Influence of 914 MHz Radiofrequency Identification
on Neuroendocrine System and Cerebral Metabolism in Rats
Radio frequency identification (RFID) is one of the currently introduced wireless radio frequency (RF) systems and is generally used in industrial and everyday life. However, the possible biologic effects of RFID radiation on human health, particularly brain function, remain unclear. Epidemiological studies suggest that exposure to RF electromagnetic field (EMF) may be a dormant risk factor in human health; therefore I expect it may affect the mammalian brain function. To study the effect of RFID exposure on rat brain function, I focused on neuroendocrine system including thyroid hormone system and melatonin, and cerebral metabolism, especially glucose metabolism. For these animal trials, a reverberation chamber was used as a whole-body exposure system. RFID exposure trial was performed during the day for the studies except for a study regarding the pineal melatonin biosynthesis, as RFID exposure during the night is more valid. The whole-body average specific absorption rate (SAR) was 4 W/kg for field of the RFID for all the experiments.
Although some transient changes in serum thyroid hormones were observed in the separate 2, 4, 8, and 16 week exposure experiments, serum level of TSH and thyroid hormones were not influenced in this study. Nocturnal 8 h RFID exposure, at SAR of 4 W/kg, caused a reduction of a 24 h urinary secretion of 6-OHMS, melatonin metabolite, and its diminution degree shows a pineal Aanat transcriptional level-dependent manner. Decreased levels of AANAT enzyme activity and protein were observed in RFID exposed group compared to sham exposed group. Moreover, level of CREB phosphorylation in pineal gland was reduced after RFID exposure. Consequently, reduced expression of Aanat mRNA was also observed in RFID-exposed group. But, No significant change was found after RFID exposure in protein kinase A (PKA) enzyme activity which is known as a key enzyme in phosphorylation of AANAT and CREB in pineal gland at night. These results indicate that nocturnal RFID exposure reduces Aanat transcription which is ultimate causes of reduction of melatonin synthesis including protein level of AANAT and, AANAT activity. I investigated the RFID exposure influence on rat cortical glucose metabolism by using 18F-deoxyglucose positron emission tomography (FDG-PET). The relative cerebral glucose metabolic rate was unchanged in the frontal, temporal and parietal cortexes of the RFID-exposed rats, compared with rats in cage-control and sham-exposed groups.
To evaluate the effect of RFID exposure on rat brain function, I had studied three different systems including cerebral glucose metabolism, thyroid system, and pineal melatonin synthesis. Taken together, my scientific data may, at least in part, provide evidence that rat brain can be influenced by RF exposure.