TUMOR PROMOTION IN A BREAST-CANCER MODEL BY EXPOSURE TO A WEAK ALTERNATING MAGNETIC-FIELD

In view of the methodological problems of epidemiological studies on associations between exposures to 50/60 Hz magnetic fields (MF) and increased incidence of cancers, laboratory studies are necessary to determine if 50/60 Hz MF are cancer promoters or can progress cancers. The objective of the present study was to determine if an alternating MF of low flux density exerts tumor-promoting or co-promoting effects in a model of breast cancer in female rats. Mammary tumors were induced by the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA). A group of 99 rats was exposed to a homogeneous MF of 50 Hz, 100 muT (microtesla), for 24 h/day 7 day/week for a period of 91 days, another group of 99 rats was sham-exposed under the same environmental conditions as the MF-exposed rats. The exposure chambers were identical for MF-exposed and sham-exposed animals, DMBA was administered orally at a dose of 5 mg/kg at the first day of exposure and at weekly intervals thereafter up to a total dose of 20 mg per rat. The animals were palpated once weekly to assess the development of mammary tumors. In controls, DMBA induced tumors in about 40% of the animals within three months of first application. Eight weeks after DMBA application the MF-exposed rats exhibited significantly more tumors than sham-exposed animals. This difference in the rate of tumor development was observed throughout the period of exposure. At the end of the three-month period of MF exposure the tumor incidence in MF-exposed rats was 50% higher than in sham-exposed rats, the difference being statistically significant. Furthermore, the size of tumors as estimated by palpation was significantly larger in the MF-exposed compared to sham-exposed rats. The data demonstrates that long-term exposure of DMBA-treated female rats to an alternating MF of low flux density promotes the growth and increases the incidence of mammary tumors, thus strongly indicating that MF exposure exerts tumor-promoting and/or copromoting effects.