Short and long-term 2100 MHz radiofrequency radiation causes endoplasmic reticulum stress in rat testis.

Long-term radiofrequency radiation (RFR) exposure, which adversely affects organisms, deteriorates testicular functions. Misfolding or unfolding protein accumulation in the endoplasmic reticulum (ER) initiates an intracellular reaction known as ER stress (ERS), which activates the unfolded protein response (UPR) for proteostasis. Since both RFR exposure and ERS can cause male infertility, we hypothesized that RFR exposure causes ERS to adversely affect testicular functions in rats. To investigate role of ERS in mediating RFR effects on rat testis, we established five experimental groups in male rats: control, short-term 2100-megahertz (MHz) RFR (1-week), short-term sham (sham/1-week), long-term 2100-MHz RFR (10-week), and long-term sham (sham/10-week). ERS markers Grp78 and phosphorylated PERK (p-Perk) levels and ERS-related apoptosis markers Chop and caspase 12 were investigated by immunohistochemistry, immunoblotting, and quantitative real-time polymerase chain reaction (qPCR). Long-term RFR exposure increased Grp78, p-Perk, and Chop levels, while short-term RFR exposure elevated Chop and caspase 12 levels. Chop expression was not observed in spermatogonia and primary spermatocytes, which may protect spermatogonia and primary spermatocytes against RFR-induced ERS-mediated apoptosis, thereby allowing transmission of genetic material to next generations. While short and long-term RFR exposures trigger ERS and ERS-related apoptotic pathways, further functional analyses are needed to elucidate whether this RFR-induced apoptosis has long-term male infertility effects.

Radiofrequency radiation reshapes tumor immune microenvironment into antitumor phenotype in pulmonary metastatic melanoma by inducing active transformation of tumor-infiltrating CD8+ T and NK cells.

Immunosuppression by the tumor microenvironment is a pivotal factor contributing to tumor progression and immunotherapy resistance. Priming the tumor immune microenvironment (TIME) has emerged as a promising strategy for improving the efficacy of cancer immunotherapy. In this study we investigated the effects of noninvasive radiofrequency radiation (RFR) exposure on tumor progression and TIME phenotype, as well as the antitumor potential of PD-1 blockage in a model of pulmonary metastatic melanoma (PMM). Mouse model of PMM was established by tail vein injection of B16F10 cells. From day 3 after injection, the mice were exposed to RFR at an average specific absorption rate of 9.7 W/kg for 1 h per day for 14 days. After RFR exposure, lung tissues were harvested and RNAs were extracted for transcriptome sequencing; PMM-infiltrating immune cells were isolated for single-cell RNA-seq analysis. We showed that RFR exposure significantly impeded PMM progression accompanied by remodeled TIME of PMM via altering the proportion and transcription profile of tumor-infiltrating immune cells. RFR exposure increased the activation and cytotoxicity signatures of tumor-infiltrating CD8+ T cells, particularly in the early activation subset with upregulated genes associated with T cell cytotoxicity. The PD-1 checkpoint pathway was upregulated by RFR exposure in CD8+ T cells. RFR exposure also augmented NK cell subsets with increased cytotoxic characteristics in PMM. RFR exposure enhanced the effector function of tumor-infiltrating CD8+ T cells and NK cells, evidenced by increased expression of cytotoxic molecules. RFR-induced inhibition of PMM growth was mediated by RFR-activated CD8+ T cells and NK cells. We conclude that noninvasive RFR exposure induces antitumor remodeling of the TIME, leading to inhibition of tumor progression, which provides a promising novel strategy for TIME priming and potential combination with cancer immunotherapy.

Expression levels of tam receptors and ligands in the testes of rats exposed to short and middle-term 2100 MHz radiofrequency radiation.

With advances in technology, the emission of radiofrequency radiation (RFR) into the environment, particularly from mobile devices, has become a growing concern. Tyro 3, Axl, and Mer (TAM) receptors and their ligands are essential for spermatogenesis and testosterone production. RFR has been shown to induce testicular cell apoptosis by causing inflammation and disrupting homeostasis. This study aimed to investigate the role of TAM receptors and ligands in the maintenance of homeostasis and elimination of apoptotic cells in the testes (weeks), short-term sham exposure (sham/1 week), and middle-term sham exposure (sham/10 weeks). Testicular morphology was assessed using hematoxylin-eosin staining, while immunohistochemical staining was performed to assess expression levels of TAM receptors and ligands in the testes of all groups. The results showed that testicular morphology was normal in the control, sham/1 week, and sham/10 weeks groups. However, abnormal processes of spermatogenesis and seminiferous tubule morphology were observed in RFR exposure groups. Cleaved Caspase 3 immunoreactivity showed statistically significant difference in 1 and 10 weeks exposure groups compared to control group. Moreover, there was no significant difference in the immunoreactivity of Tyro 3, Axl, Mer, Gas 6, and Pros 1 between groups. Moreover, Tyro 3 expression in Sertoli cells was statistically significantly increased in RFR exposure groups compared to the control. Taken together, the results suggest that RFR exposure negatively affects TAM signalling, preventing the clearance of apoptotic cells, and this process may lead to infection and inflammation. As a result, rat testicular morphology and function may be impaired.

Effects of 3.5-GHz radiofrequency radiation on energy-regulatory hormone levels in the blood and adipose tissue.

In recent years exposure of living beings to radiofrequency radiation (RFR) emitted from wireless equipment has increased. In this study, we investigated the effects of 3.5-GHz RFR on hormones that regulate energy metabolism in the body. Twenty-eight rats were divided into four groups: healthy sham (n = 7), healthy RFR (n = 7), diabetic sham (n = 7), and diabetic RFR (n = 7). Over a month, each group spent 2 h/day in a Plexiglas carousel. The rats in the experimental group were exposed to RFR, but the sham groups were not. At the end of the experiment, blood and adipose tissues were collected from euthanized rats. Total antioxidant, total oxidant, hydrogen peroxide, ghrelin, nesfatin-1, and irisin were determined. Insulin expression in pancreatic tissues was examined by immunohistochemical analysis. Whole body specific absorption rate was 37 mW/kg. For the parameters analyzed in blood and fat, the estimated effect size varied within the ranges of 0.215-0.929 and 0.503-0.839, respectively. The blood and adipose nesfatin-1 (p = 0.002), blood and pancreatic insulin are decreased, (p = 0.001), gherelin (p = 0.020), irisin (p = 0.020), and blood glucose (p = 0.040) are increased in healthy and diabetic rats exposed to RFR. While nesfatin-1 are negatively correlated with oxidative stress, hyperglycemia and insulin, ghrelin and irisin are positively correlated with oxidative stress and hyperglycemia. Thus, RFR may have deleterious effects on energy metabolism, particularly in the presence of diabetes.

Protective effect of paricalcitol in rat testicular damage induced by subchronic 1800 MHz radiofrequency radiation.

In the present study, the possible protective effects of paricalcitol (P) were investigated in testicular damage because of 1800 MHz radiofrequency radiation (RFR) exposure. Male Sprague Dawley rats 8-10 weeks old (n = 28) were randomly divided into four groups as control (C) (n = 7), RFR (n = 7, 1800 MHz RFR 1 h/day for 30 days), P (n = 7, 0.2 µg/kg paricalcitol, 3 times a week for 30 days), and RFR + P (n = 7, 1800 MHz RFR 1 h/day for 30 days +0.2 µg/kg paricalcitol, 3 times a week for 30 days). Testicular tissue was evaluated with histological and biochemical methods. No statistically significant differences were detected between the groups in seminiferous tubule diameters and germinal epithelial thicknesses. While ultrastructural changes were observed in the seminiferous tubule and Leydig cells in the RFR group, these changes were decreased in the RFR + P group. It was found that the Johnsen Score, Ki67, and p63 immunoreactivity scores (IRS), superoxide dismutase (SOD), and catalase (CAT) activities in the RFR + P group were statistically increased as compared to the RFR group and the malondialdehyde (MDA) levels were decreased statistically and significantly. These results show that paricalcitol administration may have an ameliorative effect on testicular damage occurring because of 1800 MHz RFR exposure.

Adverse effects of 900, 1800 and 2100 MHz radiofrequency radiation emitted from mobile phones on bone and skeletal muscle.

The goal of this study was to biomechanically and morphologically research both the impact of mobile phone like radiofrequency radiations (RFR) on the tibia and the effects on skeletal muscle through oxidative stress parameters. Fifty-six rats (200-250 g) were put into groups: healthy sham (n = 7), healthy RFR (900, 1800, 2100 MHz) (n = 21), diabetic sham (n = 7) and diabetic RFR (900, 1800, 2100 MHz) (n = 21). Over a month, each group spent two hours/day in a Plexiglas carousel. The rats in the experimental group were exposed to RFR, but the sham groups were not. At the end of the experiment, the right tibia bones and skeletal muscle tissue were removed. The three-point bending test and radiological evaluations were performed on the bones, and CAT, GSH, MDA, and IMA in muscles were measured. There were differences in biomechanics properties and radiological evaluations between the groups (p < .05). In the measurements in the muscle tissues, significant differences were statistically found (p < .05). The average whole-body SAR values for GSM 900, 1800 and 2100 MHz were 0.026, 0.164, and 0.173 W/kg. RFRs emitted from mobile phone may cause adverse effects on tibia and skeletal muscle health, though further studies are needed.

Very high radiofrequency radiation at Skeppsbron in Stockholm, Sweden from mobile phone base station antennas positioned close to pedestrians' heads.

In urban environment there is a constant increase of public exposure to radiofrequency electromagnetic fields from mobile phone base stations. With the placement of mobile phone base station antennas radiofrequency hotspots emerge. This study investigates an area at Skeppsbron street in Stockholm, Sweden with an aggregation of base station antennas placed at low level close to pedestrians' heads. Detailed spatial distribution measurements were performed with 1) a radiofrequency broadband analyzer and 2) a portable exposimeter. The results display a greatly uneven distribution of the radiofrequency field with hotspots. The highest spatial average across all quadrat cells was 12.1 V m⁻1 (388 mW m⁻2), whereas the maximum recorded reading from the entire area was 31.6 V m⁻1 (2648 mW m⁻2). Exposimeter measurements show that the majority of exposure is due to mobile phone downlink bands. Most dominant are 2600 and 2100 MHz bands used by 4G and 3G mobile phone services, respectively. The average radiofrequency radiation values from the earlier studies show that the level of ambient RF radiation exposure in Stockholm is increasing. This study concluded that mobile phone base station antennas at Skeppsbron, Stockholm are examples of poor radiofrequency infrastructure design which brings upon highly elevated exposure levels to popular seaside promenade and a busy traffic street.

Genotoxic effects of electromagnetic field radiations from mobile phones.

The use of wireless communication technology in mobile phones has revolutionized modern telecommunication and mobile phones have become so popular that their number exceeds the global population. Electromagnetic field radiations (EMR) are an integral part of wireless technology, which are emitted by mobile phones, mobile tower antennas, electric power stations, transmission lines, radars, microwave ovens, television sets, refrigerators, diagnostic, therapeutic, and other electronic devices. Manmade EMR sources have added to the existing burden of natural EMR human exposure arising from the Sun, cosmos, atmospheric discharges, and thunder storms. EMR including radiofrequency waves (RF) and extremely low-frequency radiation (ELF) has generated great interest as their short-term exposure causes headache, fatigue, tinnitus, concentration problems, depression, memory loss, skin irritation, sleep disorders, nausea, cardiovascular effects, chest pain, immunity, and hormonal disorders in humans, whereas long-term exposure to EMR leads to the development of cancer. The review has been written by collecting the information using various search engines including google scholar, PubMed, SciFinder, Science direct, EMF-portal, saferemr, and other websites from the internet. The main focus of this review is to delineate the mutagenic and genotoxic effects of EMR in humans and mammals. Numerous investigations revealed that exposure in the range of 0-300 GHz EMR is harmless as it did not increase micronuclei and chromosome aberrations. On the contrary, several other studies have demonstrated that exposure to EMR is genotoxic and mutagenic as it increases the frequency of micronuclei, chromosome aberrations, DNA adducts, DNA single and double strand breaks at the molecular level in vitro and in vivo. The EMR exposure induces reactive oxygen species and changes the fidelity of genes involved in signal transduction, cytoskeleton formation, and cellular metabolism.

Scientific evidence invalidates health assumptions underlying the FCC and ICNIRP exposure limit determinations for radiofrequency radiation: implications for 5G.

In the late-1990s, the FCC and ICNIRP adopted radiofrequency radiation (RFR) exposure limits to protect the public and workers from adverse effects of RFR. These limits were based on results from behavioral studies conducted in the 1980s involving 40-60-minute exposures in 5 monkeys and 8 rats, and then applying arbitrary safety factors to an apparent threshold specific absorption rate (SAR) of 4 W/kg. The limits were also based on two major assumptions: any biological effects were due to excessive tissue heating and no effects would occur below the putative threshold SAR, as well as twelve assumptions that were not specified by either the FCC or ICNIRP. In this paper, we show how the past 25 years of extensive research on RFR demonstrates that the assumptions underlying the FCC's and ICNIRP's exposure limits are invalid and continue to present a public health harm. Adverse effects observed at exposures below the assumed threshold SAR include non-thermal induction of reactive oxygen species, DNA damage, cardiomyopathy, carcinogenicity, sperm damage, and neurological effects, including electromagnetic hypersensitivity. Also, multiple human studies have found statistically significant associations between RFR exposure and increased brain and thyroid cancer risk. Yet, in 2020, and in light of the body of evidence reviewed in this article, the FCC and ICNIRP reaffirmed the same limits that were established in the 1990s. Consequently, these exposure limits, which are based on false suppositions, do not adequately protect workers, children, hypersensitive individuals, and the general population from short-term or long-term RFR exposures. Thus, urgently needed are health protective exposure limits for humans and the environment. These limits must be based on scientific evidence rather than on erroneous assumptions, especially given the increasing worldwide exposures of people and the environment to RFR, including novel forms of radiation from 5G telecommunications for which there are no adequate health effects studies.

An International Collaborative Animal Study of the Carcinogenicity of Mobile Phone Radiofrequency Radiation: Considerations for Preparation of a Global Project.

Radiofrequency radiation (RFR) was classified as a "possible" human carcinogen in 2011, which caused great public concern. A carcinogenicity study by the National Toxicology Program (NTP) found Code Division Multiple Access-and Global System for Mobile Communications-modulated mobile phone RFR to be carcinogenic to the brain and heart of male rats. As part of an investigation of mobile phone carcinogenesis, and to verify the NTP study results, a 5-year collaborative animal project was started in Korea and Japan in 2019. An international animal study of this type has two prerequisites: use of the same study protocol and the same RF-exposure system. This article discusses our experience in the design of this global study on radiofrequency electromagnetic fields (RF-EMFs).© 2022 The Authors. Bioelectromagnetics published by Wiley Periodicals LLC on behalf of Bioelectromagnetics Society.

Effect of radiofrequency exposure on body temperature: Real-time monitoring in normal rats.

Radiofrequency radiation (RFR) can generate heat in living organisms. In this study, we monitored the body temperature of healthy animals during RFR exposure in real time using an implantable iButton data logger. A reverberation chamber system for small animals was used for this radiofrequency (RF) exposure in vivo study. Healthy male Sprague-Dawley rats were divided into two groups: with versus without iButton implantation (n = 20 per group). Each group was further divided into a sham-exposed and RF-exposed group (n = 10 per subgroup). Rats were exposed to a 1,760-MHz long-term evolution (LTE) signal in the reverberation chamber system at a whole-body average specific absorption rate of 0 W/kg (sham-exposed) or 4 W/kg (RF-exposed) for 6 h. The body temperature of iButton-implanted rats was recorded using an intraperitoneally implanted iButton every minute over 6 h of RF exposure, whereas that of non-implanted rats was measured directly using a rectal thermometer immediately before and after the 6-h RF exposure period. The temperature values measured by the two types of thermometers were significantly positively correlated (r = 0.63, P < 0.01, linear regression), and changes in body temperatures recorded in iButton-implanted and non-implanted rats measured using two thermometers after 6 h of RF exposure were maintained within <1°C (P = 0.87, general linear model, followed by univariate model). Similar results were obtained for rectal thermometer measurements (P = 0.12, paired t-test). These results suggest that RF exposure at a whole-body average specific absorption rate of 4 W/kg does not induce significant changes in body temperature in healthy rats over a 6-h RF exposure period.

Non-ionizing radiation as possible carcinogen.

The advent of wireless technologies has revolutionized the way we communicate. The steady upsurge in the use of mobile phone all over the world in the last two decades, while triggered economic growth, has caused substantial damage to the environment, both directly and indirectly. The electromagnetic radiation generated from mobile phones, radio-based stations, and phone towers, high-voltage power lines have been reported which leads to the variety of health scares such as the risk of cancer in human beings and adverse effects in animals, birds, etc. Though the usage of such radiation emitting from mobile phones has risen steeply, there is a lack of proper knowledge about the associated risks. The review provides the latest research evidence based both on in vitro studies, in vivo studies, and possible gaps in our knowledge. Moreover, the present review also summarizes available literature in this subject, reports and studies which will help to form guidelines for its exposure limits to the public.Abbreviations: Continuous Wave: CW; Code Division Multiple Access: CDMA; Global System for Mobile Communications: GSM; Peripheral Blood Mononuclear Cell: PBMC; Radiofrequency: RF; Radiofrequency radiation: RFR; Universal Mobile Telecommunications System: UMTS; Wideband Code Division Multiple Access: WCDMA; Specific Absorption Rate: SAR; National Toxicology Program: NTP; amplitude-modulated or amplitude-modulation: AM; Electromagnetic frequencies: EMF; confidence interval: CI; Gigahertz: GHz; odds ratio: OR; incidence ratio: IR; reactive oxygen species: ROS; specific absorption rate: SAR; International Agency of Research on Cancer: IARC; single-strand breaks: SSB; double-strand breaks: DSB (7,12-Dimethylbenz[a]anthracene): DMBA; Hour: h; international commission on non-ionizing radiation protection: ICNIRP; extremely low frequency: ELFl; microtesla: mT; Gigahertz: GHz; hertz: Hz; decibel: dB; kilometer: Km; Watt per square meter: W/m2; Hour: h; positron emission tomography: PET.

Investigation of oxidative damage, antioxidant balance, DNA repair genes, and apoptosis due to radiofrequency-induced adaptive response in mice.

This study aims to determine whether exposure to non-ionizing radiofrequency fields could induce an adaptive response (AR) in adult mice and to reveal potential molecular mechanisms triggered by RF-induced AR. The study was performed on 24 adult male Swiss-Albino mice. The average mass of the mice was 37 g. Four groups of adult mice, each consisting of 6, were formed. The radiofrequency group (R) and the adaptive response group (RB) were exposed to 900 MHz of global system for mobile communications (GSM) signal at 0.339 W/kg (1 g average specific absorption rate) 4 h/day for 7 days, while the control group (C) and the bleomycin group (B) were not exposed. 20 minutes after the last radiofrequency field (RF) exposure, the mice in the B and RB groups were injected intraperitoneal (ip) bleomycin (BLM), 37.5 mg/kg. All the animals were sacrificed 30 minutes after the BLM injection. Oxidative damage and antioxidant mechanism were subsequently investigated in the blood samples. Changes in the expression of the genes involved in DNA repair were detected in the liver tissue. TUNEL method was used to determine the apoptosis developed by DNA fragmentation in the liver tissue. The RB group, which produced an adaptive response, was compared with the control group. According to the results, the increase of reactive oxygen species (ROS) in the RB group may have played an important role in triggering the adaptive response and producing the required minimum stress level. Furthermore, tumor suppressor 53(p53), oxo guanine DNA glycosylase (OGG-1) levels responsible for DNA repair mechanism genes expression were increased in conjunction with the increase in ROS. The change in the poly (ADP-ribose) polymerase 1 (PARP-1) and glutathione peroxidase 1 (GPx-1) gene expression were not statistically significant. The antioxidant enzyme levels of superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (TAC) were decreased in the group with adaptive response. According to the data obtained from terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis, apoptosis was decreased in the RB group due to the decrease in cell death, which might have resulted from an increase in gene expression responsible for DNA repair mechanisms. The results of our study show that exposure to RF radiation may create a protective reaction against the bleomycin. The minimal oxidative stress due to the RF exposure leads to an adaptive response in the genes that play a role in the DNA repair mechanism and enzymes, enabling the survival of the cell.

The roles of intensity, exposure duration, and modulation on the biological effects of radiofrequency radiation and exposure guidelines.

In this paper, we review the literature on three important exposure metrics that are inadequately represented in most major radiofrequency radiation (RFR) exposure guidelines today: intensity, exposure duration, and signal modulation. Exposure intensity produces unpredictable effects as demonstrated by nonlinear effects. This is most likely caused by the biological system's ability to adjust and compensate but could lead to eventual biomic breakdown after prolonged exposure. A review of 112 low-intensity studies reveals that biological effects of RFR could occur at a median specific absorption rate of 0.0165 W/kg. Intensity and exposure duration interact since the dose of energy absorbed is the product of intensity and time. The result is that RFR behaves like a biological "stressor" capable of affecting numerous living systems. In addition to intensity and duration, man-made RFR is generally modulated to allow information to be encrypted. The effects of modulation on biological functions are not well understood. Four types of modulation outcomes are discussed. In addition, it is invalid to make direct comparisons between thermal energy and radiofrequency electromagnetic energy. Research data indicate that electromagnetic energy is more biologically potent in causing effects than thermal changes. The two likely functionthrough different mechanisms. As such, any current RFR exposure guidelines based on acute continuous-wave exposure are inadequate for health protection.

Development of health-based exposure limits for radiofrequency radiation from wireless devices using a benchmark dose approach.

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.

Effects of 2600 MHz Radiofrequency Radiation in Brain Tissue of Male Wistar Rats and Neuroprotective Effects of Melatonin.

The debate on the biological effects of radiofrequency radiation (RFR) still continues due to differences in the design of studies (frequency, power density, specific absorption rate [SAR], exposure duration, cell, tissue, or animal type). The current study aimed to investigate the effects of 2,600 MHz RFR and melatonin on brain tissue biochemistry and histology of male rats. Thirty-six rats were divided into six groups randomly: cage-control, sham, RFR, melatonin, sham melatonin, and RFR melatonin. In RFR groups, animals were exposed to 2,600 MHz RFR for 30 days (30 min/day, 5 days/week) and the melatonin group animals were subcutaneously injected with melatonin (7 days/week, 10 mg/kg/day) for 30 days. SAR in brain gray matter was calculated as 0.44 and 0.295 W/kg for 1 and 10 g averaging, respectively. RFR exposure decreased the GSH, GSH-Px, and SOD levels and increased the MPO, MDA, and NOx levels (P < 0.005) significantly. RFR exposure also led to an increase in structural deformation and apoptosis in the brain tissue. This study revealed that exogenous high-dose melatonin could reduce these adverse effects of RFR. Limiting RFR exposure as much as possible is recommended, and taking daily melatonin supplements may be beneficial. Bioelectromagnetics. © 2021 Bioelectromagnetics Society.

Genetic effects of non-ionizing electromagnetic fields.

This is a review of the research on the genetic effects of non-ionizing electromagnetic field (EMF), mainly on radiofrequency radiation (RFR) and static and extremely low frequency EMF (ELF-EMF). The majority of the studies are on genotoxicity (e.g., DNA damage, chromatin conformation changes, etc.) and gene expression. Genetic effects of EMF depend on various factors, including field parameters and characteristics (frequency, intensity, wave-shape), cell type, and exposure duration. The types of gene expression affected (e.g., genes involved in cell cycle arrest, apoptosis and stress responses, heat-shock proteins) are consistent with the findings that EMF causes genetic damages. Many studies reported effects in cells and animals after exposure to EMF at intensities similar to those in the public and occupational environments. The mechanisms by which effects are induced by EMF are basically unknown. Involvement of free radicals is a likely possibility. EMF also interacts synergistically with different entities on genetic functions. Interactions, particularly with chemotherapeutic compounds, raise the possibility of using EMF as an adjuvant for cancer treatment to increase the efficacy and decrease side effects of traditional chemotherapeutic drugs. Other data, such as adaptive effects and mitotic spindle aberrations after EMF exposure, further support the notion that EMF causes genetic effects in living organisms.

Does Exposure of Smart Phones during Pregnancy Affect the Offspring's Ovarian Reserve? A Rat Model Study.

OBJECTIVE: We investigated the effect of prenatal exposure to smart phone radiation and the protective effect of omega-3 on ovarian reserve of offspring. Methods: 24 pregnant Wistar albino rats were divided into four groups. Group-I received neither radiofrequency (RF) radiation nor omega-3, group-II received RF, group-III received RF radiation and 300 mg omega-3 and group-IV received RF radiation and 600 mg Omega-3 till birth. At 42 days, bilateral oophorectomy was performed on all female offspring for follicle count and immunohistochemical staining (GDF9, FOXO1 and TUNEL). Results: Group-II had significantly lower mean number of primordial (p = 0.006), secondary follicles(p = 0.003) and a higher atresia score. Group-III variables were comparable with group-I variables. Group-IV had statistically higher median number of atretic follicles than group-I (p = 0.023). Conclusions: Ovarian reserve of offspring diminished with RF exposure during pregnancy. Omega-3 supplementation during pregnancy may reduce the potential premature ovarian failure.

Genetic susceptibility may modify the association between cell phone use and thyroid cancer: A population-based case-control study in Connecticut.

Emerging studies have provided evidence on the carcinogenicity of radiofrequency radiation (RFR) from cell phones. This study aims to test the genetic susceptibility on the association between cell phone use and thyroid cancer. Population-based case-control study was conducted in Connecticut between 2010 and 2011 including 440 thyroid cancer cases and 465 population-based controls with genotyping information for 823 single nucleotide polymorphisms (SNPs) in 176 DNA genes. We used multivariate unconditional logistic regression models to estimate the genotype-environment interaction between each SNP and cell phone use and to estimate the association with cell phone use in populations according to SNP variants. Ten SNPs had P < 0.01 for interaction in all thyroid cancers. In the common homozygote groups, no association with cell phone use was observed. In the variant group (heterozygotes and rare homozygotes), cell phone use was associated with an increased risk for rs11070256 (odds ratio (OR): 2.36, 95% confidence interval (CI): 1.30-4.30), rs1695147 (OR: 2.52, 95% CI: 1.30-4.90), rs6732673 (OR: 1.59, 95% CI: 1.01-2.49), rs396746 (OR: 2.53, 95% CI: 1.13-5.65), rs12204529 (OR: 2.62, 95% CI: 1.33-5.17), and rs3800537 (OR: 2.64, 95% CI: 1.30-5.36) with thyroid cancers. In small tumors, increased risk was observed for 5 SNPs (rs1063639, rs1695147, rs11070256, rs12204529 and rs3800537), In large tumors, increased risk was observed for 3 SNPs (rs11070256, rs1695147, and rs396746). Our result suggests that genetic susceptibilities modify the associations between cell phone use and risk of thyroid cancer. The findings provide more evidence for RFR carcinogenic group classification.

Limiting liability with positioning to minimize negative health effects of cellular phone towers.

The use of cellular phones is now ubiquitous through most of the adult global population and is increasingly common among even young children in many countries (e.g. Finland, where the market for smart phones is nearly saturated). The basic operation of cellular phone networks demands widespread human exposure to radio-frequency radiation (RFR) with cellular phone base stations providing cellular coverage in most areas. As the data needs of the population increase from the major shift in the source of Internet use from personal computers to smart phones, this coverage is widely predicted to increase. Thus, both the density of base stations and their power output is expected to increase the global human RFR exposure. Although direct causation of negative human health effects from RFR from cellular phone base stations has not been finalized, there is already enough medical and scientific evidence to warrant long-term liability concerns for companies deploying cellular phone towers. In order to protect cell phone tower firms from the ramifications of the failed paths of other industries that have caused unintended human harm (e.g. tobacco) this Current Issue summarizes the peer-reviewed literature on the effects of RFR from cellular phone base stations. Specifically the impacts of siting base stations are closely examined and recommendations are made for companies that deploy them to minimize their potential future liability.