Abstract

Purpose

The influences of radiofrequency electromagnetic exposure on animal health, particularly on serotonin metabolism, are not well-elucidated. In this in vivo study, we studied the influences of exposure to radiofrequency identification (RFID) signals on serotonin metabolism.

Materials and methods

Twenty-two male Sprague-Dawley rats were assigned to sham (n = 10) and RFID-exposed (n = 12) groups. Rats in the RFID-exposed group were exposed to RFID signals at an average whole-body specific absorption rate of 2 W/kg for 8 h/day, 5 days/week for 2 weeks. Before and after RFID exposure, 24-h urine was collected from each rat. Urinary tryptophan, 5-hydroxytryptophan, serotonin, 5-hydroxyindoleacetic acid, and 5-methoxyindole-3-acetic acid concentrations were examined using gas chromatography–mass spectrometry, and changes in the patterns of values were compared between the two groups.

Results

Urinary levels of serotonin decreased by 20% (p = 0.041, Student’s t-test) and 40% (p = 0.024, Student’s t-test) in both the sham and RFID-exposed groups, respectively. Level of 5-methoxyindole-3-acetic acid decreased by 30% in the RFID-exposed group (p = 0.039, Student’s t-test).

Conclusion

Our results indicate that exposure to RFID signals at a specific absorption rate of 2 W/kg is sufficient to alter serotonin metabolism in rats regardless of whether the exposure level is considered biohazardous.

The post Influences of exposure to 915-MHz radiofrequency identification signals on serotonin metabolites in rats: A pilot study appeared first on EMFSA.

Abstract

Environmental studies, metabolic research, and state of the art research in neurobiology point towards the reduced amount of natural day and sunlight exposure of the developing child, as a consequence of increasingly long hours spent indoors online, as the single unifying source of a whole set of health risks identified worldwide, as is made clear in this review of currently available literature. Over exposure to digital environments, from abuse to addiction, now concerns even the youngest (ages 0 to 2) and triggers, as argued on the basis of clear examples herein, a chain of interdependent negative and potentially long-term metabolic changes. This leads to a deregulation of the serotonin and dopamine neurotransmitter pathways in the developing brain, currently associated with online activity abuse and/or internet addiction, and akin to that found in severe substance abuse syndromes. A general functional working model is proposed under the light of evidence brought to the forefront in this review.

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