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Outer Hair Cell functionality and new models for noise damage NTAF’s etterutdanningskurs Hell, October 2007 Olav Kvaløy SINTEF ICT
’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
’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)
’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.
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
OHC, Gain and Protection If OHC work againstor 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)
‘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
The Cochlea http://en.wikipedia.org/wiki/Image:Cochlea-crosssection.png
The Cochlea with diffusion model Vg Iros http://en.wikipedia.org/wiki/Image:Cochlea-crosssection.png
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
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)
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