A comprehensive mechanism of biological and health effects of anthropogenic extremely low frequency and wireless communication electromagnetic fields

Abstract

Exposure to anthropogenic electromagnetic fields (EMFs), especially those of wireless communications (WC) has increased tremendously. This is an unprecedented phenomenon throughout biological evolution because, all anthropogenic EMFs, being fully polarized, coherent, and, especially WC EMFs, highly variable, differ substantially from the natural EMFs. WC EMFs consist of Microwave (MW) carrier waves, modulated, by Extremely Low Frequency (ELF) signals, and included in on/off pulses repeated at various ELF rates. Moreover, they exhibit intense random variability, mainly in the Ultra Low Frequency (ULF) band. Thus, WC EMFs are a combination of MW and ELF/ULF EMFs. The combination of polarization/coherence and intense low-frequency (ELF/ULF) variability seems to be the key to EMF-bioactivity. Epidemiological and laboratory studies highlight a connection between ELF or WC EMF exposure and cancer, infertility, electro-hypersensitivity, and various other pathologies. Studies also find DNA damage and Oxidative Stress (OS) which explain these pathologies. While man-made EMFs cannot directly ionize molecules, they are capable of doing this indirectly in biological tissue, by triggering the biosynthesis of Reactive Oxygen Species (ROS) which can damage biomolecules, including DNA. The (over)production of ROS and the consequent OS are triggered by irregular gating of Voltage-Gated Ion Channels (VGICs) in the cell membranes as described by the Ion Forced Oscillation (IFO)-VGIC mechanism: Mobile ions within VGICs forced to oscillate by the applied ELF/ULF EMFs exert forces on the voltage sensors of the VGICs, similar to or greater than the forces that physiologically gate those channels, resulting in their irregular gating (dysfunction). Dysfunction of ion channels disrupts intracellular ionic concentrations. This triggers ROS overproduction and OS by the ROS-generating systems/enzymes in the cells, such as the electron transport chain (ETC) in the mitochondria, or the NADPH/NADH oxidases (NOXs), the Nitric Oxide synthases (NOS), etc. The IFO-VGIC mechanism and the consequent OS constitute a comprehensive mechanism that explains all known adverse biological and health effects reported to be induced by anthropogenic EMFs.

Keywords: DNA damage; IFO-VGIC mechanism; ROS; electromagnetic fields; ion forced oscillation; oxidative stress; voltage-gated ion channels.

Figure 1

(A) 217 Hz (“frame repetition”) pulses from a GSM mobile phone. (B) 100 and 200 Hz pulses from a cordless domestic (DECT) phone [adapted from Pedersen (4)].

Figure 2

Schematic representation of a VGIC with its four main units, the pore, and the gate in opened state. Each main unit consists of six parallel α-helices (S1–S6). The voltage-sensors of the VGIC are the four S4 helices, one in each main unit, in symmetrical positions around the pore [adapted from Panagopoulos et al. (297)].

Figure 3

Forces dF exerted on the S4 positive charges in a VGIC due to the displacement dr of an oscillating ion in the channel pore [adapted from Panagopoulos et al. (297)].

Figure 4

Graph (in logarithmic scales) showing the bioactive combinations of EMF intensity and frequency (above line) as predicted by the IFO-VGIC mechanism. The intensity-frequency combinations of all known anthropogenic EMF sources linked to adverse bioeffects are within the predicted bioactive region (2, 302).

Figure 5

Schematic diagram of the OS processes initiated in living cells after anthropogenic EMF exposure and dysfunction of VGICs. Genetic/cell damage is executed by the generated “final” ROS [adapted from Panagopoulos et al. (210)].

Figure 6

Comprehensive mechanism of anthropogenic EMF-induced bioeffects.

Figure 7

Schematic diagram with the possible consequences of irreparable genomic DNA damage in the cells of a living organism. The arrows with dashed lines mean that the effects can be induced in a lesser degree [adapted from Panagopoulos et al. (210)].