Academic journal article Environmental Health Perspectives

Microwaves from GSM Mobile Telephones Affect 53BP1 and [Gamma]-H2AX Foci in Human Lymphocytes from Hypersensitive and Healthy Persons

Academic journal article Environmental Health Perspectives

Microwaves from GSM Mobile Telephones Affect 53BP1 and [Gamma]-H2AX Foci in Human Lymphocytes from Hypersensitive and Healthy Persons

Article excerpt

The data on biologic effects of nonthermal microwaves (MWs) from mobile telephones are diverse, and these effects are presently ignored by safety standards of the International Commission for Non-Ionizing Radiation Protection (ICNIRP). In the present study, we investigated effects of MWs of Global System for Mobile Communication (GSM) at different carrier frequencies on human lymphocytes from healthy persons and from persons reporting hypersensitivity to electromagnetic fields (EMFs). We measured the changes in chromatin conformation, which are indicative of stress response and genotoxic effects, by the method of anomalous viscosity time dependence, and we analyzed tumor suppressor p53-binding protein 1 (53BP1) and phosphorylated histone H2AX ([gamma]-H2AX), which have been shown to colocalize in distinct loci with DNA double-strand breaks (DSBs), using immunofluorescence confocal laser microscopy. We found that MWs from GSM mobile telephones affect chromatin conformation and 53BP1/[gamma]-H2AX loci similar to heat shock. For the first time, we report here that effects of MWs from mobile telephones on human lymphocytes are dependent on carrier frequency. On average, the same response was observed in lymphocytes from hypersensitive and healthy subjects. Key words: 53BP1 and [gamma]-H2AX foci, chromatin, DNA double-strand breaks, hypersensitivity to electromagnetic fields, stress response. doi:10.1289/ehp.7561 available via http://dx.doi.org/[Online 28 April 2005]

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The growing public concerns about possible effects of microwave (MW) exposure from mobile telephones have been discussed in many countries because of increasing use of wireless communication systems. Two groups have reported that increased incidence of brain tumors and acoustic neuroma is correlated with exposure to mobile telephone MWs depending on duration of mobile telephone use (Hardell et al. 2003; Lonn et al. 2004). Negative findings were also reported by other groups, but the results of these epidemiologic studies are not directly comparable because of methodologic and other differences, as has recently been reviewed (Kundi et al. 2004). The intensity levels of exposure to MWs from mobile telephones are lower than the standards adopted by the International Commission for Non-Ionizing Radiation Protection (ICNIRP 1998). These standards are based on the thermal effects of MWs resulting in heating of exposed tissues or cells. There is also evidence for nonthermal effects of MWs that suggests a possible relationship between nonthermal MW exposure and both permeability of the brain-blood barrier (Persson et al. 1997) and stress response (de Pomerai et al. 2000). Recent studies have described neuronal damage in the brains of exposed rats (Ilhan et al. 2004; Salford et al. 2003). In other studies, no effects of nonthermal MWs were observed (Meltz 2003). However, experimental data suggested that MW effects occur only under specific parameters of exposure, depending on several physical parameters and biologic variables (Adey 1999; Belyaev et al. 2000; Binhi 2002; Blackman et al. 1989). Dependence of the MW effects on several physical parameters, including frequency, polarization, and modulation, and also several biologic variables could explain various outcomes of studies with nonthermal MWs (Belyaev et al. 2000).

MWs under specific conditions of exposure induce DNA strand breaks in rat brain cells as measured by single-cell electrophoresis (Lai and Singh 1996, 1997). The mechanisms of this effect are not understood, but they could be related to induced changes in the interaction of DNA with proteins, rather than DNA damage (Belyaev et al. 1999).

Several proteins, such as the tumor suppressor p53-binding protein 1 (53BP1) and phosphorylated H2AX ([gamma]-H2AX), have been shown to produce discrete intranuclear loci, which are believed to colocalize with DNA double-strand breaks (DSBs) providing a scaffold structure for DSB repair (DiTullio et al. …

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