In the present community-based study, we analyzed impact of RFR emitted from cell phone on adult human semen quality. Results clearly indicated that there was a decrease in semen volume, linear progressive motility, sperm concentration, sperm density and percentage of normal sperm in highly exposed group in comparison to moderate and control groups. This decrease trend in all these parameters was very transpicuous from 1st year to 3rd year and it was statistically significant. On the other hand, percentage of abnormal sperm, non-motile sperm, abnormal head, midpiece and tail defects significantly increased in highly exposed group in comparison to moderately exposed and control groups with an increasing trend from 1st to 3rd year. These observations are in compliance with earlier reports [14,18,3,4,5,15,24,2,51]. Similar observations have also been reported in animal studies [27,30]. But Malyapa et al 1997 and Dasdag et al 2003 did not find adverse effect of cell phone radiation on mouse fibroblasts and sperm count, morphology, histology of rat’s testes respectively [31,13]. But it is not correct to compare a rat model to humans. This is because of the facts that rat testes are smaller in size, nonpendulous scrotum and it can migrate between the abdomen and scrotum in the inguinal canal [10].
In the present study, slight decrease in serum testosterone was noticed in highly exposed group in comparison to control and moderate groups which is statistically not significant and this trend continued during the subsequent visits 1st to 3rd in all the study groups. On the other hand, exposure to microwave have been reported to disrupts the seminiferous tubules and reduces the Leydig cell population and testosterone levels in rats [24]. It has been reported that testosterone is required for maintenance of structural morphology and physiology of seminiferous tubules, spermatogenesis and formation of spermatozoa [44,48]. Hence any changes in the concentration of testosterone will result in adverse effect on semen quality [24].
In the present study the levels of T4 in highly exposed group were showing increasing trend during the follow up visit from 1st to 3rd in highly exposed group in comparison to the moderate and control groups which is statistically significant. On the other side the level of TSH were decreasing in highly exposed group in comparison to moderately exposed and control group. Delay in spermatogenesis with maturation arrest, no pachytene spermatocytes, a decrease in seminiferous tubule diameters, an impairment of the mitochondrial activity, and a reduction in lipid concentration have been reported in hyperthyroid rats [38]. Choudhury et al (2003) reported an alteration of antioxidant systems as catalase is upregulated while GPx is downregulated in hypothyroid rats [12]. Whereas levothyroxine administration in ram have been reported to cause reduction in sperm motility and testis weight [11]. Rijntjes et al (2008) concluded that hyperthyroidism delays Leydig cell development and adversely affects spermatogenesis in rats [40].
In thyrotoxicosis patients, the high level of circulating thyroid hormones has been reported to results in asthenozoospermia in more than half of the patients, oligozoospermia and teratozoospermia in about 40% of thyrotoxic patients [1]. These abnormalities are frequently associate with a reduced semen volume (hypoposia) [1]. Hence, reduced sperm concentration &motility, and increase in abnormal morphology along with an overall decrease in semen volume have been reported to be the main semen alterations of thyrotoxic male patients [47].RW Hudson et al (1992) reported lower progressive forward motility in adult men with thyrotoxicosis due to Graves’ disease compared with euthyroid controls [41]. Krassaset al (2002) observed that hyperthyroid patients have a lower sperm motility compared to euthyroid controls [29].
As it is known that in normal man, 2% of testosterone is free, 44% is bound to sex hormone-binding globulin (SHBG), and the remaining is bound to albumin and other proteins. This is free- and albumin-bound portions testosterone which is called as bio available testosterone [8,19,53]. It has been reported that in hyperthyroidism, total testosterone and SHBG levels are increased [23,37] and free Testosterone is transiently reduced or may be within normal range [22] but mean basal bio-available Testosterone level is decreased [50]. In few thyrotoxic male subjects elevated circulating estrogen level have been reported which is because of enhanced production rate of the estrogen and increment of peripheral conversion of androgen to estrogen [39]. These reports clearly indicate that if it is confirmed hyperthyroidism then despite increased or normal total testosterone level, thyrotoxic men may have androgen deficiency due to reduced free and bioavailable testosterone and increase estrogen level. Alterations in these hormones can cause gynecomastia (24%) [1], decreased libido (70%) [52], erectile dysfunction (56%) [39], spider angiomas, spermatogenetic dysfunction [28] and reduced sperm count and/or motility. The elevated levels of thyroxin may be provoking oxidative stress on sperm including hyperthyroidism associated hyperestroginemia, enhanced nitric oxide synthase gene expression with nitric oxide overproduction following increase of cytokines stimulating ROS generation, increase turnover of mitochondrial protein, mitoptosis and increased rate of thyroid hormone induced lipolysis [36].
Several studies have been conducted to investigate the effect of RFR emitted from GSM mobile phone on levels of thyroid hormones. Baby et al (2017) conducted a cross sectional study in South India and reported a significant correlation between the total radiation and the TSH values among both individuals with or without a family history of thyroid dysfunction [7]. In a systematic review (Asl JF et al 2019) three studies reported decrease in TSH level in the subjects exposed to radiation whereas in one study an increase in TSH level was noticed [6]. Asl JF et al (2019) concluded that exposure to microwave radiations could cause cellular stress and increased thyroid gland temperature which can adversely affect the iodine uptake by the thyroid gland leading to thyroid gland disfunction [6]. In another cohort study that prolonged exposure to RFR resulted in a significant (P < 0.01) decrease in the T3 and T4 levels of the exposed subjects, indicating a possible thyroid dysfunction [16]. Mortavazi et al (2009) reported high TSH, low T4 and normal T3 concentrations in excessive mobile phone users. The authors concluded a possible hypothyroid state and thyroid dysfunction which seems to be directly proportional to the degree of duration and intensity of RFR exposure [32]. The study also concluded a possible harmful effect of cell phone RFR on the hypothalamic-pituitary-thyroid (HPT) axis [32].
To find out the effects on cell phone radiation on the thyroid gland function Bergamaschi et al (2004) conducted a study therein he divided the subjects into various groups based on their frequency of cell phone use [9]. It was reported that the subjects who had conversations on their mobile phones for > 33 hours per month had a 9.9% prevalence of low TSH values compared to a prevalence of 6% in the group who talked on their mobile phones for < 19 hours per month (P < 0.05). Based on an exploration study on this subject, Muacevic et al (2021) reported that the mobile phone radiation could negatively affect thyroid gland function and hormone production directly by disrupting the thyroid gland tissue or indirectly by disrupting the Hypothalamic-Pituitary-Thyroid (HPT) axis [33].
Current literature has established that mobile phones can exert their deleterious effects on the thyroid gland through thermal and non-thermal effects by stimulating cellular receptors and causing severance in the microtubules between cells [45]. The non-thermal effect of RFR leads to Reactive Oxygen Species (ROS) formation and accumulation of heavy metals within the cells [45,46]. It has also been reported that RFR may stimulate NADPH oxidase present on the plasma membrane of the cells which leads to ROS formation and apoptosis induction [17]. This oxidative stress may also disrupt the cellular Ca2 + ion pumps, transporters, and binding proteins [17]. In addition, RFR itself may also act on Ca2 + pumps that lead to Ca2 + efflux from cells and cellular apoptosis [17]. Other cellular stressors may be responsible for this disruption include increased cortisol levels and enzymes involved in thyroid homeostases, such as anti-thyroperoxidase, liver deiodinase, and ornithine carboxylase [21].