Within the context of noise-induced health effects, the impact of airborne acoustical phenomena on biological tissues, particularly within the lower frequency ranges, is very poorly understood. Although the human body is a viscoelastic-composite material, it is generally modeled as Hooke elastic. This implies that acoustical coupling is considered to be nonexistent at acoustical frequencies outside of the human auditory threshold. Researching the acoustical properties of mammalian tissue raises many problems. When tissue samples are investigated as to their pure mechanical properties, stimuli are not usually in the form of airborne pressure waves. Moreover, since the response of biological tissue is dependent on frequency, amplitude, and time profile, precision laboratory equipment and relevant physiological endpoints are mandatory requirements that are oftentimes difficult to achieve. Drawing upon the viscoelastic nature of biological tissue and the tensegrity model of cellular architecture, this chapter will visit what is known to date on the biological response to a variety of different acoustic stimuli at very low frequencies.
Exposure to infrasonic and lower frequency airborne pressure waves can cause cellular and tissue damage depending on frequency, dB-level, and exposure time, while the viscoelastic properties inherent to biological tissues impart a nonlinear response to this type of acoustic stressor. The complex mechanosensitive and biochemical cellular signaling pathways mediating this cellular damage have not yet been pinpointed, although fasciae structures and connective tissues (including the neuroglia) seem to be the most sensitive under longer term exposures. Immediate exposures appear to induce inflammatory processes that do not seem to be maintained with longer exposures.
Widespread vascular involvement (not limited to the biological structures addressed herein) was observed in palpebral and bulbar conjunctiva and retina, gastric mucosa, liver structures, lungs, pleura and tracheae, alveoli, pericardia, and coronary arteries. This vascular response may (unsuspectingly) be the underlying cause of many symptomatic complaints. Cognitive deficits oftentimes documented within residential field laboratories may not merely be due to sleep deprivation, but also to hippocampal neuronal damage. Fasciae morphogenesis speaks to the demand on the whole-body structural integrity elicited by this type of external mechanical insult, while collagenous growths and hemorrhagic events of a focal nature may reflect concomitant resonance phenomena.
Recovery periods are not linear, and 2-hour daily exposures imply a 22-hour nonexposure period. This presents a problem for continuous exposures, such as those encountered in some professional activities and most residential environments. The underlying objectives of most of the studies discussed herein are related to occupational exposures and do not consider continuous exposures at less than 90 dB, nor are pressure pulsed trains presented within the laboratorial acoustic environments. In residential environments, however, these attributes are often present. The simulation of residential exposures does not appear to have yet been integrated into laboratory settings and protocols.
The whole-body response also elicits the immune system, affects organs of the reproductive system, changes receptor cells in the vestibular semicanals and auditory cochlea, and induces genotoxic effects, including teratogenesis. This is a pioneering field of science, still in its infancy and urgently requiring scientists from multidisciplinary areas of study because, ultimately, the health of human populations and their offspring must be protected.