Fluoride, Cancer

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Fluoridation Side Effects

 

Fluoride, Cancer

 

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)

 

(Note by Andrew Saul: Fluoridation of water owes its

continued existence more to politics than to science.

If safety and effectiveness are truly considered,

fluoride would be questionable even as a prescription

drug. But to freely add it to public water supplies,

often without any public vote whatsoever, is far

beyond questionable. Mr. Meiers' discussion of the

dangers of fluoride is important reading.)

 

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 per-son 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 " . 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.

 

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. Further-more, the concentration

of natural fluoride varies (even in one and the same

water supply), and so does the num-ber 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 refer-ence 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 calcu-lations for the hypothetical population if

it were exposed to a carcinogen to be evaluated!

 

This is why the re-analyses 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]. 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

mor-tality 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.).

 

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 intri-cate

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 hy-drocarbon benzo(a)pyrene in

vitro [Dophuoc et al. 1981, 1983], yet addition of

fluoride to the food of experi-mental 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 ear-lier visible

and leads to earlier death if the painting solution

contains 1 ppm fluoride (as sodium fluoride) in

ad-dition to the hydrocarbon [Wagner 1981]. Beryllium

compounds are carcinogenic, but exposure of animals to

be-ryllium 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 al-leged, 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 fe-male) 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 can-cers, 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

expo-sure 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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Reprinted with permission of the author.