Recent Research on EMF and Health Risk, Twelfth report from SSM's Scientific Council on Electromagnetic Fields, 2017

Background: The Swedish Radiation Safety Authority's (SSM) Scientific Council on Electromagnetic Fields monitors current research on potential health risks with a correlation to exposure to electromagnetic fields, and provides the Authority with advice on assessing possible health risks. The Council gives guidance when the Authority must give an opinion on policy matters when scientific testing is necessary. The Council is required to submit a written report each year on the current research and knowledge situation. Objective: The report has the objective of covering the previous year's research in the area of electromagnetic fields (EMF). The report gives the Swedish Radiation Safety Authority an overview and provides an important basis for risk assessment. Results: The present annual report is the twelfth in this series and covers studies published from October 2015 up to and including March 2017. The report covers different areas of EMF (static, low frequency, intermediate, and radio frequency fields) and different types of studies such as biological, human and epidemiological studies. No new health risks have been identified. Whether mobile phone use causes brain tumours or not was mainly addressed using time trends studies in the last two years. The results were not entirely consistent but mainly point towards a lack of association. Some cell and animal studies indicate that EMF exposure may cause oxidative stress even at low exposure levels. It is unclear what relevance this may have when it comes to direct health effects in humans. A striking result was that some studies showed a stronger association between memory functions and radio wave exposure than other usage variables. The annual report also has a section covering other relevant scientific reports published recently

The carcinogenic potency of carbon particles with and without PAH after repeated intratracheal administration in the rat

The role of carcinogenic PAH in soot- and carbon black-related lung tumour induction in rats was investigated after intratracheal administration of carbon blacks (CB) and two types of diesel soot (DS) either as original or as toluene extracted particles. The total particle dose per animal was 15 mg subdivided into 16-17 weekly applications. There was one vehicle control and two groups were treated with a total dose of either 30 or 15 mg pure BaP as positive control. The main tumour results were: (a) original DS induced a higher tumour rate than extracted DS; (b) the carcinogenic potency of extracted CB probably depends on the size of the primary carbon particles and on the specific surface area of the particles; (c) extracted DS covered with 11 micrograms BaP per mg carbon particles caused a lower lung tumour rate than original DS containing only 0,9 mg BaP per mg, but a variety of other PAH and N02-PAH; (d) a total dose of 15 mg pure BaP caused a lung tumour (abstract truncated

The new born NMRI mouse, a very sensitive animal model to measure the carcinogenic potential of a PAH-containing test atmosphere by inhalation exposure

Newborn and 7-month-old NMRI and C57BL/6N mice were exposed in whole body horizontal air flow exposure chambers 17h/day for 5 days or for 4 weeks (newborn mice) and for 17 weeks (7 month old mice) to 1.1 mg/m3 of a coal tar/pitch condensation aerosol (CTP) containing 20 ug/m3 BaP among other PAH. 10 months (20 months) after starting the 4-week exposure period, the newborn NMRI mice showed a lung tumor rate of 87 (97) %. The exposure for only 5 days led to a tumor rate of 33% (30%) after 10 months (20 months) experimental time. The corresponding control groups had a lung tumor rate of 13 (17) %. These data show that the lung tumor rate after 10 months experimental time was very similar to the tumor rate found after 20 months. An increased number of malignant and multiple tumors was found after 20 months but, only in the 4-week exposure group

Role of blood-brain barrier P-glycoprotein in limiting brain accumulation and sedative side-effects of asimadoline, a peripherally acting analgaesic drug

1 Studies with knockout mice lacking mdrla P-glycoprotein (P-gp) have previously shown that blood-brain barrier P-gp is important in preventing the accumulation of several drugs in the brain. 2 Asimadoline (EMD 61753) is a peripherally selective kappa-opioid receptor agonist which is under development as a therapeutic analgaesic. From the structural characteristics of this drug and its peripheral selectivity, we hypothesized that it is transported by P-gp. 3 Using a pig-kidney polarized epithelial cell line transfected with mdr cDNAs, we demonstrate that asimadoline is transported by the mouse mdrla P-gp and the human MDRI P-gp. 4 Furthermore, we show that in mdr 1a/1b double knockout mice, the absence of P-gp leads to a 9 fold increased accumulation of asimadoline in the brain. In line with this accumulation difference, mdr 1a/1b (-/-) mice are at least 8 fold more sensitive to the sedative effect of asimadoline than wild-type mice. 5 Interestingly, the oral uptake of asimadoline was not substantially altered in mdr 1a/1b (-/-) mice. 6 Our results demonstrate that for some drugs, P-gp in the blood-brain barrier can have a therapeutically beneficial effect by limiting brain penetration, whereas at the same time intestinal P-gp is not a significant impediment to oral uptake of the drug