Ataxia telangiectasia mutated deficiency does not result in genetic susceptibility to 50 Hz magnetic fields exposure in mouse embryonic fibroblasts.

Extremely low frequency magnetic field (ELF-MF) has been classified as a possible carcinogen to humans by the International Agency for Research on Cancer [2002]. However, debate on the genotoxic effects of ELF-MF has continued due to lack of sufficient experimental evidence. Ataxia telangiectasia mutated (ATM) plays a central role in DNA damage repair; its deficiency can result in cellular sensitivity to DNA-damaging agents. To evaluate the genotoxicity of ELF-MF, we investigated the effects of 50 Hz MF on DNA damage in ATM-proficient (Atm+/+ ) mouse embryonic fibroblasts (MEFs) and ATM-deficient (Atm-/- ) MEFs, a radiosensitive cell line. Results showed no significant difference in average number of γH2AX foci per cell (9.37 ± 0.44 vs. 9.08 ± 0.28, P = 0.58) or percentage of γH2AX foci positive cells (49.22 ± 1.86% vs. 49.74 ± 1.44%, P = 0.83) between sham and exposure groups when Atm+/+ MEFs were exposed to 50 Hz MF at 2.0 mT for 15 min. Extending exposure duration to 1 or 24 h did not significantly change γH2AX foci formation in Atm+/+ MEFs. Similarly, the exposure did not significantly affect γH2AX foci formation in Atm-/- MEFs. Furthermore, 50 Hz MF exposure also did not significantly influence DNA fragmentation, cell viability, or cell cycle progression in either cell types. In conclusion, exposure to 50 Hz MF did not induce significant DNA damage in either Atm+/+ or Atm-/- MEFs under the reported experimental conditions. Bioelectromagnetics. 39:476-484, 2018. © 2018 Wiley Periodicals, Inc.

Effects of 1800 MHz RF-EMF exposure on DNA damage and cellular functions in primary cultured neurogenic cells.

PURPOSE: To systematically evaluate the effects of 1800 MHz radiofrequency electromagnetic fields (RF-EMF) exposure on DNA damage and cellular functions in primary cultured neurogenic cells. MATERIALS AND METHODS: The primary cultured astrocytes, microglia and cortical neurons were exposed to RF-EMF at a SAR of 4.0 W/kg. The DNA damage was evaluated by γH2AX foci formation assay. The secretions of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1ß) in astrocytes and microglia, microglial phagocytic activity and neuronal development were examined by enzyme-linked immunosorbent assay, phagocytosis assay and immunofluorescent staining on microtubule-associated protein tau, microtubule-associated protein 2, postsynaptic density 95 and gephyrin, respectively. RESULTS: RF-EMF exposure did not significantly induce γH2AX foci formation in three primary cultured neurogenic cells. Furthermore, RF-EMF exposure did not significantly affect the secretion of cytokines in astrocytes and microglia, and the morphological indicators of dendrites or synapses of cortical neurons. However, the exposure significantly reduced the phagocytic activity of microglia and inhibited the axon branch length and branch number of cortical neurons. CONCLUSIONS: Our data demonstrated that exposure to RF-EMF did not elicit DNA damage but inhibited the phagocytic ability of microglia and the axon branch length and branch number of cortical neurons.

Childhood pesticide poisoning in Zhejiang, China: a retrospective analysis from 2006 to 2015.

BACKGROUND: Pesticide poisoning in children has been a serious public health issue around the world, especially in the developing countries where agriculture is still one of the largest economic sectors. The purpose of this study was to analyze epidemiological characteristics of acute pesticide poisoning in children from Zhejiang province, China. METHODS: The pesticide poisoning cases for children were retrieved from Occupational Disease Surveillance and Reporting System, Zhejiang Provincial Center for Disease Control and Prevention, China. The incident cases, deaths, and fatality rate of child pesticide poisoning from 2006 through 2015 were calculated. RESULTS: During the study period, totally 2952 children were poisoned by pesticides, with 66 deaths, resulting in a fatality rate of 2.24%. Among them, there were 1607 male cases with 28 deaths, and 1345 female cases with 38 deaths. Most of the cases occurred in preschool children (1349) and adolescent age group (1269). Organophosphate and carbamate insecticides were the cause of most poisonings (1130), leading to 34 deaths. The highest fatality rate (3.13%) was due to poisoning by herbicides and fungicides, causing 14 deaths out of 448 cases. Poisoning occurred mostly in rural areas (78%). And most pesticide poisoning occurred in the summer (896) and fall (811), while fewest poisoning cases in the winter (483) but with the highest fatality rate (3.52%). CONCLUSIONS: This study shows that pesticide poisoning of children is a major health problem in Zhejiang, suggesting preventive strategies should be conducted to control childhood pesticide poisoning.

The effects of 50 Hz magnetic field exposure on DNA damage and cellular functions in various neurogenic cells.

Epidemiological studies have indicated a possible association between extremely low-frequency magnetic field (ELF-MF) exposure and the risk of nervous system diseases. However, laboratory studies have not provided consistent results for clarifying this association, despite many years of studies. In this study, we have systematically investigated the effects of 50 Hz MF exposure on DNA damage and cellular functions in both neurogenic tumor cell lines (U251, A172, SH-SY5Y) and primary cultured neurogenic cells from rats (astrocytes, microglia, cortical neurons). The results showed that exposure to a 50 Hz MF at 2.0 mT for up to 24 h did not influence γH2AX foci formation (an early marker of DNA double-strand breaks) in any of six different neurogenic cells. Exposure to a 50 Hz MF did not affect cell cycle progression, cell proliferation or cell viability in neurogenic tumor U251, A172 or SH-SY5Y cells. Furthermore, the MF exposure for 24 h did not significantly affect the secretion of cytokines (TNF-α, IL-6 or IL-1ß) in astrocytes or microglia, or the phagocytic activity of microglia. In addition, MF exposure for 1 h per day did not significantly influence expression levels of microtubule-associated protein tau, microtubule-associated protein 2, postsynaptic density 95 or gephyrin in cortical neurons, indicating an absence of effects of MF exposure on the development of cortical neurons. In conclusion, our data suggest that exposure to a 50 Hz MF at 2.0 mT did not elicit DNA damage effects or abnormal cellular functions in the neurogenic cells studied.