The temperature profile showed the expected decline over the evening but this was noticeably reversed at the times the cell phone was operating (Figures 7.4, 7.5).
The use of the cellular phone produced a significant rise (mean increase of 0.1
·c)
in aural temperature in the ear to which the phone was attached. Theopposite ear was also significantly warmer (mean increase 0.3 "C) when the phone was transmitting which suggested the temperature rise may not be simply local.
It was not possible in the present study, to determine whether the rise in temperature in the right (phone) ear was caused by conduction from heating due to the electrical internal resistance of the cell phone or as a consequence of the EMF it produced. A better design may have been to place something
between the subject and the phone, such as a leather case as Koivisto (2001) had done.
In the left ear, the temperature rise was less likely to be due to conduction. If it was caused by the RF field acting on the probe then that field would have had to pass right through the brain to get to the probe in the left auditory canal. This is contrary to the generally held stance that RF fields do not penetrate any depth. Although Bernardi et al.(2000) reported temperature increases in the brain in a model head exposed to different cellular phones.
Subsequent research has suggested that aural temperature may be effected by by the temperature of venous blood returning from the scalp and face (Jessen, 2001). If so, the readings may not accurately reflect core temperature but may be effected by localised heating produced by the phone heating up surface tissue.
Surveys and anecdotal reports have suggested heating of the tissues
surrounding a cellular phone in use. In 1998, Hansson-Mild described a dose
dependent increase in heat felt in and behind the ear during cell phone use. No laboratory studies have apparently been published on the effects of cellular phone frequencies on aural temperature in humans. However, Paredi et al.
(2001) reported a significant increase (2.3 degrees Celsius) in the skin temperature in the nostril and parietal regions on the side a GSM was
operating. This was higher than the 0.3 OC found in the present study, which is to be expected as their exposure time was 30 minutes, double that of the present study. Paredi et al. found no temperature difference in the non-phone ear, whereas the present study found a significant increase in temperature, with a mean increase of 0.3 OC. Conversely, the results do not support those of Koivisto (2001) who failed to find an increase in skin temperature. However, in that study the phone used was in a leather case to reduce heat transfer and had the speaker removed and discontinuous transmission inactivated. The rise in temperature found in the present study could be due to heating as a
consequence of electrical resistance or it may be hypothesised that it could be in some way initiated by the discontinuous transmission normally present in a
GSM phone. The Koivisto study may not have found a rise in temperature
because this feature, normally present in a cellular phone, was deactivated. The temperature difference in the phone-ear was commensurate with that reported by Bernardi et al. (2000) who found a maximum of 0.08-0.19 oc in the ear of a model head exposed to several models of cellular phone. However, the temperature increase in the non-phone ear was twice as large as predicted by the Bernardi modelling. The largest temperature difference they found was in the ear. They concluded that the rise was way below that required to
produce thermal damage. However, a lack of thermal damage does not equate with a lack of biological effects.
The difference between exposure and control sessions could also be due to the
RF interfering with the thermoscan. However, in practice trials the thermoscan beeped if it was encountering interference from the phone. Trials indicated the readings were accurate if it wasn't beeping. It didn't beep at any stage when on the non-phone side.
When the phone was not transmitting the phone ear was still significantly
warmer than the non-phone ear but the actual difference was only 0.1
oc,
which is the accuracy level of the thermoscan. This increase was not due to the difference between the thermal insulation properties of the cell phone
compared to the placebo cover used on the other ear as the difference in temperature between ears was not present in the first control session. It only occurred following the first exposure to the cell phone transmission. Thus it
was produced by the cell phone transmission. This could indicate a carry over
in heating from the exposure sessions into the subsequent control sessions which could conceivably affect the other parameters tested if effects found were due to a heating effect. It may also be why the mean difference was higher in the non-phone ear. This could suggest the time between the exposure
session and the following control (30 minutes) may have been too short.
However, the mean temperature in the three control sessions followed the expected steady decline over the course of the evening. If there was a carry over into the following control session it would be expected that this decrease would not occur.
The findings of the present study quantify the increase in aural temperature consequent to a fairly normal, extended cellular phone conversation. It should be noted that, although the increases were statistically significant the actual amount of the rise was less than the normal physiological change in
temperature during an evening. Both ears showed a steady decline of 0.4
·c
over the two and a half hours of the experiment. By contrast, the rise in the left ear was 0.1 ·