Phenotyping Noise Induced Hearing Loss with Audiometry and DPOAEs

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Presentation transcript:

Phenotyping Noise Induced Hearing Loss with Audiometry and DPOAEs Ishan Bhatt, Ph.D., NAU Susan L. Phillips, Ph.D., UNCG Mohsin Ahmed Shaikh, Ph.D. candidate, UNCG

Disclosure Dr. Susan Phillips, Mr. Mohsin Ahmed Shaikh and I have no relevant financial or nonfinancial relationships to disclose. The material presented today is based on audiometric and otoacoustic emissions (OAEs) data collected from the School of Music, University of North Carolina at Greensboro. The study was approved by the Institutional Review Board, UNCG (11-0335).

Key Factors in Noise-induced Hearing Loss Globally growing hearing health concern NIHL is a complex disorder Some individuals are more susceptible than others Gene Environment Gene-environment interaction

Importance of Phenotyping NIHL Success of gene mapping lies on the ability to define the target phenotype (i.e. trait of a disease) with accuracy and precision (Schulze & McMahon, 2004)

Early Efforts: Phenotyping NIHL Definition: Absolute audiometric thresholds at high frequencies (3 to 8 kHz) Industrial population Confounding variables (Sliwinska-Kowalska & Pawelczyk, 2013; Van Laer et al., 2006)

Recent Efforts: Phenotyping NIHL Definition: Bilateral audiometric notch within 4 to 6 kHz Collage-aged student musicians Better control over confounding variables Potential NIHL Phenotypes (Phillips et al., 2012)

Purpose of the Study To evaluate the 4-6 kHz audiometric notch using a test battery of Distortion-Product Otoacoustic Emissions (DPOAEs) Hypothesis: Musicians with 4-6 kHz audiometric notch will exhibit reduced DPOAEs compared to musicians without the notch

Method Sample 77 musicians 18-31 years Normal otoscopic examination and tympanometric findings DPOAE measured in the left ear Online Survey Primary instruments Participation in ensembles Exposure to music

DPOAE Test Battery DPOAE I/O function (ILO 292-II V6): 2 f1 - f2 DP frequency at 2, 3, 4 and 6 kHz L2 ranging from 75 to 30 dB SPL in 5 dB steps Formula-based approach: L1 = (0.4)L2+39 2f1 - f2 DPgram was measured from 2 to 8 kHz in 9 data points/octave with L1 and L2 were 60 and 40 dB SPL respectively

Statistical Analysis Repeated measure ANOVA Within subject factors: 10 DP data points, Between subject factors: Audiometric groups and music exposure Covariate: Gender

Results 55/77(23 females and 32 males) participants completed survey 18/55 showed 4-6 kHz audiometric notch 5/55 showed high frequency drop

Results continue… DPOAE I/O function: Main effect of exposure to music was statistically significant (p= 0.029) Main effect of audiometric groups was not statistically significant (p>0.05) 1 2 3 4

Results continue… Main effect of music exposure: DPgram Frequency range (2-4 kHz): F (3, 44) = 4.78, p= 0.006 Frequency range (4-8 kHz): F (3, 44) = 2.884, p= 0.046 Main effect of audiometric groups: No statistically significant effect found 1 2 3 4

DPOAEs in 3 Audiometric Configurations DPgram: 2-8 kHz (9 data points/octave)

Standing Waves in the Ear Canal Discussion No effect of audiometric configurations on DPOAEs Observation can be attributed to: DPOAE recording limitations and/or Physiological basis Standing Waves in the Ear Canal

Damage to Stria Vascularis Damage to OHCs Damage to Stria Vascularis Elevated audiometric thresholds and comparatively poor DPOAEs Elevated audiometric thresholds and comparatively better DPOAEs (Bhagat et al., 2010; Hofstetter, Ding, Powers, & Salvi, 1997; Ozturan, Jerger, Lew, & Lynch, 1996) (Mills, Norton, & Rubel, 1993; Gates et al., 2002)

Conclusion Musicians with higher music exposure are likely to show reduction in DPOAE amplitude Further research in required to investigate DPOAEs in musicians with the 4-6 kHz audiometric notch

Future Research DPOAE recording using advance calibration technique A well-defined control group of non-musicians may improve sensitivity of the future studies Animal study to validate potential sub-phenotypes Validate the music exposure survey

References Bhagat, S. P., Bass, J. K., White, S. T., Qaddoumi, I., Wilson, M. W., Wu, J., & Rodriguez-Galindo, C. (2010). Monitoring carboplatin ototoxicity with distortion-product otoacoustic emissions in children with retinoblastoma. International Journal of Pediatric Otorhinolaryngology, 74(10), 1156-1163. Gates, G. A., Mills, D., Nam, B. H., D'Agostino, R., & Rubel, E. W. (2002). Effects of age on the distortion product otoacoustic emission growth functions. Hearing Research, 163(1-2), 53-60. Hofstetter, P., Ding, D., Powers, N., & Salvi, R. (1997). Quantitative relationship of carboplatin dose to magnitude of inner and outer hair cell loss and the reduction in distortion product otoacoustic emission amplitude in chinchillas. Hearing Research,112(1-2), 199-215. Mills, D. M., Norton, S. J., & Rubel, E. W. (1993). Vulnerability and adaptation of distortion product otoacoustic emissions to endocochlear potential variation. Journal of The Acoustical Society of America, 94(4), 2108-2122. Ozturan, O., Jerger, J., Lew, H., & Lynch, G. R. (1996). Monitoring of cisplatin ototoxicity by distortion-product otoacoustic emissions. Auris Nasus Larynx, 23, 147-151. Phillips, S. L., Mace, S. T., Richter, S. J., Morehouse, R., Henrich, V. C. (2012). Genetic Bases of Noise Induced Hearing Loss. Podium presentation at the American Auditory Society conference, Scottsdale, Arizona, March. Schulze, T.G., McMahon, F.J. 2004. Defining the phenotype in human genetic studies: Forward genetics and reverse phenotyping. Hum. Hered., 58, 131-138. Sliwinska-Kowalska, M., & Pawelczyk, M. (2013). Contribution of genetic factors to noise-induced hearing loss: a human studies review. Mutation Research, 752(1), 61-65. Van Laer, L., Carlsson, P., Ottschytsch, N., Bondeson, M., Konings, A., Vandevelde, A., & Dieltjens, N. (2006). The contribution of genes involved in potassium-recycling in the inner ear to noise-induced hearing loss. Human Mutation, 27(8), 786-795.