Top Experimental and Epidemiological Studies
Top Experimental and Epidemiological Studies on Wireless Radiation
Last updated April 27, 2017
Prologue: Epidemiology only proves the past; Experimental/Toxicology Studies indicate future risks/harms
From time to time people ask, “what are the studies I should share with people who state that there is “no evidence?” On this page we have a small sampling of studies that are the evidence.
Cancer and Cancer Promotion:
Momoli, F., et al. “Probabilistic multiple-bias modelling applied to the Canadian data from the INTERPHONE study of mobile phone use and risk of glioma, meningioma, acoustic neuroma, and parotid gland tumors.” American Journal of Epidemiology, 2017.
Report confirms that Canadians who have used cellphones for 558 hours or more have more than a doubled risk of brain cancer. These important findings strengthen the association between glioma, an aggressive brain cancer, and cell phone use.
Yang, M., et al. “Mobile phone use and glioma risk: A systematic review and meta-analysis.” PLoS One, vol. 12, no. 5, 2017.
Meta-analysis found significant positive association between long-term mobile phone use (minimum, 10 years) and glioma. And there was a significant positive association between long-term ipsilateral mobile phone use and the risk of glioma. Long-term mobile phone use was associated with 2.22 times greater odds of low-grade glioma occurrence.
Carlberg, Michael and Lennart Hardell. “Evaluation of Mobile Phone and Cordless Phone Use and Glioma Risk Using the Bradford Hill Viewpoints from 1965 on Association or Causation.” BioMed Research International, vol. 2017, 2017.
When considered vis a vis deductive public health principles, the combined evidence from epidemiology and laboratory studies indicate that meningioma and glioma in the temporal lobe can be considered to be caused by cumulative RF radiation exposure. Experimental findings that RF increases production of reactive oxygen species suggest a potential mechanism.
Prasad, M., et al. “Mobile phone use and risk of brain tumours: a systematic review of association between study quality, source of funding, and research outcomes.” Neurological Sciences, 2017.
Studies with higher quality are more likely to find higher risk of brain tumour, while lower quality studies tend to indicate lower risk/protection
Grell, Kathrine, et al. “The Intracranial Distribution of Gliomas in Relation to Exposure From Mobile Phones: Analyses From the INTERPHONE Study.” American Journal of Epidemiology, vol. 184, no. 11 2016, pp. 818-28.
Similar to earlier results, we found a statistically significant association between the intracranial distribution of gliomas and the self-reported location of the phone. When we accounted for the preferred side of the head not being exclusively used for all mobile phone calls, the results were similar.
Hardell, Lennart and Michael Carlberg. “Mobile phone and cordless phone use and the risk for glioma–Analysis of pooled case-control studies in Sweden, 1997–2003 and 2007–2009.” Pathophysiology, vol. 22, no. 1, 2015, pp. 1-13.
Mobile phone and cordless phone use increased the risk of glioma, with highest risk in the >15–20 years latency group Highest ORs overall were found for ipsilateral mobile or cordless phone use, while the highest risk was found for glioma in the temporal lobe. First use of mobile or cordless phone before the age of 20 gave higher OR for glioma than in later age groups.
Carlberg, Michael and Lennart Hardell. “Decreased survival of glioma patients with astrocytoma grade IV (glioblastoma multiforme) associated with long-term use of mobile and cordless phones.” International Journal of Environmental Research and Public Health, vol. 11, no. 10, 2014, pp. 10790-805.
Elevated HR (decreased survival) for the most malignant glioma type, astrocytoma grade IV, was found for long-term use of mobile and cordless phones. Highest HR was found for cases with first use before the age of 20 years.
Coureau, Gaëlle, et al. “Mobile phone use and brain tumours in the CERENAT case-control study.” Occupational and Environmental Medicine, vol. 71, no. 7, 2014, pp. 514-22.
No association with brain tumours was observed when comparing regular mobile phone users with non-users, however, the positive association was statistically significant in the heaviest users when considering life-long cumulative duration and number of calls for gliomas. Risks were higher for gliomas, temporal tumours, occupational and urban mobile phone use.
Absorbed Exposures to Anatomical Regions of the Brain and Increased Brain Cancer Incidence Rates
Zada, Gabriel, et al. “Incidence trends in the anatomic location of primary malignant brain tumors in the United States: 1992–2006.” World Neurosurgery, vol. 77, no. 3, 2012, pp. 518-24.
Data from 3 major cancer registries demonstrate increased incidences of glioblastoma multiforme in the frontal lobe, temporal lobe, and cerebellum, despite decreased incidences in other brain regions. Although this may represent an effect of diagnostic bias, the incidence of both large and small tumors increased in these regions.
Cardis, Elisabeth, et al. “Risk of brain tumours in relation to estimated RF dose from mobile phones: results from five Interphone countries.” Occupational and Environmental Medicine, vol. 68, no. 9, 2011, pp. 631-40.
Authors found suggestions of an increased risk of glioma in long-term mobile phone users with high RF exposure and of similar, but apparently much smaller, increases in meningioma risk.
Schwann Cell Cancers
Moon et al. “Association between vestibular schwannomas and mobile phone use.” Tumour Biology, vol. 35, no. 1, 2014, pp. 581-7 .
Acoustic neuromas (vestibular schwannomas) occur more frequently on used ear of mobile phones and tumor volume showed a strong correlation with amount of mobile phone use.
Benson, V.S., et al. “Mobile phone use and risk of brain neoplasms and other cancers: prospective study.” International Journal of Epidemiology, vol. 42, no. 3, 2013, pp. 792-802.
Acoustic neuromas were 2 1/2 times more likely in long term users compared to never users (10+ years: RR = 2.46, 95% CI = 1.07-5.64, P = 0.03), with the risk increasing with duration of use (trend among users, P = 0.03).
Hardell, et al. “Pooled analysis of case-control studies on acoustic neuroma diagnosed 1997-2003 and 2007-2009 and use of mobile and cordless phones.” International Journal of Oncology, vol. 43, no. 4, 2013, pp. 1036-44.
This study confirmed previous results demonstrating an association between mobile and cordless phone use and acoustic neuroma.
Hardell, L., M. Carlberg and Mild K. Hansson. “Use of mobile phones and cordless phones is associated with increased risk for glioma and acoustic neuroma.” Pathophysiology, vol. 20, no. 2, 2012, pp. 85-110.
Regarding acoustic neuroma, ipsilateral mobile phone use in the latency group ≥10 years gave OR=1.81, 95% CI=0.73-4.45. For ipsilateral cumulative use ≥1640 h OR=2.55, 95% CI=1.50-4.40 was obtained. Also use of cordless phones increased the risk for glioma and acoustic neuroma in the Hardell group studies.
Interphone Study Group. “Acoustic neuroma risk in relation to mobile telephone use: results of the INTERPHONE international case-control study.” Cancer Epidemiology, vol. 35, no. 5, 2011, pp. 453-64.
In general, ORs were not greater in subjects who reported usual phone use on the same side of the head as their tumour than in those who reported it on the opposite side, but it was greater in those in the 10th decile of cumulative hours of use.
Hardell et al. “Mobile phones, cordless phones and the risk for brain tumours.” International Journal of Oncology, vol. 35, no. 1, 2009, pp. 5-17.
For acoustic neuroma, the highest OR was found for ipsilateral use and >10 year latency, for mobile phone OR=3.0, 95% CI=1.4-6.2 and cordless phone OR=2.3, 95% CI=0.6-8.8.
Schoemaker et al. “Mobile phone use and risk of acoustic neuroma: results of the Interphone case-control study in five North European countries.” British Journal of Cancer, vol. 93, no. 7, 2005, pp. 842-8.
Risk of a tumour on the same side of the head as reported phone use was raised for use for 10 years or longer (OR = 1.8, 95% CI: 1.1-3.1). The study suggests that there is no substantial risk of acoustic neuroma in the first decade after starting mobile phone use. However, an increase in risk after longer term use or after a longer lag period could not be ruled out.
Lonn et al. “Mobile phone use and the risk of acoustic neuroma.” Epidemiology, vol.15, no. 6, 2004, pp. 653-9
The overall odds ratio for acoustic neuroma associated with regular mobile phone use was 1.0 (95% confidence interval = 0.6-1.5). Ten years after the start of mobile phone use the estimates relative risk increased to 1.9 (0.9-4.1); when restricting to tumors on the same side of the head as the phone was normally used, the relative risk was 3.9 (1.6-9.5).
Lim et al. “Trends in Thyroid Cancer Incidence and Mortality in the United States, 1974-2013.” JAMA, vol. 317, no. 13, 2017, pp. 1338-48.
Among patients in the United States diagnosed with thyroid cancer from 1974-2013, the overall incidence of thyroid cancer increased 3% annually, with increases in the incidence rate and thyroid cancer mortality rate for advanced-stage papillary thyroid cancer. These findings are consistent with a true increase in the occurrence of thyroid cancer in the United States.
Carlberg, Michael, et al. “Increasing incidence of thyroid cancer in the Nordic countries with main focus on Swedish data.” BMC Cancer, vol. 16, no. 426, 2016.
The main finding of this register based study was an increasing incidence of thyroid cancer in Sweden during the whole study period 1970–2013 in both women and men, although not statistically significant in men. In both genders the incidence increased during the more recent study period, from 2001 in women and from 2005 in men.
Parotid Gland Cancers
Sadetzki, Siegal, et al. “Cellular Phone Use and Risk of Benign and Malignant Parotid Gland Tumors–A Nationwide Case-Control Study.” American Journal of Epidemiology, vol. 167, no. 4, 2007, pp. 457-67.
Our results suggest a relation between long-term and heavy cellular phone use and parotid gland tumors. This association was seen in analyses restricted to regular users, analyses of laterality of phone use, and analyses of area of main use.
Cancer and Cancer Promotion – Epidemiology
Momoli, F., et al. “Probabilistic multiple-bias modelling applied to the Canadian data from the INTERPHONE study of mobile phone use and risk of glioma, meningioma, acoustic neuroma, and parotid gland tumors.” American Journal of Epidemiology, 2017.
Since the 13-nation Interphone study was published in 2010, several methods papers have been published that reanalyze the data to correct for biases in the original paper. The authors of this study found that the risk estimate for glioma among the highest quartile of cell phone users increased after adjustment. Risk estimates for other types of head tumors did not change.
Siqueira, Elisa Carvalho, et al. “Cell phone use is associated with an inflammatory cytokine profile of parotid gland saliva.” Journal of Oral Pathology & Medicine, vol. 45, no. 9, 2016, pp. 682-6.
Cell phone exposure was associated with an increased level of IL-1β (a pro-inflammatory cytokine) and decreased IL-10 level (anti-inflammatory cytokine) in the exposed parotid gland saliva .
Sadetzki, Siegal, et al. “The MOBI-Kids Study Protocol: Challenges in Assessing Childhood and Adolescent Exposure to Electromagnetic Fields from Wireless Telecommunication Technologies and Possible Association with Brain Tumor Risk.” Frontiers in Public Health, vol. 2, no. 124, 2014, pp. 1-10.
MOBI-Kids, a multinational case–control study, investigates the potential effects of childhood and adolescent exposure to EMF from mobile communications technologies on brain tumor risk in 14 countries. This manuscript discusses the design of MOBI-Kids and describes the challenges and approaches chosen to address them.
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. “IARC monographs on the evaluation of carcinogenic risks to humans. Non-Ionizing Radiation, Part 2: Radiofrequency Electromagnetic Fields.” IARC Monographs on the Evaluation of Carcinogenic Risks to Humans/World Health Organization, International Agency for Research on Cancer vol. 102, 2013.
The NTP Study Shows Cancer and Cancer Promotion
Wyde, Michael, et al. “Report of Partial findings from the National Toxicology Program Carcinogenesis Studies of Cell Phone Radiofrequency Radiation in Hsd: Sprague Dawley® SD rats (Whole Body Exposure).” bioRxiv, no. 055699, 2016. (National Toxicology Program Video Presentation that includes genotoxicity results June 2016)
Exposures to cell phone equivalent RFR began for rats in-utero and during adolescence for mice, continuing through young adulthood (subchronic) or for 2 years (chronic). Researchers observed increased incidence of gliomas as well as schwannomas in both sexes, as well as significantly more rare, pre-cancerous changes in the glial cells of the brain in both sexes, while not a single one of the unexposed control animals developed these same abnormal brain cells. Male rats exposed to all levels of CDMA developed exceptional numbers of damaged, pre-cancerous brain cells (glial hyperplasia). Body weights at birth and throughout lactation in rat pups exposed in utero tended to be lower than controls. Comet assay summaries revealed statistically significant evidence of DNA damage from nonthermal exposure in mice and rats within the frontal cortex (male & female rats, male male), hippocampus (male rats), liver (male rats, female mice), and blood (male rats, female mice). The increased types of tumors found in NTP’s research rats parallel the types of increased tumors found in human long term users of cell phones.
Lerchl, Alexander, et al. “Tumor promotion by exposure to radiofrequency electromagnetic fields below exposure limits for humans.” Biochemical and Biophysical Research Communications, vol. 459, no. 4, 2015, pp. 585-90.
Numbers of tumors of the lungs and livers in exposed animals were significantly higher than in sham-exposed controls. In addition, lymphomas were also found to be significantly elevated by exposure.
Experimental Study of Pregnancy with Prenatal Exposure Affects Brain and Behavior
Aldad, Tamir S., et al. “Fetal radiofrequency radiation exposure from 800-1900 Mhz-rated cellular telephones affects neurodevelopment and behavior in mice.” Scientific Reports, vol. 2, no. 312, 2012.
In a study examining the association between prenatal cell phone use and hyperactivity in children, researchers found that mice exposed in-utero were hyperactive and had impaired memory, and in addition, recordings of excitatory postsynaptic currents revealed that these behavioral changes were due to altered neuronal developmental programming.
Kim, Ju Hwan, et al. “Long-term exposure to 835 MHz RF-EMF induces hyperactivity, autophagy and demyelination in the cortical neurons of mice.” Scientific Reports, vol. 7, 2017.
The neuronal effects of 835 MHz RF-EMF on the cerebral cortex of the mouse brain at 4.0 W/kg for 5 hours/day for 12 weeks included induction of autophaygy genes, production of proteins, accumulation of autolysosome, demyelination in cortical neurons and hyperactivity-like behavior.
Breast Cancer Case Series Report
West JG, Kapoor NS, Liao S, Chen JW, Bailey L, Nagourney RA. (2013). Multifocal Breast Cancer in Young Women with Prolonged Contact between Their Breasts and Their Cellular Phones. Case Reports in Medicine. Volume 2013, Article ID 354682.
Researchers report a four case series of women-ages from 21 to 39-with multifocal invasive breast cancer, all which regularly carried their cell phones against their breast for up to 10 hours/day for several years, had no family history of breast cancer, tested negative for BRCA1 and BRCA2, and have highly similar case pathology and morphology.
Damage to Male Reproduction
Houston, B.J., et al. “The effects of radiofrequency electromagnetic radiation on sperm function.” Reproduction, vol. 152, no. 2, 2016, pp. R263-76.
Documented impacts of RF-EMR on the male reproductive system include decreased sperm motility, elevated levels of reactive oxygen species, increased DNA damage, and decreased antioxidant levels.
Adams, Jessica A., et al. “Effect of mobile telephones on sperm quality: A systematic review and meta-analysis.” Environmental International, vol. 70, 2014, pp. 106-12.
Following a systematic review and meta-analysis to determine whether exposure to RF-EMR emitted from mobile phones affects human sperm quality, researchers found that exposure to mobile phone was associated with reduced sperm motility and overall quality.
De Iuliis, Geoffry N., et al. “Mobile phone radiation induces reactive oxygen species production and DNA damage in human spermatozoa in vitro.” PloS one, vol. 4, no. 7, 2009.
RF-EMR in both the power density and frequency range of mobile phones (1.8 GHz covering a SAR range from 0.4 to 27.5 W/kg) were shown to enhance mitochondrial reactive oxygen species generation, decrease the motility and vitality, stimulating DNA base adduct formation and ultimately cause DNA fragmentation within the human spermatozoa
Atasoy, Halil I., et al. “Immunohistopathologic demonstration of deleterious effects on growing rat testes of radiofrequency waves emitted from conventional Wi-Fi devices.” Journal of Pediatric Urology, vol. 9, no. 2, 2013, pp. 223-9.
Researchers observed significant increases in serum 8-hydroxy-2′-deoxyguanosine levels and 8-hydroxyguanosine staining in the testes of the experimental group indicating DNA damage due to exposure (p < 0.05) and effects on enzyme activity.
Avendano, Conrado, et al. “Use of laptop computers connected to internet through Wi-Fi decreases human sperm motility and increases sperm DNA fragmentation.” Fertility and Sterility, vol. 97, no. 1, 2012, pp. 39-45.
Sperm samples, mostly normozoospermic, exposed ex vivo during 4 hours to a wireless internet-connected laptop showed a significant decrease in progressive sperm motility and an increase in sperm DNA fragmentation.
Sepehrimanesh, Masood and Devra Lee Davis. “Proteomic impacts of electromagnetic fields on the male reproductive system.” Comparative Clinical Pathology, vol. 26, no. 2, 2017, pp. 309-13.
This paper reviews proteomic experimental and clinical evidence that EMF acts as a male-mediated teratogen and contributor to infertility.
Neurodevelopment and Neurological
Volkow, Nora D., et al. “Effects of cell phone radiofrequency signal exposure on brain glucose metabolism.” JAMA, vol. 305, no. 8, 2011, pp. 808-13.
Researchers concluded that compared to individuals with no exposure, 50-minute cell phone exposure was associated with increased brain glucose metabolism in the region closest to the antenna.
Bas, O., et al. “Chronic prenatal exposure to the 900 megahertz electromagnetic field induces pyramidal cell loss in the hippocampus of newborn rats.” Toxicology and Industrial Health, vol. 25, no. 6, 2009, pp. 377-84.
It was found that 900 megahertz of electromagnetic field significantly reduced the total pyramidal cell number in the cornu ammonis of the electromagnetic field group (P < 0.001).
Deshmukh, Pravin Suryakantrao, et al. “Cognitive impairment and neurogenotoxic effects in rats exposed to low-intensity microwave radiation.” International Journal of Toxicology, vol. 34, no. 3, 2015, pp. 284-90.
Rats exposed to low-intensity microwave radiation showed declined cognitive function, elevated HSP70 level, and DNA damage within the brain, compared to control animals.
Herbert, Martha R., and Cindy Sage. “Autism and EMF? Plausibility of a pathophysiological link–Part I.” Pathophysiology, vol. 20, no. 3, 2013, pp. 191-209.
Authors review pathophysiological damage to core cellular processes that are associated both with autism spectrum conditions and with biological effects of EMF/RFR exposures that contribute to chronically disrupted homeostasis
Herbert, Martha R., and Cindy Sage. “Autism and EMF? Plausibility of a pathophysiological link part II.” Pathophysiology, vol. 20, no. 3, 2013, pp. 211-34.
Authors document how behaviors in autism spectrum conditions may emerge from alterations of electrophysiological oscillatory synchronization, how EMF/RFR could contribute to these by de-tuning the organism, and policy implications of these vulnerabilities.
Odaci, E., O. Bas, and S. Kaplan. “Effects of prenatal exposure to a 900MHz electromagnetic field on the dentate gyrus of rats: a stereological and histopathological study.” Brain Research, no. 1238, 2008, pp. 224-9.
The results showed that prenatal EMF exposure caused a decrease in the number of granule cells in the dentate gyrus of the rats (P<0.01), suggesting that prenatal exposure to a 900 MHz EMF affects the development of the dentate gyrus granule cells in the rat hippocampus.
Sonmez, O.F., et al. “Purkinje cell number decreases in the adult female rat cerebellum following exposure to 900 MHz electromagnetic field.” Brain Research, no. 1356, 2010, pp. 95-101.
Results showed that the total number of Purkinje cells in the cerebellum of the EMFG was significantly lower than those of CG (p<0.004) and SG (p<0.002), suggesting that long duration exposure to 900 MHz EMF leads to decreases of Purkinje cell numbers in the female rat cerebellum.
Tang, Jun, et al. “Exposure to 900MHz electromagnetic fields activates the mkp-1/ERK pathway and causes blood-brain barrier damage and cognitive impairment in rats.” Brain Research, no. 1601, 2015, pp. 92-101.
Results demonstrate that exposure to 900 MHz EMF radiation for 28 days can significantly impair spatial memory and damage BBB permeability in rat by activating the mkp-1/ERK pathway.
Environmental Exposures Can Enhance Damage from EMFs
Kostoff, Ronald N., and Clifford GY Lau. “Combined biological and health effects of electromagnetic fields and other agents in the published literature.” Technological Forecasting and Social Change vol. 80, no. 7, 2013, no. 1331-49.
The present study examined the scope of the combined effects; i.e., identified effects on biological systems from combined exposure to electromagnetic fields/radiation and at least one other agent, concluding that EMF health impacts increase substantially when EMFs function as co-promoters and thus inclusion of co-promoters is essential for modeling real-world effects.
Byun, Yoon-Hwan, et al. “Mobile phone use, blood lead levels, and attention deficit hyperactivity symptoms in children: a longitudinal study.” PLoS One, vol. 8, no. 3, 2013.
The results suggest that simultaneous exposure to lead and RF from mobile phone use was associated with increased ADHD symptom risk, although possible reverse causality could not be ruled out.
EMF Can Interfere with Cognition
Papageorgiou, Charalabos C., et al. “Effects of wi-fi signals on the p300 component of event-related potentials during an auditory hayling task.” Journal of Integrative Neuroscience, vol. 10, no. 2, 2011, pp. 189-202.
The present study focused on the possible gender-related effects of Wi-Fi electromagnetic fields (EMF) on the attention and working memory operations of the brain, concluding that Wi-Fi exposure may exert gender-related alterations on neural activity associated with the amount of attentional resources engaged during a linguistic test.
Ntzouni, Maria P, et al. “Transient and cumulative memory impairments induced by GSM 1.8 GHz cell phone signal in a mouse model.” Electromagnetic Biology and Medicine, vol. 32, no. 1, 2013, pp. 95-120.
The data suggest that visual information processing mechanisms in hippocampus, perirhinal and entorhinal cortex are gradually malfunctioning upon long-term daily exposure, a phenotype that persists for at least 2 weeks after interruption of radiation, returning to normal memory performance levels 4 weeks later.
Theoretical and Experimental Evidence that RF Induces Specific Mechanisms
Barnes, Frank, and Ben Greenebaum. “Some Effects of Weak Magnetic Fields on Biological Systems: RF fields can change radical concentrations and cancer cell growth rates.” IEEE Power Electronics Magazine, vol. 3, no. 1, 2016, pp. 60-8.
Authors describe historical and recent concerns raised about the possible biological effects of nonionizing radiation of many different types on humans or other organisms, detailing these effects and possible mechanisms behind their induction of cellular damage.
Belyaev, Igor Y., et al. “Microwaves from UMTS/GSM mobile phones induce long‐lasting inhibition of 53BP1/γ‐H2AX DNA repair foci in human lymphocytes.” Bioelectromagnetics, vol. 30, no. 2, 2009, pp. 129-41.
Researchers described frequency-dependent effects of mobile phone microwaves on human lymphocytes from persons reporting hypersensitivity to electromagnetic fields and healthy persons, concluding that microwaves from universal global telecommunications system (UMTS) mobile phones affect chromatin and inhibit formation of DNA double-strand breaks in human lymphocytes from both hypersensitive and healthy persons.
Yakymenko, Igor, et al. “Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation.” Electromagnetic Biology and Medicine, vol. 35, no. 2, 2016, pp. 186-202.
In conclusion, our analysis demonstrates that low-intensity RFR is an expressive oxidative agent for living cells with a high pathogenic potential and that the oxidative stress induced by RFR exposure should be recognized as one of the primary mechanisms of the biological activity of this kind of radiation.
Pall, M. Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects. Journal of Cellular and Molecular Medicine, vol. 17, no. 8, 2013 pp. 958-965
This article reviews a substantially supported set of targets, voltage-gated calcium channels, whose stimulation produces non-thermal EMF responses by humans/higher animals with downstream effects involving Ca2+/calmodulin-dependent nitric oxide increases, which may explain therapeutic and pathophysiological effects of electromagnetic fields.
Hinrikus, Hiie, et al. “Mechanism of low-level microwave radiation effect on nervous system.” Electromagnetic Biology and Medicine, 2016.
Results support the proposed model of excitation by low-level microwave radiation based on the influence of water polarization on hydrogen bonding forces between water molecules, caused by this the enhancement of diffusion and consequences on neurotransmitters transit time and neuron resting potential.
Leszczynski, Dariusz, et al. “Non‐thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in human endothelial cells: Molecular mechanism for cancer‐and blood‐brain barrier‐related effects.” Differentiation, vol. 70, no. 2‐3, 2002, pp. 120-9.
Results obtained demonstrate that 1-hour non-thermal exposure of EA.hy926 cells changes the phosphorylation status of numerous, yet largely unidentified, proteins.
Markovà, Eva, Lars OG Malmgren, and Igor Y. Belyaev. “Microwaves from mobile phones inhibit 53BP1 focus formation in human stem cells more strongly than in differentiated cells: possible mechanistic link to cancer risk.” Environ Health Perspect, vol. 118, no. 3, 2010, pp. 394-9.
Microwaves from mobile phones inhibited formation of 53BP1 foci in human primary fibroblasts and mesenchymal stem cells. These data parallel our previous findings for human lymphocytes.
Pall, Martin L. “Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric effects including depression.” Journal of Chemical Neuroanatomy, vol. 75, pt. B, 2016, pp. 43-51.
Results show microwave EMFs activate voltage-gated Ca2+ channels (VGCCs) concentrated in the brain, and VGCC activity causes widespread neuropsychiatric effects in humans (genetic studies).
ELF-EMF Studies That Show Synergistic Effect
Soffritti, Morando, et al. “Synergism between sinusoidal-50 Hz magnetic field and formaldehyde in triggering carcinogenic effects in male Sprague–Dawley rats.” American Journal of Industrial Medicine, vol. 59, no. 7, 2016, pp. 509-21.
Soffritti, Morando, et al. “Life-span exposure to sinusoidal-50 Hz magnetic field and acute low-dose γ radiation induce carcinogenic effects in Sprague-Dawley rats.” International Journal of Radiation Biology, vol. 92, no. 4, 2016, pp. 202-14.
Compared to untreated controls, exposure to MF and formaldehyde causes in males a statistically significant increased incidence of malignant tumors (P ≤ 0.01), thyroid C-cell carcinomas (P ≤ 0.01), and hemolymphoreticular neoplasias (P ≤ 0.05). No statistically significant differences were observed among female groups.
Exposure Assessment Shows Greater Absorption into Younger Smaller Brains
Fernández-Rodríguez, Claudio Enrique, Alvaro Augusto Almeida De Salles, and Devra Lee Davis. “Dosimetric Simulations of Brain Absorption of Mobile Phone Radiation–The Relationship Between psSAR and Age.” IEEE Access vol. 3, 2015, pp. 2425-30.
If the peak spatial SAR (psSAR) is modeled in the entire head, as current testing standards recommend, the results for adults and children are equivalent, however the present study uses anatomically based evaluations which rely on Finite-difference time-domain simulations of different tissues within the brain, which confirm that the psSAR in a child’s brain is higher than in an adult’s brain and thus higher doses are likely to have more severe implications in the young brain.
Gandhi, Om P., et al. “Exposure limits: the underestimation of absorbed cell phone radiation, especially in children.” Electromagnetic Biology and Medicine, vol. 31, no. 1, 2012, pp. 34-51. Includes detailed history of FDA/FCC test standard evolution
Researchers indicate that the existing cell phone certification process is outdated and greatly underestimates the SAR for typical phone users, especially children, and thus call for a new certification process that incorporates different modes of use, head size, tissue properties, and anatomically based models.
Bakker, J. F., et al. “Assessment of Induced SAR in children Exposed to Electromagnetic Plane Waves Between 10 MHz and 5.6 GHz.” Physics in Medicine and Biology, vol. 55, no. 11, 2010, pp. 3115-30.
Researchers found that the basic restriction on the SAR(wb) is occasionally exceeded for children, up to a maximum of 45% in small children. The maximum SAR(10g) values, usually found at body protrusions, remain under the limit for all scenarios studied.
Ferreira, Juliana Borges, and Álvaro Augusto Almeida de Salles. “Specific Absorption Rate (SAR) in the head of Tablet users.” 7th Latin American Workshop On Communications, 2015
The psSAR simulations in heterogeneous models (adult and child) show higher levels in the children model. The possible reasons for the higher SAR estimated in the child head model compared with adult model can be due to different reasons (e.g. thinner skull, higher dielectric parameters, smaller dimensions, etc.).
Gultekin, David H., and Lothar Moeller. “NMR imaging of cell phone radiation absorption in brain tissue.” Proceedings of the National Academy of Sciences, vol. 110, no. 1, 2013, pp. 58-63.
A method is described for measuring absorbed electromagnetic energy radiated from cell phone antennae into ex vivo brain tissue.
Morris, Robert D., Lloyd L. Morgan, and Devra L. Davis. “Children Absorb Higher Doses of Radio Frequency Electromagnetic Radiation From Mobile Phones Than Adults.” IEEE Access, vol. 3, 2015, pp. 2379-87.
Authors discuss the differences between exposure and tissue absorption and re-examine the results presented by Foster and Chou. Based upon the review, authors suggest an alternative interpretation of the published literature.