EMF Health-effects Research

Iridium exposure increase c-fos expression in the mouse brain.

Morrissey JJ, Rauey S, Heasley E, Rathinavelua P, Dauphinee M, Fallon JH

Neuroscience 92:1539:1546 1999


Motorola-funded

Contractors: Goodwin Institute for Cancer Research, Plantation, Florida; and Department of Anatomy and Neurobiology, University of California at Irving, California.


The study examined expression levels of stress response and cancer-associated genes in the brains of mice exposed to one hour of RF (1.6GHz modulated Iridium) signals. No effects were observed at low levels of exposure.

An increase in c-fos mRNA levels in the brain in a pattern most consistent with thermal stress was observed only at SAR levels equal to or greater than six times the maximum peak dose and 30 times the maximum whole body average dose from an actual wireless telephone.

No change in the expression of the EGF receptor of NSCL-1 genes were observed at any dose level.


Originally published abstract.

With the rapid development of wireless communication technology over the last 20 years, there has been some public concern over possible health effects of long-term, low-level radiofrequency exposure from cellular telephones.

As an initial step in compiling a database for risk analysis by government agencies, the effects of 1-h exposure of mice to a 1.6-GHz radiofrequency signal, given as either a continuous wave or pulse modulated at 11 Hz with a duty cycle of 4:1 and a pulse duration of 9.2 ms Iridium), on c-fos gene expression in the brain was investigated. The Iridium signal is the operating frequency for a ground-to-satellite-to-ground cellular communications web which has recently become fully operational, and was named as such due to the original designed employment of the same number of low orbiting satellites as there are electrons orbiting the nucleus of an iridium atom.

The expression of c-fos was not significantly elevated in the brains of mice until exposure levels exceeded six times the peak dose and 30 times the whole body average dose as maximal cellular telephone exposure limits in humans. Higher level exposure using either continuous wave (analog) or Ieisium signals elevated c-fos to a similar extent, suggesting no obvious pulsed modulation-specific effects.

The pattern of c-fos elevation in limbic cortex and subcortex areas at higher exposure levels is most consistent with a stress response due to thermal perception coupled with restraint and/or neuron activity near thermoregulatory regions, and not consistent with any direct interaction of Iridium energy with brain tissue.

Additional Web Notes

Note to lay readers: This c-fos gene is an oncogene or cancer-causing gene. The expression of this gene is therefore of concern -- but the authors consider this to be evident "only at levels with likely result from brain heating". S.F. See also


Comment No 1: Comments on Morrissey et al., 1999

In this Motorola funded study, mice were exposed to IRIDIUM phone radiation at different intensities (SARs) for 1 hour. c-fos, a proto-oncogene, expression was determined in the brain of the animals. The conclusions, as stated in the abstract, are:

  • The expression of c-fos was not significantly elevated in the brains of mice until exposure levels exceeded six times the peak dose and 30 times the whole body average dose as maximal cellular telephone exposure limits in humans.

  • The pattern of c-fos elevation in limbic cortex and subcortex areas at higher exposure levels is most consistent with a stress response due to thermal perception coupled with restraint and/or neuron activity near thermoregulatory regions, and not consistent with any direct interaction of IRIDIUM energy with brain tissue.
Comment No 2:

Five intensities were studied that corresponded to SARs (at the frontal part of the brain) of 0.23, 0.48, 1.19, 2.99, and 7.79 W/kg. Significant increase in c-fos expression was observed in various regions of the brain at 2.99 and 7.79 W/kg. (A t-test was used in data analysis, however, ANOVA followed by a multiple range test should be used in this experiment.) It is more logical to conclude from these data that increase in c-fos expression can occur between SARs of 1.19 and 2.29 W/kg.

Even though the responses at 1.19 W/kg were not statistically significant, they were all higher than those of the sham-exposed controls. Therefore, one would expect that the threshold of effect should occur at an SAR not very much higher than 1.19 W/kg.

Even if 2.29 W/kg is taken as the level when effects occur, it is not 6 times the guideline level of partial body exposure (i.e., 1.6 W/kg).

This argument that 'if an effect is only observed at a level higher than the recommended guideline, therefore the exposure is safe" is also interesting. The RFR guideline is set at 10 times lower than the level when an effect is observed and the guideline is based on experimental results. If one observes an effect in an experiment at 2.29 W/kg, should one recommend a safety level of exposure of 0.229 W/kg?

Comment No 3:

The 'limbic cortex and subcortex areas' that showed an increase in c-fos expression in the Morrisey et al study are: anterior cingulate cortex, prepiriform cortex, medial preoptic hypothalamus, ventromedial hypothalamus, and dorsal hypothalamus. Some of these areas are involved in thermal regulation. But, the most consistent functions involving c-fos expression in these areas are sexual behavior, reward, and psychological stress.

The authors mentioned a paper by Mickley et al (Disruption of a putative working memory task and selective expression of brain c-fos following microwave induced hyperthermia, Physiol. Behav. 55, 1029-1038, 1994). They stated that "... Mickley et al. showed that c-fos expression in the brain of rats could be elevated in a pattern similar to that seen in this study by deliberate thermal exposure to 2.45-GHz microwaves."

But, there are two major differences in the patterns of brain c-fos expression reported in these two studies. Mickley et al. reported a significant effect in the thalamus, whereas no effect was observed in thalamic areas in the Morrissey et al. study. Mickley et al. also reported no c-fos induction in the ventromedial and dorsomedial hypothalamus after body heating of the rat with microwaves that increased body temperature by 2 degrees C, whereas c-fos induction was observed in these brain areas in the Morrissey et al. study.

There is another interesting finding by Morrissey et al. They found that c-fos induction was localized only to neurons and not in glial cells. (They actually stated that "...since the majority of human brain tumors are glial in origin and the cell types which respond to Iridium exposure in this study appear to be neurons, even high-dose Iridium exposure would not, from the findings of this study, appear to affect cell types which might later develop into a brain malignancy.")

However, there is a study by Dragunow et al. on heat induced c-fos in the brain of rats (Heat shock induced c-fos protein-like immunoreactivity in glial cells in adult rat brain, Experimental Neurology 106:105-109, 1989). These researchers concluded that "...heat shocking of anesthetized rats lead to a massive increase in c-fos protein-like immunoreactivity (FOS-IR) in glial-like cells in white matter and gray matter regions of the brain.

Neuronal FOS-IR was not detectibly altered by heat shock. This induction of FOS-IR was present 1 hr, but not 10 min or 24 h, after heat shock. These results demonstrate that c-fos protein is expressed in glial cells following thermal stress."

Therefore, the interpretation of Morrissey et al that 'their observation of Iridium-induced c-fos express in the mouse brain is caused by thermal stress' should be reconsidered.




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