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Richard D. Sauerheber,
Ph.D.
(Chemistry, University of California, San Diego, 1976)
Palomar Community College
1140 W. Mission Rd.
San Marcos, CA 92069
Summary
The mechanism by which fluoride's lethal poisoning of man and
animals occurs is presented. "Low" level fluoridation
of municipal water exhibits well known alterations in teeth and
bone structure and calcification of tendons and ligaments. 'Moderate'
doses cause spinal deformities and increased hip fracture tendency
and kidney and gall stones. Higher levels cause death and are
responsible for its major industrial use as a rodenticide. Solubility
calculations indicate that fluoride doses required to decrease
calcium below physiological blood levels are comparable to those
present in poisoned victims' tissues and to those causing decreased
beat rates in isolated heart cells in culture. Acute lethal poisoning
and many of the chronic 'low' level effects of fluoride are mediated
by calcium binding by the fluoride ion.
Introduction
An array of scientific findings indicate that the decision made
by many cities as early as 1956 to add fluoride (a rodenticide)
to municipal drinking water, as long as the dose is below a certain
level (usually 1 part per million, 1 milligram fluoride per liter
or 0.05 mM) to decrease the incidence of something as minor as
tooth decay, was irrational. We now know that precipitates of
calcium fluoride occur in fluoridated water cities when the acidity
is low (a pH above 7) depending on the fluoride level used. This
causes scaling of water pipes (1) and numerous biological effects
in consumers, the extent determined by the acidity and the amount
of calcium in the water.
Fluoridated municipal water
supplies in the United States have been found to contain fluoride
levels ranging anywhere from 0.012 mM to a record lethal accidental
7.5 mM (8). The biologic effects have been diverse, covering
the entire above range. In spite of lethal poisonings from municipal
water fluoridation programs, the Public Health Service retains
its mandate to fluoridate all U.S. cities as soon as possible
and to reach out to other cities throughout the world in an effort
to minimize tooth decay while fluoridating the blood of the water
consumer as though this were an acceptable alternative to topical
fluoride or to addition of fluoride to one's own consumed water.
Unfortunately, in 1992 at the
mouth of the Yukon River in Hooper Bay, Alaska the unthinkable
occurred. In what is considered an accident, an entire village
was poisoned by its own fluoridated water supply when the system
malfunctioned. This represents the first 'experiment' in which
human beings were exposed to lethal doses of fluoride. Blood
samples were measured for incorporated fluoride and calcium ion
and provided much pathologic information on the effects of high
doses of fluoride assimilated from municipal drinking water supplies
(8). 296 residents were severely poisoned with one fatality.
Most had heart malfunction-associated symptoms and severe gastrointestinal
pain.
It is now understood that the
conversion of fluoride ion into HF, hydrofluoric acid, occurred
in the stomach due to the stomach acid HCl at pH 3 and the HF
caused the intense pain. HF cannot be stored in glass since it
dissolves the container; it also dissolves leather and skin.
Also blood calcium levels dropped to 1/3 of normal in one victim,
causing a heart attack and the loss of his life. Although the
authors of the study were uncertain whether the fluoride itself
caused the effect directly or rather was due to its known ability
to precipitate magnesium or calcium ion, our recent computations
indicate that low blood calcium is responsible for the lethal
effect of acute fluoride poisoning, as indicated below.
Precipitation of calcium fluoride
into peoples' bones, tendons and ligaments (9) occurs depending
at typical doses added to municipal water. The condition known
medically as fluorosis is associated as expected with spinal
rigidity and bone fragility (2), the severity depending on the
fluoride level present in the blood and for how long.
If fluoride exposure is sufficiently
high or prolonged, formation of kidney and gall stones is known
to occur, due to the low solubility of calcium fluoride (0.04
mM at pH 7 at room temperature) (4,6). People with hyperparathyroidism
or osteosclerosis are more susceptible in this regard to chronic
consumption than others since the calcium fluoride deposits in
the soft tissues more efficiently because of lack of sufficient
binding sites in bones for it (1).
Interestingly, in children
raised on fluoridated water, teeth themselves are more rigid
while at the same time may be somewhat more resistant to cavities,
but no such effect on adult teeth occurs according to many sources
(1, chap. 39, p. 896). Thus fluoridation of adult blood is unnecessary
and indeed useless for this purpose.
The dean of Tulane University
in New Orleans indicated that fluoridated water consumption at
certain doses eventually causes gum disease and for this reason
New Orleans water was not fluoridated at the time Chicago and
New York and other cities approved it (1). Also, in 1960 under
oath in Chicago, the researcher for the Public Health Service
who started the fluoridation idea admitted that his data constituting
the scientific basis for fluoridation were invalid, shattering
its foundation (1). The original observation that people consuming
water in Texas that happened to have fluoride into it also had
whiter teeth than usual was insufficient to justify mass fluoride
addition to other public water supplies, since no one was cognizant
of the coexistence of other unhealthful effects that also occurred.
The effects of fluoride are
subtle enough to go unnoticed for most people at the levels of
fluoridation used currently in Southern California (0.012 mM)(Vallecitos
Municipal Water district handouts) and at the increased levels
proposed to be used. But since fluoride is converted completely
in the stomach to hydrofluoric acid (5), the most corrosive substance
known to man, it is likely that consumption of fluoride at levels
used in some cities is associated with ulceration of gastric
and duodenal tissue (where the pH has yet to return to basic
values that occur in the middle intestine). And many report evidence
in rats that it eventually causes cancer (1),.
Some argue these effects are
unimportant if the municipal water supply maintains very low
levels of fluoridation; but the longer the consumption occurs
for an individual and the more elderly the person with less cell
division occurring in the gastric mucosa, the more overt symptoms
become. Individuals with ulcers or heartburn are not good candidates
for the long term consumption of water containing fluoride, particularly
at doses allowed by the Public Health Service (2-4 mg/L, 0.1-0.2
mM)(VWD handouts). These high doses can be dangerous depending
on the amount of water consumed, the individual's own body chemistry,
and the ionic composition and pH of the particular cities' water
that would be fluoridated to this level.
We here determine whether and
to what extent blood levels of calcium may be affected by various
fluoride doses that are known to occur in the blood of fluoridated
water consumers to attempt to determine its modes of action.
Our calculations are consistent with the notion that fluoride's
lethal effects on the heart are due to low blood calcium subsequent
to saturation of body fluids with fluoride at its known low solubility
in the presence of physiologic levels of calcium.
Analytical Results and Discussion
Sublethal poisoning occurs at 0.1-0.2 mM fluoride in blood (3,7)
and lethal poisoning occurs in the 0.2 to 0.6 mM range due to
heart failure (3). We investigate the possibility that the margin
of safety is so slight between unnoticed effects (0.02-0.05 mM)
to sublethal (0.1-0.2 mM) and lethal poisoning (0.2-0.6 mM) is
because below the critical concentration of fluoride in the blood
that causes precipitation of calcium fluoride only chronic, often
unnoticed effects would occur. Much like being near a hot electrical
wire, one can coexist next to it for lifetimes without any difficulties.
But one false movement too close to the wire would be a disaster.
With this in mind, we calculated
the concentration of fluoride that would cause calcium fluoride
precipitates to first form from the known solubility product
constant (Ksp) for calcium fluoride (Ksp = 3.4 x 10-11 (6)) and
the known concentration of calcium ion in normal human blood
(3 mM) (5). The computed dose is 0.1 mM. Here the concentration
of fluoride is: [F-] = (Ksp/[Ca2+])1/2 from the definition of
the solubility product constant for insoluble salts where CaF2
Ca2+ + 2 F- and Ksp = [Ca2+][F-]2 (see Table I). The concentration
of fluoride where the blood calcium level would be lowered to
the lethal low level of about 1 mM is 0.2 mM fluoride.
In Table I the calculated calcium
levels that would coexist in fluid with a given fluoride level
from solubility considerations are compared with actual measurements
of blood levels of calcium and fluoride ion in the lethal poisoned
human victim from Hooper Bay, Alaska. Note the good agreement
between theoretically calculated fluoride levels, that should
lower blood calcium ion to levels below normal, with the actual
calcium and fluoride ion levels measured in the blood of this
human victim poisoned with fluoridated municipal water in Hooper
Bay.
Also note the below-normal
calculated calcium ion level that would coexist with fluoride
doses found to slow heart cell beat rates in detailed in vitro
experiments (10). Isolated beating heart cell preparations from
mammals exhibit beat rates that are proportional to the calcium
ion level in the incubation medium from .3 - 3 mM. Calcium chelating
agents EGTA and EDTA and the calcium binding site competitor
La3+ ion completely block excitation-contraction coupling in
intact beating hearts and in isolated cell preparations (11).
Further, addition of fluoride to beating heart cell preparations
slows beat rates in a dose-dependent manner that Ksp calculations
indicate would lower calcium ion levels in the incubation medium
(see Table I).
These calculated doses are
fully consistent with other published data indicating that tissue
levels of fluoride in poisoned people are in the 0.2 - 0.4 mM
range (5). Also the known human lethal dose is 1-5 grams per
adult taken at one time acutely (3,5). Since the average adult
contains about 43 liters of body fluid this corresponds to a
concentration of fluoride of 0.5 mM in such a case of instant
acute poisoning.
Wang, Zhang and Wang also found
the heart cell beat rate in cultured cells in well-controlled
experiments progressively slows with increasing fluoride levels
in a regular, concentration-dependent manner (10). Unlike skeletal
muscle, cardiac muscle requires extracellular calcium ion from
the bloodstream to couple electrical excitation of the cell membrane
with contraction of cardiac muscle fibers (11). Each time the
heart contracts, calcium fluxes into the heart cells from the
extracellular fluid (at 3 mM calcium ion normally). When the
heart relaxes, the calcium is pumped back out of the cell, allowing
the fibrils to relax. Lowered extracellular calcium ion levels
block contraction of the heart.
These data together suggest
that the mechanism by which fluoride ingestion is lethal is by
causing hypocalcemia and blockage of heart contractions. Fluoride
levels in blood below 0.1 mM do not lower calcium ion below normal
as no precipitate yet forms in the blood at this or lower doses.
But the instant fluoride exceeds this amount to any degree, calcium
ion precipitates and the blood level is lowered, unable to support
normal heart function.
Fluoride acts as an enzyme
inhibitor for all enzymes requiring calcium for function by binding
the ion and is used routinely to block sugar metabolism in red
blood cells for clinical laboratory analyses of blood specimens.
Fluoride also attaches to calcium anywhere this ion is concentrated
throughout the body, including teeth, bones, ligaments, skeletal
muscle and brain. But the most crucial function requiring calcium
that is fluoride-sensitive is the mechanism of contraction in
normal beating hearts.
That extracellular calcium
is an obligatory requirement for heart cells to undergo contraction
after electrical excitation is well known. Heart cells do not
have well-developed sarcoplasmic reticulum to store calcium for
this purpose as does all skeletal muscle, which does not exhibit
this extreme sensitivity to changes in blood calcium level. The
cellular uptake of calcium occurs during the plateau phase of
the cardiac action potential and extracellular calcium is necessary
for the development of contractile force (11). The strength of
contraction (inotropic state) of the heart depends on calcium,
where half maximal contractility occurs at 0.5 mM calcium outside
cells (12).
It is also possible that chronic
'low' level biologic effects of fluoride are also mediated exclusively
by binding and sequestration of calcium. Prior to levels of calcium
in the blood being lowered (below 0.1 mm fluoride), regions in
the body enriched in calcium would still precipitate calcium
fluoride, as in bone, teeth, ligaments and brain. The usual physiologic
response to such an insult is to increase levels of hormones
such as calcitonin to mobilize calcium from bone to fight the
sequestration. At higher fluoride doses, precipitates may be
directly responsible for the known formation of gall and kidney
stones in fluoridated consumers.
The current level of fluoride
in Southern California drinking water is 0.25 mg per liter or
0.012 mM. The blood level is typically in consumers about 1/5
to 1/8 the water level. This is below the solubility for calcium
fluoride at normal body pH, temperature and prevailing body fluid
calcium levels, and it is easy for many to assume the information
in this manuscript is irrelevant. But some cities use up to 1
or 1/5 mg/L (0.05-0.075 mM) or the Federal allowed ceiling of
2-4 mg/L (0.1-0.2 mM) and are near or at the maximum level that
would just begin precipitation of calcium, with hypocalcemia,
unless the city water happened to have so much calcium in it
that it precipitated as the fluoride preventing the fluoride
added from entering one's blood at that level. The finding that
fluoridated cities generally have increased per capita heart
attack rates is consistent with this discussion.
The fluoride level that would
precipitate calcium from Southern California water (where calcium
ion is about 2 mM) would be 0.14 mM fluoride. So before we could
reach fluoride levels approaching the Federal ceiling in water
it would precipitate calcium from our drinking water first. To
maintain a higher level of fluoride than 0.14 mM would be expensive,
requiring addition of enough to precipitate the calcium in the
water first. More would be required on top of that amount to
increase fluoride to a higher desired level. Fortunately this
would be very difficult.
Adding sodium fluoride to public
water is paid for by taxpayer adults who will not reap any measurable
benefits from it. It takes resources, time, chemicals and machinery
to continue to add it to drinking water. It is putting the water
district in charge of drugging the public and for something as
innocuous as a cavity rather than for serious effects such as
infectious illness for which we have properly chosen chlorination,
with the much less electronegative halogen.
It is not in keeping with a
free society or with proper health care practice to impose these
risks associated with fluoridating the blood of people, livestock,
and pets, and also all agricultural products, not to mention
our lawns and gardens, compared to the less significant problem
of perhaps having tooth decay. Tooth decay should be minimized
more efficiently and safely if desired with addition of fluoride
products to children's teeth carefully without swallowing or
better yet by simply brushing more vigorously and regularly.
After the death of the Brooklyn, New York boy in the dentist
chair when fluoride gel was swallowed, and after the Hooper Bay,
Alaska incident, it is clear that our blood is more important
than concern for cavities. Teeth are replaceable but lives are
not. In keeping with the Hippocratic oath, no physician reserves
the right to medicate anyone without their permission, and all
patients must remain free to withdraw from drug or other treatment
programs at any time. Forced fluoridation in public water supplies
ironically constitutes a reversal of these Public Health Service
policies. The easy way - fluoridate through the bloodstream by
drinking - is unnecessary (since topical application is possible)
and criminal (in light of the above findings). Proper dental
hygiene is much safer and achieves the desired result anyway.
The notion recently publicized that 'antifluoridationists' are
similar to earlier critics of smallpox vaccination is inconsistent
with the facts that 1) smallpox is lethal and could not be prevented
without blood vaccination, but 2) cavities are not lethal and
can be prevented with proper hygiene and if necessary the bacteria
that cause caries in the first place can be quickly destroyed
with simple methods such as hydrogen peroxide washings, etc.
without loss of life.
References
1. The Grim Truth about Fluoridation, Robert M. Buck, G.P. Putnam
& Son, New York, 1964.
2. Blakiston's Medical Dictionary, 1960, 3rd edition.
3. The Merck Index, 9th edition, Merck and Co., Inc., Rahway,
New Jersey, 1976.
4. The Handbook of Chemistry and Physics, 50th edition, Chemical
Rubber Co., Cleveland, Ohio, 1976.
5. Teitz, N., Clinical Chemistry, W.B. Saunders, Philadelphia,
1976.
6. Ebbing, D. , General Chemistry, Houghton Mifflin Co, Inc.,
Boston, 1990
7. Clinical Toxicology of Commercial Products, Gleason, M., ed.
Williams and Wilkins, Baltimore, 3rd edition, 1969.
8. Gessner, B., New England Journal of Medicine 330 p. 95, 1994
9. Goodman, L.S. and Gilman, A. The Pharmacological Basis of
Therapeutics, 5th edition, MacMillan Publishing Co., New York
10. Wang F., Zhang, D., and Wang, R. "Toxic effects of fluoride
on beating myocardial cells cultured in vitro", Fluoride
31(1) pp. 26-32, 1998.
11. Langer, G. A., Federation Proceedings, 35, p.1274, 1976.
12. Williamson, J. R., Woodrow, M. L., Scarpa, A. in: Fleckenstein,
A., Dhalla, N.S., eds., "Recent Advances in Cardiac Structure
and Metabolism", vol. 5, Baltimore, University Park Press,
p. 61, 1975.
Table I
Effects of F- on Blood Ca2+
Concentrations*
Blood [Ca2+] Blood [F-] (mM)
3.0 0.10 (F- , calculated from
Ksp, for 1st precipitation of normal blood Ca2+)
1.3 0.48 (human blood measurements,
Hooper Bay, Alaska from lethal dose victim)
1.1 0.15 (Ca2+ calculated from
Ksp for F- dose lowering heart cell beat rate 17%)
1.0 0.20 (F- calculated from Ksp to lower blood Ca2+ to 1 mM)
0.4 0.30 (Ca2+ calculated from
Ksp for F- dose lowering heart cell beat rate 27%)
*Some cities recommend 01.
- 0.2 mM fluoride be added to drinking water. Typically 1/5 or
so of the water fluoride level is the consumers' blood fluoride
level (as long as there are no accidents, equipment malfunction
as in Hooper Bay disaster, or miscalculated doses added).
As for any insoluble precipitate,
the Ksp solubility product constant determines the concentration
in solution of the ions that dissolve from the salt. For calcium
fluoride where CaF2 Ca2+ + 2F-, Ksp = [Ca2+][F-]2 = 3.4 x 10-11.
This relation was used to calculate F- levels for a given Ca2+
level or Ca2+ levels for a known F- level. Other measurements
in the table were from actual blood samples drawn from Hooper
Bay, Alaska victims where fluoridated municipal water for which
machinery malfunctioned poisoned 296 residents. Not mentioned
is the increased thirst associated with heavily fluoridated water,
a biologic response to this insult that was up to that time unknown.
The solubility of calcium fluoride
changes somewhat with temperature and pH. It is slightly more
soluble at body temperature (37oC) than room temperature but
since it also decreases in solubility with increasing basicity,
we here estimate the solubility in blood at about the published
value at pH 7 for water at room temperature because the slight
increase it actually has is offset by the higher pH of blood,
at 7.4. |
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