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Mobile phone base station radiation does not affect neoplastic transformation in BALB/3T3 cells

✍ Scribed by H. Hirose; T. Suhara; N. Kaji; N. Sakuma; M. Sekijima; T. Nojima; J. Miyakoshi


Publisher
John Wiley and Sons
Year
2008
Tongue
English
Weight
160 KB
Volume
29
Category
Article
ISSN
0197-8462

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✦ Synopsis


Abstract

A large‐scale in vitro study focusing on low‐level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT‐2000) cellular system was conducted to test the hypothesis that modulated RF fields affect malignant transformation or other cellular stress responses. Our group previously reported that DNA strand breaks were not induced in human cells exposed to 2.1425 GHz Wideband Code Division Multiple Access (W‐CDMA) radiation up to 800 mW/kg from mobile radio base stations employing the IMT‐2000 cellular system. In the current study, BALB/3T3 cells were continuously exposed to 2.1425 GHz W‐CDMA RF fields at specific absorption rates (SARs) of 80 and 800 mW/kg for 6 weeks and malignant cell transformation was assessed. In addition, 3‐methylcholanthrene (MCA)‐treated cells were exposed to RF fields in a similar fashion, to assess for effects on tumor promotion. Finally, the effect of RF fields on tumor co‐promotion was assessed in BALB/3T3 cells initiated with MCA and co‐exposed to 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA). At the end of the incubation period, transformation dishes were fixed, stained with Giemsa, and scored for morphologically transformed foci. No significant differences in transformation frequency were observed between the test groups exposed to RF signals and the sham‐exposed negative controls in the non‐, MCA‐, or MCA plus TPA‐treated cells. Our studies found no evidence to support the hypothesis that RF fields may affect malignant transformation. Our results suggest that exposure to low‐level RF radiation of up to 800 mW/kg does not induce cell transformation, which causes tumor formation. Bioelectromagnetics 29:55–64, 2008. © 2007 Wiley‐Liss, Inc.


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