ID Number		56
Study Type		In Vivo
Model		RF exposure to mice and rats and analysis of micronuclei, chromosome aberrations, gene expression and other endpoints.
Details		C3H/HeJ (female) mice were exposed to 2450 MHz CW for 20 hours/day, 7 days/wk, for 18 months at 1 W/kg (whole body average) in a circularly-polarized wave-guide system as described by Guy et al. Radio Sci 14:63-74, 1979. The mice were actually part of a larger tumor bioassay study directed by Frei (Bioelectromagnetics (1998) 19:20-31). In addition to tumor histopathology, peripheral (tail) blood and femoral bone marrow smears were prepared and scored for micronucleated polychromatic erythrocytes (PCEs). A total of 2,000 PCEs (1,000 in the blood smears and 1,000 in the bone marrow smears) were evaluated and showed a statistically significant increase of 0.5 micronuclei in 1000 in the exposed group vs the sham animals (4.6 in 1000 vs 4.1 in 1000, respectively). In a later study (performed as part of a larger bioassay by Anderson et al), pregnant Fischer 344 rats were exposed from nineteenth day of gestation to 1.6 GHz RF at an SAR of 0.036 to 0.077 W/kg for 2 hours/day, 5 days/week. After birth, rats were exposed head first in a restraining device at an SAR of 0.16 or 1.6 W/kg (brain average) for 2 hours/day, 5 days/week, for 2 years. At the end of 2 years, bone marrow smears were examined for MN in polychromatic erythrocytes. No effects of exposure were reported. In an acute exposure study using similar exposure at higher SAR for a single day, Sprague Dawley rats were exposed to 2450 MHz (CW) MW for 24 hours at an SAR of 12 W/kg (whole body average). Immediately after exposure, micronuclei incidence in peripheral blood and bone marrow cells was examined and found not to be statistically different than that of sham exposed rats. AUTHORS' ABSTRACT: Vijayalaxmi, Cao and Scarfi 2014 (IEEE #5452): Adaptive response is a phenomenon in which cells which were pre-exposed to extremely low and nontoxic doses of a genotoxic agent became resistant to the damage induced by subsequent exposure to a higher and toxic dose of the same, similar (in action) or another genotoxic agent. Such response has been well documented in scientific literature in cells exposed in vitro and in vivo to low doses of physical (especially, ionizing radiation) and chemical mutagens. The existence of similar phenomenon in mammalian cells exposed in vitro and in vivo to non-ionizing radiofrequency fields has been reported in several research publications. In in vitro studies, human blood lymphocytes exposed to radiofrequency fields and then treated with a genotoxic mutagen or subjected to ionizing radiation showed ignificantly decreased genetic damage. Similar studies in tumor cells showed significantly increased viability, decreased apoptosis, increased mitochondrial membrane potential, decreased intracellular free Ca2+ and, increased Ca2+-Mg2+-ATPase activity. In in vivo studies, exposure of rodents to radiofrequency fields and then to lethal/sub-lethal doses of g-radiation showed survival advantage, significantly decreased damage in hematopoietic tissues, decreased genetic damage in blood leukocytes and bone marrow cells, increased numbers of colony forming units in bone marrow, increased levels of colony stimulating factor and interleukin-3 in the serum and increased expression of genes related to cell cycle. These observations suggested the ability of radiofrequency fields to induce adaptive response and also indicated some potential mechanisms for the induction of such response. Several gaps in knowledge that need to be investigated were discussed. AUTHORS' ABSTRACT: Vijayalaxmi 2016 (IEEE #6485): During recent decades, researchers have used several different parameters to evaluate the biological and health effects of in vitro and in vivo exposure to non-ionizing radiofrequency fields in animals, humans and their isolated cells. The data reported in many of publications in peer-reviewed scientific journals were reviewed by the international and national expert groups of scientists for human risk assessment of exposure to radiofrequency fields. The criteria used for such assessment depended on the study design, methodology and reporting of the data in the publication. This paper describes the requirements for good study design and quality publications, and provides guidance and a checklist for researchers studying radiofrequency fields and other environmental agents.
Findings		No Effects
Status		Completed With Publication
Principal Investigator		University of Texas, USA - vijay@uthscsa.edu
Funding Agency		AF, USA
Country		UNITED STATES
References		Vijayalaxmi, et al. Radiation Research, (2004) 162:481-496 Vijayalaxmi, et al. Radiation Research, (2003) 159:558-564 Vijayalaxmi, et al. Int. J. Radiat. Biol., (2001) 77:1109-1115 Vijayalaxmi, et al. Radiat. Res., (1997) 147:495-500 Vijayalaxmi, et al. Mutation Research., (2014) S1383-5742(14)00004-0:- Vijayalaxmi, Mutation Research/Genetic Toxicology and Environmental Mutagenesis., (2016) 810:6-12 Vijayalaxmi, et al. Radiation Research., (2021) 196:417-422
Comments		* The statistical significance of the very small positive finding in the initial study in mice was first reported as no effect, then reported as a significant effect in a subsequent letter in Radiation Research to correct the original manuscript analysis (Radiation Research 149(3):308, 1998).