http://www.prnewswire.com/news-releases/popular-infant-juices-contain-too-much-f\
luoride-research-shows-114930519.html


Popular Infant Juices Contain Too Much Fluoride, Research Shows

NEW YORK, Jan. 31, 2011 /PRNewswire-USNewswire/ -- Commonly-consumed infant
fruit juices contain fluoride, some at levels higher than recommended for public
water supplies which can damage teeth, according to research to be presented on
March 17, 2011 at the International Association for Dental Research annual
meeting in San Diego.(1)

Ninety samples of three different flavors (apple, pear and grape) from three
manufacturers were tested.  All contained fluoride at concentrations ranging
from 0.11 to 1.81 parts per million (ppm).

"Children who consume excessive amounts of juice per day may be ingesting more
fluoride than the recommended daily intake," the researchers report.

Recently, the U.S. Department of Health and Human Services recommended lowering
"optimal" water fluoride levels to 0.7  ppm to decrease the epidemic of
fluoride-discolored teeth (dental fluorosis) afflicting over 41% of adolescents.
Many cities are complying; some consider ending fluoridation.

Attorney Paul Beeber, President, New York State Coalition Opposed to
Fluoridation says, "Water fluoride, along with fluoride-containing pesticide
residues, is contaminating the food supply and harming our children. Clearly,
artificial fluoridation must stop completely."

"Fluoride is neither a nutrient nor required for healthy teeth. Studies show
fluoride ingestion doesn't reduce tooth decay," says Beeber.

Earlier research shows all infant formulas, whether ready-to-feed, concentrated
or organic, contain some fluoride, (October 2009 Journal of the American Dental
Association).(2)

Researchers found fluoride in chicken products frequently eaten by children but
not listed on labels, e.g. pureed chicken, chicken sticks, and luncheon meat
made with mechanically-separated chicken. Fluoride-containing bone-dust
invariably gets into the finished product (Journal of Agricultural and Food
Chemistry September, 2001).(3)

Safe fluoride intake could "be exceeded on a recurring basis when combined with
other sources of fluoride intake such as fluoridated water, foods made with
fluoridated water, and swallowing of fluoridated toothpaste," write researchers,
Fein and Cerklewski.

"Current evidence strongly suggests that fluorides work primarily by topical
means through direct action on the teeth and dental plaque. Thus ingestion of
fluoride is not essential for caries (cavity) prevention," report Warren and
Levy in Dental Clinics of North America, April 2003. "There is no specific
nutritional requirement for fluoride," they write.(4)

New York City Council Members introduced legislation to stop fluoridation on
1/18/2011.  Show your support here: http://www.FluorideAction.Net.

References:

(1) "Fluoride Level in Commonly Consumed Infant Juices" 
http://iadr.confex.com/iadr/2011sandiego/webprogram/Paper147544.html

(2) http://jada.ada.org/cgi/content-nw/full/140/10/1228/T1

(3) http://pubs.acs.org/doi/abs/10.1021/jf0106300

(4) http://www.ncbi.nlm.nih.gov/pubmed/12699229

USDA Fluoride in Foods Database:
http://ars.usda.gov/services/docs.htm?docid=6312


SOURCE NYS Coalition Opposed to Fluoridation, Inc.

Back to top
RELATED LINKS
http://www.FluorideAction.Net

Ron here.

Deb Moore was THE person that prompted me to start the Fluoride Poisoning
Support Group.  Second Look was just getting up and running.

I would like to be included in the piolet study if at all possible. Hopefully
fluoride can be linked to fibromyalgia. The symptoms are nearly identical to
stage I and II skeletal fluorosis. Absorption through the skin and inhalation
while showering could also be addressed.

  Anyone else on board?

Alliss and /or Deb, want to include my personal story? Let's work on it!



http://www.slweb.org/ftrcresearch.html#puzzle

Pilot project to study fluoride sensitivity in people
Our pilot study on fluoride sensitivity is on hold, but not forgotten. This will
be a randomized, double-blinded, clinical trial to test for fluoride
hypersensitivity in individuals, under the direction of Dr. Hardy Limeback,
University of Toronto. While some preliminary studies were conducted by
physicians in the early years of fluoridation using specific doses of fluoride
in tablet form, no human clinical trial has focused on the hypersensitivity of
susceptible people to the usual level of fluoride (1 ppm) in drinking water.

This FTRC project will include the development of tools that will be useful for
all future research. We are also looking into the possibility of extending this
research project, based on its results, to a related study on the same subjects,
which would monitor the elimination of fluoride. These pilot studies would pave
the way for larger, more involved projects and grant funding. Universities first
require clearance from an Ethics Committee before studies involving humans can
take place. They also require extra personnel to perform the necessary work
involved. Second Look/FTRC is now attempting to raise enough funds to ensure
valid completion of these types of studies.

Recent news and events have sharply increased awareness about fluoride toxicity.
FTRC's leading-edge research will undoubtedly be recognized as having great
value when the floodgates open with information-seekers on fluoride poisoning
and hypersensitivity.

Quote from the article:  "While some preliminary studies were conducted by
physicians in the early years of fluoridation using specific doses of
fluoride in tablet form, no human clinical trial has focused on the
hypersensitivity of susceptible people to the usual level of fluoride (1
ppm) in drinking water."

I would say that isn't quite right, I've read about several double blinded
studies showing fluoride sensitivity from normal fluoridated water.  These
seem like clinical trials to me.  Here's an article from FLUORIDE that talks
about this:  http://sonic.net/kryptox/medicine/allergy.htm

These studies may not have been published in mainstream medical journals in
the U.S.  I'm thinking that may be the reason for saying "no human clinical
trial."

-Doug Cragoe

I was just reading the google news for fluoride

http://www.google.com/search?sourceid=navclient&aq=0h&oq=&ie=UTF-8&rlz=1T4GGLL_e\
nUS305US305&q=fluoride#rlz=1T4GGLL_enUS305US305&q=fluoride&um=1&ie=UTF-8&tbo=u&t\
bs=nws:1&source=og&sa=N&hl=en&tab=wn&fp=aee654dc21bede8d

Lots a press on the subject.  I just can't wait for this to blow up in their
faces. There must be a way to pour gas on this fire.

I remember Darlene Sherrell asking the ADA, CDC, DHHS, EPA, etc. to merely
produce the documents, the scientific studies, that prove the safety and
effectiveness of F- .   It never happened!!!

No one is asking these government agencies for the studies.  No individuals
comments on these newspapers sites are asking this important question.

If 10 people in Egypt can mobilize massive unrest - with the internet shut down
in that country- there has got to be a way to shine the light on the fluoride
debacle!

Any other ideas?  Will this idea work?




http://www.healthfreedomlaw.com/

LAW OFFICES OF CARLOS F. NEGRETE



  In the summer of 1998, Darlene Sherrell, challenged pro-flouridation advocates
to come forward to name a study demonstrating the safety of current fluoride
levels in drinking water and the effect excessive daily intake of fluoride as a
possible cause to chronic fluoride poisoning.

Law Offices of Carlos F. Negrete is dedicated to representing individuals and
organizations that share similar beliefs in health freedom and prevention of
toxic contamination.


http://www.laborlawtalk.com/archive/index.php/t-116636.html

name a (one) study demonstrating the safety of current fluoridation levels

Produce any studies which indicate that researchers used methods capable of
detecting cases of chronic fluoride poisoning in any U.S. city in the past --
but failed to find them.

Google search

methods capable of detecting chronic fluoride poisoning

http://www.google.com/search?sourceid=navclient&ie=UTF-8&rlz=1T4GGLL_enUS305US30\
5&q=methods+capable+of+detecting+chronic+fluoride+poisoning

I can't find one.  Did I miss it?

James R Deal - ask for the studies - they should be right at the fingertips of
all the government agencies to prove the safety and effectiveness  of all
fluoridation chemicals/medications


It will be like a dog chasing his tail - each agency refering to the next - one
big circle.

http://www.herbs4health.com/news/01oct00.htm


These men talk about hundreds of safety studies ... but when asked to name one
that didn't exclude everyone with symptoms or use inappropriate methods, there
is no response. Can you name "any published scientific article demonstrating the
safety of our current fluoride intake ... or any studies which indicate that
researchers used methods capable of detecting cases of chronic fluoride
poisoning – but failed to find them – in any fluoridated U.S. cities in the
past"? Surely if there had been such a study it would have been mentioned at
some time in the Public Health journals, or by the National Academy of Sciences
or World Health Organization. No one can name a study because none exist. There
were no legitimate long-term controlled studies; and no attempt to identify,
verify, or gather reports of suspected or confirmed cases. Chemical and
Engineering News reported: "Even if a doctor is aware of the disease, the early
stages are difficult to diagnose." Fluoridation of Water, Special report by
Bette Hileman, Chemical & Engineering News, August 1, 1988

http://www.awwa.org/files/GovtPublicAffairs/PressReleases/020111UMCFluoride.pdf

For Immediate Release: Contact: Deirdre Mueller
February 1, 2011 303-347-6140 dmueller@...
Fluoride and Public Health technical session announced for the Utility
Management Conference
(DENVER, CO) – The American Water Works Association (AWWA) announced a new
technical session, Fluoride and Public Health - Science, Safety, and
Communication to be held at the 2011 Utility Management Conference, on
Wednesday, February 9, 2011 from 1:00-2:30 p.m. at the Hyatt Regency in Denver,
Colorado.
The US Department of Health and Human Services (HHS) and the US Environmental
Protection Agency (USEPA) recently released the results of new scientific
assessments related to community water fluoridation. HHS has proposed changing
the recommended level of fluoride in drinking water to the lower end of the
current optimal range. As a result of these findings, USEPA announced it is
initiating a review of the maximum level of fluoride allowed in drinking water.
Panel members will discuss these changes and provide considerations about
effectively communicating difficult public health issues to consumers.
Session speakers will include individuals from the US Environmental Protection
Agency (USEPA) and Centers for Disease Control (CDC), and Lisa Ragain of Aqua
Vitae who will speak on environmental risk communication and strategies.
Additional information on The Utility Management Conference and registration
details are available at www.awwa.org/conferences.
# # #
AWWA is the authoritative resource for knowledge, information, and advocacy to
improve the quality and supply of water in North America and beyond. AWWA is the
largest organization of water professionals in the world. AWWA advances public
health, safety and welfare by uniting the efforts of the full spectrum of the
entire water community. Through our collective strength we become better
stewards of water for the greatest good of the people and the environment

This should be simple - just ask the ADA, CDC, DHHS, EPA and all
pro-flouridation advocates to come forward to name a study demonstrating the
safety of current fluoride levels in drinking water and the effect of excessive
daily intake of fluoride as a possible cause to chronic fluoride poisoning.

Name one that didn't exclude everyone with symptoms or use inappropriate
methods, No one can name a study because none exist. There were no legitimate
long-term controlled studies; and no attempt to identify, verify, or gather
reports of suspected or confirmed cases.


--- In FluoridePoisoning@yahoogroups.com, "ron072754" <reheman@...> wrote:
>
>
http://www.awwa.org/files/GovtPublicAffairs/PressReleases/020111UMCFluoride.pdf
>
> For Immediate Release: Contact: Deirdre Mueller
> February 1, 2011 303-347-6140 dmueller@...
> Fluoride and Public Health technical session announced for the Utility
Management Conference
> (DENVER, CO) – The American Water Works Association (AWWA) announced a new
technical session, Fluoride and Public Health - Science, Safety, and
Communication to be held at the 2011 Utility Management Conference, on
Wednesday, February 9, 2011 from 1:00-2:30 p.m. at the Hyatt Regency in Denver,
Colorado.
> The US Department of Health and Human Services (HHS) and the US Environmental
Protection Agency (USEPA) recently released the results of new scientific
assessments related to community water fluoridation. HHS has proposed changing
the recommended level of fluoride in drinking water to the lower end of the
current optimal range. As a result of these findings, USEPA announced it is
initiating a review of the maximum level of fluoride allowed in drinking water.
Panel members will discuss these changes and provide considerations about
effectively communicating difficult public health issues to consumers.
> Session speakers will include individuals from the US Environmental Protection
Agency (USEPA) and Centers for Disease Control (CDC), and Lisa Ragain of Aqua
Vitae who will speak on environmental risk communication and strategies.
> Additional information on The Utility Management Conference and registration
details are available at www.awwa.org/conferences.
> # # #
> AWWA is the authoritative resource for knowledge, information, and advocacy to
improve the quality and supply of water in North America and beyond. AWWA is the
largest organization of water professionals in the world. AWWA advances public
health, safety and welfare by uniting the efforts of the full spectrum of the
entire water community. Through our collective strength we become better
stewards of water for the greatest good of the people and the environment
>

The Food and Drug Administration (FDA) approved a drug to be used in bone scans.

Technetium-99m (Tc-99m) is traditionally used in bone scanning. This is the only
approved tracer for scanning bones as mandated by law. Since it has a shorter
life span, there was shortage of supply.

Unlike the Tc-99m, the supply for sodium fluoride F18 is abundant. Scanning of
the bones is very important for those who are suffering from cancer.  It is
especially needed by those who have breast cancer and prostate cancer. Sodium
fluoride F18 was approved in the year 1972 but because Tc-99m was less expensive
and at that time, it was still available, it was withdrawn in 1975.

Sodium fluoride F18 in terms of cost, is much higher than Tc-99m. They can be
produced through medical cyclotron that are available in various universities
and suppliers in the United States.  Using this instead of the Tc-99m, the SPECT
imaging produces better images.  Detection of any deformities can be easily seen
and can be prevented through these better scanned images.

The discontinuation of the drug was neither because of safety problems nor of
efficacy but to lower the cost of the procedure.

http://www.dailyhealthreport.org/fda-approves-new-bone-scan-drug/1586/








FDA Schedules Meeting for PET Drug Approval Applicants
The March 2 meeting will help applicants prepare new drug applications or
abbreviated new drug applications for fludeoxyglucose 18 injection, ammonia N 13
injection, and sodium fluoride F 18 injection.

Feb 05, 2011
The Food and Drug Administration announced a March 2 meeting at its White Oak
Campus in Silver Spring, Md., to help applicants prepare new drug applications
or abbreviated new drug applications for fludeoxyglucose 18 injection, ammonia N
13 injection, and sodium fluoride F 18 injection used in positron emission
tomography (PET) imaging. All producers of PET drugs for commercial clinical use
are submitting applications for marketing approval by Dec. 12, 2011.

FDA says many PET drug makers are not familiar with the drug approval process,
however, so this meeting will explain it and also FDA's general inspection
process.

Since the Food and Drug Administration Modernization Act of 1997 became law, FDA
has regulated PET drugs used in nuclear medicine. In March 2000, the agency FDA
presented its findings on the safety and effectiveness of the PET drugs it
studied and described the types of applications that can be submitted for FDG F
18 injection, ammonia N 13 injection, and sodium fluoride F 18 injection used in
PET imaging. A December 2009 regulation began a two-year timeline for PET drug
producers to submit an application for any drug used clinically.

FDA also published revised draft guidance for industry about the content and
format of the applications in the Feb. 3 Federal Register and will use it at the
meeting to explain the approval process.

http://ohsonline.com/articles/2011/02/05/fda-schedules-meeting-for-pet-drug-appr\
oval-applicants.aspx?admgarea=news


Approval Of New Drug For Use In Bone Scans
Written By: ameilia on February 4, 2011 0
The FDA has approved a New Drug Application (NDA) from the National Cancer
Institute (NCI), part of the National Institutes of Health, for a new strength
of a previously approved drug, Sodium Fluoride F18, for use in bone scans. In
contrast to Technetium-99m (Tc-99m), which has been the only approved
radioactive tracer for bone scans, Sodium Fluoride F18 is not subject to the
supply problems that have led to recent nationwide shortages of Tc-99m.

Many diagnostic imaging tests, including bone scans that utilize Single Photon
Emission Computed Tomography (SPECT), require the use of Tc-99m. Bone scans are
essential tools in the diagnosis of bone metastases in cancer patients,
especially those with cancers (such as breast and prostate) that tend to
metastasize to bone.

Sodium Fluoride F18 was approved in 1972 but withdrawn in 1975, when the less
expensive tracer Tc-99m became available. Tc-99m is derived from an isotope
called molybdenum-99 (Mo-99), which is made mostly in highly enriched uranium
nuclear reactors. Because both Mo-99 and Tc-99m have fairly short half-lives (66
hours and six hours, respectively), these drugs cannot be stockpiled.

Seven nuclear reactors worldwide currently produce Mo-99 for medical use, with
much of the United States' supply coming from a nuclear reactor in Canada that
has had frequent outages, the latest one lasting more than a year.

Although Sodium Fluoride F18 is more expensive than Tc-99, it can be produced in
medical cyclotrons, which are available at many academic universities and
commercial suppliers in the U.S. This drug also provides better images because
it uses Position Emission Tomography (PET) instead of SPECT imaging, allowing
for improved, earlier detection.

The previous strength of Sodium Fluoride F18 was discontinued for market
reasons, not for reasons of safety or efficacy. NCI hopes that multiple
companies and institutions will submit Abbreviated New Drug Applications (ANDAs)
so that generic versions of the drug can be produced, allowing for a reduction
in cost.

A decision by the Centers for Medicare & Medicaid Services regarding coverage
for Sodium Fluoride PET scans was posted on February 26, 2010. It allowed
Coverage with Evidence Development (CED), and a formal registry is being
established by the National Oncologic PET Registry (NOPR) that should help
facilitate this coverage.

Source: NCI Office of Media Relations
NIH/National Cancer Institute
.
http://biomedme.com/general/approval-of-new-drug-for-use-in-bone-scans_32698.htm\
l

This is where i lived for 8mo. helping to open a hardware store.
The county of Whatcom is currently fluoridation free.  When i told people I was
F- poisoned they got it!  Not one looked at me like I had one eye and had a
tinfoil hat!  A successful court case!

This was on Mercola.com

http://www.youtube.com/watch?v=v3STwBBOEgI&feature=player_embedded


I guess this could be the examples if spinal stenosis and chari malformation.

Ronnie

PART 1

http://www.youtube.com/watch?v=RomVuPE1A6s&feature=related

PART 2

http://www.youtube.com/watch?v=TVipx_1KR1E






Cancer Control Convention in Pasadena, California, about 1992.

TRIBUTE TO JOHN YIAMOUYIANNIS (1943-2000)

Translation from the Japanese Journal of Fluoride Research, No. 19, Nov. 2000,
p. 1, excerpts...

Dr John Yiamouyiannis, biochemist and founder of the Safe Water Foundation, USA,
died October 8, 2000, passing away peacefully in sleep at his
home in Delaware, Ohio, surrounded by members of his family.


Undergraduate degree from the University of Chicago and afterward, in 1967; PhD
in biochemistry at the University of Rhode Island. Postdoctoral research at
Western Reserve Medical School; became a biochemical editor at Chemical
Abstracts Service. There, he became aware of the health-damaging effects of
fluoride. His opposing water fluoridation prompted efforts by the National
Institute of Dental Research to have CAS silence him or risk losing substantial
US Public
Health Service funding. He resign from the CAS.

His experience is described in his book, Fluoride the Aging Factor.

Dr Ys studies with Dr Dean Burk to determine whether cancer death rates
increased after fluoridation in the 1950s caused great concern among many
Americans and prompted Congressional hearings in 1977 followed by a 21-day court
trial in Pennsylvania. There the presiding judge was compellingly convinced of
the adverse effects of fluoridation and ordered its halt as a public health
hazard. His decision, however, was overruled on jurisdictional grounds, and at
an administrative level fluoridation policy remained unchanged.

Tohru Murakami, DDS, PhD
Editor, Japanese Journal of Fluoride Research
1-5-16 Kamikoide-machi
Maebashi-shi
Gunma-ken, 371 0037, Japan

http://www.nteu280.org/Issues/Fluoride/NTEU280-Fluoride.htm



We have also taken a direct step to protect the employees we represent from the
risks of drinking fluoridated water. We applied EPA's risk control methodology,
the Reference Dose, to the recent neurotoxicity data. The Reference Dose is the
daily dose, expressed in milligrams of chemical per kilogram of body weight,
that a person can receive over the long term with reasonable assurance of safety
from adverse effects. Application of this methodology to the Varner et al.\4
data leads to a Reference Dose for fluoride of 0.000007 mg/kg-day. Persons who
drink about one quart of fluoridated water from the public drinking water supply
of the District of Columbia while at work receive about 0.01mg/kg-day from that
source alone. This amount of fluoride is more than 100 times the Reference Dose.
On the basis of these results the union filed a grievance, asking that EPA
provide un-fluoridated drinking water to its employees.

Varner et al.\4
http://www.fluoride-journal.com/98-31-2/31291-95.htm

--------------------------------------------------------------------------------
FLUORIDE 31(2),
1998, pp 91-95 International Society for Fluoride Research Table of Contents

--------------------------------------------------------------------------------


CHRONIC ADMINISTRATION OF ALUMINUM-FLUORIDE
OR SODIUM- FLUORIDE TO RATS IN DRINKING WATER:
ALTERATIONS IN NEURONAL AND CEREBROVASCULAR INTEGRITY

J A Varner, K F Jensen, W Horvath and R L Isaacson
Binghamton, New York, and Research Triangle Park, North Carolina, USA

Abstracted from Brain Research 784 284-298 1998

Objective
The question addressed in this study was to understand why 0.5 ppm of aluminum
fluoride in the drinking water of rats was associated with a larger increase in
infections and mortality than with higher concentrations of 5 ppm and 50 ppm of
aluminum fluoride in the drinking water. This higher mortality had been found in
an earlier experiment when rats were given 0.5 ppm, 5 ppm or 50 ppm aluminum for
45 weeks in their drinking water.

The earlier experiment had been done to help determine whether aluminum in
drinking water might have a role in aging-related neurological impairments. The
suggestion had been made that when both fluoride and aluminum were present in
drinking water they would form fluoroaluminum complexes, such as AlF3 in the
stomach that, compared to their ionic forms, would be transported more easily
into the blood stream and across the blood-brain barrier.

All the groups receiving AlF3 had shown the same significant reduction in the
number of cells in certain areas of the hippocampus relative to the control
group. The level of aluminum in the brains was almost double that of the control
group, while morphological abnormalities were observed throughout the brain and
its blood vessels. Dramatic behavioral differences were not seen.

One possible reason for the increased infections and mortality of animals in the
0.5 ppm AlF3 group was that the toxic agent of importance was the fluoride and
that its absorption or its effects were antagonized by the higher levels of
aluminum found with the higher doses of AlF3. The present study was undertaken
to compare 0.5 ppm of aluminum fluoride, AlF3, with a comparable level of
fluoride administered alone in the form of sodium fluoride.

Method
Twenty seven adult Long-Evans rats were administered one of three treatments for
52 weeks. All groups received double distilled deionized drinking water. No
additives were present in water for the control group. One treated group
received water containing 0.5 ppm AlF3 (Al3+) giving a fluoride concentration of
about 1 ppm. The other treated group had water containing 2.1 ppm of sodium
fluoride, to provide an equivalent amount of fluoride (about 1 ppm) as for the
AlF3 group.

Tissue aluminum levels of brain, liver, and kidney were assessed, and
histological sections of brain were examined. For the morphological evaluations
all counts and ratings were conducted by three individuals, two of whom were
always blind to the treatment of the rats from whom the tissues came.

Results
No differences were found between the body weights of rats in the different
treatment groups although more rats died in the AlF3 group (5) than in the
control group (1), P=0.05. A progressive decline in the appearance of the AlF3
animals was noted throughout the experiment, with the hair becoming sparse and
the yellowing which occurs with age. The skin became dry, flaky and of a copper
color. The aluminum levels in samples of brain were higher in both the AlF3 and
NaF groups relative to the controls, P<0.01. The kidneys of the AlF3 group had
higher aluminum levels compared to both the control and NaF groups, P<0.01.
Liver aluminum levels did not differ between groups.

The effects of the two treatments on cerebrovascular and neuronal integrity were
qualitatively and quantitatively different with the alterations being greater in
animals in the AlF3 group than in the NaF group, and greater in the NaF group
than in the controls. Examination of the distribution of the aluminum, using the
Morin method for aluminum-fluorescence, showed the distribution in sections of
brain to be exclusively associated with vasculature. This Al-fluorescence
occurred in all three groups but there were consistent treatment-related
differences in the intensity and extent of the aluminum-fluorescence. The NaF
group had less Al-fluorescence associated with the vasculature than the control
group, P<0.03. Renal changes were apparent in animals from both the NaF and AlF3
groups. More monocyte infiltration was present in the kidneys of the AlF3 group
compared to the controls, P<0.05. No morphological abnormalities were present in
the liver.

In the hippocampus, more moderately damaged and grossly abnormal cells were
present in areas of the right hippocampus in the AlF3 group than in the control
group, P<0.04, P<0.03. In neocortical layers 2 and 3 of the right hemisphere,
the AlF3 group had more moderately damaged cells than the NaF group which had
more normal cells, P<0.04. In neocortical layers 2 and 3 of the left hemisphere,
the AlF3 group had more abnormal cells than the controls, P<0.02. Corresponding
increases in the frequency of normal appearing cells were observed in the
neocortex of the control animals.

Neuronal density in the hippocampus was decreased in area CA3 in the left
hemisphere of the AlF3 group compared to the controls, P<0.05. No differences
were found in layers CA1 and CA4 in either hemisphere. Neuronal density was
decreased in neocortical layers 2 and 3 in the left hemisphere of the AlF3 group
compared to the controls and the NaF group, P<0.05. Neuronal density was also
reduced in layers 5 and 6 of the left hemisphere of the AlF3 group compared to
the controls, P<0.03, P<0.03. No differences in neuronal density were found, in
any of the groups, in layer 4 of the left hemisphere or in any of the layers of
the cortex in the right hemisphere.

While in control animals the localization of IgM was largely restricted to the
vascular lumen, indicating the integrity of the blood-brain barrier to IgM, in
the AlF3 and NaF groups staining for IgM in the neural parenchyma was increased
in the right hemisphere, P<0.03, P<0.01. No differences were found among the
groups in the left hemisphere. Minor amounts of IgM immunostaining were
detectable in the hippocampus and dentate gyrus but no significant differences
were present.

Differences in the amount of immunoreactivity for -amyloid relative to that for
amyloid A were most prominent in the vasculature of the dorsal thalamus. The
control group had few instances of immunoreactivity while the tissue of animals
from the AlF3 group demonstrated a bimodal distribution of reaction product with
either no reaction product staining or a high level. The AlF3 group had more
immunoreactivity for -amyloid in the lateral posterior thalamic areas of both
hemispheres relative to the controls, left P<0.05, right P<0.01. The NaF group
differed from the control for immunoreactivity for -amyloid in the right lateral
posterior thalamic area with the controls having low reactivity and the NaF
group having no or high levels of immunoreactivity, P<0.01.

Discussion and Conclusions
The high mortality rate in the animals receiving 0.5 ppm of aluminum in their
drinking water found in the first study was replicated in this second study.
Since the administration of sodium fluoride alone did not produce a similar
mortality rate, this effect does not appear to be directly related to fluoride
intake. The appearance of the AlF3 animals, with sparse hair and a
copper-colored hypermelanosis of the underlying skin, may be indicative of
several diseases including chronic renal failure. Histological evidence of
glomerular distortions was present in both the AlF3 and NaF groups.

The overall aluminum level of the kidneys in the AlF3 group was nearly twice
that of the NaF group and possibly may have been associated with a greater level
of physiological dysfunction. The kidney is critical to the elimination of both
aluminum and fluoride, and these changes may have impaired the elimination of
these elements, detoxification in general or homeostasis of other ions such as
calcium.

Both the AlF3 and NaF groups had increased brain aluminum levels relative to
controls. The aluminum level in the NaF group was double that of controls and
the aluminum level of the AlF3 group even greater. The aluminum detected in the
controls and NaF groups is most likely to have come from the rat chow where the
reported levels of aluminum range from 150 ppm to 8300 ppm. Fluoride commonly
occurs in food and water and is almost completely and quickly absorbed from the
gastrointestinal tract. In the present experiment, the AlF3 in the drinking
water was prepared to form optimally a fluoroaluminum species capable of
crossing the gut and vascular barriers. It is possible that the sodium
fluoride-treated group was able to form some amount of an AlF3 also capable of
becoming bioavailable.

In general, the reduction of neuronal density in the neocortex of the left
hemisphere was more prominent in the AlF3 group than the NaF and control groups.
Cellular abnormalities in the form of chromatin clumping, enhanced protein
staining, pyknosis, vacuolation, and the presence of ghost-like cells were also
more common in the AlF3 group in the left hemisphere. Vascular Al-fluorescence
was more pronounced throughout most structures of the left hemisphere of the
AlF3 group. The hippocampus was an exception to these findings with
abnormalities being found only in the right hemisphere in the CA1 and CA4 areas
of both the AlF3 and NaF groups. The right hippocampus also had higher levels of
aluminum-induced fluorescence than the left hippocampus.

Possible cellular mechanisms which might underlie the association between
regional aluminum accumulation and regional patterns of neuronal injury include
transferrin transport, calcium homeostasis and second messenger systems,
alterations in neuronal cytoskeleton, and alterations in the cerebrovasculature.
Transferrin transport carries certain metals, including aluminum, into the cells
by a receptor complex located on plasma membranes. Neurotoxic reactions to
aluminum may also result from disruption of ion homeostasis and second messenger
systems, in particular G-proteins. The activation of G-proteins in turn
initiates a chain of reactions beginning with adenylate cyclase, cAMP, and
protein kinases that ultimately result in increased phosphorylation of various
substrates. G-proteins are involved in the regulation of ion channels,
metabolism, gene expression, and cytoskeletal structures via second messenger
systems.

The deposition of aluminum in the cerebrovasculature was seen to have the
potential also to contribute to the observed neuronal injury by altering the
blood-brain barrier or cerebral blood flow. Both the AlF3 and NaF groups had
increased levels of IgM in the cortex of the right hemisphere compared to the
controls. Serum proteins, such as IgM and other antibodies, are typically
excluded from neuronal tissue by the blood-brain barrier. The increased
immunoreactivity of IgM in the present study may be indicative of a compromise
in the blood-brain barrier occurring possibly through changes in lipophilicity
or the potentiation of existing transport mechanisms.

Striking parallels were seen between aluminum-induced alterations in
cerebrovasculature and those associated with Alzheimer's disease and other forms
of dementia where microvascular abnormalities display a regional and laminar
specificity in accordance with neuronal degeneration patterns, suggesting that
the alterations in the cerebrovasculature may be a primary event in
neurodegenerative disease. Accumulation of -amyloid has been found in the
cerebrovasculature and spinal cord vasculature of elderly persons and may be a
consequence of the development of blood vessel abnormalities. Vascular tissues
produce -amyloid and the vascular deposition of -amyloid may result from
alterations in the basement membrane of blood vessels that frequently occurs
with ageing. Although it is uncertain whether -amyloid is a causative factor in
neurodegeneration or a secondary consequence of injury, aluminum appears to have
the capacity to influence the distribution and properties of -amyloid. In the
present study animals in both the AlF3 and NaF groups exhibited a bimodal
distribution of vascular -amyloid in both hemispheres in the lateral posterior
thalamus being either absent or present in high levels in both groups. This
increase in vascular -amyloid in the lateral posterior thalamus may be causally
related to the neuronal degeneration found in the area to which it is
principally connected, the superior parietal cortex.

In contrast, the control group consistently had only low levels of
immunostaining for -amyloid, a unimodal distribution. While the presence of low
levels of -amyloid in the controls was understandable as being the possible
result of a natural continuing, but limited, production of the protein
throughout life, the bimodal distribution of -amyloid in the AlF3 and NaF groups
was not understood.

While the present results do not address the causal mechanisms of
aluminum-induced neural degeneration, they do demonstrate that ingested aluminum
reaches the brain, and in such animals there exists evidence of neural injury.
While the small amount of aluminum of 0.5 ppm AlF3 in the drinking water of rats
required for neurotoxic effects was seen as surprising, the neurotoxic results
of NaF at the dose given in the present study, 2.1 ppm or about 1 ppm of
fluoride, was seen as even more so.

As dietary sources of fluoride are additive in animals it was considered that,
for the animals in the NaF group, the fluoride in rat chow, such as Purina
Rodent Laboratory Chow, together with their drinking exceeded tolerable levels.
Fluoride has diverse actions on a variety of cellular and physiological
functions including the inhibition of a variety of enzymes, a corrosive action
in acid media, and the production of hypocalcemia, hyperkalemia and possibly
cerebral impairment.

Few chronic toxicity studies of fluoride have included extensive histological
characterization of injury to the brain but have usually been limited to weight
loss, dental and skeletal changes, indicators of carcinogenesis, and damage to
soft tissues. The results of the present study indicate that more intensive
neuropathological evaluations of fluoride effects on the brain is likely to be
of value.

In summary, the chronic administration of aluminum fluoride and sodium fluoride
in the drinking water of rats resulted in distinct morphological alterations in
the brain, including effects on neurones and the cerebrovasculature. Further
studies of aluminum fluoride and sodium fluoride are needed to establish the
relative importance of a variety of potential mechanisms contributing to the
observed effects as well as to determine the potential involvement of these
agents in neurogenerative diseases.

Key words: Aluminum-fluoride; Amyloid; Brain; Cerebrovasculature; Hippocampus;
Neurotoxicity; Rat; Sodium fluoride.
Reprints: Julie A Varner, Lineberry Research Associates, PO Box 14626, Research
Triangle Park, North Carolina 27709, USA. Fax: +1-919-547-0974.
E-mail: jvarner@...



--------------------------------------------------------------------------------
FLUORIDE 31(2),
1998, pp 91-95 International Society for Fluoride Research
Home | Table of Contents | ISFR Board | Subscription
Submissions | Announcements | Authors | Subject Index

--------------------------------------------------------------------------------

Sent from my Verizon Wireless BlackBerry

GO GIRL!
I'm gettin' antsy to raise a ruckus in my town.  Maybe just a little longer for
the next inevitable media explosion!

Ronnie from Negaunee

--- In FluoridePoisoning@yahoogroups.com, Janet Pettit <jpettit@...> wrote:
>
> Aliss'
>
> So glad to hear about Calgary's decision. Time is on our side!  The
> dominoes are tipping!
>
> PALATKA, FL
>
> My little town of Palatka, FL, which is located just south of
> Jacksonville, has temporarily stopped fluoridating for now.
>
> They began fluoridation in 1999.  I moved there in 2003.   I went to
> talk to the water supervisor about 5 years ago.  He explained that the
> scale which was used to weigh the chemicals wasn't working and they
> weren't fluoridating at the time.  I saw the small house where the
> equipment was kept and where the fluoridation chemicals were added.
> Everything metal was rusted, the small window was etched and the scale
> which  they kept the storage tank on to measure the supply was very
> rusted and broken.  I spoke with him after the tour, gave him some
> literature and my spiel about the dangers of fluoridation along with
> the Connet's and Deb Moore's web sites.  I didn't followup because of
> personal  pressing problems in other areas but assumed they would soon
> fix the problem and continue fluoridation.  However, a friend of mine
> checked about a year ago and to my  surprise found out that Palatka
> still was not  adding fluoride.  I can only guess that the supervisor
> did some investigation on his own and didn't have the problem fixed.
> The scale was very small and the tank held maybe 8 or 10 gallons which
> didn't seem like a difficult problem to fix even if they had to buy a
> new scale.
>
> Right now the city is in agreement because stopping fluoridation helps
> their financial situation.  I'm reluctant to start a city wide
> campaign to have a resolution passed that would make the situation
> permanent because I'm afraid  that the dentists will jump in and
> insist on starting fluoridation again before we can educate the water
> consumers.  The dentists don't seem to know it's been stopped nor do
> many others, so far as I know.
>
>   At least, apparently, I have the supervisor on my side.  I'm going
> to begin talking with the individual commissioners quietly  to educate
> them and to get them to pass a resolution to rescind the original  one
> that began the process.
>
> 		 * * * * * *
> HENDERSONVILLE, NC
>
> My other happening is from my former home in western North Carolina
> where I led the fight beginning in 1995 when Hendersonville, NC voted
> 3 to 2 to fluoridate even though it was voted down 2 to 1 against
> about 10 years previously.  The mayor refused to put it to a vote of
> the water consumers saying that when the local health dept. told them
> to take it out was the only time it would be done.
>
> Meanwhile, unknown to me, the state did a before and after, 10 year
> study of tooth decay  in the town.  They took a baseline account of
> decay among some school children in  1997 as fluoridation was starting
> and repeated it in 2007.   After the second check in 2007, the local
> health dept. issued a statement lauding the results that tooth decay
> was much improved , thanks to fluoridation.  Tooth decay had gone
> down, they said, and the number of children with no decay had gone up.
>
> I didn't believe it... so I wrote to the state and got the actual
> results:  tooth decay had actually gone up and the number of decay-
> free children had gone down!  The local health dept. had lied!!!  They
> had made up their own numbers!  If you or anyone has a use for this
> study, I'd be glad to send copies of it and the health dept's
> resolution.  It will have to be a hard copy since my copier won't scan
> at the moment.
>
> We're having a meeting this spring in Hendersonville as a new fluoride
> fighting group is forming.  They have asked me to join them for this
> meeting.  Stay tuned.  With the new directive to reduce the amount of
> fluoride in public water maybe now the city will listen!
>
> 		 Thanks for all you do and the valuable information you share with
> us all.
>
>
>  Jan Pettit
>
>
>
>
>
>
> On Feb 8, 2011, at 9:58 PM, Aliss wrote:
>
> >
> > I just heard from Dr. Jim Beck that the votes were 9 to 3 to end
> > fluoridation. Congratulations to the mayor and councillors who made
> > a science-based ethical decision that will improve quality of
> > drinking water and public health for 1.1 million residents of Calgary.
> >
> > May this be the first domino.
> >
> > Aliss
> >
> >
> >
>

D
Send them the Paper that the EPA scientists used to get clean water at their
workplace.
http://www.nteu280.org/Issues/Fluoride/NTEU280-Fluoride.htm

We applied EPA's risk control methodology, the Reference Dose, to the recent
neurotoxicity data. The Reference Dose is the daily dose, expressed in
milligrams of chemical per kilogram of body weight, that a person can receive
over the long term with reasonable assurance of safety from adverse effects.
Application of this methodology to the Varner et al.\4 data leads to a Reference
Dose for fluoride of 0.000007 mg/kg-day. Persons who drink about one quart of
fluoridated water from the public drinking water supply of the District of
Columbia while at work receive about 0.01mg/kg-day from that source alone. This
amount of fluoride is more than 100 times the Reference Dose. On the basis of
these results the union filed a grievance, asking that EPA provide
un-fluoridated drinking water to its employees.

The implication for the general public of these calculations is clear. Recent,
peer-reviewed toxicity data, when applied to EPA's standard method for
controlling risks from toxic chemicals, require an immediate halt to the use of
the nation's drinking water reservoirs as disposal sites for the toxic waste of
the phosphate fertilizer industry\24.

This document was prepared on behalf of the National Treasury Employees Union
Chapter 280 by Chapter Senior Vice-President J. William Hirzy, Ph.D. For more
information please call Dr. Hirzy at 202-260-4683.



Re: data leads to a Reference Dose for fluoride of 0.000007 mg/kg-day.


Varner et al.\4
http://www.fluoride-journal.com/98-31-2/31291-95.htm

--------------------------------------------------------------------------------
FLUORIDE 31(2),
1998, pp 91-95 International Society for Fluoride Research Table of Contents

--------------------------------------------------------------------------------


CHRONIC ADMINISTRATION OF ALUMINUM-FLUORIDE
OR SODIUM- FLUORIDE TO RATS IN DRINKING WATER:
ALTERATIONS IN NEURONAL AND CEREBROVASCULAR INTEGRITY

J A Varner, K F Jensen, W Horvath and R L Isaacson
Binghamton, New York, and Research Triangle Park, North Carolina, USA

Abstracted from Brain Research 784 284-298 1998

Objective
The question addressed in this study was to understand why 0.5 ppm of aluminum
fluoride in the drinking water of rats was associated with a larger increase in
infections and mortality than with higher concentrations of 5 ppm and 50 ppm of
aluminum fluoride in the drinking water. This higher mortality had been found in
an earlier experiment when rats were given 0.5 ppm, 5 ppm or 50 ppm aluminum for
45 weeks in their drinking water.

The earlier experiment had been done to help determine whether aluminum in
drinking water might have a role in aging-related neurological impairments. The
suggestion had been made that when both fluoride and aluminum were present in
drinking water they would form fluoroaluminum complexes, such as AlF3 in the
stomach that, compared to their ionic forms, would be transported more easily
into the blood stream and across the blood-brain barrier.

All the groups receiving AlF3 had shown the same significant reduction in the
number of cells in certain areas of the hippocampus relative to the control
group. The level of aluminum in the brains was almost double that of the control
group, while morphological abnormalities were observed throughout the brain and
its blood vessels. Dramatic behavioral differences were not seen.

One possible reason for the increased infections and mortality of animals in the
0.5 ppm AlF3 group was that the toxic agent of importance was the fluoride and
that its absorption or its effects were antagonized by the higher levels of
aluminum found with the higher doses of AlF3. The present study was undertaken
to compare 0.5 ppm of aluminum fluoride, AlF3, with a comparable level of
fluoride administered alone in the form of sodium fluoride.

Method
Twenty seven adult Long-Evans rats were administered one of three treatments for
52 weeks. All groups received double distilled deionized drinking water. No
additives were present in water for the control group. One treated group
received water containing 0.5 ppm AlF3 (Al3+) giving a fluoride concentration of
about 1 ppm. The other treated group had water containing 2.1 ppm of sodium
fluoride, to provide an equivalent amount of fluoride (about 1 ppm) as for the
AlF3 group.

Tissue aluminum levels of brain, liver, and kidney were assessed, and
histological sections of brain were examined. For the morphological evaluations
all counts and ratings were conducted by three individuals, two of whom were
always blind to the treatment of the rats from whom the tissues came.

Results
No differences were found between the body weights of rats in the different
treatment groups although more rats died in the AlF3 group (5) than in the
control group (1), P=0.05. A progressive decline in the appearance of the AlF3
animals was noted throughout the experiment, with the hair becoming sparse and
the yellowing which occurs with age. The skin became dry, flaky and of a copper
color. The aluminum levels in samples of brain were higher in both the AlF3 and
NaF groups relative to the controls, P<0.01. The kidneys of the AlF3 group had
higher aluminum levels compared to both the control and NaF groups, P<0.01.
Liver aluminum levels did not differ between groups.

The effects of the two treatments on cerebrovascular and neuronal integrity were
qualitatively and quantitatively different with the alterations being greater in
animals in the AlF3 group than in the NaF group, and greater in the NaF group
than in the controls. Examination of the distribution of the aluminum, using the
Morin method for aluminum-fluorescence, showed the distribution in sections of
brain to be exclusively associated with vasculature. This Al-fluorescence
occurred in all three groups but there were consistent treatment-related
differences in the intensity and extent of the aluminum-fluorescence. The NaF
group had less Al-fluorescence associated with the vasculature than the control
group, P<0.03. Renal changes were apparent in animals from both the NaF and AlF3
groups. More monocyte infiltration was present in the kidneys of the AlF3 group
compared to the controls, P<0.05. No morphological abnormalities were present in
the liver.

In the hippocampus, more moderately damaged and grossly abnormal cells were
present in areas of the right hippocampus in the AlF3 group than in the control
group, P<0.04, P<0.03. In neocortical layers 2 and 3 of the right hemisphere,
the AlF3 group had more moderately damaged cells than the NaF group which had
more normal cells, P<0.04. In neocortical layers 2 and 3 of the left hemisphere,
the AlF3 group had more abnormal cells than the controls, P<0.02. Corresponding
increases in the frequency of normal appearing cells were observed in the
neocortex of the control animals.

Neuronal density in the hippocampus was decreased in area CA3 in the left
hemisphere of the AlF3 group compared to the controls, P<0.05. No differences
were found in layers CA1 and CA4 in either hemisphere. Neuronal density was
decreased in neocortical layers 2 and 3 in the left hemisphere of the AlF3 group
compared to the controls and the NaF group, P<0.05. Neuronal density was also
reduced in layers 5 and 6 of the left hemisphere of the AlF3 group compared to
the controls, P<0.03, P<0.03. No differences in neuronal density were found, in
any of the groups, in layer 4 of the left hemisphere or in any of the layers of
the cortex in the right hemisphere.

While in control animals the localization of IgM was largely restricted to the
vascular lumen, indicating the integrity of the blood-brain barrier to IgM, in
the AlF3 and NaF groups staining for IgM in the neural parenchyma was increased
in the right hemisphere, P<0.03, P<0.01. No differences were found among the
groups in the left hemisphere. Minor amounts of IgM immunostaining were
detectable in the hippocampus and dentate gyrus but no significant differences
were present.

Differences in the amount of immunoreactivity for -amyloid relative to that for
amyloid A were most prominent in the vasculature of the dorsal thalamus. The
control group had few instances of immunoreactivity while the tissue of animals
from the AlF3 group demonstrated a bimodal distribution of reaction product with
either no reaction product staining or a high level. The AlF3 group had more
immunoreactivity for -amyloid in the lateral posterior thalamic areas of both
hemispheres relative to the controls, left P<0.05, right P<0.01. The NaF group
differed from the control for immunoreactivity for -amyloid in the right lateral
posterior thalamic area with the controls having low reactivity and the NaF
group having no or high levels of immunoreactivity, P<0.01.

Discussion and Conclusions
The high mortality rate in the animals receiving 0.5 ppm of aluminum in their
drinking water found in the first study was replicated in this second study.
Since the administration of sodium fluoride alone did not produce a similar
mortality rate, this effect does not appear to be directly related to fluoride
intake. The appearance of the AlF3 animals, with sparse hair and a
copper-colored hypermelanosis of the underlying skin, may be indicative of
several diseases including chronic renal failure. Histological evidence of
glomerular distortions was present in both the AlF3 and NaF groups.

The overall aluminum level of the kidneys in the AlF3 group was nearly twice
that of the NaF group and possibly may have been associated with a greater level
of physiological dysfunction. The kidney is critical to the elimination of both
aluminum and fluoride, and these changes may have impaired the elimination of
these elements, detoxification in general or homeostasis of other ions such as
calcium.

Both the AlF3 and NaF groups had increased brain aluminum levels relative to
controls. The aluminum level in the NaF group was double that of controls and
the aluminum level of the AlF3 group even greater. The aluminum detected in the
controls and NaF groups is most likely to have come from the rat chow where the
reported levels of aluminum range from 150 ppm to 8300 ppm. Fluoride commonly
occurs in food and water and is almost completely and quickly absorbed from the
gastrointestinal tract. In the present experiment, the AlF3 in the drinking
water was prepared to form optimally a fluoroaluminum species capable of
crossing the gut and vascular barriers. It is possible that the sodium
fluoride-treated group was able to form some amount of an AlF3 also capable of
becoming bioavailable.

In general, the reduction of neuronal density in the neocortex of the left
hemisphere was more prominent in the AlF3 group than the NaF and control groups.
Cellular abnormalities in the form of chromatin clumping, enhanced protein
staining, pyknosis, vacuolation, and the presence of ghost-like cells were also
more common in the AlF3 group in the left hemisphere. Vascular Al-fluorescence
was more pronounced throughout most structures of the left hemisphere of the
AlF3 group. The hippocampus was an exception to these findings with
abnormalities being found only in the right hemisphere in the CA1 and CA4 areas
of both the AlF3 and NaF groups. The right hippocampus also had higher levels of
aluminum-induced fluorescence than the left hippocampus.

Possible cellular mechanisms which might underlie the association between
regional aluminum accumulation and regional patterns of neuronal injury include
transferrin transport, calcium homeostasis and second messenger systems,
alterations in neuronal cytoskeleton, and alterations in the cerebrovasculature.
Transferrin transport carries certain metals, including aluminum, into the cells
by a receptor complex located on plasma membranes. Neurotoxic reactions to
aluminum may also result from disruption of ion homeostasis and second messenger
systems, in particular G-proteins. The activation of G-proteins in turn
initiates a chain of reactions beginning with adenylate cyclase, cAMP, and
protein kinases that ultimately result in increased phosphorylation of various
substrates. G-proteins are involved in the regulation of ion channels,
metabolism, gene expression, and cytoskeletal structures via second messenger
systems.

The deposition of aluminum in the cerebrovasculature was seen to have the
potential also to contribute to the observed neuronal injury by altering the
blood-brain barrier or cerebral blood flow. Both the AlF3 and NaF groups had
increased levels of IgM in the cortex of the right hemisphere compared to the
controls. Serum proteins, such as IgM and other antibodies, are typically
excluded from neuronal tissue by the blood-brain barrier. The increased
immunoreactivity of IgM in the present study may be indicative of a compromise
in the blood-brain barrier occurring possibly through changes in lipophilicity
or the potentiation of existing transport mechanisms.

Striking parallels were seen between aluminum-induced alterations in
cerebrovasculature and those associated with Alzheimer's disease and other forms
of dementia where microvascular abnormalities display a regional and laminar
specificity in accordance with neuronal degeneration patterns, suggesting that
the alterations in the cerebrovasculature may be a primary event in
neurodegenerative disease. Accumulation of -amyloid has been found in the
cerebrovasculature and spinal cord vasculature of elderly persons and may be a
consequence of the development of blood vessel abnormalities. Vascular tissues
produce -amyloid and the vascular deposition of -amyloid may result from
alterations in the basement membrane of blood vessels that frequently occurs
with ageing. Although it is uncertain whether -amyloid is a causative factor in
neurodegeneration or a secondary consequence of injury, aluminum appears to have
the capacity to influence the distribution and properties of -amyloid. In the
present study animals in both the AlF3 and NaF groups exhibited a bimodal
distribution of vascular -amyloid in both hemispheres in the lateral posterior
thalamus being either absent or present in high levels in both groups. This
increase in vascular -amyloid in the lateral posterior thalamus may be causally
related to the neuronal degeneration found in the area to which it is
principally connected, the superior parietal cortex.

In contrast, the control group consistently had only low levels of
immunostaining for -amyloid, a unimodal distribution. While the presence of low
levels of -amyloid in the controls was understandable as being the possible
result of a natural continuing, but limited, production of the protein
throughout life, the bimodal distribution of -amyloid in the AlF3 and NaF groups
was not understood.

While the present results do not address the causal mechanisms of
aluminum-induced neural degeneration, they do demonstrate that ingested aluminum
reaches the brain, and in such animals there exists evidence of neural injury.
While the small amount of aluminum of 0.5 ppm AlF3 in the drinking water of rats
required for neurotoxic effects was seen as surprising, the neurotoxic results
of NaF at the dose given in the present study, 2.1 ppm or about 1 ppm of
fluoride, was seen as even more so.

As dietary sources of fluoride are additive in animals it was considered that,
for the animals in the NaF group, the fluoride in rat chow, such as Purina
Rodent Laboratory Chow, together with their drinking exceeded tolerable levels.
Fluoride has diverse actions on a variety of cellular and physiological
functions including the inhibition of a variety of enzymes, a corrosive action
in acid media, and the production of hypocalcemia, hyperkalemia and possibly
cerebral impairment.

Few chronic toxicity studies of fluoride have included extensive histological
characterization of injury to the brain but have usually been limited to weight
loss, dental and skeletal changes, indicators of carcinogenesis, and damage to
soft tissues. The results of the present study indicate that more intensive
neuropathological evaluations of fluoride effects on the brain is likely to be
of value.

In summary, the chronic administration of aluminum fluoride and sodium fluoride
in the drinking water of rats resulted in distinct morphological alterations in
the brain, including effects on neurones and the cerebrovasculature. Further
studies of aluminum fluoride and sodium fluoride are needed to establish the
relative importance of a variety of potential mechanisms contributing to the
observed effects as well as to determine the potential involvement of these
agents in neurogenerative diseases.

Key words: Aluminum-fluoride; Amyloid; Brain; Cerebrovasculature; Hippocampus;
Neurotoxicity; Rat; Sodium fluoride.
Reprints: Julie A Varner, Lineberry Research Associates, PO Box 14626, Research
Triangle Park, North Carolina 27709, USA. Fax: +1-919-547-0974.
E-mail: jvarner@...



--------------------------------------------------------------------------------
FLUORIDE 31(2),
1998, pp 91-95 International Society for Fluoride Research
Home | Table of Contents | ISFR Board | Subscription
Submissions | Announcements | Authors | Subject Index

--------------------------------------------------------------------------------

data leads to a Reference Dose for fluoride of 0.000007 mg/kg-day.

So can anyone tell me what the 0.000007 mg/kg-day would be in parts per billion?
Or should that be parts per trillion?

How about parts per googlezillion?

Seriously - can someone do the math for a fluoride poisoned, brain dead,
nin-com-poop?????

Ronnie