NOISE INDUCED HEARING LOSS

Dr.KAUSHIK SUTRADHAR

P.G.T. Deptt. Of E.N.T.

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..