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Occup. Med. Vol. 50, No. 7, pp. 492-495, 2000
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IN-DEPTH REVIEW
What: are the causes, prevention and
treatment of hearing loss in the
ageing worker?
J. Irwin
Ninewells Hospital, Dundee, UK
Hearing loss is more common in the ageing population as compared to young adults.
Individuals are not protected from other causes of hearing loss just because they are in
work. Their hearing may therefore be at risk from causes not related to their occupation.
Some factors may be synergistically linked to noise exposure, thus increasing the effect
of noise on hearing. Although some traumatic and infective causes of hearing loss are
amenable to treatment, most occupational hearing loss is not curable once present and
rehabilitative measures are the only option. General health and safety measures must
be maintained throughout a worker's employment whatever their age.
Key words: Elderly; occupational hearing loss; prevention; treatment.
Occup. Med. Vol. 50, 492-495, 2000
INTRODUCTION: CAUSES
The causes of hearing loss in adults are legion1'2 and
obviously workers are not immune from non-occupational causes. There is evidence that some illnesses and
their treatments can affect the way in which the ear
responds to potentially damaging noise trauma. Occupational noise exposure will be considered later but there
are other aspects of the workplace that may affect the
ears. Single or multiple episodes of trauma such as skull
fracture, direct trauma to the ear, blast injury or
barotrauma may affect the middle and/or inner ear.
The ageing worker may, in some cases, be more
vulnerable to accidents because of slowed reaction time,
poor vision, balance or mobility. High quality and wellmaintained general health and safety measures need to be
in place and monitored to try to minimize the risk of
accident.
Working in hot and dusty environments may predispose some employees to otitis externa but ageing
individuals are no more at risk than their younger
counterparts unless there is some predisposing factor
such as diabetes, which is commoner in older people.
Occupational noise induced hearing loss has been
recognized for hundreds of years and preventative
measures have been used for almost as long. For the
purposes of this article the natural history of this
condition is interesting. Objective studies have only been
possible since the introduction of pure tone audiome-
Correspondence to: Dr John Irwin, Area 4, Ninewells Hospital, Dundee
DD1 9SY, UK. Tel: +44 (0)1382 633867; e-mail: [email protected]
try.3'4 Initially these were all cross-sectional studies, the
progression of hearing loss was estimated by comparing
subjects of different ages and length of noise exposure.
Burns5 described how the initial effects of noise exposure
are seen between 3 kHz and 6 kHz, often at 4 kHz. With
time, the dip in hearing around 4 kHz deepens to a
maximum and then stops. The thresholds at adjacent
frequencies then become involved. Alberti6 also gave a
good account of the progression of this condition. The
hearing loss at 3 kHz and 4 kHz appears to progress at a
steady rate for the first 10 years of exposure but then the
rate of progression slows very quickly with little change
thereafter. At the other extreme it may take up to 30
years for the 1 kHz threshold to become involved to any
great extent but the rate of progress is then rapid. At
2 kHz the most rapid change in threshold occurs
between 25 and 35 years. There does seem to be
individual variation and there is* a 30 dB difference in
threshold at 2 kHz between the 25th and 75th quartiles
after 30 years of exposure.
The combined effects of noise and age have interested
researchers: are the two individual effects simply additive
or is there a more complicated interaction? The general
consensus seems to have been that there is, at worst, a
simple additive interaction and, at best, there is no
interaction.6"8 Long-term longitudinal studies following
up the same subjects have only been possible recently.
These suggest that by the age of 70 years the effects of
occupational noise exposure and other acoustic trauma
are no longer evident.9'10 This statement also applied to
the quartile that demonstrated the greatest effect of noise
on hearing (50-60 years) in Hinchliffe's work.10 This
means that noise may not cause any additional long term
hearing loss. The average exposed individual has a
J. Irwin: Hearing loss in the ageing worker
hearing loss, which occurs at an earlier age than for an
average non-exposed individual, but eventually there
may well be no difference between the two.
However, hearing loss due entirely to the ageing
process—presbyacusis—is not as common as generally
thought. If older people with hearing loss are properly
evaluated, as few as 7-15% are found to have no known
cause11'12 and if the aetiology is known, prevention may
be possible. It may also be possible to prevent some of
the hearing loss that is age related. This means that
occupational factors may be the only cause of an
individual's hearing loss and that protective measures
should be maintained.
Is there any synergism between ototraumatic agents?
This is well reviewed by Alberti6 who states that there is
probably a slight synergy between aminoglycosides at
high doses and very loud noises, but if workers are ill
enough to be on aminoglycosides they are unlikely to be
at work! There is probably no effect from loop diuretics
or salicylates. There is, however, a probable slight
synergistic effect between vibration and noise. Morata
et a/.13 have recently shown that exposure to noise at
what is currently 'safe' levels can be damaging if the
worker is also exposed to organic solvents.
Other recent articles on the aetiology of hearing loss in
old age have highlighted the importance of other easily
screened for and potentially preventable causes of
hearing loss. Brandt et al.i4 found a significant relationship between systolic blood pressure and hearing loss in
older subjects. Browning et al} found a similar relationship between plasma viscosity and sensorineural hearing
loss. Of more interest is the role of mitochondrial DNA
(mtDNA) mutation in sensorineural hearing loss. Ueda
et al}6 have studied mtDNA4977 deletions and found a
higher incidence in those subjects with hearing loss. This
suggests that these cases might be classified as mitochondrial oxidative phosphorylation diseases. This could
open the way to new treatment methods.
PREVENTION
Standard noise exposure reduction starts with education
and includes recreational as well as occupational noise
exposure.17 Despite legislation, it is not always possible
to persuade workers to use the protection provided. The
technique of positive practice overcorrection has been
shown to improve user rates, at least in military
personnel.18 Design of quieter machinery and provision
of comfortable but effective protection are also essential.
These aspects are well known to the readership of this
journal and will not be further discussed.
There are other potential means of preventing hearing
loss due both to noise exposure and ageing. This is an
exciting and potentially very fruitful area of current
research. The exact mechanism of noise induced
cochlear damage is being investigated and has been well
reviewed by Prasher.19 Glutamate is an excitatory amino
acid used as a neurotransmitter in the inner hair cells.
Excess noise stimulation leads to an excess of glutamate,
which can cause damage to primary auditory dendrites.
493
Application of kynurate (a glutamate antagonist) has so
far been shown to limit noise damage in guinea pigs. The
synaptic damage caused by excitotoxic glutamate release
is mediated by a-amino-3-hydroxy-5-methyl-4-isoxazole
proprionic acid (AMPA) and kainate receptors and the
repair mechanism involves N-methyl-D-aspartate
(NMDA) receptors. Nitric oxide (NO) is one of the
molecules involved in cell death following NMDAmediated excitotoxic damage in the central nervous
system and may be involved in the cochlea. Blockage of
NO synthesis in the cochlea could prevent damage from
loud noise exposure.
Oxygen free-radicals have also been implicated in
noise damage. These are released in the hair cells after
intense noise exposure and are converted to highly
destructive hydroxyl radicals in the stria vascularis.
Antioxidants have been shown to prevent TTS after
noise exposure. Agents used include allopurinol, lazaroids, a-D-tocopherol and mannitol (see Prasher19).
These are all well known and in current use, which
could speed up their clinical introduction.
Noise exposure leads to an increase in energy
consumption in the cochlea. This increase is dependent
on magnesium and calcium metabolism and, in particular, damage is worse if magnesium is depleted.
Magnesium supplementation has been shown to protect
against impact noise (from gunfire) in army personnel.
This work has been published by the same group in at
least three different sources. 20 " 22 Calcium channel
blockers, however, seem to have no effect.23'24
Low level exposure to an acoustic stimulus prior to
potentially damaging noise exposure - sound conditioning-seems to toughen the ear and reduce the noise
induced hearing loss.25 This seems to be due to a boost
in the endogenous antioxidant systems. Sound toughening25 is intermittent pre-exposure to sound levels that
cause TTS. This also seems to protect against permanent hearing loss but the mechanism is unknown. Sound
conditioning is a simple process and its widespread
introduction could prove very interesting.
Glial-derived neurotrophic factors (GDNF) have
been applied directly to the inner ear to prevent noise
damage. Brain-derived neurotrophic factors and neurotrophin-3 provide dose-dependent protection against
noise induced hearing loss. Research is exploring the
use of viral vectors for gene introduction of these agents
into the cochlea before noise exposure (see references 19
and 26).
TREATMENT
Outer and middle ear problems are at least theoretically
amenable to curative therapy. Occupationally induced
otitis externa may be difficult to manage if allergic factors
are involved, as repeated exposure will lead to repeated
infection. Barriers and removal from the antigen may be
necessary. Most traumatic perforations heal spontaneously but myringoplasty may be necessary. The
possibility of middle ear reconstruction after trauma is
best assessed by an experienced otologist.
494
Occup. Med. Vol. 50, 2000
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CONCLUSION
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1993; 19: 245-254.
Estimates suggest that a total of 600 million people work
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related to age-associated hearing loss in the speech
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16. Ueda N, Oshima T, Ikeda K, Aoki M, Takasaka T.
ageing will have been protected and have no noiseMitochondrial DNA deletion is a predisposing cause for
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AmJOtolatyngol 1994; 15: 26-32.
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Sensorineural problems are not yet curable but
research into auditory hair cell regeneration is in
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experiments in rats and guinea pigs using retinoic acid,
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have proved effective in improving cochleas damaged by
ototoxic medication.27 This may lead to intra-cochlear
application to treat damage after it has occurred.
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rehabilitative rather than curative. This involves amplification in the form of hearing and other aids where
needed and should address all of the communication and
psychological difficulties caused by the hearing impairment. 28 " 30 This is best dealt with by experts in the field,
such as audiological physicians.
J. Irwin: Hearing loss in the ageing worker
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