EMFs and DNA effects: potential mechanism elucidated.

For many years, scientists have suspected that long-term exposure to extremely-low-frequency electromagnetic fields (EMFs) A may be associated with increased risk of neurodegenerative diseases such as Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis. Some studies have shown that EMF exposure can damage DNA in a variety of human and animal cells, while others have shown no significant effect. Now Henry Lai and Narendra P. Singh of the University of Washington offer support for speculation that environmental exposure to EMFs is hazardous and that the effects may be cumulative [EHP 112:687-694]. They also offer a potential cellular mechanism for cell damage associated with EMF exposure that may help explain anomalies reported earlier in the literature.

Lai and Singh's findings support the so-called free radical hypothesis, which posits that extremely-low-frequency EMFs increase free radical activity in cells, thereby causing DNA damage and disturbing other cellular processes and functions. They and others had shown earlier that free radical damage can lead to cellular necrosis and apoptosis. Such effects are particularly troubling in neurons, because these cells cannot divide and are not replaced when they die--thus the potential link to neurodegenerative diseases.

Lai and Singh exposed groups of rats for 24 or 48 hours to a 60-hertz magnetic field at an intensity of 0.01 millitesla (mT)--a low intensity within the levels that a person could encounter in the environment, for example near electric blankets and hair dryers. They treated some of the groups with one of three drugs, two that are known to decrease cellular free radicals and a third, an iron chelator, that has been implicated in the generation of free radicals.

They found significantly more DNA single- and double-strand breaks in the brain cells of undosed rats that were exposed longer, indicating that the effects were cumulative. In previous research, they had exposed rats to a 0.1-mT field for 2 hours with no detectable increase in DNA double-strand breaks. This suggests a complicated interaction between intensity and duration of exposure in the biologic effects of EMFs, and could explain negative results in other studies.

Among the dosed rats, all three drugs protected against EMF-induced DNA damage. The team therefore proposes that EMF-induced effects arise through a two-stage process. Exposure first upsets iron homeostasis in certain cells, releasing free iron into the cytoplasm and nucleus. This leads to the generation of hydroxy radicals that damage DNA, lipids, and proteins. Lipid damage in the cellular membrane then leads to calcium leakage from internal sites in the cell, triggering the second step: an increase in the synthesis of the free radical nitric oxide. Nitric oxide can also cause more iron-mediated free radicals to be generated.

At that point, say Lai and Singh, if antioxidation processes fail, the cell will undergo necrosis or apoptosis. Thus, the outcome depends on the interaction of a variety of factors, including the preexisting oxidative status of the cell and the parameters of the exposure. The pair speculate that, considering the role iron seems to play in the process, iron-rich human brain tissues such as glial cells, neurons, and myelin may be more susceptible to EMF-induced damage.