Abstract: The aim of this work was to study the exposure to magnetic fields of children living at different distances from a power line and to evaluate how well theoretical calculations compared with actual exposure. Personal exposure instruments were carried for 24 h by 65 schoolchildren living 28-325 m from a 300 kV transmission line; the current load was 200-700 A. About half of the children attended a school far from the power line, whereas the other half attended a school located about 25 m from the line. Exposure to magnetic fields was analyzed for three categories of location: at home, at school, and at all other places. Time spent in bed was analyzed separately. The results indicated that children who lived close to a power line had a higher magnetic field exposure than other children. The power line was the most important source of exposure when the magnetic field due to the line was greater than about 0.2 microT. Exposure at school influenced the 24 h time-weighted average results considerably in those cases where the distance between home and power line was very different from the distance between school and power line. The calculated magnetic field, based on line configuration, current load, and distance between home and power line, corresponded reasonably well with the measured field. However, the correlation depends on whether home only or 24 h exposure is used in the analysis and on which school the children attended. The calculated magnetic field seems to be a reasonably good predictor of actual exposure and could be used in epidemiological studies, at least in Norway, where the electrical system normally results in less ground current than in most other countries.

Abstract: Based on the 'limited' evidence suggesting an association between exposure to radiofrequency fields (RF) emitted from mobile phones and two types of brain cancer, glioma and acoustic neuroma, the International Agency for Research on Cancer has classified RF as 'possibly carcinogenic to humans' in group 2B. In view of this classification and the positive correlation between increased genetic damage and carcinogenesis, a meta-analysis was conducted to determine whether a significant increase in genetic damage in human cells exposed to RF provides a potential mechanism for its carcinogenic potential. The extent of genetic damage in human cells, assessed from various end-points, viz., single-/double-strand breaks in the DNA, incidence of chromosomal aberrations, micronuclei and sister chromatid exchanges, reported in a total of 88 peer-reviewed scientific publications during 1990-2011 was considered in the meta-analysis. Among the several variables in the experimental protocols used, the influence of five specific variables related to RF exposure characteristics was investigated: (i) frequency, (ii) specific absorption rate, (iii) exposure as continuous wave, pulsed wave and occupationally exposed/mobile phone users, (iv) duration of exposure, and (v) different cell types. The data indicated the following. (1) The magnitude of difference between RF-exposed and sham-/un-exposed controls was small with some exceptions. (2) In certain RF exposure conditions there was a statistically significant increase in genotoxicity assessed from some end-points: the effect was observed in studies with small sample size and was largely influenced by publication bias. Studies conducted within the generally recommended RF exposure guidelines showed a smaller effect. (3) The multiple regression analyses and heterogeneity goodness of fit data indicated that factors other than the above five variables as well as the quality of publications have contributed to the overall results. (4) More importantly, the mean indices for chromosomal aberrations, micronuclei and sister chromatid exchange end-points in RF-exposed and sham-/un-exposed controls were within the spontaneous levels reported in a large data-base. Thus, the classification of RF as possibly carcinogenic to humans in group 2B was not supported by genotoxicity-based mechanistic evidence.

Abstract: The incidence, malignancy and treatment resistance of many types of human B-cell leukaemias (B-ALL) are directly related to patient age. A major obstacle to elucidate the contribution of age to the development and evolution of leukaemias is the lack of appropriate mouse models where precise control of the timing of oncogene expression is possible. Here we present proof-of-principle experiments showing how a conditional transgenic mouse model of BCR-ABLp190-driven B-ALL offers the opportunity to test the hypothesis that the age of the leukemic cells-of-origin of B-ALL influences B-ALL malignancy. B-ALLs generated from 12- and 20-month-old progenitors gave rise to a more invasive B-ALL than the one developed from 4-month old precursors. This was evidenced by survival analysis revealing the increased malignancy of B-ALLs generated from 20 or 12-month-old transformed progenitors compared with the 4-month equivalents (median survival of 88 days versus 50.5 and 33 days, respectively). Our study shows that the age of target cells at the time of transformation affects B-ALL malignancy.