Effect of radiofrequency radiation exposure on mouse skin tumorigenesis initiated by 7,12-dimethybenz[α]anthracene

• Published in: International journal of radiation biology Vol. 81; no. 12; pp. 861 - 867
• Main Authors: Huang, Tai-Qin, Lee, Jae-Seon, Kim, Tae-Hyung, Pack, Jeong-Ki, Jang, Ja-June, Seo, Jeong-Sun
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.12.2005; Taylor & Francis
• Subjects: 9,10-Dimethyl-1,2-benzanthracene - administration & dosage; Animals; Carcinogens - administration & dosage; Cell Phone; DMBA; Dose-Response Relationship, Radiation; Electromagnetic Fields - adverse effects; Male; Mice; Mice, Inbred ICR; Neoplasms, Radiation-Induced - physiopathology; Random Allocation; RF radiation; Skin Neoplasms - etiology; skin tumorigenesis; Tetradecanoylphorbol Acetate - administration & dosage; TPA
• ISSN: 0955-3002; 1362-3095
• DOI: 10.1080/09553000600568093

Purpose: Although radiofrequency (RF) radiation is not considered mutagenic, it has been suggested as a promoter of tumorigenesis. To study if RF radiation has a tumor promoting effect, we exposed mice with skin tumorigenesis initiated by 7,12-dimethybenz[α]anthracene (DMBA) to RF radiation. Materials and methods: Eighty male ICR mice were subjected to a single DMBA application (100 μg 100 μl acetone mouse) on shaved dorsal skin at the age of 7 weeks. After one week, the mice were randomized into four equal groups of 20 mice each: i.e., sham-, 849 MHz-, 1,763 MHz-exposed, and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated groups. The RF exposure was conducted at a whole body average specific absorption rate (SAR) of 0.4 W Kg, for 2 cycles of 45 min exposure with a 15 min interval each day, 5 days a week for 19 weeks. The TPA-treated group served as a positive control for skin tumorigenesis and were administered TPA (4 μg 100 μl acetone mouse) twice weekly without RF exposure. Results: All mice were examined weekly at a macroscopic level. No skin tumors were observed in any groups except in the TPA-treated positive control group. TPA is known tumor promoter in DMBA-induced skin carcinogenesis and tumor incidence in the TPA treated group was 95%. At week 20 after DMBA initiation, skin tissues were analyzed immunohistochemically using anti-proliferating cell nuclear antigen (PCNA) antibody. No differences were observed by pathological examination or by PCNA staining between the sham- and the RF-exposed groups. The expression of cyclin D1 and c-fos were detected only in the tumorous skin tissues of the TPA-treated group. Conclusion: No evidence was found that RF radiation serves as a tumor promoter for skin tumors. Our data suggests that 849 MHz and 1,763 MHz RF radiations, similar to those emitted from mobile phones, do not have any promoting effect on skin tumor development in DMBA-initiated mice.