Numerous mechanisms have been suggested to explain the potential for EMF to alter cellular physiology, biochemistry, and function. The most commonly cited mechanisms are 1) disruption of cellular communication, 2) modulation of cell growth via changes in calcium flux, 3) stimulation of the pineal gland leading to neuroendocrine effects, and 4) activation of specific oncogenes. Of these four mechanisms, two form unique mathematical challenges (cellular communication and calcium ion flux), one is a classical example of a biochemical pathway which could be modeled if sufficient data exists (neuroendocrine system) and the fourth (oncogene activation) is not yet ready for mathematical modeling. In this project, we propose to model the effects of EMF on the neuroendocrine system.

Modeling the effects of EMF on the neuroendocrine system will follow along classical physiological, pharmacological, and biochemical lines. In the neuroendocrine system, the pineal gland synthesizes and releases melatonin. Melatonin subsequently suppresses the activity of endocrine organs such as the gonads, pituitary gland, adrenal glands, and the thyroid. Experimental results have shown that significant nocturnal melatonin concentration decreases were caused in rats by a 60 hertz (Hz) electric field. Models developed to explain EMF-endocrine system interactions will aid us in understanding the relationship between electrical energy generated by naturally occurring processes in the body and those from environmental exposure.