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Ionising radiation can transfer sufficient energy to ionise molecules, and this can lead to chemical changes, including DNA damage in cells. Key evidence for the carcinogenicity of ionising radiation comes from: follow-up studies of the survivors of the atomic bombings in Japan; other epidemiological studies of groups that have been exposed to radiation from medical, occupational or environmental sources; experimental animal studies; and studies of cellular responses to radiation. Considering exposure to environmental ionising radiation, inhalation of naturally occurring radon is the major source of radiation in the population - in doses orders of magnitude higher than those from nuclear power production or nuclear fallout. Indoor exposure to radon and its decay products is an important cause of lung cancer; radon may cause approximately one in ten lung cancers in Europe. Exposures to radon in buildings can be reduced via a three-step process of identifying those with potentially elevated radon levels, measuring radon levels, and reducing exposure by installation of remediation systems. In the 4th Edition of the European Code against Cancer it is therefore recommended to: "Find out if you are exposed to radiation from naturally high radon levels in your home. Take action to reduce high radon levels". Non-ionising types of radiation (those with insufficient energy to ionise molecules) - including extremely low-frequency electric and magnetic fields as well as radiofrequency electromagnetic fields - are not an established cause of cancer and are therefore not addressed in the recommendations to reduce cancer risk., (Copyright © 2015 International Agency for Research on Cancer. Published by Elsevier Ltd. All rights reserved.)

Background: Although the aetiology of glioma is poorly understood, the higher incidence in males has long suggested an occupational cause., Aim: To investigate possible associations between occupational exposure to ionizing, ultraviolet (UV), radiofrequency (RF) and extremely low frequency (ELF) radiation and adult glioma risk., Methods: Case-control study using histologically confirmed cases of glioma first diagnosed between 1987 and 1991 in Melbourne, Australia, matched by age, sex and postcode of residence. A detailed occupational history was obtained for each subject. Exposure to radiation was assessed using a Finnish job exposure matrix (FINJEM) for all the radiation types as well as self-reports and expert hygienist review for RF and ionizing radiation. For ELF and UV, gender-specific FINJEM analysis was performed., Results: The study population consisted of 416 cases of glioma and 422 controls. The risk estimates given by FINJEM for ELF, RF and ionizing radiation were close to or below unity. Gender-specific analysis for UV showed odds ratios of 1.60 [95% confidence interval (CI) 0.95-2.69] and 0.54 (95% CI 0.27-1.07) for the highest exposed group of men and women, respectively (corresponding P value for trend was 0.03 and 0.04)., Conclusions: We did not find evidence of an association between glioma and occupational exposure to ELF, RF and ionizing radiation. UV radiation was associated with increased glioma risk for men but this result could have been confounded by other predominantly male occupational and lifestyle exposures associated with high UV. Further investigation of UV radiation and glioma risk is suggested.

Allele-specific competitive blocker PCR (ACB-PCR) amplification and quantification was developed for mouse p53 codon 270 CGT-->TGT base substitution and codon 244/245 AAC/CGC-->AAT/TGC tandem mutation. PCR products corresponding to p53 mutant and wild-type DNA sequences were generated. These DNAs were mixed in known proportions to construct samples with defined mutant fractions and the allele-specific detection of each mutation was systematically optimized. Each assay was used to analyze eight simulated solar light (SSL)-induced tumors. By analyzing mutant fraction (MF) standards in parallel with PCR products generated from tumor samples, p53 mutants could be quantified as subpopulations within the tumors. All eight tumors contained detectable levels of p53 codon 270 CGT-->TGT mutation. Three tumors had p53 MFs between 10(-4) and 10(-3). Five tumors had p53 MFs between 10(-3) and 10(-2). None of the eight mouse skin tumors had measurable levels of p53 codon 244/245 tandem mutation. Frequent detection of p53 codon 270 CGT-->TGT mutation provides additional evidence that a pyrimidine dinucleotide overlapping a methylated CpG site (Pyr(me)CG) is a susceptible target for SSL-induced mutagenesis. The absence of p53 codon 244/245 mutation in tumors may be explained by its mutant p53 phenotype and/or indicate that this site is not methylated. These initial results indicate that p53 codon 270 CGT-->TGT mutation may be a sensitive biomarker for SSL- or UV-induced mutagenesis. This mutational endpoint may be useful for evaluating the co-carcinogenicity of compounds administered in combination with UV or SSL.

Epidemiologic and experimental research on the potential carcinogenic effects of extremely low frequency electromagnetic fields (EMF) has now been conducted for over two decades. Cancer epidemiology studies in relation to EMF have focused primarily on brain cancer and leukemia, both from residential sources of exposure in children and adults and from occupational exposure in adult men. Because genotoxic effects of EMF have not been shown, most recent laboratory research has attempted to show biological effects that could be related to cancer promotion. In this report, we briefly review residential and occupational EMF studies on brain cancer. We also provide a general review of experimental studies as they relate both to the biological plausibility of an EMF-brain cancer relation and to the insufficiency of such research to help guide exposure assessment in epidemiologic studies. We conclude from our review that no recent research, either epidemiologic or experimental, has emerged to provide reasonable support for a causal role of EMF on brain cancer.

A nested case-control study was used to investigate the relation between a range of electromagnetic field exposures and brain tumor risk in the US Air Force. Cumulative extremely low frequency and radiofrequency/microwave electromagnetic field potential exposures were estimated from a job-exposure matrix developed for this study. Ionizing radiation exposures were obtained from personal dosimetry records. Men who were exposed to nonionizing electromagnetic fields had a small excess risk for developing brain tumors, with the extremely low frequency and radiofrequency/microwave age-race-senior military rank-adjusted odds ratios being 1.28 (95% confidence interval (Cl) 0.95-1.74) and 1.39 (95% Cl 1.01-1.90), respectively. By contrast, men who were exposed to ionizing radiation had an age-race-senior military rank-adjusted odds ratio of 0.58 (95% Cl 0.22-1.52). These results support a small association between extremely low frequency and radiofrequency/microwave electromagnetic field exposure and no association between ionizing radiation exposure and brain tumors in the US Air Force population. Military rank was consistently associated with brain tumor risk. Officers were more likely than enlisted men to develop brain tumors (age-race-adjusted odds ratio (OR) = 2.11, 95% Cl 1.48-3.01), and senior officers were at increased risk compared with all other US Air Force members (age-race-adjusted OR = 3.30, 95% Cl 1.99-5.45).

The purpose of this review is to summarize the experience gained thus far on the potential health hazards of electromagnetic radiation. Far less information is available in the medical literature on this kind of radiation than on ionizing radiation, which has been recognized as a health hazard long ago. Increased rates of cancer morbidity and mortality have been noted in populations exposed to ionizing radiation, and international quantitative safety criteria have been established. Electromagnetic radiation (radiofrequency levels between several hundred kilohertz and 300 GHz) is not an infrequent phenomenon. The literature consists mainly of epidemiological studies out of which grew the assumption that this kind of radiation may be carcinogenic. However, only limited data are available on electromagnetic radiation as a potential cancer inducer. A review of the literature does not demonstrate a direct and clear linkage between electromagnetic radiation and the occurrence of malignant tumors, but much more research and clarification are necessary before reaching any conclusions.

Non-ionizing electromagnetic radiation (NIEMR), particularly the magnetic field component, has been implicated in the development of human neoplasia. Research suggests that if these fields are part of the carcinogenic pathway, they may act as a promoter or in the progression of established cancer. Active progression of cancer cells by NIEMR negate the possible early detection of clinically silent neoplasms. We have observed the effect of non-ionizing electromagnetic fields on an established breast carcinoma cell line MCF-7, and found no stimulation of growth when exposed to a low-frequency magnetic field. The same magnetic field has been used as an adjuvant to anti-neoplastic chemotherapeutic agents. The results of this study have shown an improvement in the neoplastic cell kill by antineoplastic chemotherapy when coupled with a low frequency magnetic field. Non-ionizing electromagnetic radiation may be involved in the carcinogenic process; however, the answer to this question awaits further studies. We are exploring new methods of cancer treatment using non-ionizing electromagnetic radiation.

A number of problems become evident when we attempt to assess the data in this review. We must first acknowledge the fact that EM radiation, as opposed to some chemical and physical pollutants which can be seen, tasted, or detected by odor, is in most situations not detected by human senses. This fact alone, however, does not prove or disprove the conjecture that EMR is a potential health hazard. The studies on the effects of EMR on cell systems, animals, and human subjects, report results which promote in some and reject in others the hypothesis that EMR in the ELF and microwave range is carcinogenic. Much of the criticism of the studies on human subjects centers around (1) quantifying exposure to EM Fields; (2) the epidemiologic-statistical methods used to gather, study, and interpret the data; and (3) lack of data studying co-carcinogens. Although there is no convincing evidence that EMR is carcinogenic, the uncertainty, in addition to the ubiquity of EMR, makes study of its possible health effects and its carcinogenic potential an essential part of future medical and epidemiologic research.