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192 Disorders of the Auditory System
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20 to 69 who participated in a large survey
study were found to have noise notches
suggesting a high prevalence of NIHL
(Carroll et al., 2017). Unfortunately, NIHL
is not only isolated to the adult population. It has also been estimated that 17%
of teens present with evidence of NIHL
(Henderson, Testa, & Hartnick, 2011).
Hearing loss of this scale carries a cost of
billions in health-care dollars for coverage of diagnostic services and therapeutic management (Daniell, Fulton-Kehoe,
Smith-Weller, & Franklin, 1998). In an
effort to mitigate the damaging effects of
excessive occupational noise exposure,
OSHA instituted workplace restrictions
and regulations of noise exposure in the
Hearing Conservation Amendment of
1983. However, a generation of workers
who were employed prior to this amendment is at significant risk for NIHL. In
addition, recreational noise exposure
(music concerts and portable music players) has placed young adults at significant
risk for NIHL. In fact, in a study by Mostafapour, Lahargoue, and Gates (1998) some
degree of high-frequency hearing loss was
found in nearly one-third of a cohort of
college students.
Etiology and Pathology
There are a number of well-established
risk factors related to NIHL. These factors include smoking (Palmer, Griffin,
Syddall, & Coggon, 2004), male gender,
diabetes mellitus, cardiovascular disease
(Daniel, 2007), exposure to toxins such as
carbon monoxide or hydrogen cyanide
(Fechter, 2004), as well as various medications that are considered to be ototoxic
(Li & Steyger, 2009 ). Although these risk
factors are not the direct cause of NIHL,
they can increase an individual’s suscep-
tibility to the damaging effects of noise
and also increase the degree of hearing
loss resulting from noise exposure. In
addition, there is evidence to suggest that
genetics plays a role in increasing an individual’s susceptibility to NIHL. The gene
ahl
Cdh23
has been studied extensively and
found to promote noise injury. In addition, MNSOD, KCNQ4, KCNE1, PCDH15,
MYH14, and HSP70 have been identified
as NIHL-susceptibility genes (Wang &
Puel, 2018).
The mechanisms by which acoustic
energy damages the cochlea is via excessive stimulation of inner ear tissues, which
leads to the generation of toxic metabolic
by-products known as reactive oxygen
species and free radicals (Prasher, 1998).
These free radicals can overwhelm the
inner ear defenses, damaging hair cells
and cochlear nerve fibers (Huang et al.,
2000; Kopke et al., 1999; Kopke, Coleman,
Liu, Campbell, & Riffenburgh, 2002). The
mechanism whereby cells are destroyed
by reactive oxygen species involves damage to the mitochondria of the cell and
the initiation of a “programmed cell
death pathway,” referred to as apoptosis.
The damage caused by exposure to highnoise levels is dependent on a number
of factors including the intensity of the
noise, the frequency of the noise (higher
frequencies result in more damage), the
period of time the individual is exposed
to noise, the type and amount of hearing
protection worn by the individual, the
time spent away from noise, and genetic
factors. It has been postulated that when
exposed to high-intensity noise, capillaries in the inner ear constrict and a reduced
blood supply results (Thorne & Nuttall,
1987). This leads to metabolic exhaustion,
which is related to the free radical action
mentioned earlier (Møller, 2000). Bohne
and Harding (2000) also report that high-
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intensity sound can damage the reticular
lamina, which results in the intermingling
of cochlear fluids, creating metabolic dysfunction and hearing loss. The effects of
repeated noise exposure are additive. This
is likely a result of the fact that stereocilia
can either collapse or become fused over
time, resulting in nonoperational tip-links
(Harrison, 2001). If this occurs, the pores
cannot open and the neural firing of the
hair cell is not triggered due to the lack
of the necessary ionic exchange, which in
turn results in hearing loss. Additionally,
significant damage can arise from compromise of the supporting cells (Bohne &
Harding, 2000), which also leads to hearing deficits over time.
Site of Lesion
The primary cochlear structure affected
by noise exposure is the organ of Corti.
Specifically, the outer hair cells are damaged by oxidative stress from free radical formation, as well as from the direct
shearing trauma caused by the movement
of the high-intensity fluid waves through
the cochlea. As the intensity of noise
exposure increases, inner hair cells also
become involved, and at high intensities,
there may be excessive neurotransmitter
release that could damage nerve cells on
the receiving end of this action (Bohne &
Harding, 2000). Sound transmission into
the inner ear creates a cochlear fluid wave,
which causes a shearing force on the stereocilia of the hair cells. Interestingly, for
high-intensity sound, there is a half-octave
shift of the main damage site on the basilar membrane in reference to the specific
frequency of the stimulus (Møller, 2000).
This shift is a result of the maximum point
of displacement of the traveling wave on
the cochlea, moving in a more basal direc-
tion than for lower intensity stimuli. As
Møller (2000) summarized in his review,
in most cases of NIHL, the greatest loss
of hearing sensitivity occurs at approximately 4000 Hz. This commonly observed
finding usually results from exposure to
broad spectrum and/or impulse noise
stimuli. This finding is likely related to
the fact that the resonant frequency of the
ear canal, which typically occurs around
3000 Hz in the adult, augments the intensity of the stimulus at this frequency. If
one considers this frequency and adds the
half-octave shift, the resultant frequency
of peak damage is typically at or around
4000 Hz, where the greatest amount of
hearing loss occurs.
There are other extraneous factors
that have been found to contribute to
and/or compound hearing loss in cases
of noise exposure. For example, exposure
to ototoxic substances may increase the
injury caused by noise (Morata, Dunn,
Kretschmer, Lemasters, & Keith, 1993).
It should also be noted that there is significant evidence that insult at the level
of the cochlea will result in transsynaptic
retrocochlear degeneration, resulting in
CANS involvement (Fabiani, Mattioni,
Saponara, & Cordier, 1998). This should
be kept in mind when evaluating these
patients.
Noise-induced hearing loss is becoming an ever-increasing and widespread
hearing health problem. Noise exposure
has traditionally been linked to occupational exposure to high-noise levels, but
an increasing number of patients are being
seen today for NIHL related to recreational
activities. In particular, the use of personal
listening devices has become even more
problematic today than it ever has in the
past. A recent systematic review of the literature revealed that 58.2% of adolescents
and young adults exceed safety standards
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(100% of daily noise dose) with respect to
acceptable levels of noise exposure (Jiang,
Zhao, Guderley, & Manchaiah, 2016). As a
result, patient populations once believed
not to be at risk for noise exposure have
become target populations. Therefore,
prior to any audiologic evaluation, a carefully elicited patient history becomes critical in determining if the patient may be at
risk for NIHL.
Audiology
Audiologic evaluation of patients with
noise exposure is essential for the identification and monitoring of NIHL. It
is important to be sure the patient has
recovered completely from any noise
exposure that may have resulted in TTS
before testing for permanent hearing loss.
Usually, there is recovery from TTS within
approximately 16 hr after last exposure
to noise (i.e., assuming the TTS was not
more than 40 dB) (Gelfand, 2001). The
traditional evaluation should include —
but not be limited to — otoscopy, com-
prehensive audiometry, and immittance
testing. However, it is also recommended
that the use of ultra-high-frequency audiometry be considered as part of the battery (Korres, Balasouras, Tzagaroulakis,
Kandiloros, & Ferekidis, 2008) as it has
been demonstrated that these patients
will present with greater degrees of involvement in the high-frequency range
when compared to patients who are not
exposed to significant noise levels. In
addition, it also has been recommended
that patients with histories of noise exposure undergo otoacoustic emissions testing as this measure often demonstrates
increased sensitivity to NIHL over that
provided by the pure-tone audiogram
(Helleman, Jansen, & Dreschler, 2010).
Thus, the administration of otoacoustic
emission testing may allow earlier detection of ears at risk for NIHL; however, it
should be noted that the improved sensitivity of otoacoustic emissions over
the pure-tone audiogram has not been
convincingly demonstrated and further
research is needed in this area.
The typical configuration of hearing loss associated with noise exposure
is high frequency in nature with a “noise
notch” observed in most cases. This notch
typically occurs at or around 4000 Hz and
the width of the notch (indicating involvement of more frequencies) will spread
as the degree of hearing loss increases.
The notch in the audiogram is believed
to occur because the maximum damage
occurs at approximately 5 to 15 mm from
the oval window, which corresponds to
this particular frequency range (Jerger &
Jerger, 1981). Noise-induced hearing loss
also can affect neighboring frequencies;
therefore, the interoctaves frequencies of
3000 and 6000 Hz should be tested as the
maximum hearing loss may occur at one of
these frequencies and not only at 4000 Hz.
For example, if the stimulation frequency
is relatively narrow in spectrum and centered in the midfrequencies, the maximum loss will likely not be at 4000 Hz,
but at a lower frequency (recall the halfoctave shift) (Lim, Dunn, Ferraro, & Lempert, 1982). The hearing loss in patients
with NIHL is typically symmetric unless
there is a history of unilateral exposure
through such activities as shooting, in
which unpredictable patterns may occur
(Sataloff, Hawkshaw, & Sataloff, 2010).
At times, individuals with long-standing
conductive loss actually can preserve their
hearing as the conductive loss attenuates
the intensity of noise exposure. This some-
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times happens in only one ear, resulting in
asymmetric sensory levels.
Another factor to consider (as has
been alluded to earlier) in the evaluation
of those with a history of noise exposure
is the longer the exposure, the greater the
degree of hearing loss and the greater the
number of frequencies affected (see Gelfand, 2001). However, it is important to
recognize that there is considerable variability in humans in regard to the degree
of hearing loss related to noise exposure
(Gelfand, 2001). Susceptibility to NIHL
may be genetically determined, at least
in part, in that some auditory systems are
simply more or less resistant to the damaging effects of noise. Factors related to
this could be how well the acoustic reflex
and efferent auditory systems function,
the noise exposure history (type, intensity,
frequency, duration, etc.), the presence
or absence of any comorbid toxic exposures, and the patient’s age and general
well-being.
Medical Examination
Any patient with hearing loss should
undergo a thorough head and neck history and physical examination. The clinician must carefully document the type
and duration of occupational and recreational noise that the patient is (and/or
has been) exposed to, along with any protective measures the patient has utilized.
Inspection of the external ear and tympanic membrane is typically unremarkable; however, acoustic trauma can cause
spontaneous tympanic membrane perforation. Tuning fork evaluation should
be performed. If an asymmetry in puretone audiometry, tuning fork evaluation,
or word recognition testing is identified,
then further testing such as ABR or magnetic resonance imaging (MRI) should
be performed to rule out retrocochlear
pathology.
Audiologic Management
The management of patients with noise
exposure typically involves both counseling and amplification (depending on the
severity of the hearing loss). Knowledge
of hearing loss prevention and conservation practices is critical for any audiologist
who sees patients at risk for noise exposure (occupational and/or recreational).
Prevention and conservation of hearing
using appropriate tools such as ear plugs,
muffs, or a combination of these devices
is always recommended for patients with
significant histories of noise exposure.
Devices such as custom musicians’ ear
plugs may also be implemented depending on the specific needs of the patient.
In counseling and testing, it is important to consider the concept of damage risk
criteria and the recommendations offered
by OSHA (1983) and the National Institute of Occupational Safety and Health
(NIOSH, 1998) for noise exposure criteria.
Although a comprehensive discussion of
damage risk criteria is beyond the scope
of this section, a few comments will be
made regarding the NIOSH (1998) and
OSHA (1983) recommendations. NIOSH
has a 3 dB exchange rate for its maximum noise exposure recommendation of
85 dBA for 8 hr. This exchange rate means
that for every increase of 3 dB in the noise
level, the time of permissible exposure is
halved. For example, using this exchange
rate, the maximum exposure would be
4 hr at 88 dBA, 2 hr at 91 dBA, and only
28 sec at 115 dBA. The OSHA regulations
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have a 5 dB exchange rate starting at
90 dBA for 8 hr. Applying the exchange
rate specified in the OSHA regulations,
the maximum exposure would be 4 hr at
95 dBA, 2 hr at 100 dBA, and 15 min at 115
dBA (see Gelfand, 2001). All employees are
required to wear ear protection supplied
by the employer when steady-state noise
levels exceed these permissible exposure
levels. However, for some employees
(e.g., those who demonstrate significant
changes in their hearing thresholds dur-
ing their annual audiometric testing — see
discussion in the following text), the
threshold for action is 85 dBA for 8 hr of
exposure (or its equivalent time-weighted
average for higher intensities). The same
dB exchange rate begins at 85 dBA expo-
5
sure for 8 hr, so that the permissible noise
exposure at 90 dBA would be 4 hr and so
forth (OSHA, 1983).
Criteria are also suggested for the degree of permanent threshold shift. There
have been several approaches over the
years. These approaches account for aging
and permanent threshold shift. In evaluating individuals who have had noise exposure, NIOSH (1998) defined a significant
threshold shift as equal to or greater than
a 15 dB shift at 500, 1000, 2000, 3000, 4000,
or 6000 Hz in either ear. This criterion is
not employed as much as the OSHA criteria for pure-tone average (PTA), which
is an average threshold shift of 10 dB or
more at 2000, 3000, and 4000 Hz in either
ear. Counseling should include information on hearing protection, which should
be recommended for individuals working
in 85 dBA or greater of noise. Protection
commonly consists of ear plugs or muffs
or a combination of the two. Ear muffs
(especially those that are fluid-filled) generally provide a better noise-reduction
rating than ear plugs when worn on the
job, but this is not necessarily the case in
laboratory studies. It is important to know
that noise attenuation measured for both
plugs and muffs are greater in the lab
than in the field. For example, E-A-R foam
plugs have been reported to provide a
noise reduction rating of 14 dB in the field
and 30 dB in the lab (Berger, 1993). This
obviously reflects (among other things)
the difference between what might be
considered an ideal fitting based on the
research lab findings and a less-than-ideal
fitting in the workplace.
For patients who demonstrate hearing loss severe enough to warrant intervention beyond the fitting/provision of
personal hearing protection, traditional
amplification is typically appropriate.
However, in extreme cases of hearing loss
where hearing loss is too severe for traditional amplification, cochlear implantation may be considered.
Medical Management
At the current time, there is no known
treatment for NIHL other than better
hearing protection, reduction in exposure,
and better attention to good aural health.
Because the injury caused by noise is oxidative in nature, some researchers have
suggested the use of antioxidants, such as
N-acetylcysteine, magnesium, salicylate,
and vitamins B and E (Kopke et al., 2007;
Kramer et al., 2006; Le Prell, Yamashita,
Minami, Yamasoba, & Miller, 2007; Lynch
& Kil, 2005; Sendowski, 2006; Suckfuell,
Canis, Strieth, Scherer, & Haisch, 2007).
A variety of otoprotectants have been
shown to reduce cell death in laboratory
trials and are being investigated in preclinical trials (Le Prell, 2019). These preclinical trials are focused on the use of
medications prior to or immediately following noise exposure to prevent NIHL
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and the results are encouraging, but they
currently do not seem to have an effect on
reversing long-standing NIHL. Clearly,
this work holds promise and, in the nottoo-distant future, it is possible that medications may be available to prevent NIHL.
Case 5–2: Noise-Induced
Hearing Loss
History
A 46-year-old male was seen for evaluation
of work-related hearing loss. He reported
a 28-year history of occupational noise
exposure from working as a heavy equipment operator in underground mines and
noted a gradual decrease in hearing sensitivity with particular difficulty hearing
in the presence of background noise. He
denied the routine use of hearing protection as well as any history of recreational
noise exposure, family history of hearing
loss, or ototoxic medicine exposure, but
reported constant tinnitus bilaterally with
no other significant history.
tion levels at 500, 1000, and 2000 Hz in the
right ear and at 500 and 1000 Hz in the left
ear (a reflex was not obtained at the limits of the tympanometer at 2000 Hz in this
ear). These results were consistent with a
cochlear site of involvement for both ears.
Medical Examination
The patient presented with an essentially
normal otolaryngologic examination.
Impression
Bilateral noise-induced hearing loss.
Audiologic/Medical
Recommendations
and Management
It was recommended that the patient
obtain binaural amplification to assist with
hearing loss and difficulties. In addition,
the patient was counseled regarding the
importance of using hearing protection
both occupationally and recreationally.
Audiology
A comprehensive audiologic evaluation
indicated a mild sloping to severe sensorineural hearing loss bilaterally (Figure 5–2).
The configuration of the hearing loss was
consistent with noise exposure with a
“noise notch” observed at 4000 Hz for
both ears. Speech recognition thresholds
were in good agreement with pure-tone
averages bilaterally and word recognition
was excellent for the right ear and good
for the left ear. Tympanometry indicated
normal pressure, volume, and compliance
bilaterally, suggesting normal middle ear
status (see Figure 5–2). Acoustic reflex
thresholds were noted at reduced sensa-
Case 5–3: Noise-Induced
Hearing Loss
History
An 11-year-old female was seen following a recent failure on a school hearing screening test. The child’s mother
provided background information and
reported significant concerns regarding
her daughter’s hearing health, indicating
that her daughter had failed the school
hearing screening for 2 consecutive years.
However, the mother’s most significant
concern was the level at which her daughter listened to her MP3 player, stating that
both she and her husband could hear it
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Figure 5–2. Pure-tone thresholds, speech audiometry, and tympanometry results for a 46-year-
old male who had sustained a work-related noise-induced hearing loss (Case 5–2).
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easily from across the room. No other significant audiologic or otologic history was
reported.
Audiology
An otoscopic check was unremarkable
bilaterally. Tympanograms indicated normal pressure, volume, and compliance,
suggesting normal middle ear function for
both ears (Figure 5–3A). Results from the
audiologic examination revealed essentially normal peripheral hearing sensitivity in the low to mid frequencies with a
characteristic “noise notch” in the higher
frequencies with a maximum hearing loss
of 30 dB HL observed for 4000 Hz in both
ears. Word recognition scores were excellent bilaterally and speech recognition
thresholds were in good agreement with
the pure-tone averages. Distortion product otoacoustic emissions were performed
and demonstrated present responses
through 2000 Hz with absent responses
for the remaining frequencies bilaterally
(Figure 5–3B).
Medical Examination
The patient presented with a normal otolaryngologic examination.
Impression
Bilateral noise-induced hearing loss.
Audiologic/Medical
Recommendations
and Management
The patient and her parents were counseled regarding the importance of protecting her hearing by listening to her
music at reduced levels. It also was recommended that the patient undergo rou-
tine monitoring of her hearing sensitivity
given the pure-tone findings of a mild
hearing loss at 4000 Hz in both ears coupled with the fact that changes in cochlear
sensitivity were seen on the otoacoustic
emissions test at frequencies not reflected
on the audiogram. The otoacoustic emissions test results implicated a decrease
in cochlear function that eventually may
appear on the audiogram; therefore, these
findings were given serious consideration
when determining the management and
follow-up recommendations for this particular patient.
ototoxicity
Introduction
Ototoxicity has been defined as the effects
of certain therapeutic agents and other
chemical substances on inner ear structures, which result in cellular degeneration of the tissues of the inner ear, with
a particular propensity for damage to
the end-organs of the inner ear and the
neurons of the cochlear and vestibular branches of the eighth cranial nerve
(Hawkins, 1976). The ototoxic side effects
of medications have been known for more
than a century and were first noticed with
the use of the antimalarial medication,
quinine (Roosa, 1875). Since then, many
medicines have been implicated as being
ototoxic; however, the majority of the ototoxic medications fall into five categories
and include antibiotics, analgesics, antimalarials, antineoplastics, and diuretics.
This segment of this chapter is limited to
an overview of toxicity caused by drugs in
these categories; however, a more exhaustive background on medications/drugs
can be found elsewhere (Campbell, 2007;
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A
Figure 5–3. Pure-tone thresholds, speech audiometry, and tympanometry results (A) and distor-
tion product otoacoustic emissions (DPOAEs) (B) for an 11-year-old female with noise-induced
hearing loss (Case 5–3). continues
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B
Figure 5–3. continued Note: The heavier (upper) solid line on the DPgram indicates the cutoff
criteria for normal DPOAE values and the thinner (lower) solid line represents the average noise
floors (see text for further explanation). Key: X = left ear response, O = right ear response, triangle
= recorded noise floor response.
Offerdahl & Mishra, 2019). The term ototoxicity refers to a general toxic effect on
the inner ear, but certain medications can
be specifically cochleotoxic or vestibulotoxic. In addition, the effects of ototoxic
agents may either be temporarily ototoxic
(i.e., the damage is reversible) or largely
irreversible, depending on the specific
agent or medication. Some prescribed
medications represent the standard of
care for treating life-threatening conditions (i.e., serious infections or cancer);
thus, the benefit of using these medications outweighs the potential toxicity.
Other commonly used medications may
also carry the risk of ototoxicity, but that
risk is lowered when careful prescription
and monitoring practices are observed.
Although the majority of ototoxic medications are administered orally or intravenously, some are used in ototopic
preparations and the potential exists for
ototoxicity to develop if the drugs should
enter the middle ear through a perforation of the tympanic membrane and be
absorbed through the round window into
the inner ear.
The primary antibiotic class implicated in ototoxicity are the aminoglycosides, which include gentamicin (Moffat
& Ramsden, 1977), tobramycin (Walker,
Fazekas-May, & Bowen, 1990), amikacin
(Beaubien et al., 1990), neomycin (Murphy, 1970), kanamycin (Edson & Terrell,
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