Belyaev (2015) has discussed a number of what he describes as biophysical models which are, therefore considered here. These models are basically theoretical models of how the weak electrical forces of the EMFs can interact with biologically plausible structures to produce non- thermal effects.
The first of these Belyaev considers is Fröhlich’s theory. This is where there are “coherent longitudinal vibrations of electrically polar structures.”
A second possible mechanism involves the spin state of radical pairs.
When radical pairs are generated from the breakdown of a non-radical molecule, these radical pairs often react back with each other to form another non-radical molecule, not necessarily identical to the original non-radical. What is postulated by this theory is that EMFs can interact with one or both radicals, changing their spin state and greatly lowering their ability to react back with each other, thus generating increased free radicals and therefore increased oxidative stress. The potential strong point of this theory is that it provides an explanation for the oxidative stress found following EMF exposure. However, as noted under oxidative stress
Oxidative stress following EMF exposure is produced by peroxynitrite elevation and is not primarily produced by this radical pair mechanism.
A third mechanism discussed in Belyaev (2015) is the electrosoliton theory proposed by Brizhik and colleagues, involving a “self reinforcing solitary wave packet.” Brizhik and her colleagues discussed this in the context of reaching a threshold minimum energy state where both charged molecules and the EMF is in a coherent state, such that charge movement can ratchet from one state to another.
Belyaev (2015) discusses microwave hearing in this context. He discusses the findings showing that people can hear microwave fields that are pulsed, including pulsed low intensity EMFs. While there is no doubt that these are very interesting observations on what are clearly non-thermal effects, they do not provide a biophysical model explaining how microwave hearing may occur.
There is a literature showing that aqueous solutions of DNA absorb microwave EMFs much more efficiently than do iden- tical solutions not containing DNA.
Given the extraordinary complexity of living cells and organisms, there are only two powerful ways of demonstrating causal roles in such living cells and organisms. These are to use genetics or to use specific pharmacological agents. But these two approaches can be used when specific proteins have specific roles, not when you are looking at the role of DNA structural changes, Fröhlich’s theory, radical pair mechanisms or electrosoliton models. Fortunately the VGCC mechanism does allow this approach by studying various classes of calcium channel blockers, so here we do have hard data on widespread causal roles of VGCC acti- vation in producing EMF effects.
There are two other models which may be more compelling, each of which either produces increased [Ca2+]i.
Studies have supported the view that calcium cyclotron re- sonance, has a role in producing biological effects produced by certain specific frequencies which can interact with Ca2+ ions to produce a cy- clotron-like resonance (Foletti et al., 2010; Gaetani et al., 2009; De Carlo et al., 2012; Lisi et al., 2008; Pazur and Rassadina, 2009; Pazur et al., 2006).
In the De Carlo et al. (2012) study, the calcium channel blocker nife- dipine was shown to greatly lower the apparent calcium cyclotron re- sonance effect. This finding strongly suggests that the calcium cyclotron resonance can feed Ca2+ ions into the VGCCs, thus increasing the flow of Ca2+ ions through the VGCCs into the cell following EMF exposure. The frequencies studied here for cyclotron resonance, one was close to 7 Hz and the other was close to 50 Hz, are both in the extremely low frequency range and consequently are not relevant to microwave frequency effects.
It is now well established that there is a magnetoreception me- chanism found in many animals that can detect and respond to the very low intensity geomagnetic field. This has been most studied in bees and in birds, both of whom use it for navigation. This has been suggested to involve tiny particles of magnetite which occur in bacterial, animal and plant cells, including human cells. Kirschvink (1992) first proposed a model of how such a mechanism might act. He proposed that magnetite particles may be tethered through a microtubule and/or microfilament or perhaps other fibers to a mechanosensitive channel, such that tiny magnetic forces could open the mechanosensitive channels, allowing cation flow into the cells.
The calcium cyclotron resonance mechanism only acts with a few specific fre- quencies in the extremely low frequency range. The magnetoreception mechanism only acts, as far as one can tell, on detecting the weak geomagnetic fields and only acts, as far as one can tell, in certain spe- cific neurons. It is possible that this view may change with regard to the magnetoreception mechanism but what is clear is that the VGCC me- chanism is vastly more important than either of these mechanisms, acting in diverse cell types and acting to provide responses to a very wide frequency range and even to static electrical fields and static magnetic fields. Because static magnetic fields only place forces on moving electric charges, this produced a puzzle on how they can activate the VGCCs. Pall (2013) suggested that the solution to that puzzle is that the plasma membrane of animal cells is often moving, such that the charges in the voltage sensor are also moving and can, therefore, have forces placed on them by the static magnetic fields. These static magnetic fields, activating the VGCCs can be relative low intensity but probably must be much higher intensity than the extra- ordinarily weak geomagnetic fields. The reader is referred to Lu et al. (2015) for empirical information from an important static magnetic field study, where those static magnetic fields activate both VGCCs and voltage-gated sodium channels.
artificial EMFs are polarized with the polarization producing much larger biological effects than natural non-polarized EMFs (Belyaev, 2005, 2015; Panagopoulos et al., 2015a). The probable im- portant feature of these polarized EMFs is that they put much larger forces on electrically charged groups (Panagopoulos et al., 2015a); since such forces are central to VGCC activation via the voltage sensor,
In 24 different studies reviewed earlier (Pall, 2013) and two additional studies (Li et al., 2014; Lisi et al., 2006), microwave and lower frequency low intensity EMF effects were blocked or greatly lowered by calcium channel blockers, agents thought to be specific for blocking voltage-gated calcium channels (VGCCs). In these 26 studies, a total of 5 distinct types of channel blockers were used, with each type having a distinct structure and binding to a distinct site, such that it is essentially certain that these must be acting by blocking VGCCs, which is their only known common property.
The majority of the histological changes seen in these mostly rodent studies, are seen in the nervous system, despite its being less than 2% of the rodent cell mass. There are statements made that the nervous system, both central and peripheral, is the most highly sensitive tissue to these non-thermal microwave and lower frequency EMFs. Following the nervous system in sensitivity are the myocardium and the testis; myocardial cells are known to have very high densities of VGCCs with especially high densities in the pacemaker cells and the testis is known to have high densities specifically of the T-type VGCCs. Pulsed EMFs are more active in producing histological changes in the brain than are non-pulsed fields, in two studies reviewed; there is a much larger literature showing that in most cases pulsed fields are more biologically active (Pall, 2015; Pangopoulos et al., 2013; Belyaev, 2015).
While there were many studies of brain impact of non-thermal EMFs performed in the 1950s/60s that make the information content of Tolgskaya and Gordon (1973) quite high, there is also a substantial recent literature on brain effects of non-thermal microwave EMF exposures (see, for example: Ammari et al., 2008a,b; Bas et al., 2009; Brillaud et al., 2007; Carballo-Quinta ́s et al., 2011; Eberhardt et al., 2008; Dasdag et al., 2009, 2012; Grafstro ̈ m et al., 2008; Kumlin et al., 2007; Lo ́ pez-Martı ́n et al., 2006; Mausset-Bonnefont et al., 2004; Odaci et al., 2008; Rag ̆betli et al., 2010; Salford et al., 2003; Sonmez et al., 2010).