The year, 1995, marks the 50th anniversary of fluoridation: the deliberate addition of
fluoride to drinking water, for the avowed purpose of preventing tooth decay in
children. Differences with orthodoxy are apparent in literature
appearing from those in the dental profession and concerns over its viability
as a social program are being expressed by its strongest supporters.
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:
- 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;
- The perception by the public of dental fluorosis as a "problem" when they become increasingly aware
of the high incidence being reported;
- 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";
- The public's perception that fluoridation is environmental pollution; and
- 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 U.S. 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 U.S. 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; 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.
Thisgrossly 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
1945 better
than 99% of the children examined experienced dental decay."
This is 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”; 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
to 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?”