Previous studies have indicated a link between exposure to radiofrequency (RF) radiation and reduced sperm quality and motility, as well as increased oxidative stress in testicular tissue [1]. The 2012 BioInitiative Report emphasized that RF radiation can trigger epigenetic changes, disrupt DNA repair mechanisms, and induce new mutations, all of which can impair male fertility. However, the extent to which RF radiation exposure affects the reproductive systems of male embryos remains largely unexplored. This study addresses a significant gap in the literature by examining possible persistent damage resulting from prenatal RF radiation exposure and its impact on spermatogenesis in adulthood.
Scientists exposed pregnant Wistar rats to 3.5 GHz GSM radiation for two hours per day, either throughout the entire pregnancy (3 weeks; 3T) or during the final two weeks (2T) of pregnancy. Measured field strengths inside the cage ranged from 24 to 28 V/m, power densities from 1.53 to 2 W/m², and the maximum averaged SAR over 10 g was 0.038 W/kg. The control group was sham-exposed. After birth, six male offspring were randomly selected and kept without further exposure until adulthood (12 months). Therefore, exposure occurred only in utero. Histological analyses of the testes were performed, including the Johnson score, seminiferous tubule diameter, and epithelial height, as well as immunohistochemical analyses using markers for DNA double-strand breaks, autophagy, and apoptosis. In addition, a semen analysis of the epididymides was performed. The histological and immunohistochemical evaluations were performed blinded. The statistical ANOVA test was corrected using Holm–Bonferroni method.
Histological examinations revealed significant morphological changes in both groups of offspring exposed intrauterine, compared to the control group that was not exposed. Specifically, the diameter of the seminiferous tubules, the height of the epithelium, and the Johnson score decreased. The percentage of sperm with physiological morphology in the sham-exposed group was within the expected range (74%), whereas the number of healthy sperm decreased in the exposed groups. Apoptosis markers (TUNEL and the apoptotic index) increased in a statistically significant manner in the testicular tissue. The marker for DNA double-strand breaks, γ-H2AX, also increased in a statistically significant manner. Beclin-1, an autophagy indicator, increased statistically significantly in the 3T group.
Prenatal exposure to 3.5 GHz RF radiation below international limits can cause persistent structural and cellular changes in testicular tissue. These changes include impaired spermatogenesis, DNA damage, increased autophagy, and apoptosis that persist in offspring into adulthood. Despite being exposed only intrauterine, the tissue of the experimental animals does not recover from the damage. This suggests that mobile phone radiation during critical phases of embryonic development may pose a significant risk to male fertility. The authors point out that morphological changes in sperm are probably not artifacts because the physiological sperm morphology in the control group is within the expected range [2]. Furthermore, the authors compare their results with those of previous studies and note that nearly all of the observed adverse health effects have already been documented [3–6]. (Most of these studies have been reviewed in previous issues of the ElektrosmogReport; editor's note.)
Editor’s note:
This study stands out for its clear design (prenatal exposure), high relevance (long-term effects), validated exposure measurement, multimodal endpoint analysis, and adherence to scientific standards such as blinding, randomization, and comprehensive statistical analysis. Of particular concern is the fact that the described long-term damage is caused by chronic exposure to low field strengths to which we are exposed in everyday life. Ideally, functional fertility data such as sperm motility and other molecular markers would have been included to draw conclusions about the underlying mechanisms. Oxidative stress markers are particularly noteworthy here, as the authors discuss oxidative stress as a potential cause of the sterilizing effect of RF radiation exposure. (RH)
1. Cordelli E, Ardoino L, Benassi B, Consales C, Eleuteri P, Marino C et al. (2024). Effects of radiofrequency electromagnetic field (RF-EMF) exposure on male fertility: A systematic review of experimental studies on non-human mammals and human sperm in vitro. Environment International, 185, 108509. https://doi.org/10.1016/j.envint.2024.108509
2. van der Horst G, Skosana B, Legendre A, Oyeyipo P, du Plessis SS (2018). Cut-off values for normal sperm morphology and toxicology for automated analysis of rat sperm morphology and morphometry. Biotechnic & Histochemistry, 93(1), 49–58. https://doi.org/10.1080/10520295.2017.1380842
3. Özgen M, Take G, Kaplanoğlu İ, Erdoğan D, Seymen C M (2023). Therapeutic effects of melatonin in long-term exposure to 2100 MHz radiofrequency radiation on rat sperm characteristics. Revista Internacional de Andrologia, 21(4), 100371. https://doi.org/10.1016/j.androl.2023.100371
4. Shahin NN, El-Nabarawy NA, Gouda AS, Mégarbane B (2019). The protective role of spermine against male reproductive aberrations induced by exposure to electromagnetic field – An experimental investigation in the rat. Toxicology and Applied Pharmacology, 370, 117–130. https://doi.org/10.1016/j.taap.2019.03.009
5. Li R, Ma M, Li L, Zhao L, Zhang T, Gao X et al. (2018). The protective effect of autophagy on DNA damage in mouse spermatocyte-derived cells exposed to 1800 MHz radiofrequency electromagnetic fields. Cellular Physiology and Biochemistry, 48(1), 29–41. https://doi.org/10.1159/000491660
6. Xing F, Zhan Q, He Y, Cui J, He S, Wang G (2016). 1800MHz microwave induces p53 and p53-mediated caspase-3 activation leading to cell apoptosis in vitro. PLOS One, 11(9), e0163935. https://doi.org/10.1371/journal.pone.0163935