ID Number		1877
Study Type		In Vitro
Model		835 MHz (CDMA) and exposure to primary human lymphoctes and evaluation of DNA breaks and VDT occupational exposure and DNA damage and micronuclei frequency.
Details		Human primary lymphocytes were isolated from healthy male volunteers (n=6, 20-24 yrs old) and exposed to a combination of a CDMA modulated radiofrequency (RF) signal and Aphidicolin (APC). APC is a reversible inhibitor of the DNA repair process in eukaryotic cells by blocking DNA polymerase A/D, and was used at concentrations of either 0.2 or 2.0 ug/ml in the study. The 835 MHz CDMA RF exposure was performed for either 1 or 2 hours using a mobile phone hooked to the network and placed at an undefined orientation, distance, and transmit power level with respect to the cell culture inside the culture incubator. An SAR value of 1.1.7 W/kg was provided in the Methods section as the value reported by the manufacturer from compliance testing, although it is not clear how this SAR level is relevant to the cell culture exposure. Since Indian networks only support CDMA operation on the 800 MHz band, operation on the higher 1900 MHz carrier frequency was not possible even if the mobile phone handset (which was not identified in the study) was capable of dual band operation. DNA breaks were evaluated using the alkaline comet assay of Singh et al 1998.Exposure of lymphocytes to CDMA RF alone did not result in any significant effect on the level of DNA damage as observed by comet assay, although as expected exposure to APC alone did significantly increase the level of DNA breaks in a dose dependent manner. When used in combination, CDMA (2 hr) + APC (2.0 ug/ml) exposure further increased the amount of DNA breaks to a significant extent (p = 0.002) above the level observed with APC alone. The authors admit that on theoretical grounds, it is known that the photon energy of RF from mobile phones is insufficient to break chemical bonds in DNA and cause direct DNA damage and thus are not surprised that CDMA RF exposure alone did not result in an observable increase in comet tail length in their assay. However, they suggest the effects observed in their study in combination with a known DNA repair inhibitor are similar to other observations in the literature of synergistic effects with known mutagens (Maes et al. 2006; Zhang et al. 2002; Baohong et al. 2007), and they suggest & the potential adverse health impacts of RF exposure may not arise because the radiations alone cause any damage, but they interfere with endogenous bioprocesses deleteriously which would otherwise afford natural protection. The authors conclude The controversy that mobile phone radiation may induce DNA damage in synergism with mutagen needs to be clarified in future laboratory studies. AUTHORS' ABSTRACT: Lakshmi et al. 2010 (IEEE #6285): 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. AUTHORS' ABSTRACT: Bhargav et al. 2015 (IEEE #7311): The mobile phones (MP) are low power radio devices which work on electromagnetic fields (EMFs), in the frequency range of 900-1800 MHz. Exposure to MPEMFs may affect brain physiology and lead to various health hazards including brain tumors. Earlier studies with positron emission tomography (PET) have found alterations in cerebral blood flow (CBF) after acute exposure to MPEMFs. It is widely accepted that DNA double-strand breaks (DSBs) and their misrepair in stem cells are critical events in the multistage origination of various leukemia and tumors, including brain tumors such as gliomas. Both significant misbalance in DSB repair and severe stress response have been triggered by MPEMFs and EMFs from cell towers. It has been shown that stem cells are most sensitive to microwave exposure and react to more frequencies than do differentiated cells. This may be important for cancer risk assessment and indicates that stem cells are the most relevant cellular model for validating safe mobile communication signals. Recently developed technology for recording the human bio-electromagnetic (BEM) field using Electron photonic Imaging (EPI) or Gas Discharge Visualisation (GDV) technique provides useful information about the human BEM. Studies have recorded acute effects of Mobile Phone Electromagnetic Fields (MPEMFs) using EPI and found quantifiable effects on human BEM field. Present manuscript reviews evidences of altered brain physiology and stem cell functioning due to mobile phone/cell tower radiations, its association with increased cancer risk and explores early diagnostic value of EPI imaging in detecting EMF induced changes on human BEM.
Findings		Effects
Status		Completed With Publication
Principal Investigator		Bhavan's New Science College, India - rravindra_tiwari@yahoo.com
Funding Agency		?????
Country		INDIA
References		Tiwari, R et al. Elect Biol Med, (2008) 27:418-425 Lakshmi, N et al. Genet Mol Biol., (2010) 33:154-158 Bhargav, H et al. J Stem Cells 2015;10:287-94., (2015) 10:287-294
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