Noise Induced Hearing Loss

1. Noise Induced Hearing Loss Dr. Vishal Sharma

2. Definitions • Noise = wrong sound, in wrong place, at wrong time (Park & Park) • Acoustic Trauma =sudden, permanent sensori-neural deafness due to single exposure to an intense sound (130-140dB) of < 0.2 sec • Chronic Noise Induced Hearing Loss = gradual SNHL due to years of exposure to noise

3. History • Ramazzini (1713): reported NIHL in copper workers • NIHL recognized in US, Germany & UK in 1870s • Thomas Barrof Glasgow (1886): did first survey • Habermann(1890): histology of NIHL in cochlea • Fowler (1929): first to comment on 4 kHz dip • Bunch(1939): audiometric features of NIHL

4. Epidemiology • 30 million adults in United States are exposed to hazardous occupational sound levels (National Institute for Occupational Safety & Health, 2000). • Among these 30 million, 1 in 4 will acquire a permanent hearing loss(American Academy of Audiology, 2003). • 50 % of male miners have hearing loss by age of 50 & 70 % by age of 60 (NIOSH, 2001).

5. Classification of noise A. Based on duration:B. Frequency based: 1. Continuous: cotton spinning 1. High: sawing 2. Interrupted: traffic 2. Low:grinder 3. Transient (< 0.2 sec) 3. White noise:boiler a. Impulse: explosion b. Impact: metal to metal collision

6. Sources of noise • Industrial noise • Road traffic noise • Aircrafts & Railways noise • Entertainment noise:clubs, discos • Residential noise: alarms, music systems, home theatre, air conditioners, generators • Personal noise:personal stereos, mobile phones • Firearms & bomb blast noise

7. Agriculture Mining Construction Manufacturing Public Utilities Transportation Military Common Occupational Noise

10. Sound Thermometer

11. Clinical Features of N.I.H.L. • Similar to earlyototoxicity & presbycusis • Early NIHL limited to high frequency: no symptom • First symptom: trouble in speech comprehension with loud background noise • As NIHL progresses, patients havedifficulty in understanding high-pitched voices(women & children) even in quiet conversational situations

12. Clinical Features • Telephonic conversation is unimpaired because telephones don’t use frequencies > 3000 Hz • Many patients experience tinnitus&hyperacusis • Post-exposure tinnitus & temporary deafness are warning signs of impending permanent NIHL

13. Impact of noise on children • Household noise retards cognitive development of children b/w 7-24 months. Brains of children cope with loud noise by sound filtering which also includes human speech. This leads to retardation of intellectual skills. • Foetus also may suffer from effects of noise.

14. Characteristics of chronic NIHL (Dobie, 1990)

15. Always sensorineural, symmetric & bilateral. • Greater SNHL present at 3, 4, & 6 kHz, with recovery at 8 kHz ***. Usually greatest at 4 kHz. ***Presbyacusis has no recovery at 8 kHz • Isolated NIHL is never > 75 dB in high frequencies or > 40 dB in lower frequencies. • Rate of hearing loss in chronic NIHL is greatest during first 10-15 years of exposure & decreases later as hearing worsens. Hearing loss does not progress after noise exposure is discontinued.

16. Commonest cause of asymmetric NIHL is exposure to firearms. Right-handed shooters have more severe left ear deafness (left ear faces barrel while right ear is in acoustic shadow of head). • Similarly, Tractor operators look over their right shoulder, exposing their left ear to noise of prime mover + exhaust & their right ear gets shielded.

17. Acoustic head shadow

18. Auditory Effects of Noise • Per-stimulation fatigue or Adaptation: Noise exposure of > 90 dB elevates hearing threshold temporarily, especially at 4 kHz • Post-stimulatory fatigue: • Temporary Threshold Shift (reversible) • Permanent Threshold Shift (irreversible)

19. Temporary Threshold Shift • Exposure to loud noise for seconds to hours may cause SNHL that recovers within 16-24 hours. • Magnitude of TTS depends on: • More intense sounds lead to larger shifts. • Speech frequencies (500-3000 Hz) are most susceptible to TTS. • Interrupted exposures cause less TTS than continuous exposures.

20. Permanent Threshold Shift • Repeated TTS over weeks, months & years fail to recover completely & become noise-induced permanent threshold shift (NIPTS) • NIPTS is measured by subtracting amount of hearing loss to be expected due to aging from hearing threshold level • Amount of NIPTS & frequencies involved depend primarily on same parameters, as for TTS

21. Calculation of N.I.P.T.S.

22. Age related hearing loss

23. Progress of N.I.P.T.S.

24. Progress of N.I.P.T.S.

27. Male vs. female N.I.P.T.S.

28. Insomnia Anxiety & nervousness Coronary heart disease Lack of concentration Fatigue Irritability & impatience Indigestion Peptic ulcer Speech interference Hypertension ed heart rate ed intra-cranial tension ed breathing rate ed sweating ed color perception ed night vision Non-auditory effects of noise

29. Factors influencing N.I.H.L.

30. 1. Frequency:noise b/w 2-3 kHz  more damage 2. Intensity & duration of exposure:noise > 85 dBA for 8 hr time weighted average is unsafe 3. Intermittence:intermittent noise with quiet intervals is safer than steady noise 4. Age:children & elderly are more prone to NIHL. Presbyacusis has additive effect not synergistic. 5. Sex:males are more prone than females to NIHL

31. 6. Individual Susceptibility:Tender earsare more prone to NIHL than tough earsdue to difference in:  Genetic: Ahl gene E.A.C. skin elasticity  area ratio of TM:stapes mass of ossicles  tension of stapedius  outer hair cell density  basilar membrane stiffness cochlearvascularity  endolymph composition psychological

32. 7. Experience:Green ears have bigger NIPTS than those exposed to noise before (ripe ears). NIPTS can be reduced by adding prior exposure at lower levels (toughening or conditioning of ear). 8. Conductive deafness:gives protection (?) against NIHL as less sound gets conducted to inner ear 9. Ototoxic drugs:enhance NIHL

33. 10. Vibration:Raynaud phenomenon es NIHL 11. Absent Stapedial reflex:es NIHL for lower frequency 12. Melanization:Albinos are more prone to NIHL 13. Diabetes mellitus, Hyper-cholesterolemia, Cardiovascular disease: increase risk of NIHL (?) 14. Smoking: increase risk of NIHL (?) 15. Deep sea divers: are more prone to NIHL

34. Patho-physiology NIHL damage is explained by: • Macro-mechanical theory • Micro-mechanical theory: produced by high intensities • Biochemical theory:produced by moderate intensities

35. Macro-mechanical theory • Traveling sound wave produces movement of basilar membrane • Central part of basilar membrane undergoes maximum rocking vibration. This part houses outer hair cells (especially inner row) hence they are subjected to maximum damage.

36. Organ of Corti

37. Micro-mechanical Damage Temporary Threshold Shift: moderate swelling of hair cells + shortening of rootlets of hair cells + small vacuoles in supporting cells Permanent Threshold Shift: marked swelling of hair cells + fracture of rootlets of hair cells + large vacuoles in supporting cells + damage to outer hair cells + damage to inner hair cells

39. Biochemical Damage • Micro-mechanical damage causesinterruption of normal chemical gradient of cochlea which leads toionic poisoning • Noise activity induced vaso-constriction leads tocochlear ischaemia • Metabolic exhaustion of activated hair cells

40. Investigations A. Diagnostic B. Research only 1. Subjective Low power Microscopy  Pure Tone Audiogram Electron Microscopy 2. Objective Cyto-cochleogram  Oto-acoustic emissions  Cortical Evoked Response Audiometry  Multiple Auditory Steady-state Evoked Response

41. Audiogram in Acoustic Trauma

42. Audiogram in Chronic N.I.H.L.

43. 4 kHz (Boilermaker’s) notch, C5 dip • characteristic audiometric pattern of early NIHL. • If exposure is continued, notch gradually deepens & widens. • 4 kHz notch also seen in head injury, barotrauma or even in absence of any explanatory history.

44. Reasons for 4 kHz notch • Natural resonance of EAC being 2-3 kHz, 150% of this produces maximum damage between 3-5 kHz • Protective effect of acoustic reflex below 2 kHz • Intermittent noise is more damaging for 3-5 kHz • Outer hair cells of 3-5 kHz region are more prone to oxidative stress, have reduced vascularity (?) & ed oxygen consumption (?)

45. Acoustic gain: middle ear & pinna

46. Otoacoustic Emissions (OAE) • Spontaneous OAE:Sounds emitted without stimulus. Presence indicates hearing < 25 dB HL. • Transient evoked OAE:Sounds emitted in response to short duration click stimulus. Presence = < 35 dB HL • Distortion product OAE:Sounds emitted in response to 2 tones of different frequency & intensity. Presence = < 50 dB HL. Good for higher frequencies.

47. Normal Transient evoked OAE

48. Normal Transient evoked OAE Reproducibility should be > 75 %

49. Early detection of N.I.H.L.

50. Early stage N.I.H.L.