Previous research has suggested that exposure to radiofrequency electromagnetic fields increases electroencephalogram spectral power in non-rapid eye movement sleep. Other sleep parameters have also been affected following exposure. We examined whether aspects of sleep architecture show sensitivity to electromagnetic fields emitted by digital mobile phone handsets. Fifty participants were exposed to electromagnetic fields for 30 min prior to sleep. Results showed a decrease in rapid eye movement sleep latency and increased electroencephalogram spectral power in the 11.5–12.25 Hz frequency range during the initial part of sleep following exposure. These results are evidence that mobile phone exposure prior to sleep may promote rapid eye movement sleep and modify the sleep electroencephalogram in the first non-rapid eye movement sleep period.
1 January 2002 in International Journal of Radiation Biology
To compare the findings of the main studies that have examined the effects of GSM mobile phone radiofrequency emissions on human brain activity and sleep variables. Fourteen published studies reporting on human brain electrical activity measurements during and/or after such radiofrequency emissions were identified and compared. Although, in general, outcomes have been inconsistent and comparison between individual studies is difficult, enhanced electroencephalogram alpha-band power has been noted in several of the studies, a phenomenon also observed in some animal studies. Performance decrements observed in some recent extremely low frequency studies are consistent with enhanced alpha-band power, highlighting the possible role of extremely low frequency fields associated with battery current in mobile phone handsets. However, more complex cognitive tasks appear to show improved performance in relation to mobile phone exposure. Significant cognitive effects have been reported using both modulated and unmodulated radiofrequency carriers. The possibility of putative effects being due to extremely low frequency demodulation is therefore unlikely. There are no obvious associations between the site of exposure and regions of the brain from which effects are reported or implied. Lastly, radiofrequency effects have been reported to occur both during exposure and up to 1 h or so after cessation of exposure.
Purpose: To test whether exposure to the emissions from a digital mobile phone handset prior to sleep alters the secretion of melatonin. Materials and methods: In a double-blind cross-over design, 55 adult volunteers were both actively exposed or sham-exposed (in random order on successive Sunday nights) to mobile phone emissions for 30 min (0.25 W average power). Urine collection occurred immediately prior to retiring to bed and on rising the next morning. Melatonin output was estimated from principal metabolite concentrations (6-sulphatoxymelatonin (aMT6s) via radioimmunoassay), urine volumes and creatinine concentrations. Results: Total melatonin metabolite output (concentration×urine volume) was unchanged between the two exposure conditions (active 14.1±1.1 μg; sham 14.6±1.3 μg). The pre- and post-bedtime outputs considered separately were also not significantly different, although the pre-bedtime value was less for active versus sham exposure. When melatonin metabolite output was estimated from the ratio of aMT6s to creatinine concentrations, the pre-bedtime value was significantly less (p = 0.037) for active compared to sham. Examination of individual responses is suggestive of a small group of ‘responders’. Conclusions: Total nighttime melatonin output is unchanged by mobile phone handset emissions, but there could be an effect on melatonin onset time.