 Does long-term exposure to mobile telephones cause brain damage?
Mobile telephone use is increasing rapidly and, although these devices are held close to the head and the brain is exposed to relatively high specific absorption rates (SAR's) compared to the rest of the body, there is still some doubt as to whether mobile communication systems damage the central nervous system.
The IMVS study
Disruption of the blood-brain barrier (BBB) with a resultant increase in vascular permeability has commonly been used to determine whether mobile-telephone type radiation damages the brain. The BBB closely regulates the composition of the extracellular fluid bathing neurons by effectively controlling the movement of fluid, proteins, electrolytes and other substances between blood vessels and the neural parenchyma. The BBB is a dynamic blood-brain interface and the permeability properties of the BBB are those of the capillary endothelium. Cerebral capillary endothelium differs from endothelia elsewhere by possessing tight junctions between endothelial cells and few micropinocytotic vesicles and this protective endothelial barrier is abetted by the inductive influence of astrocytic end-feet that almost completely invest cerebral capillaries.
All previous mobile phone studies have examined short-term (5 minutes to 4 hours) exposure of the brain but, since mobile phones are used frequently over long periods of time, we wished to study the effect of prolonged exposure on BBB permeability.
In a purpose-designed exposure module with well-defined dosimetry, mice were placed in tubes arranged radially around the radiation source. All treated mice received a 60 minute far-field, whole body exposure to radiofrequency fields with similar pulsing and modulation characteristics to those used for mobile telecommunicationsons (900 MHz fields modulated at a pulse repetition frequency of 217Hz and a pulse width of 0.6ms). Mice were exposed on 5 consecutive days per week for 2 years at SAR's of 0.25, 1.0, 2.0 and 4.0 W/kg, the latter the internationally accepted maximum safe level of average whole body SAR. Control mice were either sham-exposed or permitted free movement in a cage to evaluate any stress-related effects.
At the end of the 104 week exposure period, brains were perfusion-fixed for optimal preservation and 3 coronal slices were collected for pathological examination.
Any increase in vascular permeability was detected immunohistochemically using a monoclonal antibody to endogenous albumin. The efficacy of albumin as a vascular tracer was confirmed with a positive control group exposed to a clostridial toxin known to markedly increase vascular permeability in the brain.
Results
In all exposed and control groups, albumin extravasation (shown in Figure 1) was minimal and was deemed insignificant as a maximum of 3 capillaries or venules in a given brain showed leakage from the vast array of blood vessels present in 3 coronal brain sections. There was no dose-response effect.
 
Figure 1
Conclusion
These results suggest that prolonged exposure of mice to mobile telephone-type radiofrequency fields produces negligible brain damage as assessed by disruption to BBB integrity at the light microscope level using endogenous albumin as a vascular tracer. Moreover, any increase in BBB permeability caused by these non-thermal SAR levels is probably subtle and reversible, with prompt restitution of BBB integrity and rapid oedema resolution.
This study was approved by the IMVS Animal Ethics Committee.
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