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near wind turbines report (Nissenbaum et al. 2012). The likelihood that OHC afferents are involved in the effects of low-frequency noise is further supported by observations that type II innervation is greatest in the low-frequency cochlear regions that are excited most by infrasound (Liberman et al. 1990, Salt et al. 2009).
4. Exacerbation of Noise Induced Hearing Loss
Some years ago we performed experiments to test a hypothesis that infrasound was protective against noise damage (Harding et al. 2007). We reasoned that low-frequency biasing would periodically close the mechano-electric transducer channels
of the sensory organ (reducing electrical responses as shown in the biasing studies above), and consequently reduce the amount of time that hair cells were exposed to the damaging overstimulation associated with noise exposure. The experi- mental study found that just the opposite was true. We found that simultaneous presentation of infrasound and loud noise actually exacerbated noise-induced lesions, as compared to when loud noise was presented without infrasound. Our interpretation was that low-frequency sound produced an intermixing of fluids (endolymph and perilymph) at the sites of hair cell loss resulting in lesions that were larger. A possibil- ity to be considered is therefore that long-term exposure to infrasound from wind turbines could exacerbate presbycusis and noise-induced hearing loss. Because these forms of hear- ing loss develop and progress slowly over decades, this could be a lurking consequence to human exposures to infrasound that will take years to become apparent.
5. Infrasound Stimulation of the Vestibular Sense Organs
Recent exchanges in this journal between Drs. Leventhall and Schomer concerning the direct stimulation of vestibular receptors by sound at low and infrasonic frequencies deserve comment. Dr. Leventhall asserts that both Drs. Schomer and Pierpont are incorrect in suggesting that wind turbine infra- sound could stimulate vestibular receptors, citing work by Todd in which the ear’s sensitivity was measured in response to mechanical low-frequency stimulation applied by bone
“The million-dollar question is whether the effects of wind turbine infrasound stimulation stay confined to the
ear and have no other influence on the person or animal.”
conduction. Leventhall fails to make clear that there are no studies reporting either vestibular responses, or the absence
of vestibular responses, to acoustically-delivered infrasound. This means that for all his strong assertions, Leventhall cannot refer to any study conclusively demonstrating that vestibular receptors of the ear do not respond to infrasound. Numerous studies have reported measurements of saccular and utricular responses to audible sound. Indeed, such measurements are the basis of clinical tests of saccular and utricular function through the VEMP (vestibular-evoked myogenic potentials). Some of these studies have shown that sensitivity to acoustic stimulation initially declines as frequency is lowered. On the other hand, in vitro experiments demonstrate that vestibular hair cells are maximally sensitive to infrasonic frequencies
(~1 – 10 Hz). Thus, sensitivity to acoustic stimulation may increase as stimulus frequency is lowered into the infrasonic range. Direct in vivo vestibular excitation therefore remains a possibility until it has been shown that the saccule and other vestibular receptors specifically do not respond to this stimu- lation.
Low-frequency tone-induced endolymph hydrops, as dis- cussed above, could increase the amount of saccular stimula- tion by acoustic input. Hydrops causes the compliant saccular membrane to expand, in many cases to the point where it directly contacts the stapes footplate. This was the basis of
the now superseded “tack” procedure for Ménière’s disease, in which a sharp prosthesis was implanted in the stapes footplate to perforate the enlarging saccule (Schuknecht et al., 1970). When the saccule is enlarged, vibrations will be applied to en- dolymph, not perilymph, potentially making acoustic stimu- lation of the receptor more effective. There may also be certain clinical groups whose vestibular systems are hypersensitive to very low-frequency sound and infrasound stimulation. For example, it is known that patients with superior canal dehis- cence syndrome are made dizzy by acoustic stimulation. Sub- clinical groups with mild or incomplete dehiscence could exist in which vestibular organs are more sensitive to low frequency sounds than the general population.
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