In the two studies on calcium overload following Wi-Fi exposure, such overload was measured a substantial time period following exposure. Overload was shown to be caused, to a substantial effect, by increased TRPV1 re- ceptor activity (Çiğ and Nazıroğlu, 2015; Ghazizadeh and Nazıroğlu, 2014). The TRPV1 receptor is known to be activated by oxidative stress. It is my view, discussed in detail below, that there is a central me- chanism that acts to produce excessive intracellular calcium im- mediately following EMF exposure and that the oxidative stress/TRPV1 activation is secondary.
We have then, major impacts of non-thermal EMF exposures on both of the most important intercellular regulatory systems in the body, the nervous system and the endocrine systems. We have major impacts on what may be the most important intracellular regulatory system, the calcium regulatory system. And we also have non-thermal EMFs at- tacking the DNA of our cells, putting our biological inheritance at great risk.
The most extensively reviewed of these is that pulsed EMFs are usually much more biologically active than are non-pulsed (also known as continuous wave) EMFs of identical frequency and similar average in- tensity (Osipov, 1965; Pollack and Healer, 1967; Creighton et al., 1987; Grigor’ev, 1996; Belyaev, 2005, 2015; Markov, 2007; Van Boxem et al., 2014; Pall, 2015b; Panagopoulos et al., 2015b). This pattern of action is particularly important because all wireless communication devices, including Wi-Fi (Panagopoulos et al., 2015b; Maret, 2015) commu- nicate via pulsations and are likely to be particularly dangerous as consequence of this. Panagopoulos et al., 2015b have argued that the more pulsed they are, the more damaging EMFs will be and while this may still be questioned, it may well be a roughly applicable general- ization.
It can be seen that dose-response curves are often both non-linear and non-monotone whereas industry linked groups often assume a linear and therefore monotone dose-response curve.
EMFs have been shown to be particularly active in producing effects on embryonic stem cells (Lee et al., 2014; Belyaev et al., 2009; Markovà et al., 2010; Czyz et al., 2004; Xu et al., 2016; Bhargav et al., 2015; Odaci et al., 2008; Uchugonova et al., 2008; Wang et al., 2015; Teven et al., 2012). Because such stem cells occur at much higher cell densities in children, with stem cell densities the highest in the fetus and de- creasing with increasing age (Belyaev et al., 2009; Markovà et al., 2010), impacts on young children are likely to be much higher than in adults. The decreased DNA repair and increased DNA damage following EMF exposure strongly suggest that young children may be increasingly susceptible to cancer following such exposures (Belyaev et al., 2009; Markovà et al., 2010; Czyz et al., 2004). EMF action on stem cells may also cause young children to be particularly susceptible to disruption of brain development (Xu et al., 2016; Bhargav et al., 2015), something that may be relevant to autism causation.
Redmayne and Johansson (2015) reviewed the literature showing that there are age-related effects, such that young people are more sensitive to EMF effects. It follows from these various findings that the placement of Wi-Fi into schools around the country may well be a high level threat to the health of our children as well being a threat to teachers and any very sensitive fetuses teachers may be carrying, as well.
How do EMF exposures lead to non-thermal health impacts?
The author found the answer to this question in the already published scientific literature (Pall, 2013). That study showed that in 24 different studies [there are now a total of 26 Pall (2015b)], effects of low-intensity EMFs, including microwave frequency and also extremely low frequency EMFs, static electrical fields and static magnetic fields could be blocked by calcium channel blockers, drugs that are specific for blocking voltage-gated calcium channels (VGCCs). There were 5 different types of calcium channel blockers used in these studies, each thought to be highly specific, each structurally distinct and each binding to a different site on the VGCCs. In studies where multiple ef- fects were studied, all studied effects were blocked or greatly lowered by calcium channel blockers. These studies show that EMFs produce diverse non-thermal effects via VGCC activation Pall (2013, 2014, 2015a, 2015b, 2016a, 2016b)) in many human and animal cells. In plant cells, EMFs activate somewhat similar calcium channels and produce somewhat similar effects on oxidative stress, cellular DNA damage and calcium signaling (Pall, 2016a).
The VGCCs each have a voltage sensor which is made up of 4 alpha helixes in the plasma membrane, with each such helix having 5 positive charges on it, for a total of 20 positive charges (Pall, 2015b). These voltage sensor helixes are each called S4 helixes because each is the fourth helix in a distinct multi-helix domain. Each of these voltage sensor charges is within the lipid bilayer part of the plasma membrane. The electrical forces on the voltage sensor are very high for three distinct reasons (Pall, 2015b, 2015a, 2016a). 1. The 20 charges on the voltage sensor make the forces on voltage sensor 20 times higher than the forces on a single charge. 2. Because these charges are within the lipid bilayer section of the membrane where the dielectric constant is about 1/120th of the dielectric constant of the aqueous parts of the cell, the law of physics called Coulomb’s law, predicts that the forces on those charges will be approximately 120 times higher than the forces on charges in the aqueous parts of the cell. 3. Because the plasma membrane has a high electrical resistance whereas the aqueous parts of the cell are highly conductive, the electrical gradient across the plasma membrane is estimated to be concentrated about 3000-fold. The combination of these effects means that comparing the forces on the voltage sensor with the forces on singly charged groups in the aqueous parts of the cell, the forces on the voltage sensor are approximately 20 × 120 × 3000 = 7.2 million times higher (Pall, 2015b). The physics predicts, therefore, extraordinarily strong forces activating the VGCCs via the voltage sensor. It follows that the biology tells us that the VGCCs are the main target of the EMFs and the physics tells us why they are the main target. Thus the physics and biology are pointing in the same direction.
The Tabor et al. (2014) study also used genetic probing to determine the role of the voltage-gated sodium channels. Lu et al. (2015) also used whole cell patch clamp measure- ments to measure the rapid influx of both sodium and calcium into the cell via the voltage-gated channels following EMF exposure. Sodium influx, particularly in electrically active cells, act in the normal phy- siology to depolarize the plasma membrane, leading to VGCC activation such that the voltage-gated sodium channels may act primarily via in- direct activation of the VGCCs. In summary then, we have evidence that in animal including human cells, seven distinct classes of voltage-gated ion channels are each activated by EMF exposures. From the Pall (2013) review, four classes of voltage-gated ion channels were shown from calcium channel blocker studies, to be activated by EMFs, L-type, T- type, N-type and P/Q –type VGCCs. In this paragraph we have evidence that three other channels are also activated, voltage-gated sodium channels, voltage-gated potassium channels and voltage-gated chloride channels. Furthermore the plant studies strongly suggest that the so called TPC channels, which contain a similar voltage sensor, are acti- vated in plants allowing calcium influx into plants to produce similar EMF-induced responses (Pall, 2016a). One can put those observations together with the powerful findings from the physics, that the electrical forces on the voltage-sensor are stunningly strong, something like 7.2 million times stronger than the forces on the singly charged groups in the aqueous phases of the cell. Now you have a stunningly powerful argument that the voltage sensor is the predominant direct target of the EMFs.
Why is it that the VGCCs, acting via calcium influx, seem to be much more important in producing EMF effects than are the other voltage- gated ion channels? Probably because Ca2+ ions under resting conditions in cells have about a 10,000-fold concentration gradient driving them into the cell, and over a million-fold electro- chemical gradient also driving them into the cell. Because of this, one can have huge calcium influxes upon channel activation.
Another hypothesis is that EMF-induced intracellular Ca2+-alterations might affect Ets genes, which are transcription factors expressed in different tissues