title: Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer 344 rats chronically exposed to 836 MHz modulated microwaves.
abstract: We have tested an 836.55 MHz field with North American Digital Cellular (NADC) modulation in a 2-year animal bioassay that included fetal exposure. In offspring of pregnant Fischer 344 rats, we tested both spontaneous tumorigenicity and the incidence of induced central nervous system (CNS) tumors after a single dose of the carcinogen ethylnitrosourea (ENU) in utero, followed by intermittent digital-phone field exposure for 24 months. Far-field exposures began on gestational day 19 and continued until weaning at age 21 days. Near-field exposures began at 35 days and continued for the next 22 months, 4 consecutive days weekly, 2 h/day. SAR levels simulated localized peak brain exposures of a cell phone user. Of the 236 original rats, 182 (77%) survived to the termination of the whole experiment and were sacrificed at age 709-712 days. The 54 rats (23%) that died during the study ("preterm rats") formed a separate group for some statistical analyses. There was no evidence of tumorigenic effects in the CNS from exposure to the TDMA field. However, some evidence of tumor-inhibiting effects of TDMA exposure was apparent. Overall, the TDMA field-exposed animals exhibited trends toward a reduced incidence of spontaneous CNS tumors (P < 0. 16, two-tailed) and ENU-induced CNS tumors (P < 0.16, two-tailed). In preterm rats, where primary neural tumors were determined to be the cause of death, fields decreased the incidence of ENU-induced tumors (P < 0.03, two-tailed). We discuss a possible approach to evaluating with greater certainty the possible inhibitory effects of TDMA-field exposure on tumorigenesis in the CNS.
authors.affiliation: Department of Biochemistry, University of California, Riverside, California 92521, USA.
authors.forename: W R
authors.initials: WR
authors.lastname: Adey
authors.forename: C V
authors.initials: CV
authors.lastname: Byus
authors.forename: C D
authors.initials: CD
authors.lastname: Cain
authors.forename: R J
authors.initials: RJ
authors.lastname: Higgins
authors.forename: R A
authors.initials: RA
authors.lastname: Jones
authors.forename: C J
authors.initials: CJ
authors.lastname: Kean
authors.forename: N
authors.initials: N
authors.lastname: Kuster
authors.forename: A
authors.initials: A
authors.lastname: MacMurray
authors.forename: R B
authors.initials: RB
authors.lastname: Stagg
authors.forename: G
authors.initials: G
authors.lastname: Zimmerman
authors.forename: J L
authors.initials: JL
authors.lastname: Phillips
authors.forename: W
authors.initials: W
authors.lastname: Haggren
mesh_terms: D000818:Animals; D001932:Brain Neoplasms / Q000139:chemically induced / Q000209:etiology / Q000473:pathology; D002273:Carcinogens; D016543:Central Nervous System Neoplasms / Q000139:chemically induced / Q000209:etiology* / Q000473:pathology; D003043:Cocarcinogenesis; D004195:Disease Models, Animal; D005038:Ethylnitrosourea; D005260:Female; D015994:Incidence; D008297:Male; D008872:Microwaves / Q000009:adverse effects*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011916:Rats, Inbred F344; D013120:Spinal Cord Neoplasms / Q000139:chemically induced / Q000209:etiology / Q000473:pathology
chemical_list: D002273:Carcinogens; D005038:Ethylnitrosourea