Download OHC

Outer Hair Cell functionality and
new models for noise damage
NTAF’s etterutdanningskurs
Hell, October 2007
Olav Kvaløy
SINTEF 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 damage
Assumptions 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
Vg
Iros
http://en.wikipedia.org/wiki/Image:Cochlea-crosssection.png
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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
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