Computer methods and programs in biomedicine · 2022
A comprehensive finite-element human ear model to estimate noise-induced hearing loss associated with occupational noise exposure.
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Yu You-Cheng, Wang Tang-Chuan, Shih Tzu-Ching
Аннотация
BACKGROUND AND OBJECTIVE: Noise is a common occupational and environmental hazard; however, little is known about the use of computational tools to quantitively analyze data on basilar membrane (BM) damage in noise-induced hearing loss (NIHL). Here, we established a comprehensive three-dimensional finite-element human ear model to quantify the impact of noise exposure on BM and perilymph fluid.
METHODS: We used auditory risk units (ARUs) to evaluate the BM damage for subjects (3 men and 5 women; mean age, 32.75 ± 8.86 years; age range, 24-44 years). A 90-dB sound pressure level (SPL) was normally applied at the external auditory canal (EAC) entrance to simulate sound transmission from the EAC to the cochlea at frequencies of 0.2-10.0 kHz.
RESULTS: The pressure distribution of perilymph fluid is totally different on frequency responses under low and high sound-evoked (0.013-10.0 kHz). The highest ARUs were 18.479% at the distance of 1 mm from the base, and the second-highest to fourth-highest ARUs occurred at distances of 5-7 mm from the base, where their ARUs were 9.749%, 9.176%, and 11.231%. The total of the ARUs reached 81.956% at external frequencies' sounds of 3.2-5.0 kHz. Among these, the 3.8-kHz and 3.6-kHz frequencies yielded the highest and second-highest ARUs of 20.325% and 19.873%, respectively.
CONCLUSIONS: This study would inform our understanding of NIHL associated with occupational noise exposure. We present a FE modelling and describe how it might provide a unique way to unravel mechanisms that drive NIHL due to loud noises.
METHODS: We used auditory risk units (ARUs) to evaluate the BM damage for subjects (3 men and 5 women; mean age, 32.75 ± 8.86 years; age range, 24-44 years). A 90-dB sound pressure level (SPL) was normally applied at the external auditory canal (EAC) entrance to simulate sound transmission from the EAC to the cochlea at frequencies of 0.2-10.0 kHz.
RESULTS: The pressure distribution of perilymph fluid is totally different on frequency responses under low and high sound-evoked (0.013-10.0 kHz). The highest ARUs were 18.479% at the distance of 1 mm from the base, and the second-highest to fourth-highest ARUs occurred at distances of 5-7 mm from the base, where their ARUs were 9.749%, 9.176%, and 11.231%. The total of the ARUs reached 81.956% at external frequencies' sounds of 3.2-5.0 kHz. Among these, the 3.8-kHz and 3.6-kHz frequencies yielded the highest and second-highest ARUs of 20.325% and 19.873%, respectively.
CONCLUSIONS: This study would inform our understanding of NIHL associated with occupational noise exposure. We present a FE modelling and describe how it might provide a unique way to unravel mechanisms that drive NIHL due to loud noises.