Skin Heating and Injury by Prolonged Millimeter-Wave Exposure: Theory Based on a Skin Model Coupled to a Whole Body Model and Local Biochemical Release From Cells at Supraphysiologic Temperatures

Energy dissipation by millimeter-wavelength electromagnetic-radiation (MMW; f~3-300 GHz) exposure to mammalian skin occurs within the outer surface. The penetration depth is less than 1 mm for frequencies above 25 GHz. A transport-lattice system model is used, which incorporates two spatial scales to estimate heat and chemical transport in rat skin in vivo: 1) a layered skin model involving the outer several millimeters of the body coupled to 2) a whole body model. The whole body model accounts for core-body heating, which provides a time-dependent reference temperature for blood perfusion in the skin model as well as the chemical concentration in the bloodstream and renal elimination. The model's thermal response to MMW exposure is consistent with the subcutaneous and colonic temperature measurements reported for 75 mWmiddotcm^-2 and 40-min exposures at 94 GHz in anesthetized rats. The simultaneous involvement of two biophysical mechanisms that create different chemical changes in response to the field exposure is also considered. First, a traditional nonspecific thermal-injury indicator is used to estimate denaturing molecular change due directly to heating as a function of depth in the skin. Rat skin exposed in vivo to 75 mWmiddotcm^-2 for long times (40 min) has a significant direct injury, while a 10-s exposure to 1 Wmiddotcm ^-2 results in a much less direct injury. Second, the biophysical mechanism of biochemical release through cell membranes within the tissue regions that reach supraphysiologic temperatures is also considered. The released molecules are delivered to other skin regions by diffusion and into the bloodstream by perfusion, where according to our hypothesis, the molecules interact with susceptible cells. This raises the possibility of additional indirect injury at nearby deeper skin regions that experience insignificant heating. Biochemical release may also lead to injury at distant sites within the body by perfusion clearance that transfers molecules into the systemic circulation to reach other susceptible cells. The hypothesis of simultaneous direct- and indirect-injury mechanisms is also illustrated by creating and solving didactic, coupled thermal, and chemical transport-lattice models