radiofrequency radiation
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2021 ◽  
Vol 2034 (1) ◽  
pp. 012014
Author(s):  
D B Annida ◽  
S A Oladoja ◽  
O M Oni ◽  
E L Isreal ◽  
O B Ajayi ◽  
...  

2021 ◽  
Author(s):  
Ilham Said‐Salman ◽  
Wissam Yassine ◽  
Ali Rammal ◽  
Mohammad Hneino ◽  
Hoda Yusef ◽  
...  

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Uloma Igara Uche ◽  
Olga V. Naidenko

Abstract Background Epidemiological studies and research on laboratory animals link radiofrequency radiation (RFR) with impacts on the heart, brain, and other organs. Data from the large-scale animal studies conducted by the U.S. National Toxicology Program (NTP) and the Ramazzini Institute support the need for updated health-based guidelines for general population RFR exposure. Objectives The development of RFR exposure limits expressed in whole-body Specific Absorption Rate (SAR), a metric of RFR energy absorbed by biological tissues. Methods Using frequentist and Bayesian averaging modeling of non-neoplastic lesion incidence data from the NTP study, we calculated the benchmark doses (BMD) that elicited a 10% response above background (BMD10) and the lower confidence limits on the BMD at 10% extra risk (BMDL10). Incidence data for individual neoplasms and combined tumor incidence were modeled for 5% and 10% response above background. Results Cardiomyopathy and increased risk of neoplasms in male rats were the most sensitive health outcomes following RFR exposures at 900 MHz frequency with Code Division Multiple Access (CDMA) and Global System for Mobile Communications (GSM) modulations. BMDL10 for all sites cardiomyopathy in male rats following 19 weeks of exposure, calculated with Bayesian model averaging, corresponded to 0.27–0.42 W/kg whole-body SAR for CDMA and 0.20–0.29 W/kg for GSM modulation. BMDL10 for right ventricle cardiomyopathy in female rats following 2 years of exposure corresponded to 2.7–5.16 W/kg whole-body SAR for CDMA and 1.91–2.18 W/kg for GSM modulation. For multi-site tumor modeling using the multistage cancer model with a 5% extra risk, BMDL5 in male rats corresponded to 0.31 W/kg for CDMA and 0.21 W/kg for GSM modulation. Conclusion BMDL10 range of 0.2—0.4 W/kg for all sites cardiomyopathy in male rats was selected as a point of departure. Applying two ten-fold safety factors for interspecies and intraspecies variability, we derived a whole-body SAR limit of 2 to 4 mW/kg, an exposure level that is 20–40-fold lower than the legally permissible level of 0.08 W/kg for whole-body SAR under the current U.S. regulations. Use of an additional ten-fold children’s health safety factor points to a whole-body SAR limit of 0.2–0.4 mW/kg for young children.


2021 ◽  
pp. 51-64
Author(s):  
Joshua Oladele Owolabi ◽  
Olayinka Stephen Ilesanmi

Background: The research was designed to model the exposure to radiofrequency radiation (RFR) by habitual users of RFR-enabled devices and to observe possible aberrations in tissues that are attributable to exposures. The RFR exposure regimen modelled cases of continuous, and intermittent exposures in human conditions, using Wistar rats. The primary objective of the study was to study intrauterine and postnatal exposure to RFR and study its effects on specific brain structural and functional attributes. Materials and Methods: Experimental Wistar rats were housed in facilities that enabled exposure to specific type of RFR source (the 4G RFR-emitting internet router) and for specific durations which included 21 days of pregnancy and 35 post-natal days, marking the point of puberty. Following exposure, animals were sacrificed to excise brain tissues for histological analysis using the haematoxylin and eosin technique, histochemical analysis using the Nissl technique, and immunohistochemical techniques including the IBA 1 and Caspase 3 techniques for inflammation and potential apoptosis. Representative histological and histochemical photomicrographs were analysed using principles of qualitative histology and histochemistry. Results and Conclusion: Findings from the current research showed that RFR-exposure did not produce teratogenic or neurodegenerative effects within the hippocampus. This was evident from the study of the hippocampus’ histoarchitectural organisation, morphologies of the cells as well as their spatial distribution.  Functional integrity of cells in the different regions of the hippocampal formation, namely the CA 1-4 areas as well as the dentate gyrus also showed that Nissl substance expression, which is a marker of neuron functional integrity, was relatively normally expressed across the experimental animals.  This experimental modelling of human habitual exposure to RFR showed no evidence of prenatal teratogenic effects or postnatally induced extensive neurodegeneration up until puberty. However, it would be very important to indicate that RFR-exposure enhanced apoptotic potentials via the Caspase-3 pathway. The implications of this effect on later life mental health and neurological attributes will require further investigation


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