Findings from prior studies of possible health and physiological effects from mobile phone use have been inconsistent. Exposure periods in provocation studies have been rather short and personal characteristics of the participants poorly defined. We studied the effect of radiofrequency field (RF) on self-reported symptoms and detection of fields after a prolonged exposure time and with a well defined study group including subjects reporting symptoms attributed to mobile phone use. The design was a double blind, cross-over provocation study testing a 3-h long GSM handset exposure versus sham. The study group was 71 subjects age 18-45, including 38 subjects reporting headache or vertigo in relation to mobile phone use (symptom group) and 33 non-symptomatic subjects. Symptoms were scored on a 7-point Likert scale before, after 1(1/2) and 2(3/4) h of exposure. Subjects reported their belief of actual exposure status. The results showed that headache was more commonly reported after RF exposure than sham, mainly due to an increase in the non-symptom group. Neither group could detect RF exposure better than by chance. A belief that the RF exposure had been active was associated with skin symptoms. The higher prevalence of headache in the non-symptom group towards the end of RF exposure justifies further investigation of possible physiological correlates. The current study indicates a need to better characterize study participants in mobile phone exposure studies and differences between symptom and non-symptom groups.
Several studies show increases in activity for certain frequency bands (10-14 Hz) and visually scored parameters during sleep after exposure to radiofrequency electromagnetic fields. A shortened REM latency has also been reported. We investigated the effects of a double-blind radiofrequency exposure (884 MHz, GSM signaling standard including non-DTX and DTX mode, time-averaged 10 g psSAR of 1.4 W/kg) on self-evaluated sleepiness and objective EEG measures during sleep. Forty-eight subjects (mean age 28 years) underwent 3 h of controlled exposure (7:30-10:30 PM; active or sham) prior to sleep, followed by a full-night polysomnographic recording in a sleep laboratory. The results demonstrated that following exposure, time in Stages 3 and 4 sleep (SWS, slow-wave sleep) decreased by 9.5 min (12%) out of a total of 78.6 min, and time in Stage 2 sleep increased by 8.3 min (4%) out of a total of 196.3 min compared to sham. The latency to Stage 3 sleep was also prolonged by 4.8 min after exposure. Power density analysis indicated an enhanced activation in the frequency ranges 0.5-1.5 and 5.75-10.5 Hz during the first 30 min of Stage 2 sleep, with 7.5-11.75 Hz being elevated within the first hour of Stage 2 sleep, and bands 4.75-8.25 Hz elevated during the second hour of Stage 2 sleep. No pronounced power changes were observed in SWS or for the third hour of scored Stage 2 sleep. No differences were found between controls and subjects with prior complaints of mobile phone-related symptoms. The results confirm previous findings that RF exposure increased the EEG alpha range in the sleep EEG, and indicated moderate impairment of SWS. Furthermore, reported differences in sensitivity to mobile phone use were not reflected in sleep parameters.
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