NOISE INDUCED HEARING LOSS

1. NOISE INDUCED HEARING LOSS Dr.KAUSHIK SUTRADHAR P.G.T. Deptt . Of E.N.T.

2. 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).

3. 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.

4. 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

5. 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

6. pathophysiology Metabolic Structural METABOLIC Acoustic overstimulation Excessive neurotransmitter release Transduction

7. 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

8. 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

9. 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.

10. 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.

11. Structural Changes to the micro mechanical structures like depolymerization of actin filaments in stereocilia . Changes to nonsensory elements of the cochlea swelling of the stria vascularis . swelling of afferent nerve endings. destruction of the intercilial bridges rupture of the Reissner membrane

12. 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 . 

13. gene association study for NIHL in 2 independent noise-exposed populations revealed that  PCDH15  and  MYH14  may be NIHL susceptibility genes

14. 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.

15. 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

16. Associated factors Genetic basis Smoking Diabetes Cardiovascular disease Recreational drug Exposure to ototoxic agents use Industrial solvents

17. 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.

18. 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.

19. 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.

20. Diagnosis No specific test available Audiometry Classical audiometric pattern is of a high-tone hearing loss with a notched appearance centred on 4 or 6 kHz, with some recovery at 8 kHz. However, the notch is often absent 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

21. 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 Intensity Spectral pattern of the noise(Frequency content) Temporal pattern of exposure (intermittent or continuous)

22. 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.

23. The 4k HZ notch in audiogram appears to be a consequence of several factors: The fact that human hearing is more sensitive at 1-5 kHz The fact that the acoustic reflex attenuates loud noises below 2 kHz (as demonstrated by Borg) Nonlinear middle ear function as a result of increased intensities.

24. 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.

25. 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

26. 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

27. Differential diagnosis Inner ear Autoimmune disease Genetic SNHL Autotoxicity Presbycussis Sudden hearing loss Middle ear Otosclerosis

28. 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

29. Hearing conservation programs Significant amount of individual variability exists with respect to susceptibility to NIHL Auditory system of some individuals seems to be able to withstand longer exposure times to higher loudness levels than the auditory system of others. Norms established for hearing conservation programs, although protecting the group as whole, may not protect the most sensitive individuals.   Audiograms immediately after exposure and again 24 hours later should be attained to establish the presence or absence of TTS or PTS.

30. Antioxidant therapy Glutathione sodium thiosulphate Mannitol WR-2721 desferoxamine , 2,3-dihydroxybenzoic acid Salicylate N-acetyl cysteine D- methionine Alpha tocophero1

31. 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

32. 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

33. 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.[

34. 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

35. 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: There has been exposure to excessive noise levels; The hearing loss has been a consequence of that exposure; There was a forseeable risk of injury from the exposure; The case was brought in time. The claimant must retain a solicitor to coordinate the case..