Pathology induced by excessive exposure to human-made infrasound and low frequency noise – basic concepts for the medical community [summary]

Mariana Alves-Pereira, Bruce Rapley, Huub Bakker, Rachel Summer

Presented at the Scientific Colloquium: La santé des hommes et des animaux face aux infrasons produits par les éoliennes, 16 Novembre 2018, Centre Sèvres, Paris, France

Background

Among western medicine, the human hearing threshold as defined by the Fletcher- Munson curves and translated into the dBA metric, is considered to be the only issue of concern when patients complain of ‘noise’ exposure. This position is founded in historical facts, and this philosophy of action has led to a significant minimization of hearing loss due to noise exposure, particularly among noise-exposed workers.

Infrasound and low frequency noise (≤ 200 Hz) (ILFN) are acoustical components that are not, however, covered by the Fletcher-Munson curves, or by the dBA metric. This is not usually taught in medical schools. The dBA metric reflects the human auditory threshold, and is unrelated to the threshold of health effects caused by ILFN exposure.

ILFN has been studied within military settings since the 1960’s Soviet and US space race. Today, the Russians and the Chinese scientists are studying the biological effects of ILFN exposure with controlled laboratorial studies, and in accordance with the axioms of the Scientific Method and its corollary, Evidence-based Medicine. Russia has legislation against infrasound. In Western Europe, however, ILFN has become a taboo subject leading to an uninformed medical community, and consequent misdiagnosis of disease among the general public.

The Physical Agent of Disease

In Medical Sciences, agents of disease are divided into four classes: Biological, Chemical, Physical and Psychosocial. ILFN falls into the category of Physical agents of disease because it is composed of airborne pressure waves. The World Health Organization has termed these airborne pressure waves as inanimate mechanical forces, and Infrasound is, in itself, internationally classified as non-ionizing radiation.

A propagating airborne pressure requires more than one parameter to be properly characterized. Numerical values of time-varying frequencies and time-varying amplitudes differentiate natural ILFN from human-made ILFN. This means that the physical characteristics of the ILFN emanated from natural sources are identifiably different than those emanated from human-made sources.

Physical and Biological Interface

When exposed to an environment rich in human-made ILFN, airborne mechanical forces ‘bombard’ the entire biological organism. Energy transfer occurs when there is some sort of mechanical coupling between the oncoming pressure wave and the viscoelastic material, i.e., biological tissue. Classically, it is considered that this mechanical coupling only occurs at the ear, hence we have sound. In reality, with ILFN-rich environments, mechanical coupling is occurring all over the human body, the extent of which is time-varying and frequency dependent.

Cellular Mechanical Signaling

Cellular architecture is based on tensegrity structures, i.e., composed of elements providing constant tension and others providing discontinuous compression. This is how cellular communication is achieved through mechanical signals, i.e., mechanotransduction. The physical agent of disease, ILFN, is a mechanical agent of disease, and will first be relayed into animal tissues through mechanotransduction. Pathological pathways involving the classical biochemical signaling appear in a second stage.

When the airborne pressure waves impact cells, the immediate response will depend on the direction of the force (anisotropy) and will involve cellular stretching, compression and/or torsion. Biological tissue does not respond to mechanical forces as a Hookean elastic, but rather as a viscoelastic material. This implies the existence of properties such as stress relaxation, creep and hysteresis, which are not considered when modeling a Hookean elastic. Understanding that biological tissues are viscoleastic materials is of fundamental importance to comprehend their response to the onslaught on airborne pressure waves.

Tissue Response

Structures within the biological organism exposed to ILFN tend to thicken. Cardiovascular structures, such as arterial walls, pericardia, and valves, thicken as a response to chronic ILFN exposure. This thickening is caused by the proliferation of collagen and elastin fibers in the absence of an inflammatory process. This has been seen in both human and animal models exposed to ILFN. In ILFN-exposed humans, the pericardial thickening seen through echocardiography is unrelated to pericarditis, as it occurs in the absence diastolic dysfunction, and in the absence of an inflammatory process. The peculiar organization of bundles of collagen, interspersed by elastin fibers, and the morphogenesis of a new pericardial layer of tissue (splitting the original fibrosa layer into two distinct sections), explains why diastolic function remains normal in these patients.

Actin-based structures, such as the cochlear stereocilia and respiratory brush cell microvilli, have been observed to fuse in ILFN-exposed animal models. In the cochlea, fusion occurs amongst the stereocilia and also between the stereocilia and the upper tectorial membrane. In the microvilli of respiratory brush cells, fusion increases with increasing exposure time. Tubulin-based structures were also impaired or destroyed in ILFN-exposed respiratory system cilia and pericardial cilia. Cytoskeletal changes, including the formation of vacuoles have been documented in ILFN-exposed tissue samples. The genotoxicity of ILFN has already been established through several studies quantifying the frequency of sister chromatid exchanges among ILFN-exposed humans and animals.

Health Endpoints

Within the axioms of The Scientific Method and its corollary, Evidence-based Medicine, it is compulsory that health endpoints be objective and capable of being clinically corroborated. For ILFN-induced pathology, these include: a) :cognitive deficits (P300 evoked potentials), b) :structural changes in brain (brain MRI), c) :function of the brainstem (brainstem evoked potentials and lung function tests with evaluation of the neurological control of breathing or respiratory drive), d) :structural changes of the cardiovascular structures (echo-Doppler studies).

Annoyance is not an objective parameter nor is it capable of being clinically corroborated. Cortisol levels (objective and capable of being clinically corroborated) are not particularly useful to assess health in these chronic-stress situations, i.e., occupational or residential exposures to human-made ILFN. Biomarkers associated with hemostasis and coagulation changes would, perhaps, be more appropriate.

Conclusion

ILFN is a fast-growing problem within urban and rural residential areas, occupational settings and leisure activities. Continuing to ignore the presence of ILFN as an agent of disease among human populations is dangerous, unethical and unacceptable.

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