RP302 - Noise-Induced Hearing Loss Vulnerability Correlated with External-Ear Amplification in Chinchilla

Abstract:
A difference of 14 dB-A between two otherwise identical sound-exposures would result in 3-4x increased risk of noise-induced hearing loss (NIHL). Nevertheless, attempts to explain individual NIHL vulnerability have overlooked external-ear amplification (EEA) as a significant contributor (EEA range =14 dB-A in datasets of pediatric/adolescent/adult human participants). In this study, eight chinchillas were exposed to 89 dB-SPL of 4-kHz octave-band noise for 24-hr. Relationships between EEA and auditory brainstem response (ABR) threshold shifts were analyzed. The results suggest that EEA could assist in creating individualized permissible exposure limits (PEL) to protect populations with high-vulnerability to NIHL injury.

Summary:
Rationale/Purpose
We continue to lack a clear understanding of the variables that render one individual more biologically susceptible to noise-induced hearing loss (NIHL) than another. Variable NIHL susceptibility has been evidenced in human demographic studies as well as animal studies. To date, no single factor nor combination of factors has sufficiently explained such extensive variability in NIHL susceptibility, resulting in poor ability to accurately predict the degree of auditory injury from a given noise exposure. For example, data from ISO 1999:2013 show NIHL predictions with as much as 19 dB variance (14-33 dBHL) at the conclusion of careers in similarly hazardous noise (100 dB-A). This gap in our understanding of NIHL susceptibility renders it difficult to create accurate and comprehensive guidelines for occupational and recreational hearing safety. Additionally, individually variable NIHL susceptibility poses a considerable amount of experimental noise to clinical trials that are designed to test the efficacy of otoprotective agents. If the factor(s) driving individual NIHL susceptibility could be identified, 1) public health policies could be refined to create individualized permissible exposure limits (PEL) based on pre-existing risk factors, and 2) clinical trials could control for these risk factors in subject samples or in exposure stimulus design, in order to maximize observation of the desired otoprotective agent effect.

Methods: Eight adult (4-5 yr) lanigera chinchillas were randomly selected from a larger cohort for this study. All ear and auditory measurements were conducted unilaterally in the left ear. Non-sedated animals underwent body length measurement, body weight measurement, external ear examination, and tympanometry. Animals were then sedated (ketamine, 40 mg/kg, and xylazine 2 mg/kg, subcutaneous injection [SC]) to obtain baseline auditory brainstem response (ABR) threshold measurements, and measurements of external-ear amplification (EEA) including real-ear unaided gain (REUG) and real-ear-to-coupler difference (RECD). 1-wk post-baseline, non-sedated animals underwent calibrated (+/- 2 dB) free field noise exposure (89 dB-SPL 4 kHz octave band noise encompassing 2,840-5,680 Hz for a duration of 24-hr). 24-hr post-exposure, animals were sedated and ABR measurements were obtained. ABR measurements were then repeated 4-wk post-exposure.

Results & Conclusions
Correlations between EEA and ABR threshold shift suggest that EEA could potentially be considered in the damage-risk criteria for an individual permissible exposure limit, and that clinical trial design of otoprotective agents could benefit from controlling for in-ear exposure sound level. The American Speech, Language, and Hearing Association (ASHA) guidelines state that EEA measurements are crucial in the fitting process of hearing aid output, in order to assure that enough but not too much amplification is prescribed to meet the patient’s needs. These gold-standard EEA measurements could also be used to provide consistent, evidence-based guidelines for the National Institute of Occupational Safety and Health (NIOSH) and the Occupational Safety and Health Administration (OSHA), by using EEA to improve the estimation of an individual’s NIHL-risk.