No Evidence of Persisting Unrepaired Nuclear DNA Single Strand Breaks in Distinct Types of Cells in the Brain, Kidney, and Liver of Adult Mice after Continuous Eight-Week 50 Hz Magnetic Field Exposure with Flux Density of 0.1 mT or 1.0 mT

BACKGROUND: It has been hypothesized in the literature that exposure to extremely low frequency electromagnetic fields (50 or 60 Hz) may lead to human health effects such as childhood leukemia or brain tumors. In a previous study investigating multiple types of cells from brain and kidney of the mouse (Acta Neuropathologica 2004; 107: 257-264), we found increased unrepaired nuclear DNA single strand breaks (nDNA SSB) only in epithelial cells of the choroid plexus in the brain using autoradiographic methods after a continuous eight-week 50 Hz magnetic field (MF) exposure of adult mice with flux density of 1.5 mT. METHODS: In the present study we tested the hypothesis that MF exposure with lower flux densities (0.1 mT, i.e., the actual exposure limit for the population in most European countries, and 1.0 mT) shows similar results to those in the previous study. Experiments and data analysis were carried out in a similar way as in our previous study. RESULTS: Continuous eight-week 50 Hz MF exposure with 0.1 mT or 1.0 mT did not result in increased persisting unrepaired nDNA SSB in distinct types of cells in the brain, kidney, and liver of adult mice. MF exposure with 1.0 mT led to reduced unscheduled DNA synthesis (UDS) in epithelial cells in the choroid plexus of the fourth ventricle in the brain (EC-CP) and epithelial cells of the cortical collecting duct in the kidney, as well as to reduced mtDNA synthesis in neurons of the caudate nucleus in the brain and in EC-CP. CONCLUSION: No evidence was found for increased persisting unrepaired nDNA SSB in distinct types of cells in the brain, kidney, and liver of adult mice after continuous eight-week 50 Hz magnetic field exposure with flux density of 0.1 mT or 1.0 mT

Experimental set-up of the 50 Hz MF exposure of the present study.

<p>Details are provided in the main text.</p

Representative autoradiographs of Feulgen-prestained and Light Green SF Yellowish post stained paraffin sections analyzed in the present study.

<p>The photomicrographs show details of the mouse liver after an 8-week 50 Hz MF exposure with 1.0 mT with (A, B) or without (C) injection of ³H-TdR 5 min after the end of the MF exposure. Both autoradiographs were exposed in the same box for 125 days, i.e. under completely identical conditions. In A, a few (out of many) individual silver grains found over the nucleus (arrows) and cytoplasm (arrowheads) of two hepatocytes are marked; the cell bounds are indicated. In B, the arrow points to a cell that was in S phase after injection of ³H-TdR (i.e., during the last two hours of life). In C, single silver grains found over the nucleus (arrow) or cytoplasm (arrowhead) of hepatocytes are marked, representing autoradiographic background. In all panels A to C, black dots and asterisks indicate small and larger sections of liver sinusoids, respectively. The scale bar represents 25 µm.</p

Results of the autoradiographic analyses.

<p>The graphs show mean and standard error of the mean (SEM) of grain numbers representing UDS (<b>A</b>, <b>D</b>, <b>G</b>, <b>J</b>), unrepaired nDNA SSB/ISNT (<b>B</b>, <b>E</b>, <b>H</b>, <b>K</b>) and mtDNA synthesis (<b>C</b>, <b>F</b>, <b>I</b>, <b>L</b>) of neurons in the caudate nucleus in the brain (<b>A–C</b>), epithelial cells in the choroid plexus of the fourth ventricle in the brain (<b>D–F</b>), epithelial cells of the cortical collecting duct in the kidney (<b>G–I</b>), and pericentral hepatocytes in the liver (<b>J–L</b>) after sham-exposure (open bars), MF exposure with 0.1 mT for eight weeks (gray bars), or MF exposure with 1.0 mT for eight weeks (closed bars). For a detailed description of the generation of these grain numbers and grain densities see Section “Evaluation of Autoradiographs” in the main text. Statistically significant differences between groups are indicated.</p

Diminishing benefits of urban living for children and adolescents’ growth and development

Optimal growth and development in childhood and adolescence is crucial for lifelong health and well-being1–6. Here we used data from 2,325 population-based studies, with measurements of height and weight from 71 million participants, to report the height and body-mass index (BMI) of children and adolescents aged 5–19 years on the basis of rural and urban place of residence in 200 countries and territories from 1990 to 2020. In 1990, children and adolescents residing in cities were taller than their rural counterparts in all but a few high-income countries. By 2020, the urban height advantage became smaller in most countries, and in many high-income western countries it reversed into a small urban-based disadvantage. The exception was for boys in most countries in sub-Saharan Africa and in some countries in Oceania, south Asia and the region of central Asia, Middle East and north Africa. In these countries, successive cohorts of boys from rural places either did not gain height or possibly became shorter, and hence fell further behind their urban peers. The difference between the age-standardized mean BMI of children in urban and rural areas was <1.1 kg m–2 in the vast majority of countries. Within this small range, BMI increased slightly more in cities than in rural areas, except in south Asia, sub-Saharan Africa and some countries in central and eastern Europe. Our results show that in much of the world, the growth and developmental advantages of living in cities have diminished in the twenty-first century, whereas in much of sub-Saharan Africa they have amplified