o) EPA has failed to adhere to statutes and guidelines (see Appendix
K)
1.1.
Final Rule predicated on an
inadequate and outdated standard (back
to top)
EPA's
MCL of 4 ppm, established in 1985, cannot be defended scientifically - a fact
which possibly explains why EPA has rushed to approve DOW's petition before
waiting to hear from the NRC panel which is currently reviewing the fluoride
MCL (at EPA's request!).
EPA's
decision to let DOW add another source of fluoride to the food supply is heavily
predicated on the adequacy on the 1985 MCL standard. Therefore, FAN has provided an analysis of this standard.
The analysis reveals critically important inadequacies with the MCL,
including:
a)
The MCL assumes crippling skeletal fluorosis is the only adverse bone damage
that fluoride can cause, and ignores other bone damage (arthritic symptoms,
reduced bone strength, mineralization defects, and exacerbation of bone disease
in people with kidney disease) fluoride can cause before it cripples
the skeleton.
b)
The Lowest Observed Adverse Effect Level (LOAEL) (20 mg/day) selected for
crippling fluorosis was derived from a limited set of data which provided
inadequate information on how this LOAEL may vary across the range of the
population, and across the range of pertinent exposure durations.
c)
The scientist responsible for establishing the 20 mg/day LOAEL (Harold C.
Hodge) ended up revising his estimate to 10 mg/day.
EPA, however, ignored this revision - even though it was made in 1979,
6 years before EPA issued the MCL.
d)
The 20 mg/day LOAEL has been further undermined by data published since 1985,
especially recent research on fluoride and bone strength.
e)
The safety factor underpinning the MCL is dangerously low compared with other
comparable contaminants in the environment.
f)
The MCL is based on a misrepresentation of a large body of epidemiological
data on skeletal fluorosis.
g)
The EPA has openly acknowledged that the MCL can not be considered safe for
people with kidney disease, thus violating EPA's mandate to protect
sensitive subsets of the population.
1.2.
EPA's new Final Rule has made a bad standard even worse (back
to top)
In
its risk assessment for Sulfuryl Fluoride, EPA has managed to make a bad standard
(the 1985 MCL) even worse. For, in granting DOW the right to use Sulfuryl
Fluoride, EPA has actually increased the MCL (reference dose) for children.
By
using non-conventional, poorly justified, and highly questionable assumptions,
EPA has created a "reference dose" (or "chronic safe risk assessment
dosage") for children which is up to FIVE times higher than the equivalent
dose for adults.
EPA's
use of a higher reference dose for infants and children than adults constitutes
a sudden change in policy. In
all recent risk assessments issued by EPA over the past few years, EPA has
applied the same reference dose for both children and adults. This may not have been ideal, but any adjustments made to recommended
maximum exposure levels for infants and children should have been in the direction
of lowering them, not raising them.
EPA's
sudden change in policy is as suspicious as it is unacceptable.
It
is suspicious because, had EPA not increased the reference dose for children,
then EPA's own data would show that children are already being exposed to
doses which exceed EPA's previously estimated safe level. The implications
are obvious: if children are already receiving too much fluoride, than there
is no room for additional fluoride exposures, and EPA would be compelled to
reject DOW's request to use Sulfuryl Fluoride which is known to leave fluoride
residues on food.
EPA's
manipulation of the safe fluoride dosage for children moves in exactly the
opposite direction from the intentions of the Food Quality Protection Act
(FQPA) which requires EPA to issue standards that are particularly protective
of children. In this case infants are less protected by a factor of
5 instead of more protected by a factor of 10X an overall swing against
the FQPA recommendations to protect children by a factor
of 50. This change also violates the EPA pesticide division's own requirements
for appropriate risk factors.
1.3.
EPA's exposure analysis underestimates current fluoride exposure among children
(back
to top)
Along
with increasing the allegedly safe dosage for children, EPA has also demonstrably
underestimated the level of fluoride exposure among US children. FAN's analysis
of EPA's exposure estimates reveals that:
*
EPA's supposedly conservative estimates of total fluoride exposure among children
in 2 ppm areas have recently been shown to be exceeded by the Iowa Fluoride
Project which studied children in 1 ppm areas!
*
EPA's supposedly conservative estimates of total fluoride exposure from toothpaste
severely underestimate the contribution from this source. Indeed, EPA's estimate
of the maximum daily exposure from toothpaste is a dose that is actually lower
than the average
daily exposure reported in most studies on the subject.
*
Despite EPA's assurance that children will not receive more fluoride than
the agency's newly revised MCLs, recent data from the Iowa Fluoride Project
shows that this claim is incorrect, and that some children are already receiving
more fluoride than EPA's newly revised MCLs.
*
In assessing the exposure burden among US populations, EPA has ignored critical
data on bone fluoride levels, serum fluoride levels, and urine fluoride
levels. These omissions represent serious weaknesses in EPA's analysis.
1.4.
EPA's detailed scrutiny of papers cited by FAN stands in stark contrast to
its unquestioning endorsement of the MCL (back
to top)
In
its response to papers submitted by FAN, the EPA displayed a level of intense
scrutiny which is noticeably absent in the its acceptance of the 1985 MCL.
Indeed,
if the concern at the EPA was for the "adequacy of the current MCL,"
some of EPA's time would have been more wisely spent reviewing the "scientific
literature" that underpins this standard with at least the same attention
to detail which they used in analyzing the FAN submission. Had they done so
they would have found it absurdly deficient.
There
is clearly a double standard operating here.
On the one hand, EPA blindly accepts the current MCL based upon the
flimsiest of evidence for safety, especially with respect to children, while
nitpicking numerous articles which have been peer-reviewed and published in
mainstream journals and indicate that the current MCL is unsafe . The use
of a double standard is often very revealing. It usually indicates a body
"defending" a position, rather than truly investigating an issue
objectively.
EPA's
reasons for dismissing the papers submitted by FAN are often inaccurate, inappropriate
and occasionally cavalier. Remember - we are not discussing the standard for
an additive to motor oil, but the standard for a substance which is currently
causing between 30% to 50% of American children to be impacted with dental fluorosis, a condition caused by a fluoride-induced
toxic effect on the enamel-forming cells.
While
the EPA appears content to dismiss this as a "cosmetic effect,"
at the very least this condition is a biomarker of over-exposure to a physiologically
active and cumulative toxin.
While
US health authorities, unlike those in Europe, give little credence to the
Precautionary Principle, one would have expected a little more caution from
EPA when it comes to published research which has found, among other things,
that fluoride accumulates in the human pineal gland, increases the uptake
of aluminum into rat brain, lowers children's IQ in several studies, alters
thyroid function in hyperthyroid patients, causes symptoms very similar to
arthritis, and triples hip fractures rates in China at levels in drinking
water close to the MCL.
While
we accept that there are unresolved questions and uncertainties remaining
in the literature concerning some of these health concerns, we believe that
EPA's use of the uncertainties (to dismiss the concerns) is inconsistent with
its mandate. We would argue, that the existence of uncertainty - especially
considering the seriousness of the health effects under discussion - is not unusual, and should not be reason
in and of itself to forego the need for precaution. We fear also that waiting
for more and more epidemiological studies to quantify these dangers will subject
our population to unnecessary risks and possibly irreversible harm.
2.
EPA's RISK ASSESSMENT IS BASED ON AN OUTDATED AND UNDEFENDABLE MCL (back
to top)
EPA's
Final Ruling in favor of DOW's use of sulfuryl fluoride as a fumigant on food
is based upon a standard (the 1985 MCL for fluoride of 4 ppm) which is currently
being reviewed by the NRC. The nearly 20 year old MCL does not factor in dozens
of newer studies currently under review by NRC. EPA's scientist in charge of the sulfuryl fluoride assessment
(Dennis McNeily) informed FAN, at the August 12, 2003 meeting of the NRC,
that EPA would not issue its Final Ruling until after the NRC reported
back to the EPA. Yet, EPA has
done exactly the opposite. This undue haste is puzzling and unseemly, as it
was EPA who requested the NRC to review its own 1985 standard. It was an unwise and undefendable decision
to give the DOW approval before the NRC review has been completed and it can
only indicate to the public that EPA's ruling is based on other non-scientific
considerations.
Even
without the NRC's ongoing review of the literature in place, had EPA analysts simply applied the same level of scrutiny to the
derivation of their 1985 MCL standard as
they applied to the papers FAN presented to indicate the dangers of fluoride
exposure, it would become clear to any objective analyst that the current
MCL is woefully inadequate and unprotective of the public health.
2.1
A re-examination of EPA's 1985 MCL (back
to top)
Since EPA's current risk assessment
is so heavily predicated on the adequacy of its 1985 MCL, we feel compelled
to highlight the problems and limitations with the
standard. As will be seen, this standard is so profoundly inadequate
that any risk assessment which uses this standard as its scientific basis
will be inherently flawed.
2.2
1985 MCL is designed to only protect against crippling skeletal fluorosis
(back
to top)
The
most egregious problem with EPA's 1985 MCL is that it was crafted to only
protect against a very advanced form of human fluoride toxicity - crippling
skeletal fluorosis. As common
sense alone should indicate, and as the scientific literature confirms, fluoride
causes damage to bone long before it cripples the spine. Indeed, crippling
skeletal fluorosis represents the final, most severe stage of fluoride's damage
to bone. An adequate MCL for
fluoride, therefore, would seek to protect against the bone damage which can
occur prior to the final crippling stage. These pre-crippling skeletal effects
include:
- Arthritic symptoms which mimic rheumatoid and osteoarthritis
- Reduced bone strength
- Reduced bone density
- Increased mineralization defects
- Exacerbation of bone disease in people with kidney disease
The
current 4 ppm MCL fails to protect against any of these effects.
2.3
LOAEL for EPA's MCL based on a limited, inappropriate set of data (back
to top)
Before
discussing the pre-crippling bone effects which EPA's MCL ignores, it is important
to note that EPA's MCL for crippling skeletal fluorosis was based on an inappropriately
derived LOAEL.
The
LOAEL (20 mg/day) was derived from Kaj Roholm's research on a small group
of cryolite workers working in Denmark in the 1930s (Roholm 1937; Brun 1941).
Based on Roholm's research, however, it is not possible to reach firm conclusions
about the LOAEL for crippling fluorosis. This is because:
A)
Roholm was not able to determine the dose that would not cause fluorosis
(e.g. he was not able to determine a NOAEL).
B)
The subset of the population Roholm studied (adult male workers) is not representative
of the population at large, particularly those subsets of the population known
to be more vulnerable to fluoride, including people with kidney disease, people
with chronic malnutrition, and children. Thus, based on Roholm's research,
it is simply not possible to determine the LOAEL for people with kidney disease,
for people with varying degrees of malnutrition, and for children.
C)
The workers Roholm studied who developed crippling fluorosis had only worked
at the plant for 10 to 25 years. Since skeletal fluorosis is dependent both
on dose and duration of exposure, it is not possible - based on Roholm's
research - to determine the LOAEL for people exposed to fluoride for longer
periods of time than the workers in Roholm's study. For instance, based on
Roholm's work, there is no way of determining what the LOAEL for crippling
fluorosis is for a person (healthy or not) exposed to elevated levels of fluoride
for 70+ years. It is inappropriate, therefore, for the EPA to base its MCL
on a dose that is based on people who had only worked 10 years. Needless to
say, someone living their lifetime in a 4 ppm community will be exposed to
elevated fluoride for far more than 10 years.
D)
While the LOAEL used by the EPA is based on Roholm's research, Roholm himself
never concluded that 20 mg/day was the minimum dose that could cause crippling
fluorosis (and he certainly didn't conclude that 20 mg/day was the minimum
dose for all subsets of the population and for all durations of exposure).
Roholm, who better appreciated the limitations in his data, stated that his
dose information should be used as a guide for future investigation - not
the final word!
E)
The person who reached the conclusion that Roholm's research establishes 20
mg/day as the minimum dose that can cause crippling skeletal fluorosis was
Harold C. Hodge, a prominent pro-fluoridation scientist. It should be noted,
however, that Hodge - who repeated this conclusion in numerous papers for
nearly 30 years - ended up revising his estimate towards the end of his career.
In 1979, Hodge wrote that the LOAEL for crippling skeletal fluorosis may be
as low as 10 mg/day. When the EPA established its MCL in 1985, it ignored
Hodge’s revised estimate, and stuck
with Hodge's earlier claim.
2.4.
More recent data highlights inadequacy of 20 mg/day LOAEL for crippling fluorosis
(back
to top)
Recent
research has further underscored the problem of EPA using 20 mg/day as the
LOAEL for crippling skeletal fluorosis.
In
2003, Cao published a careful analysis of the doses causing crippling skeletal
fluorosis in Tibet. According to Cao's analysis, the average dose causing
crippling fluorosis was just 12 mg/day. Meanwhile, according to a recent study
from Bo (2003), the average dose in an area of endemic skeletal fluorosis
in China was found to be just 9.4 mg/day.
These
findings from Asia are consistent with recent estimates from the National
Research Council. In 1993, the NRC estimated that crippling skeletal fluorosis
could be caused by exposure to 10 to 20 mg/day, while in 1997, the Institute
of Medicine estimated that the milder stages of crippling fluorosis could
be caused by 10+ mg/day.
Based
on this data, it is completely inappropriate for the EPA in 2004 to still
be using 20 mg/day as the LOAEL for skeletal fluorosis. The 20 mg/day LOAEL
is an anachronism. It no longer
represents the "Lowest Observed Adverse Effect Level" for crippling
fluorosis.
At
the very least, the EPA should be using
the 10 mg/day LOAEL cited by the two most recent NRC reviews (NRC 1993; IOM
1997), and by Hodge himself (Hodge 1979).
2.5.
EPA's MCL utilizes an irregular and inappropriate safety factor (back
to top)
Even
if one assumed that the 20 mg/day is an appropriate LOAEL (which it is not),
the MCL would still be completely inappropriate. This is because EPA applied
an irregular, insufficient and unjustifiable safety factor in determining
the 1985 MCL for fluoride. Normally, EPA applies a safety factor of 10 when
a LOAEL is identified within the human population. However, in the case of
crippling skeletal fluorosis, the EPA applied a safety factor of just 2.5.
We see
no reason, however, why the EPA should apply a factor less than the standard
10 for this serious endpoint. Indeed, for the following three reasons, we
believe it is imperative that if the EPA is to stick with its 20 mg/day LOAEL
for crippling fluorosis, that it apply the standard safety factor of 10.
First, as noted above, the 20 mg/day LOAEL was derived from a population that
didn't represent susceptible subsets of the population (e.g. people with kidney
disease, people with chronic malnutrition, and children).
Second, as noted above, the 20 mg/day LOAEL was derived from workers who had
been exposed to fluoride for only 10 to 25 years. Considering, however, that
skeletal fluorosis is both dose- and time-dependent, it is extremely probable
that the LOAEL will be lower for people exposed to fluoride for longer periods
of time (e.g. 70+ years).
Third, the 20 mg/day LOAEL refers to an extreme effect on bone (crippling
skeletal fluorosis) that represents the final stage of fluoride-induced bone
damage. There is ample evidence, however, that fluoride can damage bone before
it cripples the skeleton, and thus a large safety factor (e.g. at
least 10) is essential in order to protect against these pre-crippling effects.
2.6.
EPA has misrepresented epidemiological data on skeletal fluorosis (back
to top)
In its recent risk assessment, EPA provides
an entirely unacceptable defense of the 2.5 safety factor. According to the
EPA, "the typical 100x factor used by the HED to account for inter- and
intra-species variability have been removed due to the large amounts of human
epidemiological data surrounding fluoride and skeletal fluorosis" (EPA
Jan 20, 2004; p. 16).
The
problem with this statement is that when the EPA established its MCL in 1985
it ignored and misrepresented most of the epidemiological data on skeletal
fluorosis.
In
its November 14, 1985 Final Rule, the EPA made a profoundly misleading statement
concerning the epidemiological data on skeletal fluorosis. To quote:
"EPA notes that crippling skeletal fluorosis, rheumatic attack,
pain and stiffness have been observed in a large number of individuals in
other countries chronically exposed to fluoride in drinking water at levels
of 10 mg/L to 40 mg/L" (Federal Register, Nov 14, 1985, p. 47144).
Anyone
reading this statement could reasonably conclude that skeletal fluorosis was
only found in communities where the water contained fluoride above 10 ppm.
However, as had been documented repeatedly for over 40 years, skeletal fluorosis
was known to occur at levels well below 10 ppm.
Some examples:
In
two of the most frequently cited papers on skeletal fluorosis in India, (Singh
1961, 1963) crippling fluorosis was observed at 1.2 ppm and between 1 and
2 ppm.
In
1970, Siddiqui observed skeletal fluorosis at 1.2-1.4 ppm, while Jolly (1970)
reported fluorosis at 1.4 ppm.
Many
more studies reported skeletal fluorosis above 2 ppm, but far below 10 ppm,
including Pandit (3 ppm; 1940); Siddiqui (5.2 ppm; 1955); Kumar (6 ppm; 1963);
and Krishnamachari (3.5-6 ppm; 1973).
Thus,
EPA's statement in 1985 implying that skeletal fluorosis only occurred in
communities with more than 10 ppm fluoride in the water was incorrect and
misleading as it failed to acknowledge the abundant published evidence of
skeletal fluorosis at water levels far below 10 ppm .
Meanwhile,
many additional studies - published since 1985 - have confirmed the presence
of skeletal fluorosis at between 1 and 2 ppm (see Xu 1997; Choubisa 2001,
WHO 2002; Bo 2003). Indeed, in China today, any water concentration exceeding
1 ppm is considered a risk for developing skeletal fluorosis, while any concentration
exceeding 2.5 ppm is considered a "high risk" (Bo 2003).
It
is, therefore, blantantly wrong for the EPA, in 2004, to claim that the existence
of a large body of epidemiological data on skeletal fluorosis justifies its
use of a lower than standard safety factor for fluoride. Indeed, most of the data published directly contradicts and
undermines the validity of the l985 MCL
(Pandit 1940; Siddiqui 1955; Singh 1961, 1963; Kumar 1963; Sauerbrunn 1965;
Jolly 1970; Siddiqui 1970; Juncos & Donadio 1972; Krishnamachari 1973;
Johnson 1979; Xu 1997; Choubisa 2001, WHO 2002; Bo 2003; Cao 2003).
2.7.
MCL does not protect people with kidney disease (back
to top)
MCL's
are designed to protect the most susceptible subsets of the population from
harm. According to the EPA's Final Rule for fluoride's MCL:
"[T]he Agency is acutely aware of sensitive subgroups in the
population. Under the SDWA, EPA is charged with setting standards to protect
the most sensitive subgroup of a population" (Federal Register, Nov
14, 1985, p. 47151).
However,
despite being "acutely aware" of the importance of protecting sensitive
subgroups, the EPA openly acknowledged in its Final Rule that the 4 ppm MCL
could not be regarded as safe for people with kidney disease. To quote:
"The Agency feels that this RMCL provides an adequate margin
of safety except
in those very extreme cases involving severely renally impaired individuals
who consume unusually high levels of fluoride due in part to polydipsia and
other confounding factors" (emphasis added; Federal Register, Nov
14, 1985, p. 47152).
"Except"
is the key word here. It shows that the EPA in 1985 ignored its legal obligation
under the SDWA to protect a key subgroup of the population vulnerable to fluoride
harm: people with kidney disease.
Based
on the findings of Juncos & Donadio (1972) and Johnson (1979), it is clear
that if the MCL for fluoride is to protect people with kidney disease, it
needs to be set below 1.7 ppm. The
findings of Johnson (1979) are particularly important for the EPA to consider.
It appears this paper was not considered by EPA in 1985, nor was it considered
by the NRC in 1993.
Johnson
(1979) reported the Mayo Clinic's findings of fluoride-induced bone damage
in people with kidney disease. The conclusion of this paper is that fluoride
levels of 1.7 to 2.0 ppm can exacerbate the bone disease of people with kidney
disease. We believe this paper is particularly significant as it includes
measurements of fluoride levels in the patients' serum and bones. In particular,
the levels of fluoride found in the serum were greatly elevated (up to 14.1
umol/L), and, in the person with the severest case of bone disease, these
levels exceeded a) the estimated toxic threshold (10 umol/L) for fluoride-induced
bone damage (Pak 1989); b) the serum fluoride levels (9-11 umol/L) consistently
associated with reduced bone strength in animals (Turner 1995, 1996, 2001);
and c) the serum fluoride levels associated with skeletal fluorosis (5+ umol/L)
in some humans (see Table 3a in Appendix
B).
Indeed,
based just on the serum fluoride findings of this study, we believe this paper
establishes the lack of safety of 2 ppm fluoride for people with kidney disease.
Based on current knowledge, it is simply unacceptable to allow people to attain
14 umol/L fluoride in the blood.
As
such, any MCL for fluoride would need to
be below 2 ppm in order to prevent the toxic buildup of fluoride in kidney
patients' serum, as documented in the 1979 Johnson study.
2.8.
EPA's MCL Undermined by Studies Published since 1985 (back
to top)
New
research, published since 1985, has highlighted yet additional problems with
the EPA's MCL. In particular, the new research has highlighted the severe
limitations inherent in EPA's focus on crippling fluorosis as being the only
relevant adverse effect that fluoride can have on bone.
Some
examples:
In
the same year that the EPA approved the 4 ppm MCL, Arnala (1985) reported
that fluoride concentrations exceeding 1.5 ppm were associated with an increase
in mineralization defects in human bone.
A
year later, Sowers (1986) reported a statistically significant increase in
bone fractures in a 4 ppm community versus a control community with 1 ppm.
In 1991, Sowers updated her findings, and noted that in addition to an increase
in bone fractures, there was also a statistically significant reduction in
bone mass in the 4 ppm community.
A
year earlier, Phipps (1990) reported the results of a separate study which
also looked at bone mass in a 4 ppm community. As with Sowers, Phipps found
that the 4 ppm community had significantly less bone density than the 1 ppm
community in the bone that she measured (the forearm).
While
Phipps' study did not investigate bone fracture rates, a later study by Li
(2001) did. As with Sowers, Li found a statistically significant increase
in bone fracture rates, particularly hip fractures, in communities with excess
fluoride. In a community with 4.3-8 ppm, Li found that the hip fracture rate
was 3 times higher than the hip fracture
rate in the control 1 ppm community. Li also found a doubling of hip fractures
at 1.5+ ppm, however this effect was not statistically significant.
2.9.
Recent fluoride/bone strength research eviscerates 4 ppm MCL (back
to top)
The
likelihood that fluoride weakens bones and promotes fracture has been established
by two powerful lines of scientific evidence published since 1985: human clinical
trials and animal studies.
2.9a
Human clinical trials published since 1985: (back
to top)
Since
1985, a series of well-controlled clinical trials - including the much anticipated
NIH-sponsored 4 year double-blind trial (Riggs 1990) - have reported that
osteoporotic patients treated with fluoride experience a higher rate of bone
fractures (Dambacher 1986; Hedlund 1989; Bayley 1990; Orcel 1990; Riggs 1990;
Schnitzler 1990; Gutteridge 2002).
Of
particular interest are the clinical trials of Hedlund (1989); Bayley (1989),
Orcel (1990), and Gutteridge (2002), as the doses used in these trials were
only 21 to 25 mg per day.
While
EPA dismissed the relevance of these clinical trials in their recent response
to FAN, we find EPA's dismissal entirely unacceptable. Firstly, the EPA made a blatant mistake about the doses used
in these trials by failing to convert the dose of sodium fluoride into the
corresponding dose of fluoride ion. By failing to make this conversion, and
by apparently failing to read the studies in question, the EPA stated that
that the doses used in Hedlund (1989) were 50 mg/day when they were really
23 mg/day; that the doses used in Bayley were 60 mg/day when they were really
21 mg/day; and that the doses used in Gutteridge (2002) were 60 mg/day when
they were really 25 mg/day.
Secondly,
EPA dismisses the relevance of these trials by pointing out that the doses
exceed the current LOAEL of 20 mg/day. However, we believe that a more appropriate
response would be to calculate the safe dose by applying the standard margin
of safety to this data. As noted earlier, the standard margin of safety applied
when health effects have been found in humans is 10. If we apply this standard
safety factor of 10 to these trials, we get a reference dose of between 2.3
to 3.3 mg/day. Assuming 2 liters of consumption of water per day, the corresponding
MCLG for fluoride (based on bone fractures from clinical trials) would range
from 1.15 to 1.65 ppm.
2.9b
Animal studies published since 1985: (back
to top)
Complimenting
the clinical trials reporting increased bone fractures in humans receiving
fluoride has been a series of well conducted animal studies (Mosekilde 1987;
Turner 1992, 1993, 1995, 1996a, 1997, 2001; Lafage 1995; Sogaard 1995).
As
multiple authors have noted (Sogaard 1995; Turner 1996b), the majority of
animal studies investigating fluoride's impact on bone strength have found
that fluoride reduces it.
In
the extensive series of animal studies conducted by Dr. Charles Turner over
the past 12 years, an extremely consistent finding has emerged: When rats
are exposed to 50 ppm fluoride in their water, the strength of the bone is
reduced. This finding was reported by Turner in multiple groups of animals
in 3 separate studies in 1995, 1996a, and again in 2001.
The
dose of the rats receiving 50 ppm F in these studies ranged from 2.1 to 3.5
mg/kg/day (Dunipace 1995, 1998), with the estimated average dose ranging from
2.2 to 2.7 mg/kg/day.
Considering
the consistency of the finding of reduced bone strength among these rats,
it can be reasonably concluded that the LOAEL for reduced bone strength is
at, or below, 2.2 - 2.7 mg/kg/day.
If
we then apply the standard 2 UFs of 10 to account for inter- and intra-species
variations, we arrive at a safe human dose of 0.022 - 0.027 mg/kg/day. This
dose is 4.2-5.2 times lower than EPA's current MCL for adults (0.114 mg/kg/day)
and up to 26 times lower than EPA's current MCL for infants (0.571 mg/kg/day).
It
should be noted, meanwhile, that other recent animal studies have found reductions
in bone strength at doses below the doses found by Turner. For instance, Lafage
(1995) found a reduction in bone strength in minipigs at an average dose of
0.91 mg/kg/day.
It
might be appropriate, therefore, to use Lafage's dose as the LOAEL for reduced
bone strength in animals. If we apply the standard 2 UFs of 10 to Lafage's
data, we arrive at a safe human dose of 0.009 mg/kg/day, which is 12.7 times
lower than EPA's current MCL for adults (0.114 mg/kg/day) and 63 times low