Hypothesis on a casual link between EMF and an evolutionary class of cancer and spontaneous abortion.

A biophysical theory is presented that supports a causal link between EMF exposures and the different biological endpoints of cancer and spontaneous abortion. The model for time-dependent instability of DNA specificity [Biochem. Genet. 32, 383 (1994)] is assumed to have been operational since DNA became selected as the molecular structure for the genome. Species were consequently required to adapt mechanisms to protect haploid gene pools from the continuous time-dependent accumulation of evolutionary base substitutions. To this end, conserved genetic domains containing mutation-intolerance thresholds are a result of natural selection operating on time-dependent base substitutions. "P53-type" genes are examples of such conserved domains with point mutation thresholds. When the oocyte is fertilized, conserved domains express wild type keto-amino genetic information. During subsequent development and growth, time-dependent evolution events populate G-C sites with enol-imine stationary states that can be transcribed and/or replicated to express transversion and transition mutations. As the level of evolution events would approach the intolerance threshold in the haploid genome, point mutation sensitive genes from conserved diploid domains, e.g. "p53-type" genes, would generate amino acid substituted proteins that have been evolutionarily selected to participate in species preservation by removing from the gene pool those haploid genomes containing advanced levels of mutation which, if propagated, would be inconsistent with survival. Consistent with the evolutionary origin of cancer hypothesis [Cancer Biochem. Biophys: 13, 147 (1993)], perturbations that would enhance rates of populating G-C sites with enol-imine states could accelerate point mutation "activation" of "p53-type" genes that could be manifested as premature cancer in living populations or expressed as spontaneous abortion in unborn populations. The evolution event "rate constant" is (gamma/h)2 where gamma is the quantum mechanical energy shift between G-C states. This expression implies that "additional" magnetic fields could increase rates of populating enol-imine states due to Lorentz force momentum transfer to metastable proton oscillators where induced electric fields and local currents would subject elevated energy proton oscillators to collisional de-exciatations which would increase the energy density of chemical bonds that support hydrogen bonds in DNA, thereby introducing larger energy shift values in (gamma/h)2. This hypothesis is explored for "additional" magnetic fields in the range of 0.15 to 0.01 gauss where the influence of magnetic enhancement energies on rates of populating enol-imine stationary states is evaluated, using Gurney and Condon tunneling time calculations for unperturbed and magnetically enhanced protons to escape metastable keto-amino energy wells. Model calculations are qualitative and are consistent with the experimentally testable hypothesis that "additional" magnetic fields could cause increased rates of accumulating evolutionary base substitutions, thereby increasing probabilities of activating "p53-type" genes which could cause increased incidence of spontaneous abortion in unborn populations and increased incidence of cancer in living populations.