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Documents presented here are not the product of nor are they necessarily endorsed by National Wind Watch. These resource documents are provided to assist anyone wishing to research the issue of industrial wind power and the impacts of its development. The information should be evaluated by each reader to come to their own conclusions about the many areas of debate.


Date added:  April 1, 2014
Health, NoisePrint storyE-mail story

How Does Wind Turbine Noise Affect People?

Author:  Salt, Alec; and Lichtenhan, Jeffery

Introduction

Recent articles in Acoustics Today have reviewed a number of difficult issues concerning wind turbine noise and how it can affect people living nearby (Leventhall 2013, Schomer 2013; Timmerman 2013). Here we present potential mechanisms by which effects could occur.

The essence of the current debate is that on one hand you have the well-funded wind industry 1. advocating that infrasound be ignored because the measured levels are below the threshold of human hearing, allowing noise levels to be adequately documented through A-weighted sound measurements, 2. dismissing the possibility that any variants of wind turbine syndrome exist (Pierpont 2009) even when physicians (e.g., Steven D. Rauch, M.D. at Harvard Medical School) cannot otherwise explain some patients’ symptoms, and, 3. arguing that it is unnecessary to separate wind turbines and homes based on prevailing sound levels.

On the other hand you have many people who claim to be so distressed by the effects of wind-turbine noise that they cannot tolerate living in their homes. Some move away, either at financial loss or bought-out by the turbine operators. Others live with the discomfort, often requiring medical therapies to deal with their symptoms. Some, even members of the same family, may be unaffected. Below is a description of the disturbance experienced by a woman in Europe we received a few weeks ago as part of an unsolicited e-mail.

From the moment that the turbines began working I experienced vertigo-like symptoms on an ongoing basis. In many respects, what I am experiencing now is actually worse than the ‘dizziness’ I have previously experienced, as the associated nausea is much more intense. For me the pulsating, humming, noise that the turbines emit is the predominant sound that I hear and that really seems to affect me.

While the Chief Scientist [the person who came to take sound measurements in her house] undertaking the measurement informed me that he was aware of the low frequency hum the turbines produced (he lives close to a wind farm himself and had recorded the humming noise levels indoors in his own home) he advised that I could tune this noise out and that any adverse symptoms I was experiencing were simply psychosomatic.

We asked how she felt when she was away from the wind turbines, to which she replied:

I did manage to take a vacation towards the end of August and for the two weeks we were away I was perfectly fine.

The goal of our work in this field is to understand whether the physiology of the ear can, or cannot, explain the symptoms people attribute to wind turbine noise. As it is generally the case when debate influences a specific industry’s financial interests and legal well-being, the scientific objectivity of those associated with the industry can be questioned. Liability, damage claims, and large amounts of money can hang in the balance of results from empirical studies. Whether it is a chemical industry blamed for contaminating groundwater with cancer-causing dioxin, the tobacco industry accused of contributing to lung cancer, or athletes of the National Football League (NFL) putatively being susceptible to brain damage, it can be extremely difficult to establish the truth when some have an agenda to protect the status quo. It is only when sufficient scientific evidence is compiled by those not working for the industry that the issue is considered seriously.

Origins of Our Involvement in Infrasound from Wind Turbines

What is the evidence leading us to conclude that unheard infrasounds are part of the wind turbine problem, and how did we become involved in this debate? We are small group of basic and applied scientists, which means that our work addresses fundamental questions on how the ear works in normal and diseased states. While developing paradigms for our studies, we had been using a classic technique called “low-frequency biasing” – measurement of auditory responses to a test sound within the range of audibility, while simultaneously presenting a low-frequency tone (e.g., 4.8 to 50 Hz) to displace the sensory organ of the inner ear. Some auditory responses saturate when displaced by the bias tone, which can be used to establish whether the sensory organ is vibrating symmetrically or whether a fluid disturbance has displaced it to one side. A condition called “endolymphatic hydrops,” which is found in humans with Ménière’s disease, can displace the sensory organ as the space containing the fluid called endolymph swells. In our animal experiments we initially used 20 to 50 Hz bias tones, but for many reasons, and in large part based on a study in which we found that the ear responded down to 1 Hz (Salt and DeMott, 1999), we started using the lowest frequency our hardware could generate, 4.8 Hz, a frequency considered to be infrasound. Over the course of hundreds of experiments, we have found numerous biasing effects with 4.8 Hz tones at levels of 80 to 90 dB SPL (i.e., −13 to −3 dBA). We also found that the ear became about 20 dB more sensitive to infrasonic bias tones when the fluid spaces in the cochlear apex were partially occluded, as occurs with endolymphatic hydrops.

In late 2009, the first author received a report of a woman with Ménière’s disease whose symptoms – primarily dizziness and nausea – were severely exacerbated when she was in the vicinity of wind turbines. From our animal data, we knew this woman was likely hypersensitive to very low-frequency sounds. Our subsequent review of the literature on wind-turbine noise revealed two aspects that were absolutely astounding:

1. Almost all measurements of wind turbine noise are A-weighted, making the unjustified assumption that hearing is the only way by which infrasound generates physiologic effects. The few studies that reported un-weighted measurements of wind-turbine noise, or recalculated spectra by removing the A-weighting from published A-weighted spectra, clearly demonstrated increasing energy towards low frequencies with highest energy levels in the infrasound region. We were surprised that objective full-frequency measurements showed that wind turbines generate infrasound at levels capable of stimulating the ear in various ways. Under such circumstances, A-weighting measurements of turbine noise would be highly misleading.

2. Literature and websites from the wind industry often contained strong statements that wind turbine infrasound was of no significance. This view was largely based on publications by Leventhall (2006; 2007). Wind turbine noise was described as comparable to rustling leaves, flowing streams, air-conditioned offices or refrigerators heard from the next room. If wind turbine noise really was comparable to such sources then complaints would not be expected. But the turbines sounds are only comparable to these sources if the ultra-low frequencies emitted by the turbines are ignored through A-weighting. Stations that monitor infrasound or low frequency seismic (vibrational) noise for other purposes (for the detection of explosions, meteors, volcanic activity, atmospheric activity, etc.) are well-aware that low frequency sounds emanating from distant wind farms, or coupling to the ground as vibrations, can influence their measurements. The UK, Ministry of Defense has opposed wind turbines cited within 50 km of the Eskdalemuir Seismic Array. We have seen no reports of the Ministry opposing the presence of refrigerators in the region, suggesting they appreciate that sounds emitted from wind turbines and refrigerators are quite different. It was thus quite astounding to see the vast majority of wind turbine noise measurements excluding the low frequency noise content. Given the knowledge that the ear responds to low frequency sounds and infrasound, we knew that comparisons with benign sources were invalid and the logic to A-weight sound measurements was deeply flawed scientifically.

The Ear’s Response to Infrasound

Experimental measurements show robust electrical responses from the cochlea in response to infrasound (Salt and DeMott, 1999; Salt and Lichtenhan 2013). This finding was initially difficult to reconcile with measures showing that hearing was notably insensitive to such sounds but the explanation became clear from now-classic physiological studies of the ear showing that the two types of sensory cell in the cochlea had very different mechanical properties (Cheatham and Dallos 2001).

Figure 1: The sensory organ of the cochlea, showing inner and outer hair cell and neural anatomy.

Figure 1: The sensory organ of the cochlea, showing inner and outer hair cell and neural anatomy.

The auditory portion of the inner ear, the cochlea, has two types of sensory cell. The inner hair cells (IHC; shown green in Figure 1) are innervated by type I afferent nerve fibers that mediate hearing. The stereocilia (sensory hairs) of the IHCs are free-floating and do not contact the overlying gelatinous tectorial membrane (shown gray). They are mechanically displaced by fluid movements in the space below the membrane. As their input is fluid-coupled to the vibrations of the sensory organ they exhibit “velocity sensitive” responses. As the velocity of motions decreases for lower-frequency sounds, their fluid-coupled input renders the IHC insensitive to very low-frequency sounds. The other type of sensory cell, the outer hair cells (OHC; shown red in Figure 1) are innervated by type II afferent nerve fibers that are not as well understood as type I fibers and probably do not mediate conscious hearing per se. In contrast to the IHC, the stereocilia of the OHCs are inserted into the tectorial membrane. This direct mechanical coupling gives them “displacement sensitive” properties, meaning they respond well to low–frequency sounds and infrasound. The electrical responses of the ear we had been recording and studying originate from the sensitive OHCs. From this understanding we conclude that very low frequency sounds and infrasound, at levels well below those that are heard, readily stimulate the cochlea. Low frequency sounds and infrasound from wind turbines can therefore stimulate the ear at levels well below those that are heard.

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. At present, the stance of wind industry and its acoustician advisors is that there are no consequences to long-term low-frequency and infrasonic stimulation. This is not based on studies showing that long-term stimulation to low-level infrasound has no influ-ence on humans or animals. No such studies have ever been performed. Their narrow perspective shows a remarkable lack of understanding of the sophistication of biological systems and is almost certainly incorrect. As we consider below, there are many physiologic mechanisms by which long-term infrasound stimulation of the cochlea could have effects.

One important aspect of wind turbine noise that is relevant to its physiological consequences is that the duration of exposure can be extremely long, 24 hours a day and lasting for days or longer, depending on prevailing wind conditions. This is considerably different from most industrial noise where 8 hour exposures are typically considered, interspersed by prolonged periods of quiet (i.e., quiet for 16 hours per day plus all weekends). There are numerous studies of exposures to higher level infrasound for periods of a few hours, but to date there have been no systematic studies of exposure to infrasound for a prolonged period. The degree of low-frequency cochlear stimulation generated by wind turbine noise is remarkably difficult to assess, due to the almost exclusive reporting of A-weighted sound level measurements. It certainly cannot be assumed that cochlear stimulation is negligible because A-weighted level measurements are low. For example, with 5 Hz stimulation cochlear responses are generated at −30 dBA and stimulation is sufficient to cause responses to saturate (indicating the transducer is being driven to its limit) at approximately 20 dBA (Salt and Lichtenhan, 2012; Salt et al., 2013). We have also shown that 125 Hz low-pass filtered noise at just 45 dBA produces larger responses than wide band noise with the same low-frequency content presented at 90 dBA (Salt and Lichtenhan 2012). We conclude that low frequency regions of the ear will be moderately to strongly stimulated for prolonged periods by wind turbine noise. There are a number of plausible mechanisms by which the stimulation could have effects:

1. Amplitude Modulation: Low-Frequency Biasing of Audible Sounds

Modulation of the biological mechano-electric transducer of the inner ear by infrasound is completely different from the amplitude modulation of audible sounds that can be measured with a sound level meter near wind turbines under some conditions. This can be demonstrated in low-frequency biasing paradigms in which a low-frequency tone and higher-frequency audible tone are presented simultaneously to a subject.

OHCs respond to both low- and high-frequency components and modulate the high-frequency components by either saturation of the mechano-electric transducer or by cyclically changing the mechanical amplification of high frequencies. IHCs, being insensitive to the low-frequency tone, see a high pass-filtered representation of the OHC response – an amplitude modulated version of the audible probe tone, as shown in Figure 2. As hearing is mediated through the IHCs that receive approximately 90-95% of afferent innervation of the auditory nerve, the subject hears the higher-frequency probe tone varying in amplitude, or loudness. A similar biasing influence on cochlear responses evoked by low-level tone pips was explained by the low-frequency bias tone changing OHC-based cochlear amplifier gain (Lichtenhan 2012). This same study also showed that the low frequency, apical regions of the ear were most sensitive to low-frequency biasing. Studies like this raise the possibility that the amplitude modulation of sounds, which people living near wind turbines reportas being so highly annoying, may not be easily explained by measurements with an A-weighted sound level meter. Rather, the low-frequency and infrasound levels need to be considered as contributing to the perceived phenomenon. Subjectively, the perceived fluctuation from an amplitude modulated sound and from a low-frequency biased sound are identical even though their mechanisms of generation are completely different. For the subject, the summed effects of both types of amplitude modulation will contribute to their perception of modulation. Acousticians therefore need to be aware that the degree of modulation perceived by humans and animals living near wind turbines may exceed that detected by a sound level meter.

Figure 2: Demonstration of biologically-generated amplitude modulation to a non-modulated stimulus consisting of an audible tone at 500 Hz tone summed with an infrasonic tone at 4.8 Hz. The cochlear microphonic response, which is generated by the OHC, includes low and high frequency components. The IHC detect only the high frequency component, which is amplitude modulated at twice the infrasound frequency for the stimuli in this example.

Figure 2: Demonstration of biologically-generated amplitude modulation to a non-modulated stimulus consisting of an audible tone at 500 Hz tone summed with an infrasonic tone at 4.8 Hz. The cochlear microphonic response, which is generated by the OHC, includes low and high frequency components. The IHC detect only the high frequency component, which is amplitude modulated at twice the infrasound frequency for the stimuli in this example.

2. Endolymphatic Hydrops Induced by Low Frequency Tones

As mentioned above, endolymphatic hydrops is a swelling of the innermost, membrane bound fluid compartment of the inner ear. Low-frequency tones presented at moderate to moderately-intense levels for just 1.5 to 3 minutes can induce hydrops (Figure 3), tinnitus (ringing in the ears) and changes in auditory potentials and acoustic emissions that are physiological hallmarks of endolymphatic hydrops (Salt, 2004, Drexl et al. 2013).

Unlike the hearing loss caused by loud sounds, the symptoms resulting from endolymphatic hydrops are not permanent and can disappear, or at least fluctuate, as the degree of hydrops changes. Return to quiet (as in Figure 3) or relocation away from the low-frequency noise environment allow the hydrops, and the symptoms of hydrops, to resolve. This which would be consistent with the woman’s description of her symptoms given earlier. As hydrops is a mechanical swelling of the membrane-bound endolymphatic space, it affects the most distensible regions first – known to be the cochlear apex and vestibular sacculus. Patients with saccular disturbances typically experience a sensation of subjective vertigo, which would be accompanied by unsteadiness and nausea. As we mentioned above, an ear that has developed endolymphatic hydrops becomes >20 dB more sensitive to infrasound because the helicotrema becomes partially obstructed (Salt et al. 2009). The possibility of a positive feedback – low-frequency induced hydrops that causes the ear to be more sensitive to low frequencies – has to be considered. To date, all studies of low-frequency tone-induced hydrops have used very short duration (1-2 min) exposures. In humans, this is partly due to ethical concerns about the potential long-term consequences of more prolonged exposures (Drexel et al., 2013). Endolymphatic hydrops induced by prolonged exposures to moderate levels of low-frequency sound therefore remains a real possibility.

Figure 3: Brief exposures to low-frequency tones cause endolymphatic hydrops in animals (Salt, 2004) and tinnitus and acoustic emission changes consistent with endolymphatic hydrops in humans (Drexel et al, 2013). The anatomic pictures at the right show the difference between the normal (upper) and hydropic (lower) cochleae The endolymphatic space (shown blue) is enlarged in the hydropic cochlea, generated surgically in this case.

Figure 3: Brief exposures to low-frequency tones cause endolymphatic hydrops in animals (Salt, 2004) and tinnitus and acoustic emission changes consistent with endolymphatic hydrops in humans (Drexel et al, 2013). The anatomic pictures at the right show the difference between the normal (upper) and hydropic (lower) cochleae The endolymphatic space (shown blue) is enlarged in the hydropic cochlea, generated surgically in this case.

3. Excitation of Outer Hair Cell Afferent Nerve Pathways

Approximately 5-10% of the afferent nerve fibers (which send signals from the cochlea to the brain – the type II fibers mentioned above) synapse on OHCs. These fibers do not respond well to sounds in the normal acoustic range and they are not considered to be associated with conscious hearing. Excitation of the fibers may generate other percepts, such as feelings of aural fullness or tinnitus. Moreover, it appears that infrasound is the ideal stimulus to excite OHC afferent fibers given what has been learned about these neurons from in vitro recordings (Weisz et al, 2012; Lichtenhan and Salt, 2013). In vivo excitation of OHC afferents has yet to be attempted with infrasound, but comparable fibers in birds have been shown to be highly sensitive to infrasound (Schermuly and Klinke, 1990). OHC afferents innervate cells of the cochlear nucleus that have a role in selective attention and alerting, which may explain the sleep disturbances that some people living
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 experimental 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 possibility 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 hearing 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 infrasound 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 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 to 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 stimulation.

Low-frequency tone-induced endolymph hydrops, as discussed above, could increase the amount of saccular stimulation 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 endolymph, not perilymph, potentially making acoustic stimulation 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 dehiscence syndrome are made dizzy by acoustic stimulation. Subclinical groups with mild or incomplete dehiscence could exist in which vestibular organs are more sensitive to low frequency sounds than the general population.

6. Potential Protective Therapy Against Infrasound

A commonly-used clinical treatment could potentially solve the problem of clinical sensitivity to infrasound. Tympanostomy tubes are small rubber “grommets” placed in a myringotomy (small incision) in the tympanic membrane (eardrum) to keep the perforation open. They are routinely used in children to treat middle ear disease and have been used successfully to treat cases of Ménière’s disease. Placement of tympanostomy tubes is a straightforward office procedure. Although tympanostomy tubes have negligible influence on hearing in speech frequencies, they drastically attenuate sensitivity to low frequency sounds (Voss et al., 2001) by allowing pressure to equilibrate between the ear canal and the middle ear. The effective level of infrasound reaching the inner ear could be reduced by 40 dB or more by this treatment. Tympanostomy tubes are not permanent but typically extrude themselves after a period of months, or can be removed by the physician. No one has ever evaluated whether tympanostomy tubes alleviate the symptoms of those living near wind turbines. From the patient’s perspective, this may be preferable to moving out of their homes or using medical treatments for vertigo, nausea, and/or sleep disturbance. The results of such treatment, whether positive, negative, would likely have considerable scientific influence on the wind turbine noise debate.

Conclusions and Concerns

We have described multiple ways in which infrasound and low-frequency sounds could affect the ear and give rise to the symptoms that some people living near wind turbines report. If, in time, the symptoms of those living near the turbines are demonstrated to have a physiological basis, it will become apparent that the years of assertions from the wind industry’s acousticians that “what you can’t hear can’t affect you” or that symptoms are psychosomatic or a nocebo effect was a great injustice. The current highly-polarized situation has arisen because our understanding of the consequences of long-term infrasound stimulation remains at a very primitive level. Based on well-established principles of the physiology of the ear and how it responds to very low-frequency sounds, there is ample justification to take this problem more seriously than it has been to date. There are many important scientific issues that can only be resolved through careful and objective research. Although infrasound generation in the laboratory is technically difficult, some research groups are already in the process of designing the required equipment to perform controlled experiments in humans.

One area of concern is the role that some acousticians and societies of acousticians have played. The primary role of acousticians should be to protect and serve society from negative influences of noise exposure. In the case of wind turbine noise, it appears that many have been failing in that role. For years, they have sheltered behind the mantra, now shown to be false, that has been presented repeatedly in many forms such as “What you can’t hear, can’t affect you.”; “If you cannot hear a sound you cannot perceive it in other ways and it does not affect you.”; “Infrasound from wind turbines is below the audible threshold and of no consequence.”; “Infrasound is negligible from this type of turbine.”; “I can state categorically that there is no significant infrasound from current designs of wind turbines.” All of these statements assume that hearing, derived from low-frequency-insensitive IHC responses, is the only mechanism by which low frequency sound can affect the body. We know this assumption is false and blame its origin on a lack of detailed understanding of the physiology of the ear.

Another concern that must be dealt with is the development of wind turbine noise measurements that have clinical relevance. The use of A-weighting must be reassessed as it is based on insensitive, IHC-mediated hearing and grossly misrepresents inner ear stimulation generated by the noise. In the scientific domain, A-weighting sound measurements would be unacceptable when many elements of the ear exhibit a higher sensitivity than hearing. The wind industry should be held to the same high standards. Full-spectrum monitoring, which has been adopted in some reports, is essential.

In the coming years, as we experiment to better understand the effects of prolonged low-frequency sound on humans, it will be possible to reassess the roles played by acousticians and professional groups who partner with the wind industry. Given the present evidence, it seems risky at best to continue the current gamble that infrasound stimulation of the ear stays confined to the ear and has no other effects on the body. For this to be true, all the mechanisms we have outlined (low-frequency–induced amplitude modulation, low frequency sound-induced endolymph volume changes, infrasound stimulation of type II afferent nerves, infrasound exacerbation of noise-induced damage and direct infrasound stimulation of vestibular organs) would have to be insignificant. We know this is highly unlikely and we anticipate novel findings in the coming years that will influence the debate.

From our perspective, based on our knowledge of the physiology of the ear, we agree with the insight of Nancy Timmerman that the time has come to “acknowledge the problem and work to eliminate it”.

Alec N. Salt and Jeffery T. Lichtenhan
Department of Otolaryngology, Washington University School of Medicine, St. Louis, Missouri

Acoustics Today, Volume 10, Issue One, Winter 2014
doi: 10.1121/1.4870173

References

Cheatham, M.A., Dallos, P. (2001). “Inner hair cell response patterns: implications for low-frequency hearing,” Journal of the Acoustical Society of America 110:2034-2044.

Drexl, M., Überfuhr, M., Weddell, T.D., Lukashkin, A.N., Wiegrebe, L., Krause, E., Gürkov, R. (2013). “Multiple Indices of the ‘Bounce’ Phenomenon Obtained from the Same Human Ears,” Journal of the Association for Research in Otolaryngology. (e-pub, before print copy) doi:10.1007/s10162-013-0424-x

Harding, G.W., Bohne, B.A., Lee S.C., Salt A.N. (2007). “Effect of infrasound on cochlear damage from exposure to a 4 kHz octave band of noise,” Hearing Research 225:128-138.

Leventhall, G. (2006). “Infrasound From Wind Turbines – Fact, Fiction Or Deception,” Canadian Acoustics 34:29-36.

Leventhall, G. (2007). “What is infrasound?,” Progress in Biophysics and Molecular Biology 93:130–137.

Leventhall, G. (2013). “Concerns About Infrasound from Wind Turbines,” Acoustics Today 9, 3, 30-38.

Liberman, M.C., Dodds, L.W., Pierce, S. (1990). “Afferent and efferent innervation of the cat cochlea: quantitative analysis with light and electron microscopy,” Journal of Comparative Neurology 301:443-460.

Lichtenhan, J.T. (2012). “Effects of low-frequency biasing on otoacoustic and neural measures suggest that stimulus-frequency otoacoustic emissions originate near the peak region of the traveling wave,” Journal of the Association for Research in Otolaryngology 13:17-28.

Lichtenhan, J.T., Salt, A.N. (2013). “Amplitude modulation of audible sounds by non-audible sounds: Understanding the effects of wind turbine noise.” Proceedings of Meetings on Acoustics, Vol. 19: Journal of the Acoustical Society of America 133(5):3419.

Nissenbaum M.A., Aramini J.J., Hanning C.D. (2012). Effects of industrial wind turbine noise on sleep and health. Noise Health 14(60):237-243.

Pierpont, N. (2009). “Wind Turbine Syndrome.” K-Selected Books.

Salt, A.N., DeMott, J.E. (1999). “Longitudinal endolymph movements and endocochlear potential changes induced by stimulation at infrasonic frequencies,” Journal of the Acoustical Society of America. 106, 847-856.

Salt, A.N. (2004). “Acute endolymphatic hydrops generated by exposure of the ear to nontraumatic low frequency tone,” Journal of the Association for Research in Otolaryngology 5:203-214.

Salt, A.N., Brown, D.J., Hartsock, J.J., Plontke, S.K. (2009). “Displacements of the organ of Corti by gel injections into the cochlear apex,” Hearing Research 250:63-75.

Salt, A.N., Lichtenhan, J.T. (2102). “Perception-based protection from low-frequency sounds may not be enough,” Proceedings of the InterNoise Symposium, New York.

Salt, A.N., Lichtenhan, J.T., Gill, R.M., Hartsock, J.J. (2013). “Large endolymphatic potentials from low-frequency and infrasonic tones in the guinea pig,” Journal of the Acoustical Society of America 133:1561-1571.

Schermuly, L, Klinke, R. (1990). “Origin of infrasound sensitive neurones in the papilla basilaris of the pigeon: an HRP study,” Hearing Research 48:69-77.

Schomer, P. (2013). “Comments On Recently Published Article, “Concerns About Infrasound From Wind Turbines,” Acoustics Today 9, 4, 7-9.

Schuknecht, H.F. (1977). “Pathology of Ménière’s disease as it relates to the sac and tack procedures,” Annals of Otology, Rhinology and Laryngology 86:677-82.

Timmerman, N.S. (2013). “Wind Turbine Noise,” Acoustics Today 9, 3, 22-29.

Voss, S.E., Rosowski, J.J., Merchant, S.N., Peake, W.T.. (2001). “Middle-ear function with tympanic-membrane perforations. I. Measurements and mechanisms,” Journal of the Acoustical Society of America 110:1432-1444.

Weisz, C.J., Lehar, M., Hiel, H., Glowatzki, E., Fuchs, P.A. (2012). “Synaptic Transfer from Outer Hair Cells to Type II Afferent Fibers in the Rat Cochlea,” Journal of Neuroscience 32:9528-9536.

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Date added:  March 30, 2014
Noise, Regulations, U.K.Print storyE-mail story

Den Brook Amplitude Modulation Condition

Author:  National Wind Watch

Den Brook Timeline:

2005  -  RES submit planning application to West Devon Borough Council (WDBC) for nine wind turbines in the Den Brook valley between Bow, Spreyton and North Tawton
2006 Jan  -  WDBC refuses planning permission
2006 May  -  RES file Planning Appeal
2007 Feb  -  Planning Inspector grants planning permission
2007 Mar  -  Mike Hulme lodges Judicial Appeal
2008 Mar  -  Judicial Appeal refused by High Court
2008 Apr  -  Hulme appeals to Court of Appeal
2008 Aug  -  Court of Appeal requires redetermination of Planning Appeal by Inspector
2009 Dec  -  Inspector grants planning permission with conditions
2010 Jan  -  Hulme lodges appeal to Court of Appeal
2011 May  -  Court of Appeal upholds planning permission and conditions
2013 Apr  -  RES applies to amend AM conditions
2013 Aug  -  RES withdraws application to amend AM conditions
2014 Feb  -  RES submits scheme for complying with AM conditions

The “Den Brook Amplitude Modulation Condition”:

Excess amplitude modulation was defined in condition 20 of the December 2009 planning permission as any change, upon complaint, outside the dwelling, in LAeq,125ms of >3 dB in any 2-second period ≥5 times in any minute with LAeq,1min ≥28 dB and such excess occurring in ≥6 minutes in any hour.

“LAeq,125ms” is the equivalent A-weighted continuous sound level (average) over a 125-millisecond period, “LAeq,1min” over a 1-minute period.

In other words, a 125-ms pulse of 3 dBA or greater (3 dB being the difference in noise level detectable by the human ear) can not occur in any 2-second period five or more times in six or more minutes of any hour, when those minute-long average noise levels are 28 dBA or more.

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Date added:  March 30, 2014
Australia, Health, NoisePrint storyE-mail story

Letter to the AMA re its recent paper concerning wind turbines

Author:  Waite, Geoffrey

I am a retired psychologist and was a member of both the Clinical and Counselling Colleges of the Australian Psychological Society when they were active. I have been in private practice for over 25 years as well as being the principal psychologist in a large rural hospital for five years.

Recently I visited some areas of rural South Australia and Victoria and spoke with quite a number of people who claimed to be adversely affected by the operation of industrial wind turbines in their vicinity. I queried if 100% of them could be affected by this new “nocebo effect” when its opposite – the placebo effect, was usually apparent in only 30% of experimental subjects. Unfortunately there is no reputable research supporting this “nocebo effect” so it must remain a guess.

Naturally as a psychologist (retired) I was interested in the deeper story than the widely reported symptoms I was hearing about. I was greatly disturbed when I was unable to find any other cause for their suffering than the turbines. So I did some research. What became obvious was the following:

  1. Wind turbines make noise.
  2. Noise affects people.
  3. Some noise makes people happy and healthy, some noise makes people depressed and sick.

More detailed research provided some more information behind the above statements:

1. Wind turbines make noise.

Rick James, in a paper by Alec N. Salt 2010, provides graphs of recordings titled Industrial Wind Turbines Generate Infrasound (http://oto2.wustl.edu/cochlea/wt1.html). These clearly illustrate the sound generated by wind turbines, both those sounds people can hear (e.g. blade passes) and those they can not (called infrasound).

wind-turbine-infrasound

http://www.windturbinesyndrome.com/2013/acoustician-explains-wind-turbine-infrasound-low-frequency-noise-rick-james

2. Noise affects people.

The noise people can hear is obvious and affects people, some to their advantage and some to their disadvantage

The noise people can not hear is less obvious. Some is benign and some sickening.

It has been said that if a person can not hear something it can’t affect them. This is untrue. It is also untrue of the other senses – Infra red and ultraviolet light can not be seen but one burns your eyes and the other burns your skin: some poisons can not be tasted but can still kill you – e.g. tetrodotoxin (puffer fish poison), salmonella and cholera toxin: carbon monoxide, carbon dioxide can not be smelled but can kill a person.

Again noise people can hear has obvious affects – fingernails scratching a black board, a beautiful symphony, the deep beat of a rock band, the scream of a jet fighter, the brakes of a truck and so on.

www.windturbinesyndrome.com/2013

Sound that most people can not hear is either too highly pitched (high frequency) or too low (lower frequency than 20 Hz).

There is lots of anecdotal evidence that some infrasound, sound you normally don’t hear, makes you sick. Here are some of the health problems reported:

SYMPTOM/PROBLEM LIST:

1. Acute Vestibular Dysfunction/Disorder (first 12 also listed by Affadavit of Dr Owen Black, MD, May 2009, De Kalb County, Illinois) to the recent Australian Senate enquiry.

2. Acute Sympathetic Nervous System Stimulation

The following three conditions are rare, but important to mention.

3. Chronic Sleep Disturbance and Its Consequences

4. Known Clinical Consequences of Repetitive Sleep Disturbance/Deprivation

5. Combined Stress (Psychological and Physiological) and Its Consequences

6. Tissue Damage

The items below have been reported to from Germany in residents exposed for over 10 years:

The pathology is identical to that described in workers and others studied by the Portuguese researchers who first described VAD or vibroacoustic disease, (see www.wind-watch.org/documents/vibroacoustic- disease-biological-effects-of-infrasound-and-low-frequency-noise-explained-by-mechanotransduction-cellular-signalling/) now being diagnosed in others including most recently Taiwanese aviation workers (Chao et al, http://docs.wind-watch.org/chao.html).

Finally, there are growing concerns about the potential for foetal abnormalities with increasing exposures to larger wind turbines and therefore more ILFN and V. These foetal abnormalities are being reported by some farmers in their stock (cattle, sheep) at rates which are noticeably increased for them since wind turbines commenced operating. The farmers who disclosed this keep accurate records of their stock numbers and problems, and were clear in their reports. The aetiological agent is not clear, and no one is systematically collecting this data, as with human health.

There is research evidence indicating concerns about the impact of vibration on embryos (referred to previously). Vibration is being reported by some of the residents, living near wind turbines and living near coal mines in the Upper Hunter. The vibration from wind turbines is also reported by institutions with seismic arrays, which are part ofa worldwide network to detect nuclear explosions. The characteristic acoustic signature is being detected significant distances away from such institutions in Scotland and Germany. Links to those pieces of research are at: www.wind-watch.org/documents/inaudible-noise-of-wind-turbines/, www.wind-watch.org/documents/microseismic-and-infrasound-monitoring-of-low-frequency-noise-and-vibrations-from-windfarms/, and there is research done in New Zealand by Dr Bob Thorne and colleagues measuring seismic energy from larger 3MW V90 Vestas wind turbines reported to be disturbing residents, at www.wind-watch.org/documents/seismic-effect-on-residents-from-3-mw-wind-turbines/.

The long-term impact of chronic exposure to such low “dose” of vibration is unknown. It is my impression, however, that where a resident is reporting the perception of vibration, the resident’s health appears to be negatively impacted more rapidly, even when compared to others living in the same home.

All of the above problems listed have the characteristic pattern of improving partially or completely when the turbines are off, or when the residents are away from their homes. Some residents also report subsequently being affected by other sources of ILFN, such as when flying, or when exposed to LFN from heating and cooling (air conditioning) compressors, which is to be expected, as they have become “sensitized” to LFN. This phenomena of “sensitization” was noted by Professor Leventhall in 2003, where he also made it clear that if people moved away from the sources of the LFN their condition improved. What is being observed is that many sick people who do not or cannot move away, deteriorate with cumulative exposure.

Useful sources:

1. Letter to Professor Chapman, www.wind-watch.org/documents/letter-from-sarah-laurie-to-
simon-chapman/

2. Table on page 49 of Leventhall DEFRA Literature Review 2003 (reproduced from www.wind-
watch.org/documents/review-of-published-research-on-low-frequency-noise-and-its-effects/
)

3. Leventhall et al, DEFRA Literature Review, 2003, www.wind-watch.org/documents/review-of-
published-research-on-low-frequency-noise-and-its-effects/

4. NIEHS Literature Review, 2001 (www.wind-watch.org/documents/infrasound-brief-review-of-toxicological-literature/)

5. Capuccio, F et al, “Sleep Duration predicts cardiovascular outcomes: a systemic review and meta-
analysis of prospective studies” European Heart Journal (2011) 32, 1484-1492

6. McEwen, B, “Protective and Damaging Effects of Stress Mediators” New England Journal of Medicine, 1998, 338 171 – 179

7. Shannon et al, October 1994, “Effect of Vibration and Frequency Amplitude on developing chicken
Embryos” US Army Aeromedical Research Laboratory, Fort Rucker, Alabama

8. Alves Pereira et al, 2007, www.wind-watch.org/documents/vibroacoustic-disease-biological-effects-of-infrasound-and-low-frequency-noise-explained-by-mechanotransduction-cellular-signalling/

Does this fit with biology and neurology?

The vestibular system in the brain does more than just allow us to stand upright, maintain balance and move through space. It coordinates information from the vestibular organs in the inner ear, the eyes, muscles and joints, fingertips and palms of the hands, pressors on the soles of the feet, jaw, and gravity receptors on the skin and adjusts heart rate and blood pressure, muscle tone, limb position, immune responses, arousal and balance. The auditory system is also highly involved in vestibular functions. The vestibular and auditory nerves join in the auditory canal and become the eighth cranial nerve of the brain. Anything that disrupts auditory information can also affect vestibular functioning.

Dr. Alec Salt and his team at the Department of Otolaryngology, Washington University School of Medicine, St. Louis, Missouri, USA, including Stephen E. Ambrose, INCE (Brd. Cert.) Robert W. Rand, INCE Member, have conducted extensive research into vestibular response to sound pressure pulsations. (Salt, A., http://oto2.wustl.edu/cochlea/wt7.html. Stephen E. Ambrose, INCE (Brd. Cert.)) Their research shows that the ear responds to sound we cannot hear.

There are two types of hair cells in the cochlea, the inner hair cells (IHCs) and the outer hair cells (OHCs). The IHCs are fluid-connected and velocity-sensitive, responding to minute changes in the acoustic pressure variations based on frequency, with sensitivity decreasing at a rate of -6 dB per downward octave. IHCs detect audible sounds and they are insensitive to low frequency and infrasonic acoustic energy. In contrast, the OHCs are motor as well as sensory cells.

OHCs are found only in mammals. OHCs are mechanically connected, responding to small changes in displacement, with a more uniform sensitivity across the acoustic frequency spectrum. OHCs respond to and contract with infrasonic stimulus and then act to reduce vibration stimulus at the IHCs. Thus there are actually two specialized receptors, or transducers, in each ear. Furthermore this research has highlighted the importance of the vestibular system, in particular regarding low frequency (and what is generally termed ‘infrasound’). The fact that air exists within the human body including, the sinuses, the Eustachian tube and the lungs, demonstrates that the potential avenues for acoustic energy to impact on the body clearly extends beyond the ear canal. Very low frequencies, the ‘booming bass’ at rock concerts, is certainly perceived, that is felt, in the body proper. Blood gravisensors and proprioception mechanisms clearly signal the brain that acoustic vibrations are being perceived. Indeed, this is one of the main ‘attractions’ of such loud music venues. The physiological and cognitive effects of this are less clearly demonstrable.

However, Dr. Carey D. Balaban, Ph.D., Professor of Otolaryngology, Biological Sciences, Neurological Surgery at the University of Chicago, has as his primary research goal to develop a rational basis for understanding the neurobiology of the vestibular system so that new therapies for vestibular disorders can be designed. This goal is approached by: (1) identifying the organization of central vestibular circuits that mediate autonomic and somatic motor responses to vestibular stimulation; (2) identifying neurotransmitters and intracellular signal transduction proteins that are important in these brain circuits; (3) examining the role of these biochemical constituents in responses to challenges from toxins and mechanical (blast) injury; and (4) identifying contributions of these mechanisms to the clinical linkage among balance disorders, anxiety disorders (panic with agoraphobia) and migrainous vertigo. More details about how these goals were achieved by addressing the research identifications and examinations in (1) to (4) above can be found at Expert Rev Neurother. 2011 March; 11(3): 379–394. doi:10.1586/ern.11.19. These studies have a strong translational component through interactions with Drs. Joseph Furman, Rolf Jacob, Dawn Marcus, Susan Whitney, John Durrant and Mark Redfern.

The studies conclude that over the previous 20 years, clinical observations and basic research have provided evidence that the prevalent comorbidity of balance disorders, motion sickness, migraine and anxiety disorders is not a chance occurrence. Many comorbid combinations have been reported. Balance disorders (both neuro-otologic disease and chronic subjective dizziness) are often comorbid with psychiatric disorders [1–5] and with migraine [6–8]. Migraine is often associated with vertigo [10–12]. The increased motion sickness susceptibility in migraineurs [8,13–15] is attenuated by tryptan treatment [16,17]. Migraine is also associated with phobic disorders and panic disorder [9]. Migraine and balance disorders are comorbid with anxiety disorders [6,7]. We suggest that three mechanisms may contribute to the comorbidity and overlap in treatment regimens. First, the parallel patterns of serotonin, TRPV1 and purinergic receptor expression in trigeminal, vestibular and spiral ganglion cells are consistent with parallel therapeutic effects at the level of primary afferents. Second, parallel behavior of protein extravasation in inner ear, meningeal and peripheral tissues and activation of central trigeminal and vestibular pathways may contribute to comorbid migraine, vestibular disorders and hyperacusis or tinnitus. Since these migraine and audio vestibular symptoms share common peripheral mechanisms, they are expected to respond in parallel to treatment that reduces extravasation. Finally, the parallel organization of vestibular and nociceptive pathways through the parabrachial nucleus and thalamus to the amygdala and cerebral cortex is consistent with a common central representation of interoceptive well-being, which influences control of affect. The clinical picture that emerges is a balance disorder–migraine–anxiety syndrome that can manifest differentially in different patients, with comorbid components that can respond to similar treatment regimens. References numbered above are as follows:

1. Furman JM, Jacob RG. A clinical taxonomy of dizziness and anxiety in the otoneurologic setting. J Anxiety Disord. 2001; 15:9–26. [PubMed: 11388360]

2. Jacob, RG.; Furman, JM.; Balaban, CD. Psychiatric aspects of vestibular disorders. In: Baloh, RW.; Halmagyi, GM., editors. Handbook of Neurotology/Vestibular System. Oxford University Press; Oxford, UK: 1996. p. 509-528.

3. Staab JP. Chronic dizziness: the interface between psychiatry and neuro-otology. Curr Opin Neurol. 2006; 19(1):41–48. [PubMed: 16415676]

4. Staab JP, Ruckenstein MJ. Chronic dizziness and anxiety: effect of course of illness on treatment outcome. Arch Otolaryngol Head Neck Surg. 2005; 131(8):675–679. [PubMed: 16103297]

5. Staab JP, Ruckenstein MJ. Expanding the differential diagnosis of chronic dizziness. Arch Otolaryngol Head Neck Surg. 2007; 133:170–176. [PubMed: 17309987]

6. Furman JM, Balaban CD, Jacob RG, Marcus DA. Migraine-anxiety associated dizziness (MARD): a new disorder? J Neurol Neurosurg Psychiatry. 2005; 76:1–8. [PubMed: 15607984]

7. Furman JM, Marcus DA, Balaban CD. Migrainous vertigo: development of a pathogenetic model and structured diagnostic interview. Curr Opin Neurology. 2003; 16:5–13.

8. Marcus DA, Furman JM, Balaban CD. Motion sickness in migraine sufferers. Expert Opin Pharmacotherapy. 2005; 6(15):2691–2697.

9. Radat F, Swendsen J. Psychiatric morbidity in migraine: a review. Cephalagia. 2004; 25:165–178.

10. Cutrer FM, Baloh RW. Migraine-associated dizziness. Headache. 1992; 32:300–304. [PubMed: 1399552]

11. Neuhauser H, Leopold M, von Brevern M, Arnold G, Lempert T. The interrelations of migraine, vertigo, and migrainous vertigo. Neurology. 2001; 56(4):436–441. Provides the seminal clinical description of migrainous vertigo. [PubMed: 11222783]

12. Lempert T, Neuhauser H. Epidemiology of vertigo, migraine and vestibular migraine. J Neurol. 2009; 256:333–338. [PubMed: 19225823]

13. Drummond PD. Motion sickness and migraine: optokinetic stimulation increases scalp tenderness, pain sensitivity in the fingers and photophobia. Cephalagia. 2002; 22:117–124.

14. Drummond PD. Triggers of motion sickness in migraine sufferers. Headache. 2005; 45(6):653– 656. [PubMed: 15953297]

15. Drummond PD, Granston A. Facial pain increases nausea and headache during motion sickness in migraine sufferers. Brain. 2004; 127(3):526–534. [PubMed: 14749288]

16. Furman JM, Marcus DA. A pilot study of rizatriptan and visually-induced motion sickness in migraineurs. Int J Med Sci. 2009; 6:212–217. [PubMed: 19680473]

17. Furman JM, Marcus DA, Balaban CD. Rizatriptan reduces vestibular-induced motion sickness in migraineurs. J Headache Pain. 2010 (Epub ahead of print). 10.1007/s10194-010-0250-z

So to paraphrase:

  1. Primary afferent activation runs from trigeminal, vestibular and spiral ganglion cells.
  2. Second, parallel behavior of protein extravasation in inner ear, meningeal and peripheral tissues and activation of central trigeminal and vestibular pathways may contribute to comorbid migraine, vestibular disorders and hyperacusis or tinnitus.
  3. Finally, the parallel organization of vestibular and nociceptive pathways through the parabrachial nucleus and thalamus to the amygdala and cerebral cortex is consistent with… the clinical picture that emerges (as) a balance disorder–migraine–anxiety syndrome.

What is also well known from the trauma literature is that the amygdala is the primary site of warning to the brain oftentimes bringing on extreme fear, flight or fight reactions, panic and high level anxiety, and affects the thalamus to assist in reaction to threat.

Ellert R.S. Nijenhuis writes that there is evidence that the adult brain may regress to an infantile state when it is confronted with severe stress (Jacobs and Nadel, 1985, Le Doux, 1996). As Le Doux argues, the amygdala is essentially involved in very rapidly and automatically instigated physiological and behavioral responses to a major threat, as well as the classical conditioning of these threat responses. This conditioning yields probably indelible associations between unconditioned and conditioned stimuli. Extreme stress does not interfere with, and may amplify, memory processes mediated by the amygdala (Corodimas, LeDoux, Gold and Schulkin, 1994) [even if the threat comes from an infrasound stimulated Vestibular system], but it does hamper hippocampal-neocortical information processing which should inhibit or regulate emotional reactions and memories [turbine affected people may not have access to information they have been told about the bad effects of turbines – which mitigates against any so-called ‘nocebo effect’]. Chronic release of stress hormones may even damage the hippocampus. This stress-induced condition resembles the infantile state, which is characterized by functioning amygdala and a relatively immature hippocampal-neocortical system. Extreme stress may therefore evoke defensive reactions in adults which are also evoked in young children.(This text is in Ellert R.S. Nijenhuis, Somatoform Dissociation, page 117, 2004, W.W. Norton and Company, New York, as are the quoted references). It is easy to see why people exposed to a toxic stimulation of the vestibular system wake from sleep in terror.

Wind turbines make noise.

Noise affects people.

The noise you can and cannot hear from wind turbines makes you sick and sometimes very sick.

Geoffrey Waite
March 30, 2014

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Date added:  March 28, 2014
Health, NoisePrint storyE-mail story

Wind farms and health

Author:  Evans, Alun

According to the World Health Organisation’s recent report, ‘Night Noise Guidelines for Europe’ [1], environmental noise is emerging as one of the major public health concerns of the twenty-first century. It observes that, “Many people have to adapt their lives to cope with the noise at night,” and the young and the old are particularly vulnerable. This is because hearing in young people is more acute and, in older people, a loss of hearing of higher sound frequencies renders them more susceptible to the effects of low frequency noise. It is a particularly troublesome feature of the noise generated by wind turbines due to its impulsive, intrusive and incessant nature. A recent case-control study conducted around two wind farms in New England has shown [2] that subjects living within 1.4 km of an IWT had worse sleep, were sleepier during the day, and had poorer SF36 Mental Component Scores compared to those living further than 1.4 km away. The study demonstrated a strongly significant association between reported sleep disturbance and ill health in those residing close to industrial wind turbines.

The major adverse health effects caused seem to be due to sleep disturbance and deprivation with the main culprits identified as loud noise in the auditory range, and low frequency noise, particularly infrasound. This is inaudible in the conventional sense, and is propagated over large distances and penetrates the fabric of dwellings, where it may be amplified. It is a particular problem at night, in the quiet rural settings most favoured for wind farms, because infrasound persists long after the higher frequencies have been dissipated.

Sleep is a physiological necessity and the sleep-deprived are vulnerable to a variety of health problems [2,3]. particularly Cardiovascular Disease in which nocturnal noise is an important factor [4]. Sleep deprivation in children is associated with increased bodyweight [3,5], which is known to ‘track’ into later life, and predisposes to adult disease. That is why “Encouraging more sleep” is a sensible target in the Public Health Agency’s current campaign to prevent obesity in children. It also causes memory impairment because memories are normally reinforced in the later, Rapid Eye Movement, phase of sleep; again, it is the young and the old who are most affected.

Sleep deprivation is associated with an increased likelihood of developing a range of chronic diseases including Type II Diabetes, cancer (eg breast with shift work [6]), Coronary Heart Disease [7,8] and Heart Failure [9]. Although the quality of the data are mixed, those on Heart Failure reported recently from the HUNT Study [9] are quite robust as they are based on 54,279 Norwegians free of disease at baseline (men and women aged 20-89 years). A total of 1412 cases of Heart Failure developed over a mean follow-up of 11.3 years. A dose-dependent relationship was observed between the risk of disease and the number of reported insomnia symptoms: i) Difficulty in initiating sleep; ii) Difficulty in maintaining sleep; and, iii) Lack of restorative sleep. The Hazard Ratios were ‘0’ for none of these; ‘0.96’ for one; ‘1.35’ for two; and, ‘4.53’ for three; this achieved significance at the 2% level. This means that such a result could occur once by chance if the study were to be repeated 50 times, Significance is conventionally accepted at the 5% level.

Another important, recent study is MORGEN which followed nearly 18,000 Dutch men and women, free of Cardiovascular Disease at baseline, over 10-14 years [8]. In this period there were 607 events: fatal CVD, non-fatal Myocardial Infarction and Stroke. Adequate sleep, defined as at least seven hours, was a protective factor which augmented the benefits conferred by the absence of four traditional cardiovascular risk factors. For example, the benefit of adequate sleep equalled the protective contribution of not smoking cigarettes. Given that cigarette smoking is such a potent risk factor for Cardiovascular Disease, this result is striking. The findings built on earlier ones from the MORGEN study [7]. It seems that adequate sleep is important in protecting against a range of Cardiovascular Diseases which result when arteries of different sizes are compromised: large (coronary, cerebral) arteries in heart attacks and stroke, small arteries (arterioles) in heart failure.

All of these studies share the weakness that they are ‘observational’ as opposed to ‘experimental’ and, as such, their results do not constitute ‘proof.’ We now have the evidence of an experimental study carried out in human volunteers which shows that the expression of a large range of genes is affected by sleep deprivation of fairly short duration [10]. This might be the key to understanding why the health effects of sleep deprivation are so diverse. It could also shed light on the ‘Wind Turbine Syndrome,’ a cluster of symptoms which include sleep disturbance, fatigue, headaches, dizziness, nausea, changes in mood and inability to concentrate [11]. In this condition infrasound is a likely causal agent.

This group has now shown in another small intervention study that mistimed sleep desynchronized from the central circadian clock has a much larger effect on the circadian regulation of the human transcriptome (i.e., a reduction in the number of circadian transcripts from 6.4% to 1% and changes in the overall time course of expression of 34% of transcripts) [12]. This may elucidate the reasons for the large excess of cardiovascular events associated with shift work found in a meta-analysis of over 2 million subjects in 34 studies [13]. The results demonstrate that any interference in normal sleeping patterns is inimical to cardiovascular health.

The old admonition that ‘What you can’t hear won’t harm you,’ sadly isn’t true. It is now known that organ of Corti in the cochlea (inner ear) contains two types of sensory cells: one row of inner hair cells which are responsible for hearing; and, three rows of outer hair cells which are more responsive to low frequency sound [14]. The infrasound produced by wind turbines is transduced by the outer hair cells and transmitted to the brain by Type II afferent fibres. The purpose is unclear as it results in sleep disturbance. Perhaps it served some vital function in our evolutionary past which has persisted to our detriment today? In fact, many animals use infrasound for communication and navigation. This could well have a genetic basis as it is only a minority, albeit a sizable one, which is affected. This may well be the group which is also liable to travel sickness. Schomer et al have now advanced the theory that as wind turbines increase in size they increasingly emit infrasound with a frequency below 1Hz (CPS) [15]. Below this frequency the otoliths in the inner ear respond in an exaggerated way in a susceptible minority who will suffer symptoms of the Wind Farm Syndrome. Previously it was thought that the brain was only under the control of electrical and biochemical stimuli but there is new evidence that it is sensitive, in addition, to mechanical stimuli [16].

The problem of infrasound and low frequency noise was well-recognised in a report by Casella Stanger [17], commissioned by DEFRA in 2001, and since ignored: “For people inside buildings with windows closed, this effect is exacerbated by the sound insulation properties of the building envelope. Again mid and high frequencies are attenuated to a much greater extent than low frequencies.” It continued: “As the A-weighting network attenuates low frequencies by a large amount, any measurements made of the noise should be with the instrumentation set to linear.” It drew heavily upon the DOE’s Batho Report of 1990 [18]. In fact, these problems had already been elucidated and the measurement issues addressed in a trio of papers by Kelley (et al) in the 1980s [19-21]. This research again has been ignored or forgotten so the problem continues to be seriously underestimated. When measured using a tool which can detect it, levels of infrasound and low frequency noise are disturbingly high, with ‘sound pressure levels’ greater than previously thought possible [22].

There are a number of other adverse effects associated with sleep deprivation. Tired individuals are more likely to have road traffic accidents and injure themselves while operating machinery. In addition, wind turbines can, and do, cause accidents by collapsing, blade snap, ice throw, and even going on fire. They induce stress and psychological disorder from blade flicker, which also has implications for certain types of epilepsy and autism. Even the current planning process, with its virtual absence of consultation, is stress inducing, as is the confrontation between land owners, who wish to profit from erecting turbines, and their neighbours who dread the effects. Finally, wind turbines considerably reduce the value of dwellings nearby and this has a negative long term effect on their owners’ and their families’ health [23]. On top of this, increasing numbers of families will be driven into fuel poverty by spiralling electricity costs which are subsidising wind energy. It is galling that SSE’s current, seductive advertising campaign is being supported from these sources.

‘Wind Turbine Noise’ was reviewed in an editorial in the British Medical Journal in 2012 [24]. The authors concluded that “A large body of evidence now exists to suggest that wind turbines disturb sleep and impair health at distances and noise levels that are permitted in most jurisdictions.” This remains the case today. The Public Health Agency has dismissed this editorial as falling short of a ‘systematic review,’ which is fair enough, given the constraints of the format, yet ignores at least one, excellent, recent systematic review [23]. Interestingly, that review records the fact that in 1978 the British Government was found guilty in a case taken to Europe by the Irish Government of applying five techniques, including subjection to noise and deprivation of sleep. These were used in Ulster to ‘encourage’ admissions and to elicit information from prisoners and detainees. They amounted to humiliating and degrading treatment, ie torture [23].

The Public Health Agencies in the UK are now relying on a document published in April 2013 [25]. It was written by a group of acousticians at the University of Salford, which begs the question as to why such a group was selected to give advice on health issues. Since acousticians derive a significant proportion of their income from the wind industry, their scientific objectivity might be open to question. Similarly, if a profession, which worked closely with the tobacco industry, was asked to report on health, questions would be asked.

The wind industry has at times acted in a way that is reminiscent of the tobacco industry in the past. Recently a Vestas Powerpoint presentation from 2004 has surfaced [26] demonstrating that Vestas knew a decade ago that safer buffers were required to protect neighbours from wind turbine noise. They knew their pre-construction noise models were inaccurate and that “we know that noise from wind turbines sometimes annoys people even if the noise is below noise limits.” Some of this is due to the methods they use to measure noise. Presenting mean amplitude data means that 50% of the peak noise is disguised. In 2011 the CEO of Vestas wrote [27] to the Danish Minister of Environment admitting that it was not technically possible to produce wind turbines which produced less noise. Simiarly, we are repeatedly told that modern turbines are quieter and produce less ILFN which in reality is the reverse of the case [28].

The Salford Report concludes that there is “some evidence for sleep disturbance which has found fairly wide, though not universal, acceptance.” The increasing weight of evidence of sleep deprivation’s association with several chronic diseases is totally ignored. The authors of the report are at pains to deny any ‘direct’ health effects. In terms of prevention any differentiation between ‘direct’ and ‘indirect’ is irrelevant: the introduction of iodine supplementation in milking cattle to improve their “reproductive performance” during the 1960s indirectly led to a reduction in endemic goitre in humans. This was thanks to the unforeseen spillover of iodine into milk and dairy products [29].

In 2008 the distinguished American acoustic engineers George Kamperman and Richard James posed the question [30], “What are the technical options for reducing wind turbine noise emission at residences?” They observed that there were only two options: i) Increase the distance between source and receiver; or, ii) Reduce the source sound power emission. It is generally accepted that as larger and larger wind turbines are built, the noise problems are aggravated [29]. They added [30] that neither solution is compatible with the objective of the wind farm developer to maximise the wind power electrical generation within the land available.

Although the associations between noise pollution and ill health can be argued against, and there are gaps in our knowledge, there is sufficient evidence to cause grave misgivings about its safety. Further research, supported by adequate funding, remains necessary. Good and caring Government should entailcting with greater caution when its policies could jeopardise the health and human rights of its people. It is essential that the Primum non nocere, or ‘Precautionary’, principle should be applied.

In conclusion, there are serious adverse health effects associated with noise pollution generated by wind turbines. It is essential that separation distances between human habitation and wind turbines are increased. There is an international consensus emerging for a separation distance of 2 km, indeed some countries are opting for 3 km. The current guideline on separation distance is based on ETSU-R-97 and is manifestly out of date. It is only relevant to the small turbines of that era. The vastly increased scale of today’s turbines means that the current recommendation on turbine separation is grossly inadequate.

References

[1] World Health Organisation. Night noise guidelines for Europe. Copenhagen. 2009.

[2] Nissenbaum MA, Aramini JJ, Hanning CD. Effects of industrial wind turbine noise on sleep and health. Noise & Health 2012;14: 237-43.

[3] Basner M, Babisch W, Davis A et al. Auditory and non-auditory effects of noise and health. Lancet 2013, dx.doi.org/10.1016

[4] Hume KI, Brink M, Basner M. Effects of environmental noise on sleep. Noise & Health 2013:IP 193.171.77.1

[5] Carter PJ, Taylor BJ, Williams SM, Taylor RW. Longitudinal analysis of sleep in relation to BMI and body fat in children: the FLAME study. BMJ 2011;342:d2712

[6] Chung SA, Wolf TK, Shapiro CM. Sleep and health consequences of shift work in women. J Women’s Health 2009;18:965-77.

[7] Hoevenaar-Blom MP, Annemieke MW, Spijkerman AMW, Kromhout D, van den Berg JF, Verschuren WMM. Sleep Duration and Sleep Quality in Relation to 12-Year Cardiovascular Disease Incidence: The MORGEN Study. SLEEP 2011;34:1487-92.

[8] Hoevenaar-Blom MP, Annemieke MW, Spijkerman AMW, Kromhout D, Verschuren WMM. Sufficient sleep duration contributes to lower cardiovascular disease risk in addition to four traditional lifestyle factors: the MORGEN study. Eur J Prevent Cardiol 2013; doi: 10.1177/2047487313493057.

[9] Laugsand LE, Strand LB, Platou C, Vatten LJ, Janszky I. Insomnia and the risk of incident heart failure: a population study. Eur Heart J 2013 doi:10.1093/eurheartj/eht019.

[10] Möller-Levet CS, Archer SN, Bucca G, et al. Effects of insufficient sleep on circadian rhythmicity and expression amplitude of the human blood transcriptome. PNAS 2013; doi/10.1073/pnas.1217154110.

[11] Pierpont N. Wind Turbine Syndrome: A Report on a Natural Experiment. K Selected Publications, Santa Fe, New Mexico 2009.

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[26] http://aefweb.info/data/AUSWEA-2004conference.pdf

[27] See attachment to covering email message.

[28] Møller H, Pedersen CS. Low-frequency noise from large wind turbines. J Acoust Soc Am 2011;129:3727-44.

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[30] Kamperman GW, James R. The “How To” guide to siting wind turbines to prevent health risks from sound (P 8): http://www.windturbinesyndrome.com/wp-content/uploads/2008/10/kamperman-james-8-26-08-report-43-pp.pdf

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