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(Database last updated on Mar 27, 2024)
| ID Number | 52 | |
| Study Type | In Vitro | |
| Model | 900 MHz (GSM, CW), 1.748 GHz (GSM) and 1950 MHz (UMTS) exposure to cells in culture and analysis of micronuclei, DNA damage, apoptosis and other endpoints. | |
| Details | Human primary lymphocytes isolated from healthy donors (n=10) were exposed to 900 MHz (GSM) for 2 hours at either 0.3 or 1 W/kg in a waveguide (temperature controlled at 37 ± 0.1 °C). The study was simultaneously performed in two separate labs, one in Rome, Italy and the other in Naples, Italy as a CTIA sponsored replication of Hook and Tice and funded through an FDA administered CRADA. The authors report no effects on DNA damage using alkaline single cell gel electrophoresis (SCGE)/comet assay, and no effects on chromosome aberrations or sister chromatid exchange after phytohemagglutinin stimulation. Positive controls included methyl methanesulfonate (MMS) for DNA damage and mitomycin-C (MMC) for chromosome aberrations. A similar inter-laboratory study exposing cells for 24 hours was also performed using 900 MHz (GSM) exposures at 0, 1, 5, and 10 W/kg. Again, the authors report no effects of RF exposure on genotoxic or cytotoxic parameters. In earlier studies, human lymphocytes (primary cultures) were exposed to 1.748 GHz (GSM, CW) RF for 15 minutes at an average SAR of 2.25 W/kg (range 1.5 to 5 W/kg). After exposure, cells were stimulated with PHA, cultured for 72 hours, and blocked in M phase with cytocholasin B. No effects on micronuclei formation were observed following CW exposure, although a statistically significant increase in MN formation was reported with GSM exposure with an apparent dose response (SAR positions throughout the flask ranging from 1.5 - 5 W/kg were compared). No effects on proliferation were observed with either CW or GSM RF at any exposure level. Also in a preliminary study, 1800 MHz (CW) exposure to lymphocytes at 2 W/kg showed no effect, but in combination with MMC appeared to have a synergistic effect on the production of MN. These initial observations, however, are not consistent with the latest reports from this group using a more controlled and characterized exposure system. In data presented at EBEA 2001 in Helsinki Finland and BEMS (2001) in St. Paul MN, human lymphocytes were exposed to 1.748 GHz (CW, GSMK, or GSMK+TDMA) RF for 15 minutes at 2 W/kg. The authors report no effect of RF exposure on DNA damage or repair of X-ray damage under any condition. In other studies, the group exposed bovine lymphocytes to 9 GHz (CW) MW for 10 minutes at an SAR of 70 W/kg, either in the presence or absence of MMC, in a waveguide system. A maximal temperature rise of 4.5 degrees was recorded (from 29 to 33.5 C). Following exposure, cells were cultured for 5 days and analyzed for MN formation. Exposure at this thermal level resulted in a significant increase in MN incidence, both with and without MMC treatment. Human lymphocytes were also exposed to 9 GHz (AM-50 Hz) MW for 10 minutes at an SAR of 90 W/kg to achieve a final culture temperature of 37 degrees. Following exposure, cells were cultured as above and analyzed for MN formation. No consistent and statistically significant effect was observed, and variability in the assay (both increases and decreases in MN) was large. In a subsequent study, primary lymphocytes from healthy individuals (n = 6) were exposed to 2 GHz (UMTS) for 68 hours at 2.2 W/kg and evaluated by comet assay for micronuclei and DNA breaks. At the 24th hour, cells were stimulated to divide (move from G0-G1-S-G2) with PHA stimulation which allowed for testing at different synchronized stages of the cell cycle. Mitomycin C was used as a positive control. The authors reported no significant effects on micronuclei or DNA breaks at the exposure level used. In a recent study, human dermal fibroblasts (from both healthy and Turner's Syndrome subjects) were exposed to 900 MHz (GSM) at 1 W/kg for 24 hrs either +/- the co-mutagen 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX). The authors report no effect on DNA damage as analyzed by coment assay or chromosoma aberrations of RF exposure. When lymphocytes were exposed for 20 hrs at 10 W/kg and subsequently challenged with Mitomycin C, however, there was a decreased rate of micronuclei in certain samples than with MMC alone suggesting a protective or adaptive response. A similar effect has been reported for low-level ionizing radiation exposure. Sannino et al. 2009 (#4442) (Authors' abstract): The aim of this study was to investigate DNA damage in human dermal fibroblasts from a healthy subject and from a subject affected by Turner's syndrome that were exposed for 24 h to radiofrequency (RF) radiation at 900 MHz. The RF-radiation exposure was carried out alone or in combination with 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), a well-known environmental mutagen and carcinogen produced during the chlorination of drinking water. Turner's syndrome fibroblasts were also exposed for a shorter time (1 h). A signal similar to that emitted by Global System for Mobile Communications (GSM) mobile phones was used at a specific absorption rate of 1 W/kg under strictly controlled conditions of temperature and dosimetry. To evaluate DNA damage after RF-radiation exposure alone, the alkaline comet assay and the cytokinesis-block micronucleus assay were used. In the combined-exposure experiments, MX was given at a concentration of 25 microM for 1 h immediately after the RF-radiation exposure, and the effects were evaluated by the alkaline comet assay. The results revealed no genotoxic and cytotoxic effects from RF radiation alone in either cell line. As expected, MX treatment induced an increase in DNA migration in the comet assay, but no enhancement of the MX-induced DNA damage was observed in the cells exposed to RF radiation. Sannino et al. 2009 (#4478)(Authors' abstract): The incidence of micronuclei was evaluated to assess the induction of an adaptive response to non-ionizing radiofrequency (RF) radiation in peripheral blood lymphocytes collected from five different human volunteers. After stimulation with phytohemagglutinin for 24 h, the cells were exposed to an adaptive dose of 900 MHz RF radiation used for mobile ommunications at a peak specific absorption rate of 10 W/kg) for 20 h and then challenged with a single genotoxic dose of mitomycin C (100 ng/ ml) at 48 h. Lymphocytes were collected at 72 h to examine the frequency of micronuclei in cytokinesis-blocked binucleated cells. Cells collected from four donors exhibited the induction of adaptive response (i.e., responders). Lymphocytes that were preexposed to 900 MHz RF radiation had a significantly decreased incidence of micronuclei induced by the challenge dose of mitomycin C compared to those that were not pre-exposed to 900 MHz RF radiation. These preliminary results suggested that the adaptive response can be induced in cells exposed to non-ionizing radiation. A similar phenomenon has been reported in cells as well as in animals exposed to ionizing radiation in several earlier studies. However, induction of adaptive response was not observed in the remaining donor (i.e., non-responder). The incidence of micronuclei induced by the challenge dose of mitomycin C was not significantly different between the cells that were pre-exposed and unexposed to 900 MHz RF radiation. Thus the overall data indicated the existence of heterogeneity in the induction of an adaptive response between individuals exposed to RF radiation and showed that the less timeconsuming micronucleus assay can be used to determine whether an individual is a responder or non-responder. Sannino et al. 2011 (Authors' abstract): Purpose:To investigate the influence of cell cycle on the adaptive response (AR) induced by the exposure of human blood lymphocytes to radiofrequency fields (RF). Materials and methods:Human peripheral blood lymphocytes in G(0)-, G(1)- or S-phase of the cell cycle were exposed for 20 hours to an adaptive dose (AD) of 900 MHz RF at an average specific absorption rate of 1.25 W/kg and then treated with a challenge dose (CD) of 100 ng/ml mitomycin C (MMC). Un-exposed and sham-exposed controls as well as cells treated with MMC alone were included in the study. The incidence of micronuclei (MN) was evaluated to determine the induction of AR. Results:The results indicated that the cells which were exposed to AD of RF in G(0)- and G(1)-phase of the cell cycle did not exhibit AR while such a response was observed when the cells were exposed to AD of RF in S-phase of the cell cycle. Conclusions:These results confirmed the observations reported in our previous investigation where AR was observed in human blood lymphocytes exposed to AD of RF in S-phase of the cell cycle and further suggested that the timing of AD exposure of RF is important to elicit AR. AUTHORS' ABSTRACT: Zeni et al. 2012 (IEEE #5158): In this study, rat pheochromocytoma (PC12) cells were exposed, as a model of neuron-like cells, to 1950 MHz radiofrequency (RF) radiation with a signal used by the 3G wireless technology of the Universal Mobile Telecommunications System (UMTS) to assess possible adverse effects. RF exposure for 24h at a specific absorption rate (SAR) of 10 W/kg was carried out in a waveguide system under accurately controlled environmental and dosimetric parameters. DNA integrity, cell viability, and apoptosis were investigated as cellular endpoints relevant for carcinogenesis and other diseases of the central nervous system. Very sensitive biological assays were employed to assess the effects immediately after RF exposure and 24 h later, as demonstrated by the cellular response elicited in PC12 cells using positive control treatments provided for each assay. In our experimental conditions, 24h of RF exposure at a carrier frequency and modulation scheme typical of a UMTS signal was not able to elicit any effect in the selected cellular endpoints in undifferentiated PC12 cells, despite the application of a higher SAR value than those applied in the majority of the studies reported in the literature. AUTHORS' ABSTRACT: Sannino et al. 2014 (IEEE #5496): The aim of this preliminary investigation was to assess whether human peripheral blood lymphocytes which have been pre-exposed to non-ionizing radiofrequency fields exhibit an adaptive response (AR) by resisting the induction of genetic damage from subsequent exposure to ionizing radiation. Peripheral blood lymphocytes from four healthy donors were stimulated with phytohemagglutinin for 24 h and then exposed for 20 h to 1950 MHz radiofrequency fields (RF, adaptive dose, AD) at an average specific absorption rate of 0.3 W/kg. At 48 h, the cells were subjected to a challenge dose (CD) of 1.0 or 1.5 Gy X-irradiation (XR, challenge dose, CD). After a 72 h total culture period, cells were collected to examine the incidence of micronuclei (MN). There was a significant decrease in the number of MN in lymphocytes exposed to RF + XR (AD + CD) as compared with those subjected to XR alone (CD). These observations thus suggested a RF-induced AR and induction of resistance to subsequent damage from XR. There was variability between the donors in RF-induced AR. The data reported in our earlier investigations also indicated a similar induction of AR in human blood lymphocytes that had been pre-exposed to RF (AD) and subsequently treated with a chemical mutagen, mitomycin C (CD). Since XR and mitomycin-C induce different kinds of lesions in cellular DNA, further studies are required to understand the mechanism(s) involved in the RF-induced adaptive response. AUTHORS' ABSTRACT: Zeni et al. 2012 (IEEE #5509): The induction of an adaptive response (AR) was examined in human peripheral blood lymphocytes exposed to non-ionizing radiofrequency fields (RF). Cells from nine healthy human volunteers were stimulated for 24h with phytohaemagglutinin and then exposed for 20h to an adaptive dose (AD) of a 1950MHz RF UMTS (universal mobile telecommunication system) signal used for mobile communications, at different specific absorption rates (SAR) of 1.25, 0.6, 0.3, and 0.15W/kg. This was followed by treatment of the cells at 48h with a challenge dose (CD) of 100ng/ml mitomycin C (MMC). Lymphocytes were collected at the end of the 72h total culture period. The cytokinesis-block method was used to record the frequency of micronuclei (MN) as genotoxicity end-point. When lymphocytes from six donors were pre-exposed to RF at 0.3W/kg SAR and then treated with MMC, these cells showed a significant reduction in the frequency of MN, compared with the cells treated with MMC alone; this result is indicative of induction of AR. The results from our earlier study indicated that lymphocytes that were stimulated for 24h, exposed for 20h to a 900MHz RF GSM (global system for mobile communication) signal at 1.25W/kg SAR and then treated with 100ng/ml MMC, also exhibited AR. These overall data suggest that the induction of AR depends on RF frequency, type of the signal and SAR. Further characterization of RF-induced AR is in progress. AUTHORS' ABSTRACT: Sannino et al. 2017 (IEEE #6668): In this study, the effect of radiofrequency (RF) exposure to 1950 MHz, Universal Mobile Telecommunication System signal, was investigated in Chinese hamster lung fibroblast cell line (V79). Genotoxic and cytotoxic effects of 20-h exposure at specific absorption rate (SAR) values from 0.15 W/kg to 1.25 W/kg were measured by means of cytokinesis-block micronucleus (MN) assay. Exposure was carried out blinded under strictly controlled conditions of dosimetry and temperature. The effect of RF exposure alone at four SAR values was tested, that is, 0.15, 0.3, 0.6, and 1.25 W/kg. A statistically significant increase in MN frequency was found in cultures exposed to 0.15 and 0.3 W/kg (P < 0.05) compared to sham-exposed ones, in the absence of cytotoxicity. SAR values of 0.6 and 1.25 W/kg did not exert any effect. Moreover, to evaluate the ability of RF to exert protective effects with respect to a chemical mutagen, cell cultures were also pre-exposed for 20 h at 0.3 or 1.25 W/kg, and then treated with 500 ng/ml of mitomycin-C (MMC). A significant reduction in the frequency of MN was detected in cultures pre-exposed to 1.25 W/kg compared to cultures treated with MMC alone (P < 0.05), indicating induction of adaptive response. Such a decrease was not induced by pre-exposure at 0.3 W/kg SAR. Taken together, our results indicated that V79 is a sensitive cell model to evidence either adverse or beneficial effects of RF exposure, depending on experimental conditions applied. AUTHORS' ABSTRACT: Romeo, Scarfi et al. 2019 (IEEE #7263): The occurrence of modulation-specific effects after co-exposures to Radiofrequency (RF) and other agents has been discussed in the literature. In this paper, the influence of modulation and bandwidth in eliciting the DNA damage of RF alone and in combination with mitomycin-C (MMC), is analyzed in human lymphocytes. Blood cultures from healthy donors were exposed to 1950 MHz, and Continuous Wave (CW), Wideband Direct-Sequence Code Division Multiple Access (WCDMA, 4.5 MHz bandwidth), and Additive White Gaussian Noise (AWGN, 9 MHz bandwidth) signals were considered. For each signal, SAR values of 0.15, 0.3, 0.6, 1.25 W/kg were tested. RF exposure alone never induced DNA damage in the micronucleus assay. When RF exposure was followed by MMC treatment, the effect depended on modulation and bandwidth. CW exposure never altered the MMC-induced DNA damage, while such damage was reduced when either signals WCDMA at 0.3 W/kg SAR or AWGN at 0.15 and 0.3 W/kg were applied. These results indicate the influence of modulation for the occurrence of the protective effect, with a relation between the bandwidth and the power absorbed by samples. If confirmed in vivo, clinical applications using modulated RF signals could be devised, to protect cells from side effects of therapeutic treatments. |
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| Findings | No Effects | |
| Status | Completed With Publication | |
| Principal Investigator | ICEmB, CNR-IREA, Univ Naples, Italy - scarfi.mr@irea.cnr.it | |
| Funding Agency | Agency Tech, Energy, Environ, Italy, FDA, USA, CTIA, USA, CEMFEC, EU 5th Framework, Europe, CNR-IREA | |
| Country | ITALY | |
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