PMID: 

Science. 2019 11 1 ;366(6465):620-623. PMID: 31672894

Abstract Title: 

Neonicotinoids disrupt aquatic food webs and decrease fishery yields.

Abstract: 

Invertebrate declines are widespread in terrestrial ecosystems, and pesticide use is often cited as a causal factor. Here, we report that aquatic systems are threatened by the high toxicity and persistence of neonicotinoid insecticides. These effects cascade to higher trophic levels by altering food web structure and dynamics, affecting higher-level consumers. Using data on zooplankton, water quality, and annual fishery yields of eel and smelt, we show that neonicotinoid application to watersheds since 1993 coincided with an 83% decrease in average zooplankton biomass in spring, causing the smelt harvest to collapse from 240 to 22 tons in Lake Shinji, Shimane Prefecture, Japan. This disruption likely also occurs elsewhere, as neonicotinoids are currently the most widely used class of insecticides globally.

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PMID: 

Toxicology. 2019 Nov 1 ;427:152298. Epub 2019 Sep 28. PMID: 31574243

Abstract Title: 

Omethoate induces pharyngeal cancer cell proliferation and G1/S cell cycle progression by activation of Akt/GSK-3β/cyclin D1 signaling pathway.

Abstract: 

Omethoate is a broad category of organophosphorous pesticides (OPs) and has toxic effects on human health under long-term, low-dose exposure. However, the role of omethoate in cancer development remains elusive. The incidence of global head and neck squamous cell carcinomas (HNSCC) has markedly increased in recent years. Thus, we examined whether omethoate induced the proliferation of FaDu cells (a cell line of HNSCC) and if so, what the underlying mechanism was. The study revealed that omethoate induced FaDu cell growth in a dose- and time-dependent manner. Omethoate stimulated FaDu cell proliferation was mainly due to enhancing the G1 to S phase transition by flow cytometry analysis. We also found that omethoate up-regulated cyclin D1, a key gene controlling the G1-S transition. Furthermore, we showed that omethoate was capable of activating the Akt/GSK-3β signaling pathway. Blockage of Akt by siRNA or small molecule inhibitor significantly suppressed omethoate-induced cyclin D1 expression and cell proliferation. Collectively, these findings demonstrated for the first time that omethoate could induce the pharyngeal cancer cell proliferation by activation of the Akt/GSK-3β/cyclin D1 signaling pathway.

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PMID: 

Toxicology. 2019 Nov 5:152327. Epub 2019 Nov 5. PMID: 31704166

Abstract Title: 

Gestational and Perinatal Exposure to Diazinon Causes Long-lasting Neurobehavioral Consequences in the Rat.

Abstract: 

Diazinon is a widely-used organophosphate pesticide. Pulsatile exposure to diazinon during neonatal development has previously been shown cause long-term neurobehavioral impairments in rats. However, the effects of chronic low concentration exposures during perinatal development remain unclear. This experiment evaluated such effects in Sprague-Dawley rats by implanting osmotic pumps in breeder females prior to conception (N = 13-15 litters per condition) which then delivered chronic, zero order kinetic low-level infusions of 0, 114 or 228 ug/day of diazinon throughout pregnancy. One male and one female from each litter was assessed with a battery of behavioral tests that continued from four weeks of age into adulthood. Litter was used as the unit of variance for the analysis of variance test of significance, with sex as a within litter factor. Diazinon treatment condition was the between subjects factor and time or sessions were repeated measures. Chronic diazinon exposure from pre-mating until the neonatalperiod caused a significant (p 

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PMID: 

Korean J Physiol Pharmacol. 2018 May ;22(3):277-289. Epub 2018 Apr 25. PMID: 29719450

Abstract Title: 

Exposure to 835 MHz RF-EMF decreases the expression of calcium channels, inhibits apoptosis, but induces autophagy in the mouse hippocampus.

Abstract: 

The exponential increase in the use of mobile communication has triggered public concerns about the potential adverse effects of radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phones on the central nervous system (CNS). In this study, we explored the relationship between calcium channels and apoptosis or autophagy in the hippocampus of C57BL/6 mice after RF-EMF exposure with a specific absorption rate (SAR) of 4.0 W/kg for 4 weeks. Firstly, the expression level of voltage-gated calcium channels (VGCCs), a key regulator of the entry of calcium ions into the cell, was confirmed by immunoblots. We investigated and confirmed that pan-calcium channel expression in hippocampal neurons were significantly decreased after exposure to RF-EMF. With the observed accumulation of autolysosomes in hippocampal neurons via TEM, the expressions of autophagy-related genes and proteins (e.g., LC3B-II) had significantly increased. However, down-regulation of the apoptotic pathway may contribute to the decrease in calcium channel expression, and thus lower levels of calcium in hippocampal neurons. These results suggested that exposure of RF-EMF could alter intracellular calcium homeostasis by decreasing calcium channel expression in the hippocampus; presumably by activating the autophagy pathway, while inhibiting apoptotic regulation as an adaptation process for 835 MHz RF-EMF exposure.

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PMID: 

Environ Int. 2017 Apr ;101:59-69. Epub 2017 Jan 24. PMID: 28126406

Abstract Title: 

ELF exposure from mobile and cordless phones for the epidemiological MOBI-Kids study.

Abstract: 

This paper describes measurements and computational modelling carried out in the MOBI-Kids case-control study to assess the extremely low frequency (ELF) exposure of the brain from use of mobile and cordless phones. Four different communication systems were investigated: Global System for Mobile (GSM), Universal Mobile Telecommunications System (UMTS), Digital Enhanced Cordless Telecommunications (DECT) and Wi-Fi Voice over Internet Protocol (VoIP). The magnetic fields produced by the phones during transmission were measured under controlled laboratory conditions, and an equivalent loop was fitted to the data to produce three-dimensional extrapolations of the field. Computational modelling was then used to calculate the induced current density and electric field strength in the brain resulting from exposure to these magnetic fields. Human voxel phantoms of four different ages were used: 8, 11, 14 and adult. The results indicate that the current densities induced in the brain during DECT calls are likely to be an order of magnitude lower than those generated during GSM calls but over twice that during UMTS calls. The average current density during Wi-Fi VoIP calls was found to be lower than for UMTS by 30%, but the variability across the samples investigated was high. Spectral contributions were important to consider in relation to current density, particularly for DECT phones. This study suggests that the spatial distribution of the ELF induced current densities in brain tissues is determined by the physical characteristics of the phone (in particular battery position) while the amplitude is mainly dependent on communication system, thus providing a feasible basis for assessing ELF exposure in the epidemiological study. The number of phantoms was not large enough to provide definitive evidence of an increase of induced current density with age, but the data that are available suggest that, if present, the effect is likely to be very small.

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PMID: 

Int J Environ Res Public Health. 2015 May 22 ;12(5):5634-56. Epub 2015 May 22. PMID: 26006132

Abstract Title: 

Development of an RF-EMF Exposure Surrogate for Epidemiologic Research.

Abstract: 

Exposure assessment is a crucial part in studying potential effects of RF-EMF. Using data from the HERMES study on adolescents, we developed an integrative exposure surrogate combining near-field and far-field RF-EMF exposure in a single brain and whole-body exposure measure. Contributions from far-field sources were modelled by propagation modelling and multivariable regression modelling using personal measurements. Contributions from near-field sources were assessed from both, questionnaires and mobile phone operator records. Mean cumulative brain and whole-body doses were 1559.7 mJ/kg and 339.9 mJ/kg per day, respectively. 98.4% of the brain dose originated from near-field sources, mainly from GSM mobile phone calls (93.1%) and from DECT phone calls (4.8%). Main contributors to the whole-body dose were GSM mobile phone calls (69.0%), use of computer, laptop and tablet connected to WLAN (12.2%) and data traffic on the mobile phone via WLAN (6.5%). The exposure from mobile phone base stations contributed 1.8% to the whole-body dose, while uplink exposure from other people's mobile phones contributed 3.6%. In conclusion, the proposed approach is considered useful to combine near-field and far-field exposure to an integrative exposure surrogate for exposure assessment in epidemiologic studies. However, substantial uncertainties remain about exposure contributions from various near-field and far-field sources.

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PMID: 

J Biomed Phys Eng. 2018 Mar ;8(1):151-152. Epub 2018 Mar 1. PMID: 29732351

Abstract Title: 

Cancers of the Brain and CNS: Global Patterns and Trends in Incidence.

Abstract: 

Miranda-Filho et al. in their recently published paper entitled"Cancers of the brain and CNS: global patterns and trends in incidence"provided a global status report of the geographic and temporal variations in the incidence of brain and CNS cancers in different countries across continents worldwide. While the authors confirm the role of genetic risk factors and ionizing radiation exposures, they claimed that no firm conclusion could be drawn about the role of exposure to non-ionizing radiation. The paper authored by Miranda-Filho et al. not only addresses a challenging issue, it can be considered as a good contribution in the field of brain and CNS cancers. However, our correspondence addresses a basic shortcoming of this paper about the role of electromagnetic fields and cancers and provides evidence showing that exposure to radiofrequency electromagnetic fields (RF-EMFs), at least at high levels and long durations, can increases the risk of cancer.

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PMID: 

Int J Environ Res Public Health. 2015 Apr 22 ;12(4):4406-21. Epub 2015 Apr 22. PMID: 25913185

Abstract Title: 

Early exposure to intermediate-frequency magnetic fields alters brain biomarkers without histopathological changes in adult mice.

Abstract: 

Recently we have reported that intermediate-frequency magnetic field (IF-MF) exposure transiently altered the mRNA expression levels of memory function-related genes in the hippocampi of adult male mice. However, the effects of IF-MF exposure during brain development on neurological biomarkers have not yet been clarified. In the present study, we investigated the effect of IF-MF exposure during development on neurological and immunological markers in the mouse hippocampus in 3- and 7-week-old male mice. Pregnant C57BL/6J mice were exposed to IF-MF (21 kHz, 3.8 mT) for one hour per day from organogenesis period day 7 to 17. At adolescence, some IF-MF-exposed mice were further divided into exposure, recovery, and sham-exposure groups. The adolescent-exposure groups were exposed again to IF-MF from postnatal day 27 to 48. The expression of mRNA in the hippocampi was examined using a real-time RT-PCR method, and microglia activation was examined by immunohistochemical analysis. The expression levels of NR1 and NR2B as well as transcription factors (CaMKIV, CREB1), inflammatory mediators (COX2, IL-1 b,TNF-α), and the oxidative stress marker heme-oxygenase (HO)-1 were significantly increased in the IF-MF-exposed mice, compared with the control group, in the 7-week-old mice, but not in the 3-week-old mice. Microglia activation was not different between the control and other groups. This study providesthe first evidence that early exposure to IF-MF reversibly affects the NMDA receptor, its related signaling pathways, and inflammatory mediators in the hippocampus of young adult mice; these changes are transient and recover after termination of exposure without histopathological changes.

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PMID: 

Med Sci Monit. 2006 Jun ;12(6):BR215-20. Epub 2006 May 29. PMID: 16733479

Abstract Title: 

Effect of 50-Hz 1-mT magnetic field on the uterus and ovaries of rats (electron microscopy evaluation).

Abstract: 

BACKGROUND: The aim of this study was to investigate the effect of extremely low frequency magnetic fields (ELFMF) on the uterus and ovary of rats.MATERIAL/METHODS: Forty-eight female Wistar albino rats were divided into two groups, one for 50 and the other for 100 days of exposure. Each group was further divided into two groups, one sham exposed (n=12) and the other the experimental group (n=12). The experimental rats were exposed to 50-Hz 1-mT ELFMF for three hours/day for 50 or 100 days. The sham groups of rats were kept under the same circumstances without applying ELFMF. Electron microscopic examination was performed to evaluate the ovaries and uterus.RESULTS: Ultrastructural dissolution, decrease in cell organelles, cavities in cells, heterochromative appearance, and typical structural loss of the nucleus were observed in germinal epithelial cells of the rat ovaries in the 50-days ELFMF exposure group. Ultrastructural alterations in germinal epithelium and tunica albuginea of ovaries, irregularity in nucleus and nucleolus, increase in lipid vacuoles of cell cytoplasm and reduction in organelles were observed in rat ovaries in the 100-days ELFMF exposure group. Similar alterations were observed in uterus. Malondialdehyde concentration (MDA) of the ovaries and uterus increased in rats of the two exposure groups (p

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PMID: 

Can J Physiol Pharmacol. 2016 Aug ;94(8):849-57. Epub 2016 Mar 6. PMID: 27203380

Abstract Title: 

The apoptotic effect and the plausible mechanism of microwave radiation on rat myocardial cells.

Abstract: 

Microwaves may exert adverse biological effects on the cardiovascular system at the integrated system and cellular levels. However, the mechanism underlying such effects remains poorly understood. Here, we report a previously uncharacterized mechanism through which microwaves damage myocardial cells. Rats were treated with 2450 MHz microwave radiation at 50, 100, 150, or 200 mW/cm(2) for 6 min. Microwave treatment significantly enhanced the levels of various enzymes in serum. In addition, it increased the malondialdehyde content while decreasing the levels of antioxidative stress enzymes, activities of enzyme complexes I-IV, and ATP in myocardial tissues. Notably, irradiated myocardial cells exhibited structural damage and underwent apoptosis. Furthermore, Western blot analysis revealed significant changes in expression levels of proteins involved in oxidative stress regulation and apoptotic signaling pathways, indicating that microwave irradiation could induce myocardial cell apoptosis by interfering with oxidative stress and cardiac energy metabolism. Our findings provide useful insights into the mechanism of microwave-induced damage to the cardiovascular system.

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