There is a substantial body of evidence that (strongish) RF can and does cause numerous biological changes to occur which can be measured, (often effects that in other contexts are known to cause problems). Nobody who is responsible claims that RF in a cell phone usage context is "harmless" as some people do. OTOH, the benefits we get from cell phones generally are substantial. So for that reason, people have them.
What I think lies at the root of many of the problems is the fact that numerous arguably toxic - most definitely unhealthy environmental factors (various kinds of EMF can be shown to do this) cause reactive oxygen species which act as a form of depletion of a finite resource - glutathione, and at specific moments - gestation/cell differentiation (where ROS impacts expression of two genes Fyn and c-Cbl) is one, and when we get a bit older is another. Non-availability of a substance that is depleted, glutathione, can at times in the life cycle, be crucial.
Without glutathione, apoptopsis (programmed cell death) becomes the only way a cell can prevent otherwise repairable DNA damage from possibly leading to cancers.
And cell division is a finite resource - see "Hayflick Limit" etc. (An easy way exists to prevent this ROS depletion of glutathione from having as severe an impact as it would otherwise exists, supplementation with its rate-limiting precursor, the amino acid, n-acetylcysteine. (NAC) Irregardless of exposures of any kinds, as we get older the creation of AGE's in our tissue ("glycation") increases the amount of glutathione thats used up unavoidably, so NAC is a smart thing to take extra of for that reason alone.
Note: in several studies, with several changes that occur, some antioxidants may have some protective effect. melatonin was found in a few studies to be protective against some of the parameters that have been measured. In other words, melatonin taken during the daytime. Not in the evening to reduce sleep latency.
Here is how the IARC puts their summary with regard to some of these non-heat, non-cancer endpoints. Note that the studies looked at by IARC in this particular monograph (102) are also several years old.
It's worth it to read the original studies.
"5 .4 .3 Effects on genes, proteins and signalling
pathways
No studies assessing gene expression in
humans exposed to RF radiation were identified,
and only one pilot study assessed protein changes
in exposed human subjects.
Nearly 30 studies investigated gene/protein
changes in rodents exposed to RF radiation.
Many of these studies were unreliable due to
deficiencies in the exposure system or
methodological shortcomings. The data from the remaining
studies are limited and present mixed results
with no consistent pattern of response.
A large number of studies have assessed the
ability of RF radiation to affect gene/protein
expression and protein activation in human-
derived cell lines in vitro
. The majority of studies
assessing effects of RF radiation on expression
and activity of heat-shock proteins reported no
effect. A limited number of studies assessed the
ability of RF radiation to influence the activity
of signal-transduction pathways in human cells
in vitro. Three studies found changes in MAPK
signalling, while another did not. The role of
reactive oxygen species in mediating these responses
is unclear.
A total of 16 studies used high-throughput
genomics/proteomics approaches to evaluate
the effect of exposure to RF radiation on human
cell lines in vitro
. Many of these studies had
serious methodological shortcomings related to
poor exposure conditions, inadequate statistical
analysis, and lack of validation of alternative
approaches. The remaining data were limited with
no consistent pattern of response, but some studies
demonstrated changes in both gene and protein
expression, for some proteins in some cell lines.
On the basis of the above considerations,
the Working Group concluded that data from
studies of genes, proteins and changes in cellular
signalling show weak evidence of effects from RF
radiation, but did not provide mechanistic infor
-
mation relevant to carcinogenesis in humans.
5 .4 .4 Other mechanistic end-points
Several potential changes resulting from
exposure to RF radiation are summarized here.
With the exception of changes in cerebral blood
flow, many of the other studies reviewed by the
Working Group provided conflicting, nega
-
tive or very limited information, which made it
difficult to draw conclusions, especially in rela
-
tion to carcinogenesis. These studies focused on
electrical activity in the brain, cognitive func
-
tion, general sensitivity to RF radiation and
alterations in brain biochemistry. Even though
the relationship between alterations in cerebral
blood flow during exposure to RF radiation
cannot be directly related to carcinogenesis, the
Working Group concluded that the available
data were sufficiently consistent to identify them
as important findings.
Some studies were conducted in experimental
animals to explore the possibility that exposure to
RF radiation in vivo may induce the production of
reactive oxygen species in multiple organs, most
frequently brain, but also kidney, liver and eye.
Markers of oxidative stress included increases in
the concentration of malondialdehyde (related
to lipid peroxidation) and nitric oxide, enhanced
activities of antioxidant enzymes (superoxide
dismutase, catalase, glutathione peroxidase)
and pro-oxidant enzymes, and reductions in
glutathione. Many of these studies are weakened
by methodological shortcomings in design, such
as absence of sham-exposed or cage-control
groups, use of mobile phones as the exposure
source, and lack of dosimetry.
A few studies in human cells
in vitro
evalu
-
ated the possible role of exposure to RF radia
-
tion in altering levels of intracellular oxidants
or activities of antioxidant enzymes. One study
showed a marginal effect, while other studies
demonstrated an increase in activity with
increasing exposures. There were not enough
studies to make a reasonable assessment of the
consistency of these findings. Additional studies
addressed this issue in in-vitro systems with
non-human cells. While most of these did not
find changes, one study evaluated the formation
of DNA adducts from reactive oxygen species
(8-hydroxy-deoxyguanosine) and was able to
demonstrate reversal of this effect by melatonin.
While the overall evidence was inconclusive, the
results from in-vitro studies with animal models
raise some concern.
Overall, the Working Group concluded that
there was weak evidence that exposure to RF
radiation affects oxidative stress and alters the
levels of reactive oxygen species.
Numerous studies have assessed the function
of the blood–brain barrier in rodents exposed to
RF radiation at various intensities. Consistent
results from one laboratory suggest an increase
in the permeability of the blood–brain barrier,
but the majority of the studies, many of which
aimed at replicating published results, failed to
observe any effect on this point from exposure
to either continuous or pulsed RF radiation. The
evidence that exposure to RF radiation alters the
blood–brain barrier was considered weak.
A few studies dealt with alterations induced
by RF radiation in cell differentiation or induc
-
tion of apoptosis in the brain or other organs.
While most of the studies showed an association,
the Working Group was not convinced that these
data were of sufficient scientific rigour to assess
apoptotic effects in these organs. An additional
14 studies focused on apoptosis in cultured
human cells. Only two studies demonstrated an
increase in apoptosis: one compared the results
observed in treated cells with controls that were
not subject to the same conditions as the exposed
cells, while thermal effects may have had an
impact in the other study. Finally, other in-vitro
studies with non-human cells gave essentially
negative results, with the exception of one study
that demonstrated mixed results. The evidence
that exposure to RF radiation alters apoptosis
was considered weak.
Multiple assays
in vitro
were conducted to
test proliferation of primary cells or established
cell lines by analysis of cell-cycle progression
and thymidine uptake, after exposure to various
intensities of RF radiation at various time intervals.
Many of these studies used small sample
sizes and description of experimental details
was lacking in several cases. Studies with positive
results showed increases and decreases in cellular
replication, and no consistent pattern could be
discerned. The evidence that RF radiation alters
cellular replication was considered weak.
Ornithine decarboxylase is an enzyme
involved in the metabolism of polyamines,
which are critical components of cellular
replication and differentiation processes. The activity
of this enzyme was the object of several studies
in vitro in human and animal cells exposed to
GSM900 and GSM1800 signals. Some of these
studies showed significantly increased ornithine
decarboxylase activity. The result of one study
suggested that ornithine decarboxylase activities
may be reduced. It was unclear how these
changes in activity relate to human cancer. There
was weak evidence from in-vitro studies that
exposure to RF radiation alters ornithine decar
-boxylase activity.
The evidence that exposure to RF radiation, at
intensities below the level of thermal effects, may
produce oxidative stress in brain tissue and may
affect neural functions was considered weak.
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