A previous study reported thermal effects resulting from millimeter wave exposures at 35 and 94 GHz on non-human primates, specifically rhesus monkeys’ (Macaca mulatta) corneas, but the data exhibited large variations in the observed temperatures and uncertainties in the millimeter wave dosimetry. By incorporating improvements in models and dosimetry, a non-human primate experiment was conducted involving corneal exposures that agreed well with a three-layer, one-dimensional, thermodynamic model to predict the expected surface temperature rise. The new data indicated that the originally reported safety margins for eye exposures were underestimated by 41 ± 20% over the power densities explored. As a result, the expected minimal visible lesion thresholds should be raised to 10.6 ± 1.5 and 7.1 ± 1.0 J cm−2 at 35 and 94 GHz, respectively, provided that the power density is less than 6 W cm−2 for subjects that are unable to blink. If the blink reflex was active, a power density threshold of 20 W cm−2 could be used to protect the eye, although the eyelid could be burned if the exposure was long enough.

In laboratory studies of the pig Sus scrofa, hematocrit has consistently increased after conducted‐electrical‐weapon (CEW) exposures, possibly due to contraction of the spleen. Splenectomized animals and intact sham control animals were exposed, each for 30 sec, to a benchtop‐produced electrical waveform of net charge levels similar to those of some CEWs. Changes in the blood were compared statistically. Hematocrit increased significantly in both splenectomized and sham animals. There were no significant main‐effect differences between values of hematocrit from the two groups. There were, however, significant interactive effects of time and splenectomy for hematocrit, red blood cell count, and hemoglobin. After peak values were reached for these variables, values returned toward baseline levels more slowly in splenectomized animals. This may have been due to the lack of a spleen to sequester red blood cells (thereby resulting in more cells remaining in the general circulation), unlike sham animals with intact spleens.

Biological effects in the microwave band of the radiofrequency (RF) spectrum are thermally mediated. For acute high‐power microwave exposures, these effects will depend on transient time‐temperature histories within the tissue. In this article, we summarize the transient temperature response of rats exposed to RF energy emanating from an open‐ended rectangular waveguide. These exposures produced specific absorption rates of approximately 36 and 203 W/kg in the whole body and brain, respectively. We then use the experimentally measured thermal data to infer the baseline perfusion rate in the brain and modify a custom thermal modeling tool based upon these findings. Finally, we compare multi‐physics simulations of rat brain temperature against empirical measurements in both live and euthanized subjects and find close agreement between model and experimentation. This research revealed that baseline brain perfusion rates in rat subjects could be larger than previously assumed in the RF thermal modeling literature, and plays a significant role in the transient thermal response to high‐power microwave exposures. © 2021 Bioelectromagnetics Society.

IntroductionMild traumatic brain injury (mTBI) is a common injury that can lead to temporary and, in some cases, life-long disability. Magnetic resonance imaging (MRI) is widely used to diagnose and study brain injuries and diseases, yet mTBI remains notoriously difficult to detect in structural MRI. mTBI is thought to be caused by microstructural or physiological changes in the function of the brain that cannot be adequately captured in structural imaging of the gray and white matter. However, structural MRIs may be useful in detecting significant changes in the cerebral vascular system (e.g., the blood-brain barrier (BBB), major blood vessels, and sinuses) and the ventricular system, and these changes may even be detectable in images taken by low magnetic field strength MRI scanners (<1.5T).MethodsIn this study, we induced a model of mTBI in the anesthetized rat animal model using a commonly used linear acceleration drop-weight technique. Using a 1T MRI scanner, the brain of the rat was imaged, without and with contrast, before and after mTBI on post-injury days 1, 2, 7, and 14 (i.e., P1, P2, P7, and P14).ResultsVoxel-based analyses of MRIs showed time-dependent, statistically significant T2-weighted signal hypointensities in the superior sagittal sinus (SSS) and hyperintensities of the gadolinium-enhanced T1-weighted signal in the superior subarachnoid space (SA) and blood vessels near the dorsal third ventricle. These results showed a widening, or vasodilation, of the SSS on P1 and of the SA on P1–2 on the dorsal surface of the cortex near the site of the drop-weight impact. The results also showed vasodilation of vasculature near the dorsal third ventricle and basal forebrain on P1–7.DiscussionVasodilation of the SSS and SA near the site of impact could be explained by the direct mechanical injury resulting in local changes in tissue function, oxygenation, inflammation, and blood flow dynamics. Our results agreed with literature and show that the 1T MRI scanner performs at a level comparable to higher field strength scanners for this type of research.