Cellular and sub-cellular effects of microwave radiation in the simple model nematode Caenorhabditis elegans

Principal Investigator: Dr David de Pomerai (School of Life and Environmental Sciences)

Other Investigators: Dr David W. Thomas

Start Date: April 2002
Expected Date of Completion:March 2005

Cost: £323,000 (GGIEMR share £126000)

Expertise: Our groups combine expertise in assessing environmental stress using nematode worms as biosensors (DdeP) with expertise in the modelling of microwave fields and design of exposure systems (DWT). We will use expertise available at NPL for precisely measuring the field strength and temperature within our exposure system.

Approach: We have found that prolonged exposure to low-intensity microwaves switches on the so-called stress response in nematodes. This is a general protective cellular response, which is also activated by heat and toxic chemicals; it provides a measure of the stress experienced by the test worms. We will expand several aspects of this work during the MTHR-funded project. First, we will determine which of the nematode’s 19000 genes are switched on or off during microwave exposure, and will carefully compare this pattern of gene-expression changes with that caused by mild heating. Second, we will make use of the worm’s excellent genetics to unravel the genetic pathway through which microwaves switch on stress-response genes. Third, we will use temperature-sensitive mutant worm strains to ask whether certain subcellular structures are more sensitive to microwaves. We will also examine this question by determining how microwaves interact with the worms across a range of different frequencies. Detailed modelling and field measurements of the exposure system will be used to rule out the possibility that a stress response might be activated simply by microwave heating. A wide variety of control strategies will be used to eliminate other possible artefacts.

Potential Difficulties: It is important to confirm that the stress response seen in microwave-exposed worms is not simply due to heating or other artefacts (see end of 2). Once this has been done, it will be essential to confirm our findings independently in other laboratories, and to extend this work from nematode worms to vertebrate cells. Difficulties that may be encountered include very localised heating effects (not showing up as an overall temperature change) and strategies for confirming which genes are switched on or off by microwaves. The fact that these worms are very small means that stress responses are averaged over very large numbers of individuals.

Nevertheless, there are issues of reproducibility between runs; the magnitude of response observed varies considerably from one run to another. Careful definition of all conditions should help to reduce this.

Importance: Potentially, this work may provide a genuine, robust and reproducible example of a nonthermal effect of microwaves in a biological system, i.e. an effect that cannot be explained away in terms of simple heating. If so, the exact mechanism of this effect and its generality in other organisms will become key questions for future work to address. Currently, human limits for exposure to microwaves are set such that there will be no measurable increase in bulk tissue temperature. If non-thermal microwave effects can be confirmed at lower exposure levels, these current exposure limits may require re-evaluation. However, possible health hazards should not be exaggerated. Stress responses confer general protection within cells, such that mild to moderate stresses may actually prove beneficial rather than harmful, even though damage would be caused at higher exposure levels. These distinctions still remain to be clarified.