Abstract: A number of epidemiological studies have suggested that exposure to 50/60-Hz magnetic fields (MF) from power lines and electrical equipment may be associated with a modestly increased incidence of various types of cancer. Laboratory studies have indicated that nonionizing radiation has no mutagenic effect, i.e. does not initiate cancer. Thus, if 50/60-Hz MF are truly associated with an increased risk of cancer, then these fields must act as a promoter or co-promoter of cancer in cells that have already been initiated. This paper reviews the evidence produced by animal studies. As shown in this review, the available animal data on 50/60-Hz MF exposures seem to indicate that intermediate MF exposure exerts co-promoting effects in different tumor models, particularly cocarcinogenesis models of breast cancer, while chronic (up to life-time) exposure may exert promoting effects on “spontaneous” development of certain tumors. The tumor promoting or co-promoting effects of 50/60-Hz MF exposure found in several animal studies could relate to actions of MF on gene expression, immune surveillance, and Ca2+ homeostasis as demonstrated by in vitro experiments in cell cultures. However, the most plausible evidence for an in vivo effect of MF exposure which could be related to tumor promotion is reduction of circulating levels of melatonin, i.e. a hormone which is inhibitory to the growth of a wide range of cancers, particularly breast cancer. Animal studies have shown that 50-Hz MF exposure at flux densities as low as 0.3-1 mu Tesla significantly reduces nocturnal melatonin levels in plasma. While decrease of melatonin levels alone could explain tumor promoting or co-promoting effects of MF exposure, recent data indicate that MF exposure also impairs the effects of melatonin at the cellular level. Thus, the oncostatic effect of melatonin on cell proliferation of a human breast cancer cell line was antagonized by 60-Hz MF exposure at a flux density of about 1 mu Tesla. All these data indicate that interactions between 50/60-HZ MF exposure and melatonin may be the key mechanism of any carcinogenic effects. Although the existing experimental evidence is still insufficient for discerning a cause-effect relationship for MF exposure and human disease or injury, it does suggest the need for further laboratory research under well-defined laboratory exposure conditions to allow for a realistic assessment of the possible health risks and their magnitude.

Abstract: Several epidemiological studies have indicated that residential or occupational exposure to 50 or 60 Hz magnetic fields (MF) may increase the risk of breast cancer, possibly by suppression of pineal production of the oncostatic hormone melatonin. In view of the methodological problems of epidemiological studies on MF exposure and cancer risk, laboratory studies are needed to determine whether 50/60 Hz exposure can initiate, promote or copromote mammary cancer. In the present study, 216 female Sprague-Dawley rats were divided into four groups. Two of the groups (with 99 animals each) received oral applications of 7,12-dimethylbenz[a]anthracene (DMBA) and were either sham-exposed or exposed in a 50 Hz, 100 muT MF for 24 h/day 7 days/week for a period of 91 days. The other two groups (nine animals each) were either sham-exposed or MF-exposed without DMBA treatment. The exposure chambers and all other environmental factors were identical for MF-exposed and sham-exposed animals. At the end of the 3 month period of MF exposure, all rats were used for histopathological diagnosis of lesions. At the time of necropsy, significantly more MF-exposed DMBA-treated rats exhibited macroscopically visible mammary tumours than DMBA-treated controls. Furthermore, the size of mammary tumours was significantly larger in MF-exposed rats. Histopathological examination of the mammary gland showed that the number of neoplastic and non-neoplastic lesions did not significantly differ between groups, indicating that MF exposure had not altered the incidence of mammary lesions but had only accelerated tumour growth, consistent with a co-promoting effect. In the MF-exposed group, significantly more rats exhibited malignant mammary tumours than in controls, indicating that MF exposure had affected the progression of DMBA-induced lesions. The number of metastases of mammary tumours or of primary lesions in other organs in response to DMBA was not affected by MF exposure. In rats without DMBA application, no non-neoplastic or neoplastic lesions were determined. The data demonstrate that long-term exposure of DMBA-treated female rats promotes the growth and progression of mammary tumours, while tumour incidence is not affected, at least under the experimental conditions of the present study. The data thus add to the accumulating evidence that MF exposure exerts tumour co-promoting effects.

Abstract: Here, we present evidence that exposure of B-lineage lymphoid cells to low energy electromagnetic fields (EMF) stimulates the protein tyrosine kinases Lyn and Syk, results in tyrosine phosphorylation of multiple electrophoretically distinct substrates, and leads to downstream activation of protein kinase C (PKC). EMF exposure enhances protein tyrosine phosphorylation in Syk deficient but not in Lyn-deficient B-lineage lymphoid cells and stimulates Lyn kinase activity in wild-type as well as Syk-deficient B-lineage lymphoid cells. These results indicate that activation of Lyn kinase is sufficient and mandatory for EMF-induced tyrosine phosphorylation in B-lineage lymphoid cells. The PKC activity increases later than the Lyn activity and pretreatment with the PTK inhibitors genistein or herbimycin A abrogates the EMF-induced PKC signal. Thus, stimulation of Lyn is a proximal and mandatory step in EMF-induced activation of PKC in B-lineage lymphoid cells. Our observations prompt the hypothesis that a delicate growth regulatory balance might be altered in B-lineage lymphoid cells by EMF-induced activation of Lyn.