few studies have been conducted in which potential cancer risks have been evaluated using genetically engineered models in which animals demonstrate increased sensitivity to carcinogenesis. The results of such studies could be essential to assessing possible risks of RF exposure in susceptible subpopulations, including individuals with underlying disease, those with genetic alterations that predispose them to oncogenesis, and prior or simultaneous exposure to other carcinogenic or potentially carcinogenic agents. The use of genetically engineered animals may also increase the sensitivity of laboratory studies to detect weak effects, and may be particularly suitable to evaluate the possible interactions between RF fields and other agents in disease causation.

The possible risks of neoplasia (the process of tumor formation) associated with RF exposure in individuals that have been (or are currently) exposed to other environmental or occupational carcinogens may also be investigated experimentally through the use of multi-stage (“initiation-promotion” or co-carcinogenesis) cancer models (Adey et al. 1999, 2000; Zook and Simmens 2001; Bartsch et al. 2002; Anane et al. 2003; Yu et al. 2006). Several such studies have been performed in animal models for cancer in several different organ sites, with uniformly negative results. However, the overall database for RF fields and cancer would be strengthened considerably by additional studies using multi-stage model systems for cancer in tissues (such as the brain) that have been hypothesized to be targets of RF action. Currently the value of such studies is often limited by the lack of suitable animal models that demonstrate the (a) organ specificity and (b) background tumor responses to make them suitable for use in hazard identification.


As noted at the workshop (Lai 2007, Vijayalaxmi 2007), substantial effort has been put forth to evaluate the possible genetic toxicity of RF fields, both in vivo and in vitro. Although a number of positive outcomes have been reported, efforts to replicate the results of positive studies have generally failed. Furthermore, the majority of experimental studies designed to identify genotoxic effects of exposure to RF fields have not found significant mutagenic or clastogenic activity in any model system that is in broad general use for genetic toxicology evaluations. On this basis, most investigators in the field agree that no compelling body of evidence exists to support the hypothesis that RF fields are genotoxic. The committee concludes that additional studies using standard genetic toxicology test systems are unlikely to increase our understanding of the possible risks associated with RF exposure at this time.

That said, additional genetic toxicology studies may be warranted should evidence of oncogenicity be identified in any of the ongoing chronic

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