ABSTRACT
While a good number of studies have demonstrated that modern, man-made ambient electromagnetic fields can have both stimulatory and inhibitory effect on immune system function, the precise mechanisms have yet to be completely elucidated. It is hypothesized here that, depending on the parameters, one of the means by which long-term electromagnetic field exposure has the potential to eventually lead to immunosuppression is via downstream inhibition of the enzyme calcineurin - a protein phosphatase, which activates the T-cells of the immune system and can be blocked by pharmaceutical agents. Calcineurin is the target of a class of pharmaceuticals called calcineurin inhibitors (e.g., cyclosporine, pimecrolimus and tacrolimus). When organ transplant recipients take such pharmaceuticals to prevent or suppress organ transplant rejection, one of the major side effects is immunosuppression leading to increased risk of opportunistic infection: e.g., fungal, viral (Epstein-Barr virus, cytomegalovirus), atypical bacterial (Nocardia, Listeria, mycobacterial, mycoplasma), and parasitic (e.g., toxoplasmosis) infections. Frequent anecdotal reports, as well as a number of scientific studies, have shown that electromagnetic field exposures may indeed produce the same effect: a weakened immune system leading to an increase in the same or similar opportunistic infections: i.e., fungal, viral, atypical bacterial, and parasitic infections. Furthermore, numerous research studies have shown that man-made electromagnetic fields have the potential to open voltage-gated calcium channels, which can in turn produce a pathological increase of intracellular calcium, leading downstream to the pathological production of a series of reactive oxygen species. Finally, there are a number of research studies demonstrating the inhibition of calcineurin by a pathological production of reactive oxygen species. Hence, it is hypothesized here that exposures to electromagnetic fields have the potential to inhibit immune system response by means of an eventual pathological increase in the influx of calcium into the cytoplasm of the cell, which induces a pathological production of reactive oxygen species, which in turn can have an inhibitory effect on calcineurin. Calcineurin inhibition leads to immunosuppression, which in turn leads to a weakened immune system and an increase in opportunistic infection.
