Abstract
The evidence for cellular effects of exposure to power frequency electromagnetic fields (EMFs) has been considered in terms of the four main accepted stages of carcinogenesis: initiation, conversion, promotion, and progression. Tumour initiation is thought to result from genetic damage, whilst conversion is associated with large scale genetic alterations. As there is no convincing evidence that exposure induces genetic change, it is considered unlikely that it could affect either initiation or conversion. Instead, it is generally accepted that if these field do affect carcinogenesis, it is likely to be at the level of promotion, a process believed to involve a sustained increase in cell proliferation. There is some evidence for changes in cell signalling that may be relevant to tumour promotion, although such effect are generally of small magnitude and therefore unlikely to perturb most biological systems. Investigations of effects on expression of regulatory genes have been dogged by poor methodology; a small number of high quality studies suggest that effects are unlikely, at least at low flux densities. Moreover, most studies have failed to find any effect on direct measures of cell proliferation, the most relevant endpoint with respect to tumour promotion. Reports of effects on the cell surface may be relevant to tumour progression, but at present any connection remains speculative. Overall there is some evidence for effects on cell signalling, but these changes are of small magnitude and there is nothing to suggest either that they would result in increased proliferation, or that they would be sustained for the long periods necessary for tumour promotion. Hence at present there is no obvious mechanism through which EMFs are likely to affect carcinogenesis.

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