... Special care was taken to repeat the study by Tillmann et al. [4] as
accurately as possible. Male C3H/HeNCrl (n = 43) and female C57Bl/6N (n = 290)
mice were purchased in a staggered design from Charles River Germany, Sulzfeld,
Germany, at an age of 8 to 9 weeks. After acclimatization, at the age of 12
weeks (females), the males and 128 females were mated for one week (ratio 3
females: 1 male) in two rounds, thus a total of 256 potentially pregnant
females were obtained. They were distributed to the 128 cages of the exposure
devices, two animals per cage. Exposure or sham-exposure of the pregnant
females thus started at day 6 p.c. (post conception) ...
The exposure devices consisted of eight radial waveguides with 16 cages each, arranged in stacks of two and connected to power amplifiers and RF-generators. Details have been published earlier [5]. Extensive numerical calculations of the field distributions and the corresponding SAR values revealed unavoidable substantial variations for animals in different positions and within animals (local maximum SAR values) which could be as much as 3 to 5 times higher than the whole-body SAR. Two waveguides per exposure group with 16 cages each (32 cages in total, 96 animals) were one out of four groups with the following nominal whole-body SAR levels: sham-exposed (0 W/kg), 0.04 W/kg (low), 0.4 W/kg (moderate) and 2 W/kg (high) for a reference configuration of three mice (body weight 20 g each) per cage, with a standard deviation for this configuration of around 36% ...
As compared to the sham-exposed control mice, numbers of animals with bronchiolo-alveolar adenomas (lungs) were doubled at low and moderate SAR levels, and hepatocellular carcinomas were nearly or more than doubled at low, moderate, and high SAR levels, respectively. The numbers of multiple tumors were found to be significantly elevated at 0.04 W/kg (bronchiolo-alveolar adenomas, Table S1). The numbers of animals with lymphomas were increased 2.5 fold at moderate SAR levels (Fig. 1, Table 1). No increased tumor numbers were found in the brains, kidneys, and spleens of the exposed animals. Here the tumor rates were well below 10%. As expected, survival times in all ENU-treated animals were much lower than in cage controls, but not affected by exposure (Fig. S1). Body weights of (sham-) exposed animals were only slightly different from untreated, unexposed cage-control mice (Fig. S2).
The fact that both studies found basically the same tumor-promoting effects at levels below the accepted (and in most countries legally defined) exposure limits for humans is worrying. Although animal experiments are generally not easily transferable to the situation in humans, the findings are a very clear indication that--in principal--tumor-promoting effects of life-long RF-EMF exposure may occur at levels supposedly too low to cause thermal effects. The basis for defining safety guidelines regarding RF-EMF exposure by mobile phones and other RF-EMF emitting devices relies on the assumption that increases in temperature above a certain threshold are the only way how exposure can cause damage (thermal effects). These are clearly prevented by the exposure limits. However, the RF-EMF energy absorbed by the tissues or organisms, respectively, is converted to thermal energy regardless the exposure dose. As a consequence, this thermal energy influences to some extent the energy balance of tissue and the entire organism. It was shown that RF-EMF exposure at low levels (0.08 W/kg) causes increased body weights in hamsters which indicates a shift in metabolism of food [14]. Other experiments in hamsters have shown that the consumption of food and the production of CO2 is decreased by RF-EMF exposure, albeit only at relatively high SAR-levels [15]. It is therefore plausible to assume that RF-EMF energy, when absorbed and converted into thermal energy, influences metabolism and energy balance to some extent which may play a role for the observed tumor-promoting effects.
In this context it is important that the carcinogen ENU was administered to the pregnant mice at day 14 of pregnancy. We do not know at which time periods after the treatment with the carcinogen the tumor-promoting effects occurred. Early studies [16] clearly demonstrated that the prenatal time point of ENU-administration is crucial for the development of tumors in the adult. Since the carcinogen was administered to the pregnant females while being already exposed to RF-EMF, it is possible that immediately after ENU-treatment the promoting effects happened. Alternatively, they occurred during the later stages of development. Another possibility why tumor-promoting effects were seen in both studies is that the uptake of the carcinogen by the fetuses was higher in the exposed animals due to elevated metabolism. Studies addressing this question are clearly needed.
The results of our study also stress the importance of exposure conditions in replication studies which are unfortunately often slightly or substantially different from the original studies. For example, Repacholi and co-workers have shown tumor-promoting effects in transgenic mice prone for developing lymphomas [18]. Two replication studies did not confirm these effects [19] and [20]. Both replication studies, however, deviated from the original study in several ways. Not only were the exposure times different, but also were the mice in the replication studies exposed while restrained (in tubes), whereas in the original study the mice were non-restrained. While restrained animals allow exposure at comparably low SAR variations, the physiological and metabolic situations are fundamentally different in comparison to freely moving animals [21]. In fact, the unavoidable SAR variations in non-restrained, freely moving animals may turn out to be of key importance for the understanding of tumor-promoting effects.
The exposure devices consisted of eight radial waveguides with 16 cages each, arranged in stacks of two and connected to power amplifiers and RF-generators. Details have been published earlier [5]. Extensive numerical calculations of the field distributions and the corresponding SAR values revealed unavoidable substantial variations for animals in different positions and within animals (local maximum SAR values) which could be as much as 3 to 5 times higher than the whole-body SAR. Two waveguides per exposure group with 16 cages each (32 cages in total, 96 animals) were one out of four groups with the following nominal whole-body SAR levels: sham-exposed (0 W/kg), 0.04 W/kg (low), 0.4 W/kg (moderate) and 2 W/kg (high) for a reference configuration of three mice (body weight 20 g each) per cage, with a standard deviation for this configuration of around 36% ...
As compared to the sham-exposed control mice, numbers of animals with bronchiolo-alveolar adenomas (lungs) were doubled at low and moderate SAR levels, and hepatocellular carcinomas were nearly or more than doubled at low, moderate, and high SAR levels, respectively. The numbers of multiple tumors were found to be significantly elevated at 0.04 W/kg (bronchiolo-alveolar adenomas, Table S1). The numbers of animals with lymphomas were increased 2.5 fold at moderate SAR levels (Fig. 1, Table 1). No increased tumor numbers were found in the brains, kidneys, and spleens of the exposed animals. Here the tumor rates were well below 10%. As expected, survival times in all ENU-treated animals were much lower than in cage controls, but not affected by exposure (Fig. S1). Body weights of (sham-) exposed animals were only slightly different from untreated, unexposed cage-control mice (Fig. S2).
The fact that both studies found basically the same tumor-promoting effects at levels below the accepted (and in most countries legally defined) exposure limits for humans is worrying. Although animal experiments are generally not easily transferable to the situation in humans, the findings are a very clear indication that--in principal--tumor-promoting effects of life-long RF-EMF exposure may occur at levels supposedly too low to cause thermal effects. The basis for defining safety guidelines regarding RF-EMF exposure by mobile phones and other RF-EMF emitting devices relies on the assumption that increases in temperature above a certain threshold are the only way how exposure can cause damage (thermal effects). These are clearly prevented by the exposure limits. However, the RF-EMF energy absorbed by the tissues or organisms, respectively, is converted to thermal energy regardless the exposure dose. As a consequence, this thermal energy influences to some extent the energy balance of tissue and the entire organism. It was shown that RF-EMF exposure at low levels (0.08 W/kg) causes increased body weights in hamsters which indicates a shift in metabolism of food [14]. Other experiments in hamsters have shown that the consumption of food and the production of CO2 is decreased by RF-EMF exposure, albeit only at relatively high SAR-levels [15]. It is therefore plausible to assume that RF-EMF energy, when absorbed and converted into thermal energy, influences metabolism and energy balance to some extent which may play a role for the observed tumor-promoting effects.
In this context it is important that the carcinogen ENU was administered to the pregnant mice at day 14 of pregnancy. We do not know at which time periods after the treatment with the carcinogen the tumor-promoting effects occurred. Early studies [16] clearly demonstrated that the prenatal time point of ENU-administration is crucial for the development of tumors in the adult. Since the carcinogen was administered to the pregnant females while being already exposed to RF-EMF, it is possible that immediately after ENU-treatment the promoting effects happened. Alternatively, they occurred during the later stages of development. Another possibility why tumor-promoting effects were seen in both studies is that the uptake of the carcinogen by the fetuses was higher in the exposed animals due to elevated metabolism. Studies addressing this question are clearly needed.
The results of our study also stress the importance of exposure conditions in replication studies which are unfortunately often slightly or substantially different from the original studies. For example, Repacholi and co-workers have shown tumor-promoting effects in transgenic mice prone for developing lymphomas [18]. Two replication studies did not confirm these effects [19] and [20]. Both replication studies, however, deviated from the original study in several ways. Not only were the exposure times different, but also were the mice in the replication studies exposed while restrained (in tubes), whereas in the original study the mice were non-restrained. While restrained animals allow exposure at comparably low SAR variations, the physiological and metabolic situations are fundamentally different in comparison to freely moving animals [21]. In fact, the unavoidable SAR variations in non-restrained, freely moving animals may turn out to be of key importance for the understanding of tumor-promoting effects.
--
Joel M. Moskowitz, Ph.D., Director
Center for Family and Community Health
School of Public Health
University of California, Berkeley
Posted by Katie Singer
www.electronicsilentspring.com
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