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)
Meiers P. "Does Water Fluoridation have negative side effects? A critique
of
the York Review" J. Orthomol. Med. 16:2 (2001) 73-82
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:
Fig. 1: Cancer in Grand Rapids vs. U.S.A.
(Data from Swanberg, 1953)
"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".
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.
Fig. 2: Cancer Mortality in Newburgh vs. Kingston (Data from Schlesinger et al. 1956)
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.
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.
Fig. 3: Cancer Death Rates in non-fluoridated cities vs. cities fluoridated since 1952-1956
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].
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.
References:
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Fig. 2: Cancer Mortality in Newburgh vs. Kingston (Data from Schlesinger et al. 1956)
