A Free-Market Energy Blog

Industrial Wind vs. the Environment (ILFN issues in debate)

By Robert Bradley Jr. -- April 9, 2024

“Inner organs are sensitive for sound and vibration. The current state of knowledge on mechano-transduction together with known oscillatory and oxidative stress effects, point in the direction of our hypothesis and should be reason for urgent precautionary actions and further research.”

It is a very technical subject–but certainly one for deep ecologists that see humankind being a cancer to optimal, fragile Nature. Industrial wind turbines, huge and disruptive in the open space, are certainly man-made and subject to the guilty-until-proven-innocent doctrine of the “precautionary principle.”

Infrasound and low-frequency noise (ILFN) is an important issue that wind apologists do not want to discuss or debate. MasterResource posts by Stephen Cooper and others over many years have made a case that “what you cannot hear can hurt you.” As one critic put it:

More than just audible sound, grinding, whomping, blade pass whooshes, an ever-present hum, industrial wind turbines have a silent, below audible impact. It is not like a day contamination/harm at work where people can go home at night for relief. With industrial wind projects literally engulfing homes and rural areas, there is little or no escape.

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The ILFN debate continues. In the June 2023 issue of Journal of Biosciences and Medicines (Vol. 11; No. 6), “Impairment of the Endothelium and Disorder of Microcirculation in Humans and Animals Exposed to Infrasound due to Irregular Mechano-Transduction,” Ursula Maria Bellut-Staeck presented an important hypothesis for the mainstream to debate (not ignore). The Abstract and Conclusion follow.

Abstract

The microcirculation of mammals is an autoregulated and complex synchronised system according to the current demand for nutrients and oxygen. The undisturbed course of vital functions such as of growth, blood pressure regulation, inflammatory sequence and embryogenesis is bound to endothelial integrity. The sensible vasomotion is particularly dependent on it.

Mechano-transduction signalling networks play a critical role in vital cellular processes and are the decisive physiological mechanism for an adequate NO-release, main responsible for the autoregulation of vessels. Disturbed endothelial integrity, originating, e.g., from chronic oxidative stress and/or mechanic (oscillatory) stress, leads to disturbance of vasomotion as well as a disequilibrium of redox systems, recognized as main cause for the development of chronic inflammation diseases such as atherosclerosis and corresponding secondary illnesses, possibly cancer.

The endothelial cytoskeleton, which corresponds to a viscoelastic “tensegrity model”, offers the possibility for mechano-transduction via its special construction. The rapidly growing knowledge about mechanical forces in cellular sensing and regulation of the last years (that culminated in the Nobel Prize award for the decoding of pressure/vibration sensing ion channels), led us to the following hypothesis: The extern stressor “Noise” produces under certain conditions an oscillatory stress field in the physiologically laminar flow bed of capillaries, which is able to lead to irregular mechano-transductions. Findings provide a strict dependence on frequency in mechano-transduction with determination of thresholds for a 1:1 transmission.

The knowledge, recently gained on endothelial mechano-transduction, sheds a new light on the importance of low frequencies. This could indicate the long-sought pathophysiological way in which infrasound can exert a stressor effect at the cellular level. Noise-exposed citizens, who live near infrastructures such as a biogas installation, heat pumps, block-type thermal power stations and bigger industrial wind turbines (IWT’s), show worldwide mainly a symptomatology associated with microcirculatory disorder. Conceivable are also effects on insects or fishes, since the piezo-channels are recognised as conserved structures of all multicellular organism.

An experimental design is proposed to demonstrate the direct pathological influence of infrasound of defined strength, frequency, effect/time profile and duration on the sensitive vasomotion.

Conclusions

For the first time, the symptomatology of chronically infrasound exposed humans and animals can be classified pathophysiologically in a coherent hypothesis. This was made possible by the progress in knowledge of endothelial mechano-transduction, essential as vascular function of vital character in response to mechanical forces. Crucial cellular processes such as growth, differentiation, migration, angiogenesis, redox homeostasis and inflammation, are simultaneously dependent on mechanical forces and the integrity of the endothelium.

Normally, the flow in the mammalian microcirculation is laminar and not variable. This is achieved by the upstream connection of the resistance vessels in the arterioles. Persistent changes in shear stress patterns, particularly oscillatory flow, have been associated with decreased bioavailability of NO, an increase in reactive oxygen species (ROS), higher lipoprotein oxidation rates, increased endothelial apoptosis, pro-atherogenicity, chronic inflammation and possible development of cancer.

We have positive evidence for our hypothesis that a chronically acting oscillating stressor with certain conditions in frequency, time/effect profile, sound pressure and duration might induce an oscillatory stress field and therefore trigger a stress reaction on the cellular level. With the crucial basics of mechano-transduction, there is now a strong evidence with obvious indicators for a possible interaction of infrasound, especially with deep frequencies and impulsive character, as have, e.g., IWT’s or heat pumps. The elucidation for the strong dependency on mechano-transduction from the frequency of “Noise” and the identification of actin filaments and microtubules as “low-pass filters”, support our hypothesis.

In this way, the propagation of sound wave in the viscoelastic organism could become a decodable information. Regeneration, as would occur with a one-time or infrequent exposure, could not take place with chronic impact. Initially functional disturbances of the orchestrated vasomotor system, respectively of sensible vasomotion,can be expected,with longer exposure fixed anatomically recognisable pathological damages in endothelial integrity. Important in this context are the structural changes that tend to be self-reinforcing, as described in the example of remodelling of the heart.

By probably elucidating the pathophysiological pathway of how infrasound/IFLN could lead to the main health disorders, it will be possible to make steps forward in defining safe distances for living or working with emitting technical installations. Many scientific questions remain to be answered, but there is sufficient evidence to suggest that, as precautionary measurements, further technologies, involving very low frequencies and/or impulsive emissions with potential impact on living organisms, should be limited or better avoided until all issues are scientifically resolved. The possible effects on insects, which have not been clarified yet, could be of great importance, e.g., for the biodiversity and for co-affection of pollinators and thus nutrition.

The decoding of the PIEZO-1-channels should have already alerted public to the potential risks. Inner organs are sensitive for sound and vibration. The current state of knowledge on mechano-transduction together with known oscillatory and oxidative stress effects, point in the direction of our hypothesis and should be reason for urgent precautionary actions and further research.

Final Comment

So will “ExxonKnew” be replaced by “Industrial Wind Knew” in future litigation? When did the issue of infrasound and low-frequency noise first emerge, and did the trade groups in the U.S. and abroad take note and investigate the issue? The future of dilute, intermittent, inefficient, land-intensive, noise-intensive industrial wind power is part of Earth in the Balance.

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