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 spo ntaneous abortion. The model for time-dependent instability of DNA spe cificity [Biochem. Genet. 32, 383 (1994)] is assumed to have been oper ational since DNA became selected as the molecular structure for the g enome. Species were consequently required to adapt mechanisms to prote ct haploid gene pools from the continuous time-dependent accumulation of evolutionary base substitutions. To this end, conserved genetic dom ains containing mutation-intolerance thresholds are a result of natura l selection operating on time-dependent base substitutions. ''P53-type '' genes are examples of such conserved domains with point mutation th resholds. When the oocyte is fertilized, conserved domains express wil d type keto-amino genetic information. During subsequent development a nd growth, time-dependent evolution events populate G-C sites with eno l-imine stationary states that can be transcribed and/or replicated to express transversion and transition mutations. As the level of evolut ion events would approach the intolerance threshold in the haploid gen ome, 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 prese rvation by removing from the gene pool those haploid genomes containin g advanced levels of mutation which, if propagated, would be inconsist ent with survival. Consistent with the evolutionary origin of cancer h ypothesis [Cancer Biochem. Biophys. 13, 147 (1993)], perturbations tha t would enhance rates of populating G-C sites with enol-imine states c ould accelerate point mutation ''activation'' of ''p53-type'' genes th at could be manifested as premature cancer in living populations or ex pressed as spontaneous abortion in unborn populations. The evolution e vent ''rate constant'' is (gamma/(h) over bar)(2) where gamma is the q uantum mechanical energy shift between G-C states. This expression imp lies that ''additional'' magnetic fields could increase rates of popul ating enol-imine states due to Lorentz force momentum transfer to meta stable proton oscillators where induced electric fields and local curr ents would subject elevated energy proton oscillators to collisional d e-exciatations which would increase the energy density of chemical bon ds that support hydrogen bonds in DNA, thereby introducing larger ener gy shift values in (gamma/(h) over bar)(2). This hypothesis is explore d for ''additional'' magnetic fields in the range of 0.15 to 0.01 gaus s where the influence of magnetic enhancement energies on rates of pop ulating enol-imine stationary states is evaluated, using Gurney and Co ndon tunneling time calculations for unperturbed and magnetically enha nced protons to escape metastable keto-amino energy wells. Model calcu lations are qualitative and are consistent with the experimentally tes table hypothesis that ''additional'' magnetic fields could cause incre ased rates of accumulating evolutionary base substitutions, thereby in creasing probabilities of activating ''p53-type'' genes which could ca use increased incidence of spontaneous abortion in unborn populations and increased incidence of cancer in living populations.