What is Noise Induce Hearing Loss | Types of NIHL & its Etiology, Assessment and Management

NOISE INDUCE HEARING LOSS

INTRODUCTION

Noise induce hearing loss is the 2nd most common cause of hearing loss , most 

common being presbycusis millions of individuals worldwide suffered from 

NIHL

• Noise-induced hearing loss (NIHL) is a hearing impairment resulting from 

exposure to loud sound. People may have a loss of perception of a narrow 

range of frequencies or impaired perception of sound including sensitivity to 

sound or ringing in the ears . When exposure to hazards such as noise occur 

at work and is associated with hearing loss, it is referred to as occupational 

hearing loss

Hearing may deteriorate gradually from chronic and 

repeated noise exposure (such as to loud music or background 

noise) or suddenly from exposure to impulse noise, which is a 

short high intensity noise (such as a gunshot or airhorn).In 

both types, loud sound overstimulates delicate hearing cells, 

leading to the permanent injury or death of the cells. 

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)

THEORIES OF NIHL

1. Mechanical injury caused by severe motion of Basilar membrane

2. Metabolic exhaustion of cell

3. Ischemia due to vascular narrowing

 CURRENT RRENT THEORIES:-

• Mechanical theory:- alteration in the stereocilia in form of broken or 

shortened rootlets in the initial pathological process leading to Temporary 

threshold shift (TTS)

• Usually repair of the damaged stereocilia occurs within 48 hours period of 

time Due to continuous exposure of noise which leads to permanents 

threshold of hearing loss (PTS)

• In severe damage due to mechanical distruption and micro breaks in the 

structural framework of cochlear duct leads to toxic mixing of endolymph 

and perilymph leads to loss of hair cell and corresponding nerve fibers 

TYPES:-

Temporary described as Temporary Threshold Shift 
(TTS)

• It is reversible hearing loss resulting from exposure to Moderately intense sound such 

as encountered at orchestra concert , DJ party ,etc. 

• It is usually resolve between few hours to few days 

• Clinical feature:-

• Hearing impairment elevated threshold for short duration in mid frequency range 

between 3 to 6 kHz

• Tinnitus

• Loudness Recruitment

• Muffled sound

Permanent described as Permanent Threshold Shift 
(PTS) 

• If temporary threshold shift does not recover before re exposure to loud noise leads to 

permanent change in hearing known as permanent threshold shift 

• It is the irreversible elevation in hearing threshold due to structural damage to 

cochlea 

• Traditionally (PTS) caused by acoustic stimulation classified in to two types 

• 1 Acoustic Trauma:-

• Acoustic trauma is caused by single , short lasting exposure to very intense sound e.g. 

Blast injury

• 2 Noise induce hearing loss due to chronic exposure to less intense sound e.g. noise 

exposure at work place 

Clinical Presentation of Irreversible NIHL

• History of long term expousre to dangerous noise level i.e.>90 dB for 8 

hrs/day 

• Hearing loss – gradual loss, over period of 5 to 10 years

• Type of hearing loss – SNHL involving 3 to 6 kHZ frequency, such notch 

at 4kHZ

• SDS is consistent with audiometric 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 (presbycusis), 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, sawmills, mining, etc.

• Male preponderance

Metabolic 

• Structural 

• METABOLIC 

Acoustic overstimulation

Excessive neurotransmitter 

release 

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 thereby 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 signaling 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 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 non sensory elements of the cochlea 

1. Swelling of the stria vascularis.

2. Swelling of afferent nerve endings. 

3. Destruction of the inter cilial bridges 

4. Rupture of the Reisner 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 solvent

Noise Level in Different Industries
INDUSTRIES RANGE (Db)

Road traffic 60-102

Metro 70-111

Surface Rail Traffic 90-102

Fertilizer Plants 90-102

Oil & Natural Gas Complex 90-119

Air Traffic 90-112

Pharmaceutical Firms 93-103

Textile Industries 102-114

SYMPTOMS

• The first symptom of NIHL may be difficulty hearing a conversation against 

a noisy background . 

• The effect of hearing loss on speech perception has two components. 

• The first component is the loss of audibility, which may be perceived as an 

overall decrease in volume. Modern hearing aids compensate this loss with 

amplification. 

• The second component is known as "distortion" or "clarity loss" due to 

selective frequency loss. Consonants, due to their higher frequency, are typically affected first. For example, the sounds "s" and "t" are often difficult to hear for those with hearing loss, affecting clarity of speech . 

• NIHL can affect either one or both ears. Unilateral hearing loss causes 

problems with directional hearing, affecting the ability to localize sound.

• Tinnitus 

• Vertigo 

• Hypertension 

• Anxiety 

• Lack of concentration 

• Hyperacusis 

• High heart rate 

TYPES OF DIAGNOSIS 

1. Subjective Diagnosis 2. Objective Diagnosis

- Pure Tone Audiogram (PTA) - Oto Acoustic Emissions (OAEs)

- Speech Audiometry - Immittance Audiometry

DIAGNOSIS

No specific test available

Audiometry

Classical audiometric pattern is of a high-tone hearing 

loss with a notched appearance centered on 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

DIFFERENTIAL DIAGNOSIS 

Inner ear

1. Autoimmune disease 

2. Genetic SNHL 

3. Autotoxicity

4. Presbycusis

5. Sudden hearing loss

Middle ear

1. Otosclerosis

MANAGEMENT

1. Not medically or surgically treatable

2. Entirely preventable

3. Prevention includes 

• Education 

• Engineering control

• Administrative control

• Noise control programme

• Use of proper hearing protrctive devices 

(both ear plugs & ear-muffs)

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

• Deferoxamine, 

• 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