Select "NOTES" Tab below to Read - Download "APP Enhanced RF DBASE" Version
LIST- Bio/Phys Effct
|Click Here - DIRECTIONS to FILTER DBASE||To View & Enlarge Abstract Cells- CLICK|
|No.||Bio/Phys Effcts||Sub Catg||Authors||Title||View Abstr|
|Type of Stdy||Year||Country||Srch Abstrct|
|1||Cancer ; (NE)Brain effct||Carlberg M, Hardell L||Decreased Survival of Glioma Patients with Astrocytoma Grade IV (Glioblastoma Multiforme) Associated with Long-Term Use of Mobile and Cordless Phones||View Abstr||case-control/ cohort||2014||Sweden||1. On 31 May 2011 the WHO International Agency for Research on Cancer (IARC) categorised radiofrequency electromagnetic fields (RF-EMFs) from mobile phones, and from other devices that emit similar non-ionising electromagnetic fields, as a Group 2B, i.e., a "possible", human carcinogen. A causal association would be strengthened if it could be shown that the use of wireless phones has an impact on the survival of glioma patients. We analysed survival of 1678 glioma patients in our 1997-2003 and 2007-2009 case-control studies. Use of wireless phones in the >20 years latency group (time since first use) yielded an increased hazard ratio (HR) = 1.7, 95% confidence interval (CI) = 1.2-2.3 for glioma. For astrocytoma grade IV (glioblastoma multiforme; n = 926) mobile phone use yielded HR = 2.0, 95% CI = 1.4-2.9 and cordless phone use HR = 3.4, 95% CI = 1.04-11 in the same latency category. The hazard ratio for astrocytoma grade IV increased statistically significant per year of latency for wireless phones, HR = 1.020, 95% CI = 1.007-1.033, but not per 100 h cumulative use, HR = 1.002, 95% CI = 0.999-1.005. HR was not statistically significant increased for other types of glioma. Due to the relationship with survival the classification of IARC is strengthened and RF-EMF should be regarded as human carcinogen requiring urgent revision of current exposure guidelines.||https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC4211006||Int J Environ Res Public Health 11(10):10790-10805, 2014|
|2||Cancer ; (NE)Brain effct||Hardell L, Carlberg M, Hansson Mild K||Mobile phone use and the risk for malignant brain tumors: A case-control study on deceased cases and controls||View Abstr||case-control/ cohort||2010||Sweden||2. We investigated the use of mobile or cordless phones and the risk for malignant brain tumors in a group of deceased cases. Most previous studies have either left out deceased cases of brain tumors or matched them to living controls and therefore a study matching deceased cases to deceased controls is warranted. Recall error is one issue since it has been claimed that increased risks reported in some studies could be due to cases blaming mobile phones as a cause of the disease. This should be of less importance for deceased cases and if cancer controls are used. In this study brain tumor cases aged 20-80 years diagnosed during 1997-2003 that had died before inclusion in our previous studies on the same topic were included. Two control groups were used: one with controls that had died from another type of cancer than brain tumor and one with controls that had died from other diseases. Exposure was assessed by a questionnaire sent to the next-of-kin for both cases and controls. Replies were obtained for 346 (75%) cases, 343 (74%) cancer controls and 276 (60%) controls with other diseases. Use of mobile phones gave an increased risk, highest in the >10 years' latency group yielding odds ratio (OR) = 2.4, and 95% confidence interval (CI) = 1.4-4.1. The risk increased with cumulative number of lifetime hours for use, and was highest in the >2,000 h group (OR = 3.4, 95% CI = 1.6-7.1). No clear association was found for use of cordless phones, although OR = 1.7, 95% CI = 0.8-3.4 was found in the group with >2,000 h of cumulative use. This investigation confirmed our previous results of an association between mobile phone use and malignant brain tumors.||https://www.ncbi.nlm.nih.gov/pubmed/20551697||Neuroepidemiology 35(2):109-114, 2010|
|3||Cancer ; Skin||Hardell L, Carlberg M, Hansson Mild K, Eriksson M||Case-control study on the use of mobile and cordless phones and the risk for malignant melanoma in the head and neck region||View Abstr||case-control/ cohort||2011||Sweden||3. The incidence of cutaneous malignant melanoma has increased during the last decades in Sweden as in many other countries. Besides of ultraviolet radiation and constitutional factors such as light-sensitive skin and poor ability to tan few risk factors are established. Some studies indicate that electromagnetic fields might be of concern. In this case-control study we assessed use of mobile and cordless phones in 347 cases with melanoma in the head and neck region and 1184 controls. These subjects constituted 82% and 80%, respectively, that answered the questionnaire. Overall no increased risk was found. However, in the most exposed area; temporal, cheek and ear, cumulative use >365h of mobile phone yielded in the >1-5-year latency group odds ratio (OR)=2.1, 95% confidence interval (CI)=0.7-6.1 and cordless phone use gave OR=2.1, 95% CI=1.1-3.8. Highest OR was calculated for first use of mobile or cordless phone before the age of 20 years regardless of anatomical localisation in the head and neck region. No interaction was found with established risk factors such as red, medium blond or fair hair colour, blue eyes, skin type I or II (never or sometimes tanned), severe sunburns as teenager or heredity. The results must be interpreted with caution due to low numbers and potential methodological shortcomings in a case-control study. However, the findings might be consistent with a late carcinogenic effect from microwaves, i.e. tumour promotion, but need to be confirmed.||https://www.ncbi.nlm.nih.gov/pubmed/21764571||Pathophysiology 18(4):325-333, 2011|
|4||Cancer ; (NE)Brain effct||Hardell L, Carlberg M, Söderqvist F, Mild KH||Case-control study of the association between malignant brain tumours diagnosed between 2007 and 2009 and mobile and cordless phone use||View Abstr||case-control/ cohort||2013||Sweden||4. Previous studies have shown a consistent association between long-term use of mobile and cordless phones and glioma and acoustic neuroma, but not for meningioma. When used these phones emit radiofrequency electromagnetic fields (RF-EMFs) and the brain is the main target organ for the handheld phone. The International Agency for Research on Cancer (IARC) classified in May, 2011 RF-EMF as a group 2B, i.e. a 'possible' human carcinogen. The aim of this study was to further explore the relationship between especially long-term (>10 years) use of wireless phones and the development of malignant brain tumours. We conducted a new case-control study of brain tumour cases of both genders aged 18-75 years and diagnosed during 2007-2009. One population-based control matched on gender and age (within 5 years) was used to each case. Here, we report on malignant cases including all available controls. Exposures on e.g. use of mobile phones and cordless phones were assessed by a self-administered questionnaire. Unconditional logistic regression analysis was performed, adjusting for age, gender, year of diagnosis and socio-economic index using the whole control sample. Of the cases with a malignant brain tumour, 87% (n=593) participated, and 85% (n=1,368) of controls in the whole study answered the questionnaire. The odds ratio (OR) for mobile phone use of the analogue type was 1.8, 95% confidence interval (CI)=1.043.3, increasing with >25 years of latency (time since first exposure) to an OR=3.3, 95% CI=1.6-6.9. Digital 2G mobile phone use rendered an OR=1.6, 95% CI=0.996-2.7, increasing with latency >15-20 years to an OR=2.1, 95% CI=1.2-3.6. The results for cordless phone use were OR=1.7, 95% CI=1.1-2.9, and, for latency of 15-20 years, the OR=2.1, 95% CI=1.2-3.8. Few participants had used a cordless phone for >20-25 years. Digital type of wireless phones (2G and 3G mobile phones, cordless phones) gave increased risk with latency >1-5 years, then a lower risk in the following latency groups, but again increasing risk with latency >15-20 years. Ipsilateral use resulted in a higher risk than contralateral mobile and cordless phone use. Higher ORs were calculated for tumours in the temporal and overlapping lobes. Using the meningioma cases in the same study as reference entity gave somewhat higher ORs indicating that the results were unlikely to be explained by recall or observational bias. This study confirmed previous results of an association between mobile and cordless phone use and malignant brain tumours. These findings provide support for the hypothesis that RF-EMFs play a role both in the initiation and promotion stages of carcinogenesis.||https://www.ncbi.nlm.nih.gov/pubmed/24064953||https://www.ncbi.nlm.nih.gov/pmc/articles/: PMC3834325||Int J Oncol 43(6):1833-1845, 2013||DIRECTIONSo FILTER the DBASE|
|5||Cancer ; (NE)Brain effct||Hardell L, Eriksson M, Carlberg M, Sundstrom C, Mild KH||Use of cellular or cordless telephones and the risk for non-Hodgkin's lymphoma||View Abstr||;1,15;126,8;385,8;1014,12||case-control/ cohort||2005||Sweden||5. OBJECTIVES:|
To evaluate the use of cellular and cordless telephones as the risk factor for non-Hodgkin's lymphoma (NHL).
Male and female subjects aged 18-74 years living in Sweden were included during a period from 1 December 1999 to 30 April 2002. Controls were selected from the national population registry. Exposure to different agents was assessed by questionnaire.
In total, 910 (91%) cases and 1016 (92%) controls participated. NHL of the B-cell type was not associated with the use of cellular or cordless telephones. Regarding T-cell NHL and >5 year latency period, the use of analogue cellular phones yielded: odds ratio (OR) = 1.46, 95%; confidence interval (CI) = 0.58-3.70, digital: OR=1.92, 95%; CI=0.77-4.80 and cordless phones: OR=2.47; CI=1.09-5.60. The corresponding results for certain, e.g. cutaneous and leukaemia, T-cell lymphoma for analogue phones were: OR=3.41, 95%; CI=0.78-15.0, digital: OR=6.12, 95%; CI=1.26-29.7 and cordless phones: OR=5.48, 95%; CI=1.26-23.9.
The results indicate an association between T-cell NHL and the use of cellular and cordless telephones, however based on low numbers and must be interpreted with caution. Regarding B-cell NHL no association was found.
|https://www.ncbi.nlm.nih.gov/pubmed/16001209||Int Arch Occup Environ Health 78(8):625-632, 2005|
|6||Cancer ; (NE)Brain effct||Hardell, L, , Carlberg, M, , Mild, K, , 2005,||Case-control study of the association between the use of cellular and cordless telephones and malignant brain tumors diagnosed during 2000-2003||View Abstr||case-control/ cohort||2006||Sweden||6. We performed a case–control study on the use of cellular and cordless telephones and the risk for brain tumors diagnosed during 2000–2003. We report the results for malignant brain tumors with data from 317 cases (88%) and 692 controls (84%). The use of analog cellular phones yielded odds ratio (OR) of 2.6 and a 95% confidence interval (CI) of 1.5–4.3, increasing to OR=3.5 and 95% CI=2.0–6.4 with a >10-year latency period. Regarding digital cellular telephones, the corresponding results were OR=1.9, 95% CI=1.3–2.7 and OR=3.6, 95% CI=1.7–7.5, respectively. Cordless telephones yielded OR=2.1, 95% CI=1.4–3.0, and with a >10-year latency period, OR=2.9, 95% CI=1.6–5.2. The OR increased with the cumulative number of hours of use and was highest for high-grade astrocytoma. A somewhat increased risk was also found for low-grade astrocytoma and other types of malignant brain tumors, although not significantly so. In multivariate analysis, all three phone types studied showed an increased risk.||https://www.ncbi.nlm.nih.gov/pubmed/16023098||Environ Res 100(2):232-241, 2006|
|7||Cancer ; (NE)Brain effct||Lonn S, Ahlbom A, Hall P, Feychting M||Mobile phones and head tumours. The discrepancies in cause-effect relationships in the epidemiological studies - how do they arise?||View Abstr||;6,11;379,8;971,8;1864,12||MetaAnalysis||2011||Italy||7. |
BACKGROUND: Whether or not there is a relationship between use of mobile phones (analogue and digital cellulars, and cordless) and head tumour risk (brain tumours, acousticneuromas, and salivary gland tumours) is still a matter of debate; progress requires a critical analysis of the methodological elements necessary for an impartial evaluation of contradictory studies.
METHODS: A close examination of the protocols and results from all case-control and cohort studies, pooled- and meta-analyses on head tumour risk for mobile phone users was carried out, and for each study the elements necessary for evaluating its reliability were identified. In addition, new meta-analyses of the literature data were undertaken. These were limited to subjects with mobile phone latency time compatible with the progression of the examined tumours, and with analysis of the laterality of head tumour localisation corresponding to the habitual laterality of mobile phone use.
RESULTS: Blind protocols, free from errors, bias, and financial conditioning factors, give positive results that reveal a cause-effect relationship between long-term mobile phone use or latency and statistically significant increase of ipsilateral head tumour risk, with biological plausibility. Non-blind protocols, which instead are affected by errors, bias, and financial conditioning factors, give negative results with systematic underestimate of such risk. However, also in these studies a statistically significant increase in risk of ipsilateral head tumours is quite common after more than 10 years of mobile phone use or latency. The meta-analyses, our included, examining only data on ipsilateral tumours in subjects using mobile phones since or for at least 10 years, show large and statistically significant increases in risk of ipsilateral brain gliomas and acoustic neuromas.
CONCLUSIONS: Our analysis of the literature studies and of the results from meta-analyses of the significant data alone shows an almost doubling of the risk of head tumours induced by long-term mobile phone use or latency.
|https://www.ncbi.nlm.nih.gov/pubmed/21679472||Environ Health. 10:59, 2011.|
|8||Cancer ; (NE)Brain effct||Lonn S, Ahlbom A, Hall P, Feychting M||Use of mobile phones and cordless phones is associated with increased risk for glioma and acoustic neuroma||View Abstr||MetaAnalysis||2012||Sweden||8. The International Agency for Research on Cancer (IARC) at WHO evaluation of the carcinogenic effect of RF-EMF on humans took place during a 24-31 May 2011 meeting at Lyon in France. The Working Group consisted of 30 scientists and categorised the radiofrequency electromagnetic fields from mobile phones, and from other devices that emit similar non-ionising electromagnetic fields (RF-EMF), as Group 2B, i.e., a 'possible', human carcinogen. The decision on, mobile phones was based mainly on the Hardell group of studies from Sweden and the IARC Interphone study. We give an overview of current epidemiological evidence for an increased risk for brain tumours including a meta-analysis of the Hardell group and Interphone results for mobile phone use. Results for cordless phones are lacking in Interphone. The meta-analysis gave for glioma in the most exposed part of the brain, the temporal lobe, odds ratio OR)=1.71, 95% confidence interval (CI)=1.04-2.81 in the ≥10 years (>10 years in the Hardell group) latency group. Ipsilateral mobile phone use ≥1640h in total gave OR=2.29, 95% CI=1.56-3.37. The results for meningioma were OR=1.25, 95% CI=0.31-4.98 and OR=1.35, 95% CI=0.81-2.23, respectively. 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 ≥1640h 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. Survival of patients with glioma was analysed in the Hardell group studies yielding in the >10 years latency period hazard ratio (HR)=1.2, 95% CI=1.002-1.5 for use of wireless phones. This increased HR was based on results for astrocytoma WHO grade IV (glioblastoma multiforme. Decreased HR was found for low-grade astrocytoma, WHO grades I-II, which might be caused by RF-EMF exposure leading to tumour-associated symptoms and earlier detection and surgery with better prognosis. Some studies show increasing incidence of brain tumours whereas other studies do not. It is concluded that one should be careful using incidence data to dismiss resultsn i analytical epidemiology. The IARC carcinogenic classification does not seem to have had any significant impact on governments' perceptions of their responsibilities to protect public health from this widespread source of radiation.||https://www.ncbi.nlm.nih.gov/pubmed/23261330||Pathophysiology 2012 Dec 20|
|9||Cancer ; (NE)Brain effct||Myung SK, Ju W, McDonnell DD, Lee YJ, Kazinets G, Cheng CT, Moskowitz JM||Mobile Phone Use and Risk of Tumors: A Meta-Analysis||View Abstr||;5,8;196,8;387,8;1428,11||MetaAnalysis||2009||Korea||9. |
PURPOSE: Case-control studies have reported inconsistent findings regarding the association between mobile phone use and tumor risk. We investigated these associations using a meta-analysis.
METHODS: We searched MEDLINE (PubMed), EMBASE, and the Cochrane Library in August 2008. Two evaluators independently reviewed and selected articles based on predetermined selection criteria.
RESULTS: Of 465 articles meeting our initial criteria, 23 case-control studies, which involved 37,916 participants (12,344 patient cases and 25,572 controls), were included in the final analyses. Compared with never or rarely having used a mobile phone, the odds ratio for overall use was 0.98 for malignant and benign tumors (95% CI, 0.89 to 1.07) in a random-effects meta-analysis of all 23 studies. However, a significant positive association (harmful effect) was observed in a random-effects meta-analysis of eight studies using blinding, whereas a significant negative association (protective effect) was observed in a fixed-effects meta-analysis of 15 studies not using blinding. Mobile phone use of 10 years or longer was associated with a risk of tumors in 13 studies reporting this association (odds ratio = 1.18; 95% CI, 1.04 to 1.34). Further, these findings were also observed in the subgroup analyses by methodologic quality of study. Blinding and methodologic quality of study were strongly associated with the research group.
CONCLUSION: The current study found that there is possible evidence linking mobile phone use to an increased risk of tumors from a meta-analysis of low-biased case-control studies. Prospective cohort studies providing a higher level of evidence are needed.
|https://www.ncbi.nlm.nih.gov/pubmed/19826127||J Clin Oncol 27:5565-5572, 2009|
|10||(CE)Enzmyes & Proteins||Leszczynski D, Joenväärä S, Reivinen J, Kuokka R,||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||View Abstr||In Vitro||2002||Finland||10. Abstract We have examined whether non-thermal exposures of cultures of the human endothelial cell line EA.hy926 to 900 MHz GSM mobile phone microwave radiation could activate stress response. Results obtained demonstrate that 1-hour non-thermal exposure of EA.hy926 cells changes the phosphorylation status of numerous, yet largely unidentified, proteins. One of the affected proteins was identified as heat shock protein-27 (hsp27). Mobile phone exposure caused a transient increase in phosphorylation of hsp27, an effect which was prevented by SB203580, a specific inhibitor of p38 mitogen-activated protein kinase (p38MAPK). Also, mobile phone exposure caused transient changes in the protein expression levels of hsp27 and p38MAPK. All these changes were non-thermal effects because, as determined using temperature probes, irradiation did not alter the temperature of cell cultures, which remained throughout the irradiation period at 37/±/0.3/°C. Changes in the overall pattern of protein phosphorylation suggest that mobile phone radiation activates a variety of cellular signal transduction pathways, among them the hsp27/p38MAPK stress response pathway. Based on the known functions of hsp27, we put forward the hypothesis that mobile phone radiation-induced activation of hsp27 may (i) facilitate the development of brain cancer by inhibiting the cytochrome c/caspase-3 apoptotic pathway and (ii) cause an increase in blood-brain barrier permeability through stabilization of endothelial cell stress fibers. We postulate that these events, when occurring repeatedly over a long period of time, might become a health hazard because of the possible accumulation of brain tissue damage. Furthermore, our hypothesis suggests that other brain damaging factors may co-participate in mobile phone radiation-induced effects.||https://www.ncbi.nlm.nih.gov/pubmed/12076339||Differentiation 70:120–129, 2002|
|11||Cancer||Richter E, Berman T, Ben-Michael E, Laster R, Westin JB,||Cancer in Radar Technicians Exposed to Radiofrequency/Microwave Radiation: Sentinel Episodes||View Abstr||case-control/ cohort||2000||Israel||11. Controversy exists concerning the health risks from exposures to radiofrequency/microwave irradiation (RF/MW). The authors report exposure-effect relationships in sentinel patients and their co-workers, who were technicians with high levels of exposure to RF/MW radiation. Information about exposures of patients with sentinel tumors was obtained from interviews, medical records, and technical sources. One patient was a member of a cohort of 25 workers with six tumors. The authors estimated relative risks for cancer in this group and latency periods for a larger group of self-reported individuals. Index patients with melanoma of the eye, testicular cancer, nasopharyngioma, non-Hodgkin's lymphoma, and breast cancer were in the 20-37-year age group. Information about work conditions suggested prolonged exposures to high levels of RF/MW radiation that produced risks for the entire body. Clusters involved many different types of tumors. Latency periods were extremely brief in index patients and a larger self-reported group. The findings suggest that young persons exposed to high levels of RF/MW radiation for long periods in settings where preventive measures were lax were at increased risk for cancer. Very short latency periods suggest high risks from high-level exposures. Calculations derived from a linear model of dose-response suggest the need to prevent exposures in the range of 10-100 muw/cm(2).||https://www.ncbi.nlm.nih.gov/pubmed/10926722||Int J Occup Environ Health 6(3):187-193, 2000|
|12||Cancer ; (NE)Brain effct||Richter ED, Berman T, Levy O||Brain cancer with induction periods of less than 10 years in young military radar workers||View Abstr||case-control/ cohort||2002||Israel||12. The authors have reported on 5 young patients who had brain tumors that appeared within 10 yr of initial occupational exposures to radar. Four of the patients were less than 30 yr of age when the diagnoses were initially made. Brief induction periods that follow high exposures in individual sentinel patients are a recognized indicator of impending group risk, and these periods call attention to the need for precautionary measures. Similarly, reports of short induction periods for brain cancer on the side of the head in which there has been prior use of cell phones may also indicate increased risk.||https://www.ncbi.nlm.nih.gov/pubmed/12530592||Arch Environ Health 57(4):270-272, 2002|
|13||(CE)genetic effct||Mashevich M, Folkman D, Kesar A, Barbul A, Korenstein R, Jerby E, Avivi L,||Exposure of human peripheral blood lymphocytes to electromagnetic fields associated with cellular phones leads to chromosomal instability||View Abstr||In Vitro||2003||Israel||13. Whether exposure to radiation emitted from cellular phones poses a health hazard is at the focus of current debate. We have examined whether in vitro exposure of human peripheral blood lymphocytes (PBL) to continuous 830 MHz electromagnetic fields causes losses and gains of chromosomes (aneuploidy), a major /somatic mutation/ leading to genomic instability and thereby to cancer. PBL were irradiated at different average absorption rates (SAR) in the range of 1.6-8.8 W/kg for 72 hr in an exposure system based on a parallel plate resonator at temperatures ranging from 34.5-37.5 °C. The averaged SAR and its distribution in the exposed tissue culture flask were determined by combining measurements and numerical analysis based on a finite element simulation code. A linear increase in chromosome 17 aneuploidy was observed as a function of the SAR value, demonstrating that this radiation has a genotoxic effect. The SAR dependent aneuploidy was accompanied by an abnormal mode of replication of the chromosome 17 region engaged in segregation (repetitive DNA arrays associated with the centromere), suggesting that epigenetic alterations are involved in the SAR dependent genetic toxicity. Control experiments (i.e., without any RF radiation) carried out in the temperature range of 34.5-38.5 °C showed that elevated temperature is not associated with either the genetic or epigenetic alterations observed following RF radiation - the increased levels of aneuploidy and the modification in replication of the centromeric DNA arrays. These findings indicate that the genotoxic effect of the electromagnetic radiation is elicited via a non-thermal pathway. Moreover, the fact that aneuploidy is a phenomenon known to increase the risk for cancer, should be taken into consideration in future evaluation of exposure guidelines.||https://www.ncbi.nlm.nih.gov/pubmed/12524674||Bioelectromagnetics 24:82-90, 2003|
|14||(CE)genetic effct ; (CE)Mutagenic effect||Akhavan-Sigari R, Baf MM, Ariabod V, Rohde V, Rahighi S||Connection between Cell Phone use, p53 Gene Expression in Different Zones of Glioblastoma Multiforme and Survival Prognoses||View Abstr||CHECK NO ABSTRACT||In Vivo - Human||2014||Germany||14. The aim of this paper is to investigate p53 gene expression in the central and peripheral zones of glioblastoma multiforme using a real-time reverse transcription polymerase chain reaction (RT-PCR) technique in patients who use cell phones ≥3 hours a day and determine its relationship to clinicopathological findings and overall survival. Sixty-three patients (38 males and 25 females), diagnosed with glioblastoma multiforme (GBM), underwent tumor resection between 2008 and 2011. Patient ages ranged from 25 to 88 years, with a mean age of 55. The levels of expression of p53 in the central and peripheral zone of the GBM were quantified by RT-PCR. Data on p53 gene expression from the central and peripheral zone, the related malignancy and the clinicopatholagical findings (age, gender, tumor location and size), as well as overall survival, were analyzed. Forty-one out of 63 patients (65%) with the highest level of cell phone use (≥3 hours/day) had higher mutant type p53 expression in the peripheral zone of the glioblastoma; the difference was statistically significant (P=0.034). Results from the present study on the use of mobile phones for ≥3 hours a day show a consistent pattern of increased risk for the mutant type of p53 gene expression in the peripheral zone of the glioblastoma, and that this increase was significantly correlated with shorter overall survival time. The risk was not higher for ipsilateral exposure. We found that the mutant type of p53 gene expression in the peripheral zone of the glioblastoma was increased in 65% of patients using cell phones ≥3 hours a day.||https://www.ncbi.nlm.nih.gov/pubmed/25276320||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4178273||Rare Tumors 2014 Aug 8;6(3):5350 doi: 104081/rt20145350|
|15||(CE)Cellular effct||Ozgur E, Guler G, Kismali G, Seyhan N||Mobile Phone Radiation Alters Proliferation of Hepatocarcinoma Cells||View Abstr||In Vitro||2014||Turkey||15. This study investigated the effects of intermittent exposure (15 min on, 15 min off for 1, 2, 3, or 4 h, at a specific absorption rate of 2 W/kg) to enhanced data rates for global system for mobile communication evolution-modulated radiofrequency radiation (RFR) at 900- and 1,800-MHz frequencies on the viability of the Hepatocarcinoma cells (Hep G2). Hep G2 cell proliferation was measured by a colorimetric assay based on the cleavage of the tetrazolium salt WST-1 by mitochondrial dehydrogenases in viable cells. Cell injury was evaluated by analyzing the levels of lactate dehydrogenase (LDH) and glucose released from lysed cells into the culture medium. Morphological observation of the nuclei was carried out by 4',6-diamidino-2-phenylindole (DAPI) staining using fluorescence microscopy. In addition, TUNEL assay was performed to confirm apoptotic cell death. It was observed that cell viability, correlated with the LDH and glucose levels, changed according to the frequency and duration of RFR exposure. Four-hour exposure produced more pronounced effects than the other exposure durations. 1,800-MHz RFR had a larger impact on cell viability and Hep G2 injury than the RFR at 900 MHz. Morphological observations also supported the biochemical results indicating that most of the cells showed irregular nuclei pattern determined by using the DAPI staining, as well as TUNEL assay which shows DNA damage especially in the cells after 4 h of exposure to 1,800-MHz RFR. Our results indicate that the applications of 900- and 1,800-MHz (2 W/kg) RFR cause to decrease in the proliferation of the Hep G2 cells after 4 h of exposure. Further studies will be conducted on other frequency bands of RFR and longer duration of exposure.||https://www.ncbi.nlm.nih.gov/pubmed/24817642||Cell Biochem Biophys 2014 May 11 [Epub ahead of print]|
|16||(CE)Enzmyes & Proteins ; Cancer||Zeng QL, Weng Y, Chen GD, Lu DQ, Chiang H, Xu ZP||[Effects of GSM 1800 MHz radiofrequency electromagnetic fields on protein expression profile of human breast cancer cell MCF-7.]||View Abstr||;5,10;257,8;729,8;1482,12||In Vitro||2006||China||16. |
OBJECTIVE: To study the effects of GSM 1800 MHz radiofrequency electromagnetic fields (RF EMF) exposure on protein expression profile of human breast cancer cell line (MCF-7), as to exploring the possible effects on normal cell physiological function.
METHODS: MCF-7 cells were continuously or intermittently (5 minutes field on followed by 10 minutes off) exposed to RF EMF for different duration (1 hour, 3 hours, 6 hours, 12 hours, or 24 hours) at an average specific absorption rate (SAR) of 3.5 W/kg. The extracted proteins were separated by 2-dimensional electrophoresis and the protein-spot distribution of the sliver-stained gels was analyzed by using PDQuest software 7.1. Each experiment was repeated three times.
RESULTS: On the average, around 1100 proteins were detected using pH 4 - 7 IPG strip. There were no differential proteins found under continuous exposure at SAR of 3.5 W/kg for 6 hours. Under other exposure conditions, we found various differentially expressed proteins in exposure groups as compared with the sham-exposed controls. Especially in 3 hours intermittent exposure and 12 hours continuous exposure, eighteen and seven differential proteins were detected, respectively. The categories and functions of these differentially expressed proteins were analyzed by searching of SWISS-PROT protein database, which suggested that these proteins should be related to the functions of biosynthesization, signal transduction, and DNA damage and repair.
CONCLUSIONS: Data indicated that the protein expression changes induced by RF radiation might depend on exposure duration and mode. Many biological processes might be affected by RF exposure.
|https://www.ncbi.nlm.nih.gov/pubmed/16836875||Zhonghua Yu Fang Yi Xue Za Zhi. 40(3):153-158, 2006.|
|17||(CE)Mutagenic effect||Marinelli F, La Sala D, Cicciotti G, Cattini L, Trimarchi C, Putti S, Zamparelli A, Giuliani L, Tomassetti G, Cinti C||Exposure to 900 MHz electromagnetic field induces an unbalance between pro-apoptotic and pro-survival signals in T-lymphoblastoid leukemia CCRF-CEM cells||View Abstr||In Vitro||2004||Italy||17. It has been recently established that low-frequency electromagnetic field (EMFs) exposure induces biological changes and could be associated with increased incidence of cancer, while the issue remains unresolved as to whether high-frequency EMFs can have hazardous effect on health. Epidemiological studies on association between childhood cancers, particularly leukemia and brain cancer, and exposure to low- and high-frequency EMF suggested an etiological role of EMFs in inducing adverse health effects. To investigate whether exposure to high-frequency EMFs could affect in vitro cell survival, we cultured acute T-lymphoblastoid leukemia cells (CCRF-CEM) in the presence of unmodulated 900 MHz EMF, generated by a transverse electromagnetic (TEM) cell, at various exposure times. We evaluated the effects of high-frequency EMF on cell growth rate and apoptosis induction, by cell viability (MTT) test, FACS analysis and DNA ladder, and we investigated pro-apoptotic and pro-survival signaling pathways possibly involved as a function of exposure time by Western blot analysis. At short exposure times (2-12 h), unmodulated 900 MHz EMF induced DNA breaks and early activation of both p53-dependent and -independent apoptotic pathways while longer continuous exposure (24-48 h) determined silencing of pro-apoptotic signals and activation of genes involved in both intracellular (Bcl-2) and extracellular (Ras and Akt1) pro-survival signaling. Overall our results indicate that exposure to 900 MHz continuous wave, after inducing an early self-defense response triggered by DNA damage, could confer to the survivor CCRF-CEM cells a further advantage to survive and proliferate.||https://www.ncbi.nlm.nih.gov/pubmed/14603534||J Cell Physiol 198(2):324-332, 2004|
|18||(CE)Mutagenic effect ; Cancer||Repacholi, MH, Basten, A, Gebski, V, Noonan, D, Finnie, J, Harris, AW,||Lymphomas in E mu-Pim1 transgenic mice exposed to pulsed 900 MHZ electromagnetic fields||View Abstr||In Vivo - Animal||1997||Australia||18. Whether radiofrequency (RF) fields are carcinogenic is controversial; epidemiological data have been inconclusive and animal tests limited. The aim of the present study was to determine whether long-term exposure to pulse-modulated RF fields similar to those used in digital mobile telecommunications would increase the incidence of lymphoma in E mu-Pim1 transgenic mice, which are moderately predisposed to develop lymphoma spontaneously. One hundred female E mu-Pim1 mice were sham-exposed and 101 were exposed for two 30-min periods per day for up to 18 months to plane-wave fields of 900 MHz with a pulse repetition frequency of 217 Hz and a pulse width of 0.6 ms. Incident power densities were 2.6-13 W/m2 and specific absorption rates were 0.008-4.2 W/kg, averaging 0.13-1.4 W/kg. Lymphoma risk was found to be significantly higher in the exposed mice than in the controls (OR = 2.4. P = 0.006, 95% CI = 1.3-4.5). Follicular lymphomas were the major contributor to the increased tumor incidence. Thus long-term intermittent exposure to RF fields can enhance the probability that mice carrying a lymphomagenic oncogene will develop lymphomas. We suggest that such genetically cancer-prone mice provide an experimental system for more detailed assessment of dose-response relationships for risk of cancer after RF-field exposure.||https://www.ncbi.nlm.nih.gov/pubmed/9146709||Radiat Res 147(5):631-640, 1997|
|19||Cancer||Hruby R, Neubauer G, Kuster N, Frauscher M||Study on potential effects of "902-MHz GSM-type Wireless Communication Signals" on DMBA-induced mammary tumours in Sprague-Dawley rats.||View Abstr||In Vivo - Animal||2008||Austria||19. The aim of the study was to detect whether long-term exposure to "902-MHz GSM-type Wireless Communication Signals" ("radio-frequency (RF)-exposure") would affect 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumours in female Sprague-Dawley rats. Five hundred female rats were each given a single oral dose of 17mg DMBA per kg body weight (bw) at an age of 46-48 days. Three groups of 100 animals each were RF-exposed (902MHz; crest factor 8; pulse width=0.57ms) from the next day onwards to normal whole-body averaged doses (expressed as specific absorption rate, SAR) of 0.4, 1.3 or 4.0W/kg bw (low/mid/high-dose group) for 4h/d, 5d/week, during 6 months. A sham-exposed and a cage-control group remained without RF-exposure (<<0.01mW/kg). Animals were weekly weighed and palpated for mammary tumours; all mammary glands were examined histopathologically. There were several statistically significant differences between RF-exposed groups and the sham-exposed group, as follows: All RF-exposed groups had, at different times, significantly more palpable tissue masses. There were fewer animals with benign neoplasms, but more with malignant tumours in the high-dose group. In addition, there were more adenocarcinomas in the low-dose group, more malignant neoplasms in the low- and high-dose groups, more animals with adenocarcinomas in the high-dose group, and fewer animals with fibroadenomas in the low- and mid-dose groups. The cage-control group had, when compared with the sham-exposed group, statistically significantly more palpable tissue masses, more benign and also more malignant neoplasms. The cage-control group had in most aspects the highest incidence and malignancy of neoplasms among all groups. None of the above findings in RF-exposed animals produced a clear dose-response relation and the responses of the cage-control group were either similar to or stronger than those of any of the RF-exposed group. The significant differences between the sham-exposed animals and one or more RF-exposed groups may be interpreted as evidence of an effect of RF-exposure. In the context of the results of the cage-control group, in the light of controversial results reported in the literature, and given the fact that the DMBA-mammary tumour model is known to be prone to high variations in the results, it is the authors' opinion that the differences between the groups are rather incidental ones.||https://www.ncbi.nlm.nih.gov/pubmed/17981079||Mutat Res. 649(1-2):34-44, 2008.|
|20||(CE)Cellular effct; Cancer||Yang L, Hao D, Wang M, Zeng Y, Wu S, Zeng Y||Cellular Neoplastic Transformation Induced by 916 MHz Microwave Radiation||View Abstr||In Vitro||2012||China||20. There has been growing concern about the possibility of adverse health effects resulting from exposure to microwave radiations, such as those emitted by mobile phones. The purpose of this study was to investigate the cellular neoplastic transformation effects of electromagnetic fields. 916 MHz continuous microwave was employed in our study to simulate the electromagnetic radiation of mobile phone. NIH/3T3cells were adopted in our experiment due to their sensitivity to carcinogen or cancer promoter in environment. They were divided randomly into one control group and three microwave groups. The three microwave groups were exposed to 916 MHz EMF for 2 h per day with power density of 10, 50, and 90 w/m(2), respectively, in which 10 w/m(2) was close to intensity near the antenna of mobile phone. The morphology and proliferation of NIH/3T3cells were examined and furthermore soft agar culture and animal carcinogenesis assay were carried out to determine the neoplastic promotion. Our experiments showed NIH/3T3cells changed in morphology and proliferation after 5-8 weeks exposure and formed clone in soft agar culture after another 3-4 weeks depending on the exposure intensity. In the animal carcinogenesis study, lumps developed on the back of SCID mice after being inoculated into exposed NIH/3T3cells for more than 4 weeks. The results indicate that microwave radiation can promote neoplastic transformation of NIH/3T3cells.||https://www.ncbi.nlm.nih.gov/pubmed/22395787||Cell Mol Neurobiol32(6):1039-1046, 2012|
|21||(CE)genetic effct||Trivino Pardo JC, Grimaldi S, Taranta M, Naldi I, Cinti C||Microwave electromagnetic field regulates gene expression in T-lymphoblastoid leukemia CCRF-CEM cell line exposed to 900 MHz||View Abstr||In Vitro||2012||Italy||21. Electric, magnetic, and electromagnetic fields are ubiquitous in our society, and concerns have been expressed regarding possible adverse effects of these exposures. Research on Extremely Low-Frequency (ELF) magnetic fields has been performed for more than two decades, and the methodology and quality of studies have improved over time. Studies have consistently shown increased risk for childhood leukemia associated with ELFmagnetic fields. There are still inadequate data for other outcomes. More recently, focus has shifted toward Radio Frequencies (RF) exposures from mobile telephony. There are no persuasive data suggesting a health risk, but this research field is still immature with regard to the quantity and quality of available data. This technology is constantly changing and there is a need for continued research on this issue. To investigate whether exposure to high-frequency electromagnetic fields (EMF) could induce adverse health effects, we cultured acute T-lymphoblastoid leukemia cells (CCRF-CEM) in the presence of 900 MHz MW-EMF generated by a transverse electromagnetic (TEM) cell at short and long exposure times. We evaluated the effect of high-frequency EMF on gene expression and we identified functional pathways influenced by 900 MHz MW-EMF exposure.||https://www.ncbi.nlm.nih.gov/pubmed/22332889||Electromagn Biol Med 31(1):1-18, 2012|
|22||Cancer ; (NE)Brain effct||Hartikka H, Heinävaara S, Mäntylä R, Kähärä V, Kurttio P, Auvinen A||Mobile phone use and location of glioma: A case-case analysis||View Abstr||case-control/ cohort||2009||Finland||22. We assessed a new approach for evaluating the glioma risk among users of mobile phones to focus on the part of the brain most heavily exposed to radiofrequency electromagnetic fields from mobile phones. The tumor midpoint was defined from radiological imaging. A case-case analysis with 99 gliomas was performed using logistic regression. The exposed cases were those with the tumor mid-point within 4.6 cm from the line between the mouth and the external meatus of the ear, representing the most likely location of the mobile phone (the source of exposure). Alternative analyses based on various indicators of mobile phone use as the outcome were also carried out. The majority of cases were regular mobile phone users. A slightly higher proportion of gliomas among mobile phone users than non-users occurred within 4.6 cm from the presumed location of the mobile phone (28% vs. 14%). Modestly elevated odds ratios were observed for several indicators of mobile phone use, but without an exposure gradient. The highest odds ratios were found for contralateral and short-term use.Our results, though limited by the small sample size, demonstrate that detailed information on tumor location allows evaluation of the risk related to the most heavily exposed part of the brain, representing direct evaluation of the possible local carcinogenic effects of the radiofrequency fields. However, field strength varies between users and over time also within a given anatomic site, due to the output power of the phone. Collaborative analysis of a larger sample is planned.||https://www.ncbi.nlm.nih.gov/pubmed/19142876||Bioelectromagnetics 30(3):176-182, 2009|
|23||Cancer||de Vocht F, Hannam K, Buchan I||Environmental risk factors for cancers of the brain and nervous system: the use of ecological data to generate hypotheses||View Abstr||;5,12;428,12;650,10;1686,12||Commentary/Hypothesis||2013||England||23. |
BACKGROUND: There is a public health need to balance timely generation of hypotheses with cautious causal inference. For rare cancers this is particularly challenging because standard epidemiological study designs may not be able to elucidate causal factors in an early period of newly emerging risks. Alternative methodologies need to be considered for generating and shaping hypotheses prior to definitive investigation.
OBJECTIVES: To evaluate whether open-access databases can be used to explore links between potential risk factors and cancers at an ecological level, using the case study of brain and nervous system cancers as an example.
METHODS: National age-adjusted cancer incidence rates were obtained from the GLOBOCAN 2008 resource and combined with data from the United Nations Development Report and the World Bank list of development indicators. Data were analysed using multivariate regression models. RESULTS: Cancer rates, potential confounders and environmental risk factors were available for 165 of 208 countries. 2008 national incidences of brain and nervous system cancers were associated with continent, gross national income in 2008 and Human Development Index Score. The only exogenous risk factor consistently associated with higher incidence was the penetration rate of mobile/cellular telecommunications subscriptions, although other factors were highlighted. According to these ecological results the latency period is at least 11-12 years, but probably more than 20 years. Missing data on cancer incidence and for other potential risk factors prohibit more detailed investigation of exposure-response associations and/or explore other hypotheses.
CONCLUSIONS: Readily available ecological data may be underused, particularly for the study of risk factors for rare diseases and those with long latencies. The results of ecological analyses in general should not be overinterpreted incausal inference, but equally they should not be ignored where alternative signals of aetiology are lacking.
|https://www.ncbi.nlm.nih.gov/pubmed/23343858||Occup Environ Med 2013 Jan 23 [Epub ahead of print]|
|24||(CE)genetic effct||Czyz J, GuanK, ZengQ, NikolovaT, MeisterA, SchönbornF, SchudererJ, KusterN, WobusAM,||High frequency electromagnetic fields (GSM signals) affect gene expression levels in tumor suppressor p53-deficient embryonic stem cells||View Abstr||In Vivo - Animal||2004||Germany||24. Effects of electromagnetic fields (EMF) simulating exposure to the Global System for Mobile Communications (GSM) signals were studied using pluripotent embryonic stem (ES) cells in vitro. Wild-type ES cells and ES cells deficient for the tumor suppressor p53 were exposed to pulse modulated EMF at 1.71 GHz, lower end of the uplink band of GSM 1800, under standardized and controlled conditions, and transcripts of regulatory genes were analyzed during in vitro differentiation. Two dominant GSM modulation schemes (GSM-217 and GSM-Talk), which generate temporal changes between GSM-Basic (active during talking phases) and GSM-DTX (active during listening phases thus simulating a typical conversation), were applied to the cells at and below the basic safety limits for local exposures as defined for the general public by the International Commission on Nonionizing Radiation Protection (ICNIRP). GSM-217 EMF induced a significant upregulation of mRNA levels of the heat shock protein, hsp70 of p53-deficient ES cells differentiating in vitro, paralleled by a low and transient increase of c-jun, c-myc, and p21 levels in p53-deficient, but not in wild-type cells. No responses were observed in either cell type after EMF exposure to GSM-Talk applied at similar slot-averaged specific absorption rates (SAR), but at lower time-averaged SAR values. Cardiac differentiation and cell cycle characteristics were not affected in embryonic stem and embryonic carcinoma cells after exposure to GSM-217 EMF signals. Our data indicate that the genetic background determines cellular responses to GSM modulated EMF.||https://www.ncbi.nlm.nih.gov/pubmed/15114639||Bioelectromagnetics 25:296-307, 2004|
|25||Cancer||Auvinen A, Hietanen M, Luukkonen R, Koskela R-S,||Brain tumors and salivary gland cancers among cellular telephone users||View Abstr||;5,11;128,8;375,8;552,12||EPIDEMIOLOGY||2002||Finland||25. |
BACKGROUND: Possible risk of cancer associated with use of cellular telephones has lately been a subject of public debate.
METHODS: We conducted a register-based, case-control study on cellular phone use and cancer. The study subjects were all cases of brain tumor (N = 398) and salivary gland cancer (N = 34) diagnosed in Finland in 1996, with five controls per case.
RESULTS: Cellular phone use was not associated with brain tumors or salivary gland cancers overall, but there was a weak association between gliomas and analog cellular phones.
CONCLUSIONS: A register-based approach has limited value in risk assessment of cellular phone use owing to lack of information on exposure.
|https://www.ncbi.nlm.nih.gov/pubmed/11964939||Epidemiology 13:356-359, 2002.|
|26||Cancer ; (NE)Brain effct||Berg G, Spallek J, Schuz J, Schlehofer B, Bohler E, Schlaefer K, Hettinger I, Kunna-Grass K, Wahrendorf J, Blettner M||Occupational exposure to radio frequency/microwave radiation and the risk of brain tumors: Interphone Study Group, Germany||View Abstr||EPIDEMIOLOGY||2006||Germany||26. It is still under debate whether occupational exposure to radio frequency/microwave electromagnetic fields (RF/MW-EMF) contributes to the development of brain tumors. This analysis examined the role of occupational RF/MW-EMF exposure in the risk of glioma and meningioma. A population-based, case-control study including 381 meningioma cases, 366 glioma cases, and 1,494 controls aged 30-69 years was performed in three German regions in 2000-2003. An exposure matrix for occupational activity was constructed by using information on RF/MW-EMF exposure collected in a computer-assisted personal interview. "High" exposure was defined as an occupational exposure that may exceed the RF/MW-EMF exposure limits for the general public recommended by the International Commission on Non-Ionizing Radiation Protection. Multiple conditional logistic regressions were performed separately for glioma and meningioma. No significant association between occupational exposure to RF/MW-EMF and brain tumors was found. For glioma, the adjusted odds ratio for highly exposed persons compared with persons not highly exposed was 1.21 (95% confidence interval: 0.69, 2.13); for meningioma, it was 1.34 (95% confidence interval: 0.64, 2.81). However, the slight increase in risk observed with increasing duration of exposure merits further research with larger sample sizes.||https://www.ncbi.nlm.nih.gov/pubmed/16873421||Am J Epidemiol164(6):538-548, 2006|
|27||(CE)Cellular effct; (CE)genetic effct||Caraglia M, Marra M, Mancinelli F, D'Ambrosio G, Massa R, Giordano A, Budillon A, Abbruzzese A, Bismuto E||Electromagnetic fields at mobile phone frequency induce apoptosis and inactivation of the multi-chaperone complex in human epidermoid cancer cells||View Abstr||In Vivo - Human||2005||Italy||27. The exposure to non-thermal microwave electromagnetic field (MW-EMF) at 1.95 MHz, a frequency used in mobile communication, affects the refolding kinetics of eukaryotic proteins (Mancinelli et al., 2004). On these basis we have evaluated the in vivo effect of MW-EMF in human epidermoid cancer KB cells. We have found that MW-EMF induces time-dependent apoptosis (45% after 3 h) that is paralleled by an about 2.5-fold decrease of the expression of ras and Raf-1 and of the activity of ras and Erk-1/2. Although also the expression of Akt was reduced its activity was unchanged likely as a consequence of the increased expression of its upstream activator PI3K. In the same experimental conditions an about 2.5-fold increase of the ubiquitination of ras and Raf-1 was also found and the addition for 12 h of proteasome inhibitor lactacystin at 10 microM caused an accumulation of the ubiquitinated isoforms of ras and Raf-1 and counteracted the effects of MW-EMF on ras and Raf-1 expression suggesting an increased proteasome-dependent degradation induced by MW-EMF. The exposure of KB cells to MW-EMF induced a differential activation of stress-dependent pathway with an increase of JNK-1 activity and HSP70 and 27 expression and with a reduction of p38 kinase activity and HSP90 expression. The overexpression of HSP90 induced by transfection of KB cells with a plasmid encoding for the factor completely antagonized the apoptosis and the inactivation of the ras --> Erk-dependent survival signal induced by MW-EMF. Conversely, the inhibition of Erk activity induced by 12 h exposure to 10 mM Mek-1 inhibitor U0126 antagonized the effects induced by HSP90 transfection on apoptosis caused by MW-EMF. In conclusion, these results demonstrate for the first time that MW-EMF induces apoptosis through the inactivation of the ras --> Erk survival signaling due to enhanced degradation of ras and Raf-1 determined by decreased expression of HSP90 and the consequent increase of proteasome dependent degradation.||https://www.ncbi.nlm.nih.gov/pubmed/15754340||J Cell Physiol 204(2):539-548, 2005|
|28||Cancer ; Skin||Heikkinen P, Kosma VM, Alhonen L, Huuskonen H, Komulainen H, Kumlin T, Laitinen JT, Lang S, Puranen L, Juutilainen J||Effects of mobile phone radiation on UV-induced skin tumourigenesis in ornithine decarboxylase transgenic and non-transgenic mice||View Abstr||;5,8;5,8;190,22;996,9;1541,12||In Vivo - Animal||2003||Finland||28. |
PURPOSE: The effects of low-level radiofrequency radiation (RFR) on ultraviolet (UV)-induced skin tumorigenesis were evaluated in ornithine decarboxylase (ODC) and non-transgenic mice.
MATERIALS AND METHODS: Transgenic female mice over-expressing the human ODC gene and their non-transgenic littermates (20 animals in the cage control group, and 45-49 animals in the other groups) were exposed for 52 weeks to UV radiation or a combination of UV radiation and pulsed RFR. The UV dose was 240 Jm(-2) (1.2 x human minimum erythemal dose) delivered three times a week. One group of animals was exposed to Digital Advanced Mobile Phone System (DAMPS)-type RFR, the other group to Global System for Mobile (GSM)-type RFR at a nominal average specific absorption rate of 0.5 W kg(-1), 1.5 h day(-1), for 5 days a week. The skin was carefully palpated weekly for macroscopic tumours. Histopathological analyses of all skin lesions and of a specified dorsal skin area were performed on all animals.
RESULTS: UV exposure resulted in development of macroscopic skin tumours in 11.5 and 36.8% of non-transgenic and transgenic animals, respectively. The RFR exposures did not give a statistically significant effect on the development of skin tumours in either transgenic or non-transgenic animals, or in combined analysis, but tumour development appeared slightly accelerated especially in non-transgenic animals. No effects of RFR exposures were found on excretion of 6-hydroxymelatonin sulphate into urine or on polyamine levels in dorsal skin.
CONCLUSION: RFR exposures did not significantly enhance skin tumourigenesis. However, the slightly accelerated tumour development may warrant further evaluation.
|https://www.ncbi.nlm.nih.gov/pubmed/12775446||Int J Radiat Biol 79(4):221-233, 2003|
|29||(CE)DNA effct||Franzellitti S, Valbonesi P, Ciancaglini N, Biondi C, Contin A, Bersani F, Fabbri E||Transient DNA damage induced by high-frequency electromagnetic fields (GSM 1.8 GHz) in the human trophoblast HTR-8/SVneo cell line evaluated with the alkaline comet assay||View Abstr||In Vitro||2010||Italy||29. One of the most controversial issue regarding high-frequency electromagnetic fields (HF-EMF) is their putative capacity to affect DNA integrity. This is of particular concern due to the increasing use of HF-EMF in communication technologies, including mobile phones. Although epidemiological studies report no detrimental effects on human health, the possible disturbance generated by HF-EMF on cell physiology remains controversial. In addition, the question remains as to whether cells are able to compensate their potential effects. We have previously reported that a 1-h exposure to amplitude-modulated 1.8 GHz sinusoidal waves (GSM-217 Hz, SAR=2 W/kg) largely used in mobile telephony did not cause increased levels of primary DNA damage in human trophoblast HTR-8/SVneo cells. Nevertheless, further investigations on trophoblast cell responses after exposure to GSM signals of different types and durations were considered of interest. In the present work, HTR-8/SVneo cells were exposed for 4, 16 or 24h to 1.8 GHz continuous wave (CW) and different GSM signals, namely GSM-217 Hz and GSM-Talk (intermittent exposure: 5 min field on, 10 min field off). The alkaline comet assay was used to evaluate primary DNA damages and/or strand breaks due to uncompleted repair processes in HF-EMF exposed samples. The amplitude-modulated signals GSM-217 Hz and GSM-Talk induced a significant increase in comet parameters in trophoblast cells after 16 and 24h of exposure, while the un-modulated CW was ineffective. However, alterations were rapidly recovered and the DNA integrity of HF-EMF exposed cells was similar to that of sham-exposed cells within 2h of recovery in the absence irradiation. Our data suggest that HF-EMF with a carrier frequency and modulation scheme typical of the GSM signal may affect the DNA integrity.||https://www.ncbi.nlm.nih.gov/pubmed/19822160||Mutat Res 683(1-2):35-42, 2010|
|30||(CE)DNA effct||Hekmat A, Saboury AA, Moosavi-Movahedi AA,||The toxic effects of mobile phone radiofrequency (940MHz) on the structure of calf thymus DNA||View Abstr||In Vitro||2012||Iran||30. Currently, the biological effects of nonionizing electromagnetic fields (EMFs) including radiofrequency (RF) radiation have been the subject of numerous experimental and theoretical studies. The aim of this study is to evaluate the possible biological effects of mobile phone RF (940MHz, 15V/m and SAR=40mW/kg) on the structure of calf thymus DNA (ct DNA) immediately after exposure and 2h after 45min exposure via diverse range of spectroscopic instruments. The UV-vis and circular dichroism (CD) experiments depict that mobile phone EMFs can remarkably cause disturbance on ct DNA structure. In addition, the DNA samples, immediately after exposure and 2h after 45min exposure, are relatively thermally unstable compared to the DNA solution, which was placed in a small shielded box (unexposed ct DNA). Furthermore, the exposed DNA samples (the DNA samples that were exposed to 940MHz EMF) have more fluorescence emission when compared with the unexposed DNA, which may have occurred attributable to expansion of the exposed DNA structure. The results of dynamic light scattering (DLS) and zeta potential experiments demonstrate that RF-EMFs lead to increment in the surface charge and size of DNA. The structure of DNA immediately after exposure is not significantly different from the DNA sample 2h after 45min exposure. In other words, the EMF-induced conformational changes are irreversible. Collectively, our results reveal that 940MHz can alter the structure of DNA. The displacement of electrons in DNA by EMFs may lead to conformational changes of DNA and DNA disaggregation. Results from this study could have an important implication on the health effects of RF-EMFs exposure. In addition, this finding could proffer a novel strategy for the development of next generation of mobile phone.|
|https://www.ncbi.nlm.nih.gov/pubmed/23164448||Ecotoxicol Environ Saf 2012 Nov 16 pii: S0147-6513(12)00368-5 doi: 101016/jecoenv201210016 [Epub ahead of print]|
|31||(CE)genetic effct||Sekeroğlu V, Akar A, Sekeroğlu ZA||Cytotoxic and genotoxic effects of high-frequency electromagnetic fields (GSM 1800MHz) on immature and mature rats||View Abstr||In Vivo - Animal||2012||Turkey||31. We investigated the cytogenotoxic effects of high frequency electromagnetic fields (HF-EMF) for 45 day and the effect of a recovery period of 15 day after exposure to EMF on bone marrow cells of immature and mature rats. The animals in treatment groups were exposed to 1800MHz EMF at SAR of 0.37 W/kg and 0.49 W/kg for 2h/day for 45 day. Two recovery groups were kept for a recovery period of 15 day without EMF after exposure to HF-EMF. Two control groups for both immature and mature rats were also included. Significant differences were also observed in chromosome aberrations (CA), micronucleus (MN) frequency, mitotic index (MI) and ratio of polychromatic erythrocytes (PCEs) in all treatment groups. The cytogenotoxic damage was more remarkable in immature rats and, the recovery period did not improve this damage in immature rats. Because much higher and irreversible cytogenotoxic damage was observed in immature rats than in mature rats, further studies are needed to understand effects of EMF on DNA damage and DNA repair, and to determine safe limits for environment and human, especially for children.||https://www.ncbi.nlm.nih.gov/pubmed/22405939||Ecotoxicol Environ Saf 80:140-144, 2012|
|32||(CE)DNA effct ; (CE)oxidative stress||Tomruk A, Guler G, Dincel AS||The influence of 1800 MHz GSM-like signals on hepatic oxidative DNA and lipid damage in nonpregnant, pregnant, and newly born rabbits||View Abstr||In Vivo - Animal||2010||Turkey||32. The aim of our study is to evaluate the possible biological effects of whole-body 1800 MHz GSM-like radiofrequency (RF) radiation exposure on liver oxidative DNA damage and lipid peroxidation levels in nonpregnant, pregnant New Zealand White rabbits, and in their newly borns. Eighteen nonpregnant and pregnant rabbits were used and randomly divided into four groups which were composed of nine rabbits: (i) Group I (nonpregnant control), (ii) Group II (nonpregnant-RF exposed), (iii) Group III (pregnant control), (iv) Group IV (pregnant-RF exposed). Newborns of the pregnant rabbits were also divided into two groups: (v) Group V (newborns of Group III) and (vi) Group VI (newborns of Group III). 1800 MHz GSM-like RF radiation whole-body exposure (15 min/day for a week) was applied to Group II and Group IV. No significant differences were found in liver 8 OHdG/10(6) dG levels of exposure groups (Group II and Group IV) compared to controls (Group I and Group III). However, in Group II and Group IV malondialdehyde (MDA) and ferrous oxidation in xylenol orange (FOX) levels were increased compared to Group I (P < 0.05, Mann-Whitney). No significant differences were found in liver tissue of 8 OHdG/10(6) dG and MDA levels between Group VI and Group V (P > 0.05, Mann-Whitney) while liver FOX levels were found significantly increased in Group VI with respect to Group V (P <0.05, Mann-Whitney). Consequently, the whole-body 1800 MHz GSM-like RF radiation exposure may lead to oxidative destruction as being indicators of subsequent reactions that occur to form oxygen toxicity in tissues.||https://www.ncbi.nlm.nih.gov/pubmed/19851891||Cell Biochem Biophys 56(1):39-47, 2010|
|33||(CE)genetic effct||Schwarz C, Kratochvil E, Pilger A, Kuster N, Adlkofer F, Rüdiger HW||Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic effects in vitro in human fibroblasts but not in lymphocytes||View Abstr||;5,11;479,7;1157,7;1665,12||In Vitro||2008||Austria||33. |
OBJECTIVE: Universal Mobile Telecommunication System (UMTS) was recently introduced as the third generation mobile communication standard in Europe. This was done without any information on biological effects and genotoxic properties of these particular high-frequency electromagnetic fields. This is discomforting, because genotoxic effects of the second generation standard Global System for Mobile Communication have been reported after exposure of human cells in vitro.
METHODS: Human cultured fibroblasts of three different donors and three different short-term human lymphocyte cultures were exposed to 1,950 MHz UMTS below the specific absorption rate (SAR) safety limit of 2 W/kg. The alkaline comet assay and the micronucleus assay were used to ascertain dose and time-dependent genotoxic effects. Five hundred cells per slide were visually evaluated in the comet assay and comet tail factor (CTF) was calculated. In the micronucleus assay 1,000 binucleated cells were evaluated per assay. The origin of the micronuclei was determined by fluorescence labeled anticentromere antibodies. All evaluations were performed under blinded conditions.
RESULTS: UMTS exposure increased the CTF and induced centromere-negative micronuclei (MN) in human cultured fibroblasts in a dose and time-dependent way. Incubation for 24 h at a SAR of 0.05 W/kg generated a statistically significant rise in both CTF and MN (P = 0.02). At a SAR of 0.1 W/kg the CTF was significantly increased after 8 h of incubation (P = 0.02), the number of MN after 12 h (P = 0.02). No UMTS effect was obtained with lymphocytes, either unstimulated or stimulated with Phytohemagglutinin.
CONCLUSION: UMTS exposure may cause genetic alterations in some but not in all human cells in vitro.
|https://www.ncbi.nlm.nih.gov/pubmed/18278508||Int Arch Occup Environ Health 81(6):755-767, 2008|
|34||(CE)Cellular effct; (CE)genetic effct||Pesnya DS, Romanovsky AV,||Comparison of cytotoxic and genotoxic effects of plutonium-239 alpha particles and mobile phone GSM 900 radiation in the Allium cepa test||View Abstr||N/A||2012||Russia||34. The goal of this study was to compare the cytotoxic and genotoxic effects of plutonium-239 alpha particles and GSM 900 modulated mobile phone (model Sony Ericsson K550i) radiation in the Allium cepa test. Three groups of bulbs were exposed to mobile phone radiation during 0 (sham), 3 and 9h. A positive control group was treated during 20min with plutonium-239 alpha-radiation. Mitotic abnormalities, chromosome aberrations, micronuclei and mitotic index were analyzed. Exposure to alpha-radiation from plutonium-239 and exposure to modulated radiation from mobile phone during 3 and 9h significantly increased the mitotic index. GSM 900 mobile phone radiation as well as alpha-radiation from plutonium-239 induced both clastogenic and aneugenic effects.However, the aneugenic activity of mobile phone radiation was more pronounced. After 9h of exposure to mobile phone radiation, polyploid cells, three-groups metaphases, amitoses and some unspecified abnormalities were detected, which were not registered in the other experimental groups. Importantly, GSM 900 mobile phone radiation increased the mitotic index, the frequency of mitotic and chromosome abnormalities, and the micronucleus frequency in a time-dependent manner. Due to its sensitivity, the A. cepa test can be recommended as a useful cytogenetic assay to assess cytotoxic and genotoxic effects of radiofrequency electromagnetic fields.||https://www.ncbi.nlm.nih.gov/pubmed/23059817||Mutat Res 2012 Oct 8 pii: S1383-5718(12)00291-4 doi: 101016/jmrgentox201208010 [Epub ahead of print]|
|35||(CE)genetic effct||Souza LD, Cerqueira ED, Meireles JR||Assessment of nuclear abnormalities in exfoliated cells from the oral epithelium of mobile phone users||View Abstr||In Vivo - Human||2013||Brazil||35. Transmission and reception of mobile telephony signals take place through electromagnetic wave radiation, or electromagnetic radiofrequency fields, between the mobile terminal and the radio base station. Based on reports in the literature on adverse effects from exposure to this type of radiation, the objective of this study was to evaluate the genotoxic and cytotoxic potential of such exposure, by means of the micronucleus test on exfoliated cells from the oral epithelium. The sample included 45 individuals distributed in 3 groups according to the amount of time in hours per week (t) spent using mobile phones: group I, t > 5 h; group II, t > 1 h and ≤ 5 h; and group III, t ≤ 1 h. Cells from the oral mucosa were analyzed to assess the numbers of micronuclei, broken egg structures and degenerative nuclear abnormalities indicative of apoptosis (condensed chromatin, karyorrhexis and pyknosis) or necrosis (karyolysis in addition to these changes). The occurrences of micronuclei and degenerative nuclear abnormalities did not differ between the groups, but the number of broken egg (structures that may be associated with gene amplification) was significantly greater in the individuals in group I (p < 0.05).||https://www.ncbi.nlm.nih.gov/pubmed/23713418||Electromagn Biol Med 2013 May 28 [Epub ahead of print]|
|36||(CE)DNA effct||66, Diem E, Schwarz C, Adlkofer F, Jahn O, Rudiger H,||Non-thermal DNA breakage by mobile-phone radiation (1800MHz) in human fibroblasts and in transformed GFSH-R17 rat granulosa cells in vitro||View Abstr||In Vivo - Animal||2005||Austria||36. Cultured human diploid fibroblasts and cultured rat granulosa cells were exposed to intermittent and continuous radiofrequency electromagnetic fields (RF-EMF) used in mobile phones, with different specific absorption rates (SAR) and different mobile-phone modulations. DNA strand breaks were determined by means of the alkaline and neutral comet assay. RF-EMF exposure (1800MHz; SAR 1.2 or 2W/kg; different modulations; during 4, 16 and 24h; intermittent 5min on/10min off or continuous wave) induced DNA single- and double-strand breaks. Effects occurred after 16h exposure in both cell types and after different mobile-phone modulations. The intermittent exposure showed a stronger effect in the comet assay than continuous exposure. Therefore we conclude that the induced DNA damage cannot be based on thermal effects.||https://www.ncbi.nlm.nih.gov/pubmed/15869902||Mutat Res 583:178-183, 2005|
|37||(CE)DNA effct ; (CE)oxidative stress||Yao K, Wu W, Wang K, Ni S, Ye P, Yu Y, Ye J, Sun L||Electromagnetic noise inhibits radiofrequency radiation-induced DNA damage and reactive oxygen species increase in human lens epithelial cells||View Abstr||;5,8;358,8;821,8;1409,12||In Vitro||2008||China||37. |
PURPOSE: The goal of this study was to investigate whether superposing of electromagnetic noise could block or attenuate DNA damage and intracellular reactive oxygen species (ROS)increase of cultured human lens epithelial cells (HLECs) induced by acute exposure to 1.8 GHz radiofrequency field (RF) of the Global System for Mobile Communications (GSM).
METHODS: An sXc-1800 RF exposure system was used to produce a GSM signal at 1.8 GHz (217 Hz amplitude-modulated) with the specific absorption rate (SAR) of 1, 2, 3, and 4 W/kg. After 2 h of intermittent exposure, the ROS level was assessed by the fluorescent probe, 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA). DNA damage to HLECs was examined by alkaline comet assay and the phosphorylated form of histone variant H2AX (gammaH2AX) foci formation assay.
RESULTS: After exposure to 1.8 GHz RF for 2 h, HLECs exhibited significant intracellular ROS increase in the 2, 3, and 4 W/kg groups. RF radiation at the SAR of 3 W/kg and 4 W/kg could induce significant DNA damage, examined by alkaline comet assay, which was used to detect mainly single strand breaks (SSBs), while no statistical difference in double strand breaks (DSBs), evaluated by gammaH2AX foci, was found between RF exposure (SAR: 3 and 4 W/kg) and sham exposure groups. When RF was superposed with 2 muT electromagnetic noise could block RF-induced ROS increase and DNA damage.
CONCLUSIONS: DNA damage induced by 1.8 GHz radiofrequency field for 2 h, which was mainly SSBs, may be associated with the increased ROS production. Electromagnetic noise could block RF-induced ROS formation and DNA damage.
|https://www.ncbi.nlm.nih.gov/pubmed/18509546||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2391079||Mol Vis 14:964-969, 2008|
|38||(CE)genetic effct||Zhang SZ, Yao GD, Lu DQ, Chiang H, Xu ZP||[Effect of 1.8 GHz radiofrequencyelectromagnetic fields on gene expression of rat neurons]||View Abstr||;5,10;267,8;915,8;1906,11||In Vitro||2008||China||38. |
To investigate the changes of gene expression in rat neuron induced by 1.8 GHz radiofrequencyelectromagnetic fields (RF EMF) to screen for RF EMF-responsive genes and the effect of different exposure times and modes on the gene expression in neuron.
Total RNA was extracted immediately and purified from the primary culture of neurons after intermittent exposed or sham-exposed to a frequency of 1.8 GHz RF EMF for 24 hours at an average special absorption rate (SAR) of 2 W/kg. Affymetrix Rat Neurobiology U34 array was applied to investigate the changes of gene expression in rat neuron. Differentially expressed genes (Egr-1, Mbp and Plp) were further confirmed by semi-quantitative revere transcription polymerase chain reaction (RT PCR). The expression levels of Egr-1, Mbp and Plp were observed at different exposure times (6, 24 h) and modes (intermittent and continuous exposure).
Among 1200 candidate genes, 24 up-regulated and 10 down-regulated genes were found by using Affymetrix microarray suite software 5.0 which are associated with multiple cellular functions (cytoskeleton, signal transduction pathway, metabolism, etc.) after functional classification. Under 24 h and 6 h intermittent exposure, Egr-1 and Plp in experiment groups showed statistic significance (P < 0.05) compared with the control groups, while expression of Mbp did not change significantly (P > 0.05). After 24 h continuous exposure, Egr-1 and Mbp in experiment groups showed statistic significance (P < 0.05) compared with the control group, while expression of Plp did not change significantly (P > 0.05). Under the same exposure mode 6 h, expression of all the 3 genes did not change significantly. Different times (6, 24 h) and modes (intermittent and continuous exposure) of exposure exerted remarkable different influences on the expression of Egr-1, Mbp, Plp genes (P < 0.01).
The changes of many genes transcription were involved in the effect of 1.8 GHz RF EMF on rat neurons; Down-regulation of Egr-1 and up-regulation of Mbp, Plp indicated the negative effects of RF EMF on neurons; The effect of RF intermittent exposure on gene expression was more obvious than that of continuous exposure; The effect of 24 h RF exposure (both intermittent and continuous) on gene expression was more obvious than that of 6 h (both intermittent and continuous).
|https://www.ncbi.nlm.nih.gov/pubmed/19358751||Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 26(8):449-452, 2008|
|39||(CE)DNA effct||Cam ST, Seyhan N||Single-strand DNA breaks in human hair root cells exposed to mobile phone radiation||View Abstr||;5,8;156,22;465,9;810,12||In Vitro||2012||Turkey||39. |
PURPOSE: To analyze the short term effects of radiofrequency radiation (RFR) exposure on genomic deoxyribonucleic acid (DNA) of human hair root cells.
SUBJECTS AND METHODS: Hair samples were collected from 8 healthy human subjects immediately before and after using a 900-MHz GSM (Global System for Mobile Communications) mobile phone for 15 and 30 minutes. Single-strand DNA breaks of hair root cells from the samples were determined using the 'comet assay'.
RESULTS: The data showed that talking on a mobile phone for 15 or 30 minutes significantly increased (p< .05) single-strand DNA breaks in cells of hair roots close to the phone. Comparing the 15-min and 30-min data using the paired t-test also showed that significantly more damages resulted after 30 minutes than after 15 minutes of phone use.
CONCLUSIONS: A short-term exposure (15 and 30 minutes) to RFR (900-MHz) from a mobile phone caused a significant increase in DNA single-strand breaks in human hair root cells located around the ear which is used for the phone calls.
|https://www.ncbi.nlm.nih.gov/pubmed/22348707||Int J Radiat Biol88(5):420-424, 2012|
|40||(CE)DNA effct ; (CE)oxidative stress||Campisi A, Gulino M, Acquaviva R, Bellia P, Raciti G, Grasso R, Musumeci F, Vanella A, Triglia A||Reactive oxygen species levels and DNA fragmentation on astrocytes in primary culture after acute exposure to low intensity microwave electromagnetic field||View Abstr||In Vitro||2010||Italy||40. The exposure of primary rat neocortical astroglial cell cultures to acute electromagnetic fields (EMF) in the microwave range was studied. Differentiated astroglial cell cultures at 14 days in vitro were exposed for 5, 10, or 20min to either 900MHz continuous waves or 900MHz waves modulated in amplitude at 50Hz using a sinusoidal waveform and 100% modulation index. The strength of the electric field (rms value) at the sample position was 10V/m. No change in cellular viability evaluated by MTT test and lactate dehydrogenase release was observed. A significant increase in ROS levels and DNA fragmentation was found only after exposure of the astrocytes to modulated EMF for 20min. No evident effects were detected when shorter time intervals or continuous waves were used. The irradiation conditions allowed the exclusion of any possible thermal effect. Our data demonstrate, for the first time, that even acute exposure to low intensity EMF induces ROS production and DNA fragmentation in astrocytes in primary cultures, which also represent the principal target of modulated EMF. Our findings also suggest the hypothesis that the effects could be due to hyperstimulation of the glutamate receptors, which play a crucial role in acute and chronic brain damage. Furthermore, the results show the importance of the amplitude modulation in the interaction between EMF and neocortical astrocytes.||https://www.ncbi.nlm.nih.gov/pubmed/20156525||Neurosci Lett31 473(1):52-55, 2010|
|41||(CE)DNA effct ; (CE)oxidative stress||Wu W, Yao K, Wang KJ, Lu DQ, He JL, Xu LH, Sun WJ||[Blocking 1800 MHz mobile phone radiation-induced reactive oxygen species production and DNA damage in lens epithelial cells by noise magnetic fields||View Abstr||;5,10;216,9;482,7;765,11||In Vitro||2008||China||41. |
OBJECTIVE: To investigate whether the exposure to the electromagnetic noise can block reactive oxygen species (ROS) production and DNA damage of lens epithelial cells induced by 1800 MHz mobile phone radiation.
METHODS: The DCFH-DA method and comet assay were used respectively to detect the intracellular ROS and DNA damage of cultured human lens epithelial cells induced by 4 W/kg 1800 MHz mobile phone radiation or/and 2microT electromagnetic noise for 24 h intermittently.
RESULTS: 1800 MHz mobile phone radiation at 4 W/kg for 24 h increased intracellular ROS and DNA damage significantly (P<0.05). However, the ROS level and DNA damage of mobile phone radiation plus noise group were not significant enhanced (P>0.05) as compared to sham exposure group.
CONCLUSION: Electromagnetic noise can block intracellular ROS production and DNA damage of human lens epithelial cells induced by 1800 MHz mobile phone radiation.
|https://www.ncbi.nlm.nih.gov/pubmed/18275117||] Zhejiang Da Xue Xue Bao Yi Xue Ban 37(1):34-38, 2008|
|42||(CE)DNA effct ; (CE)Mutagenic effect||Ji S, Oh E, Sul D, Choi JW, Park H, Lee E||DNA Damage of Lymphocytes in Volunteers after 4 hours Use of Mobile Phone||View Abstr||;5,11;408,8;1126,8;1340,12||In Vivo - Human||2004||Korea||42. |
OBJECTIVES: There has been gradually increasing concern about the adverse health effects of electromagnetic radiation originating from cell phones which are widely used in modern life. Cell phone radiation may affect human health by increasing free radicals of human blood cells. This study has been designed to identify DNA damage of blood cells by electromagnetic radiation caused by cell phone use.
METHODS: This study investigated the health effect of acute exposure to commercially available cell phones on certain parameters such as an indicator of DNA damage for 14 healthy adult volunteers. Each volunteer during the experiment talked over the cell phone with the keypad facing the right side of the face for 4 hours. The single cell gel electrophoresis assay (Comet assay), which is very sensitive in detecting the presence of DNA strand-breaks and alkali-labile damage in individual cells, was used to assess peripheral blood cells (T-cells, B-cells, granulocytes) from volunteers before and after exposure to cell phone radiation. The parameters of Comet assay measured were Olive Tail Moment and Tail DNA %.
RESULTS: The Olive Tail Moment of B-cells and granulocytes and Tail DNA % of B-cells and granulocytes were increased by a statistically significant extent after 4- hour use of a cell phone compared with controls.
CONCLUSIONS: It is concluded that cell phone radiation caused the DNA damage during the 4 hours of experimental condition. Nonetheless, this study suggested that cell phone use may increase DNA damage by electromagnetic radiation and other contributing factors.
|https://www.ncbi.nlm.nih.gov/pubmed/25175620||J Prev Med Public Health 37(4):373-380, 2004|
|43||(CE)DNA effct ; (CE)Mutagenic effect||Tice RR, Hook GG, Donner M, McRee DI, Guy AW||Genotoxicity of radiofrequency signals. I. Investigation of DNA damage and micronuclei induction in cultured human blood cells||View Abstr||In Vitro||2002||USA||43. As part of a comprehensive investigation of the potential genotoxicity of radiofrequency (RF) signals emitted by cellular telephones, in vitro studies evaluated the induction of DNA and chromosomal damage in human blood leukocytes and lymphocytes, respectively. The signals were voice modulated 837 MHz produced by an analog signal generator or by a time division multiple access (TDMA) cellular telephone, 837 MHz generated by a code division multiple access (CDMA) cellular telephone (not voice modulated), and voice modulated 1909.8 MHz generated by a global system of mobile communication (GSM)-type personal communication systems (PCS) cellular telephone. DNA damage (strand breaks/alkali labile sites) was assessed in leukocytes using the alkaline (pH>13) single cell gel electrophoresis (SCG) assay. Chromosomal damage was evaluated in lymphocytes mitogenically stimulated to divide postexposure using the cytochalasin B-binucleate cell micronucleus assay. Cells were exposed at 37±1°C, for 3 or 24 h at average specific absorption rates (SARs) of 1.0-10.0 W/kg. Exposure for either 3 or 24 h did not induce a significant increase in DNA damage in leukocytes, nor did exposure for 3 h induce a significant increase in micronucleated cells among lymphocytes. However, exposure to each of the four RF signal technologies for 24 h at an average SAR of 5.0 or 10.0 W/kg resulted in a significant and reproducible increase in the frequency of micronucleated lymphocytes. The magnitude of the response (approximately four fold) was independent of the technology, the presence or absence of voice modulation, and the frequency (837 vs. 1909.8 MHz). This research demonstrates that, under extended exposure conditions, RF signals at an average SAR of at least 5.0 W/kg are capable of inducing chromosomal damage in human lymphocytes.||https://www.ncbi.nlm.nih.gov/pubmed/11835258||Bioelectromagnetics 23:113-126, 2002|
|44||(CE)DNA effct||Sun LX, Yao K, Jiang H, He JL, Lu DQ, Wang KJ, Li HW||[DNA damage and repair induced by acute exposure of microwave from mobile phone on cultured human lens epithelial cells]||View Abstr||;5,10;189,8;920,8;1733,12||In Vitro||2006||China||44. |
OBJECTIVE: To investigate the effects of acute exposure of low-power 217 Hz modulated 1. 8 GHz microwave radiation on the DNA damage of human lens epithelial cells (hLECs) and repair.
METHODS: Cultured hLECs were exposed to 217 Hz modulated 1. 8 GHz microwave radiation at SAR (specific absorption rate) of 1. 0, 2. 0, 3. O0 and 4. 0 W/kg for 2 hours in an sXc-1800 incubator and irradiate system, the DNA single strand breaks were detected with comet assay ( single-cell gel electrophoresis) in sham-irradiated cells and irradiated cells incubated for varying periods: 0, 30 and 60 minutes after irradiation. Images of comets were digitized and analyzed using an Imagine-pro plus software, and the indexes used in this study were tail length (TL) and tail moment (TM). BrdU was added into the medium with additional one hour incubation after radiation, the cell proliferation rate was determined using a BrdU-kit.
RESULTS: The difference of DNA-breaks between the exposure and sham exposure groups induced by 1.0 and 2.0 W/kg irradiation were not significant in each time points (P > 0.05) ; there were significant difference in both groups at the exposure dose of 3. 0 and 4. 0 W/kg immediately and at the time of 30 minutes after irradiation (P <0. 01) ; if the radiation exposure time was beyond one hour no differences were be able to detected in 3.0 W/kg group (P > 0. 05) compared with control, but the evidence of significant DNA damage still existed in 4. 0 W/kg group at the same time point. Cell proliferation rate had no significant difference when the application of SAR was < or = 3. 0 W/kg (P >0. 05) , however the cell proliferation was decreased significantly at the dose of 4. 0 W/kg irradiation ( P < 0. 01).
CONCLUSIONS: No effective DNA damage was induced using comet assay after 2 hours irradiation of 1. 8 GHz microwave on hLECs at the dose SAR < or = 3.0 W/kg. 4.0 W/kg irradiation caused significantly DNA damage and inhibition of hLECs proliferation.
|https://www.ncbi.nlm.nih.gov/pubmed/17415965||Zhonghua Yan Ke Za Zhi. 2006 Dec;42(12):1084-8.||Eye Center of the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou|
|45||(CE)genetic effct||Zhao TY, Zou SP, Knapp PE||Exposure to cell phone radiation up-regulates apoptosis genes in primary cultures of neurons and astrocytes.||View Abstr||In Vitro||2007||USA||45. The health effects of cell phone radiation exposure are a growing public concern. This study investigated whether expression of genes related to cell death pathways are dysregulated in primary cultured neurons and astrocytes by exposure to a working Global System for Mobile Communication (GSM) cell phone rated at a frequency of 1900MHz. Primary cultures were exposed to cell phone emissions for 2h. We used array analysis and real-time RT-PCR to show up-regulation of caspase-2, caspase-6 and Asc (apoptosis associated speck-like protein containing a card) gene expression in neurons and astrocytes. Up-regulation occurred in both "on" and "stand-by" modes in neurons, but only in "on" mode in astrocytes. Additionally, astrocytes showed up-regulation of the Bax gene. The effects are specific since up-regulation was not seen for other genes associated with apoptosis, such as caspase-9 in either neurons or astrocytes, or Bax in neurons. The results show that even relatively short-term exposure to cell phone radiofrequency emissions can up-regulate elements of apoptotic pathways in cells derived from the brain, and that neurons appear to be more sensitive to this effect than astrocytes.||https://www.ncbi.nlm.nih.gov/pubmed/17187929||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2713174||Neurosci Lett. 412(1):34-38, 2007.|
|46||(CE)oxidative stress ; (CE)genetic effct||Hou Q, Wang M, Wu S, Ma X, An G, Liu H, Xie F||Oxidative changes and apoptosis induced by 1800-MHz electromagnetic radiation in NIH/3T3 cells||View Abstr||In Vitro||2014||China||46. To investigate the potential adverse effects of mobile phone radiation, we studied reactive oxygen species (ROS), DNA damage and apoptosis in mouse embryonic fibroblasts (NIH/3T3) after intermittent exposure (5 min on/10 min off, for various durations from 0.5 to 8 h) to an 1800-MHz GSM-talk mode electromagnetic radiation (EMR) at an average specific absorption rate of 2 W/kg. A 2',7'-dichlorofluorescin diacetate fluorescence probe was used to detect intracellular ROS levels, immunofluorescence was used to detect γH2AX foci as a marker for DNA damage, and flow cytometry was used to measure apoptosis. Our results showed a significant increase in intracellular ROS levels after EMR exposure and it reached the highest level at an exposure time of 1 h (p < 0.05) followed by a slight decrease when the exposure continued for as long as 8 h. No significant effect on the number of γH2AX was detected after EMR exposure. The percentage of late-apoptotic cells in the EMR-exposed group was significantly higher than that in the sham-exposed groups (p < 0.05). These results indicate that an 1800-MHz EMR enhances ROS formation and promotes apoptosis in NIH/3T3 cells.||https://www.ncbi.nlm.nih.gov/pubmed/24665905||Electromagn Biol Med 2014 Mar 25 [Epub ahead of print]|
|47||(CE)DNA effct||Zhang DY, Xu ZP, Chiang H, Lu DQ, Zeng QL||[Effects of GSM 1800 MHz radiofrequency electromagnetic fields on DNA damage in Chinese hamster lung cells||View Abstr||;5,10;151,8;1317,8;1673,11||In Vitro||2006||China||47. |
OBJECTIVE: To study the effects of GSM 1800 MHz radiofrequency electromagnetic fields (RF EMF) on DNA damage in Chinese hamster lung (CHL) cells.
METHODS: The cells were intermittently exposed or sham-exposed to GSM 1800 MHz RF EMF (5 minutes on/10 minutes off) at a special absorption rate (SAR) of 3.0 W/kg for 1 hour or 24 hours. Meanwhile, cells exposed to 2-acetaminofluorene, a DNA damage agent, at a final concentration of 20 mg/L for 2 hours were used as positive control. After exposure, cells were fixed by using 4% paraformaldehyde and processed for phosphorylated form of H2AX (gammaH2AX) immunofluorescence measurement. The primary antibody used for immunofluorescence was mouse monoclonal antibody against gammaH2AX and the secondary antibody was fluorescein isothiocyanate (FITC)-conjugated goat anti-mouse IgG. Nuclei were counterstained with 4, 6-diamidino-2-phenylindole (DAPI). The gammaH2AX foci and nuclei were visualized with an Olympus AX70 fluorescent microscope. Image Pro-Plus software was used to count the gammaH2AX foci in each cell. For each exposure condition, at least 50 cells were selected to detect gammaH2AX foci. Cells were classified as positive when more than five foci were detected. The percentage of gammaH2AX foci positive cells was adopted as the index of DNA damage.
RESULTS: The percentage of gammaH2AX foci positive cell of 1800 MHz RF EMF exposure for 24 hours (37.9 +/- 8.6)% or 2-acetylaminofluorene exposure (50.9 +/- 9.4)% was significantly higher compared with the sham-exposure (28.0 +/- 8.4)%. However, there was no significant difference between the sham-exposure and RF EMF exposure for 1 hour (31.8 +/- 8.7)%.
CONCLUSION: 1800 MHz RF EMF (SAR, 3.0 W/kg) for 24 hours might induce DNA damage in CHL cells.
|https://www.ncbi.nlm.nih.gov/pubmed/16836873||] Zhonghua Yu Fang Yi Xue Za Zhi 40(3):149-152, 2006|
|48||(CE)Enzmyes & Proteins||Zhao R, Zhang SZ, Yao GD, Lu DQ, Jiang H, Xu ZP.||[Effect of 1.8 GHz radiofrequency electromagnetic fields on the expression of microtubule associated protein 2 in rat neurons]||View Abstr||;5,10;190,8;1094,8;1436,11||In Vitro||2006||China||48. |
OBJECTIVE: To investigate the changes of gene expression in rat neurons induced by 1.8 GHz radiofrequency electromagnetic fields (RF EMF) and to screen for the RF EMF-responsive genes.
METHODS: Newly-born SD rats in 24 hours were sacrificed to obtain cortex and hippocampus neurons. The cells were divided randomly into two groups: the experiment group (the irradiation group) and the control group (the false irradiation group). In the irradiation group, after twelve days' culture, neurons were exposed to 1.8 GHz RF EMF modulated by 217 Hz at a specific absorption rate (SAR) of 2 W/kg for 24 hours (5 minutes on/10 minutes off) while in the false control group, the neurons were put in the same waveguide as in the irradiation group, but were not exposed to any irradiation. The total RNA was isolated and purified immediately after exposure. The affymetrix rat neurobiology U34 assay was used for detecting the changes in gene expression profile according to the manufacturer's instruction. RF EMF-responsive candidate gene was confirmed by using ribonuclease protection assay (RPA).
RESULTS: Among 1200 candidate genes, the expression levels of 34 genes were up or down regulated. Microtubule associated protein 2 (Map2) gene was selected as the candidate and subjected to further analysis. RPA data clearly revealed that Map2 was statistically significantly up-regulated after neurons were exposed to the RF EMF (P < 0.05).
CONCLUSION: The modulation of gene expression and function of Map2 as a neuron specific cytoskeleton protein is crucial to maintain the normal framework and function of neurons. The finding that 1.8 GHz RF EMF exposure increases the expression of Map2 might indicate some unknown effects of RF EMF on neurons.
|https://www.ncbi.nlm.nih.gov/pubmed/16701035||Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 24(4):222-225, 2006.|
|49||(CE)DNA effct||Trosić I, Pavicić I, Milković-Kraus S, Mladinić M, Zeljezić D||Effect of electromagnetic radiofrequency radiation on the rats' brain, liver and kidney cells measured by comet assay||View Abstr||In Vivo - Animal||2011||Croatia||49. The goal of study was to evaluate DNA damage in rat's renal, liver and brain cells after in vivo exposure to radiofrequency/microwave (Rf/Mw) radiation of cellular phone frequencies range. To determine DNA damage, a single cell gel electrophoresis/comet assay was used. Wistar rats (male, 12 week old, approximate body weight 350 g) (N = 9) were exposed to the carrier frequency of 915 MHz with Global System Mobile signal modulation (GSM), power density of 2.4 W/m2, whole body average specific absorption rate SAR of 0.6 W/kg. The animals were irradiated for one hour/day, seven days/week during two weeks period. The exposure set-up was Gigahertz Transversal Electromagnetic Mode Cell (GTEM--cell). Sham irradiated controls (N = 9) were apart of the study. The body temperature was measured before and after exposure. There were no differences in temperature in between control and treated animals. Comet assay parameters such as the tail length and tail intensity were evaluated. In comparison with tail length in controls (13.5 +/- 0.7 microm), the tail was slightly elongated in brain cells of irradiated animals (14.0 +/- 0.3 microm). The tail length obtained for liver (14.5 +/- 0.3 microm) and kidney (13.9 +/- 0.5 microm) homogenates notably differs in comparison with matched sham controls (13.6 +/- 0.3 microm) and (12.9 +/- 0.9 microm). Differences in tail intensity between control and exposed animals were not significant. The results of this study suggest that, under the experimental conditions applied, repeated 915 MHz irradiation could be a cause of DNA breaks in renal and liver cells, but not affect the cell genome at the higher extent compared to the basal damage.||https://www.ncbi.nlm.nih.gov/pubmed/22397269||Coll Antropol 35(4):1259-1264, 2011|
|50||(CE)genetic effct||Gandhi G, Singh P||Cytogenetic damage in mobile phone users: preliminary data||View Abstr||case-control/ cohort||2005||India||50. Mobile telephones, sometimes called cellular (cell) phones or handies, are now an integral part of modern life. The mobile phone handsets are low-powered radiofrequency transmitters, emitting maximum powers in the range of 0.2 to 0.6 watts. Scientific concenrns have increased sufficiently over the possible hazard to health from using cell phones. The reported adverse health effects include physiological, behavioural and cognitive changes as well as tumour formation and genetic damage. However findings are controversial and no consensus exists. Genotoxicity has been observed either in lower organisms or in vitro studies. The aim of the present study hence was to detect any cytogenertic damage in mobile phone users by analysing short term peripheral lymphocyte cultures for chromosomal aberrations and the buccal mucosal cells for micronuclei (aneugenicity and clastogenicity). The results revealed increased number of micronucleated buccal cells and cytological abnormalities in cultured lymphocytes indicating the genotoxic response from mobile phone use.||http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.525.6707&rep=rep1&type=pdf||Int J Hum Genet 5(4):259-265, 2005|
|51||(CE)DNA effct||Sykes PJ, McCallum BD, Bangay MJ, Hooker AM, Morley AA||Effect of Exposure to 900 MHz Radiofrequency Radiation on Intrachromosomal Recombination in pKZ1 Mice||View Abstr||In Vivo - Animal||2001||Australia||51. Radiofrequency (RF) radiation emitted from mobile phones is not considered to be directly genotoxic, but it may have downstream effects on cellular DNA. We studied the effect of 4 W/kg pulsed 900 MHz RF radiation on somatic intrachromosomal recombination in the spleen in the pKZ1 recombination mutagenesis model. Somatic intrachromosomal recombination inversion events were detected in spleen tissue of pKZ1 mice by histochemical staining for E. coli beta-galactosidase protein in cells in which the lacZ transgene has undergone an inversion event. pKZ1 mice were exposed daily for 30 min to plane-wave fields of 900 MHz with a pulse repetition frequency of 217 Hz and a pulse width of 0.6 ms for 1, 5 or 25 days. Three days after the last exposure, spleen sections were screened for DNA inversion events. There was no significant difference between the control and treated groups in the 1- and 5-day exposure groups, but there was a significant reduction in inversions below the spontaneous frequency in the 25-day exposure group. This observation suggests that exposure to RF radiation can lead to a perturbation in recombination frequency which may have implications for recombination repair of DNA. The biological significance of a reduction below the spontaneous frequency is not known. The number of mice in each treatment group in this study was small (n = 10 or n = 20). Therefore, repetition of this study with a larger number of animals is required to confirm these observations.||https://www.ncbi.nlm.nih.gov/pubmed/11604062||Radiat Res 156(5):495-502, 2001|
|52||(CE)DNA effct ; (CR)Other Agents - Protect Efct||Gajski G, Garaj-Vrhovac V.||Radioprotective effects of honeybee venom (Apis mellifera) against 915-MHz microwave radiation-induced DNA damage in wistar rat lymphocytes: in vitro study||View Abstr||In Vitro||2009||Croatia.||52. The aim of this study is to investigate the radioprotective effect of bee venom against DNA damage induced by 915-MHz microwave radiation (specific absorption rate of 0.6 W/kg) in Wistar rats. Whole blood lymphocytes of Wistar rats are treated with 1 microg/mL bee venom 4 hours prior to and immediately before irradiation. Standard and formamidopyrimidine-DNA glycosylase (Fpg)-modified comet assays are used to assess basal and oxidative DNA damage produced by reactive oxygen species. Bee venom shows a decrease in DNA damage compared with irradiated samples. Parameters of Fpg-modified comet assay are statistically different from controls, making this assay more sensitive and suggesting that oxidative stress is a possible mechanism of DNA damage induction. Bee venom is demonstrated to have a radioprotective effect against basal and oxidative DNA damage. Furthermore, bee venom is not genotoxic and does not produce oxidative damage in the low concentrations used in this study.||https://www.ncbi.nlm.nih.gov/pubmed/19482833||Int J Toxicol 28(2):88-98, 2009|
|53||(CE)oxidative stress ; (CE)antioxidant/oxidants||Furtado-Filho OV, Borba JB, Dallegrave A, Pizzolato TM, Henriques JA, Moreira JC, Saffi J||Effect of 950 MHz UHF electromagnetic radiation on biomarkers of oxidative damage, metabolism of UFA and antioxidants in the livers of young rats of different ages||View Abstr||;5,8;286,23;902,8;1183,13||In Vivo - Animal||2013||Brazil||53. |
PURPOSE: To assess the effect of 950 MHz ultra-high-frequency electromagnetic radiation (UHF EMR) on biomarkers of oxidative damage, as well as to verify the concentration of unsaturated fatty acids (UFA) and the expression of the catalase in the livers of rats of different ages.
MATERIALS AND METHODS: Twelve rats were equally divided into two groups as controls (CR) and exposed (ER), for each age (0, 6, 15 and 30 days). Radiation exposure lasted half an hour per day for up to 51 days (21 days of gestation and 6, 15 or 30 days of life outside the womb). The specific absorption rate (SAR) ranged from 1.3-1.0 W/kg. The damage to lipids, proteins and DNA was verified by thiobarbituric acid reactive substances (TBARS), protein carbonyls and comets, respectively. UFA were determined by gas chromatography with a flame ionization detector. The expression of catalase was by Western blotting.
RESULTS: The neonates had low levels of TBARS and concentrations of UFA after exposure. There was no age difference in the accumulation of protein carbonyls for any age. The DNA damage of ER 15 or 30 days was different. The exposed neonates exhibited lower expression of catalase.
CONCLUSIONS: 950 MHz UHF EMR does not cause oxidative stress (OS), and it is not genotoxic to the livers of neonates or those of 6 and 15 day old rats, but it changes the concentrations of polyunsaturated fatty acid (PUFA) in neonates. For rats of 30 days, no OS, but it is genotoxic to the livers of ER to total body irradiation.
|https://www.ncbi.nlm.nih.gov/pubmed/23789976||Int J Radiat Biol 2013 Jul 25 [Epub ahead of print]|
|54||(CE)Cellular effct||Donnellan M, McKenzie DR, French PW||Effects of exposure to electromagnetic radiation at 835 MHz on growth, morphology and secretory characteristics of a mast cell analogue, RBL-2H3||View Abstr||In Vitro||1997||Sydney||54. A mast cell line, RBL-2H3, was exposed to 835 MHz for 20 minutes, three times per day for 7 days at a power density of 8.1 +/- 3 mW/cm2. From day 4 onwards, it was observed that the rate of DNA synthesis and cell replication increased, that actin distribution and cell morphology became altered, and the amount of beta-hexosaminidase (a marker of granule secretion) released in response to a calcium ionophore was significantly enhanced, in comparison to unexposed cultures. There were no effects seen on levels of cytoskeletal protein synthesis or of beta-actin mRNA. Morphological changes persisted following subculture for at least 7 days in the absence of further exposure. It is hypothesized that effects of exposure to an electromagnetic field at 835 MHz may be mediated via a signal transduction pathway.||https://www.ncbi.nlm.nih.gov/pubmed/9313343||Cell Biol Int 21:427-439, 1997|
|55||(CE)oxidative stress||Belyaev IY, Hillert L, Protopopova M, Tamm C, Malmgren LO, Persson BR, Selivanova G, Harms-Ringdahl M||915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci in human lymphocytes from hypersensitive and healthy persons||View Abstr||In Vitro||2005||Sweden||55. We used exposure to microwaves from a global system for mobile communication (GSM) mobile phone (915 MHz, specific absorption rate (SAR) 37 mW/kg) and power frequency magnetic field (50 Hz, 15 muT peak value) to investigate the response of lymphocytes from healthy subjects and from persons reporting hypersensitivity to electromagnetic field (EMF). The hypersensitive and healthy donors were matched by gender and age and the data were analyzed blind to treatment condition. The changes in chromatin conformation were measured with the method of anomalous viscosity time dependencies (AVTD). 53BP1 protein, which has been shown to colocalize in foci with DNA double strand breaks (DSBs), was analyzed by immunostaining in situ. Exposure at room temperature to either 915 MHz or 50 Hz resulted in significant condensation of chromatin, shown as AVTD changes, which was similar to the effect of heat shock at 41 degrees C. No significant differences in responses between normal and hypersensitive subjects were detected. Neither 915 MHz nor 50 Hz exposure induced 53BP1 foci. On the contrary, a distinct decrease in background level of 53BP1 signaling was observed upon these exposures as well as after heat shock treatments. This decrease correlated with the AVTD data and may indicate decrease in accessibility of 53BP1 to antibodies because of stress-induced chromatin condensation. Apoptosis was determined by morphological changes and by apoptotic fragmentation of DNA as analyzed by pulsed-field gel electrophoresis (PFGE). No apoptosis was induced by exposure to 50 Hz and 915 MHz microwaves. In conclusion, 50 Hz magnetic field and 915 MHz microwaves under specified conditions of exposure induced comparable responses in lymphocytes from healthy and hypersensitive donors that were similar but not identical to stress response induced by heat shock.||https://www.ncbi.nlm.nih.gov/pubmed/15768430||Bioelectromagnetics 26(3):173-184, 2005|
|56||(CE)genetic effct||Belyaev IY, Koch CB, Terenius O, Roxstrom-Lindquist K, Malmgren LO, H Sommer W, Salford LG, Persson BR||Exposure of rat brain to 915 MHz GSM microwaves induces changes in gene expression but not double stranded DNA breaks or effects on chromatin conformation||View Abstr||In Vivo - Animal||2006||Sweden||56. We investigated whether exposure of rat brain to microwaves (MWs) of global system for mobile communication (GSM) induces DNA breaks, changes in chromatin conformation and in gene expression. An exposure installation was used based on a test mobile phone employing a GSM signal at 915 MHz, all standard modulations included, output power level in pulses 2 W, specific absorption rate (SAR) 0.4 mW/g. Rats were exposed or sham exposed to MWs during 2 h. After exposure, cell suspensions were prepared from brain samples, as well as from spleen and thymus. For analysis of gene expression patterns, total RNA was extracted from cerebellum. Changes in chromatin conformation, which are indicative of stress response and genotoxic effects, were measured by the method of anomalous viscosity time dependencies (AVTD). DNA double strand breaks (DSBs) were analyzed by pulsed-field gel electrophoresis (PFGE). Effects of MW exposure were observed on neither conformation of chromatin nor DNA DSBs. Gene expression profiles were obtained by Affymetrix U34 GeneChips representing 8800 rat genes and analyzed with the Affymetrix Microarray Suite (MAS) 5.0 software. In cerebellum from all exposed animals, 11 genes were upregulated in a range of 1.34-2.74 fold and one gene was downregulated 0.48-fold (P < .0025). The induced genes encode proteins with diverse functions including neurotransmitter regulation, blood-brain barrier (BBB), and melatonin production. The data shows that GSM MWs at 915 MHz did not induce PFGE-detectable DNA double stranded breaks or changes in chromatin conformation, but affected expression of genes in rat brain cells||https://www.ncbi.nlm.nih.gov/pubmed/16511873||Bioelectromagnetics27(4):295-306,2006|
|57||(CE)DNA effct||Phillips, J, L, , Ivaschuk, O, , Ishida-Jones, T, , Jones, R, A, , Campbell-Beachler, M, and Haggren, W,||DNA damage in Molt-4 T- lymphoblastoid cells exposed to cellular telephone radiofrequency fields in vitro||View Abstr||In Vivo - Animal||1998||USA||57. Molt-4 T-lymphoblastoid cells have been exposed to pulsed signals at cellular telephone frequencies of 813.5625 MHz (iDEN signal) and 836.55 MHz (TDMA signal). These studies were performed at low SAR (average = 2.4 and 24 microwatt/g for iDEN and 2.6 and 26 microwatt/g for TDMA) in studies designed to look for athermal RF effects. The alkaline comet, or single cell gel electrophoresis, assay was employed to measure DNA single-strand breaks in cell cultures exposed to the radiofrequency (RF) signal as compared to concurrent sham-exposed cultures. Tail moment and comet extent were calculated as indicators of DNA damage. Statistical differences in the distribution of values for tail moment and comet extent between exposed and control cell cultures were evaluated with the SKolmogorov-Smirnoff distribution test. Data points for all experiments of each exposure condition were pooled and analyzed as single groups. It was found that: 1) exposure of cells to the iDEN signal at an SAR of 2.4 microwatt/g for 2 h or 21 h significantly decreased DNA damage; 2) exposure of cells to the TDMA signal at an SAR of 2.6 microwatt/g for 2 h and 21 h significantly decreased DNA damage; 3) exposure of cells to the iDEN signal at an SAR of 24 microwatt/g for 2 h and 21 h significantly increased DNA damage; 4) exposure of cells to the TDMA signal at an SAR of 26 microwatt/g for 2 h significantly decreased DNA damage. The data indicate a need to study the effects of exposure to RF signals on direct DNA damage and on the rate at which DNA damage is repaired.||http://www.sciencedirect.com/science/article/pii/S0302459898000749||http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.666.910&rep=rep1&type=pdf||Bioelectrochem Bioenerg 45:103-110, 1998|
|58||(CE)DNA effct||Belyaev IY, Markovà E, Hillert L, Malmgren LO, Persson BR||Microwaves from UMTS/GSM mobile phones induce long-lasting inhibition of 53BP1/gamma-H2AX DNA repair foci in human lymphocytes||View Abstr||In Vitro||2009||Sweden||58. We have recently described frequency-dependent effects of mobile phone microwaves (MWs) of global system for mobile communication (GSM) on human lymphocytes from persons reporting hypersensitivity to electromagnetic fields and healthy persons. Contrary to GSM, universal global telecommunications system (UMTS) mobile phones emit wide-band MW signals. Hypothetically, UMTS MWs may result in higher biological effects compared to GSM signal because of eventual "effective" frequencies within the wideband. Here, we report for the first time that UMTS MWs affect chromatin and inhibit formation of DNA double-strand breaks co-localizing 53BP1/gamma-H2AX DNA repair foci in human lymphocytes from hypersensitive and healthy persons and confirm that effects of GSM MWs depend on carrier frequency. Remarkably, the effects of MWs on 53BP1/gamma-H2AX foci persisted up to 72 h following exposure of cells, even longer than the stress response following heat shock. The data are in line with the hypothesis that the type of signal, UMTS MWs, may have higher biological efficiency and possibly larger health risk effects compared to GSM radiation emissions. No significant differences in effects between groups of healthy and hypersensitive subjects were observed, except for the effects of UMTS MWs and GSM-915 MHz MWs on the formation of the DNA repair foci, which were different for hypersensitive (P < 0.02[53BP1]//0.01[gamma-H2AX]) but not for control subjects (P > 0.05). The non-parametric statistics used here did not indicate specificity of the differences revealed between the effects of GSM and UMTS MWs on cells from hypersensitive subjects and more data are needed to study the nature of these differences.||https://www.ncbi.nlm.nih.gov/pubmed/18839414||Bioelectromagnetics30(2):129-141, 2009|
|59||(CE)DNA effct||Belyaev IY||Radiation-induced DNA repair foci: Spatio-temporal aspects of formation, application for assessment of radiosensitivity and biological dosimetry||View Abstr||Commentary/Hypothesis||2010||Slovak Republic||59. Several proteins involved in DNA repair and DNA damage signaling have been shown to produce discrete foci in response to ionizing radiation. These foci are believed to co-localize to DSB and referred to as ionizing radiation-induced foci (IRIF) or DNA repair foci. Recent studies have revealed that some residual IRIF remain in cells for a relatively long time after irradiation, and have indicated a possible correlation between radiosensitivity of cells and residual IRIF. Remarkably, residual foci are significantly larger in size than the initial foci. Increase in the size of IRIF with time upon irradiation has been found in various cell types and has partially been correlated with dynamics and fusion of initial foci. Although it is admitted that the number of IRIF reflect that of DSB, several studies report a lack of correlation between kinetics for IRIF and DSB and a lack of co-localization between DSB repair proteins. These studies suggest that some proportion of residual IRIF that depend on cell type, dose, and post-irradiation time may represent alternations in chromatin structure after DSB have been repaired or misrepaired. While precise functions of residual foci are presently unknown, their possible link to remaining chromatin alternations, nuclear matrix, apoptosis, delayed repair and misrejoining of DSB, activity of several kinases, phosphatases, and checkpoint signaling has been suggested. Another intriguing possibility is that some of DNA repair foci may mark break-points at chromosomal aberrations (CA). While this possibility has not been confirmed substantially, the residual foci seem to be useful for biological dosimetry and estimation of individual radiosensitivity in radiotherapy of cancer.||https://www.ncbi.nlm.nih.gov/pubmed/20096808||Mutat Res 704(1-3):132-141, 2010|
|60||(CE)Enzmyes & Proteins||de Pomerai DI, Smith B, Dawe A, North K, Smith T, Archer DB, Duce IR, Jones D, Candido EP||Microwave radiation can alter protein conformation without bulk heating||View Abstr||In Vitro||2003||UK||60. Exposure to microwave radiation enhances the aggregation of bovine serum albumin in vitro in a time- and temperature-dependent manner. Microwave radiation also promotes amyloid fibril formation by bovine insulin at 60 degrees C. These alterations in protein conformation are not accompanied by measurable temperature changes, consistent with estimates from field modelling of the specific absorbed radiation (15-20 mW kg(-1)). Limited denaturation of cellular proteins could explain our previous observation that modest heat-shock responses are induced by microwave exposure in Caenorhabditis elegans. We also show that heat-shock responses both to heat and microwaves are suppressed after RNA interference ablating heat-shock factor function.||https://www.ncbi.nlm.nih.gov/pubmed/12753912||http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(03)00413-7/abstract||FEBS Lett 543(1-3):93-97, 2003|
|61||(CE)DNA effct ; (CE)oxidative stress||Tkalec M, Stambuk A, Srut M, Malarić K, Klobučar GI||Oxidative and genotoxic effects of 900 MHz electromagnetic fields in the earthworm Eisenia fetida||View Abstr||In Vivo - Animal||2013||Croatia||61. Accumulating evidence suggests that exposure to radiofrequency electromagnetic field (RF-EMF) can have various biological effects. In this study the oxidative and genotoxic effects were investigated in earthworms Eisenia fetida exposed in vivo to RF-EMF at the mobile phone frequency (900 MHz). Earthworms were exposed to the homogeneous RF-EMF at field levels of 10, 23, 41 and 120 V m(-1) for a period of 2h using a Gigahertz Transversal Electromagnetic (GTEM) cell. At the field level of 23 V m(-1) the effect of longer exposure (4h) and field modulation (80% AM 1 kHz sinusoidal) was investigated as well. All exposure treatments induced significant genotoxic effect in earthworms coelomocytes detected by the Comet assay, demonstrating DNA damaging capacity of 900 MHz electromagnetic radiation. Field modulation additionally increased the genotoxic effect. Moreover, our results indicated the induction of antioxidant stress response in terms of enhanced catalase and glutathione reductase activity as a result of the RF-EMF exposure, and demonstrated the generation of lipid and protein oxidative damage. Antioxidant responses and the potential of RF-EMF to induce damage to lipids, proteins and DNA differed depending on the field level applied, modulation of the field and duration of E. fetida exposure to 900 MHz electromagnetic radiation. Nature of detected DNA lesions and oxidative stress as the mechanism of action for the induction of DNA damage are discussed.||https://www.ncbi.nlm.nih.gov/pubmed/23352129||Ecotoxicol Environ Saf 90:7-12, 2013|
|62||(NE)behavior, memory & learning||Ntzouni MP, Skouroliakou A, Kostomitsopoulos N, Margaritis LH.||Transient and cumulative memory impairments induced by GSM 1.8 GHz cell phone signal in a mouse model.||View Abstr||In Vivo - Animal||2013||Greece||62. This study was designed to investigate the transient and cumulative impairments in spatial and non-spatial memory of C57Bl/6J mice exposed to GSM 1.8 GHz signal for 90 min daily by a typical cellular (mobile) phone at a specific absorption rate value of 0.11 W/kg. Free-moving male mice 2 months old were irradiated in two experimental protocols, lasting for 66 and for 148 days respectively. Each protocol used three groups of animals (n = 8 each for exposed, sham exposed and controls) in combination with two behavioural paradigms, the object recognition task and the object location task sequentially applied at different time points. One-way analysis of variance revealed statistically significant impairments of both types of memory gradually accumulating, with more pronounced effects on the spatial memory. The impairments persisted even 2 weeks after interruption of the 8 weeks daily exposure, whereas the memory of mice as detected by both tasks showed a full recovery approximately 1 month later. Intermittent every other day exposure for 1 month had no effect on both types of memory. 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. It is postulated that cellular repair mechanisms are operating to eliminate the memory affecting molecules.The overall contribution of several possible mechanisms to the observed cumulative and transient impairments in spatial and non-spatial memory is discussed.||https://www.ncbi.nlm.nih.gov/pubmed/23320614||Electromagn Biol Med. 2013 Jan 15. [Epub ahead of print]|
|63||(CE)DNA effct ; (NE)Brain effct||Deshmukh PS, Megha K, Banerjee BD, Ahmed RS, Chandna S, Abegaonkar MP, Tripathi AK||Detection of Low Level Microwave Radiation Induced Deoxyribonucleic Acid Damage Vis-à-vis Genotoxicity in Brain of Fischer Rats||View Abstr||;5,11;217,10;392,22;1123,8;1235,11||In Vivo - Animal||2013||India||63. |
BACKGROUND: Non-ionizing radiofrequency radiation has been increasingly used in industry, commerce, medicine and especially in mobile phone technology and has become a matter of serious concern in present time.
OBJECTIVE: The present study was designed to investigate the possible deoxyribonucleic acid (DNA) damaging effects of low-level microwave radiation in brain of Fischer rats.
MATERIALS AND METHODS: Experiments were performed on male Fischer rats exposed to microwave radiation for 30 days at three different frequencies: 900, 1800 and 2450MHz. Animals were divided into 4 groups: Group I (Sham exposed): Animals not exposed to microwave radiation but kept under same conditions as that of other groups, Group II: Animals exposed to microwave radiation at frequency 900 MHz at specific absorption rate (SAR) 5.953 × 10(-4) W/kg, Group III: Animals exposed to 1800 MHz at SAR 5.835 × 10(-4) W/kg and Group IV: Animals exposed to 2450MHz at SAR 6.672 × 10(-4) W/kg. At the end of the exposure period animals were sacrificed immediately and DNA damage in brain tissue was assessed using alkaline comet assay.
RESULTS: In the present study, we demonstrated DNA damaging effects of low level microwave radiation in brain.
CONCLUSION: We concluded that low SAR microwave radiation exposure at these frequencies may induce DNA strand breaks in brain tissue.
|https://www.ncbi.nlm.nih.gov/pubmed/23833433||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3702122||Toxicol Int 20(1):19-24, 2013|
|64||(CE)oxidative stress ; (NE)Neurological effct||Kesari KK, Meena R, Nirala J, Kumar J, Verma HN||Effect of 3G cell phone exposure with computer controlled 2-D stepper motor on non-thermal activation of the hsp27/p38MAPK stress pathway in rat brain||View Abstr||In Vivo - Animal||2014||India,||64. Cell phone radiation exposure and its biological interaction is the present concern of debate. Present study aimed to investigate the effect of 3G cell phone exposure with computer controlled 2-D stepper motor on 45-day-old male Wistar rat brain. Animals were exposed for 2 h a day for 60 days by using mobile phone with angular movement up to zero to 30°. The variation of the motor is restricted to 90° with respect to the horizontal plane, moving at a pre-determined rate of 2° per minute. Immediately after 60 days of exposure, animals were scarified and numbers of parameters (DNA double-strand break, micronuclei, caspase 3, apoptosis, DNA fragmentation, expression of stress-responsive genes) were performed. Result shows that microwave radiation emitted from 3G mobile phone significantly induced DNA strand breaks in brain. Meanwhile a significant increase in micronuclei, caspase 3 and apoptosis were also observed in exposed group (P < 0.05). Western blotting result shows that 3G mobile phone exposure causes a transient increase in phosphorylation of hsp27, hsp70, and p38 mitogen-activated protein kinase (p38MAPK), which leads to mitochondrial dysfunction-mediated cytochrome c release and subsequent activation of caspases, involved in the process of radiation-induced apoptotic cell death. Study shows that the oxidative stress is the main factor which activates a variety of cellular signal transduction pathways, among them the hsp27/p38MAPK is the pathway of principle stress response. Results conclude that 3G mobile phone radiations affect the brain function and cause several neurological disorders.||https://www.ncbi.nlm.nih.gov/pubmed/23949848||Cell Biochem Biophys 68(2):347-358, 2014|
|65||(CE)Enzmyes & Proteins||Zhijian C, Xiaoxue L, Wei Z, Yezhen L, Jianlin L, Deqiang L, Shijie C, Lifen J, Jiliang H.||Studying the protein expression in human B lymphoblastoid cells exposed to 1.8-GHz (GSM) radiofrequency radiation (RFR) with protein microarray.||View Abstr||In Vitro||2013||China||65. In the present study, the protein microarray was used to investigate the protein expression in human B-cell lymphoblastoid cells intermittently exposed to 1.8-GHz GSM radiofrequency radiation (RFR) at the specific absorption rate (SAR) of 2.0W/kg for 24h. The differential expression of 27 proteins was found, which were related to DNA damage repair, apoptosis, oncogenesis, cell cycle and proliferation (ratio >1.5-fold, P<0.05). The results validated with Western blot assay indicated that the expression of RPA32 was significantly down-regulated (P<0.05) while the expression of p73 was significantly up-regulated in RFR exposure group (P<0.05). Because of the crucial roles of those proteins in DNA repair and cell apoptosis, the results of present investigation may explain the biological effects of RFR on DNA damage/repair and cell apoptosis.||https://www.ncbi.nlm.nih.gov/pubmed/23454122||Biochem Biophys Res Commun. 433(1):36-39, 2013.|
|66||(CE)DNA effct||Khalil AM, Gagaa M, Alshamali A||8-Oxo-7, 8-dihydro-2'-deoxyguanosine as a biomarker of DNA damage by mobile phone radiation||View Abstr||In Vivo - Animal||2012||Saudi Arabia||66. We examined the effect of exposure to mobile phone 1800 MHz radio frequency radiation (RFR) upon the urinary excretion of 8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxodG), one major form of oxidative DNA damage, in adult male Sprague-Dawley rats. Twenty-four rats were used in three independent experiments (RFR exposed and control, 12 rats, each). The animals were exposed to RFR for 2 h from Global System for Mobile Communications (GSM) signal generator with whole-body-specific absorption rate of 1.0 W/kg. Urine samples were collected from the rat while housed in a metabolic cage during the exposure period over a 4-h period at 0.5, 1.0, 2.0 and 4.0 h from the beginning of exposure. In the control group, the signal generator was left in the turn-off position. The creatinine-standardized concentrations of 8-oxodG were measured. With the exception of the urine collected in the last half an hour of exposure, significant elevations were noticed in the levels of 8-oxodG in urine samples from rats exposed to RFR when compared to control animals. Significant differences were seen overall across time points of urine collection with a maximum at 1 h after exposure, suggesting repair of the DNA lesions leading to 8-oxodG formation.||https://www.ncbi.nlm.nih.gov/pubmed/22249391||Hum Exp Toxicol31(7):734-740, 2012|
|67||(CE)Mutagenic effect||Anghileri LJ, Mayayo E, Domingo JL, Thouvenot P||Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering factor||View Abstr||In Vivo - Animal||2005||France||67. The aim was to study the effects of radiofrequency (Rf) in a mice strain characterized by age-determined carcinogenesis of lymphatic tissues. Mice were treated with a 1 h/week Rf exposure for 4 months. A group submitted to sham exposure was used as control animals. The evolution of carcinogenesis was followed up to 18 months. The maximal life span of control mice was about 24 months. All dead animals were clinically and histologically examined to give an age-determined comparative quantification of the evolving carcinogenesis. A radiocalcium tracer method permitted the evaluation of Rf effects on transmembrane transport of extracellular calcium at 1 and 24 h after exposure. The determination of induced lipid peroxidation completed this second study. The findings show that Rf provoked an earlier general lymphocyte cell infiltration, formation of lymphoblastic ascites and extranodal tumours of different histological types, as well as an increased early mortality. The results suggest that in Rf-exposed mice, carcinogenesis may be induced earlier and with different pathological forms than in control animals. The modifications in cellular calcium homeostasis and the age-determined thymus involution appear to be important factors involved in this carcinogenesis process.||https://www.ncbi.nlm.nih.gov/pubmed/16019929||InterJ RadBiol 81(3):205-209, 2005|
|68||(CE)Mutagenic effect||Anghileri LJ, Mayayo E, Domingo JL, Thouvenot P||Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance of processes driven by the calcium ion signal||View Abstr||Commentary/Hypothesis||2006||France||68. The acceleration of carcinogenesis, which was induced either by radio frequency radiation from a cellular telephone or by the ferric-ATP complex, was similar in a mouse strain characterized by age-determined carcinogenesis of lymphoid tissues. Organ hypertrophy, the presence of lymphoid blood and ascites, the development of solid tumours, and mortality were very different to those found in control animals. These results emphasize the role of calcium ion signal influx in the activation of oncogenes and the failure of thymus-determined immune defences.||https://www.ncbi.nlm.nih.gov/pubmed/16679860||Eur J Cancer Prev 15(3):191-195, 2006|
|69||(CE)oxidative stress; (CE)Cellular effct||Lu YS, Huang BT, Huang YX||Reactive oxygen species formation and apoptosis in human peripheral blood mononuclear cell induced by 900 MHz mobile phone radiation||View Abstr||In Vivo - Animal||2012||China||69. We demonstrate that reactive oxygen species (ROS) plays an important role in the process of apoptosis in human peripheral blood mononuclear cell (PBMC) which is induced by the radiation of 900MHz radiofrequency electromagnetic field (RFEMF) at a specific absorption rate (SAR) of ~0.4 W/kg when the exposure lasts longer than two hours. The apoptosis is induced through the mitochondrial pathway and mediated by activating ROS and caspase-3, and decreasing the mitochondrial potential. The activation of ROS is triggered by the conformation disturbance of lipids, protein, and DNA induced by the exposure of GSM RFEMF. Although human PBMC was found to have a self-protection mechanism of releasing carotenoid in response to oxidative stress to lessen the further increase of ROS, the imbalance between the antioxidant defenses and ROS formation still results in an increase of cell death with the exposure time and can cause about 37% human PBMC death in eight hours.||https://www.ncbi.nlm.nih.gov/pubmed/22778799||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384892/||Oxid Med Cell Longev 2012:740280, 2012|
|70||(CE)DNA effct ; (FR)Fertility & Reproduction||Tsybulin O, Sidorik E, Brieieva O , Buchynska L, Kyrylenko S, Henshel D, IYakymenko I,||GSM 900 MHz cellular phone radiation can either stimulate or depress early embryogenesis in Japanese quails depending on the duration of exposure||View Abstr||;5,9;225,21;734,9;1286,12||In Vivo - Animal||2013||Ukraine||70. |
PURPOSE: Our study was designed to assess the effects of low intensity radiation of a GSM (Global System for Mobile communication) 900 MHz cellular phone on early embryogenesis in dependence on the duration of exposure.
MATERIALS AND METHODS: Embryos of Japanese Quails were exposed in ovo to GSM 900 MHz cellular phone radiation during initial 38 h of brooding or alternatively during 158 h (120 h before brooding plus initial 38 h of brooding) discontinuously with 48 sec ON (average power density 0.25 µW/cm2, specific absorption rate 3 µW/kg) followed by 12 sec OFF intervals. A number of differentiated somites was assessed microscopically. Possible DNA damage evoked by irradiation was assessed by an alkaline comet assay.
RESULTS: Exposure to radiation from a GSM 900 MHz cellular phone led to a significantly altered number of differentiated somites. In embryos irradiated during 38 h the number of differentiated somites increased (p<0.001), while in embryos irradiated during 158 h this number decreased (p<0.05). The lower duration of exposure led to a significant (p<0.001) decrease in a level of DNA strand breaks in cells of 38-hour embryos, while the higher duration of exposure resulted in a significant (p<0.001) increase in DNA damage as compared to the control.
CONCLUSION: Effects of GSM 900 MHz cellular phone radiation on early embryogenesis can be either stimulating or deleterious depending on the duration of exposure.
|https://www.ncbi.nlm.nih.gov/pubmed/23578013||Int J Rad Biol Posted online on April 11, 2013 (doi:103109/095530022013791408)|
|71||(CE)DNA effct; (FR)Fetal Dev & Expos||Panagopoulos DJ, Chavdoula ED, Nezis IP, Margaritis LH||Cell death induced by GSM 900-MHz and DCS 1800-MHz mobile telephony radiation.||View Abstr||In Vivo - Animal||2007||Greece||71. In the present study, the TUNEL (Terminal deoxynucleotide transferase dUTP Nick End Labeling) assay - a well known technique widely used for detecting fragmented DNA in various types of cells - was used to detect cell death (DNA fragmentation) in a biological model, the early and mid stages of oogenesis of the insect Drosophila melanogaster. The flies were exposed in vivo to either GSM 900-MHz (Global System for Mobile telecommunications) or DCS 1800-MHz (Digital Cellular System) radiation from a common digital mobile phone, for few minutes per day during the first 6 days of their adult life. The exposure conditions were similar to those to which a mobile phone user is exposed, and were determined according to previous studies of ours [D.J. Panagopoulos, A. Karabarbounis, L.H. Margaritis, Effect of GSM 900-MHz mobile phone radiation on the reproductive capacity of D. melanogaster, Electromagn. Biol. Med. 23 (1) (2004) 29-43; D.J. Panagopoulos, N. Messini, A. Karabarbounis, A.L. Philippetis, L.H. Margaritis, Radio frequency electromagnetic radiation within "safety levels" alters the physiological function of insects, in: P. Kostarakis, P. Stavroulakis (Eds.), Proceedings of the Millennium International Workshop on Biological Effects of Electromagnetic Fields, Heraklion, Crete, Greece, October 17-20, 2000, pp. 169-175, ISBN: 960-86733-0-5; D.J. Panagopoulos, L.H. Margaritis, Effects of electromagnetic fields on the reproductive capacity of D. melanogaster, in: P. Stavroulakis (Ed.), Biological Effects of Electromagnetic Fields, Springer, 2003, pp. 545-578], which had shown a large decrease in the oviposition of the same insect caused by GSM radiation. Our present results suggest that the decrease in oviposition previously reported, is due to degeneration of large numbers of egg chambers after DNA fragmentation of their constituent cells, induced by both types of mobile telephony radiation. Induced cell death is recorded for the first time, in all types of cells constituting an egg chamber (follicle cells, nurse cells and the oocyte) and in all stages of the early and mid-oogenesis, from germarium to stage 10, during which programmed cell death does not physiologically occur. Germarium and stages 7-8 were found to be the most sensitive developmental stages also in response to electromagnetic stress induced by the GSM and DCS fields and, moreover, germarium was found to be even more sensitive than stages 7-8.||https://www.ncbi.nlm.nih.gov/pubmed/17045516||Mutat Res.626(1-2):69-78, 2007.|
|72||Cancer ; (NE)Central Nervous System||Sato, Y., Kiyohara, K., Kojimahara, N. and Yamaguchi, N.||Time trend in incidence of malignant neoplasms of the central nervous system in relation to mobile phone use among young people in Japan||View Abstr||EPIDEMIOLOGY||2016||Japan||72. The aim of this study was to examine whether incidence of malignant neoplasms of the central nervous system from 1993 to 2010 has increased among young people in Japan, and whether the increase could be explained by increase in mobile phone use. Joinpoint regression analysis of incidence data was performed. Subsequently, the expected incidence rate was calculated assuming that the relative risk was 1.4 for those who used mobile phones more than 1640 h cumulatively. Annual percent change was 3.9% (95% confidence interval [CI], 1.6–6.3) for men in their 20s from 1993 to 2010, 12.3% (95% CI, 3.3–22.1) for women in their 20s from 2002 to 2010, 2.7% (95% CI, 1.3–4.1) for men in their 30s from 1993 to 2010, and 3.0% (95% CI, 1.4–4.7) for women in their 30s from 1993 to 2010. Change in incidence rates from 1993 to 2010 was 0.92 per 100,000 people for men in their 20s, 0.83 for women in their 20s, 0.89 for men in their 30s, and 0.74 for women in their 30s. Change in expected incidence rates from 1993 to 2010 was 0.08 per 100,000 people for men in their 20s, 0.03 for women in their 20s, 0.15 for men in their 30s, and 0.05 for women in their 30s. Patterns in sex-, age-, and period-specific incidence increases are inconsistent with sex-, age-, and period-specific prevalence trends, suggesting the overall incidence increase cannot be explained by heavy mobile phone use.||https://www.ncbi.nlm.nih.gov/pubmed/27197787||Bioelectromagnetics. doi: 10.1002/bem.21982. japan|
|73||Cancer||Wolf R, Wolf D||Increased incidence of cancer near a cell-phone transmitter station||View Abstr||EPIDEMIOLOGY||2004||Israel||73. Significant concern has been raised about possible health effects from exposure to radiofrequency (RF) electromagnetic fields, especially after the rapid introduction of mobile telecommunication systems. Parents are especially concerned with the possibility that children might develop cancer after exposure to the RF emissions from mobile telephone base stations erected in or near schools. The few epidemiologic studies that did report on cancer incidence in relation to RF radiation have generally presented negative or inconsistent results, and thus emphasized the need for more studies that should investigate cohorts with high RF exposure for changes in cancer incidence. The aim of this study is to investigate whether there is an increased cancer incidence in populations, living in a small area, and exposed to RF radiation from a cell-phone transmitter station.|
This is an epidemiologic assessment, to determine whether the incidence of cancer cases among individuals exposed to a cell-phone transmitter station is different from that expected in Israel, in Netanya, or as compared to people who lived in a nearby area. Participants are people (n=622) living in the area near a cell-phone transmitter station for 3-7 years who were patients of one health clinic (of DW). The exposure began 1 year before the start of the study when the station first came into service. A second cohort of individuals (n=1222) who get their medical services in a clinic located nearby with very closely matched, environment, workplace and occupational characteristics was used for comparison.
In the area of exposure (area) eight cases of different kinds of cancer were diagnosed in a period of only one year. This rate of cancers was compared both with the rate of 31 cases per 10,000 per year in the general population and the 2/1222 rate recorded in the nearby clinic (area B). Relative cancer rates for female were 10.5 for area A. 0.6 for area B and 1 for the whole town of Netanya. Cancer incidence of women in area A was thus significantly higher (p<0.0001) compared with that of area B and the whole city. A comparison of the relative risk revealed that there were 4.15 times more cases in area than in the entire population. The study indicates an association between increased incidence of cancer and living in proximity to a cell-phone transmitter station
|https://www.emf-portal.org/en/article/19820||http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.527.1036&rep=rep1&type=pdf||Inter J Cancer Prev 1(2):123-128,|
|74||Cancer; (CE)Cellular effct||Yakymenko I, Sidorik E, Kyrylenko S, Chekhun V||Long-term exposure to microwave radiation provokes cancer growth: evidences from radars and mobile communication systems||View Abstr||MetaAnalysis||2011||Ukraine||74. In this review we discuss alarming epidemiological and experimental data on possible carcinogenic effects of long term exposure to low intensity microwave (MW) radiation. Recently, a number of reports revealed that under certain conditions the irradiation by low intensity MW can substantially induce cancer progression in humans and in animal models. The carcinogenic effect of MW irradiation is typically manifested after long term (up to 10 years and more) exposure. Nevertheless, even a year of operation of a powerful base transmitting station for mobile communication reportedly resulted in a dramatic increase of cancer incidence among population living nearby. In addition, model studies in rodents unveiled a significant increase in carcinogenesis after 17-24 months of MW exposure both in tumor-prone and intact animals. To that, such metabolic changes, as overproduction of reactive oxygen species, 8-hydroxi-2-deoxyguanosine formation, or ornithine decarboxylase activation under exposure to low intensity MW confirm a stress impact of this factor on living cells. We also address the issue of standards for assessment of biological effects of irradiation. It is now becoming increasingly evident that assessment of biological effects of non-ionizing radiation based on physical (thermal) approach used in recommendations of current regulatory bodies, including the International Commission on Non-Ionizing Radiation Protection (ICNIRP) Guidelines, requires urgent reevaluation.We conclude that recent data strongly point to the need for re-elaboration of the current safety limits for non-ionizing radiation using recently obtained knowledge. We also emphasize that the everyday exposure of both occupational and general public to MW radiation should be regulated based on a precautionary principles which imply maximum restriction of excessive exposure||https://www.ncbi.nlm.nih.gov/pubmed/21716201||Exp Oncol 33(2):62-70,|
|75||Cancer||Li CY, Liu CC, Chang YH, Chou LP, Ko MC||A population-based case-control study of radiofrequency exposure in relation to childhood neoplasm||View Abstr||EPIDEMIOLOGY||2012||Taiwan||75. This population-based case-control study in Taiwan considered incident cases aged 15 years or less and admitted in 2003 to 2007 for all neoplasm (ICD-9-CM: 140-239) (n=2606), including 939 leukemia and 394 brain neoplasm cases. Controls were randomly selected, with a case/control ratio of 1:30 and matched on year of birth, from all non-neoplasm children insured in the same year when the index case was admitted. Annual summarized power (ASP, watt-year) was calculated for each of the 71,185 mobile phone base stations (MPBS) in service between 1998 and 2007. Then, the annual power density (APD, watt-year/km(2)) of each township (n=367) was computed as a ratio of the total ASP of all MPBS in a township to the area of that particular township. Exposure of each study subject to radio frequency (RF) was indicated by the averaged APD within 5 years prior to the neoplasm diagnosis (cases) or July 1st of the year when the index case was admitted (controls) in the township where the subject lived. Unconditional logistic regression model with generalized estimation equation was employed to calculate the covariate-adjusted odds ratio [AOR] of childhood neoplasm in relation to RF exposure. A higher than median averaged APD (approximately 168 WYs/km(2)) was significantly associated with an increased AOR for all neoplasms (1.13; 1.01 to 1.28), but not for leukemia (1.23; 0.99 to 1.52) or brain neoplasm (1.14, 0.83 to 1.55). This study noted a significantly increased risk of all neoplasms in children with higher-than-median RF exposure to MPBS. The slightly elevated risk was seen for leukemia and brain neoplasm, but was not statistically significant. These results may occur due to several methodological limitations||https://www.ncbi.nlm.nih.gov/pubmed/22885353||Sci Total Environ 435-436:472-478,|
|76||Cancer||Dode AC, Leão MM, Tejo Fde A, Gomes AC, Dode DC, Dode MC, Moreira CW, Condessa VA, Albinatti C, Caiaffa WT||Mortality by neoplasia and cellular telephone base stations in the Belo Horizonte municipality, Minas Gerais state||View Abstr||EPIDEMIOLOGY||2011||Brazil||76. Pollution caused by the electromagnetic fields (EMFs) of radio frequencies (RF) generated by the telecommunication system is one of the greatest environmental problems of the twentieth century. The purpose of this research was to verify the existence of a spatial correlation between base station (BS) clusters and cases of deaths by neoplasia in the Belo Horizonte municipality, Minas Gerais state, Brazil, from 1996 to 2006 and to measure the human exposure levels to EMF where there is a major concentration of cellular telephone transmitter antennas. A descriptive spatial analysis of the BSs and the cases of death by neoplasia identified in the municipality was performed through an ecological-epidemiological approach, using georeferencing. The database employed in the survey was composed of three data banks: 1. death by neoplasia documented by the Health Municipal Department; 2. BSs documented in ANATEL ("Agência Nacional de Telecomunicações": 'Telecommunications National Agency'); and 3. census and demographic city population data obtained from official archives provided by IBGE ("Instituto Brasileiro de Geografia e Estatística": 'Brazilian Institute of Geography and Statistics'). The results show that approximately 856 BSs were installed through December 2006. Most (39.60%) of the BSs were located in the "Centro-Sul" ('Central-Southern') region of the municipality. Between 1996 and 2006, 7191 deaths by neoplasia occurred and within an area of 500 m from the BS, the mortality rate was 34.76 per 10,000 inhabitants. Outside of this area, a decrease in the number of deaths by neoplasia occurred. The greatest accumulated incidence was 5.83 per 1000 in the Central-Southern region and the lowest incidence was 2.05 per 1000 in the Barreiro region. During the environmental monitoring, the largest accumulated electric field measured was 12.4 V/m and the smallest was 0.4 V/m. The largest density power was 40.78 μW/cm(2), and the smallest was 0.04 μW/cm(2)||https://www.ncbi.nlm.nih.gov/pubmed/21741680||Brazil.Sci Total Environ 409(19):3649-3665|
|77||(CE)genetic effct ; (CE)DNA effct||Gandhi G, Kaur G, Nisar U||A cross-sectional case control study on genetic damage in individuals residing in the vicinity of a mobile phone base station||View Abstr||EPIDEMIOLOGY||2014||India||77. Mobile phone base stations facilitate good communication, but the continuously emitting radiations from these stations have raised health concerns. Hence in this study, genetic damage using the single cell gel electrophoresis (comet) assay was assessed in peripheral blood leukocytes of individuals residing in the vicinity of a mobile phone base station and comparing it to that in healthy controls. The power density in the area within 300 m from the base station exceeded the permissive limits and was significantly (p = 0.000) higher compared to the area from where control samples were collected. The study participants comprised 63 persons with residences near a mobile phone tower, and 28 healthy controls matched for gender, age, alcohol drinking and occupational sub-groups. Genetic damage parameters of DNA migration length, damage frequency (DF) and damage index were significantly (p = 0.000) elevated in the sample group compared to respective values in healthy controls. The female residents (n = 25) of the sample group had significantly (p = 0.004) elevated DF than the male residents (n = 38). The linear regression analysis further revealed daily mobile phone usage, location of residence and power density as significant predictors of genetic damage. The genetic damage evident in the participants of this study needs to be addressed against future disease-risk, which in addition to neurodegenerative disorders, may lead to cancer||https://www.ncbi.nlm.nih.gov/pubmed/25006864||Electromagn Biol Med 2014 Jul 9:1-11 [Epub ahead of print]|
|78||(CE)genetic effct||Kim JY, Hong SY, Lee YM, Yu SA, Koh WS, Hong JR, Son T, Chang SK, Lee M||In vitro assessment of clastogenicity of mobile-phone radiation (835 MHz) using the alkaline comet assay and chromosomal aberration test||View Abstr||In Vitro||2008||Korea||78. Recently we demonstrated that 835-MHz radiofrequency radiation electromagnetic fields (RF-EMF) neither affected the reverse mutation frequency nor accelerated DNA degradation in vitro. Here, two kinds of cytogenetic endpoints were further investigated on mammalian cells exposed to 835-MHz RF-EMF (the most widely used communication frequency band in Korean CDMA mobile phone networks) alone and in combination with model clastogens: in vitro alkaline comet assay and in vitro chromosome aberration (CA) test. No direct cytogenetic effect of 835-MHz RF-EMF was found in the in vitro CA test. The combined exposure of the cells to RF-EMF in the presence of ethylmethanesulfonate (EMS) revealed a weak and insignificant cytogenetic effect when compared to cells exposed to EMS alone in CA test. Also, the comet assay results to evaluate the ability of RF-EMF alone to damage DNA were nearly negative, although showing a small increase in tail moment. However, the applied RF-EMF had potentiation effect in comet assay when administered in combination with model clastogens (cyclophosphamide or 4-nitroquinoline 1-oxide). Thus, our results imply that we cannot confidently exclude any possibility of an increased risk of genetic damage, with important implications for the possible health effects of exposure to 835-MHz electromagnetic fields||https://www.ncbi.nlm.nih.gov/pubmed/18214898||Environ Toxicol 23(3):319-327,|
|79||Synergistic effct ; (CE)DNA effct||Baohong W, Lifen J, Lanjuan L, Jianlin L, Deqiang L, Wei Z, Jiliang H||Evaluating the combinative effects on human lymphocyte DNA damage induced by ultraviolet ray C plus 1.8GHz microwaves using comet assay in vitro||View Abstr||In Vivo - Animal||2007||china||79. The objective of this study was to observe whether 1.8GHz microwaves (MW) (SAR, 3 W/kg) exposure can influence human lymphocyte DNA damage induced by ultraviolet ray C (UVC). The lymphocytes, which were from three young healthy donors, were exposed to 254 nm UVC at the doses of 0.25, 0.5, 0.75, 1.0, 1.5 and 2.0 J m(-2), respectively. The lymphocytes were irradiated by 1.8GHz MW (SAR, 3 W/kg) for 0, 1.5 and 4 h. The combinative exposure of UVC plus MW was conducted. The treated cells were incubated for 0, 1.5 and 4 h. Finally, comet assay was used to measure DNA damage of above treated lymphocytes. The results indicated that the difference of DNA damage induced between MW group and control group was not significant (P>0.05). The MTLs induced by UVC were 1.71+/-0.09, 2.02+/-0.08, 2.27+/-0.17, 2.27+/-0.06, 2.25+/-0.12, 2.24+/-0.11 microm, respectively, which were significantly higher than that (0.96+/-0.05 microm) of control (P<0.01). MTLs of some sub-groups in combinative exposure groups at 1.5-h incubation were significantly lower that those of corresponding UVC sub-groups (P<0.01 or P<0.05). However, MTLs of some sub-groups in combinative exposure groups at 4-h incubation were significantly higher that those of corresponding UVC sub-groups (P<0.01 or P<0.05). In this experiment it was found that 1.8GHz (SAR, 3 W/kg) MW exposure for 1.5 and 4 h did not enhance significantly human lymphocyte DNA damage, but could reduce and increase DNA damage of human lymphocytes induced by UVC at 1.5-h and 4-h incubation, respectively||http://www.sciencedirect.com/science/article/pii/S0300483x07000601||Toxicology 232(3):311-316,|
|80||(CE)DNA effct ; (CR)Other Agents - Protect Efct||Lai, H, Carino, MA, Singh, NP||Naltrexone blocks RFR-induced DNA double strand breaks in rat brain cells||View Abstr||In Vivo - Animal||1997||USA||80. Previous research in our laboratory has shown that various effects of radiofrequency electromagnetic radiation (RFR) exposure on the nervous system are mediated by endogenous opioids in the brain. We have also found that acute exposure to RFR induced DNA strand breaks in brain cells of the rat. The present experiment was carried out to investigate whether endogenous opioids are also involved in RFR-induced DNA strand breaks. Rats were treated with the opioid antagonist naltrexone (1 mg/kg, IP) immediately before and after exposure to 2450-MHz pulsed (2 ?s pulses, 500 pps) RFR at a power density of 2 mW/cm2 (average whole body specific absorption rate of 1.2 W/kg) for 2 hours. DNA double strand breaks were assayed in brain cells at 4 hours after exposure using a microgel electrophoresis assay. Results showed that the RFR exposure significantly increased DNA double strand breaks in brain cells of the rat, and the effect was partially blocked by treatment with naltrexone. Thus, these data indicate that endogenous opioids play a mediating role in RFR-induced DNA strand breaks in brain cells of the rat.||https://link.springer.com/article/10.1023/A%3A1019154611749||Wireless Networks 3:471-476, 1997|
|81||(CE)Mutagenic effect||Kesari KK, Behari J, Kumar S||Mutagenic response of 2.45 GHz radiation exposure on rat brain.||View Abstr||;5,8;108,21;983,8;1542,11||In Vivo - Animal||2010||India||81. |
PURPOSE: To investigate the effect of 2.45 GHz microwave radiation on rat brain of male wistar strain.
MATERIAL AND METHODS: Male rats of wistar strain (35 days old with 130 +/- 10 g body weight) were selected for this study. Animals were divided into two groups: Sham exposed and experimental. Animals were exposed for 2 h a day for 35 days to 2.45 GHz frequency at 0.34 mW/cm(2) power density. The whole body specific absorption rate (SAR) was estimated to be 0.11 W/Kg. Exposure took place in a ventilated Plexiglas cage and kept in anechoic chamber in a far field configuration from the horn antenna. After the completion of exposure period, rats were sacrificed and the whole brain tissue was dissected and used for study of double strand DNA (Deoxyribonucleic acid) breaks by micro gel electrophoresis and the statistical analysis was carried out using comet assay (IV-2 version software). Thereafter, antioxidant enzymes and histone kinase estimation was also performed.
RESULTS: A significant increase was observed in comet head (P < 0.002), tail length (P < 0.0002) and in tail movement (P < 0.0001) in exposed brain cells. An analysis of antioxidant enzymes glutathione peroxidase (P < 0.005), and superoxide dismutase (P < 0.006) showed a decrease while an increase in catalase (P < 0.006) was observed. A significant decrease (P < 0.023) in histone kinase was also recorded in the exposed group as compared to the control (sham-exposed) ones. One-way analysis of variance (ANOVA) method was adopted for statistical analysis.
CONCLUSION: The study concludes that the chronic exposure to these radiations may cause significant damage to brain, which may be an indication of possible tumour promotion (Behari and Paulraj 2007 ).
|https://www.ncbi.nlm.nih.gov/pubmed/20353343||Int J Radiat Biol. 86(4):334-343, 2010|
|82||(CE)DNA effct ; (CR)Other Agents - Protect Efct||Lai, H, Singh, NP,||Melatonin and a spin-trap compound block radiofrequency electromagnetic radiation-induced DNA strand breaks in rat brain cells||View Abstr||In Vivo - Animal||1997||USA||82. Effects of in vivo microwave exposure on DNA strand breaks, a form of DNA damage, were investigated in rat brain cells. In previous research, we have found that acute (2 hours) exposure to pulsed (2 microseconds pulses, 500 pps) 2450-MHz radiofrequency electromagnetic radiation (RFR) (power density 2 mW/cm2, average whole body specific absorption rate 1.2 W/kg) caused an increase in DNA single- and double-strand breaks in brain cells of the rat when assayed 4 hours post exposure using a microgel electrophoresis assay. In the present study, we found that treatment of rats immediately before and after RFR exposure with either melatonin (1 mg/kg/injection, SC) or the spin-trap compound N-tert-butyl-alpha-phenylnitrone (PBN) (100 mg/kg/injection, i.p.) blocks this effects of RFR. Since both melatonin and PBN are efficient free radical scavengers it is hypothesized that free radicals are involved in RFR-induced DNA damage in the brain cells of rats. Since cumulated DNA strand breaks in brain cells can lead to neurodegenerative diseases and cancer and an excess of free radicals in cells has been suggested to be the cause of various human diseases, data from this study could have important implications for the health effects of RFR exposure.||https://www.ncbi.nlm.nih.gov/pubmed/9261542||Bioelectromagnetics 18(6):446-454, 1997|
|83||(CE)DNA effct||Lai H, Singh NP,||Interaction of Microwaves and a Temporally Incoherent Magnetic Field on Single and Double DNA Strand Breaks in Rat Brain Cells||View Abstr||In Vivo - Animal||2005||USA||83. The effect of a temporally incoherent magnetic field ('noise') on microwave-induced DNA single and double strand breaks in rat brain cells was investigated. Four treatment groups of rats were studied: microwave-exposure (continuous -wave 2450-MHz microwaves, power density 1 mW/cm2, average whole body specific absorption rate of 0.6 W/kg), 'noise'-exposure (45 mG), 'microwave + noise'-exposure, and sham-exposure. Animals were exposed to these conditions for 2 hrs. DNA single and double strand breaks in brain cells of these animals were assayed 4 hrs later using a microgel electrophoresis assay. Results show that brain cells of microwave-exposed rats had significantly higher levels of DNA single and double strand breaks when compared with sham-exposed animals. Exposure to 'noise' alone did not significantly affect the levels (i.e., they were similar to those of the sham-exposed rats). However, simultaneous 'noise' exposure blocked microwave-induced increases in DNA strand breaks. These data indicate that simultaneous exposure to a temporally incoherent magnetic field could block microwave-induced DNA damage in brain cells of the rat.||http://www.tandfonline.com/doi/full/10.1081/JBC-200055046?scroll=top&needAccess=true||Electromag Biol Med 24:23-29, 2005|
|84||(CE)DNA effct||Paulraj R, Behari J||Single strand DNA breaks in rat brain cells exposed to microwave radiation||View Abstr||In Vivo - Animal||2006||India||84. This investigation concerns with the effect of low intensity microwave (2.45 and 16.5GHz, SAR 1.0 and 2.01W/kg, respectively) radiation on developing rat brain. Wistar rats (35 days old, male, six rats in each group) were selected for this study. These animals were exposed for 35 days at the above mentioned frequencies separately in two different exposure systems. After the exposure period, the rats were sacrificed and the whole brain tissue was dissected and used for study of single strand DNA breaks by micro gel electrophoresis (comet assay). Single strand DNA breaks were measured as tail length of comet. Fifty cells from each slide and two slides per animal were observed. One-way ANOVA method was adopted for statistical analysis. This study shows that the chronic exposure to these radiations cause statistically significant (p<0.001) increase in DNA single strand breaks in brain cells of rat.||https://www.ncbi.nlm.nih.gov/pubmed/16458332||Mutat Res. 596:76-80, 2006|
|85||Eyes ; Cancer||Behrens T, Lynge E, Cree I, Sabroe S, Lutz JM, Afonso N, Eriksson M, Guénel P, Merletti F, Morales-Suarez-Varela M, Stengrevics A, Févotte J, Llopis-González A, Gorini G, Sharkova G, Hardell L, Ahrens W||Occupational exposure to electromagnetic fields and sex-differential risk of uveal melanoma||View Abstr||;5,11;195,8;805,8;1336,11||case-control/ cohort||2010||Germany||85. |
OBJECTIVES: The association between occupational exposure to electromagnetic fields (EMF) and the risk of uveal melanoma was investigated in a case-control study in nine European countries.
METHODS: Incident cases of uveal melanoma and population as well as hospital controls were included and frequency matched by country, 5-year birth cohort and sex. Subjects were asked whether they had worked close to high-voltage electrical transmission installations, computer screens and various electrical machines, or in complex electrical environments. Measurements of two Scandinavian job-exposure matrices were applied to estimate lifelong cumulative EMF exposure. Unconditional logistic regression analyses, stratified by sex and eye colour were calculated, adjusting for several potential confounders.
RESULTS: 293 patients with uveal melanoma and 3198 control subjects were interviewed. Women exposed to electrical transmission installations showed elevated risks (OR 5.81, 95% CI 1.72 to 19.66). Positive associations with exposure to control rooms were seen among men and women, but most risk increases were restricted to subjects with dark iris colour. Application of published EMF measurements revealed stronger risk increases among women compared to men. Again, elevated risks were restricted to subjects with dark eye colour.
CONCLUSION: Although based on a low prevalence of exposure to potential occupational sources of EMF, our data indicate that exposed dark-eyed women may be at particular risk for uveal melanoma.
|https://www.ncbi.nlm.nih.gov/pubmed/20798011||Occup Environ Med.67(11):751-759, 2010|
|86||(FR)Fertility & Reproduction ; (CE)DNA effct||Atasoy HI, Gunal MY, Atasoy P, Elgun S, Bugdayci G||Immunohistopathologic demonstration of deleterious effects on growing rat testes of radiofrequency waves emitted from conventional Wi-Fi devices||View Abstr||;5,10;166,8;769,8;1165,12||In Vivo - Animal||2013||Turkey||86. |
OBJECTIVE: To investigate effects on rat testes of radiofrequency radiation emitted from indoor Wi-Fi Internet access devices using 802.11.g wireless standards.
METHODS: Ten Wistar albino male rats were divided into experimental and control groups, with five rats per group. Standard wireless gateways communicating at 2.437 GHz were used as radiofrequency wave sources. The experimental group was exposed to radiofrequency energy for 24 h a day for 20 weeks. The rats were sacrificed at the end of the study. Intracardiac blood was sampled for serum 8-hydroxy-2'-deoxyguanosine levels. Testes were removed and examined histologically and immunohistochemically. Testis tissues were analyzed for malondialdehyde levels and prooxidant-antioxidant enzyme activities.
RESULTS: We 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). We also found decreased levels of catalase and glutathione peroxidase activity in the experimental group, which may have been due to radiofrequency effects on enzyme activity (p < 0.05).
CONCLUSIONS: These findings raise questions about the safety of radiofrequency exposure from Wi-Fi Internet access devices for growing organisms of reproductive age, with a potential effect on both fertility and the integrity of germ cells.
|https://www.ncbi.nlm.nih.gov/pubmed/22465825||J Pediatr Urol. 9(2):223-229, 2013|
|87||(FR)Fertility & Reproduction ; (CE)DNA effct||Avendano C, Mata A, Sanchez Sarmiento CA, Doncel GF||Use of laptop computers connected to internet through Wi-Fi decreases human sperm motility and increases sperm DNA fragmentation||View Abstr||In Vivo - Human||2012||Argentina||87. OBJECTIVE: To evaluate the effects of laptop computers connected to local area networks wirelessly (Wi-Fi) on human spermatozoa.DESIGN: Prospective in vitro study.SETTING: Center for reproductive medicine.PATIENT(S): Semen samples from 29 healthy donors.INTERVENTION(S): Motile sperm were selected by swim up. Each sperm suspension was divided into two aliquots. One sperm aliquot (experimental) from each patient was exposed to an internet-connected laptop by Wi-Fi for 4 hours, whereas the second aliquot (unexposed) was used as control, incubated under identical conditions without being exposed to the laptop.MAIN OUTCOME MEASURE(S): Evaluation of sperm motility, viability, and DNA fragmentation.RESULT(S): Donor 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. Levels of dead sperm showed no significant differences between the two groups.CONCLUSION(S): To our knowledge, this is the first study to evaluate the direct impact of laptop use on human spermatozoa. Ex vivo exposure of human spermatozoa to a wireless internet-connected laptop decreased motility and induced DNA fragmentation by a nonthermal effect. We speculate that keeping a laptop connected wirelessly to the internet on the lap near the testes may result in decreased male fertility. Further in vitro and in vivo studies are needed to prove this contention.||https://www.ncbi.nlm.nih.gov/pubmed/22112647||https://www.fertstert.org/article/S0015-0282(11)02678-1/fulltext||Fertil Steril. 97(1):39-45, 2012|
|88||Cancer; (CE)Cellular effct||Paulraj R, Behari J||The effect of low level continuous 2.45 GHz waves on enzymes of developing rat brain.||View Abstr||In Vivo - Animal||2002||India||88. The present work describes the effect of low level continuous microwaves (2.45 GHz) on developing rat brain. Some 35-day-old Wistar rats were used for this study. The animals were exposed 2 hr/day for 35 days at a power density of 0.34 mW/cm2 [specific absorption rate (SAR), 0.1 W/kg] in a specially made anechoic chamber. After the exposure, the rats were sacrificed and the brain tissue was dissected out and used for various biochemical assays. A significant increase in calcium ion efflux and ornithine decarboxylase (ODC) activity was observed in the exposed group as compared to the control. Correspondingly, a significant decrease in the calcium-dependent protein kinase activity was observed. These results indicate that this type of radiation affects the membrane bound enzymes, which are associated with cell proliferation and differentiation, thereby pointing out its possible role as a tumor promoter.||http://www.tandfonline.com/doi/abs/10.1081/JBC-120015993||Electromag Biol Med 21:221-231, 2002|
|89||Cancer ; (ME)Metabolic efct||Singh N, Rudra N, Bansal P, Mathur R, Behari J, Nayar U,||Poly ADP ribosylation as a possible mechanism of microwave--biointeraction||View Abstr||In Vivo - Animal||1994||India||89. Electromagnetic fields (EMFs) affect the metabolism of the body including the nervous, endocrine, cardiovascular, hematological as well as the reproductive system. EMFs are environmental pollutants, thus posing a health hazard which can cause steric changes in the molecule located at the cell surface. Microwaves are known to cause chromosomal abberations and act as tumor promoters. The process involves a stream of signals from cell membrane to nucleus and other organelles. The present investigations aim to understand the mechanism of biological effects of microwaves (2.45 GHz). The effect was studied on poly ADP-ribosylation, which is a post translational modification of chromatin protein catalysed by the enzyme poly ADPR polymerase using NAD+ as the substrate. Poly ADP-ribosylation has been shown to be involved in several aspects of chromatin structure and function. Twenty-three days old rats weighing 42-48 gms were exposed at a microwave dose level of 1.0 mW/cm2. After exposure for sixty days the animals were sacrificed and an estimation of poly ADPR polymerase activity was undertaken in different organs of these animals. There was an increase of 20% in its activity in liver, 35% in testis, whereas brain showed a 53% decrease in diencephalon and 20% decrease in the cortex in the exposed animals as compared to their respective controls. There was no change in enzyme activity in spleen and kidney. This was accompanied by concomitant changes in NAD+ levels. The above results may be cited as important events in carcinogenesis and tumor promotion related to microwave exposure and the signal transduction mechanism involved. The goal is to shed light on complex ecogenetic interactions leading to cancer modulation of gene expression by epigenetic mechanism.||https://www.ncbi.nlm.nih.gov/pubmed/7814078||Indian J Physiol Pharmacol 38(3):181-184, 1994|
|90||(CE)Mutagenic effect||Balcer-Kubiczek EK, Harrison GH||Neoplastic transformation of C3H/10T1/2 cells following exposure to 120-Hz modulated 2.45-GHz microwaves and phorbol ester tumor promoter.||View Abstr||In Vitro||1991||USA||90. Some recent epidemiological studies have shown a positive association between cancer incidence and exposure to electromagnetic (EM) fields. Evidence from in vitro studies indicates that this effect could be due to synergistic interaction between EM fields and tumor promoters. However, no dose-response data related directly to carcinogenesis have been published. In this study, actively growing cultures of C3H/10T1/2 cells were exposed for 24 h to 2.45-GHz microwaves pulse-modulated at 120 Hz. Conditions of EM-field exposure were designed to simulate low-field exposures (specific absorption rate 0.1, 1, or 4.4 W/kg; the corresponding peak amplitudes were electric field 18, 56, or 120 V/m, magnetic field 0.09, 0.27, or 0.56 muT, respectively). In separate experiments, a 24-h EM- field exposure at 4.4 W/kg was preceded or followed by X irradiation at 0.5, 1, or 1.5 Gy. Cells were assayed for cell survival and neoplastic transformation with or without post-treatment administration of 0.1 micrograms/ml of 12-O-tetradecanoylphorbol-13-acetate (TPA) for the duration of the assay. The EM fields alone had no effect on cell survival or induction of neoplastic transformation. However, enhancement of transformation due to EM fields plus TPA was highly significant and ranged up to a level equivalent to that produced by 1.5 Gy of X rays. The frequency of neoplastic transformation was dependent on the level of EM exposure and was additive with doses of X rays given as a cocarcinogen.||https://www.ncbi.nlm.nih.gov/pubmed/2020740||Radiat Res 126(1):65-72, 1991|
|91||(CE)DNA effct||Sarkar S, Ali S, Behari J,||Effect of low power microwave on the mouse genome: a direct DNA analysis||View Abstr||In Vivo - Animal||1994||India||91. The potential mutagenic effect of low power microwave at the DNA sequence level in the mouse genome was evaluated by direct DNA analysis. Animals were exposed to microwave at a power density of 1 mW/cm2 for 2 h/day at a frequency of 2.45 GHz over a period of 120, 150 and 200 days. HinfI digested DNA samples from testis and brain of control and exposed animals were hybridized with a synthetic oligo probe (OAT 36) comprising nine repeats of 5'-GACA-3'. As compared to control animals, band patterns in exposed animals were found to be distinctly altered in the range of 7-8 kb which was also substantiated by densitometric analysis. Though the mechanism of this rearrangement is not yet clear, the results obtained at the present dose are of significance. This dose, which has been set as the safe limit for general public exposure by the Non-Ionizing Radiation Committee of the International Radiation Protection Association, may imply a need for (re)evaluation of the mutagenic potential of microwaves at the prescribed safe limit for the personnel and people who are being exposed.||https://www.ncbi.nlm.nih.gov/pubmed/7506381||Mutat Res 320(1-2):141-147, 1994|
|92||(CE)DNA effct||Lai H, Singh NP,||Single- and double-strand DNA breaks in rat brain cells after acute exposure to radiofrequency electromagnetic radiation||View Abstr||In Vivo - Animal||1996||USA||92. We investigated the effects of acute (2-h) exposure to pulsed (2-micros pulse width, 500 pulses s(-1)) and continuous wave 2450-MHz radiofrequency electromagnetic radiation on DNA strand breaks in brain cells of rat. The spatial averaged power density of the radiation was 2mW/cm2, which produced a whole-body average-specific absorption rate of 1.2W/kg. Single- and double-strand DNA breaks in individual brain cells were measured at 4h post-exposure using a microgel electrophoresis assay. An increase in both types of DNA strand breaks was observed after exposure to either the pulsed or continuous-wave radiation, No significant difference was observed between the effects of the two forms of radiation. We speculate that these effects could result from a direct effect of radiofrequency electromagnetic energy on DNA molecules and/or impairment of DNA-damage repair mechanisms in brain cells. Our data further support the results of earlier in vitro and in vivo studies showing effects of radiofrequency electromagnetic radiation on DNA.||https://www.ncbi.nlm.nih.gov/pubmed/8627134||Int J Radiat Biol 69(4):513-521, 1996|
|93||(CE)DNA effct||Lai H, Singh NP,||Acute low-intensity microwave exposure increases DNA single-strand breaks in rat brain cells||View Abstr||In Vivo - Animal||1995||USA||93. Levels of DNA single-strand break were assayed in brain cells from rats acutely exposed to low- intensity 2450 MHz microwaves using an alkaline microgel electrophoresis method. Immediately after 2 h of exposure to pulsed (2 microseconds width, 500 pulses/s) microwaves, no significant effect was observed, whereas a dose rate-dependent [0.6 and 1.2 W/kg whole body specific absorption rate (SAR)] increase in DNA single-strand breaks was found in brain cells of rats at 4 h postexposure. Furthermore, in rats exposed for 2 h to continuous-wave 2450 MHz microwaves (SAR 1.2 W/kg), increases in brain cell DNA single-strand breaks were observed immediately as well as at 4 h postexposure.||https://www.ncbi.nlm.nih.gov/pubmed/7677797||Bioelectromagnetics 16(3):207-210, 1995|
|94||(CR)Other Agents - Protect Efct ; (CE)DNA effct||Hatice S, Gürler, Birsen Bilgici, Aysegül K, Akar, Leman Tomak & Abdülkerim Bedir.||Increased DNA oxidation (8-OHdG) and protein oxidation (AOPP) by low level electromagnetic field (2.45 GHz) in rat brain and protective effect of garlic||View Abstr||;6,8;183,9;708,9;935,11||In Vitro||2014||Turkey||94. |
PURPOSE: To investigate the oxidative damage and protective effect of garlic on rats exposed to low level of electromagnetic fields (EMF) at 2.45 GHz Microwave radiation (MWR).
METHODS: Thirty-six Wistar rats were divided into three groups. Group I was the control group and not exposed to EMF. Group II and III were exposed to low level EMF (3.68 ± 0.36 V/m) at 2.45 GHz MWR for 1 hour/day for 30 consecutive days. Daily 500 mg/kg garlic was given to Group III during the study period. At the end of the study, thiobarbituric acid reactive substances (TBARS), advanced oxidation protein products (AOPP) and 8-hydroxydeoxyguanosine (8- OHdG) levels were investigated in brain tissue and blood samples.
RESULTS: Exposure to low level of EMF increased 8-OHdG level in both plasma and brain tissue whereas it increased AOPP level only in plasma. Garlic prevented the increase of 8-OHdG level in brain tissue and plasma AOPP levels.
CONCLUSIONS: It may be concluded that low level EMF at 2.45 GHz MWR increases the DNA damage in both brain tissues and plasma of the rats whereas it increases protein oxidation only in plasma. It may also be argued that the use of garlic decreases these effects.
|https://www.ncbi.nlm.nih.gov/pubmed/24844368||International Journal of Radiation Biology. Posted online on August 4, 2014|
|95||(CE)DNA effct ; (CE)Mutagenic effect||Lakshmi N, Tiwari R, Bhargava S, Ahuja Y||Investigations on DNA damage and frequency of micronuclei in occupational exposure to electromagnetic fields (EMFs) emitted from video display terminals (VDTs)||View Abstr||case-control/ cohort||2010||India||95. The potential effect of electromagnetic fields (EMFs) emitted from video display terminals (VDTs) to elicit biological response is a major concern for the public. The software professionals are subjected to cumulative EMFs in their occupational environments. This study was undertaken to evaluate DNA damage and incidences of micronuclei in such professionals. To the best of our knowledge, the present study is the first attempt to carry out cytogenetic investigations on assessing bioeffects in personal computer users. The study subjects (n = 138) included software professionals using VDTs for more than 2 years with age, gender, socioeconomic status matched controls (n = 151). DNA damage and frequency of micronuclei were evaluated using alkaline comet assay and cytochalasin blocked micronucleus assay respectively. Overall DNA damage and incidence of micronuclei showed no significant differences between the exposed and control subjects. With exposure characteristics, such as total duration (years) and frequency of use (minutes/day) sub-groups were assessed for such parameters. Although cumulative frequency of use showed no significant changes in the DNA integrity of the classified sub-groups, the long-term users (> 10 years) showed higher induction of DNA damage and increased frequency of micronuclei and micro nucleated cells.||https://www.ncbi.nlm.nih.gov/pubmed/21637620||Gen Mol Biol 33(1): 154-158, 2010||UGC Research Unit, Bhavan's New Science College, Hyderabad, Andhra Pradesh India.|
|96||(CE)oxidative stress ; (CE)Mutagenic effect||Naziroglu M, Cig B, Dogan S, Uguz AC, Dilek S, Faouzi D||2.45-Gz wireless devices induce oxidative stress and proliferation through cytosolic Ca²? influx in human leukemia cancer cells.||View Abstr||;6,8;309,22;626,8;1136,12||In Vitro||2012||Turkey||96. |
PURPOSE: Electromagnetic radiation from wireless devices may affect biological systems by increasing free radicals. The present study was designed to determine the effects of 2.45 GHz radiation on the antioxidant redox system, calcium ion signaling, cell count and viability in human leukemia 60 cells.
MATERIALS AND METHODS: Twelve cell cultures were equally divided into two main groups as controls (n =?6) and irradiated (n =?6) and then subdivided into four different subgroups depending on the duration of exposure, namely 1, 2, 12 and 24 hours. The samples were analyzed immediately after the experimental period.
RESULTS: The extent of lipid peroxidation, cytosolic free Ca²? and cell numbers were higher in 2.45 GHz groups than in the controls. The increase of cytosolic free Ca²? concentrations was radiation time-dependent and was highest at 24-h exposure. The reduced glutathione, glutathione peroxidase, vitamin C and cell viability values did not show any changes in any of the experimental groups. 2-aminoethyl diphenylborinate inhibits Ca²? ions influx by blockage of the transient receptor potential melastatin 2.
CONCLUSIONS: 2.45 GHz electromagnetic radiation appears to induce proliferative effects through oxidative stress and Ca²? influx although blocking of transient receptor potential melastatin 2 channels by 2-aminoethyl diphenylborinate seems to counteract the effects on Ca²? ions influx.
|https://www.ncbi.nlm.nih.gov/pubmed/22489926||Int J Radiat Biol. 88(6):449-456, 2012.|
|97||(CE)oxidative stress; (CE)Cellular effct||Cig B, Nazıroglu M||Investigation of the effects of distance from sources on apoptosis, oxidative stress and cytosolic calcium accumulation via TRPV1 channels induced by mobile phones and Wi-Fi in breast cancer cells||View Abstr||In Vitro||2015||Turkey||97. TRPV1 is a Ca2+ permeable channel and gated by noxious heat, oxidative stress and capsaicin (CAP). Some reports have indicated that non-ionized electromagnetic radiation (EMR)-induces heat and oxidative stress effects. We aimed to investigate the effects of distance from sources on calcium signaling, cytosolic ROS production, cell viability, apoptosis, plus caspase-3 and -9 values induced by mobile phones and Wi-Fi in breast cancer cells MCF-7 human breast cancer cell lines were divided into A, B, C and D groups as control, 900, 1800 and 2450MHz groups, respectively. Cells in Group A were used as control and were kept in cell culture conditions without EMR exposure. Groups B, C and D were exposed to the EMR frequencies at different distances (0cm, 1cm, 5cm, 10cm, 20cm and 25cm) for 1h before CAP stimulation. The cytosolic ROS production, Ca2+ concentrations, apoptosis, caspase-3 and caspase-9 values were higher in groups B, C and D than in A group at 0cm, 1cm and 5cm distances although cell viability (MTT) values were increased by the distances. There was no statistically significant difference in the values between control, 20 and 25cm. Wi-Fi and mobile phone EMR placed within 10cm of the cells induced excessive oxidative responses and apoptosis via TRPV1-induced cytosolic Ca2+ accumulation in the cancer cells. Using cell phones and Wi-Fi sources which are farther away than 10cm may provide useful protection against oxidative stress, apoptosis and overload of intracellular Ca2+. This article is part of a Special Issue entitled: Membrane channels and transporters in cancers||http://www.ncbi.nlm.nih.gov/pubmed/25703814||http://emfrefugee.blogspot.com/2015/02/investigation-of-effects-of-distance.html||Biochim Biophys Acta. 2015 Feb 19. pii: S0005-2736(15)00053-X. doi: 10.1016/j.bbamem|