In humans, there is significant variability in susceptibility to noise-induced hearing loss (NIHL) across individuals, even when exposed to the same or similar degrees of noise hazard [1,2,3,4,5]. Data from the International Standards Organization (ISO) 1999:2013 (2013) showed variable hearing loss ranging from 14 to 33 dB HL in workers with careers of a similar 100 dB-A occupational noise exposure. In a prospective experimental study of young adults exposed to 100 dB-SPL of headphone music for four hours [6], temporary threshold shift (TTS) ranged from − 5 to 14 dB HL at 15-min post-exposure testing, thereby confirming the presence of significant, individual variability in risk of NIHL in a controlled study exposure.

Remarkably, efforts to relate anatomical external-ear differences have not been a part of the risk assessment of NIHL, even though external-ear amplification differences are well-documented [7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22]. Multiple reports have shown that there can be major differences in the external-ear amplification of infants relative to adults [23], and it has long been established that variable head and ear size among adults alone suggest that significant differences in external-ear amplification are present across the adult population [24]. Holding duration of a noise exposure constant, the risk of NIHL doubles with every 3 dB-A increase in exposure level (NIOSH, 1998) [25] or 5 dB-A increase in noise exposure (OSHA, 1983) [26]; therefore, it is likely that external-ear amplification differences of up to 14 dB between two individuals [15] play a significant role in individual susceptibility to NIHL.

Experiments in animals also show significant variability to NIHL susceptibility despite strictly controlled study designs, reduced biological and environmental variability, and careful adherence to experimental protocols. Among animal studies, one of the most established models of NIHL is the chinchilla. This model has been used repeatedly to study NIHL because of the similarities between human and chinchilla hearing. Chinchilla hearing sensitivity, frequency range, and cochlear anatomy closely correlates to that of humans [27]. However, the chinchilla demonstrates higher susceptibility to NIHL relative to other species [28, 29]. Despite this relative susceptibility, the chinchilla has been a reliable and robust model for NIHL. For example, studies observing the anatomical and threshold effects of impulse noise on chinchillas found that whereas some animals experienced no permanent threshold shift (PTS), other animals demonstrated threshold shifts as high as 40 dB [30]. This variability suggests that other factors, such as EEA, could play a role in NIHL. A major study that integrated multiple data sets to create a relationship between temporary threshold shift (TTS) and PTS from over 900 noise-exposed chinchillas found PTS variability as high as 60 dB across animals, independent of differences in experimental procedures [31,32,33,34,35]. Although these studies were not designed to focus on PTS differences among animals, it is clear that individual susceptibility to NIHL critically impacts overall hearing outcomes following noise exposure. Thus far, individual variability has been considered a byproduct of animal noise exposure experiments that parallels human correlates, but has not been explicitly investigated.

To date, no single factor has sufficiently explained NIHL variability across individuals who experience similar exposure to noise. This gap in our understanding of NIHL susceptibility makes it difficult to create comprehensive public health guidelines and regulations for NIHL prevention. Existing Occupational Health and Safety Administration (OSHA) guidelines on NIHL can fall short of adequately protecting up to 25% of the workforce population [36]. These risk estimates are based on only two variables: (1) noise exposure duration and (2) noise exposure sound level. Current NIHL risk guidelines do not take into account any individual differences, such as external-ear amplification (EEA). Undoubtedly, genetics plays some role in NIHL susceptibility, as genetically modified mice have demonstrated higher susceptibility to NIHL than wildtype controls [37, 38]. In humans, however, research in this area has been limited, although researchers have identified as many as 34 gene variants associated with NIHL [39]. Whereas genetic testing may eventually become an effective predictor of NIHL susceptibility, EEA could be used as an immediate, efficient, cost-effective, and direct mean of predicting individual susceptibility to NIHL.

EEA refers to sound amplification contributed by external-ear structures (e.g., pinna, concha, and ear canal) as sound waves encounter them. Estimates of EEA can be derived from a probe microphone placed near (within 2–5 mm) the eardrum. These in-ear probe measurements consistently reveal higher and more accurate sound levels of a noise exposure than those measured outside the ear in the free field. For example, the sound level of a live music concert measured with a sound level meter held near two concert attendee’s ears standing in the same location might reflect similar dB-SPL, but may differ by as much as 5–19 dB-A if measured at the level of the eardrum, according to recent findings in EEA variability across children, adolescents, and adults [14, 15].

NIOSH scientific guidelines for hearing conservation are more conservative than OSHA federal guidelines. NIOSH promotes a lower, daily permissible noise exposure limit and estimates NIHL risk using a 3-dB exchange rate. This means that the noise dose (i.e., quantified estimation of NIHL risk) of a given exposure doubles with each 3-dB increase. Grinn and Le Prell [15] recently showed that individual EEA can differ by 14 dB (range 5–19 dB) between individuals in a dataset of pediatric, adolescent, and adult participants. If we hypothetically explore the difference in noise dose between two individuals exposed to free field noise at 90 dB for two hours, given an EEA difference of 14 dB between the two of them, one individual would hypothetically accrue 79% in-ear noise dose (i.e., 95 dB for 2 h), and the other individual would theoretically accrue a 2.016% in-ear noise dose (i.e., 104 dB for 2 h). Although the two individuals in this hypothetical scenario were exposed to the exact same free field sound level and duration of noise exposure, EEA differences would have profound effects on their individual noise doses, and thus, their susceptibility to NIHL.

The contributions of EEA are well-established in the study of hearing and hearing loss [40]. In fact, in-ear probe microphone measurement of EEA has been the “gold standard” of clinical hearing aid verification (real-ear probe microphone spectrum measurement analysis) since the early 1980s [18, 41,42,43]. However, the relationship between EEA and NIHL risk has been largely overlooked. Current NIHL regulations and guidelines (OSHA, 1983 and NIOSH, 1998) do not provide for individual differences in EEA when setting permissible or recommended noise exposure limits. Despite the lack of adoption by OSHA and NIOSH, a link between EEA and individual NIHL risk from free field exposures has been suggested in at least one major study [44].

If EEA accounts for a significant portion of individual variability to NIHL, EEA measurements (or proxy measurements) could be used to successfully and pragmatically identify high-risk individuals (i.e., individuals with high-EEA). It is possible to imagine that individuals with high-EEA may be incurring risk of NIHL at exposure levels that are currently considered to be “permissible” or “safe” by OSHA and NIOSH (in other words, these may be the “tender” ears). To evaluate the relationship between EEA and NIHL, we developed an animal model based on the chinchilla. We hypothesized that animals with higher EEA would exhibit more severe temporary threshold shift (TTS) and permanent threshold shift (PTS) following a 24-h laboratory noise exposure. We hypothesized that EEA measurements alone could account for a significant portion of individual differences in NIHL susceptibility.