on “EMFacts Consultancy”.
From Cindy Sage on the CHE-EMF list:
EMF at only 12 mG has been shown to reduce the protective effect of melatonin on human breast cancer cells. This is the latest in a series of at least seven (7) papers reporting similar results. These EMF (magnetic field) levels of exposure can be found in homes and offices near transmission lines or with faulty wiring, or near large electrical appliances or electric panels. 1.2 uT (microTesla) is the same as 12 milligauss (12 mG).
Girgert, R Hanf V Emons G Grundker, 2010. Signal Transduction of the Melatonin Receptor
MT1Is Disrupted in Breast Cancer Cells by Electromagnetic Fields.
Bioelectromagnetics 31:237- 245 (2010)
The growth of estrogen-receptor positive breast cancer cells is
inhibited by the pineal gland hormone, melatonin. Concern has been
raised that power-line frequency and microwave electromagnetic fields
(EMFs) could reduce the efficiency of melatonin on breast cancer
cells. In this study we investigated the impact of EMFs on the signal
transduction of the high-affinity receptor MT1 in parental MCF-7 cells
and MCF-7 cells transfected with the MT1 gene. The binding of the
cAMP-responsive element binding (CREB) protein to a promoter sequence
of BRCA-1 after stimulation with melatonin was analyzed by a gel-shift
assay and the expression of four estrogen-responsive genes was
measured in sham-exposed breast cancer cells and cells exposed to a
sinusoidal 50 Hz EMF of 1.2 uT for 48 h. In sham-exposed cells,
binding of CREB to the promoter of BRCA-1 was increased by estradiol
and subsequently diminished by treatment with melatonin. In cells
exposed to 1.2 uT, 50 Hz EMF, binding of CREB was almost completely
omitted. Expression of BRCA-1, p53, p21WAF, and c-myc was increased by
estradiol stimulation and subsequently decreased by melatonin
treatment in both cell lines, except for p53 expression in the
transfected cell line, thereby proving the antiestrogenic effect of
melatonin at molecular level. In contrast, in breast cancer cells
transfected withMT1exposed to 1.2 uT of the 50 Hz EMF, the expression
of p53 and c-myc increased significantly after melatonin treatment but
for p21WAF the increase was not significant. These results
convincingly prove the negative effect of EMF on the antiestrogenic
effect of melatonin in breast cancer cells. Bioelectromagnetics
31:237–245, 2010. 2009 Wiley-Liss, Inc.
Key words: breast cancer; electromagnetic fields
The BioInitiative Report, Chapter 13, Evidence for Breast Cancer
Promotion (2007) summarizes earlier studies. Note that the author of
this paper – Girgert – also published on the negative effect of EMF on
tamoxifen. Please contact Cindy Sage if you would like copies of any
of these articles.
II. Melatonin and ELF-EMF
Evidence which supports a possible mechanism for ELF-EMF and breast
cancer is the consistent finding (in five separate labs) that
environmental levels of ELF-EMF can act at the cellular level to
enhance breast cancer proliferation by blocking melatonin’s natural
oncostatic action in MCF-7 cells (Liburdy, 1993; Luben et al, 1996;
Morris et al, 1998; Blackman et al, 2001; Ishido, et al, 2001).
ELF-EMF levels between 0.6 and 1.2 µT have been shown to consistently
block the protective effects of melatonin.
The series of papers reporting increased breast cancer cell
proliferation when ELF-EMF at environmental levels negatively affects
the oncostatic actions of melatonin in MCF-7 cells should warrant new
public exposure guidelines or planning target limits for the public,
and for various susceptible segments of the population.
Liburdy, R. P., T. R. Sloma, et al, 1993. ELF magnetic fields, breast
cancer, andmelatonin: 60 Hz fields block melatonin’s oncostatic
action on ER+ breast cancer cell proliferation. J of Pineal Research.
Luben et al, 1996. Replication of 12 mG EMF effects on melatonin
responses of MCF-7 breast cancer cells in vitro. Abstract A-1 of the
1996 Annual review of research on biological effects of electric and
magnetic fields from the generation, delivery and use of electricity,
November 17-21, 1996. San Antonio, Texas, p.1
Luben et al, 1998. Independent replication of 60-Hz 1.2 µT EMF
effects on melatonin and tamoxifen responses of MCF-7 cells in vitro.
Abstract A-3.4, Bioelectromagnetics Society Annual Meeting, St. Pete
Beach, FL. June 7-11, p 17-18.
Morris et al, 1998. In vitro exposure of MCF-7 human breast cancer
cells to 60-Hz magnetic fields. Abstract p-125A, Bioelectromagnetics
Society Annual Meeting, St. Pete Beach, FL. June 7-11, p 204-205.
Ishido et al, 2001. Magnetic fields (MF) of 50 Hz at 1.2 µT as well
as 100 µT cause uncoupling of inhibitory pathways of adenylyl cyclase
mediated by melatonin 1a receptor in MF-sensitive MCF-7 cells.
D.E. Blask, S.M. Hill, Effects of melatonin on cancer: studies on
MCF-7 human breast cancer cells in culture, J. Neural Transm. Suppl.
21 (1986) 433–449.
Loberg LI et al 1999. Gene expression in human breast epithelial cells
exposed to 60 Hz magnetic fields, Carcinogenesis 20 1633–1636.
III. Tamoxifen and ELF-EMF
Girgert et al (2005) reported that “the anti-estrogenic activity of
tamoxifen is reduced in two subclones of MCF-7 cells under the
influence of ELF/EMF to different extent. Dose-response curves of the
growth-inhibitory effect of tamoxifen are shifted towards higher
concentrations leading to a reduced growth inhibition at a given
concentration. Our observations confirm results from a previous
report describing a reduced inhibitory effect of tamoxifen at 1—7 M
from 40% to only 17% by exposure to an EMF of 1.2 µT” (Harland t
al, 1997). Further, Girgert et al conclude that “From a medical
point of view, it is disturbing that maximal induction of cell
proliferation by tamoxifen at a field strength of 1.2 µT is observed
at concentration of 10-6 M. This is exactly the serum concentration
achieved in BC patients under standard oral therapy.” (De Cupis et
The Girgert et al paper confirms prior findings that environmental
level ELF-EMF inhibits the antiproliferative action of tamoxifen in
MCF-7 human breast cancer cells. Four other papers reporting this
effect include Liburdy et al, 1997; Harland et al, 1997; Harland et
al, 1999; and Blackman et al, 2001).
Liburdy et al, 1997. Magnetic Fields, Melatonin, Tamoxifen, and Human
Breast Cancer Cell Growth. In: Stevens R. G., Wilson B. W., Anderson
L.E. (Eds). The Melatonin Hypothesis – Breast Cancer and Use of
Electric Power. Battelle Press, Columbus, Richland 1997: 669- 700.
Harland et al, 1997. Environmental magnetic fields inhibit the
antiproliferative action of tamoxifen and melatonin in a human breast
cancer cell line. Bioelectromagnetics, 18, 555-562.
Harland et al, 1999. Evidence for a slow time-scale of interaction for
magnetic fields inhibiting tamoxifen’s antiproliferative action in
human breast cancer cells. Cell Biochemistry Biophysics, 31(3),
Blackman et al, 2001. The influence of 1.2 μT, 60 Hz magnetic fields
on melatonin and tamoxifen-induced inhibition of MCF-7 cell growth.
Bioelectromagnetics, 22(2), 122-128.
Girgert et al, 2005. Induction of tamoxifen resistance in breast
cancer cells by ELF electromagnetic fields. Biochemical Biophysics
Research Communications, 336, 1144-1149.
A. De Cupis et al, 1997. Oestrogen/growth factor cross-talk in breast
carcinoma: a specific target for novel antioestrogens, TIPS 18