Health risks related to 900 MHz 2 G frequency exposure remain inconclusive under current regulatory standards. Research into potential long-term effects is ongoing, particularly as the use of mobile networks and wireless devices increases. This study investigates the effects of non-thermal exposure levels of mobile phone 900 MHz radiofrequency electromagnetic field (RF-EMF) on rodent neurodevelopment. In vivo, the effects of pre- and post-natal 0.08 and 0.4 W/kg specific absorption rate (SAR) exposure were assessed for their impact on the proteomic profile at postnatal day 0 (PND 0). Brain-derived neurotrophic factor (BDNF), BrdU+ proliferative cells, synaptogenesis, and oxidative stress in the hippocampus and cortex of rat pups were studied at PND 8 and PND 17. Effects of the lowest SAR (0.08 W/kg) were assessed in vitro to afford mechanistic data regarding neural stem cells (NSCs) differentiation. In vivo results showed a decrease in BDNF level and BrdU+ proliferative cells with a decrease in synapse balance (excitatory synapses/inhibitory synapses). In vitro, at 0.08 W/kg there was an increase in Ki-67 + proliferative cells, apoptosis, and double-strand DNA breaks in NSCs. A lower ratio of B1 cells (primary progenitors of NSCs) among total cerebral cells and a higher ratio of oligodendrocyte progenitor cells and astrocytes were observed in the exposed NSCs. Our findings suggest that key cellular events for brain ontogenesis are likely to undergo changes with RF-EMF 900 MHz exposure during early development. These support the hypothesis that the developing central nervous system is vulnerable to RF-EMF exposures in rodents at regulatory thresholds.

The widespread use of wireless technologies has raised public health concerns about the biological effects of radiofrequency (RF) exposure. Children have a higher specific absorption rate (SAR) of radiation energy compared to adults. Furthermore, brown adipose tissue (BAT) is more prevalent in infants and tends to decrease with age. Previous animal studies demonstrated a cold sensation in rats exposed to 900 MHz (second generation, 2G). UCP1-dependent thermogenesis and BAT hyperplasia are two fundamental adaptive mechanisms initiated in response to cold. This study investigated the impact of short-term exposure to 2G and fifth generation (5G) on key thermogenic and adipogenic markers related to these mechanisms while considering age and exposure duration. Juvenile and young adult Wistar rats were randomized into three subgroups: a 5G group (3.5 GHz), 2G group (900 MHz), and a control group (SHAM). They were exposed to their respective continuous-wave RF signals for 1 or 2 weeks at an intensity of 1.5 V/m, with two exposure sessions of 1 h per day. After the exposure period, a RT-qPCR was carried out to evaluate the genetic markers involved in BAT thermogenesis and adipogenesis. Two adipogenic biomarkers were affected; a fold change reduction of 49% and 32% was detected for PRDM16 (p = 0.016) and C/EBP β (p = 0.0002), respectively, after 5G exposure, regardless of age and exposure duration. No significant RF effect was found on UCP1-dependent thermogenesis at a transcriptional level. These findings suggest that exposure to a 5G radiofrequency may partially disrupt brown adipocyte differentiation and thermogenic function by downregulating PRDM16 and C/EBP β, possibly leading to higher cold sensitivity.