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Outer Hair Cell functionality and new models for noise damage

NTAF’s etterutdanningskursHell, October 2007

Olav KvaløySINTEF ICT

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’State of the Art’ of understanding of damage risk

At levels from 85dBA to <130dBA:

Damage = dBlevel * time (dose)

At higher levels >150dB instantaneous damage (legislation states max 130dBCpeak)

Our model works on the continuous noise integration

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’State of the Art’ understanding of OHC

OHC is damaged by continuous high noise

OHC hearing loss is often accompanied by hyperacusis

OHC represents +57dB gain at threshold (Moore)

OHC is not active above 90dB (Moore)

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’State of the Art’ questioned

Why is OHC damaged at high levels if they are inactive above 90dB?

We is know these are the dangerous levels.

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Beyond ’State of the Art’

OHC is damaged by high noise

OHC hearing loss is often accompanied by hyperacousis

OHC represents +57dB gain at threshold

New hypothesis: OHC is active above 90dB

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OHC, Gain and Protection

If OHC work against or dampen the movement at high levels this would explain:

Why OHC are damaged at high levels (they work harder!)

Hyperacousis when OHC damage (no OHC to restrict the level)

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Recruitment and Outer Hair Cells (OHC)

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‘Diffusion’ model for HOC damageAssumptions in the model: OHC work to protect cochlea during high noise and are

‘worn out’ by to much work

Some substance ‘X’ is needed for the cells to work Some substance ‘Y’ needs to be carried away from cells If the X or Y concentration goes beyond certain limits the

cells will be damaged

These substances must be transported to / fro the cells by diffusion

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The Cochlea

http://en.wikipedia.org/wiki/Image:Cochlea-crosssection.png

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The Cochlea with diffusion model

http://en.wikipedia.org/wiki/Image:Cochlea-crosssection.png

Iros

Vg

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Diffusion model of HOC damage

Literature shows that Reactive Oxygen Specimen (ROS) is produced in the cells and will destroy them

Antioxidants protect the ear against noise (Vitamin C will reduce ROS concentration and protect)

The model will give credit to resting periods between noise

Literature shows destructive levels start <70dB if no rest

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Diffusion model of HOC damage

x(t) is instantaneous sound pressure

h(t) is the ROS production function

Vg is antioxidant source

We assume TTS is a sign increased ROS concentration (by this we can calibrate the model)

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Thank you for listening

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How to prove OHC hypothesis?

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Protocol for OHC hypothesis test: Gather young healthy subjects (students?) Expose them to high noise (produce TTS)

concerts or brass-band practice as exposure source (students own choice!) Measure Threshold and UnComfortable Level (UCL)

before and after sound exposure

Threshold levels and/or OAE to document OHC activity ’Loudness Scaling’ and/or ’Reflex Measurement’ used to measure

UCL

Lower OHC activity and lower UCL after exposure proves hypothesis

Main Problem: Ethics in exposing subjects to potentially hazardous sound levels