Abstract

Exposure of living organisms to man-made electromagnetic fields (EMFs) causes a variety of adverse biological and health effects including oxidative stress (OS), genetic damage, cell death, and cancer, as is today documented by a great number of indisputable scientific studies. How does this happen? Key signaling molecules in all cells are the mobile ions, the concentrations of which control all cellular functions. The mobile ions move in and out of the cells through ion channels. A most important class of ion channels are the voltage-gated ion channels (VGICs) which open or close by polarized forces on the electric charges of their voltage-sensors generated by changes ≥ 30 mV in the membrane voltage. Polarization, coherence, and existence of Extremely Low Frequencies (ELFs) are common features of all man-made EMFs. Polarized and coherent oscillating EMFs force mobile ions to oscillate in parallel and in phase with them. This coordinated oscillation generates electrical forces on neighboring charges. The forces increase with increasing EMF intensity and decreasing EMF frequency. The oscillating ions close to the voltage-sensors of VGICs generate similar forces on them as those generated by 30 mV changes in the membrane voltage, causing irregular opening and closing of the VGICs. Continuance of such a dysfunction disrupts intra-cellular ionic concentrations, which determine the cell's electrochemical balance and homeostasis. Impairment of this balance triggers overproduction of reactive oxygen species (ROS) in cells which create OS and can damage DNA and other critical biomolecules. Since no convincing corresponding non-thermal mechanism exists for Radio Frequency (RF) EMFs, and because all RF EMFs employed in wireless communications (WC) and other applications are necessarily combined with ELF pulsation, modulation, and random variability, it seems that all non-thermal biological effects of man-made EMFs attributed, until now, to RF EMFs are actually due to their ELF components and can be explained by this mechanism.

Full Text
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