Responses of the Human Inner Ear to Low-Frequency Sound

Abstract

The perceptual insensitivity to low frequency (LF) sound in humans has led to an underestimation of the physiological impact of LF exposure on the inner ear. It is known, however, that intense, LF sound causes cyclic changes of indicators of inner ear function after LF stimulus offset, for which the term "Bounce" phenomenon has been coined.Here, we show that the mechanical amplification of hair cells (OHCs) is significantly affected after the presentation of LF sound. First, we show the Bounce phenomenon in slow level changes of quadratic, but not cubic, distortion product otoacoustic emissions (DPOAEs). Second, Bouncing in response to LF sound is seen in slow, oscillating frequency and correlated level changes of spontaneous otoacoustic emissions (SOAEs). Surprisingly, LF sound can induce new SOAEs which can persist for tens of seconds. Further, we show that the Bounce persists under free-field conditions, i.e. without an in-ear probe occluding the auditory meatus. Finally, we show that the Bounce is affected by contralateral acoustic stimulation synchronised to the ipsilateral LF sound. These findings clearly demonstrate that the origin of the Bounce lies in the modulation of cochlear amplifier gain. We conclude that activity changes of OHCs are the source of the Bounce, most likely caused by a temporary disturbance of OHC calcium homeostasis. In the light of these findings, the effects of long-duration, anthropogenic LF sound on the human inner ear require further research.

A Review of the Possible Perceptual and Physiological Effects of Wind Turbine Noise

“…In contrast to the original estimates of OHC threshold (∼40 dB lower than IHC at 5 Hz; Salt & Hullar, 2010 ), gain calculations in the later work suggest that the human apical cochlea could be similarly activated at around 55 dB to 65 dB SPL (corresponding to −38 to −28 dBA). This surprisingly high level of sensitivity of OHCs to LF (when compared with IHC activation and perceptual threshold) is strongly supported by recent work examining the spontaneous otoacoustic emissions in humans ( Drexl, Krause, Gürkov, & Wiegrebe, 2016 ; see also Drexl, Otto, et al., 2016 ; Jeanson, Wiegrebe, Gürkov, Krause, & Drexl, 2017 ; Kugler et al., 2014 ). It has been known for quite some time using human distortion product otoacoustic emissions (e.g., Hensel, Scholz, Hurttig, Mrowinski, & Janssen, 2007 ) as well as in vivo animal data ( Patuzzi, Sellick, & Johnstone, 1984 ) that LF and IS do affect cochlear processing and that the cochlea aqueduct does pass IS frequencies into the inner ear ( Traboulsi & Avan, 2007 ).…”

“…Given, however, the range of technical issues in making such acoustic measurements and the diversity of reported levels reviewed earlier, this claim is similarly limited by the available acoustic data. Furthermore, the recent work examining the guinea pig endocochlear potential ( Salt et al., 2013 ) and human otoacoustic emissions (e.g., Drexl, Otto, et al., 2016 ; Kugler et al., 2014 ) indicate even greater levels of sensitivity of OHCs to LF when compared with the perceptual threshold mediated by IHC activity than first predicted. This suggests the need for a review of such conclusions.…”