells to complete the process of degeneration. Remaining supporting cells participate in the formation of scars on the endolymphatic surface of the organ of Corti (i.e., reticular lamina) and on the basilar membrane. This period can be termed the chronic phase of noise damage because hearing thresholds have stabilized and most organ of Corti degeneration resulting from the exposure has been completed. The exact appearance of a chronic noise-damaged ear depends on the millimeter extent (apex-to-base) of the initial damage and the rapidity with which the reticular lamina scars over. Some variability in the extent of damage in the chronic noise-exposed ear appears to have a genetic component (i.e., variation in susceptibility to noise).

DAMAGING EFFECTS OF NOISE ON HEARING ABILITY

Intense short-duration exposures such as explosions result in an immediate noticeable hearing loss. This injury is termed acoustic trauma. Shortly after the exposure, the individual has what has been termed a 'compound threshold shift' (CTS), which suggests that the hearing loss has both temporary and permanent components. Thresholds partially recover over 1-2 weeks post-exposure. This recovery represents the disappearance of the TTS. The individual so exposed is often left with a 60 dB PTS at one or more high frequencies. A classic study by Ward and Glorig (1961) documented the severe, permanent hearing loss resulting from a single exposure to an exploding firecracker.

Exposure to moderate-intensity noise for several minutes or hours initially results in a TTS only. If thresholds are measured after the individual has been away from the noise for 18-24 hours, his/her thresholds will have returned to pre-exposure levels. However, repeated exposure to moderate-intensity noise gradually results in a permanent deterioration of auditory thresholds. This type of injury is termed noise-induced hearing loss (NIHL). A classic study by Taylor et al. (1965) reported the progressive loss of hearing in a cross-sectional study of workers in the jute-weaving industry. The noise associated with jute weaving looms is broadband with SPLs ranging from 87-102 dB. Jute weavers with 1-2 years of employment had 15- and 10-dB median hearing losses at 4 and 6 kHz, respectively. With continued employment, hearing loss increased at these frequencies and gradually spread to involve other frequencies as well. With 40-52 years of employment, the median hearing loss was 50 dB at 3 and 4 kHz, 46 dB at 2 kHz, 39 dB at 6 kHz and 15 dB for frequencies below 1 kHz. Taylor's study was conducted before the mandatory use of hearing protectors in noisy industries so the measured hearing losses could be directly related to the workers' years of employment. Because most of the jute weavers were female and had very little exposure to noise other than that in the workplace, the magnitude and pattern of their hearing losses represent the audiometric effect of prolonged exposure to moderately intense industrial noise.

An interrupted exposure to noise (e.g., 6 hours a day for 36 days) initially produces the same magnitude of TTS as a continuous exposure. However, as the interrupted exposure paradigm is continued, thresholds begin to improve and may eventually return to within 10-15 dB of pre-exposure baseline (Clark et al., 1987; Sinex et al., 1987; Clark and Bohne, 1992). The phenomenon of recovery of thresholds during an interrupted exposure may indicate that the cells of the ear can become more resistant to the effects of noise based on their prior auditory history. This has been termed the "toughening" phenomenon (Canlon et al., 1988; 1992).

Despite extensive research on noise and its effects since World War II, the incidence of NIHL has not diminished (Gasaway, 1990). There are several reasons for this. First, although federal regulations exist to protect the hearing of workers in many industries (OSHA, 1983), these regulations do not cover all workers (Plakke, 1990) and are not uniformly enforced (Dobie, 1993). Other people, including babies and children, are routinely exposed to hazardous levels of noise at play or during their leisure activities (Clark, 1991; McClymont and Simpson, 1989). Second, local and national campaigns about the hazards of noise have not been very effective (Florentine, 1990). Finally, although there are several hypotheses about how noise damages hearing and the structure of the inner ear, the pathogenesis of NIHL is still unknown.

Current hypotheses regarding the pathogenesis of NIHL include: 1) Reduced blood flow during the exposure (Hawkins, 1971) leading to hypoxia (i.e., reduced oxygen) and the release of reactive oxygen species in the cochlea (Quirk et al., 1992); 2) Metabolic exhaustion of the stimulated sensory cells (Lim and Dunn, 1979); 3) Excessive release of neurotransmitter during the exposure leading to excitotoxic damage of afferent nerve fibers and terminals (Pujol, 1992); 4) Intermixing of cochlear fluids through the damaged reticular lamina (Bohne and Rabbitt, 1983). Although data supporting each hypothesis have been published, conflicting data also exist. This report summarizes some of the major results obtained in this laboratory over the past 25 years.

MATERIALS AND METHODS

SUBJECTS: One- to three-year-old chinchillas were continuously exposed to an octave band of noise (OBN) with a center frequency of either 0.5 or 4 kHz and a sound pressure level (SPL) of 57-95 dB for 2-432 days. The hearing ability of the animals was determined prior to, during and after their exposures to noise using behavioral techniques or auditory brainstem response thresholds. At various intervals post-exposure, the chinchillas were anesthetized, their cochleas were surgically exposed and preserved by perfusing fixative (buffered solution of 1% osmium tetroxide) through the perilymphatic spaces. This in-vivo fixation technique virtually eliminates the possibility of post-mortem artifacts in the sensory epithelium (Bohne, 1972).

HISTOLOGICAL TECHNIQUE: The cochleas with most of the cochlear bone intact were dehydrated and embedded in Durcupan, a plastic which is compatible with transmission electron microscopy (TEM). After the plastic polymerized, the bone was removed and the cochlear duct was divided into 16-24 segments which ranged in length from 0.5-1.5 mm. This dissection technique preserves the entire cochlear duct, including the basilar membrane, osseous spiral lamina, stria vascularis, Reissner's membrane and contents of scala media, and minimizes the chances of producing artifactual damage in the soft tissue (Bohne, 1972; Bohne and Harding, 1993). The dissected segments of the cochlear duct were first examined as flat preparations by phase contrast microscopy so that losses of inner (IHC) and outer (OHC) hair cells, inner (IP) and outer (OP) pillar cells could be counted and amount of myelinated nerve fiber (MNF) loss in the osseous spiral lamina could be estimated. For each cochlea, a graph or cytocochleogram was prepared showing the percentage loss of IHC, OHC and MNF, and regions of stria-vascularis (SV) degeneration as a function of percentage distance from the apex of the organ of Corti (OC). The structural damage was correlated with functional measures of hearing using the frequency-place map for the chinchilla cochlea (Eldredge et al., 1981). After collecting quantitative data, selected organ of Corti segments were semi-thick and thin-sectioned at a radial or tangential angle and examined by bright-field and TEM, respectively.

RESULTS

THE PATTERNS OF CELL LOSS ARE DIFFERENT AT THE BASE & APEX: A major finding in our studies is that the patterns of cell loss following excessive exposure to noise are quite distinct in the apical and basal halves of the cochlea (Bohne, 1976b) and have a different relation to functional measures of hearing (Clark and Bohne, 1978; Bohne and Clark, 1982; Nordmann et al., submitted). Exposure to a 4-kHz OBN at 86 dB SPL for two days produces acute hair-cell degeneration which consists of one to several focal losses of OHC and beginning loss of OP, IP and IHC in the 4-8 kHz region of the cochlea.

Fig. 1: High-frequency region after a 2-day exposure to a high-frequency noise

This phomicrograph depicts the organ of Corti in the basal turn shortly after termination of a 4-kHz OBN at 86 dB SPL for two days. In the center, there is a defect (arrow) in the reticular lamina involving focal loss of OHC (1, 2, 3), OP and IP and a few IHC. Bar = 10 um.


Fig. 2: Graph of cochlear damage after a 2-day exposure to a high-frequency noise



This cytocochleogram is from the ear shown in Fig. 1. At 70-83% distance (4-8-kHz), there is about 10% OHC loss and a narrow IHC lesion. There is a beginning focal lesion in the high-frequency region (base) of the cochlea.

With nine or more days of exposure to the 4-kHz OBN, the damage progresses to total loss of the organ of Corti (i.e., OC wipeout) in one or more regions of the basal turn.

Fig. 3: High-frequency region after a 36-day exposure to a high-frequency noise

This illustration shows the organ of Corti in the basal turn shortly after exposure to 4-kHz OBN at 86 dB SPL for 36 days. An OC wipeout is visible in the center (between arrows). The nerve fibers (MNF) adjacent to the wipeout have also degenerated. Undifferentiated epithelium (E) covers basilar membrane and seals open ends of tunnel. Bar = 50 um.

Fig. 4: Graph of cochlear damage after a 36-day exposure to the 4-kHz OBN


Cytocochleogram from the ear shown in Fig. 3. Between 84-93% distance (8-12-kHz), there is an OC wipeout (tall black bar) and a region of 100% loss of IHC and OHC. Each of these lesions has an associated loss of adjacent MNF (short black bars).

When at least six adjacent IHC are missing, secondary degeneration of MNF in the adjacent region of the osseous spiral lamina can be detected within a few days post-exposure (Bohne et al., 1987). MNF degeneration extends medially toward Rosenthal's canal adjacent to all OC wipeouts that are present for more than two weeks. Chronic lesions involving focal losses of IHCs and MNFs are always associated with a permanent elevation of auditory thresholds for one or more high-frequency tones (Normann et al., submitted).

Beginning damage in the low-frequency region of the organ of Corti consists of loss of OHCs scattered over a broad area in the 0.25-1-kHz region of the cochlea.

Fig. 5: Low-frequency region after a 2-day exposure to a low-frequency noise

This illustration shows the organ of Corti in the apical turn shortly after exposure to 0.5-kHz OBN at 95 dB SPL for two days. Scattered OHC are missing in rows 2 and 3 and are replaced by phalangeal scars (arrows). First row OHC, IHC and pillar cells are intact. Bar = 20 um.

Fig. 6: Graph of cochlear damage after a 2-day exposure to the 0.5-kHz OBN


Cytocochleogram from the ear shown in Fig. 5. OHC loss averages about 7% in the apical cochlea (0.25-1-kHz). At the same location, most IHC are present and all MNF are intact.

Lengthening the exposure to nine or more days increases OHC loss in the low-frequency region while most IHC, IP, OP and MNF remain intact. This broad OHC lesion in the apical half of the cochlea is not associated with a decrement in the thresholds for low-frequency tones until the OHC loss exceeds 30% (Clark and Bohne, 1978; Bohne and Clark, 1982). Exposure to the 0.5-kHz OBN for nine or more days also damages the basal half of the cochlea near the 4-kHz region (Fried et al., 1976). The basal-turn lesions which result from exposure to the 0.5-kHz OBN are indistinguishable from those caused by exposure to the 4-kHz OBN (Bohne, 1976). Once basal-turn damage appears following prolonged exposure to the 0.5-kHz OBN, the damage grows faster than that in the low-frequency region (Bohne and Clark, 1982).

Fig. 7: Low-frequency region after a 36-day exposure to a low-frequency noise

The organ of Corti in the apical turn shortly after exposure to 0.5-kHz OBN at 95 dB SPL for 36 days. Only a few OHC (arrows) remain, while the rest of the organ of Corti (e.g., IHC, OP) and MNFs are intact. Bar = 50 um.

Fig. 8: Graph of cochlear damage after a 36-day exposure to the 0.5-kHz OBN

Cytocochleogram from the ear shown in Fig. 7. OHC loss averages about 35% in the apical portion (0.15-1.5-kHz) of the cochlea while all IHC and MNF are intact. Between 75-85% distance (6-10-kHz), there are multiple focal losses of IHC and OHC and an area of stria vascularis degeneration (cross-hatched bar).

SPREADING OR PROGRESSIVE DEGENERATION OF THE ORGAN OF CORTI AFTER A DAMAGING NOISE EXPOSURE: Another major finding involves the progressive degeneration that the organ of Corti undergoes after termination of a damaging noise exposure. Noise damage begins as scattered losses of hair cells. With short-duration, moderate-level exposures, the damage does not appear to spread to adjacent cells. In the reticular lamina, degenerated hair cells are replaced by phalangeal scars (e.g., Fig. 5) which are formed by enlarged processes from outer pillar cells, Deiters' cells or inner phalangeal cells. When the hair cells initially degenerate, defects or holes are left in the reticular lamina for a period of time before the phalangeal scars form. These holes provide a route for endolymph to enter the fluid spaces of the organ of Corti (Bohne, 1976c; Bohne and Rabbitt, 1983). When most OHC degenerate in a focal region, the intermixing of endolymph and Cortilymph produces secondary loss of adjacent supporting cells and other sensory cells (e.g., Fig. 1). With the appearance of large defects in the reticular lamina, additional sensory and supporting cells and nerve fibers undergo progressive degeneration until an entire region of the organ of Corti has been lost (e.g., Fig. 3). The intermixing of endolymph and Cortilymph terminates when the boundary between scala media and the fluid spaces of the organ of Corti is re-established. Within OC wipeouts, the endolymph boundary consists of a single layer of squamous epithelium which replaces the organ of Corti on the basilar membrane, and inner sulcus, Claudius', Hensen's and Deiters' cells which seal the open ends of the tunnel and Nuel spaces (e.g., Fig. 3).

DISCUSSION

CHOICE OF ANIMAL: Chinchillas are used as our experimental model for the following reasons. First, the audibility curve of the chinchilla (Miller, 1970; Fay, 1988) is similar to that of humans (Sivian and White, 1933; Fay, 1988), both in the range of audible frequencies and in the frequencies (i.e., 1-4 kHz) to which the animals are maximally sensitive. Second, the chinchilla has a life span of 15-20 years. Thus, it can be used in experiments involving prolonged exposures (e.g., more than 1 year) to moderate-intensity noises, exposures which more closely resemble industrial noise. Finally, the chinchilla's middle and inner ears are surgically accessible so that one inner ear can be protected from noise by disarticulating the ossicular chain (Clark and Bohne, 1987), thereby providing an internal control for each animal (Bohne et al., 1986; Sun et al., 1994; Bohne et al., 1998).

CHOICE OF HISTOLOGICAL PREPARATION TECHNIQUE: A number of different histological techniques are available for examining the normal and damaged inner ear. These include: celloidin or paraffin-embedding of the decalcified temporal bone followed by serial sectioning (e.g., McGill and Schuknecht, 1976), "wet dissection" of the cochlea and examination of organ of Corti samples as flat preparations (e.g., Johnsson and Hawkins, 1976; Raphael and Altschuler, 1991), scanning electron microscopy (e.g., Hunter-Duvar, 1977) and the plastic-embedding technique described above. All histological techniques have positive and negative features. We use the plastic-embedding technique almost exclusively because it minimizes dissection artifacts in the delicate cochlear epithelia, it permits cell loss and damage to be evaluated throughout the entire organ of Corti and related to distance in the cochlea, and it allows TEM examination of cytological changes in specimens in which cell losses were quantified in the flat preparations.

PATTERNS OF HEARING LOSS AND UNDERLYING HISTOPATHOLOGY IN THE NOISE-DAMAGED COCHLEA: In chinchillas subjected to long exposures, cell loss in the low-frequency region of the cochlea is generally limited to OHC. In contrast, once damage begins in the high-frequency region, it grows more rapidly than that in the low-frequency region and often involves losses of OHC, IHC and afferent nerve fibers. The histopathological differences between cochlear damage in the low- and high-frequency regions may explain why the first functional manifestation of damage in the noise-exposed chinchilla is a permanent hearing loss for one or more high-frequency tones.

Noise-induced hearing loss in humans commonly begins in the high frequencies around 4 kHz, regardless of the frequency content of the noise. With continued exposure, the threshold at 4 kHz worsens and the hearing loss spreads to involve higher and lower frequencies (Taylor et al., 1965). Examination of noise-damaged human temporal bones has shown that lesions in the high-frequency region consist of near total loss of the organ of Corti and its afferent innervation (Bredberg, 1968; Johnsson and Hawkins, 1976) while damage in the low-frequency region is largely confined to the OHC (Bredberg, 1968). Our findings in noise-exposed chinchillas with respect to the patterns of cochlear damage and their relation to functional measures of hearing agree quite well with data from humans. On this basis, the noise-exposed chinchilla is an excellent model for investigating the mechanisms of degeneration and repair in noise-exposed humans.

CONCLUSIONS

The noise-exposed cochlea undergoes histopathological alterations which can be separated into primary and secondary events. Primary histopathological events consist of degeneration of hair cells, especially OHC. Secondary events follow primary events and consist of progressive degeneration of supporting cells, afferent nerve fibers and additional hair cells. Currently, the best way in which to minimize primary noise damage in your ears is to limit your cumulative exposure to loud noises. Many secondary noise effects develop after termination of a noise exposure. Thus, one goal of our research is to develop therapeutic measures which increase the rate of healing of the organ of Corti after primary noise damage. If successful, treatments which minimize secondary damage in the organ of Corti may reduce the severity of NIHL in individuals who are often exposed to excessive noise.

REFERENCES

* Bohne BA: Location of small cochlear lesions by phase contrast microscopy prior to thin sectioning. Laryngoscope 82:1-16, 1972.
* Bohne, BA: Mechanisms of noise damage in the inner ear. In: The Effects of Noise on Hearing. Eds.: D Henderson, RP Hamernik, DS Dosanjh, JH Mills. Raven Press, New York, pp. 41-68, 1976a.
* Bohne BA: Safe level for noise exposure. Ann Otol Rhinol Laryngol 85:711-724, 1976b. * Bohne BA: Mechanisms of noise damage in the inner ear, in Henderson D, Hamernik RP, Dosanjh DS, Mills JH (eds): Effects of Noise on Hearing. New York, Raven, 1976c, pp 41-68.
* Bohne BA, Bozzay DG, Harding, GW: Interaural correlations in normal and traumatized cochleas: Length and sensory cell loss. J Acoust Soc Am 80:1729-1736, 1986.
* Bohne BA, Clark WW: Growth of hearing loss and cochlear lesion with increasing duration of noise exposure, in Hamernik RP, Henderson D, Salvi R (eds): New Perspective on Noise- Induced Hearing Loss. New York, Raven, 1982, pp 283-302.
* Bohne, BA, Clark, WW: Studies of noise-induced hearing loss using an animal model. Hear Instrmts 41:13-16 and 58, 1990.
* Bohne BA, Harding, GW: Combined organ of Corti/ modiolus technique for preparing mammalian cochleas for quantitative microscopy. Hear Res 71:114-124, 1993.
* Bohne BA, Maghami EG, Bahadori RS, et al: The role of micro-noise trauma in the etiology of aging-related changes in the inner ear. Hear Res 124:132-145, 1998.
* Bohne BA, Rabbitt KD: Holes in the reticular lamina after noise exposure: implications for continued damage in the organ of Corti. Hear Res 11:41-53, 1983.
* Bohne BA, Yohman L, Gruner MM: Cochlear damage following interrupted exposure to high-frequency noise. Hear Res 29:251-264, 1987.
*Bohne, BA, Zahn, SJ, Bozzay, DG: Damage to the cochlea following interrupted exposure to low-frequency noise. Ann Otol Rhinol Laryngol, 94:122-128, 1985.
* Bredberg G: Cellular pattern and nerve supply of the human organ of Corti. Acta Otolaryngol Suppl 236, 1-135, 1968.
* Canlon, B, Borg, E, Flock, A: Protection against noise trauma by pre-exposure to a low-level acoustic stimulus. Hear Res, 34:197-200, 1988.
* Canlon, B, Borg, E, Lofstrand, P: Physiologic and morphologic aspects to low-level acoustic stimulation. In: Noise-Induced Hearing Loss, eds.: AL Dancer, D Henderson, RJ Salvi, RP Hamernik. Mosby Year Book, pp. 489-499, 1992.
* Clark WW: Noise exposure from leisure activities: A review. J Acoust Soc Am 90:175-181, 1991.
* Clark WW, Bohne BA: Animal model for the 4-kHz tonal dip. Ann Otol Rhinol Laryngol, Suppl 51, pp 1-16, 1978.
* Clark WW, Bohne BA: Attenuation and protection provided by ossicular removal. J Acoust Soc Am 81:1093-1099, 1987.
* Clark, WW, Bohne, BA, Boettcher, FA: Effect of periodic rest on hearing loss and cochlear damage following exposure to noise. J Acoust Soc Amer, 82:1253-1264, 1987.
* Clark, WW, Bohne, BA: Effects of periodic rest on cochlear damage and hearing loss. In: Noise-Induced Hearing Loss, eds.: A.L Dancer, D Henderson, RJ Salvi, RP Hamernik. Mosby Year Book, pp. 445-455, 1992.
* Dobie RA: Medical-Legal Evaluation of Hearing Loss. New York, NY, Van Nostrand Reinhold, 1993.
* Eldredge DH, Miller JD, Bohne BA: A frequency-position map for the chinchilla cochlea. J Acoust Soc Am 69:1091-1095, 1981.
* Fay RR: Hearing in Vertebrates: A Psychophysics Databook. Winnetka, IL, Hill-Fay Associates, 1988, pp 327-330 and 357-361.
* Florentine M: Education as a tool to prevent noise-induced hearing loss. Hear Instrms 41:33-34, 1990.
* Fried MP, Dudek SE, Bohne BA: Basal turn cochlear lesions following exposure to low-frequency noise. Trans Am Acad Ophth Otol 82:285-298, 1976.
* Gasaway DC: Noise in the military and its effect on hearing. Hear Instrms 41:21-22, 1990.
* Hawkins, JE, Jr: The role of vasoconstriction in noise-induced hearing loss. Ann Otol Rhinol Laryngol 80:903-913, 1971.
* Hunter-Duvar IM: Morphology of the normal and the acoustically damaged cochlea. Scan Elect Micros 2:421-428, 1977.
* Johnsson L-G, Hawkins JE Jr: Degeneration patterns in human ears exposed to noise. Ann Otol Rhinol Laryngol 85:725-739, 1976.
* Kim, J, Morest, DK, Bohne, BA: Degeneration of axons in the brain stem of the chinchilla after auditory overstimulation Hear Res, 103:169-191, 1997.
* Lim DJ, Dunn DE: Anatomical correlates of noise induced hearing loss. Otolaryngol Clinics N Am 12:493-513, 1979.
* Lurie, MH: The degeneration and absorption of the organ of Corti in animals. Ann Otol Rhinol Laryngol, 51:712-717, 1942.
* McClymont LG, Simpson DC: Noise levels and exposure patterns to do-it-yourself power tools. J Laryngol Otol 103:1140-1141, 1989.
* McGill TJI, Schuknecht HF: Human cochlear changes in noise-induced hearing loss. Laryngoscope 86:1293-1302, 1976.
* Miller JD: The audibility curve of the chinchilla. J Acoust Soc Am 48:513-523, 1970.
* Morest DK, Kim J, Potashner SJ, Bohne BA: Long-term degeneration in the cochlear nerve and cochlear nucleus of the adult chinchilla following acoustic overstimulation. Micro Res Tech 41:205-216, 1998.
* National Institute on Deafness and other Communication Disorders: Fact sheet - Noise- Induced Hearing Loss. NIH Pub. No. 97-4233, April, 1999.
* Nordmann AS, Bohne BA, Harding GW: Histopathological differences between temporary and permanent threshold shift. Hear Res (submitted 4/99).
* Plakke BL: Noise in agriculture and its effect on hearing. Hear Instrms 41:22-24, 1990.
* Pujol R: Sensitive developmental period and acoustic trauma: Facts and hypotheses, in Dancer AL, Henderson D, Salvi R, et al (eds): Noise-Induced Hearing Loss. St. Louis, MO, Mosby, 1992, pp 196-203.
* Quirk WS, Avinash, G, Nuttall, AL, et al: The influence of loud sound on red blood cell velocity and blood vessel diameter in the cochlea. Hear Res 63:102-107, 1992.
* Raphael Y, Altschuler RA: Reorganization of cytoskeletal and junctional proteins during cochlear hair cell degeneration. Cell Mot Cytoskel 18:215-227, 1991.
* Sinex, DG, Clark, WW, Bohne, BA: Effect of periodic rest on physiological measures of auditory sensitivity following exposure to noise. J Acoust Soc Amer, 2:1265-1273, 1987.
* Sivian LJ, White SD: On minimum audible fields. J Acoust Soc Am 4:288-321, 1933.
* Sun JC, Bohne, BA, Harding, GW: Is the older ear more susceptible to noise damage? Laryngoscope 104:1251-1258, 1994.
* Taylor W, Pearson J, Mair A, : Study of noise and hearing in jute weaving. J Acoust Soc Am 38:113-120, 1965.
* US Department of Labor - Occupational Safety and Health Administration: Occupational noise exposure: Hearing conservation Amendment; Final rule. Fed Register 48:9738-9784, 1983.
* Ward, WD, Glorig, A: A case of firecracker-induced hearing loss. Laryngoscope, 71:1590-1596, 1961.


Copyright © 1997, 1999 Barbara A. Bohne. and Gary W. Harding

Last updated 6/14/99.

Back to Index