“Supplements 1 and 2 show that the majority of studies reported genetic effects of EMF (66% for RFR and 79% for static/ELF-EMF). Thus, it is safe to conclude that genotoxic effects of EMF have been reported. The most common effects found are: DNA strand breaks, micronucleus formation, and chromosomal structural changes. There are not many studies on mutation. Thus, it is not known whether these genotoxic effects transform into mutation and involved in carcinogenesis. Interestingly, available data do not suggest mutagenic effect after RFR exposure (Chang et al., 2005; Meltz et al., 1990; Ono et al., 2004; Takahashi et al., 2002); whereas most static/ELF-EMF studies (Chahal et al., 1993; Mairs et al., 2007; Miyakoshi, 1997; Miyakoshi et al., 1998, 1996; Potenza et al., 2004; Wilson et al., 2015) suggested some mutagenic effects….”

To prove an effect, one should look for consistency in data. Genetic damage studies have shown similar effects with different set-up and in various biological systems. And, the gene expression results (Supplement 3) also support the studies on genetic damages. Expression of genes related to cell differentiation and growth, apoptosis, free radical activity, DNA repair, and heat-shock proteins have been reported. These changes could be consequences of EMF-induced genetic damages…. In conclusion, there are enough reasons to believe that genetic effects of EMF are real and possible.

During cell phone use, a relatively constant mass of tissue in the brain is exposed to the radiation at relatively high intensity (peak specific absorption rate (SAR) of 4–8 W/kg). Many papers have reported genetic effect/DNA damage at much lower SAR (or power density) (see Supplement 4). This questions the wisdom of the several exposure standard-setting organizations in using the obsolete data of 4 W/kg (whole-body averaged SAR) as the threshold for exposure-standard setting. Furthermore, since critical genetic mutations in one single cell are sufficient to lead to cancer and there are millions of cells in a gram of tissue, it is inconceivable that some standards have changed the SAR from averaged over 1 gm to 10 gm of tissue. (The limit of localized tissue exposure has been changed from 1.6 W/kg averaged over 1 gm of tissue to 2 W/kg over 10 gm of tissue. Since distribution of radiofrequency energy is non-homogenous inside tissues, this change allows a higher peak level of exposure.) What is actually needed is a better refinement of SAR calculation to identify ‘peak values’ of SAR inside the brain.

Any effect of EMF has to depend on the energy absorbed by a biological entity and on how the energy is delivered in space and time. Aside from influences that are not directly related to experimentation (Huss et al., 2007), many factors could influence the outcome of an experiment in bioelectromagnetics research. Frequency, intensity, exposure duration, and the number of exposure episodes can affect the response, and these factors can interact with each other to produce different effects. In addition, in order to understand the biological consequences of EMF exposure, one must know whether the effect is cumulative, whether compensatory responses result, and when homeostasis will break down. A drawback in the interpretation and understanding of experimental data from bioelectromagnetic research is that there is no general accepted mechanism on how EMF affects biological systems. Since the energy level is not sufficient to cause direct breakage of chemical bonds within molecules, the effects are probably indirect and secondary to other induced chemical changes in the cell. The mechanisms by which EMF causes genetic effects are  unknown. This author suspects that biological effects of EMF exposure are caused by multiple inter-dependent biological  mechanisms.”