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"Hidden dangers from cell phones"
Bjorn Cedervall wrote
"Hidden cancer danger from cellular phones"
Yesterday, a Swedish scientist warned against the danger of cellular
phones in "Dagens Nyheter" - the largest Swedish morning paper (main
article on debate page). The headline reads "Hidden cancer danger from
cellular phones" - the somewhat smaller second headline reads "The
consequences of cellular phones may/can become tragic if measures are
not taken in time".
Then, as introduction text in bold: "Nothing says that microwaves from
cellular phones should be harmless. It is rather the opposite: research
shows association between this kind of radiation and different diseases
- anything from cancer, brain damage and high blood pressure to sleeping
disturbances and asthma. When it comes to microwave radiation we
furthermore risk getting harmful levels without seeing any warning
signals. The risk is that future historians will ask themselves: "Why
didn't we take any measures in time?"..."
Then the main article (six columns) begins. The text is quite
suggestive. The works referred to in the article:
"Professor Henry Lai" (Univ. Wash, Seattle) - the rat brain story.
Dr. John Holt and Professor Peter French, St. Vincent's Hospital, Sydney
Australia (mast cells, asthma and EMF).
Dr. Neil Cherry at Lincoln University, Lincoln, New Zeeland
(epidemiological studies of "cellular phone fields" (0.1 microwatt per
square centimeter - discussion about cancer, insomnia, immune defense,
miscarriage and changes in blood pressure).
Med dr S. Braunes, Freiburgs University, Germany (ref. to article in The
lancet, 1998 blood pressure)
Michael Repacholi, Royal Adelaide Hospital, Adelaide, Australia (900 MHz
distant field (0.008 - 4.2 watt per kg tissue where the risk was
statistically significant at a level of 2.4 times after 18 months of
exposure, 30 min. in the morning and 30 min. in the evening).
Bruce Hocking, Camberwell, Australia (0.2 - 8 microwatt per square
centimeter up to 4 kms distance (2.5 U.S. miles) from TV masts in
Australia).
Ioannis Magras and Thomas Xenos, Thessalonikis University, Greece
(embryonal development of mice, 0.2 to 1 microwatt per square
centimeter).
//My question: Are any of you able to comment the studies above from a
scientific point? Some people above lack titles because they have not
been given in the article I am referring to.//"
I can comment on some of the studies.
Lai and Singh claimed to have observed double strand DNA breaks after
exposure to RF radiation at SARs of around 1 W/kg, but this work has not
been replicated in other laboratories and methodological deficiencies have
been pointed out; ie no one really accepts this finding.
The study by Hocking et al showed some association between the incidence of
childhood leukemia and distance from TV transmitters. Assosiation is not
causation, although this has not prevented Neil Cherry running around New
Zealand (and the world?) saying "the North Sydney study showed children near
the tower are 264% more likely to get leukemia" (the figure may not be exact
but the general nature of his comment is correct). Cherry has a background
in meteorology and is a bag of wind. I include a lengthier comment on the
North Sydney study below. In fact the distribution of leukemia incidence is
unrelated to the TV towers and there are no plausible mechanisms whereby
such RF power flux densities could have any effect on health.
The study by Repacholi is of more substance. Exposure of transgenic mice to
900 MHz fields pulsed at 217 Hz with pulse widths of 0.6 microseconds for up
to 18 months (simulating mobile phone transmissions) produced an increase in
lymphoma (which the animals were prone to) compared with controls. There
was quite a variation in SAR in the exposed animals which were free to roam
in cages , so no dose response was found. Also the relevance of the study
for normal mice, let alone humans is unknown. The methodology of the study
has been criticised on a number of grounds. One of these is that it
violated its own study design. For this strain of mice an applied chemical
carcinogen is reported to induce lymphoblastic lymphomas in a large number
of the treated animals. These lymphomas appear within a year after
initiating treatment. In the Repacholi et al study the experiment was
continued for a longer time (18 months), and as the animals aged a different
type of tumour (a follicular lymphoma) appeared. This is known to occur
with inbred strains of mice. However,the study did not show a statistically
significant difference in the number of lymphoblastic lymphomas in the RF
exposed group compared with the sham exposed group at 1 year, when these
lymphomas stopped appearing. The study has not been replicated. Concerns
have also been raised about animal health, absence of a positive control
treatment group, and exposure variation during the study.
North Sydney study - a follow up analysis
Hocking et al. compared an inner group of three aggregated local government
areas (LGAs) close to the transmission tower with an outer ring of
aggregated LGAs. Hocking et al. excluded some other LGAs also quite close
to the towers, on socioeconomic grounds, although at the same time they
stated that there was little evidence of a relationship between
socioeconomic levels and acute lymphoblastic leukaemia (ALL) in New South
Wales. The new study therefore looked individually at 16 LGAs in
relationship to likely exposures from the North Sydney television stations.
The study used all cases from 1972 to 1990. Three LGAs, Willoughby, Lane
Cove and North Sydney are those closest to the towers, and these authors
identified seven other LGAs in North Sydney and six in other areas of Sydney
as being of comparable distances to the *outer ring* used by Hocking et al.
The authors calculated the signal strengths by a formula dependent on the
distance from the tower and the angle of depression from the horizontal, and
also carried out site measurements using a Holaday Instruments broad band
isotropic field strength meter. They present a graph comparing observed
with calculated signal strength which shows reasonable correlation for free
space conditions at roof height, with other areas subject to shadowing
having lower observed strengths, and two points near the base of the
antennae being of greater emissions than calculated. They present an
average RFR exposure levels for the different LGAs based on calculated
signal strengths for a random sample of 20 residences in the high signal
strength areas, and at other distances by an average of fewer measurements.
Signal strength in the three closest LGAs are given as 1.46 microwatts/cm2
in Lane Cove, 1.40 in Willoughby, and 0.66 in North Sydney. These are the
highest three measurements, most other areas showing average strengths of
less than 0.25, apart from Hunters Hill, which gives 0.46. They found
maximum levels in streets immediately below the antennae of up to 100
microwatts/cm2. A measure of socioeconomic status was calculated from
census data, the *Ross index*; the three LGAs with high RFR exposure had
slightly higher average socioeconomic status than the rest.
Incidence rates of ALL and of total leukaemia in childhood were calculated
for each LGA. For ALL these ranged from 0.9 to 14.8 cases per 100,000
population. The rate was highest in Lane Cove, a high exposure area, but
the rates in North Sydney and Willoughby, the other two high exposure areas,
were similar to the less exposed areas. A regression line of incidence
versus estimated RFR exposure shows a positive trend; a similar regression
against the socioeconomic status measure also shows a positive trend. The
analysis is dependent on the three higher intensity areas, and particular on
Lane Cove and Willoughby, as these have the highest estimated RFR exposures.
The ALL rate in Lane Cove is considerably higher than the general trend,
and that in Willoughby is considerably lower, suggesting no regular
relationship with RFR exposure. The trend for ALL based on all LGAs gives a
relative risk of 1.45 (95% confidence limits, 0.96-2.19) for a change in
average area RFR exposure of 1 microwatt/cm2 , that is, an almost
significant positive association. For total childhood leukaemia, the result
is very similar, with a relative risk of 1.38 (limits 0.99-1.91). Exclusion
of the Lane Cove area removes this trend so that there is virtually no
relationship, relative risk 0.83 (limits 0.45-1.55) for ALL, and similarly,
0.90 for total leukaemia.
The analysis further shows that combining the three higher exposure areas,
and comparing them to an outer ring of areas as was done by Hocking et al.,
produces an excess risk similar to that recorded by Hocking et al., but this
excess is abolished if Lane Cove is excluded. As the 1 microwatt/cm2 unit
is about equivalent to the difference in exposure levels between the inner
and the outer ring of areas, the results simply comparing the inner to the
outer ring are similar: relative risk 1.53 (limits 0.92 - 2.53), reducing to
0.90 (0.46 - 1.75) when Lane Cove is excluded.
Further comparison of Lane Cove with all the other LGAs shows a much higher
rate for Lane Cove at ages 0-4, mainly seen in the earlier and later times,
1972-78, and 1985-90, and a less marked excess in 10-14 year olds in Lane
Cove in the 1979-84 period.
The main result is therefore the considerable contrast between high rates in
Lane Cove (14.8 per 100,000) and low rates in Willoughby, 3.4 per 100,000.
These two areas had the highest and similar estimated RFR exposures, and
also had similar housing stocks and socioeconomic status.
The basic conclusion is that leukaemia rates do vary in different localities
in Sydney, and in particular, during the years studied, the leukaemia
incidence in Lane Cove appears to have been abnormally high. This is very
unlikely to be due to RFR exposure, as the other two areas with high RFR
exposures, Willoughby and North Sydney, do not show any increase in
leukaemia. The previously noticed relationship depends on this excess in
Lane Cove, and there is no relationship with estimated RFR exposure and
leukaemia rates in the Sydney LGAs with the exception of Lane Cove. The
logical conclusion is that the excess in Lane Cove must be due either to
chance or to some factor apart from radiofrequency radiation. For it to be
related to RFR exposure, actual exposures of children who live in Lane Cove
would have to be much higher than those calculated in this paper, and
correspondingly actual exposures in Willoughby would have to be much lower
than those calculated. The authors suggest that further studies are needed
to examine the excess rates in Lane Cove.
This study is an improvement on the first North Sydney study by Hocking and
colleagues because it looks at the data in more detail, giving a greater
ability to see if there is a regular association between leukaemia
occurrence and estimated radiofrequency exposures. The estimation of
exposure is still based primarily on distance, although the measurements
performed do confirm that the three areas closest to the transmitters do
have measurably higher exposure levels when measured at a few open air sites
than do the other areas. The study does still show an association between
leukaemia incidence and estimated RFR exposure. However it shows that, of
three areas with high RFR exposure levels, only one of these three has an
elevated risk. This makes it more likely that some factor other than RFR is
responsible for the excess.
Andrew McEwan
_________________________
Andrew C McEwan PhD
National Radiation Laboratory
PO Box 25-099
Christchurch, New Zealand
Ph 64 3 366 5059
Fax 64 3 366 1156
acmcewan@nrl.moh.govt.nz
________________________
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