Timothy C. Hain, MD Page last modified: February 16, 2014
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Noise is a common cause of hearing loss in the US. Twenty-five percent of the US work force is regularly exposed to potentially damaging noise (Suter and von Gierke, 1987). Because of occupational risk of noise induced hearing loss, there are government standards regulating allowable noise exposure. People working before the mid 1960's may have been exposed to higher levels of noise where there were no laws in the USA mandating use of devices to protect hearing. An example of an audiogram showing noise induced hearing loss is shown below. There is a clear "notch" at 3000 hz, with better hearing at both lower and higher frequencies. NIHL is usually slightly worse on the left side, possibly due to less efficient protective reflexes (Nageris et al, 2007).
|Example audiogram showing noise induced notch.||Another example of a noise notch (between 2K and 6K).|
Noise notches often have a corresponding notch in the sweep OAE.
|Notch in OAE corresponding to notch in hearing (on figure above, R). On this figure, the "strength" of the OAE response is proportional to the vertical distance between the red and black lines above. There is no distance at all between about 3000 and 4500 Hz -- the same place as the hearing notch. There is also no OAE at high frequencies. This is a common pattern in persons who have experienced noise induced hearing loss.|
Noise can also cause a reversible hearing loss, called a temporary threshold shift (TTS). This typically occurs in individuals who are exposed to gunfire or firecrackers, and hear ringing in their ears after the event (tinnitus). TTS can be caused by listening to ordinary digital music devices at volumes that are not especially high -- e.g. 100 dB (Le Prell et al, 2012). Sound pressure levels can routinely reach levels of 126 db (Breinbauer et al, 2012). Non-occupational noise are also regularly encountered during recreational activities and are a source of premature hearing reduction. Peak noise levels, in DB, are provided in the following table taken from Smith et al, 1999).
A more dramatic illustration of loudness can be found on the AAO site, by clicking here.
Motorcycle riding is an example of an activity that is associated with hearing loss. Temporary threshold shifts occur after a run of 1 hour at 80 mph. The greatest TTS was repoted to occur at 1KHz, with a mean loss of 10.3 Db (McCombe et al, 1995). Hearing in motorcyclists has been reported to be worse than age-matched controls, with the most marked changes at 0.5 to 1 Khz (i.e. lower frequencies).
Airbag deployment and Blast injury.
Airbag deployment in auto accidents is a potential source for noise induced hearing loss or tinnitus. (McFeely, Bojrab et al. 1999; Price and Kalb 1999; Yaremchuk and Dobie 2001). This is a type of "impulse noise", similar to a fire-cracker or explosion. The intensity of an airbag noise is high -- about 160-180 dB. There can be a 10dB difference between ears due to the head shadow effect. Presumably there is a bigger difference when the airbag deployment is very close to one ear. We have not yet encountered a patient with a PLF post airbag deployment, but as airbags can cause TM perforations, this seems possible.
There is an obvious similarity between airbag and blast injuries. The main difference is that the impulse in blast injuries can be louder, and perforations are more common. Damage to the hair cells, and possibly also spiral ganglion neurons is the main source of hearing disturbance in experimental models (Cho et al, 2013).
Axelsson et al (1981) studied the effect of listening to loud music in 538 teenagers at vocational schools. Hearing loss correlated with family history of hearing loss.
It has long been realized that hearing aids and hearing assistive devices are potential sources of noise induced hearing injury. At this writing, while the possibility is there, evidence suggests that this is not a significant problem for hearing aids. See the hearing aid page for more on this topic. We find the argument that hearing aids do not cause hearing loss very suspicious, as we do not see why hearing loss should be a consequence of recreational listening, but not due to hearing aids which are even more highly powered devices. Our thought is that any loud device can cause hearing loss, whether it is sold by an audiologist or bought to use as a musical reproduction device.
Hearing loss and tinnitus (usually temporary), can also be associated with high doses of aspirin or other ototoxic drugs such as the nonsteroidal anti-inflammatory drugs.
Race -- according to Jerger et al (1986), who tested 28 firefighters exposed to high levels of ambulance siren noise. They found that whites are more susceptible to noise than blacks.
Musical instruments can generate considerable sound and thus can also cause hearing loss. The most damaging type of sounds is in the high-frequencies. Violins and violas can be sufficiently loud to cause permanent hearing loss. This is typically worse in the left ear which is nearer the instrument. Unlike other instruments, the ability to hear the high-frequency harmonics is crucial to these musicians. Mutes can be used while practicing to reduce long term exposure.
There are a number of strategies that can be used to reduce the change of noise injury from other instrumentalists. Musicians ear plugs are generally "flat" so that bass and treble notes are not relatively favored, thus distorting perception. Nevertheless, a"vented" ear plug can be used to tune the ear cavity to low frequencies, which are less damaging. Drummers should use musicians ear plugs, such as the ER-25. Guitarists and vocalists can use the less attenuating ER-15. Too much ear protection can result in overplaying and not enough protection can result in hearing loss.
Plexiglass baffles can be used to reduce the noise from other instruments.These are particularly relevent for drummer's high-hat cymbals. Drums and brass can be particularly a problem. Ear monitors are small in-the-ear devices that look like hearing aids, that can be used to electronically protect hearing, while allowing the musicians to hear themselves. Acoustic monitors are stethescope like devices that block sound from other in the group, but allow the instrumentalist to hear their own instrument.
Loudspeakers produce both high and low frequency sounds. High frequencies tend to emanate in almost a straight line, while low frequencies are present in nearly all directions. Thus, standing besides a high-frequency source may provide some protection. Humming just prior to, and through a loud noise such as a cymbal crash or rim shot may provide some protection. Small protective muscles in the ear contract naturally when we sing or hum, and thus humming may protect from other noises.
Strategies that reduce the loudness of sound to the ear reduce the chance of damage. As people routinely increase the volume of what they are hearing when there is outside noise, one strategy that can help is simply to use devices that reduce outside noise such as "ear bud" earphones or supra-aural earphones (Breinbauer et al, 2012).
(Most of this material comes from two articles by Chasin M, 2000. According to his articles, Mr. Chasin has published a book entitled "musicians and the prevention of hearing loss", which is available from Singular Publishing group, San Diego).
Unlike the situation with hearing, noise is not generally recognized as a common cause of dizziness or vestibular disturbances. This likely results from the difference in "tuning" between the hair cells of the cochlea and the vestibular labyrinth -- cochlear hair cells are "tuned" to respond to frequencies between about 20 and 20,000 hz, while vestibular hair cells are "tuned" to respond to input between 0 and 10 hz. Nevertheless, there are several contexts in which noise can cause vestibular damage.
Goltz and associates (2001) reported on 258 military subjects who had been heavily exposed to noise. They found that vestibular damage caused by intense noise exposure might be expressed clinically in subjects with asymmetrical hearing loss. There was a strong correlation between the subjects' complaints and the results of the vestibular function tests. There was no correlation between the severity of the hearing loss and the vestibular symptomatology and pathology. They concluded that subjects exposed to intense noise may have evidence of vestibular pathology only when there is an asymmetrical hearing loss. Whenever hearing loss is symmetrical, an equal damage to the vestibular system of both ears is most probably responsible for the absence of abnormal findings on the vestibular function tests The results of this study have important medicolegal implications for individuals exposed to intense noises.
Oosterveld and others (1982) carried out an extensive vestibular examination in a group of 29 noise-exposed technicians. A spontaneous nystagmus was found in 18 persons, and 24 had a positional nystagmus exceeding a velocity of the slow phase of 5 degrees/s in three or more positions. In 17 subjects a cervical nystagmus could be provoked, while a nystagmus preponderance of more than 20% in the rotation test was found in seven persons. A difference in excitability between the labyrinths of more than 20% was shown by seven subjects. None of the subjects showed pathology in the tests for central vestibular disorders. s. No correlation was found between the grade of the hearing loss and the vestibular function disturbance. This can be explained in terms of the adaptive properties of the vestibular system. All subjects showed pathology in one or more of the vestibular tests. The medico-legal aspects of vestibular involvement in noise-induced hearing loss can be of some importance. Hearing loss itself does not affect work capability directly; however, a vestibular disorder might well do so. In consequence, noise-exposed individuals could be disabled because of vertigo or balance disorder--an important and perhaps neglected aspect of noise-induced hearing damage. PMID: 6984349 [PubMed - indexed for MEDLINE]
Manabe and others (1995) reported results in Thirty-six NIHL patients were divided into two groups according to the presence (vertigo group) or absence (non-vertigo group) of vestibular complaints. Electrocochleograms were recorded from all subjects after pure tone audiometry. A higher incidence of increased -summating potential (SP)/action potential (AP) ratio was observed in the vertigo group than in the non-vertigo group. Caloric tests were performed in the vertigo group, and a reduced response was observed in 47.1% of ears. It is generally considered that the -SP/AP ratio is a useful indicator of endolymphatic hydrops. Therefore, episodic vertigo in NIHL patients may result from a pathophysiological mechanism similar to that of Meniere's disease.
Shupak and others (1994) evaluated vestibular function in a group of subjects with documented NIHL, employing electronystagmography (ENG) and the smooth harmonic acceleration (SHA) test. Subjects were 22 men suffering from NIHL and 21 matched controls. Significantly lower vestibulo-ocular reflex gain (p = 0.05), and a tendency towards decreased caloric responses were found in the study group. No differences in the incidence of vertigo symptoms, spontaneous, positional and positioning nystagmus, directional preponderance and canal paresis in the ENG, or the SHA test phase and asymmetry parameters were observed between the groups. These results demonstrated a symmetrical centrally compensated decrease in the vestibular end organ response which is associated with the symmetrical hearing loss measured in the study group. Statistically significant correlations were found between the average hearing loss, the decrement in the average vestibulo-ocular reflex gain (p = 0.01), and ENG caloric lateralization (p = 0.02). These correlations might indicate a single mechanism for both cochlear and vestibular noise-induced injury. The results imply subclinical, well compensated malfunction of the vestibular system associated with NIHL.
Likoski et al (1988) reported results in sixty patients with varying degrees of noise-induced hearing loss (NIHL) after long-term exposure to intense impulse noise from firearms, but without manifest clinical symptoms of vestibular pathology, were tested for body sway using a stable platform. The results were compared with those from 115 healthy referents examined in the same way. Subjects with NIHL showed significantly more body sway, estimated as movement of the centre of gravity in the horizontal plane, than did the referents. Subjects with more severe NIHL showed more sway than subjects with milder acoustic trauma. The results show that body sway is increased in patients with NIHL from exposure to impulse noise of high intensity in a way suggesting an exposure-effect relationship. This suggests subclinical disturbances of the vestibular system in these patients.
Aantaa et al (1977) reported findings in 49 male workers, mean age 30 years, who had been working in conditions of extreme noise and vibration for between 6 months and 10 years. Vestibular disturbances could be shown (in the form of spontaneous nystagmus, lowered caloric excitability, or pathology in rotatory tests) in as high as 44.9%. The lesions were believed to have arisen in the peripheral vestibular organ as a consequence of the low frequency vibration.
Excessively loud noise can also induce perilymph fistulae and cause Meniere's disease to worsen.
Airbag and blast references:
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