Possible cocarcinogenic effects of ELF electromagnetic fields may require repeated long-term interaction with known carcinogenic factors

Abstract

Literature on cancer‐related biological effects of extremely low frequency (ELF) magnetic fields (MF) is discussed in the light of the current understanding of carcinogenesis as a multistep process of accumulating mutations. Different animal models and study designs have been used to address possible cocarcinogenic effects of MFs. Based on a comparison of the results, we propose a hypothesis that MF exposure may potentiate the effects of known carcinogens only when both exposures are chronic. We also discuss possible mechanisms of MF effects on carcinogenesis and the adequacy of the classical two‐step intiation/promotion animal experiments for simulating human exposure to the complex mixture of environmental carcinogens. We conclude that experiments designed according to the two‐step concept may not be sufficient for studying the possible role of MF in carcinogenesis. Possible further animal studies are more likely to be productive if they include models that combine chronic exposure to MFs with long‐term exposures to known carcinogens. Bioelectromagnetics 21:122–128, 2000. © 2000 Wiley‐Liss, Inc.

Cell Type Specific Redox Status is Responsible for Diverse Electromagnetic Field Effects

“…It has to be taken into account that experimental approaches regarding EMFexposure show short-term conditions because of technical limitation, which never reflect the real situation, such as longterm exposure and the influence of other environmental noxes. It has been stated [112,190] that current in vivo experiments on the possible carcinogenicity of EMF are inadequate for environmental exposure of carcinogens to humans when common experimental initiator/promoter design was used. Since environmental exposure of the general public may well comprise several types of carcinogens, including continuous exposure to a wide spectrum of EMF, it seems important to note that the exact time point of initiation during EMF exposure may be of crucial importance.…”

Effects on G2/M Phase Cell Cycle Distribution and Aneuploidy Formation of Exposure to a 60 Hz Electromagnetic Field in Combination with Ionizing Radiation or Hydrogen Peroxide in L132 Nontumorigenic Human Lung Epithelial Cells

“…Many studies have reported possible associations between ELF-MF exposure and an increased risk of cancer, genomic instability, and reproductive dysfunction [1,2,3,4]. However, the association between ELF-MFs and cancer remains controversial since different results have been obtained depending on the type of cancer studied; moreover, methodological problems have been identified in some of the studies [5,6]. Furthermore, one in vitro study found that a 50/60 Hz ELF-MF was unable to induce mutations [7].…”

The effects of extremely low frequency magnetic fields on mutation induction in mice

“…Since humans are exposed to various combinations of an array of different carcinogens at changeable levels, exposure to ELF-MF could potentially act in a promotor, co-promotor or enhancer through either simultaneous or sequential exposure, ultimately contributing towards tumour progression (Juutilainen et al, 2000). Indeed a study had previously reported that mice experienced enhanced skin tumorigenesis when exposed to UV radiation in conjunction with magnetic fields (Kumlin et al, 1998).…”

“…However the majority of these co-carcinogenicity studies are either inconclusive or negative in their findings (Juutilainen et al, 2000;Vijayalaxmi & Obe, 2005), despite using numerous cytogenic assays (comet, MN and SCE) and combined treatments with multiple mutagens (mitomycin C or X-rays) at a range of high 50 Hz flux densities (80-1740 mT) (Maes et al, 2000). Similarly, a recent series of studies performed by the same laboratory demonstrated that 4 or 16 hour exposure to 60 Hz, 1 mT ELF-MF in combination with ionising radiation (1 Gy X-rays) or H 2 O 2 or cellular myelocytomatosis oncogene (c-Myc) activation did not have either an enhancing or synergistic effect on MN formation (Jin et al, 2012) or primary DNA damage (Jin et al, 2014).…”

“…Correspondingly, persistent or excessive cellular oxidative stress may ultimately induce oxidative damage to the macromolecules and lipid peroxidation which, if left unrepaired and subsequent genomic stability fails to be restored, could result in cell death via apoptosis (Kim et al, 2010). Apoptosis is a protective mechanism through which damaged, infected or potentially cancerous cells are removed to maintain normal homeostasis of multicellular organisms (Lacy-Hulbert et al, 1998;Juutilainen et al, 2000). In fact the alteration of the cells redox state to a more oxidative environment has been shown to occur immediately prior to the final phase of caspase activation in numerous models of apoptosis (reviewed in Kannan & Jain, (2000)).…”