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30th Oct 2000: Peter Meiers
NB. The following paper has been published in the
Journal of Orthomolecular Medicine, Vol. 16, No. 2 (2001) pp. 73-82.
Does
water fluoridation have negative side effects?
A critique of the York Review
Objective 4, Sections 9.1 – 9.6 :
– CANCER STUDIES –
by Peter Meiers, Saarbruecken, Germany
(October 30, 2000)
The National Health Service (NHS) Centre
for Reviews and Dissemination at the University of York recently released a
review perceived to be "the final word on fluoridation" [McDonagh et al.
2000]. To judge from the course of a discussion about the layout of this
York review [Schuld 2000], the result was to be expected: benefits (though
smaller than previously claimed) with regard to caries prophylaxis, at the
cost of some "cosmetic defects" (dental fluorosis), no harm to general
health. This report is just one of many made in the past apparently aimed at
giving support to preoccupied views of the proponents of fluoridation. Like
other sections, the evaluation of the fluoridation-cancer link in this
report is far from presenting "a summary of the best available and most
reliable evidence on the safety and efficacy of water fluoridation". Not
only did the York team disregard all relevant experimental data (a
prerequisite to decide what effects of fluoride should be looked for), it
also, quite obvious to anyone knowing the relevant literature, distorted
facts to make its point.
This is not a new experience. Fears of
undesired effects of the controversial "public health measure" have never
been taken serious by its promoters. Even though animal experimentation on
fluoride and cancer, performed long before any fluoridation experiment was
started in the United States [Meiers 1984, 1986], could have given reason
for concern, investigations into possible fluoride effects on human cancer
victims were not initiated by promoters of the measure prior to any
fluoridation efforts nor in the course of the first experimental trials, but
by opponents whose charges posed a threat to the continuing supply of public
funds and thus necessitated appropriate replies [American Dental Association
1952]. For example, at government hearings in 1952, Taylor [1952] presented
evidence that fluoride shortens the lifespan of cancer-prone mice. Perkins
[1952] speculated on this basis that people in fluoridated cities might die
of cancer at an earlier age because of their fluoride exposure: If a person
would die of cancer at the age of 80, 70, 60, 50, or 40 on a water intake
free from fluorine, the same person would die at the age of 65.6, 57.4,
49.2, 41, or 32.8 years, respectively, on a water intake containing
approximately 1 ppm of sodium fluoride.
Relative to the city of Grand Rapids,
fluoridated since January 1945, Perkins wrote:
"The vital
statistics provided by the health authorities of that city to the United
States Public Health Service and published in ´Vital Statistics of the
United States´, Part II, Table 14, for the year 1945 (the year
fluoridation was installed in Grand Rapids)
show that 252 persons died of cancer. Four years later, the same sources
showed that the deaths in that city from cancer totaled 349. This is an
increase of approximately 39 percent in cancer deaths during the first
five years of fluoridation in Grand Rapids. It is significant that the
records for the five years previous to the adoption of fluoridation
showed an actual decrease in the cancer death rate of approximately 6
percent."
It was these claims
that prompted Swanberg [1953] to evaluate the cancer data of Grand
Rapids and to compare them with cancer mortality data for the United
States as a whole. The York
Committee describes this study [Section 9.4] as showing that:
"The death rate from
cancer in the study area decreased during the study period whereas the
death rate from cancer in the whole of the US (the control area)
increased over the same period" and excludes it from the main analysis
because the "whole of the US includes areas with fluoride in the water
supplies and so [is] not a suitable control area".
Fig. 1: Cancer in Grand
Rapids vs. U.S.A. (Data from Swanberg, 1953)
While this was a wise decision [see
Ziegelbecker 1987] the team did not realize, apparently, that the Swanberg
study actually revealed something quite different from the author's
conclusion: the number of cancer deaths per 100,000 residents per year
increased in Grand Rapids as it did in the U.S.A. (Fig.1, upper graph). As
to the large rise during the years of World War II and the decrease
afterwards, Swanberg explains that
"it is known that in
the early forties there was a migration away from Grand Rapids toward the
center of war industries. After 1945 there was a migration back"
which fact is illustrated in the lower
graph of Fig.1 (data taken from Swanberg´s publication). If this migration
involved just the younger residents it led to a relative increase of the
fraction of older people "per 100,000 residents" during the years of war,
thus increasing the crude cancer death rate. Though Swanberg, editor of the
journal that published his study, gave the full set of data, he selected for
his conclusion those data points appropriate to show a decrease in cancer
death rate after the start of fluoridation:
"The death rate from
cancer in Grand
Rapids in 1944,
the year before fluoridation was adopted, is given as 206.2 per 100,000
population. In 1952, after 8 years of fluoridation, the cancer death rate
was 185.3 per 100,000, a decrease of 10 per cent. In the 9-year period
between 1944 and 1952 in the United States as a
whole, the cancer death rate rose from 124 per 100,000 population in 1944 to
143.9 per 100,000 in 1952, an increase of 16 per cent."
The York review committee either did not
realize this fraud or it chose to mention the unjustified conclusions of the
author to put some undeserved weight to other studies which apparently found
a decrease in cancer death rates after fluoridation started.
Likewise, the York team used a very special approach to evaluate data
from the Newburgh-Kingston study by Schlesinger et al. [1956]. Table 12
in the Schlesinger et al. publication lists the number of cancer deaths
per 100,000 people in fluoridated Newburgh and the non-fluoridated
control city of Kingston for 1942 to 1954, an up and down so that hardly
any difference can be ascertained between the two cities (Fig. 2). Yet,
the York review team [see App. C10, p. 196] excerpted from this list
data for 1944 (219.0 for Newburgh vs. 169.0 for Kingston) and the last
year reported (221.2 for Newburgh, 264.4 for Kingston) when the number
of cancer deaths was in favor of fluoridated Newburgh (while in 1952,
for example, it was lower in Kingston). With this data selection the
York team created the picture that cancer mortality went way up in
non-fluoridated Kingston, while it remained nearly unchanged in
fluoridated Newburgh.
Fig. 2: Cancer Mortality in Newburgh vs.
Kingston (Data from Schlesinger et al. 1956)
Several studies published after the 1956
Newburgh-Kingston "final report" focused on possible effects of natural
fluoride waters on the incidence or mortality of cancer and revealed some
major shortcomings. They were essentially static (comparing data of just one
year) as opposed to the time-trend analyses quoted above. Furthermore, the
concentration of natural fluoride varies (even in one and the same water
supply), and so does the number of registered water supplies within each
municipality [Heasman and Martin 1962; Glattre and Wiese 1979]. Therefore,
it seems to make no sense to compare areas with a water fluoride level of
0.06-0.10 mg/l to areas with 0.11-0.5 mg/l, as Glattre and Wiese do, nor to
arrange fluoride cities into groups based on a difference of one hundredth
mg/l (i.e. 0,5-0,99 vs.1 mg/l and more) as Kinlen [1974, 1975] does. Where
more than one water source supplies a local authority some authors
calculated "weighted means" [Chilvers and Conway 1985]. On this basis, the
latter authors found some of the areas used by Kinlen [1974, 1975] to be
misclassified (see also Heasman and Martin 1962; Nixon and Carpenter 1974).
While these facts should have been reason enough to exclude the Kinlen paper
from the main analysis in the York review, his method of standardization
should have given it the final blow. But as to the Standard population used
by Kinlen the York team claims: "Not stated" (Appendix C10, p. 191). The
Kinlen paper has appendices, among them Appendix B which reads:
"The method for
obtaining the ratios shown in table I was to calculate for each sex and each
age group the number of cases that would be expected in the population in
question in each fluoride category if the total number of cases in all areas
combined was distributed uniformly."
That means, he pooled the groups to
calculate his "expected" cancer deaths and thus used a reference population
partly exposed to the variable to be tested! While the York team excluded
the Swanberg study on this basis, it did ignore the same mistake made by
Kinlen.
In case fluoride increases the number of
deaths, inclusion of exposed people in the reference population would raise
the number of (speculative) "expected" deaths in the groups to be examined
(depending on population structure). As Standardized Mortality Ratios (SMR´s)
are calculated by dividing the number of observed cancer deaths per 100,000
people (O) by the number of "expected" cancer deaths per 100,000 people (E),
the SMR (O:E) becomes the lower the higher the "expected" (E) rate. This
kind of SMR calculation applied in time-trend studies to populations of
different size and structure (fluoridated vs. non-fluoridated cities) using
a shifting reference population (USA 1950, 1960, 1970 as the standard for
the corresponding census years) creates the artifact of decreasing cancer
death rates in fluoridated cities.
An example: In a hypothetical population
with no change both in population structure and the number of cancer deaths
during 1950 to 1970, applying U. S. data in 1950 by age, gender and race to
calculate the number of deaths expected for 1950 in that population, and
likewise U.S. data in 1960 and 1970 for those respective years, will result
in an increasing number of expected deaths in the time span 1950 to 1970,
since cancer death rates rose in the U.S. during that time. As the number of
deaths expected in the hypothetical population will increase, i.e. "E"
becomes higher, the O:E ratio (SMR) becomes lower. Thus one will be able to
show that the cancer death rates decreased in that population (while, as
presupposed above, nothing happened at all with the actual rates). What a
large increase in cancer death rates would be required just to balance the
misleading SMR calculations for the hypothetical population if it were
exposed to a carcinogen to be evaluated!
This is why the reanalyses by Smith
[1980] as well as Kinlen and Doll [1981] of the Yiamouyiannis and Burk
[1977] study on the fluoridation-cancer link are useless. Of these, the
Smith paper got a high ranking according to the York
validity checklist for it "did not include the error in the NCI data"
(Section 9.1.1) – which isn´t true, of course. After all, how can one expect
the York committee members to know the details of that year-long discussion
of the 20-cities study to evaluate properly the relevance of Smith´s
re-analysis?
As the Grand Rapids and
Newburgh/Kingston data show, there are large fluctuations of cancer death
rates over time in individual cities so that it isn´t appropriate to select
just two data points for statistical evaluation, but the best approach would
be to make a linear regression analysis to compare rates before and after
fluoridation started. As differences might be small it seems to be a good
idea to pool the data of several fluoridated cities and to compare them to a
set of non-fluoridated ones.
In
1975, Yiamouyiannis and Burk reported to the U.S. Congress that a set of
20 U.S. central cities had almost identical cancer mortality rates
(cancer deaths per 100,000 people per year) between 1940 and 1950, but
that since fluoridation started (in 1952-1956) in a group of ten of
these cities their cancer death rate increased faster than that of the
ten cities remaining non-fluoridated (Fig. 3). The study was later
published in the Journal "Fluoride" [Yiamouyiannis and Burk 1977] and
caused quite a stir.
Early in 1976, a representative of the National Cancer Institute (NCI)
claimed in a letter to Congressman Delaney that the NCI´s re-analysis
showed that the increase was entirely due to changes in the age, race
and sex structure of the population in question [Fredrickson 1976].
While refusing congressional requests for detailed data (weighted or
unweighted rates used? Which reference population? etc.), the NCI
clandestinely has passed this data on to other scientists [Yiamouyiannis
1977] who reported them as their "independent analysis" [Doll and Kinlen
1977; Oldham and Newell 1977].
Fig. 3: Cancer Death Rates in
non-fluoridated cities vs. cities fluoridated since 1952-1956
However, the NCI data submitted
contained two characteristic errors reproduced in both papers: (A) The
non-white females, age 65-74 in 1970, in the non-fluoridated population
should be 46.1 (not 51.1; thousands) so that the total population becomes
7342.7 (thousands) instead of 7347.7. As a result the expected number of
cancer deaths in non-fluoridated cities in 1970 is 12,384 (instead of
12,407). (B) Total cancer deaths in the non-fluoridated cities in 1970
should be 14,272 (and not 14,487) [Kinlen and Doll, 1977; Oldham and Newell
1979]. The Smith [1980] paper eliminated error (B) of the NCI data, but
still contains error (A).
However, the main point of disagreement
between the statisticians is that whereas Burk and his group derived
putative "observed Cancer Death Rates" (CDRo) by linear regression analysis
of all available and pertinent data, i.e. the crude CDR´s characterizing the
observation period of 1953 to 1968, and extrapolation to 1950 and 1970,
other investigators have taken reported or pericensal CDRo figures for 1950
and 1970. "If, as they say, only the censal or pericensal data for 1950 or
1970 ought to be taken into account, the association between fluoridation
and cancer is wiped away by adjustment. If instead, as we insist, the
intermediate data for 1953 through 1968 must be used, a large association
remains, notwithstanding adjustment" [Graham et al. 1987]. Neither
regression analysis of cancer death rates [Mahoney et al. 1991] nor
calculation of intercensal population by interpolation of data acquired in
census years [Cohn 1992] seem to be unacceptable methods. Furthermore, a
look at age-specific cancer mortality data for the twenty cities,
unfortunately only available for 1970, indicates a higher cancer mortality
at an earlier age in the fluoridated group (Fig. 4). The difference is
obvious in these large populations even though people in non-fluoridated
cities are exposed to fluoride from sources other than drinking water
(tablets, drops, mouthwashes, topical applications, canned foods prepared in
fluoridated cities, etc.).
Fig. 4: Age-specific cancer
mortality rates (cancer deaths per 100,000 people of each age group) in
white males, white females, nonwhite males and nonwhite females in
fluoridated vs. non-fluoridated cities in 1970 (Data from Kinlen and Doll
1981)
While epidemiologists hitherto
essentially looked for evidence in human populations of a per se
carcinogenic effect of fluoride, substantiated by more recent in-vitro
experiments [Tsutsui et al. 1984; Jones et al. 1988; Lasne et al. 1988], the
question raised by Perkins in 1952 relative to the promoter effects of
fluorides has still not been addressed, neither by health officials in
general nor by the York team. Humans today are exposed to not one but many
different carcinogenic agents (including chemicals, viruses, ionizing
radiation) which interact in very intricate ways. Fluoride is known to
inhibit some enzymes and to activate others. Fluoride inhibits the enzymatic
deacetylation of N-Hydroxy-Acetylaminofluorene [Irving 1966] and thus leaves
more of the substrate for a sulfotransferase enzyme that builds the ultimate
carcinogen from that compound. Fluoride activation of dimethyl-nitrosamine
demethylase in liver microsomes [Dophuoc et al. 1981, 1983] increases the
carcinogenic potential of dimethylnitrosamine. It has no obvious influence
on the oxidative activation of the ubiquitous carcinogenic hydrocarbon
benzo(a)pyrene in vitro [Dophuoc et al. 1981, 1983], yet addition of
fluoride to the food of experimental animals injected with this compound
leads to increased incidence of malignant tumors [Tannenbaum and Silversone
1949]. Likewise, skin cancer induced in animals by skin painting with
benzo(a)pyrene becomes earlier visible and leads to earlier death if the
painting solution contains 1 ppm fluoride (as sodium fluoride) in addition
to the hydrocarbon [Wagner 1981]. Beryllium compounds are carcinogenic, but
exposure of animals to beryllium fluoride enhances the growth of lung tumors
induced by the beryllium [Schepers 1961]. Fluoride and fluorophosphate
promote tumor growth induced in vitro by benzo(a)pyrene and many other
compounds [Jones et al. 1988]. In this assay the promoter effect came to a
halt as soon as the fluoride was omitted from the culture medium. Thus the
early experiments of Taylor [1952, 1954, 1965] are fully supported by more
recent evidence.
According to a WHO scientific group "the
occurrence of tumors earlier than in the controls, without increased
incidence" is among the types of responses "used to classify chemicals as
carcinogens" [WHO 1969].
Enhancing effects are also apparent from
some life table data published in the National Toxicology Program
carcinogenicity test of sodium fluoride [NTP 1990]. This test had been
requested by the U.S. Congress during hearings in 1977. Back then, NCI
representative Kraybill [1977] presented a list of publications which, he
alleged, had already shown that sodium fluoride has no carcinogenic
activity. However, not a single one of the publications on his list had
anything to do with fluoride and cancer. Anyway, the start of the
carcinogenicity test requested by Congress was announced four years later [Whitmire
1981]. After another four years, a first result was declared inadequate
because the low fluoride semisynthetic diet "was deficient in several
vitamins and minerals" [NTP 1985]. Another two-year study was scheduled to
begin in October 1985. The report, released in 1990, focused on the
occurrence of a rare form of cancer, osteosarcoma, in several of the male
(but not the female) dosed rats used in the study [NTP 1990]. This evidence
of carcinogenicity was downgraded to be "equivocal".
Nevertheless, a few epidemiological
studies addressed a possible influence of water fluoridation on the
incidence of osteosarcoma in humans. It occurs in less than one in 100,000
people or about 0.1 percent of all reported cancers, and therefore it would
be hard to detect small increases in risk (on the order of five to ten
percent) [USPHS 1991]. Examinations in a very limited number of afflicted
people led to conflicting results. The study designs (e.g. exclusion of
people formerly exposed to some radiation) reveal that still the search for
a per se carcinogenic effect of fluoride was in the foreground. There seems
to be agreement that osteosarcoma incidence in the U. S. increased in people
below age 30 with some decrease at later age. A contribution by water
fluoridation could not be ascertained by these limited studies, but obvious
difficulties in classification of exposure to fluoridated drinking water and
examination of exposure from other sources need to be more carefully
addressed in more thorough future investigations. The York team apparently
was not aware of these shortcomings.
In summary,
the York review fits well in a history of attempts to downgrade possible
risks associated with exposure to fluoride. Selection of data, inconsistent
use of exclusion criteria, disregard of experimental studies which could
have offered a clue to proper evaluation of epidemiological investigations
render the York
review useless. Either the York
team was not really interested (to say the least), aimed at supporting
proponents´ views, or was hopelessly lost in its task.
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"Washington News Letter", J. Am. Dent. Assoc. 44: 461
Cohn P.D. (1992): "A brief report on the
association of drinking water fluoridation and the incidence of osteosarcoma
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(1981): "Effects of hydrogen fluoride on benzo(a)pyrene and
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