Discussion Paper on Hearing Loss

Prepared for the Veterans Review and Appeal Board - June 2010. Updated December 2011.

3. Overview of Hearing Loss

a. Types of Hearing Loss

Hearing loss in any individual at any given time is a combination of the following factors:

  • a. Congenital (what were they born with)
  • b. Acquired (what they developed as a result of pathological exposures or processes during their lifetime)

The entities of nosiocusis (hearing loss from pathologic processes), sociocusis (from everyday noise exposure) and presbycusis (from age related change) form the subgroups of acquired hearing loss.

Conceptually three types of hearing loss exist:

  1. Sensorineural
  2. Conductive
  3. Mixed (a combination of sensorineural and conductive hearing loss)

A sensorineural hearing loss exists with injury to the cochlea or the cochlear nerve. This is the type of hearing loss that is found in routine, unprotected daily exposure to loud noise potentially injurious to hearing in the occupational work force or from recreational exposure.

A conductive hearing loss occurs when there is some interference of sound transmission or vibration due to pathology involving the external and/or middle ear. +This type of loss might be found in an individual for example with a large tympanic membrane (TM) perforation where mechanical vibrations along the ossicular chain are dampened.

A mixed hearing loss occurs when both a sensorineural and conductive hearing loss are present at the same time. For example, an individual with a large TM perforation who received topical antibiotic ear drops for the treatment of a middle ear infection that caused inadvertent toxicity to the inner ear in addition (i.e. topical ototoxicity).

Conductive Hearing Loss Sensorineural Hearing Loss
1. External otitis (acute and chronic) 1. Occupational or Noise Induced Hearing Loss (NIHL)
2. Wax 2. Presbycusis
3. Exostoses/osteomas 3. Menière's Disease
4. Acute Otitis Media 4. Ototoxicity (Systemic and Topical)
5. Otitis Media with Effusion 5. Cochlear Otosclerosis
6. TM perforations 6. Trauma
7. Chronic Suppurative Otitis Media (CSOM)
   a. Safe or mucosal CSOM
   b. Cholesteatoma
7. Acoustic neuromas (vestibular schwannomas)
8. Otosclerosis 8. Sudden Sensorineural Loss

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b. Common Causes for a Sensorineural Hearing Loss

i. Noise induced Hearing Loss

According to the 1990 Noise and Hearing Loss Consensus Conference, “Noise Induced Hearing Loss (NIHL) results from damage to the ear from sounds of sufficient intensity and duration that a temporary or permanent sensorineural hearing loss is produced. The hearing loss may range from mild to profound, may result in tinnitus (unwanted head noise) and is cumulative over a lifetime.” Occupational NIHL and presbycusis (degenerative hearing from aging change) represent the two most common causes of sensorineural hearing loss in society today.

Two types of noise exposure are associated with NIHL: transient and continuous.

Impact (i.e. the collision of two solid objects as might occur in a forge plant) or impulse (i.e. the sudden noise of an explosion) noise are examples of transient noise where there is a rapid rise in sound pressure and very quick decline over 0.2 seconds. Constant (continuous) or steady state noise by comparison remains relatively constant and lasts longer although fluctuations in sound intensity may occur. Although short lived, most impact/impulse noise typically has peak intensity levels much higher than found in steady state noise exposure. All things being equal, most noise in industry is a combination of continuous and superimposed impact noise.

When susceptible, unprotected ears are exposed to loud noise potentially injurious to hearing , the inner ear seems to react in one of three ways: by adapting to the noise (i.e. the inner ear seems to “toughen” in some individuals), by developing a transient threshold shift (TTS) or a permanent threshold shift (PTS).

TTS refers to a transient sensorineural hearing loss lasting hours to a few days. Hearing thresholds are depressed until the metabolic activity in the cochlea recovers. For this reason, workers ideally should be out of noise for at least 24 if not 48 hrs prior to audiometric testing to avoid the effects of TTS on hearing.

PTS refers to a permanent loss of sensorineural hearing which is the direct result of irreparable injury to the organ of Corti. Noise induced deafness generally affects hearing between 3000-6000 Hz with maximal injury centering around 4000 Hz initially, an important point to remember.

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a. The 4000 Hz Audiometric Dip

The 4000 Hz “notch” or “dip” in sensorineural hearing has been a classic finding in NIHL over the years. Some noise sources, however, such as gunfire, may maximally affect hearing at 6000 Hz. Noise exposure from chipping machines and jackhammers characteristically damage the higher frequencies severely before affecting the lower frequencies.

Why the 4000 Hz frequency appears more affected than other frequencies continues to generate some controversy. There is good pathologic evidence, however, that demonstrates maximal cochlear hair cell loss in the tonal areas where the 4000 Hz hair cells normally reside in both animals and humans.

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b. Individual Susceptibility to Noise

Individuals vary in their susceptibility to noise and the damage it may cause to the cochlea.

To date, susceptibility has not been shown to be dependent on gender (males vs. females), skin colour, any known diseases, pre-exposure hearing loss and smoking.

Of interest, one near universal finding is that on average, hearing threshold levels (HTL's) in the right ear are better than the left ear by about 1 dB. This, however, is of no practical importance clinically.

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c. Asymmetry of Sensorineural Hearing Loss from Noise

In general terms NIHL usually demonstrates a 4000 Hz dip. It should be also symmetric bilaterally.

Whether one ear is more resilient to noise in the same individual (the so-called “tough vs. tender” ear argument), while of academic curiosity, is not based on any known pathologic basis to date. Nevertheless some individuals exposed to noise not infrequently demonstrate some asymmetry in their hearing loss. This, however, is usually related to the fact that one ear receives a greater exposure to the noise source than the other. For example, truck drivers in North America not infrequently have a greater degree of hearing loss in their left ear (when the window is rolled down the left ear would be exposed to more sound from the engine). Those who fire guns often demonstrate a greater degree of hearing loss in the ear closest to the barrel (the left ear in a right-handed shooter) because that ear would be closest to the explosion and the other ear would be protected by a “head shadow.”

Please remember that when an asymmetric sensorineural hearing loss exists, steps often need to be taken to exclude pathologic causes (i.e. tumours, other inner ear disorders etc.).

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d. Basic Facts Concerning Noise Induced Hearing Loss

The following statements tend to reflect what is agreed upon by the majority of scientists and physicians who deal with NIHL.

  1. Noise exposure can produce a permanent hearing loss that may affect speech communication.
  2. Noise induced hearing loss (NIHL) may produce a temporary threshold shift (TTS), permanent threshold shift (PTS) or a combination of both.
  3. A PTS is caused by destruction of certain inner ear structures that cannot be replaced or repaired.
  4. The amount of hearing loss produced from a given noise varies from person to person.
  5. NIHL typically affects higher frequency hearing than those frequencies essential for communication (i.e. 500, 1000 and 2000 Hz) initially.
  6. Four major factors determine the effects of exposure to noise overall:
  7. Exposure to noise:

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ii. Presbycusis

Progressive age related sensorineural hearing loss is often called presbycusis. In susceptible individuals, the early effects of presbycusis are occasionally seen around age 40 years. Around age 55-60 years, an individual's hearing starts to worsen at a faster rate. For this reason a correction factor for presbycusis is applied in occupational hearing loss claims depending on the jurisdiction (in the province of Ontario, for example, a correction factor of 0.5dB/year of age > 60 years).

The pathologic basis for presbycusis appears to be one of gradual devascularization of the cochlea and loss of functioning hair cells. Secondary to the hair cell loss, one can often see progressive neuronal dropout along the cochlear nerve. The majority of changes histopathologically are noted in the basal turn of the cochlea where the high frequency hair cells and their corresponding cochlear nerve neurons are found. Nevertheless, the changes seen in presbycusis are typically non-specific and can also be seen in a vast number of pathologies including the effects of noise upon the inner ear.

Clinically, hearing loss from presbycusis appears to be an accelerating process unlike hearing loss in NIHL. In this regard, the effects of aging in the absence of other factors cause a loss of hearing at all frequencies whose rate of growth becomes more rapid as age increases (especially after 60 years): an important point to remember in this context.

Unfortunately, there is no specific treatment available that will prevent age related hearing loss at present. To a large degree hearing loss with age is genetically primed; in other words, the hearing your parents had as they aged is often passed on to you – usually, but not always.

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a. Controversies between presbycusis and NIHL

In the adjudication process of an occupational NIHL claim, it is often difficult to separate the total amount of hearing loss from noise and age-related change.

For example, not everyone as they age will experience age-related presbycutic change (changes from presbycusis are variable with some individuals experiencing greater degrees of age-related change than others).

Moreover, exposure to high level noise early on may produce hearing loss more rapidly than aging, such that the aging process has a negligible effect (i.e. the more that has been lost early on, the less there is to lose later on) and so on and so forth.

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b. Dobie's and Corso's Theorems

The effects of noise exposure and aging on hearing when not combined are reasonably well understood. When the two processes are combined, the resultant pathology and their effects upon hearing are not as well understood.

Although it seems logical to “subtract” the age-related effects from the total hearing loss in order to quantify the amount of hearing loss due to noise, this is really quite simplistic when one considers that aging effects and noise exposure can at times be practically indistinguishable from one another.

Because compensation claims have required some consideration of presbycusis and its role in the total hearing loss of an individual, various correction factors have been applied.

Dobie's theorem states that the total hearing loss from noise and age are essentially additive (this is the theory put into practice when a standard correction factor after age 60 years is applied, in the Province of Ontario for example).

Corso's theorem on the other hand states that any correction for age should be based on a variable ratio (as individuals age, the assumption is that the effects of presbycusis variably accelerate by decade). This certainly generates a more complicated mathematical model but probably more closely approaches what is happening physiologically.

Nevertheless, quantification of hearing loss attributable to age when occupational NIHL is present is really quite a complex phenomenon.

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iii. Meniere's Disease

This is an inner ear disorder characterized by episodes of vertigo (an illusion of movement) lasting minutes to hours, fluctuant hearing loss and tinnitus (unwanted head noise). Frequently there is a sense of pressure or fullness in the ear during attacks.

Usually one ear is involved initially although, over time, the other ear becomes involved in nearly 50% of cases. The hearing loss is typically a low-frequency sensorineural loss that fluctuates initially, often reverting close to normal between attacks in the early stages. Over time the severity of the hearing loss progresses. Occasionally both a low-frequency and a high-frequency loss occur, but not usually the type of high-frequency hearing loss seen following noise exposure.

Pathologically there is distension of the inner ear membranes by excess endolymph. It is not known if this results from excess production or inadequate drainage/re-absorption of endolymph. When the distended membranes rupture, the resulting admixture of inner (endolymph) and outer (perilymph) fluids causes electrolyte disturbances (i.e. the so-called Na+ - K+ intoxication theory) leading to dizziness. After its collapse the membrane heals and the cycle recommences. However, the natural history in Meniere's remains enigmatic with unpredictable periods of exacerbation and remission.

Treatment is medical in most cases involving a low salt diet and diuretics and vestibular sedatives. Currently there is research into the application of intermittent pressure/pulses to the inner ear via the eardrum (i.e. the Meniett device). When vertigo is incapacitating, the balance function of the inner ear may be destroyed by transtympanic instillation of gentamicin with varying hearing preservation. As a last resort, the whole inner ear can be destroyed surgically by a procedure called a labyrinthectomy.

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iv. Cochlear Otosclerosis

Otosclerosis usually results in a conductive hearing loss from stapes footplate fixation when new bone grows in this area. Nevertheless the otosclerotic foci can involve any part of the hard bone (otic capsule) surrounding the inner ear. When the foci primarily affect the cochlea, the patient may present with a chronic progressive sensorineural hearing loss in one or both ears. If the footplate as well as the cochlea is involved then a mixed (conductive and sensorineural) loss might occur.

The diagnosis of cochlear otosclerosis is usually made when a familial history of otosclerosis exists and other rare causes for a chronic progressive loss can be excluded. The presence of a pink-flamingo hue to the middle ear on otoscopy (so-called Schwartze's sign), absent stapedial reflexes on audiometry and bone density changes involving the surrounding bone of the inner ear best appreciated on high-resolution CT scanning, also helps in the diagnosis. As otosclerosis is a lifelong condition, the sensorineural hearing loss from cochlear otosclerosis is often superimposed on hearing loss from advancing age (i.e. presbycusis). The sensorineural hearing loss from otosclerosis progresses at an average rate of 5.5 dB/decade, higher than that seen in presbycusis.

Although no medical treatment can ever reverse the sensorineural hearing loss, treatment with oral sodium fluoride may minimize and possibly stabilize an affected individual's hearing.

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v. Trauma

Physical injury to the ear is usually the result of blunt trauma in the circumstances of a significant head injury. Most patients suffering deafness by this mechanism will have had at least transient unconsciousness and have been admitted to hospital.

When physical trauma is severe enough to cause a temporal bone fracture (the temporal bone is the larger part of the skull bone that houses all the structures of the ear), two types of fractures occur: longitudinal and transverse. In general terms longitudinal fractures are much more common and tend to result in a fracture line through the roof of the middle ear and ear canal. Bleeding from the ear is not unusual at the time. The hearing loss noted is usually conductive and arises from a discontinuity of the ossicular chain although any combination of conductive and sensorineural hearing loss can occur. The pathognomatic sign of a longitudinal temporal bone fracture is the so-called “step deformity” in the deep ear canal. Exploration of the middle ear surgically with correction of the ossicular chain discontinuity or insertion of a prosthesis is called an ossiculoplasty.

Transverse fractures of the temporal bone occur when the fracture lines run directly through the hard bone of the otic capsule. A fracture through this bone (which is reportedly the hardest bone in the body) implies the force of the injury was severe and often incompatible with survival. If the individual survives, there is usually complete loss of hearing and vestibular function on the involved side. Facial paralysis from injury to the facial nerve (a nerve that runs in close approximation to the inner ear) typically occurs. On examination, blood is usually seen in the middle ear behind an intact ear drum (a hemotympanum).

Trauma, however, can also be penetrating (i.e. a Q-tip through the ear drum), thermal (i.e. a welder's spark down the ear canal), electrical (accidental electrocution or lightening strikes), explosive and implosive (i.e. professional bell and scuba divers who try to “pop” their ears too vigorously) etc. The resultant hearing loss, depending on the mechanism, can be conductive, sensorineural or a combination thereof.

When a column of air is forced down the ear canal in an explosive fashion (i.e. a slap to the ear, a bomb blast etc.) the TM often ruptures in its central portion and the hearing loss is usually conductive until the drum repairs itself. Persistence of a conductive hearing loss after the TM has healed would suggest continued problems with the ossicular chain.

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vi. Ototoxicity

Ototoxicity is defined as the tendency of certain substances to cause functional impairment and cellular damage to the tissues of the inner ear, especially to the cochlea and the vestibular apparatus. Toxic substances can be delivered systemically either via the blood stream or topically through perforations/ventilation tubes in the ear drum.

Aminoglycoside antibiotics are powerful weapons in the treatment of certain bacterial infections. Unfortunately these antibiotics can cause varying degrees of cochlear, vestibular and renal toxicity. Careful and regular monitoring of auditory function (especially in the ultra high frequencies > 8000 Hz) and serum antibiotic levels may help the physician prevent ototoxic effects from occurring. The prolonged use of topical aminoglycoside antibiotics to treat middle ear pathology in the presence of a TM perforation is not without some risk which should always be kept in mind.

Anti-malarial drugs such as quinine and chloroquin unfortunately have ototoxicity as side effects if taken in excess. Reversibility however is relatively common once the medications have been discontinued. Platinum-based chemotherapeutic drugs (i.e. cisplatin) for the treatment of malignancy (cancer of the breast, lung etc.) have been especially well documented to cause cochleotoxicity. Of interest, the first course of cisplatin often demonstrates which patients are vulnerable to cochlear damage and what may happen in future if continued treatment courses are required.

Heavy metal, asphyxiant and solvent exposure at certain levels have all been implicated to cause chemical induced hearing loss. Solvents, especially toluene have been identified to cause hearing loss alone and in individuals with combined simultaneous exposure to noise. All frequencies of hearing can be affected. In one longitudinal study over 20 years, a remarkably large proportion of workers in the chemical sector showed pronounced hearing loss (23%) compared to groups from non-chemical environments (5-8%). The effect was found despite lower noise levels in the chemical department (80-90 dBA) compared to other divisions in the factory (95-100dBA).

According to an analysis by Morata et al, the adjusted relative risk for hearing loss in a group of workers for noise alone was 4.1, for noise and toluene was 10.9, and for a solvent mixture alone was 5.0. Solvents, heavy metals and asphyxiants can also affect central auditory pathways additionally.

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vii. Acoustic Neuroma (AN) or Vestibular Schwannoma

This is a pathologic misnomer since this tumour is strictly a schwannoma of the vestibular nerve. It arises in the internal auditory canal for the most part where the nerves run between the inner ear and the brainstem. Pressure on the nerve or devascularization of the acoustic nerve or inner ear causes hearing loss, which usually is a high frequency loss with reduced speech discrimination. The loss is typically progressive but occasionally may be sudden (40% of patients with a known AN will have a sudden loss of hearing during the observation period). AN's are overwhelmingly unilateral, but when in association with a rare genetic disorder, neurofibromatosis type 2, they may be bilateral.

Although benign, this tumour has serious health implications for the patient and is sought by otolaryngologists when there is an undiagnosed asymmetry in hearing. The Auditory Brainstem Response (ABR) is used as a screening test while a gadolinium enhanced Magnetic Resonance Imaging (MRI) study is considered the gold standard investigation.

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viii. Sudden Sensorineural Hearing Loss

This diagnosis is given to an individual who experiences a sudden hearing loss in one ear. The extent of the loss varies from a partial loss at one frequency right up to a profound loss at all frequencies with a profound discrimination loss. Patients can sometimes identify the moment of occurrence, or wake with it, or appreciate it only when they use the phone.

These sudden losses are considered by the profession to be most likely viral or inflammatory in origin. Many recover spontaneously, generally within a six month time frame. Severe losses and those associated with vertigo have a worse prognosis. Patients if seen early enough (i.e. within a 2-3 weeks) are usually treated with a tapering schedule of prednisone (a potent steroid). Anti-virals are often prescribed. Recently there has been a move to provide the patient with intratympanic injections of a concentrated steroid such as dexamethasone which has the theoretical advantage of providing the inner ear with a higher concentration of the steroid without the side effects associated with an oral steroid.

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4. Audiology

The formal recording of an individual's hearing forms the basis of the audiogram. For the purposes of compensation, the best audiograms will most likely be performed by an audiologist who typically has a master's degree or doctorate in audiology.

The following audiometric tests form the foundation for most assessments of hearing. These include what is called conventional audiometry and impedance (immitance) testing with tympanometry.

a. Conventional Audiometry

i. Pure Tone Audiogram (PTA)

An individual's threshold hearing to pure tones at different frequencies (250-8000 Hz) is performed.

Air conduction (AC) thresholds are delivered via headphones and the individual is asked to respond to the sound of the lowest intensity (in dB) they hear at the frequency being tested. When a conductive hearing loss is suspected the ear canal and inner ear mechanisms for transmission of sound energy to the inner ear are bypassed by placing a bone vibrator over the mastoid which directly stimulates the inner ear. Bone conduction (BC) thresholds are obtained in this fashion. In complex situations (mixed hearing losses), it may be necessary to “mask” the ear not being tested (to prevent crossover of sound to the other ear).

In a pure sensorineural hearing loss, AC thresholds should be the same as BC thresholds. In a pure conductive hearing loss, BC thresholds will be better than AC thresholds. In a mixed hearing loss, elements of both sensorineural and conductive hearing loss are present. When AC thresholds are better than BC thresholds in a tested ear, this usually implies an exaggerated hearing loss is present.

The pure tone audiogram forms the basis for assessing if an individual qualifies for compensation benefits. A weighted pure tone average (usually taken at 500, 1000, 2000 + 3000 Hz), depending on the provincial/territorial criteria, is required for this determination from AC thresholds if a pure sensorineural hearing loss is present or from BC thresholds if any conductive element to hearing loss is present.

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ii. Speech Reception Threshold (SRT)

Complex words with equal emphasis on both syllables (so-called spondaic words such as “hotdog,” “uptown,” “baseball” etc.) are given to an individual at the lowest intensity they can hear. As a general rule the SRT value should roughly equal the pure tone average in the speech frequencies at 500, 1000 and 2000 Hz. If there is a significant discrepancy, this could imply an exaggerated hearing loss is present as well.

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iii. Speech Discrimination Scores (SDS)

A list of phonetically balanced single syllable words (these are words commonly found in the English language in everyday speech such as “fat,” “as,” “door” etc.) are presented to an individual at 40dB above their speech reception threshold (SRT) in the ear being tested. Most individuals with normal sensorineural hearing should get over 80% of the words correct at this level. When speech discrimination scores are especially poor, this implies that there may be a lesion involving the cochlear nerve ( i.e. acoustic neuroma) and that further investigation may be necessary.

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b. Impedance Testing with Tympanometry

In this test, a probe is placed into the ear canal that both emits a sound and can vary pressure within the canal which causes the ear drum to move.

i. Middle ear pressure measurements (acoustic immitance)

This tells whether the pressure in the middle ear is within normal limits and provides some indirect measurement of Eustachian tube function. Pressures between -100 to +100 are considered normal. In general terms if the Eustachian tube is functioning normally, pressure on both sides of the ear drum should be similar (i.e. a “0” reading).

ii. Stapedial reflex testing

Stiffening of the ear drum from loud noise occurs when the stapedius muscle contracts in the middle ear. Most individuals with normal sensorineural hearing will exhibit a reflex at 70-80 dB above their normal hearing threshold level at the frequency being tested.

Absent stapedial reflexes are usually seen in middle ear pathology such as otitis media with effusion or otosclerosis. When reflexes occur at less than a difference than 70-80 dB above hearing threshold at the frequency tested, this is indirect evidence of a phenomenon called recruitment which is usually seen in cochlear pathology (i.e. Meniere's disease, superior semicircular canal dehiscence syndrome etc.).

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iii. Tympanometry and Types of Curves

If one measures how the ear drum moves when pressure is changed in the external ear canal from negative to positive, a series of curves can be attained. Clinical correlation has demonstrated that the following curves usually are seen in these pathologies.

Figure 5: Schematic representation of tympanometry curves

(D)

Figure 5: Schematic representation of tympanometry curves

  • A - Normal
  • As - Otosclerosis or ossicular fixation
  • AD - Ossicular discontinuity
  • C - Eustachian tube dysfunction
  • B - Middle ear atelectasis (the TM is rigidly fixed to the middle ear) or otitis media with effusion (glue ear)

If a TM perforation is present, it is impossible to obtain a “seal” of the middle ear or a tympanogram.

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c. Evoked Response Audiometry

The ability to measure minute electrical potentials following sound stimulation of the cochlea (i.e. evoked response) provides us with information concerning the cochlea (i.e. electrocochleography), the cochlear nerve and brainstem (i.e. the auditory brainstem response or ABR) and higher cortical auditory pathways (i.e. threshold evoked potentials, cortical evoked response audiometry). An experienced tester, typically an audiologist, is required to perform these technically demanding tests.

The indications and relative importance of these tests are described below.

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i. Electrocochleography (ECoG)

This test measures electrical activity in the cochlea during the first 2 msec of cochlear stimulation. ECoG's chief value lies in its ability to demonstrate wave 1 of the auditory brainstem response (ABR) and whether waveform morphology is suggestive of changes thought to occur in endolymphatic hydrops, the pathophysiologic substrate of Meniere's disease.

ii. Auditory Brainstem Response (ABR)

This term is synonymous with the term brainstem evoked potential (BEP) or the brainstem evoked response audiogram (BERA). This test measures electrical waveforms obtained in the first 10 msec from cochlear stimulation. Waveform morphology is thought to arise from the cochlear nerve and the various relay stations in the brainstem the electrical response has to travel through.

Changes in waveform morphology and latency of the ABR can be quite helpful in the assessment of an individual with an asymmetric sensorineural hearing loss if an acoustic neuroma is suspected.

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iii. Threshold Evoked Potentials (TEP's)

These electrical waveforms are usually identified between 50-200 msec following cochlear stimulation and are thought to represent cortical pathways of electrical activity.

One advantage of TEP testing is that the electrical waves can provide us with information concerning the actual threshold at a certain frequency an individual hears and, as such, gives us some objective measurement of an individual's hearing that is not dependent on a voluntary response. The test is often indicated in an individual if there are concerns regarding an exaggerated hearing loss.

d. Otoacoustic emissions

Otoacoustic emissions (OAEs) are actual minute sounds produced by the active vibration of the basilar membrane generated by the outer hair cells. In response to an acoustic stimulus, there is stimulation of efferent nerves that travel back to the cochlea from the brainstem which cause the outer hair cells to vibrate the basilar membrane. The vibrations are passed though the cochlear to the ossicular chain where the tympanic membranes move, creating a sound that can be amplified and recorded. Any pathology that affects the middle ear (i.e. an effusion, ossicular chain fixation etc.) or tympanic membrane (i.e. a perforation) could adversely affect the response.

OAE's occur spontaneously without stimulation (spontaneous OAEs) or can be found as an evoked response to stimulation. There are 2 types of evoked OAEs commonly identified: transiently evoked OAEs and distortion product OAEs (DPOAEs).

With transient OAEs, a broad stimulus is provided to the ear and most of the basilar membrane becomes involved. Conditions known to cause a sensorineural hearing loss reduce or eliminate the response at a threshold of 30dB or higher, making the test an ideal screening technique for hearing loss, especially in the newborn and those receiving possible ototoxic medication.

With DPOAE testing, single frequency emissions are produced in response to 2 simultaneous stimulus tones. As specific frequencies can be tested, a distortion product audiogram can be generated similar to a pure tone audiogram. The response seems to be suppressed at intensities greater than 50dB or higher. Under certain circumstances DPOAEs could be applied as a general screening test in those suspected to have an exaggerated hearing loss (malingering).

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5. Common Audiometric Configurations in Certain Disease Pathologies

Figure 6: Normal Audiogram

Figure 6: Normal Audiogram

a. Noise Induced Hearing Loss

In its classic presentation, a notched sensorineural hearing loss is noted at 4000 Hz that should be relatively symmetric. Middle ear pressures should be normal, stapedial reflexes present and a normal A tympanogram noted.

Figure 7: Audiogram in NIHL

Figure 7: Audiogram in NIHL

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b. Presbycusis

Age-related hearing loss typically presents with a bilateral symmetric high frequency sensorineural hearing loss.

Figure 8: Audiogram in presbycusis case

Figure 8: Audiogram in presbycusis case.

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c. Meniere's Disease

A low frequency sensorineural hearing loss is pathognomonic for this condition. Fluctuation in hearing is often noted on sequential audiometry.

Figure 9: Audiogram in Meniere's Disease (right side affected)

Figure 9: Audiogram in Meniere's Disease (right side affected).

d. Congenital Hearing Loss

Individuals usually present with a hearing loss early in life. A mid-frequency loss is sometimes noted. This is often called a “cookie-bite” audiogram.

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e. Exaggerated Hearing Loss

There are often numerous discrepancies noted such as the presence of acoustic reflexes at levels below volunteered pure tone thresholds; discrepancies between the volunteered pure tone average and speech reception thresholds etc. Repeat testing and evoked response audiometry is often helpful.

Figure 10: Audiogram in exaggerated hearing loss case

Figure 10: Audiogram in exaggerated hearing loss case.

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6. Tinnitus

Tinnitus (from the Latin, “to ring a bell”) by definition is unwanted head noise. It is a common problem that affects an estimated 20% of the population at any given time. Tinnitus can be either subjective or objective.

Subjective tinnitus can only be appreciated by the affected individual, is usually associated with a sensorineural hearing loss of some type and is the most common type noted. It is usually described as a constant sound (i.e. ring, buzz, hum, etc.) that is worse in the absence of competing background noise (i.e. at night when it is quiet).

Objective tinnitus, on the other hand, is quite rare but by definition is a noise that can be appreciated by an observer. Usually the tinnitus here is described as being pulsatile or clicking. Causes for objective tinnitus include the presence of vascular middle ear tumours (i.e. glomus tumours), aneurysms near the inner ear/ skull base or from repetitive contractions of middle ear muscles (so-called middle ear myoclonus).

Regardless of cause, tinnitus can be quite disturbing for many individuals and can certainly affect their well being. Treatment for tinnitus includes the use of more pleasurable competing background noise strategies (i.e. keeping the radio on at night, wearing an Ipod or Sony Walkman etc.), aids to improve hearing or masking devices that dampen unwanted head noise. Tinnitus maskers are noise generators worn like a hearing aid that produces a sound of similar frequency to an individual's tinnitus. When tinnitus is severe enough to affect an individual's well being, a trial of pharmacologic treatment is generally recommended. Certain anticonvulsants (medications used for seizure control) have been effective for some individuals. New therapies involving tinnitus retraining strategies (tinnitus retraining therapy) have recently been promoted when simpler measures seem to fail to provide relief.

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Tinnitus in NIHL Claims

In the context of a NIHL claim, tinnitus is not infrequently noted. Compensation is available for a non-economic loss (NEL). The problem with tinnitus, however, is that it is difficult to quantify objectively and to fully appreciate how it affects an individual's well being. In general terms when a claim for tinnitus exists, the medical assessor ideally would like to have the following criteria (as suggested by the Veteran's Administration [VA] in the United States) present before an NEL award is made:

  1. The claim for tinnitus should be unsolicited.
  2. The tinnitus must accompany a compensable level of hearing loss (i.e. a tinnitus match audiometrically).
  3. The tinnitus should be present for at least 2 years.
  4. The individual affected has undergone treatments to try and alleviate their perceived unwanted head noise (i.e. medication trials, prosthetic devices, psychiatric intervention etc.).
  5. Evidence to support a personality change or a sleep disorder as a result of the tinnitus.
  6. No history of substance abuse.
  7. A history of tinnitus supported by statements from the family.

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Questions regarding Tinnitus

1. In Veterans Affairs Canada's Entitlement Eligibility Guidelines, one of the causes of tinnitus is stated to be "Exposure to noise that is of sufficient intensity and duration to cause a hearing loss of 25 decibels (dB) or more at the 3000, 4000 or 6000 hertz (Hz) frequencies (in the ear(s) with tinnitus) prior to clinical onset." In your opinion, to be caused or contributed to by the above-described noise-exposure, must the tinnitus occur within any particular time frame? e.g. - can it occur years or even decades later and still be caused or contributed to by that particular noise exposure?

This question is difficult to answer in a black and white fashion. Usually tinnitus is associated with some degree of sensorineural hearing loss but not always. Unprotected exposure to injurious noise levels does affect the higher frequencies of hearing initially and in the classic clinical description has been associated with a notched 4000 Hz hearing loss (but not always).

The question is easy to answer if tinnitus occurs at the time an individual is working and exposed to noise or perhaps occurs shortly thereafter (let's say within a 1 year time frame – this is the time frame that many studies have used looking at the effects of acute acoustic trauma in an affected ear).

It becomes more difficult to answer when the individual leaves a noisy environment (e.g. at retirement) and other factors (e.g. presbycusis, recreational noise exposure, other pathologies involving the ears, etc.) come into play, especially if it occurs years later.

Without sufficient evidence-based medicine to guide us, the decision of whether the delayed onset of tinnitus was caused in part by prior exposure to noise while in employment becomes to some degree the decision of the adjudicator. Using the VAC Entitlement Eligibility Guidelines one could reasonably accept that noise exposure which had caused a permanent loss of over 25dB at 3000, 4000 and 6000 Hz prior to leaving a noisy environment should be considered a contributing factor. If the noise exposure had not caused a loss of over 25dB then one perhaps should not consider the exposure as being considered a significant factor to the individual's tinnitus.

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2. If there is an audiogram which shows a loss of 25 decibels or more at the 3000, 4000 or 6000 hertz frequency and a subsequent audiogram shows a drop to less than 25 decibels at the same frequency, could the noise exposure which caused the 25dB or more loss still cause or contribute to tinnitus? Or, to put it another way, must the 25dB or more hearing loss continue at the same frequency if the tinnitus is to be attributed to the noise exposure which first lead to the 25dB loss?

The answer to the first part of the question is yes it could (despite my recommendations in question 1) but the scenario described seems more akin to the phenomenon of a temporary threshold shift (TTS). As mentioned in my answer to question 1 it is not black and white. It would certainly require documentation of the individual that their noise had occurred when the threshold hearing was > 25 dB and that it persisted despite an improvement in their hearing. Again one is somewhat guided by the VAC Entitlement Eligibility Guidelines. I unfortunately do not have the source information to know how this decision came to be made and what criteria were used specifically for a loss > 25dB at 3000,4000 and 6000 Hz.

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3. Are hearing aids considered to be a prescribed masking device when used for tinnitus only?

Hearing aids on their own would not be considered to be the most appropriate tinnitus masker if there was no significant hearing loss present. They however work best in combination with a patient who has both a hearing loss and related tinnitus that can receive benefit from amplification and for tinnitus management. For tinnitus alone one might reasonably consider masking devices (which generally produce a white band noise) or even the wearing of commercially available products such as MP3 players, iPods etc.

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7. Hyperacusis

Hyperacusis is a curious phenomenon where an individual describes an uncomfortable, sometimes painful, hypersensitivity to sounds that would be normally well tolerated in daily life. In some instances it can be quite disabling for the affected individual who tends to withdraw from any exposure to uncomfortable noise. Most individuals affected often have normal hearing. The term “phonophobia” has been used interchangeably.

Why hyperacusis arises is poorly understood. It has been documented at times to follow an incident of acute acoustic trauma. Sometimes it arises without a cause being identified. Investigations such as a magnetic resonance imaging (MRI) are generally required to exclude the unlikelihood of central nervous system pathology. Mean comfort levels (MCL's) and uncomfortable loudness levels (ULL's) during audiometry provide some information concerning the threshold intensity of sound an individual can tolerate.

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8. Questions and Controversies in NIHL

1. Why are the frequencies of 0.5, 1, 2 and 3 kHz used for NIHL awards when hearing loss is often greater at 4, 6 and 8 kHz?

This is a very relevant question that is based on the definition of how hearing loss causes a handicap for the affected individual in their ability to identify spoken words or sentences under everyday conditions of normal living.

Although the higher frequencies are initially affected in NIHL, an individual will really only begin to demonstrate a significant handicap to hearing everyday speech in a quiet surrounding when the average of the hearing thresholds at 500, 1000, 2000 ( + 3000) Hz is above 25 dB. The prediction for a handicap did not appear to be improved by the inclusion of other frequencies > 4000 Hz.

The inclusion of the 3000 Hz threshold value for NIHL awards is not always required depending on the jurisdiction. It should be appreciated that while a decrease in hearing sensitivity at 3000 Hz has little effect upon hearing speech in quiet circumstances, it produces a handicap in the presence of competing background noise (i.e. restaurants, family gatherings, church etc.) or when speech is distorted. Most would not be expected to have problems with the telephone (most telephones rarely transmit sounds > 3000 Hz).

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2. What do other jurisdictions consider to be disabling hearing loss (provincial, national and international)?

In the province of Ontario, the Workplace Safety and Insurance Board (WSIB)'s Operation Policy Manual (OPM) Document No. 04-03-10, entitled “Noise Induced Hearing Loss, On/After January 2, 1990” states that workers with an occupational noise induced hearing loss sufficient to cause a hearing impairment may be entitled to benefits when there is a hearing loss of 22.5 dB in each ear when the four speech frequencies (500, 1000, 2000 and 3000 Hz) are averaged.

The WSIB accepts the following circumstances as persuasive evidence of work-related conditions in claims for sensorineural hearing loss:

  • Continuous exposure to 90dB (A) of noise for 8 hrs per day, for a minimum of 5 years, or the equivalent; and
  • A pattern of hearing loss consistent with noise induced sensorineural hearing loss.

A presbycusis (aging) correction factor of 0.5 dB is deducted from the measured hearing loss (averaged over the 500, 1000, 2000 and 3000 Hz frequencies) for every year the worker is over the age of 60 years at the time of the audiogram. The hearing loss that remains after the presbycusis adjustment is then used to determine entitlement to benefits. Entitlement to health care and rehabilitation benefits is available when the adjusted hearing loss is at least 22.5 dB in each ear.

It is important to appreciate that decisions can also be made on an exceptional basis which the WSIB has recognized.

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Exceptions

Since individual susceptibility to noise varies, if the evidence of noise exposure does not meet the above exposure criteria, claims will be adjudicated on the real merits and justice of the case, having regard to the nature of the occupation, the extent of the exposure, and any other factors peculiar to the individual case.

A list of Provincial and Territorial Comparisons for NIHL is provided below:

Province Exposure Requirements a. Entitlement Criteria
b. Minimum hearing loss level for hearing aid benefits
Presbycusis correction factor (or other) Tinnitus compensation
a. In Claim
b. In PI
British Columbia (BC) 85 dBA-8h/day over 2 years a. Average at 500, 1000 and 2000 Hz
b. Hearing loss > 30 dB/30dB bilaterally for hearing loss benefits
Use of Robinson's Tables a. Yes
b. No
Alberta (AB) 85 dB-8h/day over2 years a, b. Average at 500, 1000, 2000 and 3000 Hz >140dB to be considered for hearing aids and/or pension award Use of Robinson's Tables a. Yes
b. NA
Saskatchewan (SK) 85 dB-8h/day over 2 years a. Average at 500, 1000, 2000 and 3000 Hz
b. Hearing loss > 35 dB bilaterally
No deduction a. Yes
b. 2%
Manitoba (MB) 85 dB-8h/day over 2 years a. Average at 500, 1000, 2000 and 3000 Hz
b. Hearing loss > 26.25 dB bilaterally for benefits
2 dB/year after age 60 a. Yes
b. 2%
Ontario (ON) 90 dB-8h/day over 5 years a. Average at 500, 1000, 2000 and 3000 Hz
b. Hearing loss > 22.5 dB for benefits
0.5 dB/year after age 60 a. Yes- medical opinion and tinnitus match required
b. 2%
Quebec (QB) NA a. NA
b. Hearing loss > 30 dB for benefits
NA a.b. NA
New Brunswick (NB) NA a. Average at 500, 1000, 2000 and 3000 Hz
b. Hearing loss >25 dB for benefits
NA a. Yes
b. NA
Prince Edward Island (PEI) 85 dBA-8h/day over 2 years a. Average at 500, 1000, 2000 and 3000 Hz
b. Hearing loss >25 dB in one ear for benefits
0.5 dB/year after age 60 a. Yes
b. 2%
Nova Scotia (NS) NA a.b. Average at 500, 1000, 2000 and 3000 Hz > 100 dB 2 dB/year after age 60 a. Yes
b. NA
Newfoundland (NF) 85 dBA-8h/day over 2 years a. NA
b. Hearing loss >25 dB for benefits
0.5 dB/year after age 60 a. Yes
b. NA
Yukon 85 dB-8h/day over 5 years ( but must have worked for 2 years in the Yukon) a. Average at 500, 1000, 2000 and 3000 Hz
b. Hearing loss must be >25 dB for benefits
None accounted for a. Yes
b. 2%
Northwest Territories and Nunavut 90 dBA-8h/day over 5 years a.b. NA NA a.b. NA

NA - Not available, PI - permanent impairment

The above list does demonstrate a lack of uniformity in NIHL claims and benefits within Canada.

A comprehensive list of US comparisons for NIHL and benefits can be found in Table 35.1 pages 797-799 in the Chapter concerning State and Federal Formulae Differences in Occupational Hearing Loss, 3rd Edition. Sataloff and Sataloff. 2006

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3. Does previous noise exposure make an ear more sensitive to future noise exposure?

Apparently it does not. It is generally thought that if an ear has suffered a permanent threshold shift from a noise induced etiology, then further noise exposure will cause less damage than would occur in a normal ear to a similar exposure. This is based primarily on animal modes which have demonstrated that at the frequency range of maximum damage, the increase in a noise induced PTS from the second exposure was smaller for ears with greater pre-existing loss (the so-called “you can't further damage what has already been damaged” rule).

The following example illustrates this rule:

Person A and Person B were both exposed to a similar event.

Person A had a pre-existing PTS to 20 dB. Person B had no previous noise exposure and had no PTS.

Following similar noise exposure at the same instance.

Person A displayed a TTS to 45 dB - a loss of 25 dB. Person B (who had no dB loss due to noise exposure) displayed a TTS to 45 dB - a loss of 45dB.

Person A's loss was 20 dB while Person B's loss was 45dB. Person B's previously unaffected hearing received the most damage.

To conclude, this is really defined by what is called Corso's theorem, which implies that the majority of noise induced hearing loss occurs early on in noise exposure. Once the hearing loss has occurred one would not anticipate further injury to what has already been lost. Continued exposure, however, would be expected to continue to worsen hearing (albeit at a slower rate) and for that reason the use of hearing protection would still be recommended.

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4. Does previous NIHL accelerate the onset of presbycusis?

This is question that continues to intrigue auditory research scientists. As previously noted, the effects of noise exposure and aging on hearing when not combined are reasonably well understood. When the two processes are combined, the resultant pathology and its effects upon aging are not as well understood.

It is likely that the two effects are not additive (Corso's theorem) but from a practical point of view this is how they are usually viewed with regards to compensation claims (Dobie's theorem).

Some generally accepted principles (according to the American Academy of Otolaryngology (AAO) - Head and Neck Surgery 1994 Guidelines) with regards to age-related change note that:

  • a. At any given age for frequencies above 1000 Hz men will have more age-related hearing loss than women.
  • b. Age-related hearing loss affects all frequencies, although the higher frequencies are usually more affected.
  • c. Age-related hearing loss is an accelerating process where the rate of change increases with age.

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5. Does permanent damage to the cochlear hair cells caused by noise exposure contribute to the eventual development of a hearing disability?

There is a significant redundancy within the inner ear as it pertains to hearing. In other words, many hair cells in a similar region of the cochlea will encode for a certain frequency response to sound stimulation. Hair cell loss can continue until a certain critical point is breeched with the individual unaware of any hearing deficit. Once the critical loss of hair cells occurs, however, the individual will notice a hearing loss.

One can speculate that this might be one of the reasons an individual early on in their exposures may not be aware of a hearing loss, only to appreciate a hearing loss later in life when other factors such as presbycutic change occur.

The issue can be debated but at present we have no means of actually knowing on clinical grounds the degree of hair cell damage that has occurred on a microscopic basis from noise exposure in a living individual if hearing is still deemed as normal. As previously mentioned there is a certain redundancy of cochlear hair cells for tonal awareness and one can probably have significant loss of hair cells yet maintain normal hearing. Once noise exposure has stopped other factor(s) would need to be involved to therefore worsen hearing. Nevertheless the cochlear hair cells reserve is probably not as great as it once was. That usually is the reason why we state that following noise exposure other factor(s) would be likely to cause further hearing loss in an individual.

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6. At what age does presbycusis begin to make a material difference to hearing disability and at what age can its effects be seen on an audiogram?

When we are born we can hear frequencies up to 20,000 Hz. Over the years we hear less and less. Because we tend to make little use of frequencies > 8000 Hz we do not become aware of a hearing loss in general until the frequencies < 8000 Hz are affected.

Although we think of presbycusis as an age-related event, not all individuals will develop this condition. Moreover, we really don't have a lot of good prospective long-term studies over 4-5 decades that can ultimately answer this question completely. Upon saying this, however, we can actually demonstrate that many individuals will start to show early changes in hearing as early as age 40 years (in subjects screened to rule out other ear disease and noise exposure).

With regards to the rate of hearing loss noted in presbycusis, recent evidence from longitudinal prospective studies from Denmark and the UK indicate that the actual rate of deterioration seems to be influenced by age; those over 55 years showed a higher rate of deterioration of up to 9 dB/decade against a deterioration of 3 dB/decade for those under 55 years.

Future genetic studies may provide us with further information concerning those at greater risk for progressive hearing loss from presbycusis in future.

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7. Can moderate workplace noise exposure causing a TTS and repeated exposures later cause a PTS?

Yes. Repeated noise exposure that causes a temporal threshold shift (TTS) can ultimately lead to a permanent threshold shift (PTS) with repeated exposures. It is agreed that hearing loss and injury to the ear increases with the noise level, the duration of exposure, the number of exposures and the susceptibility of the individual.

A TTS is considered to represent a pathological metabolically induced fatigue of the hair cells or other structures within the Organ of Corti. Its development and recovery are proportional to the logarithm of exposure time. It reverses slowly over a period of hours. The practical “cutoff point” for a TTS is approximately 40dB. Below this threshold, value recovery is relatively swift; above this, it appears delayed. If a person experiences repeated TTS with a shift in excess of 40 dB, the recovery time is longer and can result, over time, in a PTS.

In a PTS the destruction and eventual cochlear hair cell loss is thought to arise from direct mechanical destruction from high-intensity sound and from metabolic decompensation with subsequent degeneration of sensory elements.

While one would normally expect full recovery of hearing function after a TTS, there is one important consideration that needs to be taken into account. Some of this is based on the redundancy principle within the inner ear: not all hair cells possibly recover following a TTS but enough do so as to prevent hearing loss. Continued exposure to excessive noise will therefore result in further hearing loss.

In other words, when an ear sustains a TTS, it is conceivable that there may be some permanent injury to some of the inner/outer hair cells at the frequencies tested that is not reversible. Thankfully there is a significant amount of redundancy in the inner ear. It is only when a quantum number of hair cells are injured irreparably that we then begin to clinically notice a permanent threshold shift (PTS) in hearing.

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8. Following acute acoustic trauma, what is the natural history of the subsequent hearing loss?

The position in the world literature continues to support that any progressive hearing loss from acute trauma ceases unless the individual is re-exposed to more acute acoustic trauma or some other factor(s) occurs (i.e. concomitant presbycusis, head injury etc.).

The classic studies of acute acoustic trauma by Segal et al (1988) and Kellerhals (1991) are often used to support this position.

In the cohort study by Segal et al, 841 individuals from either the regular US army or military reserve sustained a permanent sensorineural hearing loss from acute acoustic trauma without subsequent re-exposure. Audiometric evaluations were performed on these individuals at 6 months, 1, 2 and 4 years after initial exposure. Hearing remained stable at 1 year in approximately 90-91.3%, improved in 7.7%, and appeared to worsen in 2.2%. Follow-up beyond the 1 year mark did not reveal any further deterioration of hearing in any individual. Of interest, in a parallel series of control patients who were further exposed to repeated episodes of acute acoustic trauma during the same study period, by the end of 4 years, 30% of these individuals had demonstrated significant hearing deterioration.

The importance of the Segal study is that after 1 year, one would not expect further worsening of hearing in subjects who ceased to have further noise exposure.

Kellerhals' study reviewed a much smaller series of individuals who were exposed to acute acoustic trauma but looked at them over a 20 year duration. In his study cohort only 1% of individuals following acute acoustic trauma demonstrated deterioration of hearing of more than 20 dB in at least 1 frequency. The findings also indicate that the late progression of hearing loss following a single episode of acute acoustic trauma did not exist.

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9. Are certain individuals more predisposed to developing NIHL than others?

Large susceptibilities in NIHL occur in persons exposed to the same noise environment. A review of endogenous factors related to individual sensitivity by Ward did not find any effects other than those related to the acoustic energy reaching the cochlea or the oxygen supply to the cochlea.

While there has been concern that smoking and elevated serum cholesterol levels might play a role by affecting blood flow and hence oxygen delivery to the cochlea, this has not been validated. Pigmentation differences in subjects grouped by eye color (on the basis that pigmentation in the stria vascularis of the cochlea is similar) and race have been inconclusive as well. Curiously, however, within-race differences in hearing levels and eye colour group are present and cross-racial differences in hearing are substantial.

Other studies have failed to show any effect on vulnerability caused by diabetes, silicosis or leprosy. There is some slight evidence that Meniere's disease might increase vulnerability. Whether deficiencies in vitamins render an individual more sensitive is also not certain.

In summary, susceptibility has not been shown to be dependent on gender, skin color, any known diseases, mental attitude towards noise, exposure history, pre-exposure hearing loss and even a history of smoking.

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10. From a medical assessor's perspective, why are many NIHL claims contentious?

Most contentious claims arise for the following reasons which include:

  • The absence of a proper pre-employment audiogram.
  • The absence of a proper exit audiogram, especially when a worker leaves their employment.
  • Poor quality audiograms performed either by a tester not appropriately trained or in facilities not up to the ANSI or ISO recommended standards.
  • The configuration of the audiogram is not typical for NIHL, especially when the 4000 Hz loss is not present; there is a greater than expected loss of hearing in the lower frequencies; and when significant asymmetries to hearing loss occur without reasonable explanation.
  • Differing opinions between the treating physician and the medical assessor. It is always important to remember that, “while all NIHL is sensorineural in nature, not all sensorineural hearing loss is Occupational.”

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11. Is it true that there can be a + or - 5% margin of error in audiograms?

There are three main components to look at when an audiogram seems to be contentious:

  • a. what are the facility standards for this particular facility?
  • b. is the equipment calibrated regularly to specified standards?
  • c. was the tester well skilled?

Audiograms are not specific science in that the responses from the patient/Applicant are subjective. The margin of error - outside of one of the three above-noted criteria would lie with the patient. When audiogram results are brought into question, another audiogram is conducted. This would not be applicable to audiograms being reviewed in the historic sense (conducted during service, pertinent to a specific time frame, etc.). Patients can be suggestible - the difference shouldn't be huge, and it is a well recognized phenomenon.

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9. References

Selected Texts

  1. American Academy of Otolaryngology - Head and Neck Surgery Foundation Subcommittee on the Medical Aspects of Noise. Evaluation of People Reporting Occupational Hearing Loss 1998.
  2. American Academy of Otolaryngology - Head and Neck Surgery Foundation: Guide for Conservation of Hearing in Noise. Edited by David Osguthorpe 1988.
  3. American Medical Association: Guidelines to the Evaluation of Permanent Impairment. 3rd Edition 1990.
  4. Occupational Hearing Loss. 3rd Edition. Robert Thayer Sataloff and Joseph Sataloff. Taylor and Francis. New York 2006.
  5. Hearing Loss. 4th Edition. Robert Thayer Sataloff and Joseph Sataloff. Taylor and Francis, New York 2005.
  6. Ototoxicity. Peter S Roland and John A Rutka. BC Decker Inc, Hamilton 2004.
  7. Occupational Medicine: State of the Art Review. Occupational Hearing Loss. Volume 10(3): July-September, Philadelphia, Hanley and Belfus 1995.
  8. Noise Induced Hearing Loss by Lonsbury - Martin BL, Martin GK and Telischi FF. Volume 4,Chapter 126 in Otolaryngology - Head and Neck Surgery 3rd Edition. Charles Cummings, John Fredriksson et al, Mosby Press 1998.
  9. Medicolegal Evaluation of Hearing Loss by Robert Dobie. Van Nostrand Reinhold, New York 1993.
  10. Diseases of the Ear: Clinical and Pathological Aspects by Michael Hawke and Anthony Jahn. Lea and Febiger, Philadelphia 1987.

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Selected Papers and Supplements

  1. Borg E, Canlon B, Engstom B. Noise Induced Hearing Loss. Scan Audiol 1995; Suppl 40:1
  2. Lutman ME, Spencer HS. Occupational Noise and Demographic Factors in Hearing. Actga Otolaryngol (Stockh) 1991; Suppl 476 : 74-84.
  3. Hinchcliffe R. The Age Function of Hearing - Aspects of the Epidemiology. Acta Otolaryngol (Stockh) 1991; Suppl 476 :7-11.
  4. Davis AC, Ostri B and Parving A. A Longitudinal Study of Hearing. Acta Otolaryngol (Stockh) 1991; Suppl 476: 12-17.
  5. Clark WW: Hearing: The Effects of Noise. Otolaryngol Head Neck Surg 1992; 106: 669-676.
  6. Segal S, Harrell M, Sharar A et al. Acute Acoustic Trauma: Dynamics of Hearing Loss Following Cessation of Exposure. Am J Otol 1998; 9(4): 293-298.
  7. Corso JF. Age and Sex Difference in Pure Tone Threshold. Arch Otolaryngol 1963; 77: 385-392.
  8. Corso JF. Support for Corso's Hearing Loss Model Relating Aging and Noise Exposure. Audiol 1992; 31: 162-167.
  9. Rosler G. Progression of Hearing Loss Caused by Occupational Noise. Scan Audiol 1994; 23: 13-37.
  10. Dobie RA. The Relative Contributions of Occupational Noise and Aging in Individual Cases of Hearing Loss. Ear and Hearing 1992; 13(1): 19-27.
  11. Kellerhals B. Progressive Hearing Loss After Single Exposure to Acute Acoustic Trauma. Eur Arch Otorhinolaryngol 1991; 248:289-292.
  12. Morata TC, Dunn DE, Kretschmer LK et al: Occupational exposures to organic solvents and noise. Effects on Hearing. Scan J Work Environ Health 1993; 19: 245-254.

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