Medscape www.medscape.com

Tables for:
Scientific Progress - Wireless Phones and Brain Cancer: Current State of the Science

[Medscape General Medicine 2(2), 2000. © 2000 Medscape Portals, Inc]


Table 1. In Vitro Toxicologic Studies Identified Through Literature Surveillance


AuthorsBiological ModelBiological End PointExposure ConditionsResultsIntervention Indicated (y/n)
Flipo et al, 1998 (Canada) Murine macrophages, spleen lymphocytes, and thymic cells of micealteration of cellular functions of immunocom-petent cells250-1500 G static magnetic fields 24 hourssignificant effects recorded include: decreased macrophage phagocytosis inhibited lymphocyte miyogenic response enhanced apoptotic death of thymocytes y
Ivaschuk et al, 1997 (United States)nerve growth factor-treated PC12 Rat pheochromocytoma cellseffects on c-jun and c-fos expression836.55 MHz generated by time division multiple access (TDMA) up to 60 minutesno change in c-fos transcript levels transcript levels for c-jun altered only after 20 min. exposure to 9 mW/cm2n
Maes et al, 1997 (Belgium)human whole blood cellschromosome aberrations, sister chromatid exchanges, DNA single-strand breaks935.2 MHz (GSM) generated by code division multiple access (CDMA) alone and in combination with mitomycin C 2 hours 0.3-0.4 W/kgno direct cytogenic effect was found (alkaline comet assay was used)n
Vijayalaxmi et al, 1997 (United States) Human blood lymphocytesincidence of chromosomal aberrations and micronuclei2450 MHz 90 minutes 12.46 W/kg no significant differences between radiofrequency radiation (RFR)-exposed and sham-exposed lymphocytes with regard to: mitotic indices, incidence of cells showing chromosomal damage, exchange aberrations, acentric fragments, binucleate lymphocytes, micronuclein
Antonopoulos et al, 1997 (Germany) Human peripheral lymphocytescell-cycle progression and frequencies of sister-chromatid exchanges380 MHz 0.08 W/kg 900 MHz 0.208 W/kg 1800 MHz 1.7 W/kg no differences between treated and control cultures n
Stagg et al, 1997 (United States)Rat glioma cellsDNA synthesis rates836.55 MHz generated by TDMA 24 hours 0.15-59 uW/g no increase in cell proliferationn
Cain et al, 1997 (United States) 10T I/L cells and 10e cellsintercellular communication disruption836.55 MHz generated by TDMA 28 days 0.15, 1.5, 15 uW/g no influence on tumor promotionn
Malyapaet al, 1997 (United States)human glioblastoma and mouse cellsDNA damage as measured by alkaline comet assay2450 MHz up to 24 hours 0.7 and 1.9 W/kg no DNA damage in mammalian cellsn
Malyapaet al, 1997 (United States) human glioblastoma and mouse cellsDNA damage as measured by alkaline comet assay835.62 frequency-modulated continuous wave (FMCW) and 847.74 MHz generated by CDMA 24 hours 0.6 W/kg no DNA damage in mammalian cellsn
Garaj-Vrhovac et al, 1996 (Croatia) human blood lymphocytesfrequency of micronuclei415 MHz up to 30 minutes increased frequency of micronucleiy
Cleary et al, 1996 (United States)cytolytic T lymphocytes (in the absence or presence of interleukin-2)lymphocyte proliferation2450 MHz 2 hours 5-50 W/kg RFR may affect membrane signal transduction in the absence of heating, resulting in altered proliferationy
Wolke et al, 1996 (Germany)cardiac myocytes of guinea pigscalcium homeostasis of isolated ventricular cardiac myocytes900 MHz 1300 MHz 1800 MHz 500 sno significant differences between sham exposure and high-frequency field exposure of cellsn
Malyapa et al, 1998 (United States) rat brain cells DNA single-strand breaks2450 MHz 2 hours 1.2 W/kg no significant differences between groups in comet length or comet moment of cells. Euthanasia by guillotine is most appropriate in studies of DNA damage in brain cellsn
Harris et al, 1998 (Australia)transgenic micemalignant lymphoma induction50 Hz 18 months no tumorigenic effectn
Imaida et al, 1998 (Japan)ratsrat liver carcinogenesis929.2 MHz generated by TDMA 6 weeks 0.8-0.58 W/kg no significant effect on rat liver carcinogenesisn
Imaida et al, 1998 (Japan)ratsrat liver carcinogenesis1.5 GHz generated by TDMA 6 weeks .680-.453 W/kg no significant effect on rat liver carcinogenesisn
Frei et al, 1998 (United States) cancer-prone micelatency, incidence, growth rate of mammary tumors, animal longevity2450 MHz 18 months 0.3 W/kg no significant effect on: mammary tumor incidence, latency to tumor onset, tumor growth rate, or animal longevity n
Frei et al, 1998 (United States)cancer-prone micelatency, incidence, growth rate of mammary tumors, animal longevity2450 MHz 18 months 1.0 W/kg no significant effect on: mammary tumor incidence, latency to tumor onset, tumor growth rate, or animal longevity n
Toler et al, 1997 (United States) cancer-prone micelatency, incidence, growth rate of mammary tumors, animal longevity435 MHz 21 months 0.32 W/kg no significant effect on: mammary tumor incidence, latency to tumor onset, tumor growth rate, or animal longevityn
Vijayalaxmi et al, 1997 (United States) cancer-prone miceincidence of micronuclei in polychromatic erythrocytes (PCEs)2450 MHz 18 months 1.0 W/kg no statistically significant differences between RFR-exposed and sham-exposed mice in incidence of micronuclei in PCEsn
Lai, Singh, 1997 (United States)rat brain cellsDNA single-strand breaks60 Hz 2 hours flux densities of 0.1, 0.25, 0.5 mT a dose-dependent increase in single- and double-strand DNA breaks in rat brain cells (euthanasia by dry ice)y
Lai, Singh, 1997 (United States) rat brain cells treated with melatonin or a spin trap compound (PBN)blocking effects of RFR2450 MHz 2 hours 1.2 W/kg melatonin and PBN blocked the RFR-induced increases in DNA breaks in rat brain cellsn
Repacholiet al, 1997 (Australia)transgenic miceincidence of lymphoma900 MHz 18 months 0.3-1.4 W/kg lymphoma risk found to be significantly higher in exposed group ( odds ratio = 2.4, P < .006)y
Vollrath et al, 1997 (Germany)rats and hamsterspineal melatonin synthesis900 MHz up to 6 hours 0.06-0.36 W/kg--rats 0.04 W/kg--hamsters no notable short-term effect on pineal melatonin synthesisn
Fritze et al, 1997 (Germany)ratsblood brain barrier permeability900 MHz 4 hours 0.3 to 7.5 W/kg no pathologically significant changes of the blood-brain barrier permeabilityn
Singh, Bate, 1996 (Canada)pigspulmonary intravascular macrophage (PIM) response915 MHz (infrared, low and high microwave) 24 hours results suggest enhanced secretory activity in the PIMs of low microwave treated pigs high microwave treatment induced some damage to pulmonary interstitium y
Balode, 1996 (Latvia) cows living in the Skrunda radio location station (RLS) radiation zoneincidence of micronuclei in bovine peripheral erythrocytes154-162 MHz impulse RFR exposure from an RLS for at least 2 yearsstatistically significant differences between the control and exposed groups in the frequency distribution of micronuclei in peripheral erythrocytesy
Lai, Singh, 1995 (United States) rat brain cellsDNA single-strand breaks2450 MHz 2 hours 1.2 W/kg an increase in single- and double-strand DNA breaks in rat brain cells (euthanasia by dry ice)y
Brusick et al, 1998 (United States) literature reviewgenotoxicity of RFR800-3000 MHz RFRdata from over 100 studies were subjected to a weight-of-evidence evaluation and suggest that RFR is not directly mutagenic and that adverse effects from organism exposure to RFR are predominantly the result of hypothermian
Verschaeve, Maes, 1998 (Belgium) literature reviewgenetic toxicology of RFRmobile telephone frequenciesmajority of research shows that such exposure does not induce genetic effects in vivo or in vitro and does not seem to be teratogenic or induce cancer; however, more research should be donen
Hermann, Hossmann, 1997 (Germany)literature reviewneurologic effectsmicrowave exposureno positive evidence that pulsed or continuous microwave exposure confers elevated risk to brainn

Table 1 is adapted from Wireless Phones and Health II: State of the Science. Norwell, Mass: Kluwer Academic Publishers; 2000. In press.


Table 2. Current Epidemiology Studies Identified Through Literature Surveillance


Investigators/AuthorsStudy Type/SizeOutcomeWireless TechnologyResultsInter-vention (y/n)More Research (y/n)
Mann et al, 1997 (Germany)cross-over design/22 healthy subjectsnocturnal hormone profiles of growth hormone, cortisol, luteinizing hormone, and melatoninGSM mobile phone system, 900 MHZ., Pulsed with 217 Hz., average power density 0.02 mW/cm2 at 40 cm distanceno significant effects except for a slight, transient elevation in cortisol productionnn
Mild et al, 1998 (Sweden, Norway)cross-sectional/ 9114 Swedes and 3200 Norwegians subjective symptoms (headaches, fatigue, warmth behind/on the ear, burning of the skin); covariates considered were gender, age, VDT work and an index of psychosocial work loadGSM and NMT900 mobile phonesthe prevalence of fatigue and headaches was similar for GSM and NMT users in Norway, whereas it was lower for GSM users in Sweden. In both countries, GSM users reported a lower frequency of feeling of warmth on/behind the ear compared to NMT users. There was a positive relationship between prevalence of symptoms and number of calls per day and total number of minutes using the phone per day for both transmitter systemsnn
Wagner et al, 1998 (Germany) cross-over design experiment/22 malessleepGSM mobile phone system, 900 MHz, pulsed with 217 Hz, average power density 0.2 W/m2 at 40 cm distancesleep-onset latency and duration of REM sleep tended to be reduced while the occurrence of first REM episode tended to be prolonged with exposure to the radiofrequency field. None of these changes were statistically significantnn
De Seze et al, 1998 (France) cross-over design experiment/18 malesanterior pituitary hormones (adrenocorticotropic hormone , thyroid-stimulating hormone [TSH], growth hormone , prolactin, luteinizing hormone, and follicle stimulating hormone); covariates considered were age, seasonal variation, smoking status, and time of exposure GSM cellular phones (890-900 MHz, max. Power 2 W)no persistent or cumulative changes in the secretion of the anterior pituitary hormones were detected. Only a 21% decrease of TSH concentration was detected during the radiotelephone exposure period, which remained within the physiologic range and recovered fully during the post-exposure periodnn
Braune et al, 1998 (Germany) in vivo experiment/7 males, 3 femalesblood pressure, heart rate, capillary perfusion, and subjective well-beingGSM, 900 MHz, 2 W, 217 Hz frame repetition rateexposure to the phone caused an increase in sympathetic efferent activity with increases in blood pressure between 5 and 10 mm Hg, probably due to more pronounced vasoconstriction. No statistically significant effects on subjective parameters were foundnn
Freude et al, 1998 (Germany)in vivo experiment/ 16 males human slow brain potentialsGSM, 916.2 MHz, 350 mW average powerelectromotive force exposure produced a significant decrease of slow brain potentials at central and temporo-parieto-occipital brain regions, but not at the frontal regionnn

Table 2 is adapted from Wireless Phones and Health II: State of the Science. Norwell, Mass: Kluwer Academic Publishers; 2000. In press.


Table 3. Toxicology Completed Within the WTR Program


IN VITRO TOXICOLOGY

LabBiological ModelBiological End PointExposure ConditionsResultsIntervention Indicated (y/n)Tier III R-search Warranted (y/n)
ILSbacterial cultures (salmonella typhimurium/Escherichia coli)reverse mutation induction837 MHz in analog, TDMA, CDMA mode 3 hours at 1, 2.5, 5, 10 W/kg not mutagenicnn
ILSbacterial cultures (salmonella typhimurium/E coli)reverse mutation induction1909.8 MHz in PCS mode 3 hours at 1.0-1.5, 2.5-3.3, 5.0-5.1, 9.6-11.0 W/kg not mutagenicnn
SRIbacterial cultures (salmonella typhimurium/E coli)reverse mutation induction837 MHz in analog mode 3 hours at 1, 2.5, 5, 10 W/kg not mutagenicnn
ILSmammalian cell culture (mouse lymphoma cells)deletions and point mutation induction837 MHz in analog, TDMA, CDMA mode 3 hours at 1, 2.5, 5, 10 W/kg not mutagenicnn
ILSmammalian cell culture (mouse lymphoma cells)deletions and point mutation induction1909.8 MHz in PCS mode 3 hours at 1.3, 3.3, 5.3, 10.3 W/kg not mutagenicnn
SRImammalian cell culture (mouse lymphoma cells)deletions and point mutation induction837 MHz in analog mode 3 hours at 1, 2.5, 5, 10 W/kg not mutagenicnn
ILShuman blood lymphocyteschromosomal aberrations837 MHz in analog, TDMA, CDMA mode 3 hours at 1, 2.5, 5, 10 W/kg and 21 hours at 10 W/kg not clastogenicnn
ILShuman blood lymphocyteschromosomal aberrations1909.8 MHz in PCS mode 3 hours at 1.2, 2.9, 5.0, 10.1 W/kg and 21 hours at 10.2 W/kg not clastogenicnn
SRIhuman blood lymphocyteschromosomal aberrations837 MHz in analog mode 3 hours at 1, 2.5, 5, 10 W/kg and 21 hours at 10 W/kg not clastogenicnn
ILShuman blood leukocytesDNA damage in eukaryote cells837 MHz in analog, TDMA mode 3 hours at 1, 2.5, 5, 10 W/kg and 24 hours at 10 W/kg no DNA damage inducednn
ILS interim reporthuman blood leukocytesDNA damage in eukaryote cells837 MHz in CDMA mode 3 hours at 1, 2.5, 5, 10 W/kg and 24 hours at 10 W/kg there was an equivocal increase in DNA migration for a 3-hour exposure; however, additional testing is needed. No DNA damage was induced for the 24-hour exposureny
ILShuman blood leukocytesDNA damage in eukaryote cells1909.8 MHz in PCS mode 3 hours at 1.6, 2.9, 5.1, 10.3 W/kg and 24 hours at 10.1 W/kg no DNA damage inducednn
ILShuman lymphocyte binucleate micronucleus cellsstructural and/or numerical chromosomal damage; micronuclei formation837 MHz in analog, TDMA mode 3 hours at 1, 2.5, 5, 10 W/kg and 24 hours at 5, 10 W/kg there was no increase in lymphocyte frequency for a 3-hour exposure. There was a statistically significant increase in lymphocyte frequency for a 24-hour exposure suggesting genotoxicityny
ILS interim reporthuman lymphocyte binucleate micronucleus cellsstructural and/or numerical chromosomal damage837 MHz in CDMA mode 3 hours at 1, 2.5, 5, 10 W/kg and 24 hours at 10 W/kg there was no increase in lymphocyte frequency for a 3-hour exposure. There was a statistically significant increase in lymphocyte frequency for a 24-hour exposure; however, additional testing is neededny
ILS interim reporthuman lymphocyte binucleate micronucleus cellsstructural and/or numerical chromosomal damage1909.8 MHz in PCS mode 3 hours at 1.6, 2.9, 5.1, 10.1 W/kg and 24 hours at 10.3 W/kg there was no increase in lymphocyte frequency for a 3-hour exposure. There was a statistically significant increase in lymphocyte frequency for a 24-hour exposure; however, additional testing is neededny

IN VITRO TOXICOLOGY

LabBiological ModelBiological End PointExposure ConditionsResultsIntervention Indicated (y/n)Tier III R-search Warranted (y/n)
ILSrat brain cellsDNA damage in eukaryote cells837 MHz in analog mode 3 hours at 1, 5, 10 W/kg no statistically significant increase in DNA migrationny
UW interim reportrat brain cellsDNA damage in eukaryote cells837 MHz in analog mode 3 hours at 1, 5, 10 W/kg additional testing with a larger sample size is needed before conclusion can be madeny

Table 3 is adapted from Wireless Phones and Health II: State of the Science. Norwell, Mass: Kluwer Academic Publishers; 2000. In press.


Table 4. Epidemiology Completed Within the WTR Program


Investigator/ Authors Study Type/ Size OutcomeWireless TechnologyResultsIntervention (y/n)More Research (y/n)
Rothman et al, Epidemiology Resources, Inc., 1996 (United States) questionnaire-based pilot study on 5000 phone usersassess utility of information from billing records; assess questionnaire validity; evaluate handedness as a surrogate for laterality of phone use analog phonesbilling records are useful; high correlation between answers to questionnaire and billing records; handedness was not associated with laterality of phone use ny
Rothman et al, Epidemiology Resources, Inc., 1996 (United States) record-based cohort of 250,000 cellular telephone usersoverall mortality among users of hand-held vs nonhand-held telephoneshand-held portable vs nonhand-heldage-specific rates were similar; long-term increase in mortality is not associated with radiofrequency exposure over the short term ny
Rothman et al, Epidemiology Resources, Inc., 1998 (United States) record-based cohort of 496,460 cellular telephone userscause-specific risk of death among users of hand-held vs nonhand-held telephoneshand-held portable vs nonhand-heldmost striking increase among handheld cellular telephone users was due to motor vehicle accidents. Deaths from brain cancer were greater than expected, but there were only 2 cases, too few to draw any firm conclusionny
Muscat et al, American Health Foundation, 1999 (United States) case-control; 465 patients with newly diagnosed brain cancer and 421 age-matched controls brain tumors (meningiomas excluded)self-reported phone use 1) frequency of use, 2) duration of use (years) and 3) cumulative frequency (frequency X duration) no association was observed between brain cancer risk and cell phone use. A histologic-specific analysis showed a significant association for 34 patients with ganglioneuromas/ ganglioneuroblastomas. 14 of 34 were cell phone users. No association with frequency or duration variables ny

Table 4 is adapted from Wireless Phones and Health II: State of the Science. Norwell, Mass: Kluwer Academic Publishers; 2000. In press.