To study whether higher irradiation doses and/or pulse modulation can cause measurable heat-shock protein reporter gene induction in Caenorhabditis elegans (nematodes) in the absence of heating artefacts, transgenic worms were exposed to 1.8 GHz electromagnetic fields at SAR values of 1.8 W/kg for 2.5 h at 25°C.
|Chamber||The fully automated exposure system consisted of two identical chambers for RF or sham exposure, mounted in the same incubator, and enabled well-controlled exposures of cells in monolayers or in suspension [Schuderer et al., 2004].|
|Setup||The Petri dishes were exposed in H-polarization. The induced E-fields had a pronounced polarization parallel to the bottom and in the direction of the waveguide axis. The induced H-fields were orthogonal to the induced E-fields, both of which were dominantly parallel to the bottom of the dish.|
|Sham exposure||A sham exposure was conducted.|
GSM Talk signal characterized by a random change between the DTX and non-DTX or GSM Basic modes. The distribution in time was exponential with a mean duration of 10.8 s for non-DTX and 5.6 s for DTX. The dominant modulation components of this signal are 2, 8, 217, 1733 Hz, and higher harmonics [Tillmann et al., 2007].
For both continuous wave and pulsed radiofrequency exposures, there was no indication that radiofrequency exposure could induce reporter gene expression above sham exposure levels. Thus, at much higher induced radiofrequency field strength (compared to previous studies and close to the maximum permitted exposure from a mobile phone handset), this particular nematode heat-shock protein gene is not up-regulated.