Introduction:The increasing scientific evidence of various health hazards on exposure of Radiofrequency Radiation (RFR) emitted from both the cell phones and base stations have caused significant media attention and public discussion in recent years. The mechanism of interaction of RF fields with developing tissues of children and fetuses may be different from that of adults due to their smaller physical size and variation in tissue electromagnetic properties. The present study may provide an insight into the basic mechanisms by which RF fields interact with developing tissues in an embryo.

A Mobile phone in operation emits a pulsed radiofrequency electromagnetic field which is absorbed into the user's body particularly the head region. Contradictory scientific reports on the health effect of nonionizing radiations on biological tissues have prompted to undertake the present study to evaluate the damage in the developing lens of a chick embryo following exposure to radiation emitted from a 2G cell phone. Fertilized chick embryos were incubated in two groups in a standard egg incubator. The experiment group was exposed to radiation emitted from a 2G cell phone. On completion of scheduled duration, the embryos were collected and processed for routine histological studies. The 9th to 12th day chick embryo eyes were processed for assessment of DNA damage using the alkaline comet assay technique. The lens thickness and the equatorial diameter were measured using oculometer and statistically compared for both groups. In the present study, the exposure of chick embryos to a 2G cell phone caused structural changes in lens epithelial cells, formation of cystic cells and spaces, distortion of lens fibers, and formation of posterior aberrant nuclear layer. The DNA damage in the developing eyes of the experiment group assessed by comet assay was highly significant.

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Background and Objectives: The role of genomic instability resulting from chromosomal aberrations, gene mutations due to deletions, translocations and single gene defects is a known phenomenon leading to DNA damage. A deficient repair process is also attributed to the perpetuation of this damage. Placental insufficiency in pregnancy during late embryonic or early fetal period resulting in DNA damage gives rise to malformed phenotypes. An attempt was made to study the extent of DNA damage in non syndromic congenital malformations. Materials and Methods: A total of 20 children were studied. 10 of them, between 10 days to 5 years of age, presenting with non syndromic congenital anomalies formed the cases. An equal number of children matched for age criteria formed the controls. Lymphocytes collected from peripheral blood of these children were subjected to the standard comet assay, an highly sensitive, reliable, relatively inexpensive and reproducible single cell layer electrophoretic technique, where damaged DNA migrates out of the cell towards the anode forming a comet. The length of the tail is a measure of the DNA damage. Results: The malformations observed were those of urogenital, craniofacial and nervous systems. The mean comet tail lengths were 24.744 μm, 20.649 μm and 27.402 μm respectively. Comparing this to the mean tail length in controls with 1.992 μm, there was high statistical significance (P value <0.0001). Conclusion: Gene mutations, particularly involving Sex Region Determining (SRD) genes and Superoxide Dismutase (SOD) enzyme imbalances, have been implicated in these congenital malformations. Thus the comets seen in this study reflect the DNA damage due to the gene defects.