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DEFINITION
Reduction in auditory acuity associated with noise
exposure.
Typical NIHL is of a sensorineural type
Involves injury to the inner ear.
Usually bilateral and symmetrical.
affects the higher frequencies (3k, 4k or 6k Hz)
and then spreading to the lower frequencies (0.5k,
1k or 2k Hz).
TYPES
Temporary described as Temporary Threshold Shift
(TTS), or
Permanent described as Permanent Threshold
Shift (PTS)
Acoustic trauma where a single exposure to an
intense sound leads to an immediate hearing loss.
INCIDENCE
About 10% of the world population work in
hazardous levels of noise
Worldwide, 16% of the disabling hearing loss in
adults is attributed to occupational noise, ranging
from 7 to 21% in the various subregions.
NIHL is the second most common form of acquired
hearing loss after age-related loss (presbyacusis),
with studies showing that people who are exposed
to noise levels higher than 85 db suffered from
NIHL
Its one of the most common military occupational
disabilities
In India, occupational permissible exposure limit for
8 h time weighted average is 90 dBA
Major industries responsible for excessive noise
and exposing workers to hazardous levels of noise
are textile, printing, saw mills, mining, etc.
Male preponderance
PATHOPHYSIOLOGY
Metabolic
Structural
METABOLIC
Acoustic overstimulation
Excessive neurotransmitter release
Transduction
Stimulation with sound of moderate intensity
increases cochlear blood flow, whereas sound of
high intensity decreases cochlear blood flow
Outer hair cell (OHC) plasma membrane fluidity
Role of glucocorticoid receptors
Recent studies shown the presence of
glucocorticoid signaling pathways in the cochlea
and their protective roles against noise-induced
hearing loss
Oxidative stress:
overstimulation of tissues by noise causes
excess production of reactive oxygen species,
including superoxide and hydroxyl radicals which
oxidize cellular targets such as lipids, proteins
and DNA by virtue of a highly reactive unpaired
electron therby causing necrotic changes or
apoptotic cell death
Activity of ROS is antagonized by the antioxidant system consisting of small molecules (e.g. glutathione, vitamin C, vitamin E) and protective enzymes (e.g. glutathione peroxidase, superoxide dismutase).
The balance determines the cellular redox status.
Overstimulation by noise can increase the production of ROS resulting in a shift of the redox balance and triggering the activation of signalling pathways and gene expression.
Depending on the severity of the insult, the cell may activate survival pathways (e.g. synthesis of antioxidant enzymes) or invoke death pathways of necrosis or apoptosis.
Acoustic overstimulation activates multiple
transcription factors in the cochlea, including the
transcription factor AP-l and thus potentially
apoptotic pathways via jun kinase
Greatest area of injury in occupational NIHL
appears to be to that portion of a cochlea sensitive
to frequencies of about 4k Hz
Continuous stimuli are more damaging than
interrupted stimuli.
Intermittent noise defined as loudness levels that
fluctuate more than 20 dBA is more protective for
apical lesions induced by low frequencies than for
basal lesions induced by high frequencies.
STRUCTURAL
Changes to the micro mechanical structures
like depolymerization of actin filaments in
stereocilia.
Changes to nonsensory elements of the cochlea
1. swelling of the stria vascularis.
2. swelling of afferent nerve endings.
3. destruction of the intercilial bridges
4. rupture of the Reissner membrane
Outer hair cells are more susceptible to noise
exposure than inner hair cells.
Temporary threshold shifts (TTS) decreased
stiffness of the stereocilia of outer hair cells. The
stereocilia become disarrayed and floppy. they
respond poorly.
Permanent threshold shifts (PTS) are associated
with fusion of adjacent stereocilia and loss of
stereocilia.
gene association study for NIHL in 2 independent
noise-exposed populations revealed
that PCDH15 and MYH14 may be NIHL
susceptibility genes
ACOUSTIC TRAUMA
Caused by an extremely loud noise usually
resulting in immediate, permanent hearing loss.
Such transient noise stimuli are generally less than
0.2 seconds in duration.
TYPES OF TRANSIENT NOISE
Impulse noise usually due to blast effect and the
rapid expansion of gases
Impact noise which results from a collision (usually
metal on metal). Impact noises are often associated
with echoes and reverberations, which produce
acoustic peaks and troughs.
The sound stimuli generally exceed 140 dB
Mechanical tearing of membranes and physical
disruption of cell walls with mixing of perilymph and
endolymph.
Damage from impulse noise appears to be a direct
mechanical disruption of inner ear tissues because
their elastic limit is exceeded
ASSOCIATED FACTORS
Genetic basis
Smoking
Diabetes
Cardiovascular disease
Recreational drug
Exposure to ototoxic agents use
Industrial solvents
SYMPTOMS
Trouble in normal and telephone conversation
Turning up the radio/television volume
Tinnitus
Many patients experience tinnitus associated
with both TTS and PTS. Postexposure tinnitus and
TTS serve as warning signs of impending
permanent NIHL.
NIHL, especially ONIHL, is generally symmetrical.
Occasionally, a work environment results in
asymmetrical noise exposure, as seen in tractor
drivers.
Tractor operators have to monitor equipment
mounted on the rear side, most operators look over
their right shoulder, exposing their left ear to the
noise of the prime mover and exhaust while their
right ear is shielded by head shadow.
The most common cause of asymmetric NIHL is exposure
to firearms, particularly long guns.
Right-handed shooters have a more severe hearing loss
in the left ear because the left ear faces the barrel while
the right ear is tucked into the shoulder and is in the
acoustic shadow of the head.
Study of impulse noise in soldiers exposed to weapon-
related noise levels (1.6-16 kHz) found that, after their
military service, the soldiers' hearing had significantly
deteriorated (an average of 6 dB exclusively at 10 and 12
kHz).
Transiently evoked otoacoustic emission (TEOAE)
reduction was registered predominantly at 2, 3, and 4 kHz,
with greatest decrease at 2 kHz (P < 0.02).
Reduced TEOAE levels in soldiers exposed to noise may
be the first sign of potential hearing loss.
DIAGNOSIS
No specific test available
Audiometry
1. Classical audiometric pattern is of a high-tone hearing loss with a notched appearance centredon 4 or 6 kHz, with some recovery at 8 kHz. However, the notch is often absent
2. Significant audiometric loss at frequencies below 2 kHz is extremely uncommon
Tympanometry
Cortically evoked reflex audiometry may be required in those individuals in whom a significant nonorganic component (feigned thresholds) is suspected
NIHL begins with a temporary threshold shift (TTS)
which recovers almost completely once the noxious
stimulus is removed. The amount of time over which
recovery occurs is unclear and controversial, but a 24
hr period is generally considered.
extent of a NIHL (TTS/PTS) is predictable on
1. Intensity
2. Spectral pattern of the noise(Frequency content)
3. Temporal pattern of exposure (intermittent or
continuous)
Duration of exposure to the noise (time weighted
average [TWA])
Individual susceptibility to the noise
Pure-tone and narrow-band stimuli result in a
maximum TTS at or slightly above the center
frequency of the noise producing it
In occupational situations, TTSs are almost always
greatest between 3000-6000 Hz and are often quite
narrowly focused at 4000 Hz.
The 4k HZ notch in audiogram appears to be a
consequence of several factors:
1. The fact that human hearing is more sensitive at
1-5 kHz
2. The fact that the acoustic reflex attenuates loud
noises below 2 kHz (as demonstrated by Borg)
3. Nonlinear middle ear function as a result of
increased intensities.
On separating the effects of ageing from the
effects of noise using the reference to one or
more of the many standardized reference tables
detailing hearing thresholds with age for typical
screened and unscreened populations, e.g. The
NPL tables, ISO 7029, IS01999 or the National
Study of Hearing, removal of an 'average' value
for age-related hearing loss has left an assumed
noise-induced hearing loss.
Use of a highly screened control group, with
better hearing thresholds, may suggest a significant
hearing loss due to noise, while a less highly
screened control group (with poorer thresholds)
may suggest near-normal hearing for an individual
of that age.
The control group should be free of other otological
pathology, such as ear disease, head injuries,
positive family history of hearing loss
CALCULATION OF THE HEARING IMPAIRMENT
From the audiogram,the average of the thresholds of
hearing for frequencies of 500, 1000, 2000, 4000 and 6000
Hz is calculated
25 dB is deducted from the value (as there is no impairment
up to 25 dB).
1.5 is then multiplied to it.
This is the percentage of hearing impairment for one ear
Percentage handicap= (Better ear%×5)+(worse ear%)
6
DIFFERENTIAL DIAGNOSIS
Inner ear
1. Autoimmune disease
2. Genetic SNHL
3. Autotoxicity
4. Presbycussis
5. Sudden hearing loss
Middle ear
1. Otosclerosis
PREVENTION
Therapeutic intervention should target early parts
of the toxic molecular cascades
The protectant must be present in the inner ear
in sufficiently high amounts at the time of noise
trauma
Protective medication should not have any side
effects of its own.
Hearing protectors should be used when
engineering controls and work practices are not
feasible for reducing noise exposure to safe levels
Hearing conservation programs
1. Significant amount of individual variability exists with respect to susceptibility to NIHL
2. Auditory system of some individuals seems to be able to withstand longer exposure times to higher loudness levels than the auditory system of others.
3. Norms established for hearing conservation programs, although protecting the group as whole, may not protect the most sensitive individuals.
4. Audiograms immediately after exposure and again 24 hours later should be attained to establish the presence or absence of TTS or PTS.
ANTIOXIDANT THERAPY
Glutathione
sodium thiosulphate
Mannitol
WR-2721
desferoxamine,
2,3-dihydroxybenzoic acid
Salicylate
N-acetyl cysteine
D-methionine
Alpha tocophero1
NEUROTROPHIC FACTORS
noise trauma may affect the spiral ganglion cells
Viability of the spiral ganglion cells is required for
the success of cochlear implant in the profoundly
deaf
Neurotrophic factors regulate cellular homeostasis
including the cellular redox state and modulate
gene transcription and cell cycle activities
Brain-derived neurotrophic factor, neurotrophin-3
and glial-derived neurotrophic factor
OCCUPATIONAL NIHL
( INDIAN SCENARIO) Studies of NIHL in India are limited
Study was conducted in heavy engineering
industry, which included machines shop and press
divisions. The sound levels ranged from 83 to 116
dBA. Hearing impairment was progressive in all the
study groups.
In a textile mill weavers study, the sound levels
were around 102-104 dBA . NIHL at 4000 Hz was
as high as 30 dB in the age range 25-29 years, 40
dB in the age range 30-34 years and 45 dB in the
age range 35-39 years
Noise pollution on traffic policemen in the city of
Hyderabad, India, was carried out by the Society to
Aid the Hearing Impaired, revealed that 76% had
NIHL
The National institute of miners’ health (NIMH) has
carried out NIHL studies in various mines. NIHL
was prevalent among 12.8% of the employees.
Moderate NIHL was detected in 10.2% and severe
NIHL was observed in 2.6% of the employees.[
COMPENSATION
In India, NIHL has been a compensable disease
since 1948 under the Employees State Insurance
Act (1948) and the Workmen's Compensation Act
(1923). But still there is very little awareness
regarding this fact.
Nearly 3 billion dollars has been paid as
compensation for NIHL in the USA in the last two
decades.
In India, it was only in 1996 that the first case got
compensation
About 250 workers are receiving compensation for
NIHL
PURSUING A CLAIM
The common option is to pursue a civil claim where the
burden of proof is on the claimant. For such a case
to succeed the claimant must demonstrate “on the
balance of probabilities” (i.e. more likely than not)
that:
1. There has been exposure to excessive noise levels;
2. The hearing loss has been a consequence of that
exposure;
3. There was a forseeable risk of injury from the
exposure;
4. The case was brought in time.
The claimant must retain a solicitor to coordinate the
case..