Ave studies on laboratory animals revealed an increased cancer risk?
In the past, a number of studies on laboratory animals looked at the possibility of radio frequency (RF) energy causing cancer, and most found no causal link. One exception was a 1997 study that exposed a strain of mice prone to lymphoma to radio frequency signals similar to those transmitted by GSM-type handsets every day over 18 months. The researchers reported more new lymphoma cases among exposed mice.
Other researchers who carried out a similar experiment in 2002 found no significant effect on the number of new lymphoma cases in mice. Other studies had tested whether exposure to radio frequency fields alone could trigger any type of cancer in normal or genetically predisposed animals. Other studies have investigated whether exposure to RF fields could enhance the development of tumours triggered by cancer-causing chemicals, X-rays or UV radiation. No significant increase in the number of tumour cases has been reported among exposed laboratory animals, but most of these studies used relatively low exposure.
In the last few years, a number of lifetime and long-term exposure studies were performed on laboratory animals by exposing them to 900 MHz GSM signals and other higher frequency signals at higher exposure levels than previous studies. All studies concluded that there was no effect of radiofrequency fields on the risk of developing tumours even at the higher exposures. One study found a reduced survival rate in exposed animals, but this finding remains unexplained.
What was already known on this subject?
The possible carcinogenicity of RF field exposure has been investigated in a number of experimental systems, with essentially negative results. The positive finding of increased lymphoma incidence in the lymphoma-prone transgenic Eµ-Pim1 mouse strain (Repacholi et al. 1997) is an interesting exception. The previous opinion of 2007 discussed a study (Utteridge et al. 2002) that failed to confirm the results of the Repacholi study, as well as several other studies that had evaluated carcinogenicity of RF fields in a variety of experimental models. Several studies had tested carcinogenicity of RF fields alone in normal or genetically predisposed animals, and several other studies had tested possible co-carcinogenicity together with known chemical or physical carcinogens. No statistically significant (p<0.05) increase of tumour incidence was found in any of the studies reviewed. Questions that remained were relevance of the experimental models to human carcinogenesis and the relatively low exposure levels used in most of the studies. What has been achieved since then?
A number of lifetime and chronic exposure studies have been performed on laboratory animals. The study reported by Oberto et al. (2007) was another replication and an extension of the Repacholi et al. (1997) study with Eµ-Pim1 transgenic mice exposed to a GSM-type signal. There were several methodological improvements compared to the original study by Repacholi et al. (1997) including use of several exposure levels (0.5, 1.4 or 4.0 W kg/kg), well-defined dosimetry and more uniform exposure (achieved by restraining the animals) and extensive histopathology of all animals. Compared to the sham-exposed controls, survival was reduced in the animals exposed to RF fields. The intergroup differences were statistically significant (p<0.05) in the male animals, but there was no trend with increasing exposure level (lowest survival at 0.5 W/kg). No increase in lymphoma incidence was observed in the RF exposed groups. Concerning other neoplastic findings, Harderian gland adenomas were increased in male mice, with a significant dose-related trend (p<0.01). However, this trend was not supported by the findings on female animals, i.e. no tumours were observed in the highest exposure groups. For the statistical analysis, the cage control and the sham-exposed control groups were combined, which is not a valid procedure given the differences in body weight development and tumour incidence between these groups (these differences are most likely related to restraint of the sham-exposed animals). However, based on the data reported in the paper, a different analysis strategy (comparison to the sham- exposed group only) would not essentially change the conclusion that there was no effect of RF electromagnetic fields on tumours at any site. The reduced survival in the exposed animals is not thoroughly discussed by the authors; this finding remains unexplained and difficult to interpret without detailed information about the causes of death.
In another study with lymphoma-prone animals (Sommer et al. 2007), unrestrained AKR/J mice, 160 animals per group, were chronically sham-exposed or exposed to a generic UMTS test signal for 24 h/day, 7 days/week at a SAR of 0.4 W kg/kg. No effect from exposure to RF electromagnetic fields was seen on lymphoma incidence, survival time or severity of the disease.
Two studies evaluated carcinogenicity of both a GSM signal at 902 MHz and a DCS signal at 1,747 MHz in conventional laboratory animals including B6C3F1 mice (Tillmann et al. 2007) and Wistar rats (Smith et al. 2007). Three exposure levels from 0.4 to 4 W/kg (and sham exposure) were used. The study on mice (Tillman et al. 2007) produced no evidence that RF field exposure increased the incidence or severity of neoplastic or non- neoplastic lesions, or resulted in any other Interestingly however, the incidence of liver adenomas in males decreased with increasing exposure level, with a statistically significant (p<0.05) difference between the highest exposure and the sham exposed group. However, comparison with published tumour rates in untreated mice revealed that the observed tumour rates were within the range of historical control data. The study on rats (Smith et al. 2007) was a combined chronic toxicity and carcinogenicity study, and some of the animals (15 males and 15 females per group) were killed at 52 weeks from the start of the study. There were no significant differences in the incidence, multiplicity, latency or severity of neoplasms, or any other adverse responses to RF field exposure.
Saran et al. (2007) used Patched1 heterozygous knockout mice, an animal model in which exposure of newborn animals to ionizing radiation enhances development of brain tumours (medulloblastoma). Newborn Patched1 mice and their wild-type siblings were exposed to 900 MHz GSM-type radiation at 0.4 W/kg for 30 min twice a day for 5 days. No differences in survival were found between exposed and sham-exposed animals. Medulloblastomas (in 7 animals) and rhabdomyosarcomas (in 56 animals) were found in the Patched1 mice but not in the wild-type animals. The incidence of rhabdomyosarcoma was higher (68%, 36 animals) in the exposed group than in the sham-exposed group (51%, 20 animals), but this difference was not statistically significant (p>0.05). The incidences of medulloblastomas, other tumours or preneoplastic skin lesions did not differ between the exposed and sham-exposed groups.
Shirai et al. (2007) investigated possible promoting effect of 1.95 MHz RF fields (W- CDMA signal) on ethylnitrosourea (ENU)-induced brain tumours in Fischer 344 rats. The brain tumour incidences of both females and males tended to be higher in the two RF exposed groups (0.67 and 2 W/kg) than in the sham-exposed group, but no statistically significant (p<0.05) effects were reported. Moreover, an opposite trend (decreasing incidence with increasing exposure level) was observed in a previous similar study (Shirai et al. 2005), indicating that the trends observed are most likely incidental.
Hruby et al. (2008) treated 100 female Sprague-Dawley rats per group with 7,12- Dimethylbenz(a)anthracene (DMBA) to induce mammary tumours and then exposed the animals to 900 MHz GSM signals. The exposure groups included cage controls, sham- exposed controls and three exposure groups (0.4, 1.3 and 4.0 W/kg). The exposed and sham exposed animals were restrained during exposure. There were several statistically significant (p<0.05) differences between RF field-exposed groups and the sham-exposed group. All RF-exposed groups had significantly more palpable mammary gland tissue masses than the sham-exposed group, but there was no clear increase with increasing exposure level (no dose-response relationship). The incidence of malignant mammary tissue tumours was lowest in the sham-exposed group, and significantly increased in the high exposure group. However, the incidence of benign tumours was significantly lower in the three RF exposed groups than in the sham-exposed group. The number of animals with benign or malignant neoplasms was similar in the sham-exposed group and in the three RF-exposed groups. Given that the DMBA mammary tumour model is known to be prone to high variations in the results, the authors concluded that the differences between the groups were most likely incidental. Comparison with the results of the almost identical study of Yu et al. (2006) supports this conclusion: both studies reported similar development of mammary tumours in three groups, but lower rate of development (seen in the appearance of palpable tumours and/or reduced malignancy) in one group. Hruby et al. (2008) found the lowest rate of development in the sham- exposed group, while Yu et al. (2006) found it in the 0.44 W kg-1 groups. Both studies consistently reported highest incidence of tumours in the cage control group, which is most likely related to the different handling of the cage control animals (different stress level, differences in food intake).
Morales R. Karelis
CI 18089995
CAF
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