The cancer hazard associated with lifetime exposure to radiofrequency radiation (RFR) was examined in Sprague Dawley (SD) rats at the Ramazzini Institute (RI), Italy. There were increased incidences of gliomas and cardiac schwannomas. The translational relevance of these rare rat tumors for human disease is poorly understood. We examined the genetic alterations in RFR-derived rat tumors through molecular characterization of important cancer genes relevant for human gliomagenesis. A targeted next-generation sequencing (NGS) panel was designed for rats based on the top 23 orthologous human glioma-related genes. Single-nucleotide variants (SNVs) and small insertion and deletions (indels) were characterized in the rat gliomas and cardiac schwannomas. Translational relevance of these genetic alterations in rat tumors to human disease was determined through comparison with the Catalogue of Somatic Mutations in Cancer (COSMIC) database. These data suggest that rat gliomas resulting from life-time exposure to RFR histologically resemble low grade human gliomas but surprisingly no mutations were detected in rat gliomas that had homology to the human IDH1 p.R132 or IDH2 p.R172 suggesting that rat gliomas are primarily wild-type for IDH hotspot mutations implicated in human gliomas. The rat gliomas appear to share some genetic alterations with IDH1 wildtype human gliomas and rat cardiac schwannomas also harbor mutations in some of the queried cancer genes. These data demonstrate that targeted NGS panels based on tumor specific orthologous human cancer driver genes are an important tool to examine the translational relevance of rodent tumors resulting from chronic/life-time rodent bioassays.
Excerpt
In summary, our results demonstrate that regardless of their etiology (due to lifetime RFR exposure or arising spontaneously), rat gliomas are primarily Idh1/2 wild type unlike most human gliomas. Histologically, most of the rat gliomas resemble diffuse low-grade gliomas in humans and such gliomas that do not harbor IDH1/2 mutations in humans are known to have poor prognosis. The genetic alterations in other cancer genes evaluated in this panel provide novel insights into tumor progression in rat gliomas and cardiac schwannomas. The relevance of specific mutations to human cancers is variable, with some genes (Tp53, Cdkn2a, Erbb2, Chek2, Kras and Pik3r1) harboring many alterations with COSMIC relevance while the opposite is true for other target genes (Idh1/2, Atrx, Notch1, Pten, Rb1 and Setd2). Several of these conserved mutations in rat tumors do not have comparable alterations in the COSMIC database, suggesting that the orthologous mutations could have different functional consequences in rat carcinogenesis and deserve further study. An important consideration is that molecular differences underlying mutational processes contribute to distinct mutational patterns which could be the result of similar etiology, albeit by different mechanisms.
Several of the variants that were detected in gliomas were also observed in non-tumor brain tissues from interim time point providing an insight into the molecular pathogenesis in rodent carcinogenicity studies and these strategies may be utilized to potentially estimate the cancer hazard risk in shorter term animal studies. Finally, this targeted mutation panel may be refined using data from whole genome or exome sequencing of rat tumors and performing error corrected duplex sequencing to increase the sensitivity to detect rare mutations in exposed non-tumor tissues from early time points.
A newly-published study by the Ramazzini
Institute (RI) replicates the heart tumor result from the NationalToxicology Program (NTP) study of cell phone radiation on rats.The RI study found increased incidence of heart schwannoma in male rats despite the
use of different frequencies and much lower intensity radio frequency radiation
(RFR) than the NTP study. This suggests that the primary health effect found in the NTP study is robust.
rats to evaluate the carcinogenic effects of cell phone radiation.
Among male rats, the overall incidence of heart schwannoma and
hyperplasia (precancerous cells) was 0.7% (3 of 412) in the control group, 1.2% (5/401) in the 5
volts/meter (V/m) group, 1.0% (2/209) in the 25 V/m group, and 3.9% (8/207) in
the 50 V/m group. The 50 V/m group had significantly greater incidence than the
control group (p < .02).
Among male rats, the overall incidence of glioma and glial cell
hyperplasia in the control group was 0.0% (0 of 412), 0.7% (3/401) in the 5 V/m group, 1.4% (3/209) in the 25 V/m group, and 0.0% (0/207) in
the 50 V/m group. However, these differences were not statistically significant.
frequency (1800 MHz vs. 900 MHz) and much lower intensity microwave radiation
exposures than the NTP study. The Specific Absorption Rates ranged from 0.001 –
0.1 W/kg SAR in the RI study as compared to 1.5 – 6.0 W/kg in the NTP study.
Bologna, Italy that has conducted scientific research for more than
two decades to identify and quantify environmental toxic and carcinogenic risks
and evaluate the effectiveness of drugs to prevent the onset or development of
cancer.
The abstract for the paper and the press release appear below.
P.S. In our six-nation study of RFR exposure, the average total RFR exposure (not just cell tower RFR) was highest in Los Angeles where it ranged from 0.72 to 1.60 V/m across eight different outdoor microenvironments (Sagar et al., 2018). The highest average total RFR value measured in our study was 1.85 V/m which was found on a university campus in Australia and was attributable to FM radio transmissions.
Background: In 2011, IARC
(International Agency for Research on Cancer) classified radiofrequency radiation (RFR) as possiblehuman carcinogen (Group 2B). According to IARC, animals studies, as well as
epidemiological ones, showed limited evidence of carcinogenicity. In 2016, the
NTP published the first results of its long-term bioassays on near field RFR,
reporting increased incidence of malignant glial tumors of the brain and heart
Schwannoma in rats exposed to GSM – and CDMA –modulated cell phone RFR. The
tumors observed in the NTP study are of the type similar to the ones observed
in some epidemiological studies of cell phone users.
Objectives: The Ramazzini Institute (RI) performed a life-span carcinogenic
study on Sprague-Dawley rats to evaluate the carcinogenic effects of RFR in the
situation of far field, reproducing the environmental exposure to RFR generated
by 1.8 GHz GSM antenna of the radio base stations of mobile phone. This is the
largest long-term study ever performed in rats on the health effects of RFR,
including 2448 animals. In this article, we reported the final results
regarding brain and heart tumors.
Methods: Male and female Sprague-Dawley rats were exposed from prenatal life
until natural death to a 1.8 GHz GSM far field of 0, 5, 25, 50 V/m with a
whole-body exposure for 19 h/day.
Results: A statistically significant increase in the incidence of heart
Schwannomas was observed in treated male rats at the highest dose (50 V/m).
Furthermore, an increase in the incidence of heart Schwann cells hyperplasia
was observed in treated male and female rats at the highest dose (50 V/m),
although this was not statistically significant. An increase in the incidence
of malignant glial tumors was observed in treated female rats at the highest
dose (50 V/m), although not statistically significant.
Conclusions: The RI findings on far field exposure to RFR are consistent with
and reinforce the results of the NTP study on near field exposure, as both
reported an increase in the incidence of tumors of the brain and heart in
RFR-exposed Sprague-Dawley rats. These tumors are of the same histotype of
those observed in some epidemiological studies on cell phone users. These
experimental studies provide sufficient evidence to call for the reevaluation of IARC conclusions regarding
the carcinogenic potential of RFR in humans.
https://pubmed.ncbi.nlm.nih.gov/29530389/
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Title: World’s Largest Animal Study on Cell Tower Radiation Confirms Cancer Link
https://www.saferemr.com/2018/03/RI-study-on-cell-phone.html
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