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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

2007; Wiley; Volume: 28; Issue: 7 Linguagem: Inglês

10.1002/bem.20324

1521-186X

Tomoyuki Shirai, Toshio Ichihara, Kanako Wake, Soichi Watanabe, Yukio Yamanaka, Mayumi Kawabe, Masao Taki, Osamu Fujiwara, Jianqing Wang, Satoru Takahashi, Seiko Tamano,

Noise Effects and Management

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. Bioelectromagnetics 28:562–572, 2007. © 2007 Wiley‐Liss, Inc.