Evaluation of the potential of mobile phone specific electromagnetic fields (UMTS) to produce micronuclei in human glioblastoma cell lines

Halh Al-Serori, Michael Kundi, Franziska Ferk, Miroslav Mišík, Armen Nersesyan, Manuel Murbach, Tamara T. Lah, and Siegfried Knasmüller. Toxicology In Vitro, Volume 40, pp. 264–271, April 2017, online 24 January 2017, DOI: 10.1016/j.tiv.

Recent epidemiological studies indicate that exposure to mobile-phone-specific electromagnetic fields (EMF) causes development of glioblastomas in humans. In this study, the effects of the universal mobile telecommunications system radiofrequency (UMTS-RF) signal – also known as 3G – on the formation of micronuclei (MN) due to structural and numerical chromosomal aberrations and other anomalies, such as nuclear buds (NB) that reflect gene amplification were assessed. Human glioblastoma cell lines, which were cultivated for 16 h in the presence and absence of fetal calf serum, were exposed to EMF with the well-characterized sXc1950 exposure system designed by the IT’IS Foundation. No evidence for induction of MN or other anomalies was found when the cells were exposed to EMF at specific absorption rate (SAR) levels of 0.25, 0.50, and 1.00 W/kg, which suggests that the UMTS-RF signal does not cause chromosomal damage in glioblastoma cells. However, at the highest exposure dose of 1.00 W/kg, morphological features observed in U251 cells indicate the induction of programmed cell death (apoptosis). The mechanisms that may lead to apoptosis induction will be investigated in follow-up studies.

The scientific and technical impact of the study can be summarized as:

• • The double-blinded exposure protocols of the sXc1950 system were used in RF exposure experiments on human glioblastoma cells to investigate possible RF mobile-phone-specific radiation effects on chromosomal stability.
  • No evidence was found for induction of MN formation or several other nuclear anomalies.
  • Induction of apoptosis was observed in a p53-mutated cell line (U251), while, in p53-proficient cells (U87), the apoptosis rate was not increased.

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