Scientific studies and reports showing rises in cancer risk from EMF exposure
The effects of radiofrequency electromagnetic radiation on sperm function (2016); American Center for Reproductive Medicine, Cleveland Clinic, Department of Urology, Weill Cornell Medicine – Qatar, Department of Urology, Hamad Medical Corporation, Doha, Faculty of Dentistry, MAHSA University; Arab Journal of Urology
|Meta-analysis of 27 studies||various EMF|
Among a total of 27 studies investigating the effects of RF-EMR on the male reproductive system, negative consequences of exposure were reported in 21. Within these 21 studies, 11 of the 15 that investigated sperm motility reported significant declines, 7 of 7 that measured the production of reactive oxygen species (ROS) documented elevated levels and 4 of 5 studies that probed for DNA damage highlighted increased damage due to RF-EMR exposure. Associated with this, RF-EMR treatment reduced the antioxidant levels in 6 of 6 studies that discussed this phenomenon, whereas consequences of RF-EMR were successfully ameliorated with the supplementation of antioxidants in all 3 studies that carried out these experiments. In light of this, we envisage a two-step mechanism whereby RF-EMR is able to induce mitochondrial dysfunction leading to elevated ROS production.
Radiofrequency radiation (900 MHz)-induced DNA damage and cell cycle arrest in testicular germ cells in swiss albino mice (2016); Molecular Cytogenetic Laboratory, Department of Life Science and Bioinformatics; Toxicology and Industrial Health
|Male mice||900 MHz for 4 hours/day and 8 hours/day for 35 days|
EMF exposure caused depolarization of mitochondrial membranes resulting in destabilized cellular redox homeostasis. Statistically significant increases in the damage index in germ cells and sperm head defects were also noted in exposure groups. Flow cytometric estimation of germ cell subtypes in mice testis revealed 2.5-fold increases in spermatogonial populations with significant decreases in spermatids. Almost fourfold reduction in spermatogonia to spermatid turnover (1C:2C) and three times reduction in primary spermatocyte to spermatid turnover (1C:4C) was found indicating arrest in the premeiotic stage of spermatogenesis, which resulted in loss of post-meiotic germ cells apparent from testis histology and low sperm count in exposed groups. Histological alterations such as sloughing of immature germ cells into the seminiferous tubule lumen, epithelium depletion and maturation arrest were also observed. To conclude, exposure-induced oxidative stress causes DNA damage in germ cells, which alters cell cycle progression leading to low sperm count in mice.
All these changes showed recovery following the post-exposure period indicating that the adverse effects of exposure are detrimental but reversible.