Decayed, Missing and Filled Teeth

In 1987, Dr. Allan Gray, then Director, Division of Dental Health Services
for the province of British Columbia, Canada, published an article in the
Journal of the Canadian Dental Association (vol 10, 763-764) pointing out
that it was "time for a new baseline." He pointed to the finding that tooth
decay, as measured by DMFT (Decayed, Missing and Filled Teeth) rates were
falling "drastically" in non-fluoridated areas as well as fluoridated.
Six years later, in 1993, Dr. D. Christopher Clark, Associate Professor,
Faculty of Dentistry, University of British Columbia, wrote in the same
journal (vol 59, 3, 272-279) that "[T]he traditional thinking about the way
fluorides prevent dental caries has changed. Recent studies have
demonstrated that the role of fluorides in the prevention of dental caries
is predominantly through remineralization, which is primarily a
posteruptive phenomenon. The primary effect from fluorides is
post-eruptive, not pre-eruptive, and more therapeutic than preventive."
These "recent studies" are represented by those of Doctors O. Fejerskov and
F. Manji of the Royal Dental College, Aarhus, Denmark and Dr. A. Thylstrup,
Royal Dental College, Copenhagen, Denmark and others such as Dr. J.M. Ten
Cate of the Academic Center for Dentistry, Amsterdam, the Netherlands.
These European dental scientists contributed their views to an
international symposium on fluorides that was held March 21-24, 1989 in
Pine Mountain, Georgia, U.S.A. The proceedings of this Conference were
published as a "Special Issue" in the February 1990 edition (Vol 69) of the
Journal of Dental Research.

Special Issue of Journal of Dental Research

In the same Special Issue, Doctors H. Kalsbeek and G.H.W. Verrips of the
Netherlands Institute for Preventive Health Care reported on their studies
of dental caries prevalence and the use of fluorides in different European
countries. They stated (on page 731) that "no significant association was
found between the availability of fluoridated water and fluoride
dentifriceand the DMFT in 12 year-old children." They found, also, that
"[I]n most European countries, the 12 year-old DMFT index is now
(1985-1988) relatively low as compared with figures from 1970-1974."
Their findings agree with those found in the smaller population studied by
Dr. Gray in 1987. Does this indicate a shift away from fluoridation on the
basis of new scientific findings? Is science the nemesis of fluoridation?
Herschel S. Horowitz, of the National Institute of Dental Research,
National Institutes of Health, Bethesda, Maryland U.S.A., could
appropriately be called a "crusader" for the cause of fluoridation. He
summarized (p760-764) his concern regarding the many factors that could
influence public acceptance of the procedure. Horowitz classifies the
factors as "socio-political."

These factors are:
1. The change in allocating Federal (U.S.) funds to States that prevents
the "earmarking" of money for fluoridation as opposed to "block funding" in
which fluoridation must compete with other public health priorities;
2. The perception by the public of dental fluorosis as a "problem" when
they become increasingly aware of the high incidence being reported;
3. The publicity being given to the results of studies such as the
1986-1987 oral health survey of U.S. schoolchildren which showed a
continuing decline in caries prevalence in both fluoridated and
non-fluoridated groups, which called forth a declaration, by those
reporting the data, that "caries is no longer a public health problem";
4. The public's perception that fluoridation is environmental pollution;
and
5. The increase in public anxiety with regard to the many possible adverse
health effects.

Dr. Horowitz expresses his exasperation with the democratic process. "In
some localities," he writes, "politicians are empowered to make such
decisions (i.e., to fluoridate) but, frequently, in order to protect their
perceived reelection potential, they decide that a public vote should be
held on community water fluoridation, which, in effect, transfers the
responsibility to an uninformed or misinformed public."
His opinion of those professionals who do not possess his zeal for
fluoridation is not much higher than his perception of the public. "The
public and health care practitioners," he writes, "are ill-informed or
misinformed about the value and appropriate uses of fluoride, and about the
relative benefits produced by fluoride compared with other methods
promulgated for the prevention of caries."
Dr. Horowitz's first point appears to be an admission that the fluoridaters
have had, in the past, a potent way to bribe financially strapped
communities to add fluoride to their water supplies. This "incentive" has
worked well in the past to tie fluoridation in with Federal grants for
upgrading community water systems. It is noteworthy that he is not
mentioning any curtailment of Federal funds that are used to promote
fluoridation both in the U.S. and abroad.

Fluorosis

His second point concerns dental fluorosis. This has long been painted as a
"mild cosmetic" change in the teeth of children and adults who were exposed
to fluoride during dental development. There is sufficient understanding of
the process underlying dental fluorosis and the implication of deposition
of fluoride in the skeleton and soft tissues in papers that accompany
Horowitz's in the Special Issue.
Fejerskov states (p693) that "[the clinical features reflect that fluoride
given in low concentrations over the long period of tooth development
results in various degrees of enamel porosity (or hypomineralization)." He
continues, "[I]n its mildest forms, the porosity is to be found in the
outermost enamel only, but the entire tooth surface is involved. With
increasing severity, both the depth of enamel involvement and degree of
porosity increase. Assuming a relatively constant exposure level (most
commonly water-borne fluoride), all surfaces of a given tooth will be
equally affected.
"In more severe forms of dental fluorosis" Fejerskov continues (p694), "the
tooth erupts into the oral cavity entirely chalky white. The degree of
porosity (hypomineralization) of such teeth result in diminished physical
strength of the enamel, and parts of the superficial enamel may break
away."
Dr. G. M. Whitford, of the School of Dentistry, Medical College of Georgia,
U.S.A., well-known for his work on the metabolism and toxicity of fluoride
and support of water fluoridation, has this to say about prevalence (p546).
"There is a growing body of evidence which indicates that the prevalence
and, in some cases, the severity of dental fluorosis is increasing in both
fluoridated and non-fluoridated regions in the U.S."
Later, he continues, "This trend is undesirable for several reasons: (1) it
increases the risk of esthetically objectionable enamel defects; (2) in
more severe cases, it increases the risks of harmful effects to dental
function; (3) it places dental professionals at an increased risk of
litigation; and (4) it jeopardizes the perception of safety and, therefore,
the public acceptance of the use of fluorides."
In countries such as China and India, that have large populations living in
endemic fluorosis areas, the various degrees of dental fluorosis are seen
as a continuum with accompanying bone deposition which leads, in many
cases, to crippling skeletal fluorosis, paralysis and soft tissue disease.
If dental fluorosis were to be "officially" recognized as an "adverse
effect" by senior Government, it would be "game over" for fluoridation as a
"safety factor" would be required that would lower the Environmental
Protection Agency's (EPA) Maximum Contaminant Level (MCL) for drinking
water to 0.2 mg/L fluoride (from its present 4.0 mg F/L). This would be
very much lower than the "optimal" concentration of 0.7-1.2 mg/L fluoride
recommended for water fluoridation. This lower figure would be based on the
2.0 mgF/L concentration established (by EPA) as the level to produce dental
fluorosis and a safety factor of 10. In actuality, dental fluorosis is
related to total ingestion of fluoride of 0.75-1.0 mg fluoride per day
(Whitford in The Metabolism and Toxicity of Fluoride, Karger, 1989).
It is of interest that a recent Canadian review, Inorganic Fluorides,
carried out by the Ministries of Environment and Health under the Canadian
Environmental Protection Act and published in 1993, declined to assess
either dental fluorosis or the beneficial effects of fluoride in the
prevention of dental caries, the subject of Dr. Horowitz's third concern.
Dental fluorosis, to sum up, is a noticeable and undesirable cosmetic
change due only to the influence of fluoride on developing teeth. Because
it is associated with damage to the teeth and deposition of fluoride in the
skeleton and soft tissues, it is an adverse effect with psychological as
well as physical implications.
The injury to the enamel, described by Fejerskov, must predispose toward
caries, not act as a preventive.
Dr. Horowitz and his pro-fluoridationist colleagues have good cause to be
concerned about recent studies of effectiveness.

Cost Effectiveness

By the very nature of statistical science, selective, small scale studies
can show reductions in caries as measured by the DMFT or DMFS (tooth
surfaces) of 40% or better, the figure used to calculate
"cost-effectiveness." For example, a British Columbia study compared the
DMFS of 109 children in fluoridated Kelowna and 93 children in
non-fluoridated Vernon. The DMFS of these 10 year-olds was 1.65 and 2.5
respectively. The "benefit" for the fluoridated group was 34%. But, the
difference was 0.85 of a tooth surface! This is not clinically significant
and is within "examiner error" that has been shown to be, typically,
between 15-20%. Dorothea F. Radusch wrote in the Journal of the American
Dental Association (28, 1959-62) as long ago as December 1941 that this may
be as high as 74% for carious tooth surfaces.
When studies based on large populations are reported honestly, "the truth
will out." Such is the case with the 1986-87 oral health survey of U.S.
schoolchildren (39,207 children ages 5-17 years). This, as Horowitz pointed
out, showed a continuing decline in caries prevalence in both fluoridated
and non-fluoridated groups. Analysis of the data (obtained through the
Freedom of Information Act) by Dr. John Yiamouyiannis, a well-known
biochemist from Delaware, showed no significant differences in decay rates
of permanent teeth or the percentages of decay-free children in
fluoridated, partially fluoridated or non-fluoridated areas. This study was
published in Fluoride, the journal of the International Society for
Fluoride Research (vol 23, 2) in April 1990.
Analysis of the same data by Doctors J. A. Brunelle and J. P. Carlos of the
National Institute of Dental Research (NIDR) and published by the U. S.
Public Health Service in Health Benefits and Risks February 1991, the
promoter's "Bible," showed a "benefit" of 17.7% which is within both
mathematical error exhibited in their paper (Yiamouyiannis) and within
"examiner error" and is, therefore, not significant.
Prof. Y. Imai of Japan studied 22,000 schoolchildren in 1972 in naturally
occurring fluoride areas (nat) and found increased caries with increased
levels of fluoride. A study of 23,000 elementary schoolchildren in Tucson,
Arizona, by Dr. Cornelius Steelink in 1992, showed increased caries with
increased levels of fluoride (nat) in drinking water as did Prof. S.P.S.
Teotia of India who reported on a study (nat) of 400,000 children from 1973
to 1993.
Dr. John Colquhoun found in a study of 26,405 12-13 year old schoolchildren
in New Zealand, in 1989, that those living in artificially fluoridated
areas had slightly more caries than those living in non-fluoridated areas.
Furthermore, both Colquhoun and Steelink showed in their studies that there
was a definite positive correlation between low family income and the
prevalence of caries. This was independent of the level of fluoride in
drinking water and whether it was artificially added or occurred naturally.

Why is the public not better informed about this? Why do Dr. Horowitz and
his colleagues, especially in the U.S., Canada, the U.K., Ireland,
Australia and New Zealand, the major fluoridating countries, continue not
only to hang on to this scientifically bankrupt procedure but also to
promote it actively.
It is of interest to note that dental researchers in largely unfluoridated
Europe no longer consider that the systemic use of fluoride has a place in
the primary prevention of tooth decay. Some of these, consider that topical
application, under specific conditions, may prevent caries formation by
"remineralization" of incipient lesions.
Fluoridation does not prevent tooth decay but it contributes to dental
fluorosis and other adverse health effects that will be discussed later.
Can it be perceived as environmental pollution?

Environmental Pollution

Fluorine is the 13th most abundant element on earth. It is so volatile that
it is found in nature as fluoride in combination with other elements, such
as calcium, magnesium, phosphates etc.
Fluoride is not an "essential element" so far as human nutrition is
concerned. It is not recognized as such by the U.S. Food and Drug
Administration (FDA) and has never been demonstrated as "essential" by
animal experimentation. However, fluoride is essential for modern industry,
the fluoride wastes of which are responsible for pollution of the air, land
and water.
The fluoride placed into the majority of drinking water supplies for the
purpose of increasing natural levels, if any, to the "optimal
concentration" required by fluoridation is in the form of hydrofluosilicic
acid or sodium silicofluoride. These are waste products of the phosphorous
and phosphate fertilizer industries. These products are obtained from
scrubbing factory stacks to remove wastes such as sulphur hexafluoride that
would, otherwise, cause atmospheric pollution.
These products are introduced into public drinking water systems with
little regard to other contaminants that may be present such as lead,
mercury, arsenic and radionucleides. In the US, a Water Chemicals Codex
addresses the Recommended Maximum Impurity Content (RMIC) for lead and
arsenic but not radionucleide levels.
George Glasser, reviewing the subject for the Sarasota Eco Report (Vol 4,
No 12,) of December, 1994, states: "[A]nother coproduct from phosphate
fertilizer manufacture is yellow-cake uranium. The radioactive coproduct is
used in the manufacture of nuclear weapons and the nuclear power industry.
The wastes from the manufacture of phosphate fertilizers are also
contaminated with radium and are among the most concentrated radioactive
wastes produced from natural materials. These radioactive wastes are
referred to as naturally occurring radioactive materials (NORM) and the EPA
has no regulations for NORM waste disposal."
Neither the publication Toxicological Profile for Fluorides, Hydrogen
Fluoride and Fluorine (F), prepared for the U.S. Department of Health in
December 1991 nor the Canadian Government's 1993 review, Inorganic
Fluorides, provide estimates of the amount of fluoride entering the
environment via the fluoridation of water supplies. The Canadian report
does contain sufficient "clues" to enable an estimate.
The example of Tacoma (population 250,400 (1990 census) in Washington
State, gives an idea of the amounts. Fluoride plants' monthly reports were
collected from the Tacoma City Water Department. The data are recorded in
US gallons, pounds and "short," or US tons.
The daily amounts, on average, are: 57,000,000 gallons of water processed
through the system; 2,300 pounds (1.15 tons) of hydrofluosilicic acid and
4,100 pounds (2.05 tons) of sodium hydroxide are added. The
hydrofluosilicic acid is "commercial strength," 24.20%. The daily amount of
fluoride ion added to the water, and therefore, into the environment, is
estimated to be 424.62 pounds (0.2 tons). Annual discharge of
hydrofluosilicic acid into the Tacoma water system, on average, is 419
tons. The annual amount of fluoride ion is 73 tons.
It can be calculated that on the basis of an intake of one pint of water
per day for children aged 0-11 years, the "target group" of fluoridation,
as estimated by Dr. F.J. McClure in 1943 and Dr. J.S. Walker, in 1963,
children consume about 0.06% of the water supply. Therefore, 99.04% is used
exclusively to carry fluoride elsewhere, largely through the sewer system
where it is a source of pollution to the environment.
One can truthfully state that "for every $1000 spent for fluoridation
chemicals, less than fifty cents goes to children."

Fluoride Discharged into Environment

On the basis of the Tacoma data, it can be calculated that for every one
million persons living in a fluoridated area, 292 tons of fluoride ions are
discharged into their water supplies each year. For the population of 134
million Americans the A.D.A. states, who are on fluoridated water supplies,
this is an estimated 39,000 tons of fluoride annually.
The Canadian study, mentioned previously, permits a calculation of 2000
tonnes (1 tonne = 2240 lbs.) of fluoride annually discharged into the
environment from fluoridated water supplies. This amount places this source
of fluoride discharged in water second only to phosphate fertilizer
manufacturing, but ahead of chemical production, coal-fired power, primary
aluminum production, and others that are identified.
Fluoride, in community water systems, enters the environment in various
ways. Surface runoff from fire fighting, washing cars, watering gardens may
enter streams directly or through storm sewers at the "optimal
concentration" of one part per million (ppm) or 1 milligram per liter
(mg/L). Most enters during waste water treatment.
T.T. Masuda reported in 1964, after studying a large number of US cities,
that concentrations of fluoride in sewage effluent in fluoridated cities
even after secondary treatment was 1.16-1.25 mg/L. This compares to 0.38
mg/L fluoride in unfluoridated sewage effluent.
Studies by L.L. Bahls, reported in 1973, and L. Singer and W.D. Armstong,
in 1977, demonstrated that the elevation of fluoride levels in sewage
effluent could persist for a considerable distance, up to 16 km. in one
instance.
The promoters of fluoridation argue that dilution reduces concentration
over distance. But, the amount of fluoride is deposited in sediment, either
locally or, in the case of rivers, in the estuary. Fluoride in sediment may
persist for 1-2 million years. It may recontaminate water if dredging takes
place. It also has a direct toxic effect on sediment-dwelling organisms.
Those responsible for the 1993 Canadian Government Review, Inorganic
Fluorides, concluded that inorganic fluorides are entering the Canadian
environment at concentrations that may cause long-term harmful effects to
biota in aquatic and terrestial ecosystems.
With regard to the effects on aquatic organisms, the authors extrapolate
laboratory findings to the field, to yield estimated adverse effects
thresholds (lethal, growth impairment and decreased egg production) of 0.28
mg/L fluoride for fresh water species and 0.5 mg/L for marine species.
These are exceeded by surface runoff and sewage effluent from fluoridated
water systems.
The author of this article and Anne Anderson published a review in Fluoride
(Vol 7 No 4, 1994) showing how effluent from fluoridated water systems in
British Columbia and Washington State could be contributing to the loss of
salmon species in the Fraser and Columbia-Snake river systems. This could
be attributed not only to direct toxic effects on all stages of fish
development and their feed; but also, to the inhibition of migration. This
latter was shown by Drs. D. Daemker and D.B. Dey in their study of the John
Day Dam on the Columbia river published in 1989.
Fluoride is toxic in low concentrations to all living things. The authors
of the Canadian review, in a section entitled "Ecotoxicity," present a
review of the effect of inorganic fluoride, airborne in particular, on
plants and animals, especially herbivores.

Fluoride More Toxic than Lead

Fluoride is known to be more toxic than lead and only slightly less toxic
than arsenic. Recently, in 1994, N.P. Gritsan, G.W. Miller and G.G.
Shmalkov reported their study on the effect of various pollutants on
abnormal plant development in Southeast Ukraine. They found that among 17
elements, including fluoride, cadmium, lead and aluminum, fluoride was the
most toxic.
Since humans share the same enzyme systems and DNA mechanisms as other
biota and fluoride is a proven enzyme and DNA repair inhibiting agent, why
would anyone think that humans are immune from its toxic effects?
Dr. Horowitz appears to be more concerned about the "increase in public
anxiety" that may lead to lack of public acceptance of fluoridation, than
about the possible adverse effects of fluoride on humans.
In September 1994, the 20th Conference of the International Society for
Fluoride Research was held in Beijing, China. This Conference was jointly
sponsored by the Ministry of Health, People's Republic of China, the World
Health Organization and The National Natural Science Foundation of China.
In attendance were 200 researchers from the host country and about 150 from
other countries.
The major area of concern was the prevalence of fluorosis in China. The
"endemic fluorosis" areas of China contain a population of 100 million. Of
these, 43 million people have dental fluorosis of all degrees of severity;
2.4 million have skeletal fluorosis, a severe crippling disease with bone
deformities.
The Chinese presented papers using observations from studies of both
experimental animals and humans showing the relationship between poor diet,
especially calcium deficiency, repeated childbirth and duration of
exposure, to the severity of the effects of chronic fluoride poisoning.
The Chinese reported not only adverse effects on teeth and bones but also
those involving soft tissues. Some of these occur at surprisingly low
levels of total fluoride ingestion, some of which were within the range of
total intake reported for fluoridated areas of the U.S. and Canada.
They presented evidence of increased fractures, poor fracture healing and
bone outgrowths (exostoses) as some of the skeletal effects.
With regard to soft tissue involvement, studies were presented that dealt
with neurological lesions. They ascribed paralysis to direct action of
fluoride on the central nervous system in addition to the effect of
pressure on motor nerves by encroachment of fluorotic bone. Studies also
showed that thyroid dysfunction, heart disease and abnormal
electrocardiograms and cerebrovascular disease were more prevalent in the
endemic fluorosis areas.
An association was shown between chronic fluoride intoxication and lowered
intelligence as measured by IQ tests; chromosomal abnormalities; decreased
immunity; increased senile cataracts; and cancer.
The Chinese scientists also reported higher infant death rates due to
congenital abnormalities and higher death rates generally in endemic
fluorosis areas. They also reported variable synergistic effects between
fluoride and aluminum, fluoride and arsenic, fluoride and selenium.
The foregoing would almost appear to be the table of contents of Dr. John
Yiamouyiannis' book, Fluoride, the Aging Factor (Health Action Press,
Delaware, Ohio), and the older publication, Fluoridation, the Great
Dilemma, by Drs. George L. Waldbott, Albert W. Burgstahler and H. Lewis
McKinney (Coronado Press, 1978).
Dr. Horowitz and his colleagues can be expected to attempt to refute this
evidence of the potential harm from fluoridation by arguing that the
endemic fluorosis areas in China are largely rural and that the people are
impoverished, with poor nutrition, especially calcium deficiency. They
would also point to the higher levels of fluoride in water, 2.5-5 mg/L, and
to additional sources of fluoride such as coal burning for cooking and for
drying corn, wheat and millet. They would deny that these adverse effects
occur in the US where fluoridation has been practiced since 1945.
To do this successfully, they would have to refute the many studies
published in peer-reviewed journals, that show that in the US there is a
significant relationship between residence in fluoridated areas and most of
the problems described by the Chinese.
These studies show increases in chromosomal abnormalities such as Down's
Syndrome (mongolism) as demonstrated by Dr. Ional Rapaport in 1954 and
1957. They show, also, increased overall cancer deaths, (Drs. Dean Burk and
John Yiamouyiannis, 1977); and deaths from osteosarcoma, a rare bone
cancer, in young men reported by Dr. R. N. Hoover and others in 1991 and
Dr. P.D Cohn in 1992.
The studies on osteosarcoma were inspired by the finding of the US National
Toxicology Program in 1989 that there was a dose-related relationship
between fluoride and osteosarcoma in male rats. The study found, also, a
relationship between fluoride and an extremely rare form of liver cancer in
the experimental animals as well as cancers of other areas such as the
mouth. When the findings were "peer reviewed," the conclusions were termed
"equivocal," a term that gave rise to the controversy that continues to
this day.

Fluoridation and Hip Fractures

They would also have to refute the studies that show a higher incidence of
hip fracture in residents of fluoridated areas. This includes U.S. studies
published in the Journal of the American Medical Association (JAMA) by Dr.
S.J. Jacobsen in 1990 and Christa Danielson and others in 1992.
Studies from abroad have shown the same relationship between fluoridation
and hip fractures: Dr. C. Cooper (UK) in JAMA, July 24, 1991 and Dr. J.
Colquhoun, New Zealand Medical Journal, August 1991. There are also studies
showing the effect of low concentrations of fluoride on the immune system
such as that in Complementary Medicine, 1992, by Dr. Shiela L. M. Gibson of
the Glasgow Homeopathic Hospital. There are studies from India where
endemic fluorosis is a major public health problem. Publications from this
country cover many aspects for which their extensive literature must be
consulted. One important area of research in India deals with one of the
most frequently encountered symptoms that occurs long before skeletal
fluorosis becomes clinically obvious ­p; gastrointestinal discomfort.
Outstanding work on this has been carried out by Dr. A.K. Susheela and her
co-workers at the All India Institute of Medical Sciences, Delhi. One of
her papers, published in Fluoride (Vol 25, No 1) 1992 shows, by means of
photographs taken through an endoscope, the unhealthy appearance of stomach
mucosa when it is exposed to very low concentrations of fluoride.
These texts should be consulted for further examples of scientific studies
that counter the false notion that fluoride, even at optimal concentration,
is without harm. Those individuals and institutions that promote
fluoridation have by their actions, created endemic fluorosis in the US,
Canada and other countries that have adopted the practice.
Like China, before defluoridation, 43% (or more in some studies) of
children in these fluoridated areas exhibit dental fluorosis. Is it
possible that 2.4% of the public have largely unrecognized skeletal
fluorosis? How many deaths from congenital abnormalities could be laid at
the doorstep of fluoridation?
How many tons of antacids are consumed by North Americans for "functional
dyspepsia" (that is, stomach ulcer pain without demonstrable ulcers) caused
by drinking fluoridated water and beverages?
People living in endemic fluorosis areas, such as China and India,
frequently exhibit as "early" signs of the development of later skeletal
deformity, back stiffness along with joint and tendon pain. How many
persons residing in fluoridated areas have these symptoms caused by
fluoride? How many are misdiagnosed as "repetitive stress syndrome,"
"tendonitis" or "arthritis" of unknown type or cause?

Physicians Have Low Index of Suspicion

That we do not have a full picture is due to two major factors.
The first, is that physicians (and other health professionals) have a low
index of suspicion that fluoridation could be associated with disease. They
have been assured by the promoters that fluoride is safe and they cannot
find fluoride listed in the commonly used texts in the differential
diagnosis of various related diseases; for example, articles dealing with
"functional dyspepsia," thyroid dysfunction, arthritis etc. do not present
fluorosis as a possibility.
Second, the reason that we, in the U.S. and Canada do not see as many of
the deformed and damaged teeth and severe bone deformities as in countries
such as China and India may be owing to our good fortune in having adequate
dietary calcium, magnesium and vitamin C, the deficiencies of which have
been demonstrated to increase severity of fluorosis.
Dr. Albert Schatz reported on the increased infant death rates due to
congenital malformations in Chile that were associated with water
fluoridation. In his paper, published in the Journal of Arts, Science and
Humanities in January 1976, he made the following statement:
"The large scale, overall statistical studies which compare total
populations in fluoridated and control cities in the United States actually
conceal the very information that is purportedly being sought. This occurs
because the relatively well-nourished majority numerically overwhelms those
groups in the undernourished minority which are the most susceptible to
fluoride toxicity."
When are in-depth studies going to be carried out on the adverse effects of
fluoridation in the population of our own "third world," the impoverished
living in the slums of fluoridated cities in the US? When is Canada going
to do likewise?
The Canadian Government review of inorganic fluorides, after condemning
fluoride as a threat to both aquatic and terrestial plant and animal life
and possibly affecting global warming, nevertheless adopt the view of the
promoters that "inorganic fluorides (i.e., fluoride ions) are not entering
the environment in quantities or conditions that may constitute a danger to
human life or health." The reader may recall that those responsible for
this study deliberately avoided discussion of dental fluorosis in humans
(although they did present it as a problem in their discussion of
herbivores).
The authors of the Canadian review state that, in spite of their
conclusions, they cannot lightly dismiss the implications of the
dose-response trend in the occurrence of osteosarcoma in rat experiments.
They also express reservations regarding the potential of adverse effects
upon human reproduction, development, the central nervous and immune
systems; but only at levels required to produce skeletal effects.

Poor Nutrition Increases Risk of Fluoride Toxicity

In both countries, there is cause for concern about the relationship
between poverty and poor nutrition and what we know about its increasing
the severity of fluoride intoxication.
In the US, a Report issued January 30, 1995 by the privately funded
National Center for Children in Poverty stated that "more than a quarter of
American children under age 6 were living in poverty in 1992." This is 6
million children. How many of these live in fluoridated cities?
In Canada, the Canadian Institute for Child Health, a nonprofit
organization funded in part by Health Canada, reported, in 1994, that 21%
of Canada s children, 1.2 million, live in poverty.
It is ironic that the poor are the group that are frequently pointed to as
being best served by fluoridation. This is very wrong on several counts.
First, these are the most vulnerable to severe adverse health effects of
all types. Second, if we were to accept the most recent rationalization for
fluoridation, to establish the means for "remineralization," the poor are
the least likely to meet the preconditions laid down by such advocates as
Drs. G. Rolla, D. Gaare and Bogaard of the Dental Faculty of Oslo, Norway.
These researchers write in their abstract on page 158 of the Proceedings of
the Beijing Conference: "It can be concluded that fluoride is most
effective in subjects with reasonably good, but not necessarily perfect,
oral hygiene."
Without the means to pay for dental care, it is hardly likely that the
children of the poor, especially the "working poor,'' would employ oral
hygiene to the standard described by Dr. Rolla et al.
Nation's Health, the official newspaper of the American Public Health
Association, one of the organizations that continue to endorse
fluoridation, contains a relevant item in its issue for January 1995. The
newspaper reports the findings of a study conducted at Harold Washington
Elementary School in Chicago. This study involved 128 first, second, third
and fourth grade graders that were given oral examinations in November 1993
and June 1994.
"During the initial exam," the article relates, "dentists found 135
cavities. Parents were notified and given names of public aid dentists.
However, when dentists conducted the second exam seven months later, they
found 127 cavities, representing both untreated cavities found in the first
exam and new cavities. Altogether 23 students experienced an increase in
cavities, while 32 experienced a decrease, meaning they received dental
treatment. The remaining students experienced no change."
The author of the study, Susan Diamond MS, RD, concluded that many students
at this inner city elementary school have never visited a dentist's office.
She observed that only the occurrence of pain alerts many students' parents
to bring them to the dentist. She attributes the low priority of dental
care to lack of dental instruction at school and in the home. "Many
students," she is quoted as saying, "do not own tooth brushes, and others
must share them with family members." We must add that Chicago, according
to the U.S.P.H.S. Fluoridation Census, 1985 has been fluoridated to 1 ppm
since November 1968.
In order that the foregoing is not interpreted as an endorsement of the
topical use of fluoride, the reader is invited to look up the paper of
Kalsbeek and Verrips presented in Georgia in 1989 where they found no
significant relation between the decline in caries and the availability of
fluoridated water or fluoride dentifrices. Other investigators have
reported similar findings: Dr. M. Diesendorf, who presented a study in
Nature (July 1986) involving eight developed countries over a period of 30
years; and, Dr. John Colquhoun who reported in New Zealand Environment in
1991 that study of dental caries over time in New Zealand showed that a
sharp decline was in evidence before fluoridation and before the
availability of fluoridated tooth paste.

Toxic Dose is Probably 5 mg

Furthermore, some methods of applying topical fluorides to the teeth of
children may be life-endangering. Dr. G. M. Whitford's paper presented to
the Georgia symposium and included in the "Special Issue" of the Journal of
Dental Research, concluded that the "probable toxic dose" (PTD) is
approximately 5 milligrams (mg) of fluoride for each kilogram (kg) of body
weight (1 kg =2.2 lbs).
For a 2 year-old child (average weight 11.3 kg) the PTD is 57 mg. This
quantity, according to Whitford, is contained in 57 grams (2 ounces) of a
1000 ppm fluoride tooth paste, 38 grams of 1500 ppm tooth paste, 248
milliliters (mL) (8 ounces) of a 0.5% sodium fluoride mouth rinse and only
4.6 mL (less than 1 teaspoon) of 1.23% Acidulated Phosphate Fluoride (APF)
gel.
A young child is expected to hold this highly toxic (12,300 ppm) material,
poured into 2 trays of 2.5 mL each, for 5 minutes. How many parents are
told by the dentist that if the child were to swallow the APF gel, he could
die?
Whitford's Probable Toxic Dose may be lowered in the future. A mass
poisoning with fluoride from a faulty water system in Hooper Bay, Alaska in
1993 indicated that the PTD may be as low as 0.3 mg of fluoride per kg body
weight. The implication of this finding should be clear.
If these facts concerning the possible adverse health effects of fluoride
were to become known to the general public, it should increase the "public
anxiety" that worries Dr. Horowitz and his fellow promoters. So far, little
interest has been shown by the press. To the contrary, the media dutifully
repeats verbatim the press releases put out by the endorsing agencies such
as the American and Canadian Dental Associations (CDA and ADA).
A good example is the treatment accorded the 50th Anniversary of
fluoridation. The press release from the ADA with its dateline "Chicago,
January 24,1995" bears the caption: 50 Years of Fighting Tooth Decay with
Fluoride: 1945-1995. "On January 25, 1945," the text begins, "Grand Rapids
Michigan embarked on a trend-setting study and became the first community
to adjust the amount of fluoride in its water to an optimum level."
The press release makes the statement that "more than 134 million Americans
across the country are served by water supplies where the fluoride
concentration has been adjusted to the optimal level for dental health. In
Grand Rapids in 1945 before fluoridation, better than 99% of the children
examined experienced dental decay. After the famed 'Grand Rapids Study',
dental decay plummeted 65%."
Let us take a closer look at this landmark event. Prior to 1945, a search
took place for the cause of dental staining in states such as Colorado and
Texas. During the course of study, observations were made that this
disfigurement appeared to confer some type of increased resistance to
dental caries. The causative agent for the tooth discoloration ("mottling")
was discovered to be fluoride naturally occurring in drinking water.
A number of studies of this reported phenomenon were undertaken. The most
important of these was the study of 21 U.S. cities by Dr. H. Trendley Dean
of the U.S. Public Health Service. These studies would not be given much
credence today; they would not pass through the gates of peer review to
enter the scientific literature. Dean's work, in particular, that is still
pointed to as the "classic" basis for the fluoridation hypothesis, did not
meet even Dean's own criteria for constancy of water supply. Mathematical
errors abound. "Variation" and "examiner error," the latter well-known to
Dean, negated the results.
Dr. F.B. Exner, of Seattle, a Radiologist who became an international
authority on fluoride and strong opponent of fluoridation, prepared a
report for the City of New York in 1955 entitled Fluoridation of Public
Water Supplies. This was an analysis of the published studies of Dr. F.J.
McClure and Dr. H. Trendley Dean, both of whom were "pioneers" in the early
days of research on the dental effects of fluoride. Exner described their
reports as being unscientific and inaccurate. Exner even suspected fraud.
It was, perhaps, inevitable that Dr. Exner was given the opportunity to aid
Mr. Kirkpatrick Dilling in his questioning of Dr. Dean, under oath as a
witness in a suit to enjoin fluoridation of Chicago's water supply
(Schuringa et al. vs City of Chicago) in 1960.
Dr. Dean was forced to admit that the studies of Galesburg, Quincy,
Monmouth and Macomb and the studies of 21 cities with 7,257 children did
not meet his own criteria and were, therefore, worthless. Of course, this
revelation took place 15 years after the trials began; but it is difficult
to believe that there were not those in high positions in the U.S.P.H.S.,
including Dean himself, who recognized the defects in these studies.
Dr. Philip R.N. Sutton, of the Dental School of the University of
Melbourne, in his monograph Fluoridation, Errors and Omissions in
Experimental Trials (Melbourne University Press 1959, 1960), pointed out
that the trials which took place not only in Grand Rapids but also in
Newburgh and Evanston in the U.S. and in Brantford, Canada, constitute the
main experimental evidence that has led to fluoridation as a public health
measure.
The hypothesis that was to be tested was that "a concentration of about 1
part per million of fluoride in the drinking water, mechanically added,
inhibits the development of dental caries in the user."

Criteria for a Proper Trial

To carry out such a study properly, certain conditions must be met. First,
the investigator must select the participating communities with a view to
ensuring that when two groups, fluoridated and non-fluoridated are to be
compared, the water supply to both the trial population and the control
population must be similar in all respects except for the mechanically
added fluoride. If it is desirable to compare the results of mechanically
fluoridated water at 1 ppm with the results from a naturally fluoridated
water supply it is important that the latter also be at a concentration of
1 ppm and that the analysis of both water supplies are similar with regard
to other components such as calcium, magnesium etc.
Second, the populations under study must be similar in all important
respects: age, socioeconomic status and, if it is significant, racial
composition. It should go without stating that residence in either the test
area or the control area must be constant.
Third, such a trial, if it is to mean anything, must be of sufficient
duration to measure the dental status of permanent teeth after exposure for
at least a "10 year lifetime.''
Fourth, the common-sense "rules" of research must be followed. Attention
must be paid to the size of the sample population. There must be uniformity
in what is measured; for example, DMFT. Examinations of both the test
population and the control population must be undertaken before the trial
begins and at predetermined intervals. Mathematics must be accurate and the
results corrected for "variation" and "examiner error."
Finally, as in any study of the possible effect of any treatment,
statistical methods must be used to evaluate whether the results obtained
are due to "chance" or to the treatment, in this case fluoride at 1 ppm in
drinking water.
Dr. Sutton's study of the fluoridation trials is meticulously documented
with reference to the written reports prepared by the investigators and an
examination of data that was made available. On publication, the Australian
Dental Association sent copies to each of the principal investigators for
review. The second edition (1960) contains a section in which these reviews
are reprinted and the objections are answered by Sutton.
In general, not one of the experimental trials met the criteria presented
previously. Each had one or more errors or omissions that invalidate any
results that are purported as being supportive of the hypothesis. The
following deals superficially with the defects. Sutton's work must be
consulted for details.

Grand Rapids Study

Grand Rapids had Muskegon for its control. There were large differences in
sample size so that variability was high. In the test city, for example,
samples varied from 1,806 children to 3; in the control, in 12 categories
less than 20 children were examined. One "group" in the control city
consisted of one child. This grossly affects the reliability of a mean
rate.
Different methods of sampling were used and changes in examiners took place
with no assessment of examiner variability. The first examination of caries
in Muskegon did not take place until after Grand Rapids was fluoridated.
This was a poor beginning.
Finally, the coup de grace, the control city Muskegon, was fluoridated in
July 1951, six and one-half years after the commencement of fluoridation in
Grand Rapids. This rendered Muskegon useless as a control and occurred at a
time when few of the permanent teeth had erupted in the fluoridated test
city.
The promoters of fluoridation have stated repeatedly that "at Muskegon
Michigan, the control city where fluoride-free water is used, the incidence
of dental caries is unchanged." Sutton points out that some of those
presenting this statement in 1954 and 1955 seemed unaware that the
experiment had ended in 1951 with the fluoridation of the control.
But, was this statement true? The authors of the study (Arnold et al.),
mentioned, according to Sutton, that "a similar comparison (to Grand
Rapids) of results at Muskegon shows the percentage reduction to range from
1.5% in 6 year olds to a high of 15.5% in 11 year olds in the permanent
teeth. The percentage reductions used were obtained by expressing the
difference between the most recent and the original DMF rate as a
percentage. Variations in DMF rates obtained in intervening years are
ignored. If the results for Muskegon had been computed in 1946 instead of
1951, the reduction would have been 40.7% instead of 1.5% in the six
year-old group, and 32.7% instead of 15.5% in the 11 year-old children.
The Grand Rapids trial did nothing to support the case for the fluoridation
hypothesis. The children of both artificially fluoridated Grand Rapids and
the fluoride-free control, Muskegon, experienced a decline in dental caries
during the period of the trial from January 1945 to July 1951.
This should come as no surprise today in the light of the studies of
Kalsbeek and Verrips, Diesendorf, Gray and Yiamouyiannis mentioned
previously in this review.
Several questions arise. Was Muskegon's water fluoridated to terminate the
experiment because it was discovered that DMF rates were declining in both
cities? Why did "reputable" members of the dental profession repeat to
audiences in major dental meetings that there had been no change in
Muskegon when they should have known the facts? Why did some of these
appear to be unaware that the trial had been terminated?
The "result" stated in the ADA press release of a reduction in tooth decay
in Grand Rapids as a result of fluoridation is deceptive advertising. The
authors should be brought to account by the authorities. The same order of
decline may have been demonstrated for Muskegon if a properly constructed
study had been allowed to run its course!

Other Trials

The Evanston, Illinois study with Oak Park, Illinois as control, got off to
a bad start. A United Kingdom Mission (1953) that studied the Evanston
trial observed that in Evanston the economic level was high and dental care
was "outstandingly good." But, comparison of the caries rates before
fluoridation showed that the control area, Oak Park, was found to have a
lower caries rate than Evanston.
Sutton uses 21 pages of his 73-page original report to attempt to come to
an understanding of the many manipulations of the student groups that took
place, in order to compensate for the lower caries rates encountered in the
control throughout the test period.
The United Kingdom Mission was informed that yearly examinations had been
carried out since the commencement of fluoridation on February 11, 1947 and
would be continued until 1962. At the time of the UK Mission report, no
examination of the control city had taken place (since February 26, 1947);
and, in Evanston, only one age group was examined each year. Sutton points
out that the design of the trial provided for only two examinations, 11
years apart, to be made in the control city.
The second examination, scheduled for 1958, was commenced in 1956 when it
was apparent that the water supply of Oak Park would be fluoridated. This
examination was completed November 1956 soon after the fluoridation of Oak
Park on 1 August.
The data from this study were not published for 10 years. Much of the data
had not been released at the time of Sutton's book in 1959!
The authors reporting on this study made incompatible statements regarding
sample size and what Sutton describes as "extraordinary changes of opinion
regarding the significance of results based on the same data.''
Of some note is the evidence in the data of the effect of fluoride in
delaying tooth eruption. The results of examinations carried out in
Evanston 1946-1951 suggest a progressive decline in the number of erupted
first permanent molar teeth in six year-old children. The results obtained
in examinations conducted in 1953 and 1955 were omitted from the published
reports.
Brantford, Ontario, Canada was the site of two independent trials. One was
conducted by the City Health Department, the other by The National Health
and Welfare Ministry. There were so many mathematical and other errors in
the City report that its results, as Sutton states, must be treated with
caution. The National Study is reputed to be the most complete of the
10-year North American trials.
Again, a bad start. The trial began over two and one-half years after the
commencement of fluoridation of the Brantford water supply. Those
responsible for the study probably reasoned that little change was to be
expected in DMF rates until about six years after the commencement of
fluoridation - the so-called "structural theory" popular at the time that
has now, as indicated by the ADA Press Release, been replaced by the
"remineralization" rationalization.
Sarnia, Ontario was selected as the "fluoride-free" control and Stratford,
Ontario as the control city with natural fluoride to 1.3 ppm.
The City of Brantford, over a period of 15 years, had provided more free
dental services for children than most Canadian cities. As a result, the
children of Brantford compared to those in the controls had both a higher
treatment and a better oral hygiene status. This was recognized by the
authors of the report.
No pre-fluoridation survey was carried out in this study. The initial
examination in 1948, not surprisingly, showed that tooth mortality (teeth
which are missing or which must be extracted) was much higher in the
controls.
As in the other studies, there are marked deficiencies and omissions in the
compilation and reporting of data. This, along with the absence of caries
rates in Brantford and Sarnia prior to fluoridation, makes it impossible to
establish that there was a marked reduction in the test city due to
fluoridation.
The City of Newburg,, New York was the test area; Kingston, New York was
the "fluoride-free" control. These two cities situated on the Hudson River
about 30 miles apart were said to be comparable in all ways, including
comparable water supplies, except that Newburg's would have an addition of
sodium fluoride.
Again, as in other studies, the control city had no examinations until
after fluoridation started in the test city on May 2, 1945.
However, the major problem was that the water supplies were not comparable.
The source of Newburg's water was surface water; Kingston's was obtained
from mountain spring impounded. Analysis carried out by the US Geological
Survey showed them to be of vastly different composition. The water in
Newburgh (N) had much higher values than Kingston (K) in the following:
calcium (N 35.0 ppm, K 6.6 ppm), magnesium (N 3.6 ppm, K 0.9 ppm) and
hardness (N 102 ppm, K 20.0 ppm). Eight other characteristics of Newburgh
water were at least 4 times higher than those of Kingston.
A 1949 statement from the American Waterworks Association (quoted by
Sutton) is to the effect that the experimental verification of the
fluoride-dental caries hypothesis "obviously necessitates the use of a
nearby 'control' city with a water supply comparable in all respects to
that to which fluoride is being added."
In spite of this the study proceeded with, as Sutton describes it, a wide
variation in the methods used in data collection and result presentation.
There were changes in examiners and statisticians. The study was also
confounded by uncertainty with regard to shifts in the population of both
the test and control areas.
The final report of the study (1956) found a decrease in the "percent
difference" between the DMF rate per 100 erupted teeth of children aged six
to nine years in Newburgh and Kingston compared to the previous (1955)
report. A trial period of 10 to 12 years was originally mentioned in the
first report of the study. Sutton states that "in view of the decrease in
the 'percent difference'...it is unfortunate that the trial was stopped as
soon as the minimum period proposed by the authors had elapsed."
In May 1989, Dr. J. V. Kumar and others of the New York State Department of
Health, published a study of the current situation in Newburgh and Kingston
in the American Journal of Public Health (Vol 79, 50). Their analysis of
dental caries data revealed that caries prevalence declined in both
Newburgh and Kingston. The difference in terms of DMFT for 7-14 year old
children was shown graphically to be less than one tooth; i.e., Newburgh
1.5, Kingston 2.0. This is probably within examiner error and not
significant. They pointed out the confounding effect of other sources of
fluoride such as fluoride drops, tablets and dentifrices that have
contributed to dental fluorosis in the children of both cities.
It is not difficult to imagine the reception that Sutton's monograph
encountered in some circles. He records in an editorial in the January 1990
issue of Fluoride that the distributors of the book were approached by the
Nutrition Foundation and others to suppress the monograph in the U.S.A. In
addition, the printer's type of edition was destroyed without authority. He
notes, also, that his book was omitted from the Index to Dental Literature
published by the ADA.
Dr. Sutton adds, almost as a footnote, that in 1984 emphasis was shifted by
the World Health Organization, a major promoter, from the Newburgh etc.
trials to the further 128 studies listed in a book written by Murray and
Rugg-Gunn in 1982. Sutton investigated the scientific status of their
references in 1988. His conclusion: "Murray and Rugg-Gunn, in what appears
to have been a comprehensive worldwide search, were unable to locate even
one study which demonstrated that fluoridation reduced dental caries."
Why, after the expenditure of what must have been millions of dollars and
uncountable man-years has it been impossible to demonstrate proof of the
fluoridation-caries hypothesis?

Fluoridation Does Not Prevent Caries!

The answer is simple: fluoridation does not prevent dental caries!
Dr. Rudolph Ziegelbecker, Director of the Institute for Environmental
Research, Graz, Austria, ran through his computer the results of all
published studies of the relationship between fluoride in water and dental
caries. These studies included Trendley Deans' 21 cities and 23 others. He
reported in Fluoride in 1981 that he found no relationship.
Ziegelbecker followed up this study on what he felt were selected data,
with data from the World Health Organization's (WHO) Oral Health Data Bank
and Oral Health Pathfinder Study. Using these data, collected in 1987, he
again contradicted the reports that there was an inverse relationship
between dental caries incidence and water fluoride levels. His findings,
reported in Fluoride (Vol 26, No4) October 1993 pointed out that in most
countries the relationship tends to be direct rather than inverse; that is,
dental caries increases as water fluoride increases.
This finding conflicts with the belief of the promoters of fluoridation;
but it is in accord with other studies, some of which were mentioned
previously. Noteworthy in this respect are those of Imai (Japan), Colquhoun
(New Zealand), S.P.S. and M. Teotia (India) and Steelink (USA).
Ziegelbecker adds the studies of S.K. Ray et al. in India (1981) and O.
Chibole in Kenya (1988).
Let us return again to the A.D.A. press release. The manipulated numerical
values (one hesitates to call them statistics) that are used in the press
release are reminiscent of those seen in such advertisements as: "Three out
of four Doctors prefer Camel cigarettes," or, more recently "choose Tylenol
over Aspirin."
"Half of the children entering first grade today have never had a single
cavity." This may be true; but as may be seen from studies of caries over
time, this has nothing to do with either fluoridation or fluoride
dentifrice.
"In Grand Rapids, in 1945better than 99% of the children examined
experienced dental decay." This presented to us without any details
regarding the age of the children, the size of the sample or whether this
is a mean or average. As Sutton pointed out, there was enormous variation
in the size of samples so that variation as well as examiner error made
exact determinations impossible.
If we accept that only one child in one hundred was caries-free, the next
statement is deliberately ambiguous. "After the famed 'Grand Rapids Study,'
dental decay plummeted 65%." We have to ask: "where did this take place and
when did this take place?"
The figure probably comes from the 1956 final report on the Grand Rapids
Study by Drs. F.A. Arnold, H.T. Dean et al. in Public Health Reports in
which they stated: "In children born since fluoridation was put into
effect, the caries rate for the permanent teeth was reduced on the average
by about 60%."
This claim has been used since by the ADA, the WHO and other promoters; but
such reduction, as we have seen, could be equally true of the children in
Muskegon, the control that was fluoridated before any proper comparisons
could be made.
The studies made subsequent to 1956, demonstrate that there has been a
general decline in dental caries in the developed world and that the number
of decayed, missing and filled teeth in children who had been fluoridated
all their lives are no fewer than those children reared in non-fluoridated
areas.
Several paragraphs of the press release tell us in gushing terms how
"incredible" the "benefits" are. The emotive statements tone down the
reductions to "20 to 40%" and inform us about "remineralization" ­p; not
telling us, of course, that the original concept of "restructuring,'' the
rationalization for systemic fluorides, has been abandoned.
There is an appeal to adults that fluoride helps decrease root decay for
which properly structured studies are lacking. The press release lists a
number of organizations that, it is implied, assure us that fluoridation
can benefit all "in a safe and extremely cost-effective manner."
When we know that fluoride does not prevent dental caries,
cost-effectiveness is nill. To the contrary, fluoridation is costing us
dearly, more than we can calculate at the present time, to treat its dental
and other adverse effects.
The figure given for cost effectiveness is calculated from the per capita
expenditure for fluoridation chemicals, the average cost of a filling and a
reduction in caries of 40%. Most of which collapses like a deck of cards
when it is recognized that the reduction of caries is a "statistical
illusion.''
Not illusory, however, is the large amounts of taxpayers' money that is
being spent to supply the chemicals for this purpose. If the hypothesis
were proven to be genuine, the facts remain: for every $1,000 spent on
chemicals, less than fifty cents goes to children and adverse effects on
humans and other creatures in the ecosystem would greatly overbalance the
"benefits.''
The press release ends with the "national health objective" for the year
2000 to increase to at least 75% of the portion of US population served by
community water systems providing optimal levels of fluoride.
In view of all the evidence currently available, such contemplated action
is a disgrace!
Dr. Herschel Horowitz, in a paper published in the Journal of Public Health
Dentistry (Vol 52, 4) in 1992, stated: "When Grand Rapids, Michigan, began
to fluoridate its water supply in 1945, relatively few other sources of
fluoride existed in the United States. At that time only about 1.7% of the
US population lived in communities in which the natural amounts of fluoride
in drinking water were at optimal or greater than optimal concentrations
and few food products had appreciable concentrations of fluoride, e.g. tea
and seafood."
He pointed out that by 1955, more than 15% of the U.S. population had
access to drinking water with optimal or greater concentrations of
fluoride; by 1965, 30%; by 1975, 49%. He estimated that at the time of his
writing (1991), more than 130 million persons or 53% of the U.S. population
lived in areas with "optimal" or greater concentrations of fluoride in
their drinking water.
He recognized that this has caused total fluoride consumption to rise in
both fluoridated and non-fluoridated areas because of the incorporation of
fluoride in beverages and foods prepared in fluoridated areas.
In an editorial in Fluoride (Vol 24 No 1) 1991, Roy R. Kintner reviewed
studies to that date of total fluoride intake. A total intake baseline
prior to fluoridation projects in the U.S. was estimated at 0.45-0.55 mg
fluoride per day for an adult. These were based on studies predating 1950.
Subsequent studies show increases in both fluoridated and non-fluoridated
areas. The rise in low fluoride cities "came about due to contamination of
food and beverages through the importation of commercial products produced
and/or prepared in neighboring communities when they adopted fluoridation."

Mean Adult Intake, 2.7mg Fluoride

Kintner reported that the mean adult male intake, in a fluoridated
community in 1991, was 2.7 mg fluoride per day. The estimated daily
fluoride exposure for young adults (11-19 years), adults (20-64 years) and
male adults (20-64 years) in the upper 1st percentile were, in mean values,
respectively: greater than 4.3 mg fluoride per day (mg F/day); greater than
5.6 mg F/day; and, greater than 6.0 mg F/day.
Estimates presented in the USPHS publication Review of Fluoride Benefits
and Risks 1991 (tables 10 and 11) show that 2 year-old (20kg) children may
ingest 2.3 mg F/day in low fluoride areas (less than 0.3 ppm) and 3.6 mg
F/day in optimal (0.7-1.2 ppm) fluoridated areas. These estimates include
fluoride obtained from the use of fluoride dentifrice twice a day and
fluoride supplements (0.5 mg/day) in low fluoride areas.
It can be calculated from these tables that a 50 kg adult has a total
intake of 2.2 mg fluoride per day in low fluoride areas and greater than
6.0 mg fluoride per day in optimal fluoridated areas.
The intake of a 200 pound (91 kg) male athlete or heavy industrial worker
replenishing himself with food and water in a fluoridated area is,
conceivably, in excess of 12 mg fluoride per day!
Kinder points out that these total intakes of fluoride places a significant
portion of the U.S. population at or above the 4-5 mg fluoride per day
level. Dr. F.J. McClure in a 1945 paper published in the Journal of
Industrial Hygiene and Toxicology recommended that this not be exceeded.
It should come as no surprise that children consuming these amounts of
fluoride during their tooth-forming years in both low fluoride and
fluoridated areas develop dental fluorosis. In British Columbia, for
example, 65% of the children in the sample from fluoridated Kelowna had
mild or moderate dental fluorosis of one or more tooth surfaces; in
non-fluoridated Vernon, 55% were similarly afflicted.
Adults do not have a "marker" of intoxication such as dental fluorosis to
signal a high level of fluoride intake.
It may be the case that the original dental and public health promoters did
not anticipate that their actions would raise total fluoride levels to
their present high values. In their haste to initiate the artificial
addition of fluoride to drinking water, they failed to carry out the
projections required to predict the consequences. Lack of adequate
information at the time may excuse mistakes of the past; but failure to
learn from these mistakes and take appropriate action could be interpreted
as negligence.
Dr. Horowitz and his fellow fluoridation promoters consider the increased
numbers of fluoridated communities as "progress" along the path to a
society that will, ultimately, be freed from tooth decay.
Those who are familiar with the historical development of the concept of
fluoridation and the evidence of its lack of effectiveness and of its
adverse effects on teeth, the skeletal system and soft tissues, must
disagree.

Endemic Fluorosis

All of the evidence points to fluoridation as the deliberate creation in
the United States and elsewhere of an extensive area of endemic fluorosis.
Endemic fluorosis, not dental caries, is a major public health problem in
1995. This could be as serious as it is in China, India and elsewhere. The
population at risk is more than 130 million in the United States alone.
The year 1995 does mark a 50th anniversary. To anyone who knows the facts,
this is not a celebration of the conquest of tooth decay by some "magic
bullet." It is an event marking the beginning of a period of fraud,
deception and betrayal.
There are those in the dental profession who call for "a new baseline" or a
"change in traditional thinking" and a general acceptance in Continental
Europe that the systemic use of fluoride to prevent dental caries is passé.
There has been an obvious switch on the part of the ADA elite from the
"structural" to the "remineralization" rationalization. However, in the US,
Canada, Ireland and the United Kingdom, orthodoxy regarding fluoridation is
entrenched.
Fluoridation, especially in the United States, has been established as a
"National Goal" or "Mission.'' Billions of taxpayers' dollars have been
spent over the past 50 years to fulfill this mission. As is typical of so
many government sponsored endeavors, this mission will continue even though
there is ample evidence that the fluoride-caries hypothesis is invalid and
that fluoridation has created a major public health problem, endemic
fluorosis. And, in spite of the fact that fluoridation poses a definite
threat to the environment.
Only the withdrawal of public support can end such an institutionalized
government program as fluoridation, supported as it is by professional
elites. Dr. Horowitz is correct. The public will call for a halt to
fluoridation when they learn that the program is a misuse of increasingly
scarce resources. The program is a failure and costing us dearly in terms
of treatment for adverse effects and losses in the ecosystem due to
fluoride pollution.
How can the public continue support once they learn that dental fluorosis
is not merely cosmetic but a sign that we have poisoned our children? How
can they continue support when they learn that the adverse effects of
fluoride are well-founded, especially when total fluoride intake is
considered?
There is a disturbing tendency on the part of many in the research
community to search only for "positive" results. These, especially when
they deal with human health, are more likely than "negative" findings to
lead to the staking out of a special territory. Cynthia Crossen, in her
book Tainted Truth, the Manipulation of Fact in America (Simon and
Schuster, 1994) presents many examples of cases in which this has occurred;
for example, the "Oat Bran Miracle" that wasn't.
Once an idea such as "1 ppm fluoride, artificially added to drinking water,
prevents dental caries" becomes desired territory, only those studies
supporting or enhancing it are the coin of the realm. Research that
produces results that are contrary is dross. If the research does not
support the hypothesis, the latter remains sound but the research "doesn't
work.''
The early research of Dean and others are examples of manipulating the
results, either intentionally or through ignorance of scientific method to
obtain positive support for the hypothesis underlying fluoridation.
The "trials" in Rapid City, Evanston, etc. were a graphic example of
research that "didn't work." Again, either through ineptitude or calumny.
Some defenders have intimated that these were not scientific studies to
compare the results of a fluoridated population with controls, but were
demonstrations that fluoride could indeed be added to the water supply
without any immediate mechanical problems or apparent adverse effects.
Like any commercial product, fluoridation has been promoted over the past
fifty years to the point that to millions it is "truth."
Built upon the early trumpeting of the power of fluoride to banish tooth
decay, a number of applications have arisen over the past half century:
dentifrices for use in the home and in the dental office; oral fluoride
tablets, drops and mouth rinses.
The companies manufacturing/marketing these products commission their own
research and fund dental meetings on the subject. The list of corporate
sponsors of the International Conference held in Pine Mountain, Georgia
that has been referred to a number of times in this article, includes many
familiar names: Chesebrough-Ponds; Unilever; Johnson and Johnson; Procter
and Gamble; Colgate-Palmolive; Bristol Myers; and others. One other name
that has an interest and publishes a magazine for dentists is the Princeton
Resource Center; this has nothing to do with the university of the same
name but is financed by M&M/Mars.
Standing in the background letting others work for them are those
industries that supply the raw materials used for fluoridation or who
benefit from the image of fluoride as benign. Without fluoridation,
millions of tons of hydrofluosilicic acid would have to be funneled into
holding ponds and treated at great expense, rather than have it turn a
profit.
Smelter operators, faced with legal suits concerning fluoride damage to the
ecosystem, including humans, can shrug their shoulders and say "it's good
for children's teeth, isn't it?"

Additional references for studies cited in the text available on request.

Correspondence:

Richard G. Foulkes, MD
P.O. Box 278
Abbotsford, British Columbia
Canada V2S 4N9
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Fluoride, teeth and the Atomic Bomb