Robert Dobie, MD
Occupational hearing loss may be partial or (rarely) total, unilateral or bilateral, and conductive, sensorineural, or mixed (conductive and sensorineural). Conductive hearing loss involves the external or middle ear, and impairs the passage of sound to the inner ear; sensorineural hearing loss (SNHL) results from dysfunction of the inner ear, auditory nerve, or brain. In the workplace, conductive and mixed hearing loss can be caused by blunt or penetrating head injuries, explosions, and thermal injuries such as slag burns sustained when a piece of welder’s slag penetrates the eardrum. SNHL usually results from damage to the cochlea, especially loss of hair cells from the organ of Corti. Among the causes of occupational SNHL are continuous exposure to noise in excess of 85 dBA, blunt head injury, and exposure to ototoxic substances.
PHYSIOLOGY OF HEARING
Sound waves consist of alternating periods of compression and rarefaction within a medium such as air. The stronger the pressure variation, the louder the sound. Measurement of hearing in terms of sound pressure in micropascals (μPa) is cumbersome because of the enormous dynamic range of normal hearing (for the frequencies humans hear best, pressures between 20 and 20,000,000 μPa can be heard and tolerated). For this reason, the logarithmic decibel (dB) scale is used, compressing a million-fold pressure variation into a range of 120 dB. Since humans hear some frequencies better than others, audiometers are calibrated in “hearing level” (HL), a scale that defines 0 dB HL—at each frequency—as the faintest sound that the average healthy young person can detect.
Sound frequency (the number of waves passing a fixed point each second, measured in Hertz [Hz]) correlates with pitch. The normal human ear can detect sounds across the frequency range from approximately 20–20,000 Hz. The most important range for human speech communication is between 500 and 3000 Hz.
When sound traveling in air strikes water, almost all of it is reflected, because air and water have very different acoustic impedances. To allow efficient transmission of air-conducted sound into the fluid-filled inner ear, the impedance-matching middle ear has evolved; when the ear canal is open, and the tympanic membrane and the three ossicles (malleus, incus, and stapes) are working properly, the inner ear can respond to sounds that are up to 60 dB less intense than would otherwise be the case.
The transduction of mechanical vibrations to nerve impulses by the inner hair cells takes place in the inner ear (cochlea) at the organ of Corti. The hair cells of the organ of Corti rest on the basilar membrane, and the stereocilia of the three rows of outer hair cells oscillate against the tectorial membrane. A shearing action between the stereocilia and the tectorial membrane, caused by the traveling wave motion of the basilar membrane, results in release of neurotransmitters by a single row of inner hair cells to the auditory nerve fibers that innervate them.
As the wave travels from base (high frequency) to apex (low frequency) along the basilar membrane, it reaches a peak amplitude that correlates directly with the frequency of the sound. Each point along the basilar membrane is frequency specific (tonotopically organized). The electromotility of the outer hair cells enhances the frequency tuning of the traveling wave.
EVALUATION OF HEARING
Clinical Observation
The simplest form of hearing evaluation occurs during medical history taking in the examination room without any sophisticated equipment. Can the patient converse adequately face-to-face at a normal distance (about 1 meter)? At lesser or greater distances? When the examiner is speaking normally, loudly, or (in cases of very severe hearing loss) shouting? When the examiner’s back is turned and visual cues are lost? During handwashing, with the interfering noise of running water? While no substitute for audiometry, simple gross observations of this type should correlate with—and can serve to validate or invalidate—the results of formal hearing tests.
“Whispered-voice” tests are still used in some contexts (eg, they are permitted as a substitute for audiometry for commercial drivers’ licenses).
Tuning Fork Tests
Tuning fork tests should be performed with a 512-Hz tuning fork because lower frequencies may elicit a tactile response.
A. Rinne Test
In cases where the patient hears air conduction (tuning fork placed by the opening of the ear canal) better than via bone conduction (tuning fork placed on the mastoid bone), a sensorineural hearing loss or normal hearing is usually indicated in the test ear. When bone conduction is louder than air conduction, a conductive hearing loss is usually present (a severe unilateral sensorineural loss may show the same pattern unless masking is used to exclude the better ear).
B. Weber Test
When the tuning fork is placed on the forehead or front teeth, sound should lateralize toward the ear with a conductive loss and away from the ear with a sensorineural loss (in cases of unilateral or asymmetric hearing loss).
Pure-Tone Audiometry
In a clinical audiogram, sensitivity to pure tones is measured at 250, 500, 1000, 2000, 3000, 4000, 6000, and 8000 Hz for air conduction (head phones) and, if necessary, bone conduction (bone oscillator). The threshold of hearing (the softest tone that is audible) can be measured by adjusting tone intensity either manually, or automatically under computer control; the latter is common in occupational hearing conservation programs (HCPs). Thresholds are expressed in decibels, with the normal range (for young adults) at each frequency from 0 to 20 dB HL. Because loud sounds may stimulate the opposite ear, masking that ear with competing noise is necessary when asymmetry exists. When both air and bone conduction are decreased, a sensorineural hearing loss exists. Conductive losses are indicated by an “air-bone gap,” in which the air-conduction threshold exceeds the bone-conduction threshold. Results may be presented numerically or shown graphically (Figures 13–1 to 13–5).
Figure 13–1. Normal to mild noise-induced hearing loss. The audiogram shows typical bilateral high-frequency sensorineural hearing loss, which is most severe at 4000 Hz. Note the normal speech discrimination score.
Figure 13–2. Normal to severe noise-induced hearing loss plus age-related hearing loss. The audiogram shows moderate to severe high-frequency sensorineural hearing loss but preservation of the lower tones. Note the moderate decrease in the speech discrimination score.
Figure 13–3. Presbycusis. The audiogram shows moderate to severe gently sloping sensorineural hearing loss. Note that the hearing threshold at 4000 Hz is better than at 8000 Hz, a pattern suggestive, but not diagnostic, of an aging change rather than exposure to noise.
Figure 13–4. Moderate conductive hearing loss. The audiogram shows a disparity between the thresholds of bone conduction and air conduction. This “air-bone gap” represents the degree of hearing impairment caused by dysfunction of the external or middle ear. Tympanogram shows an increase in left middle ear compliance. The audiogram is typical of a left ossicular chain disruption.
Figure 13–5. Nonorganic hearing loss. The audiogram shows pure-tone thresholds that are significantly worse than the speech reception thresholds recorded on the same data.
Bekesy (Self-Recording) Audiometry
Pure-tone thresholds also may be measured by Bekesy audiometry in which the patient uses self-directed techniques that involve pressing and releasing a signal button. This procedure used to be widespread in occupational HCPs.
Speech Audiometry
Two routine tests are performed to assess speech reception and comprehension, which are the most important aspects of audition.
A. Speech Reception Threshold
The speech reception threshold (SRT) is the intensity (in decibels) at which the listener is able to repeat 50% of balanced two-syllable words known as spondee words (eg, baseball, playground, and airplane). The threshold is usually in close agreement (within 6–10 dB) with an average of the pure-tone thresholds for frequencies between 500 and 2000 Hz. The normal range for young adults is between 0 and 20 dB, with thresholds of 25–40 dB termed mild hearing loss, 40–55 dB termed moderate, 55–70 termed moderately severe, 70–90 dB termed severe, and greater than 90 dB termed profound hearing loss.
B. Word Recognition Score
In the word recognition score (WRS), also referred to as speech discrimination score, monosyllabic words that are phonetically balanced are presented at intensities usually well above the speech reception threshold (SRT plus 30–40 dB) in order to test speech comprehension. Results are expressed as a percentage of words repeated correctly. The normal range of WRSs for young adults is 88–100%. Word lists are available for most languages. Severe depression of the WRS usually indicates socially significant disability, but WRSs display high test-retest variability.
Impedance (Immittance) Audiometry
The mechanical aspects of the middle ear sound transformer system can be assessed by tympanometry and acoustic reflex testing.
A. Tympanometry
Tympanometry employs an acoustic probe to measure the impedance of the eardrum and ossicular chain. Reduced middle ear compliance usually indicates a partial vacuum owing to auditory tube dysfunction, whereas noncompliance suggests either a tympanic membrane perforation or middle ear effusion. An increase in compliance suggests either laxity of the tympanic membrane or disruption of the ossicular chain.
B. Acoustic Reflex Testing
Contraction of the middle ear muscles in response to a loud noise results in a measurable rise of middle ear impedance. Interpretation of acoustic reflex testing also may yield information regarding the integrity of the auditory portion of the central nervous system. It is also an indirect measurement of recruitment (abnormal growth of loudness) that frequently accompanies sensorineural hearing loss.
Evoked-Response Audiometry (Brain Stem Audiometry)
In patients who demonstrate unilateral or asymmetric sensorineural hearing loss, retrocochlear lesions (lesions of the eighth cranial nerve, brain stem, or cortex) must be ruled out. Evoked potentials, which typically are elicited in response to clicking noises and recorded via scalp electrodes, provide information about the location of sensorineural lesions. For individuals with normal hearing, as well as most patients with cochlear hearing losses, a series of five electroencephalographic waves may be detected, representing the central auditory system from the eighth cranial nerve (wave I) to the inferior colliculus (wave V). Any significant delay or even a complete absence of response may indicate a cerebellopontine angle tumor (eg, acoustic neuroma) or a lesion of the brain stem. More definitive diagnosis of retrocochlear lesions requires computed tomographic (CT) scanning or magnetic resonance imaging (MRI).
Stenger Test
This test is useful for detecting feigned unilateral hearing loss. The Stenger principle states that when tones of the same frequency but of different intensities are presented to both ears simultaneously, only the louder tone will be heard. When the louder tone is presented to the ear with a feigned hearing loss, the patient stops responding because the patient perceives that all the sound is coming from that side. Patients with true unilateral loss indicate that they continue to hear the sound in the opposite ear.
Otoacoustic Emissions
Otoacoustic emissions (OAEs) are a recent addition to objective hearing testing. OAEs are produced when the cochlea receives an external sound stimulus, and the mechanical properties of the outer hair cells act in a manner in which a measurable sound is produced and transmitted laterally through the middle ear to be recorded in the external auditory canal. There are two types of evoked OAEs used clinically today. They are transient-evoked otoacoustic emissions (TEOAEs) and distortion-product otoacoustic emissions (DPOAEs). Individuals with hearing better than 35 dB (TEOAEs) and 50 dB (DPOAEs) will usually produce OAEs, unless there is middle ear pathology. If an individual generates OAEs but does not admit to hearing, the middle ear and cochlea are assumed to be functional, and thus a nonorganic or retrocochlear origin must be assumed. OAEs are useful in forensic examination because OAEs are rapid (30 seconds to 3 minutes), reproducible, frequency specific (1000–10,000 Hz), and sensitive to outer hair cell dysfunction, such as the damage caused by noise. OAEs may someday prove useful in hearing conservation programs, but have not been shown to be more effective than pure-tone audiometry, and cannot detect worsening hearing in people with even mild hearing loss who have already lost their OAEs.
Fitness for Work
The Hearing In Noise Test (HINT) has been proposed as a direct measure of functional speech perception in noise, for use in screening applicants for hearing-critical jobs. The HINT measures speech intelligibility in quiet and in spectrally matched noise at suprathreshold levels using sentence materials. The testing is done in quiet and in three background-noise environments (noise front, noise right, and noise left). The noise level is fixed at 65 dBA while the sentence (signal) level is varied; the signal-to-noise ratio (SNR) is the difference in decibels between the sentence level and the noise level at which performance is 50% correct. Young adults can usually repeat the sentences even when the noise is louder than the sentences, while people with hearing loss often require the sentences to be considerably louder than the noise. For the quiet test condition, ability to repeat 50% of sentences at a level of 28 dBA is proposed as the passing criterion. In noise, the SNRs are used to determine a percentile score based on norms for normal listeners. Some governmental employers use a fifth percentile criterion (95% of young normal listeners perform better than the subject) as a barely passing score. Tests like this are attractive because they use more realistic speech than conventional speech tests (sentences rather than isolated words) and incorporate background noise, which is important in some jobs. However, they cannot claim to simulate any specific occupational hearing situation (many jobs have unique vocabularies and types of noise) and have not been shown to correlate with or to predict job performance. There is no simple way to estimate fitness to work from hearing tests.
DIFFERENTIAL DIAGNOSIS OF SENSORINEURAL HEARING LOSS
Nonoccupational Hearing Loss
In attempting to determine the extent of occupational hearing loss in a subject, the following nonoccupational hearing-loss disorders must be considered.
A. Age-Related Hearing Loss
Age-related hearing loss (ARHL) is a slow and progressive deterioration of hearing that is associated with aging and not attributable to other causes (see Figure 13–3). It is often referred to as presbycusis and is associated with a variety of inner ear pathologies, including atrophy of the inner and outer hair cells, stria vascularis, and spiral ganglion in the cochlea. Other features that occur histologically include atrophy or degeneration of central auditory pathways and possibly mechanical changes in the cochlear duct affecting movement of the basement membrane. Usually the hearing loss is a gradual, more or less symmetric, progressive, high-frequency sensorineural loss associated with gradually deteriorating speech discrimination. In the US population, age is by far the most important predictor of hearing loss; the odds of having significant hearing impairment increase about threefold with every decade from age 25 to age 65. The severity of ARHL at any given age is highly variable, depending in part upon independent risk factors such as male sex, white race, lower socioeconomic status, heavy smoking, diabetes, and noise exposure (occupational and nonoccupational). ARHL has a large genetic component; heritability is close to 50%.
B. Hereditary Hearing Impairment
In developed countries, congenital and early-onset deafness has an important genetic origin, and at least 60% of the cases are inherited. Hereditary hearing impairment (HHI) can be conductive, mixed, or sensorineural impairment, and the pattern of inheritance can be dominant, recessive, X-linked, or mitochondrial. HHI may be accompanied by a positive family history, consanguity, and/or physical findings consistent with a hereditary syndrome known to include hearing loss. Currently, more than 100 genes are involved in the different types of inherited deafness (syndromic and nonsyndromic). HHI is usually detected in early childhood, particularly if it is associated with syndromes (eg, autosomal-recessive Usher syndrome, autosomal-dominant branchio-oto-renal syndrome, or X-linked mixed hearing loss with stapes gusher). Autosomal-recessive nonsyndromic HHI accounts for 80% of nonsyndromic early-onset hearing loss. A single gene locus, DFNB1, accounts for a high proportion of the recessive cases, with variability depending on the population. The gene involved in this type of deafness is GJB2, which encodes the gap-junction protein connexin 26. Connexins are transmembrane proteins that form channels that allow rapid transport of ions or small molecules between cells. Autosomal-dominant nonsyndromic HHI usually presents in early or middle adulthood and often is progressive. Genetic screening is available clinically for several of the nonsyndromic and syndromic mutations.
C. Metabolic Disorders
Progressive hearing loss may be related to diabetes mellitus, heavy smoking, severe thyroid dysfunction, renal failure, autoimmune disease, and perhaps hyperlipidemia. In diabetes mellitus, the pathology is varied, involving primary neuropathy and/or small-vessels disease. Other metabolic disorders may involve pathology in the stria vascularis, which is important in maintaining the ion balance and the electrical potentials within the cochlea.
D. Idiopathic Sudden Sensorineural Hearing Loss
This is differentiated by its sudden onset, usually developing within 24 hours, in the absence of precipitating factors. The hearing loss is almost always unilateral. The hearing-loss pattern in idiopathic sudden sensorineural hearing loss (ISSNHL) is variable. The degree of hearing loss is unpredictable, ranging from mild to profound; partial or total spontaneous recovery is typical. Vertigo is present in some cases of ISSNHL and suggests a worse prognosis.
The etiology of ISSNHL is unknown; viral cause, vascular insult, and inner ear membrane rupture (Reissner membrane, tectorial membrane) have been postulated. This disorder warrants a thorough evaluation in order to rule out any other known pathology.
The treatment of ISSNHL is debatable. The most common therapies are observation versus steroids (oral or intratympanic). Vasodilators, anticoagulants, and diuretics also have been used in the treatment of some ISSNHL.
E. Infectious Origin
This includes bacterial or viral infections, including meningitis and encephalitis, that may cause hearing loss. Spirochete infections such as congenital or acquired syphilis and Lyme disease can result in hearing loss and vestibular dysfunction. The congenital syphilis sufferer may develop symptoms in infancy or later in life that also may be associated with vestibular symptoms similar to Ménière syndrome; the hearing loss can be unilateral but usually is bilateral. Late syphilis may present a slowly progressive sensorineural hearing loss and also may exhibit associated vestibular problems.
Mumps may cause a rather severe, most typically unilateral sensorineural hearing loss. Other childhood viral exanthems also can cause sensorineural hearing loss. Congenital hearing loss also can be caused by rubella virus and cytomegalovirus.
F. Central Nervous System Disease
Cerebellopontine angle tumors, especially vestibular schwannoma (acoustic neuroma), may present with progressive sensorineural hearing loss that is unilateral. This is in contrast to noise-induced hearing loss and ARHL, which are usually symmetric. Patients with unilateral or asymmetric sensorineural hearing loss require further investigation to rule out these tumors. This investigation may require detailed audiometric studies and CT scan or MRI. Demyelinating diseases (eg, multiple sclerosis) may present a sudden unilateral hearing loss that typically recovers to some degree.
G. Ménière Disease (Endolymphatic Hydrops)
Ménière disease and its variants generally present a fluctuating low-frequency or flat unilateral sensorineural hearing loss, fullness or pressure in the affected ear, tinnitus, and episodic disabling vertigo. In the early stages, the hearing loss usually affects the low frequencies, but over time it may progress to a flat severe hearing loss. Although the etiology is unknown, histopathology reveals a hydropic dilatation of the endolymphatic chambers of the cochlea and membranous labyrinth.
H. Nonorganic Hearing Loss
Functional hearing loss for purposes of secondary gain is quite frequent. This may be seen in people with normal hearing and in those who embellish an existing organic hearing loss. With skillful audiometric techniques, it is usually possible to distinguish organic from nonorganic hearing loss, but this may require referral to an audiologic center with considerable experience with this problem.
There are various indications of nonorganic hearing loss. Poor correlation between the speech reception thresholds and the average of the air conduction thresholds at 500, 1000, and 2000 Hz is the most common indication of functionality (see Figure 13–5). The speech reception thresholds are generally within 6 dB of the average of the “speech frequencies.” Excessive test-retest variability is also suggestive. In cases of suspected unilateral functional hearing loss, the Stenger test is useful. Evoked-response audiometry, otoacoustic emissions tests, or both also may be useful for objectively establishing hearing thresholds in patients unable or unwilling to cooperate with conventional testing.
NOISE-INDUCED HEARING LOSS
Etiology & Pathogenesis
Noise-induced hearing loss (NIHL) is a complex disorder probably caused by an interaction between genetic and environmental factors. NIHL results mechanically from trauma to the sensory epithelium of the cochlea and metabolically from the generation of reactive oxygen species. The sensory epithelium of the cochlea consists of one row of stereociliated inner hair cells and three rows of stereociliated outer hair cells supported by supporting cells (Hansen and Deiter cells). The most obvious injury is to the stereocilia of the inner and outer hair cells (the electromechanical transducers of sound energy), which may become distorted or even disrupted under acoustically generated shearing forces of the tectorial membrane. All structures of the organ of Corti, however, can be affected. Vascular, chemical, and metabolic changes occurring in the sensory cells cause loss of stereocilia stiffness possibly as the result of contraction of the rootlet structures that anchor the stereocilia to the cuticular plate at the top of the hair cell.
Initially the vascular, chemical, and metabolic changes are potentially reversible, and given time, the hearing will recover. This is known as a temporary threshold shift (TTS). TTS can last for several hours. However, when there is permanent loss of stereocilia with apparent fracture of the rootlet structures and destruction of the sensory cells, which are replaced by nonfunctioning scar tissue, an audiogram will show permanent threshold shift (PTS). The outer hair cells, which are important in tuning, generally are affected before the inner hair cells. A retrograde degeneration of cochlear nerve fibers occurs progressing centrally. Noise can involve other structures in the cochlea, including vascular change in the area of the metabolically active stria vascularis. Because TTS may mimic PTS, individuals should be given audiometric tests after a recovery period of 12–24 hours following exposure to hazardous levels of noise. PTS may be caused by a brief exposure to extremely high-intensity sounds, but it is caused more commonly by prolonged repetitive exposure to lower levels of hazardous noise.
Susceptibility to NIHL is rather variable. While some individuals are able to tolerate high noise exposures for prolonged periods of time with minimal hearing loss, others who are subjected to the same environment can develop considerable hearing loss. Risk of permanent hearing impairment is related to the duration and intensity of exposure (Table 13–1) and probably to genetic susceptibility.
Table 13–1. Relative intensity of common noises.
Generally, prolonged exposure to sounds louder than 85 dBA (ie, an 85-dB noise level determined by using the A scale) is potentially injurious. Although there has been no recent nationwide noise exposure survey, it is still true that millions of workers in the United States are exposed to hazardous noise that could result in hearing loss. Continuous exposure to hazardous levels of noise tends to have its maximum effect in the high-frequency regions of the cochlea. Noise-induced hearing loss is usually most severe around 4000 Hz, with downward extension toward the “speech frequencies” (500–3000 Hz) occurring only after prolonged or severe exposure. Interestingly, this tendency of noise-induced hearing loss to preferentially affect the high-frequency regions of the cochlea remains true regardless of the frequency of the injurious noise and may be related to the resonance of the ear canal.
The inner ear is partially protected from the effects of continuous noise by the acoustic reflex. This reflex, which is triggered when the ear is subjected to noise louder than 90 dB, causes the middle ear muscles (the stapedius and tensor tympani) to contract, thereby stiffening the conductive system and reducing the amount of sound that enters the inner ear (this occurs only from frequencies below about 2 kHz). Because this protective reflex is neurally mediated, it is delayed in onset for a period ranging from 25 to 150 ms, depending on the intensity of the sound. Therefore, the biologic effect of impulse noise is not as dampened as the effect of continuous noise.
Acoustic Trauma
While most noise-induced hearing loss is a result of long-term exposure, acoustic trauma, defined as a permanent threshold shift from a single exposure, may result from a brief exposure to extremely loud noise. In some cases, this may follow intense impulse noises; in other cases, it may follow a single explosion. Blast injuries from explosions can result in pressures that injure middle ear structures such as the tympanic membrane. Blast injuries not only generate impulse noise but also may injure the ear through generation of overpressures and even hot combustion products that can disrupt the tympanic membrane. Although it is less common, an acute decrease in hearing also may occur following single periods of exposure to continuous noise. For example, several hours of unprotected exposure to a jet turbine producing sounds in the 120–140 dB range may result in permanent cochlear damage.
Clinical Findings in NIHL and ARHL
Patients with NIHL and/or ARHL frequently complain of gradual deterioration in hearing. The most common complaint is difficulty in comprehending speech, especially in the presence of competing background noise. Because these patients have a high-frequency bias to their hearing loss, they hear vowel sounds better than consonant sounds. This leads to a distortion of speech sounds when they are listening to people with higher-pitched voices (eg, women and children). Background noise, which is usually low frequency in bias, masks the better-preserved portion of the hearing spectrum and further exacerbates the problems with speech comprehension.
All types of hearing loss are frequently accompanied by tinnitus. Most often patients describe a high-frequency tonal sound (ringing), but the sound is sometimes lower in tone (buzzing, blowing, or hissing) or even nontonal (popping or clicking). This sensation may be intermittent or continuous and may be exacerbated by further exposure to noise. Tinnitus is usually most bothersome to patients when there is little ambient noise present. Therefore, some patients may complain of inability to fall asleep or to concentrate when in a very quiet room.
On tuning fork examination, the patient hears air conduction better than bone conduction, which indicates a sensorineural hearing loss. Audiometric examination usually reveals a bilateral, predominantly high-frequency sensorineural hearing loss in both NIHL and ARHL; in NIHL there is usually a maximum drop of the pure-tone thresholds occurring at or around 4000 Hz on the pure-tone audiogram (see Figures 13–1 and 13–2).
The 4000-Hz notch, which frequently develops relatively early in the worker’s exposure to hazardous noise, generally will widen as further exposure continues; thus lower and higher frequencies become affected somewhat later if the exposure continues. Because the most important thresholds for comprehension of human speech are between 500 and 3000 Hz, significant conversational difficulties do not begin until frequencies of 3000 Hz and below are affected. The speech discrimination score is normal in the early stages of noise-induced hearing loss but may deteriorate as the loss becomes more severe. Because of great variability, the diagnosis of noise-induced hearing loss cannot always be eliminated or established by the shape of the audiogram.
Although the hearing loss in NIHL is bilateral, asymmetry can exist, particularly when the source of the noise is lateralized (eg, rifle or shotgun firing). Tinnitus (ringing or buzzing) may or may not be present. Tinnitus is a subjective complaint, and measurements of tinnitus are based on the patient’s ability to match the ringing in loudness and frequency. Often the tinnitus pitch is close to the frequency of the maximum hearing loss seen on the audiogram and is about 5 dB above that threshold in loudness. Tinnitus frequently is blocked out by ambient noise. Tinnitus in the absence of hearing loss is probably not related to noise exposure.
Individuals who have acoustic trauma can present with a variety of audiometric patterns. These patients frequently experience tinnitus, and a few will have symptoms of hyperacusis and, occasionally, vertigo.
Prevention
The Occupational Safety and Health Administration (OSHA) regulates exposure to noise at or above an 8-hour time-weighted average (TWA) of 85 dBA, the approximate biologic threshold above which permanent shifts in hearing are possible. Above 85-dBA TWA, OSHA requires enrolment in a hearing conservation program.
A HCP is the recognized method of preventing noise-induced hearing loss in the occupational environment. While there is a tendency to think of “hearing conservation” as the provision of audiometric tests and hearing protection, much more is required. An effective HCP integrates the following program elements:
1. Noise monitoring
2. Engineering controls
3. Administrative controls
4. Worker education
5. Selection and use of hearing-protection devices (HPDs)
6. Periodic audiometric evaluations
Record keeping is also important, and OSHA requires that NIHL be recorded on the OSHA 300 Log of Injuries and Illnesses. If an employee’s audiogram reveals a work-related standard threshold shift (10-dB shifts in hearing acuity) in one or both ears, and the employee’s total hearing level is 25 dB or more above audiometric zero (averaged at 2000, 3000, and 4000 Hz) in the same ear(s) as the STS, then the employer must record the case in Section M(5) of the OSHA 300 Log. For the purposes of injury and illness recording, this sometimes may be referred to as a recordable threshold shift. It should be noted that prior to recording a hearing loss, employers may seek the advice of a physician or other licensed health care professional to determine if the loss is work related, make adjustments for presbycusis, and perform additional hearing tests to verify the persistence of the hearing loss. HCP elements are outlined briefly below.
A. Noise Monitoring
If there is reason to believe that worker noise exposure will equal or exceed a TWA of 85 dBA, then noise monitoring is required. A sampling strategy must be designed to identify all workers who need to be included in the HCP. If there is a change in production, process, equipment, or controls that would affect workers’ exposures, noise monitoring tests should be repeated.
B. Engineering Controls
The information collected during noise monitoring (particularly octave-band analysis, which indicates the sound level at selected frequencies) may be used to design engineering noise controls. Designers conceptualize possible engineering solutions in terms of the source (what is generating the noise), the path (the route(s) the generated noise may travel), and the receivers (the workers exposed to the noise). The noise controls may involve the use of enclosures (to isolate sources or receivers), barriers (to reduce acoustic energy along the path), or distance (to increase the path and ultimately reduce the acoustic energy at the receiver) to reduce worker noise exposure. In general, engineering controls are preferred but are not always feasible because of their costs and limits in technology.
C. Administrative Controls
Administrative controls include (1) reducing the amount of time a given worker might be exposed to a noise source in order to prevent the TWA noise exposure from reaching 85 dBA and (2) establishing purchasing guidelines to prevent introduction of equipment that would increase worker noise dose. While simple in principle, the implementation of administrative controls requires management’s commitment and constant supervision, particularly in the absence of engineering or personal-protection controls. In general, administrative controls are used as an adjunct to existing HCP noise-control strategies rather than as the exclusive approach for controlling noise exposure.
D. Worker Education
Workers and management must understand the potentially harmful effects of noise in order to satisfy OSHA and, most important, to ensure that the HCP is successful in preventing noise-induced hearing loss. A good worker education program describes (1) program objectives, (2) existing noise hazards, (3) how hearing loss occurs, (4) purpose of audiometric testing, and (5) what workers can do to protect themselves. In addition, roles and responsibilities of the employer and the workers should be stated clearly. Training is required to be provided annually to all workers included in the HCP. Opportunities for maintaining awareness occur during periodic safety meetings, as well as during audiometric testing appointments when testing results are explained.
E. Hearing Protection Devices
Hearing protection devices (HPDs) are available in a variety of types from a number of manufacturers. There are three basic types of HPDs: (1) ear plugs, or aurals (premolded, formable, and custom-molded), (2) canal caps, or semiaurals (with a band that compresses each end against the entrance of the ear canal), and (3) ear muffs, or circumaurals (which surround the ear). Each of these types of devices has advantages and disadvantages that vary according to worker activity, equipment and facility noise characteristics, and the work environment (Figure 13–6). Selection of appropriate HPDs should ideally include input from the industrial hygienist, the audiologist, the occupational medicine physician, and of course, the workers who will use these devices. Although the HCP is triggered by the presence of noise levels equal to or greater than an 8-hour TWA of 85 dBA, HPDs must attenuate worker exposure to an 8-hour TWA at or below 90 dBA, the OSHA 8-hour permissible exposure level (PEL) for noise.
Figure 13–6. Comparison of the attenuation properties of a molded-type earplug and an earmuff protector. Note that the earplug offers greater attenuation of the lower frequencies, whereas the earmuff is better at the higher frequencies.
It is important to note that—where hazardous noise levels are present—HPDs must attenuate exposure to an 8-hour TWA of 85 dBA or below for employees who have experienced a standard threshold shift. This requirement also applies to employees who have not yet had baseline audiograms. In general, the use of HPDs by employees exposed to TWA noise levels of 85 dBA or greater is recommended.
F. Audiometric Evaluations
Audiometric testing provides the only quantitative means of assessing the overall effectiveness of a hearing-conservation program. A properly managed audiometric testing program supervised by a certified audiologist or physician who is trained and experienced in occupational hearing conservation will detect changes in response to environmental noise that otherwise might be overlooked. Results of audiometric testing must be shared with employees to ensure effectiveness. The overall results or trends noted in an audiometric testing program can be used to fine-tune the HCP, that is, to determine which types of HPDs to offer to employees or to identify where additional employee training is needed.
Noise Reduction Ratings & Selection of Hearing-Protection Devices
All HPDs sold in the United States are assigned a standardized value known as the noise reduction rating (NRR). Manufacturers of HPDs are required by the Environmental Protection Agency to have their products tested in order to obtain an NRR prior to placing them on the market. NRRs (listed in decibels) are based on laboratory attenuation data achieved under ideal conditions. Actual noise reduction achieved under field conditions using any HPD will be much lower than the NRR. Adjustment of the NRR is appropriate before a device is chosen for field use, as explained below.
A. Weighting-Scale Adjustment
Depending on the monitoring method used to determine noise exposure, an initial adjustment to the NRR of a selected device may be necessary. For example, if workplace noise levels are determined by using the C scale (dBC) on the monitoring instrumentation, the assigned NRR may be subtracted directly from the actual measured TWA noise levels to determine the legal “adequacy” of the device selected relative to the regulatory 90-dBA TWA exposure criterion (or for employees who either [1] have standard threshold shifts or [2] have not yet had baseline audiograms, the 85-dBA TWA exposure criterion).
If workplace noise levels are determined by using the A scale (dBA) on the monitoring instrumentation, the assigned NRR should be reduced by 7 dB before being subtracted from the actual measured TWA noise levels to determine the legal “adequacy” of the device selected relative to the 90-dBA TWA exposure criterion (or for employees who either [1] have standard threshold shifts or [2] have not yet had baseline audiograms, the 85-dBA TWA exposure criterion).
The A-scale adjustment is necessary because this scale approximates the response of the human ear to speech frequencies and discounts much of the acoustic energy from the low and high frequencies that are present in the work environment. Because the C scale is essentially flat (unweighted) across the audible frequency spectrum, all the acoustic energy present is integrated into the measurement, and no adjustment is necessary.
B. Derating
The effectiveness of HPDs depends on whether they are used properly. NRRs are obtained in the laboratory under ideal conditions and reflect the attenuation that would be achieved or exceeded by 98% of subjects in this “best-case” situation. To predict the NRR of HPDs during actual use more accurately (and conservatively), the product’s NRR should be derated. In auditing hearing conservation programs, OSHA derates the assigned NRR (after weighting-scale adjustment, if necessary) by one-half (50%) for all types of HPDs to determine the “relative performance.” As a typical example, if a device has an NRR of 29 and workplace noise measurements were made using the A scale, then OSHA’s predicted field attenuation of the device would be (29 – 7)/2 = 11 dB. Such a device would be expected to provide protection (per the legal OSHA 90-dBA PEL) where 8-hour TWA noise levels of up to 101 (90 + 11) dBA are present. As a worse-case example, failure to make an adjustment for A-scale noise measurements, along with a failure to apply a 50% derating, could lead an uninformed evaluator to falsely believe that this same HPD would provide protection in environments with 8-hour TWA noise levels of up to and including 119 (90 + 29) dBA.
The National Institute for Occupational Safety and Health (NIOSH) recommends a variable scheme for derating NRRs. For example, earmuffs are derated 25%, formable earplugs are derated 50%, and all other earplugs are derated 70%. This scheme may more accurately reflect the attenuation that can be expected for various types of HPDs under “real world” conditions. Remember that the derating of an HPD is not strictly required by OSHA, but it does provide a conservative estimate of the likely field attenuation that will be provided.
C. Combining HPDs
HPDs may be combined (ie, wearing earplugs and earmuffs) to provide more protection in high-noise environments. However, the NRRs of the combined devices are not added together to determine the total noise reduction. Under such circumstances, OSHA advises its inspectors that 5 dB is to be added after the weighting-scale adjustment is applied to the device with the higher NRR (again, OSHA does not require the 50% derating described earlier). This is a conservative approach to determining combined attenuation, and actual field attenuation (and protection) probably is higher. As a practical matter, double protection may be inadequate when TWA noise exposures exceed 105 dBA.
D. HPD Provision Versus HPD Enforcement
When 8-hour TWA noise levels are equal to or greater than 85 dBA (a 50% noise dose) but less than 90 dBA (a 100% noise dose), HPDs must be made available to the exposed workers. For 8-hour TWA noise dose levels at or above 90 dBA, however, HPDs must be provided to workers, and their proper use must be enforced by the employer (exceptions: [1] employees with standard threshold shifts must be provided with HPDs when the 8-hour TWA noise levels are equal to or greater than 85 dBA, and [2] employees who have not yet had baseline audiometric tests must be provided with HPDs). A suitable variety of HPDs must be provided. The weighting-scale adjustment of the NRR must be applied, and it is advisable to apply a derating scheme that will adjust the NRR to ensure adequate protection of the worker.
Treatment
There is no medical or surgical treatment available to reverse the effects of NIHL. After the diagnosis has been established by otologic examination and performance of an audiometric test battery, the physician should counsel the patient on the likely consequences of continued exposure to excessive noise and should recommend techniques for avoidance of further noise-induced damage. Hearing amplification is reserved for patients with socially impaired hearing.
Hearing aids must be fitted carefully to optimally meet the needs of the individual with regard to frequency bias and gain. In bilateral hearing losses, bilateral amplification usually provides more satisfactory rehabilitation. Whether or not to try hearing amplification is the patient’s decision. A reasonable criterion for referral to a professional for hearing aid evaluation is a speech reception threshold greater than 25 dB or a speech discrimination score of less than 80% when words are presented at a normal conversation level of 50 dB HL. In patients with high-frequency hearing loss and relatively normal low-frequency hearing, hearing aids generally are most helpful in those who have a significant hearing loss at 2000 Hz on the pure-tone audiogram. A borderline candidate may be an individual with normal hearing through 1500 Hz, a mild loss at 2000 Hz, and a moderate or greater loss at 3000 Hz and above.
Earlier hearing aids used analog circuitry, which had limited ability to match a patient’s audiometric configuration and to compensate for recruitment. Almost all current hearing aids use digital circuitry, which modifies incoming sound to enhance speech and reduce ambient background noise. This noise suppression allows greater gain before producing audible feedback (suppression). Digital hearing aids also allow for multiple and directional microphones. Programmable hearing aids can retain various programs to allow the user to adjust to various noise environments.
Hearing aids are also differentiated by style. The largest and most powerful and adjustable is the behind-the-ear (BTE) aid. There is also an in-the-ear (ITE) aid, an in-the-canal (ITC) aid, and a completely in-the-canal (CIC) aid. The CIC is the smallest but is harder to adjust and is the least powerful.
Before purchasing a hearing aid, the patient should have a hearing aid evaluation and a trial period with the patient wearing the hearing aids in various circumstances. A patient’s willingness to wear a hearing aid will depend on many factors, including cosmetic considerations and concerns about the ability to insert the hearing aid and to manipulate its controls. Numerous other clever instruments, known as assistive listening devices, are available to enhance comprehension in small or large groups (eg, at business meetings or conventions), with telephone use, and with various audio or visual media, such as television. Most of these devices work by wireless transmission of FM signals or infrared light beams. Aural rehabilitation classes designed to enhance the patient’s ability to comprehend speech also may be helpful and usually are available in urban areas.
There is no cure for tinnitus resulting from noise-induced hearing loss or any other cause, although numerous amelioration measures are available. In the absence of further inner ear injury, tinnitus may diminish gradually, usually over a course of weeks to months. A subtle degree of tinnitus often persists and is especially obvious when the patient is in a quiet room. For the few patients who find this to be extremely troublesome, sound therapy, in which music or other sounds are presented, is often helpful. In patients with significant hearing loss, the most successful treatment may be appropriate hearing amplification. Modified hearing aids (tinnitus maskers) designed to produce masking noises generally have been of limited success. Use of biofeedback or counseling (eg, cognitive-behavioral therapy) has helped some patients suppress their tinnitus. Sound therapy and counseling are often combined in programs such as “tinnitus retraining therapy.” Psychiatric referral to manage associated depression sometimes is necessary.
Prognosis
Hearing in patients with NIHL will stabilize if the patient is removed from the noxious stimulus. If it does not stabilize, hearing will continue to deteriorate, ultimately resulting in severe high-frequency hearing impairment. Although adequate hearing protection is essential and always should be recommended, other factors also may play a role in the patient’s prognosis. ARHL will add to the noise-induced loss as the patient grows older.
Future Therapies
In the mammalian auditory system, hair cell loss resulting from aging, ototoxic drugs, infections, noise, and other causes is irreversible and leads to permanent sensorineural hearing loss. To restore hearing, it is necessary to generate new functional hair cells. The advent of new approaches such as gene therapy, neural stem cell and embryonic stem cell transplantation, and genomics may lead to methods for inducing hair cell regeneration and repair in the mammalian cochlear and vestibular systems.
HEARING LOSS CAUSED BY PHYSICAL TRAUMA
Etiology & Pathogenesis
A broad spectrum of injuries may cause trauma to the ears. Blunt head injury is by far the most common cause of traumatic hearing loss. A blow to the head creates a pressure wave in the skull that is transmitted through bone in a manner similar to the way a pressure wave in air is carried by the conducting mechanism of the ear. The cochlear injury observed following blunt head trauma closely resembles both histologically and audiologically that which is induced by high-intensity acoustic trauma. Motor vehicle accidents are the major cause of blunt head trauma and account for about 50% of temporal bone injuries. Penetrating injuries of the temporal bone are relatively rare, accounting for fewer than 10% of cases. Other occupational causes of ear injury include falls, explosions, and burns from caustic chemicals, open flames, or welder’s slag that enters the ear canal.
Examination & Treatment
In the conscious patient, hearing should be assessed immediately with a 512-Hz tuning fork. Even in an ear severely traumatized and filled with blood, sound will lateralize toward a conductive hearing loss and away from a sensorineural one. Complete audiometric examinations (see the section “Evaluation of Hearing”) can be performed after the patient has been stabilized. Patients also should be checked for signs of vestibular injury (nystagmus) and facial nerve trauma (paralysis).
A. Injuries Causing Conductive Hearing Loss
1. Blunt head trauma with or without temporal bone fracture may cause hematotympanum—a collection of blood in the middle ear. If this is the sole injury, hearing usually recovers over several weeks. Blunt head trauma on rare occasion may result in separation of the bones of the middle ear (ossicular chain disruption).
2. Burns sustained when a piece of welder’s slag penetrates the eardrum often heal poorly, and chronic infection often results.
3. Barotrauma can result in a conductive hearing loss with fluid or blood behind the tympanic membrane. This is generally transitory and resolves in a few days to a few weeks.
4. Traumatic membrane perforations usually heal spontaneously if secondary infection does not develop (patients should be instructed not to get the ear wet during the healing period), although hearing loss may persist.
Conductive hearing loss that persists more than 3 months after injury is usually the result of a tympanic membrane perforation or disruption of the ossicular chain (see Figure 13–4). These lesions are suitable for surgical repair, usually on a delayed basis. Repair is by grafting the tympanic membrane or by reconstructing the ossicular chain with homograft or prosthetic materials or both.
B. Injuries Causing Sensorineural Hearing Loss
Trauma to the inner ear results most commonly from blunt head injury. Labyrinthine concussion frequently occurs with transient vertigo, potentially permanent hearing loss, and tinnitus. Treatment is expectant, with vestibular suppressants such as meclizine offering symptomatic relief of vertigo.
Trauma also may cause rupture of the round or oval window membranes, which can lead to leakage of inner ear fluids into the middle ear (perilymph fistula). Most perilymphatic fistulas heal spontaneously. Persistent perilymphatic leakage is difficult to diagnose and requires surgical treatment, with autogenous material used to repair the defect. Most patients with surgically confirmed fistulas suffer recurrent episodes of vertigo and hearing loss, often temporally related to vigorous physical exercise.
C. Injuries Causing Mixed Conductive and Sensorineural Hearing Loss
Temporal bone injuries sometimes involve both the middle and inner ear, resulting in mixed, conductive, and sensorineural hearing loss. Fractures of the temporal bone tend to occur along lines that connect points of weakness in the skull base. Clinically, these fractures may be divided into two patterns: longitudinal and transverse. Longitudinal fractures are much more common (80% of cases) and usually result from a blow to the lateral aspect of the head. They frequently involve the structures of the middle ear but characteristically spare the inner ear, resulting in a conductive or mixed hearing loss. Transverse fractures are less common (20% of cases) and usually result from a severe occipital blow. Serious intracranial injury frequently accompanies transverse fractures. Typically, they traverse the inner ear and cause total sensorineural hearing loss and labyrinthine death. Fractures through the inner ear often are accompanied by severe vertigo that lasts for weeks or even months.
Temporal bone fractures are recognized clinically by the presence of blood, cerebrospinal fluid, or both in the ear canal or by the presence of blood in the middle ear behind an intact tympanic membrane. The ear canal should be cleaned carefully, using sterile suction to assess the integrity of the tympanic membrane. Under no circumstances should a recently traumatized ear be irrigated. Battle sign (ecchymosis over the mastoid region) is seen occasionally. Definitive diagnosis requires high-resolution CT scanning to demonstrate the fracture lines.
OTOTOXIC HEARING LOSS
Etiology & Pathogenesis
Ototoxic hearing loss is the result of exposure to chemical substances that injure the cochlea. Most ototoxins injure hair cells either directly or through disruption of cochlear homeostatic mechanisms. In the vast majority of cases, ototoxic hearing loss stems from the use of medications such as aminoglycoside antibiotics (eg, neomycin), platinum-containing antineoplastic agents (eg, cisplatin), loop diuretics (eg, furosemide), and salicylates (eg, aspirin). The latter two classes of drugs cause only temporary hearing loss that resolves when the drug is stopped.
In industries with noisy work environments, workers who are being treated with potentially ototoxic medications may be at increased risk for hearing loss because the combination of some ototoxic drug treatments and noise trauma can lead to a greater degree of hearing loss than either would produce by itself. Aspirin, however, is probably not associated with an increased likelihood of NIHL.
Hearing loss also may result from exposure to ototoxic substances in the workplace. Heavy metals, including arsenic, cobalt, lead, lithium, mercury, and thorium, have been reported to have ototoxic potential. Other chemicals that may be ototoxic include cyanide, benzene, aniline dyes, iodine, chlorophenothane, dimethyl sulfoxide, dinitrophenol, propylene glycol, methylmercury, potassium bromate, carbon disulfide, carbon monoxide, carbon tetrachloride, and industrial solvents such as styrene and toluene.
Prevention
Medicinal ototoxins should be administered in the lowest dose compatible with therapeutic efficacy. Serum peak and trough levels of aminoglycosides should be monitored to reduce the risk of excessive dosages. Simultaneous administration of multiple ototoxic drugs should be avoided when possible to minimize synergistic effects. Persons with preexisting sensory hearing loss and compromised renal or hepatic function are at substantially increased risk. Identification of those at heightened risk of ototoxic hearing loss is important to avoid this complication. Audiometric evaluation is appropriate to identify and monitor ototoxic exposure.
MEDICOLEGAL ISSUES
Calculation of Binaural Hearing Impairment
Only one method for calculating the severity of hearing loss is in widespread use. The current method developed by the American Academy of Otolaryngology and Head and Neck Surgery (AAO-HNS) is as follows: (1) The average hearing threshold level at 500, 1000, 2000, and 3000 Hz is calculated for each ear. (2) The percentage of the impairment for each ear (the monaural loss) is calculated by multiplying the amount by which the preceding average exceeds 25 dBA (low fence) by 1.5, up to a maximum of 100%, which is reached at 92 dBA (high fence). (3) The hearing handicap (binaural assessment) then should be calculated by multiplying the smaller percentage (better ear) by 5, adding this figure to the larger percentage (poorer ear), and dividing the total by 6.
The AMA Guides to the Evaluation of Permanent Impairment (6th edition) describe identical calculations for rating a “binaural hearing impairment” (BHI) percentage as the AAO-HNS. In addition, the AMA Guides allow adding up to 5% for tinnitus if the tinnitus impacts the ability to perform activities of daily living. The AMA method of estimating BHI has been validated against patient’s self-report of hearing disability and is used in most state and federal workers compensation programs.
For the preceding calculations to be valid, the audiometer employed must be checked daily and calibrated periodically by an independent agency. The booth used for testing must meet the standards of background noise levels established by the American National Standards Institute (ANSI) in 1977.
A note of caution is needed regarding the calculation of percentage of hearing loss based on older audiograms. Different standards for the measurement of hearing were in use prior to establishment of the current standard by the ANSI in 1969. From 1964 to 1969, the standard of the International Standards Organization (ISO) was widely used; this is essentially the same as the current ANSI standard, and no conversion is needed. However, from 1951 to 1964, and in some cases up through 1969, the standard of the American Standards Association (ASA) was used, and audiograms obtained in this period require conversion for use in the preceding formula. To convert an audiogram from the ASA to the ANSI standard, add 14 dB at 500 Hz, 10 dB at 1000 Hz, 8.5 dB at 2000 Hz, 8.5 dB at 3000 Hz, 6 dB at 4000 Hz, and 9.5 dB at 6000 Hz. In cases where the 3000-Hz threshold was not measured, the average of 2000 and 4000 Hz may be substituted.
Assessment of Impairment
As indicated previously, the normal range of speech reception threshold is between 0 and 20 dB, with losses of 25–40 dB termed mild, 40–55 dB termed moderate, 55–70 termed moderately severe, 70–90 dB termed severe, and greater than 90 dB termed profound. Of course, the extent of disability suffered by the patient depends on many psychological, social, and work-related factors. Assessment of an individual’s fitness to work requires knowledge about the various duties performed by that individual. Some typical work-related issues for consideration include the amount of communication with coworkers and others that is required on the job, the type of communication (eg, in person or via the telephone), and the need to hear alerting signals or emergency warning alarms.
To meet the Social Security Administration’s guidelines for total disability as a result of hearing impairment, an individual must have either (1) an average hearing threshold of 90 dB or greater for the better hearing ear, based on both air and bone conduction at 500, 1000, and 2000 Hz or (2) a speech discrimination score of 40% or less in the better-hearing ear. In both cases, hearing must not be restorable by hearing amplification devices.
Compensation for Occupational Hearing Loss
There is no national surveillance or injury reporting system for hearing loss. As such, comprehensive data on the economic impact of hearing loss are not available. The U.S. Department of Labor (DOL) reports that the average settlement a government worker receives for hearing loss is about $6000. This is considerably larger than the average settlement received by workers under state workers’ compensation programs. The DOL treats aggravated or accelerated hearing losses in the same manner as losses entirely precipitated or proximally caused by the patient’s employment. In other words, the amount of preemployment hearing loss is not subtracted when the percentage of loss is calculated. In contrast, local and state government regulations frequently take into account the level of preexisting hearing loss and some use formulas to correct for the anticipated progression of ARHL when calculating compensation awards.
The relationship between NIHL and ARHL is complex. Many studies have tried to address the issue of the aging worker who has been exposed to hazardous noise for a long period of time. The most widely held opinion is that ARHL and NIHL are essentially additive.
REFERENCES
CDC: Workplace Safety and Health Topics. Noise and Hearing Loss Prevention. http://www.cdc.gov/niosh/topics/noise/.
Marlenga B: Determinants of early-stage hearing loss among a cohort of young workers with 16-year follow-up. Occup Environ Med 2012;69:479 [PMID: 22447644].
Thurston FE: The worker’s ear: a history of noise-induced hearing loss. Am J Ind Med 2013. 56:367. [PMID: 22821731].
Tufts JB: Auditory fitness for duty. J Am Acad Audiol 2009;20:539 [PMID: 19902702].
SELF-ASSESSMENT QUESTIONS
Select the one correct answer to each question.
Question 1: In a clinical audiogram
a. sensitivity to pure tones is measured for air conduction using a bone oscillator
b. thresholds are expressed in decibels, with the normal range (for young adults) at each frequency from 0 to 40 dB HL
c. when either air or bone conduction is decreased, a sensorineural hearing loss exists
d. conductive losses are indicated by an “air-bone gap,” in which the air-conduction threshold exceeds the bone-conduction threshold
Question 2: Speech reception threshold (SRT)
a. is the intensity (in decibels) at which the listener is able to repeat all of balanced two-syllable words known as spondee words
b. is usually not in close agreement with an average of the pure-tone thresholds for frequencies between 500 and 2000 Hz
c. has a normal range for young adults between 0 and 20 dB
d. of greater than 50 dB is termed profound hearing loss
Question 3: The hearing in noise test (HINT)
a. measures speech intelligibility but does not incorporate background noise
b. uses more realistic speech than conventional speech tests (sentences rather than isolated words)
c. is not used to test government employees
d. simulates specific occupational hearing situations
Question 4: Age-related hearing loss (ARHL)
a. is a rapid and progressive deterioration of hearing associated with aging
b. should be distinguished from what is called presbycusis
c. is seldom associated with other inner ear pathologies
d. has a large genetic component; heritability is close to 50%
Question 5: Idiopathic sudden sensorineural hearing loss (ISSHL)
a. usually develops within 24 hours, in the absence of precipitating factors
b. is almost always bilateral
c. seldom has partial or total spontaneous recovery
d. when accompanied by vertigo, has a better prognosis
Question 6: Noise-induced hearing loss (NIHL)
a. results mechanically from trauma to the sensory epithelium of the cochlea and metabolically from the generation of reactive oxygen species
b. is not related to the duration and intensity of exposure
c. is first measured around 500–3000 Hz
d. is usually most severe around 8000 Hz
Question 7: The acoustic reflex
a. fully protects the inner ear from the effects of continuous noise
b. is triggered when the ear is subjected to noise louder than 30 dB
c. increases the amount of sound that enters the inner ear
d. is delayed in onset depending on the intensity of the sound
Question 8: The Occupational Safety and Health Administration (OSHA)
a. regulates exposure to noise at or above an 8-hour time-weighted average (TWA) of 85 dBA
b. requires enrolment in a hearing conservation program for noise above 50-dBA TWA
c. has no jurisdiction over private company employees
d. provides a national surveillance reporting system for hearing loss
Question 9: Hearing protective devices
a. must be made available to the exposed workers when 8-hour TWA noise levels are equal to or greater than 85 dBA (a 50% noise dose) but below 90 dBA (a 100% noise dose)
b. must be provided by OSHA or state agencies to all exposed workers
c. must be provided to employees with any standard threshold shifts
d. must be provided to employees who have not yet had baseline audiometric tests
Question 10: Ototoxic hearing loss
a. is the result of exposure to chemical substances that injure the cochlea
b. does not result from the use of medications
c. does not result from exposure to heavy metals
d. is readily reversible with chelating agents