Auteurs
Tiwari R, Lakshmi NK, Surender V, Rajesh AD, Bhargava SC, Ahuja YR. (2008). Combinative exposure effect of radio frequency signals from CDMA mobile phones and aphidicolin on DNA integrity. Electromagn Biol Med 27(4):418-425.

Background
Public exposure to radiofrequency (RF) electromagnetic fields (EMFs) from mobile phones (MPs) is growing exponentially worldwide. In addition to environmental exposure to EMFs, occupational exposure to DNA-damaging agents, such as mutagenic chemicals and drugs, is also possible. In vitro studies of possible genotoxic effects of RF EMFs on cells have been of value in supplementing epidemiologic evidence about human disease.

Objective
The aim of the present study was to assess the effect of Code Division Multiple Access (CDMA) mobile phone signals on DNA integrity in human leukocytes. The effect of aphidicolin (APC), a chemical compound with anti-mitotic properties and a known DNA repair inhibitor, on possible DNA damage induced by RF signals, was also evaluated.

Methods
Blood samples were drawn from six healthy males aged 20-24 years, of the same socioeconomic status, non-smokers and non-drinkers of alcohol. The samples were exposed to RF signals of CDMA mobile phone at 835 MHz and specific absorption rate (SAR) of 1.17 W/kg for 1 hour. The effects of combined exposure were studied with two aphidicolin concentrations: 0.2 and 2 mg/ml. Sham exposure was used as a control. Alkaline comet assay was used to study DNA damage. DNA repair efficiency of the samples was studied after 2 hours of exposure in the incubator.

Results
No increase in DNA damage in the peripheral blood lymphocytes was detected after exposure to RF EMFs compared to sham exposure. Aphidicolin at 2 mg/ml concentration showed highly significant DNA damage levels, whereas the damage levels at 0.2 mg/ml were insignificant. Significant DNA damage levels were seen after combined exposure to RF signals and aphidicolin at both concentrations, compared to the sham exposure. DNA repair efficiency did not change significantly after either RF EMF or aphidicolin exposure. Combined exposure to RF EMF and aphidicolin at both concentrations resulted in significant variations in DNA repair efficiency.

Interpretation
Similar to many other in vitro studies, the results of this study did not suggest any increase in DNA damage in the peripheral blood leukocytes due to RF EMF exposure. On theoretical grounds, it is known that the photon energy of RF EMFs from mobile phones is insufficient to break chemical bonds in DNA and cause direct DNA damage. The enhancing effect of aphidicolin on DNA damage in combination with RF signals may be attributed to aphidicolin anti-mitotic properties. The results of this study also suggest that the DNA damage is repairable at both aphidicolin concentrations.
Conclusion
It can be inferred from the results of this study that in vitro exposure to RF EMFs alone does not induce significant DNA damage, while combined exposure to RF EMFs and DNA repair inhibitor aphidicolin induces reversible DNA damage.

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