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14 August 2017

Female Infertility & Cell Phone Radiation

(Choice of photo by "Towards Better Health"
from Pinterest)
Female Infertility & Cell Phone Radiation
Electromagnetic Radiation Safety,
11 August 2017

Although we have considerable evidence that cell phone radiation damages sperm and is associated with male infertility, little attention has been paid to studying the effects of cell phone radiation on female infertility.*

A newly published study by Courtney Lynch and her colleagues found for women trying to get pregnant that stress as measured by the alpha-amylase levels in their saliva predicted whether they were successful. The researchers found that women with the highest levels of this enzyme in their saliva had a 29 percent lower probability of pregnancy compared to those with the lowest levels.

Although this study did not examine EMF exposure, earlier research published by Christoph Augner and his colleagues found that people who lived within 100 meters of cell phone towers had greater salivary alpha-amylase levels. In an experimental study, the researchers found that exposure to higher levels of GSM cell tower radiation increased the levels of this salivary enzyme.

In a 2013 review paper, Nazıroğlu and colleagues examined research on the effects of Wi-Fi and mobile phone radiation on reproductive signaling pathways. They reported that this radiation is related to "oxidative stress and overproduction of free oxygen radicals in female and male infertility." The authors concluded that "the role of EMR from mobile phones and wireless devices in female and male fertility should be investigated."

The news story and study abstracts appear below.

References (Last update: 8/11/2017)

Shahin S, Singh SP, Chaturvedi CM. Mobile Phone (1800MHz) Radiation Impairs Female Reproduction in Mice, Mus musculus, through Stress Induced Inhibition of Ovarian and Uterine Activity. Reprod Toxicol. 2017 Aug 2. pii: S0890-6238(17)30167-3.


• Mice exposed to mobile phone radiation (MPR) in different operative modes.
• Ovarian & uterine histopathology, steroidogenesis & stress parameters were checked.
• Degenerative changes & reduced follicle count were observed in MPR exposed ovary.
• MPR resulted significant decrease in ovarian steroidogenic proteins & sex steroids.
• MPR induced oxidative & nitrosative stress impairs reproductive functions in mice.


Present study investigated the long-term effects of mobile phone (1800MHz) radiation in stand-by, dialing and receiving modes on the female reproductive function (ovarian and uterine histo-architecture, and steroidogenesis) and stress responses (oxidative and nitrosative stress). We observed that mobile phone radiation induces significant elevation in ROS, NO, lipid peroxidation, total carbonyl content and serum corticosterone coupled with significant decrease in antioxidant enzymes in hypothalamus, ovary and uterus of mice. Compared to control group, exposed mice exhibited reduced number of developing and mature follicles as well as corpus lutea. Significantly decreased serum levels of pituitary gonadotrophins (LH, FSH), sex steroids (E2 and P4) and expression of SF-1, StAR, P-450scc, 3β-HSD, 17β-HSD, cytochrome P-450 aromatase, ER-α and ER-β were observed in all the exposed groups of mice, compared to control. These findings suggest that mobile phone radiation induces oxidative and nitrosative stress, which affects the reproductive performance of female mice.



Experimental group mice were exposed to non-thermal (for body as a whole) mobile phone radiation (1800 MHz) by using Nokia 100 (2G, GSM) dual-band mobile phones continuously for four months (3 h/day for 120 days) in different operative modes i.e., dialing (dialing was performed), receiving (dialing signals from D-group was received) and stand-by (mobile phone was kept in just switched on mode) modes. From D-group mobile phones, only dialing signals (and not speech signals) were sent to the mobile phones of R-group. Dialing signals on the mobile phones of R-group were received so that both D- and R-group animals were in continuous condition of connectivity for 1½ hrs, then after a very small break (∼10–15 s) again the dialing was initiated from the mobile phones of D-group and signals were received at the mobile phones of R-group and the continuity between the signal transmission and reception is maintained for another 1½ hrs. SB-group mice were kept beneath the “switched-on” mobile phones continuously for 3 h. Before the start of exposure, silent profile with no vibration was set for the mobile phones of all groups. To neutralize the box related and other external constraints, one sham control group was taken into account in each study. The control group mice were subjected to sham exposure in the same mobile phone exposure set-up for same time each day but with the mobile phones in “switched-off” condition.

This study demonstrate the deleterious effects of long-term 1800 MHz mobile phone radiation exposure in different operative modes i.e. dialing (D), receiving (R) and stand-by (SB) modes on female reproduction. Present experimental findings clearly elucidate that mobile phone radiation has a negative impact on female reproductive system. Outcome of the study demonstrates that long-term mobile phone irradiation causes alteration in ovarian and uterine morphology, histoarchitecture and activity. Mobile phone irradiated mice ovary revealed less number of developing and mature follicles with few corpus lutea and increased number of atretic/degenerative follicles. Although marked changes were observed in all the three experimental groups, the effects were more pronounced and severe in cases of R- and SB-groups of mice.

Overall, our study clearly elucidates that the long-term 1800 MHz mobile phone exposure impairs female reproductive system possibly via inducing both oxidative and nitrosative stress. Our study also suggests that mobile phone exposure produces deleterious effect on hypothalamus, ovary and uterus, and thus affects the ovarian and uterine activity and histoarchitecture adversely. Mobile phone radiation may result in ovarian and uterine dysfunction by increasing ROS and RNS production and disturbing antioxidant status. Oxidative and nitrosative stress created at the hypothalamus and peripheral level (ovary and uterus) as a consequence of long-term mobile phone exposure may severely reduce both steroidogenesis and folliculogenesis in the ovary as well as the structural and functional status of the uterus.

These results led us to conclude that chronic exposure to long-term mobile phone radiation may severely affect the ovarian and uterine activity of female mice and thus may lead to infertility. The effects were more pronounced/deleterious in stand-by and receiving conditions. Further, the results of this study performed on the rodent model, Mus musculus, may not be extrapolated to human being as the SAR value delivered to human at the ovary or uterus end will be much less than (and not comparable to) the value for the rodent at the desired site due to greater depth of the site from the skin surface of human being, assuming large body size ratio between two type of subjects, i.e., human being and rodent. However, if the human being is exposed to mobile phone radiation over longer duration, there may be the possibility of the radiation producing similar effect on human female reproductive system, on the assumption, that the total energy absorbed in the two cases is of same order of magnitude. Therefore, we anticipate that, these findings will improve our understanding of the etiology of female infertility due to heavy mobile phone usage.

The rise in female infertility problems may be, at least in part, due to a contribution from mobile phone radiation exposure to females. Hence, we anticipate that the outcome of the present study will not only contribute in framing of proper guidelines for safer use of mobile phone, which is an unavoidable device of present life style but may also assist in deciding the threshold limits to minimize adverse effects of the long term exposure to mobile phone radiations for females. However, further investigation is required in humans and non-human primates to determine whether the risks are similar and to establish safe exposure limits.

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