Lack of promoting effects of chronic exposure to 1.95-GHz W-CDMA signals for IMT-2000 cellular system on development of N-ethylnitrosourea-induced central nervous system tumors in F344 rats |
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Authors: | Shirai Tomoyuki Ichihara Toshio Wake Kanako Watanabe So-ichi Yamanaka Yukio Kawabe Mayumi Taki Masao Fujiwara Osamu Wang Jianqing Takahashi Satoru Tamano Seiko |
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Affiliation: | Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan. tshirai@med.nagoya-cu.ac.jp |
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Abstract: | The present study was performed to evaluate effects of a 2-year exposure to an electromagnetic near-field (EMF) equivalent to that generated by cellular phones on tumor development in the central nervous system (CNS) of rats. For this purpose, pregnant F344 rats were given a single administration of N-ethylnitrosourea (ENU) on gestational day 18. A total of 500 pups were divided into five groups, each composed of 50 males and 50 females: Group 1, untreated controls; Group 2, ENU alone; Groups 3 to 5, ENU + EMF (sham exposure and two exposure levels). A 1.95-GHz wide-band code division multiple access (W-CDMA) signal, which is a feature of the International Mobile Telecommunication 2000 (IMT-2000) cellular system was employed for exposure of the rat head starting from 5 weeks of age, 90 min a day, 5 days a week, for 104 weeks. Brain average specific absorption rates (SARs) were designed to be .67 and 2.0 W/kg for low and high exposures, respectively. The incidence and numbers of brain tumors in female rats exposed to 1.95-GHz W-CDMA signals showed tendencies to increase but without statistical significance. Overall, no significant increase in incidences or numbers, either in the males or females, was detected in the EMF-exposed groups. In addition, no clear changes in tumor types in the brain were evident. Thus, under the present experimental conditions, exposure of heads of rats to 1.95-GHz W-CDMA signals for IMT-2000 for a 2-year period was not demonstrated to accelerate or otherwise affect ENU-initiated brain tumorigenesis. |
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Keywords: | electromagnetic field brain tumor rat ENU IMT‐2000 |
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