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SUBMITED
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ACCEPTED
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VOLUME
Vol.07 Issue 05 2025
CITATION
Karim Chubin. (2025). Water Fluoridation Reconsidered: Minimal Benefits,
Mounting Risks, and Ethical Dilemmas. The American Journal of Medical
Sciences
and
Pharmaceutical
Research,
7(05),
06
–
13.
https://doi.org/10.37547/tajmspr/Volume07Issue05-02
COPYRIGHT
© 2025 Original content from this work may be used under the terms
of the creative commons attributes 4.0 License.
Water Fluoridation
Reconsidered: Minimal
Benefits, Mounting Risks,
and Ethical Dilemmas
Karim Chubin
British-Trained Anthropologist. Swiss and German -trained
Naturopath and Nutritionist
Abstract:
Public water fluoridation, once a celebrated
preventive dentistry milestone, is increasingly being
reevaluated in light of current scientific, ethical, and
policy considerations. While initially justified based on
data suggesting systemic benefits from ingestion,
current evidence demonstrates
fluoride’s primary
anticaries mechanism is topical, not systemic.
Simultaneously, recent studies have linked fluoride
ingestion
—
even at levels considered safe (0.7 mg/L) by
the U.S. Department of Health and Human Services
(HHS)
—
to neurodevelopmental harm, endocrine
disruption, and musculoskeletal risks. This article
presents a review of the scientific literature addressing
fluoride’s mechanisms of action, its systemic risks, and
the ethical challenges posed by involuntary mass
medication. Based on recent epidemiological findings,
policy developments, and bioethical principles, the
continued practice of public water fluoridation appears
scientifically outdated and ethically untenable.
INTRODUCTION:
Fluoridation of public water supplies began in the
United States in the 1940’s as a novel approach to
preventing
dental
caries.
Spurred
by
early
observational studies of communities with naturally
fluoridated water, fluoridation was seen as an effective,
low-cost intervention to reduce tooth decay in children.
In 1945, Grand Rapids, Michigan became the first U.S.
city to fluoridate its water. By the 1960s, the U.S. Public
Health Service endorsed the practice nationwide,
thereby spreading rapid adoption.
Today, approximately 63% of the U.S. population
receives fluoridated water. However, the same trend
has not been observed globally. Western European
countries have largely rejected or discontinued water
fluoridation. For instance, Austria, Belgium, Denmark,
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Finland, France, Germany, Italy, the Netherlands,
Norway, Sweden, and Switzerland have all opted
against fluoridation, citing concerns about safety,
ethics, or the lack of demonstrable benefits. Despite
similar or lower rates of tooth decay in these countries,
they have achieved oral health improvements through
alternative strategies such as topical fluoride use,
education, and dietary interventions.
The divergence in global fluoridation policy invites
scrutiny and critical questions. For example, has
fluoridation become an outdated relic of public health
policy? Do its claimed benefits outweigh the risks,
particularly when fluoridated toothpaste is nearly
universal? And finally, is it ethically defensible to
administer a potentially harmful chemical via public
utilities, without individual consent?
Systemic vs. Topical Fluoride: Mechanism and Efficacy
Reconsidered
Historically, the rationale for water fluoridation
originated from the belief that fluoride has systemic
benefits, namely that fluoride ingested during
childhood integrates into developing enamel,
rendering
teeth
more
resistant
to
acid
demineralization. This paradigm has dominated public
health doctrine for decades. However, research over
the past 25 years has decisively shifted the scientific
consensus toward topical action as the principal
mechanism of fluoride efficacy while highlighting
significant systemic risks pertaining to ingested
fluoride.
The CDC, despite calling water fluoridation “one of the
ten greatest public health achievements of the
twentieth century,
” acknowledged as early as 1999 that
“Fluoride prevents dental caries predominantly after
eruption of the tooth into the mouth, and its actions
primarily are topical for both adults and children” [1].
This mirrors the findings of Featherstone et al., who
c
oncluded in their seminal 2000 study, “Fluoride, the
key agent in battling caries, works primarily via topical
mechanisms…Fluoride incorporated during tooth
development is insufficient to play a significant role in
caries protection” [2].
Moreover, a 2004 review in
Caries Research
further
asserted that systemic incorporation of fluoride during
enamel formation provides negligible resistance to
decay, compared to topical applications: “A dogma has
existed for many decades, that fluoride has to be
ingested and acts mainly pre-eruptively. However,
recent studies concerning the systemic effect of
fluoride supplementation concluded that the caries-
preventive effect of fluoride is almost exclusively
posteruptive” [3].
If fluoride works best when applied topically, then
ingesting it through water becomes an inefficient and
potentially hazardous route of administration. Topical
application via toothpaste (1000
–
1500 ppm fluoride)
provides controlled and effective exposure with
minimal systemic absorption. In contrast, fluoridated
drinking water (~0.7 ppm) results in widespread
systemic distribution, affecting every organ and
accumulating in tissues like bone and the pineal gland.
The topical benefits of fluoride from drinking water are
minor compared to those from toothpaste. Drinking
water
only
briefly
contacts
enamel
during
consumption. The Cochrane Collaboration’s 2015
systematic
review
found
that
most
studies
demonstrating caries reduction were conducted before
1975, when fluoridated toothpaste use was far less
common [4]. In modern populations, the evidence of
significant additional benefit from water fluoridation is
weak, especially when controlling for confounding
variables such as socioeconomic status, diet, and access
to dental care.
Moreover, the 2024 Cochrane update concluded that
among studies published after 1975, the mean
reduction in decayed, missing, or filled primary teeth
(DMFT) was only 0.24 teeth per child
—
a negligible
effect [5]. In terms of public health return on
investment, this minor benefit does not justify
widespread and indiscriminate exposure to ingested
fluoride and its many health risks.
In the next sections, these risks are explored in detail,
beginning with perhaps the most concerning:
neurotoxicity and the implications for childhood
cognitive development and intelligence quotient (IQ).
Neurodevelopmental Risk: Fluoride and Brain Health
Among the most consequential findings in fluoride
research are those regarding its effects on the
developing brain. Mounting evidence points to fluoride
being a potential neurotoxin, particularly when
exposure occurs during prenatal and early postnatal
development. Concerning evidence linking fluoride to
reductions in intelligence quotient (IQ) and altered
neurobehavioral
outcomes
also
merits
close
examination.
Numerous
observational
studies
from
varied
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geographic regions have associated higher fluoride
exposure with lower IQ scores in children. A 2012 meta-
analysis by Choi et al., published in
Environmental
Health Perspectives
, analyzed 27 studies and found a
consistent association between elevated fluoride levels
in drinking water and an average IQ reduction of 6.9
points in children [6]. While many of these studies were
conducted in regions with naturally high fluoride
concentrations (e.g., China, Iran, and India), the
implication of fluoride as a neurotoxin is biologically
plausible and consistent across cohorts.
Crucially, more recent studies have focused on
populations with fluoride exposures comparable to
those found in fluoridated North American water
systems (~0.7 mg/L). The ELEMENT study in Mexico, for
example, followed mother-child pairs and found that a
1 mg/L increase in maternal urinary fluoride during
pregnancy was associated with a 5
–
6 point reduction in
child IQ by ages 4
–
12 [7]. This was not a small or
isolated effect
—
it remained significant after controlling
for multiple confounders including socioeconomic
status, maternal education, and lead exposure.
The Canadian MIREC study, a government-funded
cohort of over 500 mother-child pairs, similarly found
that a 1 mg/L increase in maternal urinary fluoride
corresponded to a 4.5-point IQ decrease in male
offspring at ages 3
–
4, with a smaller, non-significant
effect in girls [8]. Another analysis from the same
cohort reported that infants who were formula-fed
with fluoridated water scored significantly lower in
performance IQ than those fed with non-fluoridated
water, particularly boys [9].
Finally, a 2023 dose-response meta-analysis by
Grandjean and Veneri published in
Environmental
Research
provided a more granular understanding of
the relationship. This team calculated a benchmark
dose level (BMDL) at which fluoride exposure would
lead to a 1-point IQ loss. The BMDL was approximately
0.2 mg/L in maternal urine fluoride
—
far below the
average levels observed in fluoridated populations [10].
These findings suggest that even current “optimal”
fluoridation levels may exceed reasonable thresholds
for neurotoxicity in vulnerable populations.
The biological plausibility of fluoride as a neurotoxin is
also supported by animal studies. Fluoride readily
crosses the placenta and accumulates in fetal tissue,
including the brain. In rodents, prenatal fluoride
exposure has been linked to oxidative stress, altered
neurotransmitter levels, and histological changes in the
hippocampus
—
a region critical for memory and
learning [11].
In response to mounting concerning evidence, the U.S.
National Toxicology Program (NTP) completed a
systematic review in 2020, concluding that fluoride is
“presume
d to be a cognitive developmental hazard to
humans” [12]. This classification was based on
moderate to high confidence in the human evidence
and some supporting animal studies. Notably, the NTP
found consistent associations between fluoride
exposure and lower IQ in children, even in studies of
water fluoride levels below 1.5 mg/L.
Opponents of these findings argue that ecological
studies are subject to bias and confounding. However,
the strongest studies
—
such as ELEMENT and MIREC
—
are prospective birth cohorts with individual-level
fluoride measurements and extensive adjustment for
potential confounders. Their findings cannot be easily
dismissed or blamed on poor design.
The implications of fluoride-induced neurotoxicity are
far-reaching. Even a modest average IQ reduction
across a population can shift the curve of intellectual
ability, reducing the number of high-performers and
increasing the number of individuals requiring special
educational services. According to Grandjean, a
population-wide IQ loss of 5 points equates to a
profound economic and societal burden, including
reduced productivity and increased social support
needs [13].
Given that fluoride’s primary dental benefits are
topical, not systemic, and that systemic exposure offers
only very minor cavity prevention, the tradeoff
between significant cognitive damage and negligible
dental health benefits becomes medically and ethically
indefensible.
Endocrine Disruption: Fluoride’s Effects on Thyroid
and Pineal Gland Function
Fluoride’s interaction w
ith the endocrine system,
particularly the thyroid and pineal glands, is well
documented in toxicological and epidemiological
research. The thyroid gland plays a critical role in
regulating metabolism, brain development, and mood.
Fluoride, as a halogen in the same chemical family as
iodine, competes with iodine uptake in the thyroid. This
competition can reduce the synthesis of thyroid
hormones
—
especially in iodine-deficient individuals.
Historically,
sodium
fluoride
was
used
pharmacologically to treat hyperthyroidism due to its
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known suppressive effects on thyroid activity. The
mechanism involves inhibition of thyroid peroxidase
(TPO), an enzyme essential for the iodination of
tyrosine residues and the subsequent synthesis of T3
and T4 hormones.
Modern epidemiological studies have
reignited
concern
about
fluoride’s
impact on the thyroid. A 2015 study by
Peckham et al., conducted in England,
used a large dataset from primary care
providers to compare hypothyroidism
prevalence in fluoridated versus non-
fluoridated areas. The results revealed
that those in areas with fluoride levels
≥0.7 mg/L were nearly twice as likely to
report high rates of hypothyroidism,
even after adjusting for age and sex [14].
Further evidence comes from cross-sectional analyses
conducted in the United States and Canada. Malin AJ,
et al. found that adolescents living in fluoridated
regions had statistically lower free T4 concentrations
than those in non-fluoridated regions, despite no
difference in TSH levels, suggesting subtle suppression
of thyroid hormone production [15]. This pattern may
be particularly consequential during periods of rapid
development, such as adolescence or pregnancy.
In animal models, fluoride exposure has consistently
resulted in thyroidal changes. Rats exposed to 1
–
5 mg/L
fluoride in drinking water exhibited decreased serum
T3 and T4 levels and increased TSH, mirroring
hypothyroidism in humans. These endocrine effects
have
downstream
implications
for
cognitive
development, growth, and energy metabolism.
The pineal gland is another endocrine organ profoundly
affected by fluoride. Located near the center of the
brain, the pineal gland secretes melatonin
—
a hormone
that regulates circadian rhythm and the sleep-wake
cycle. Melatonin is also implicated in antioxidant
activity and immune modulation.
In 2001, University of Surrey researcher Dr. Jennifer
Luke demonstrated that fluoride accumulates in the
pineal gland in quantities similar or greater than
fluoride accumulation in the bones and teeth [16]. Her
autopsy-based
study
found
pineal
fluoride
concentrations averaging over 300 mg/kg, with the
degree of calcification correlated with decreased
melatonin production in adolescents. Luke proposed
that this could partly explain the earlier onset of
puberty observed in fluoridated populations, as
melatonin suppresses reproductive hormone secretion
during childhood.
Other studies corroborate Luke’s conclusions. A 2019
ecological study in the U.S. found that adolescents in
fluoridated communities reported more sleep
disturbances and delayed bedtimes than those in non-
fluoridated regions [17]. Melatonin assays in small
cohorts have shown reductions in overnight levels
among individuals with high cumulative fluoride
exposure, though larger controlled studies are still
needed.
Given the widespread nature of thyroid disease and the
critical function of melatonin in regulating mood, sleep,
and immune response, fluoride’s potential role as an
endocrine disruptor raises serious public health
questions. While subtle at the individual level, the
population-level effects
—
particularly on vulnerable
groups
—
appears to be substantial.
Musculoskeletal Effects: Bone Quality, Fractures, and
Joint Health
Fluoride’s impact on the musculoskeletal system is
multifaceted, with negative effects accumulating over
time. Unlike most environmental toxins, which are
excreted relatively quickly, the div retains
approximately 50% of ingested fluoride, primarily in the
bones and teeth. This cumulative effect raises concerns
about skeletal fluorosis, impaired bone quality,
increased risk of fractures, and arthritic symptoms.
Skeletal fluorosis is a chronic metabolic bone disease
caused by prolonged ingestion of high levels of fluoride.
It is characterized by increased bone density
(osteosclerosis), joint pain, stiffness, and in severe
cases, crippling deformities. While endemic skeletal
fluorosis is rare in fluoridated countries, research
indicates that subtler skeletal effects may occur even at
exposure levels typical of municipal fluoridation (0.7
–
1.5 mg/L).
Clinical trials and observational studies have produced
mixed results on fluoride’s effects on bone mineral
density (BMD) and fracture risk. For example,
randomized controlled trials using high-dose fluoride
(20
–
40 mg/day) for osteoporosis showed increases in
spinal BMD but paradoxically led to an increased rate of
non-spinal fractures, suggesting that fluoride-
incorporated bone may be denser but structurally
inferior [18].
In population-based studies, similar concerns have
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emerged. A cohort study from Sweden followed 4,306
postmenopausal women for over a decade and found
that those with the highest fluoride exposure (~2.5
mg/day from water and food) had a 1.59-fold increased
risk of hip fracture compared to those with the lowest
exposure [19]. Importantly, the fluoride levels in this
study were within the range considered safe by U.S.
standards.
Additional data from the U.S. suggest that water
fluoridation may correlate with higher rates of bone
fracture in children and adolescents. A 2021 ecological
study comparing pediatric fracture rates across the
country found that those with water fluoride levels at
or above 0.7 mg/L had statistically higher incidences of
forearm, elbow, and lower-limb fractures [20]. While
the ecological design limits causal interpretation, the
findings are consistent with animal studies showing
compromised bone microarchitecture from chronic
fluoride exposure.
Fluoride also affects joint health. In regions with
moderate to high fluoride in drinking water (~1.5
–
3.0
mg/L), several case-control studies have found a strong
association between urinary fluoride levels and the
prevalence
of
radiographically
confirmed
osteoarthritis. A 2020 Chinese study reported that each
1 mg/L increase in urinary fluoride was associated with
a 27% increased occurrence of knee osteoarthritis [21].
Subjects in the highest exposure quartile had more than
double the risk compared to those in the lowest.
Furthermore, skeletal fluoride burden is known to
increase with age, water intake, and renal insufficiency.
Individuals with impaired kidney function
—
such as the
elderly or those with chronic kidney disease
—
are
especially vulnerable, as their ability to excrete fluoride
is reduced. Over decades, this may predispose to earlier
onset of osteoporosis, degenerative joint disease, and
even spinal stenosis.
Taken together, the evidence suggests that fluoride’s
skeletal effects are dose- and duration-dependent.
Even at current fluoridation levels, long-term
accumulation may subtly alter bone quality and joint
function. When juxtaposed against the marginal
benefits of water fluoridation for dental health, these
musculoskeletal risks merit serious public health
consideration.
Ethical Considerations of Involuntary Fluoridation
The practice of fluoridating public water supplies raises
pressing ethical questions regarding autonomy,
consent, risk distribution, and public health
governance. Central to the debate is whether it is
appropriate for governments to administer a
biologically active compound to entire populations
without individual consent
—
particularly when the
compound’s primary benefits are topical and when
solid evidence suggests ingestion has substantial health
risks.
Informed Consent and Autonomy
Modern bioethics emphasizes the principle of informed
consent, especially in the context of medical or quasi-
medical interventions. By fluoridating municipal water,
public health agencies bypass the individual’s right to
choose regarding consuming a pharmacologically active
substance. Unlike vaccines or medications, which
require informed consent and often involve targeted
application based on health status, fluoridation treats
all individuals identically, irrespective of age, pre-
existing conditions, or personal preferences.
This is particularly problematic for vulnerable
populations, such as infants, pregnant women, people
with renal insufficiency, and people with thyroid
disorders, all of whom may be more susceptible to
fluoride’s adverse effects. Yet flu
oridation policies
provide no mechanism for opt-out except through
intentional filtration initiatives or bottled water
—
often
at significant personal cost.
Disproportionate Burden on the Economically
Disadvantaged
Ironically, one of the primary justifications for water
fluoridation is to protect low-income populations,
under the assumption that they are less likely to access
professional dental care or fluoridated toothpaste.
However, these same groups are often the least able to
avoid fluoride exposure when desired. Water filters
capable of removing fluoride (such as reverse osmosis
systems) are expensive, and reliance on bottled water
poses a financial and environmental burden.
This asymmetry effectively forces economically
disadvantaged individuals to bear both the brunt of
fluoride exposure and the cost of avoiding it. Thus,
fluoridation may inadvertently deepen health
inequities rather than reduce them.
Medicalization Without Oversight
Fluoridation constitutes a form of mass medication, yet
it is implemented without the regulatory and ethical
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oversight typical of pharmaceutical interventions.
Unlike prescription drugs, fluoride administered via
drinking water does not undergo dose individualization,
safety screening, or monitoring for side effects. Nor
does it account for total fluoride exposure from all
sources (e.g., toothpaste, food, tea, air pollution),
which can push individuals
—
especially children
—
well
beyond recommended daily intake limits.
Furthermore, no distinction is made between
individuals who already receive adequate topical
fluoride through oral hygiene and those who do not.
The result is systemic overexposure in many cases, with
dental fluorosis now affecting more than 40% of
adolescents in the United States according to CDC data.
[22]
Legal and International Precedents
Several legal cases and international conventions
challenge the permissibility of fluoridation. The
Nuremberg Code, formulated after World War II to
guard against unethical experimentation, mandates
voluntary consent for medical interventions. Some
bioethicists argue that fluoridation violates this
principle. While court decisions in the U.S. have
generally upheld fluoridation, courts in other nations
(such as the Netherlands and Israel) have ruled against
the practice, citing human rights violations.
Internationally, most Western European countries have
chosen not to fluoridate, not necessarily because they
believe it is unsafe, but because they view it as ethically
and legally inappropriate to medicate an entire
population via the water supply without explicit
consent.
Public Trust and the Role of Government
Finally, continued fluoridation in the face of mounting
evidence of adverse effects risks eroding public trust in
health authorities. As awareness grows around
fluoride’s
risks, public resistance is also increasing.
Lawsuits have been filed against the U.S. Environmental
Protection Agency (EPA), and several municipalities
have repealed or suspended their fluoridation
programs, including the entire state of Utah.
Respect for bodily autonomy and transparent risk
communication are cornerstones of modern public
health ethics. Policies that obscure risks or impose
irreversible exposures without consent run counter to
these principles.
CONCLUSIONS AND RECOMMENDATIONS
The continued fluoridation of public water supplies,
while historically rooted in noble public health
intentions, no longer aligns with the best available
science, ethical principles, or global practices. Initially
introduced to address dental caries through systemic
fluoride incorporation into developing teeth, the
rationale for water fluoridation has been substantially
weakened by newer evidence indicating that fluoride’s
primary benefit is topical
—
not systemic
—
and that its
ingestion carries significant risks.
The scientific literature presents a strong case that
systemic
fluoride
exposure
contributes
to
neurodevelopmental harm, particularly during prenatal
and early childhood windows. Cohort studies and meta-
analyses have consistently reported IQ reductions
associated with fluoride levels currently found in
fluoridated water. Similarly, fluoride’s impact on
thyroid function and pineal gland calcification suggests
broader endocrine disruption that could contribute to
subclinical hypothyroidism, altered sleep patterns, and
early onset of puberty.
Skeletal effects, including compromised bone quality,
higher fracture risk, and osteoarthritic changes, further
demonstrate that fluoride acts as a cumulative toxin
with chronic exposure. These risks disproportionately
affect subgroups such as infants, those with kidney
disease, and the elderly.
Ethically, fluoridation represents an outdated model of
public health
—
one that overrides individual consent
and imposes risk without mechanisms for opt-out. It
places the burden of avoidance disproportionately on
low-income populations and lacks the regulatory
scrutiny expected of medical interventions.
Given these findings, the following recommendations
are proposed:
•
Public health agencies should reclassify water
fluoridation as a legacy policy, subject to sunset or
phase-out in favor of targeted topical fluoride
(toothpaste) and improved dental access.
•
Policy makers should prioritize informed consent
and individual choice, ensuring that fluoride
exposure is voluntary and adjustable by the
individual
rather
than
compulsory
via
infrastructure.
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•
Further large-scale, government-funded studies
should be conducted to monitor cumulative
fluoride intake and investigate its effects on
sensitive subpopulations.
•
Healthcare providers should receive education and
training regarding the risks of fluoride ingestion,
particularly for pregnant women and young
children.
Fluoridation’s place in public health must be
reexamined based on modern science as well as
through the lens of human rights, bodily autonomy, and
environmental responsibility. A policy once lauded for
preventing cavities now poses broader public health
concerns
—
concerns
that
demand
an
honest
reevaluation and targeted action.
REFERENCES
Centers for Disease Control and Prevention.
Achievements in public health, 1900
–
1999: fluoridation
of drinking water to prevent dental caries.
MMWR
Morb Mortal Wkly Rep
. 1999;48(41):933
–
940.
Featherstone JDB. The science and practice of caries
prevention.
J Am Dent Assoc
. 2000;131(7):887
–
899.
Marthaler TM. Changes in dental caries 1953
–
2003.
Caries Res
. 2004;38(3):173
–
181.
Iheozor-Ejiofor Z, Worthington HV, Walsh T, et al.
Water fluoridation for the prevention of dental caries.
Cochrane Database Syst Rev
. 2015;(6):CD010856.
Iheozor-Ejiofor Z, Worthington HV, Walsh T, O'Malley L,
Clarkson JE, Macey R, et al. Water fluoridation for the
prevention of dental caries.
Cochrane Database Syst
Rev
.
2021;10(10):CD010856.
doi:10.1002/14651858.CD010856.pub3.
Choi AL, Sun G, Zhang Y, Grandjean P. Developmental
fluoride neurotoxicity: a systematic review and meta-
analysis.
Environ Health Perspect
. 2012;120(10):1362
–
1368.
Bashash M, Thomas D, Hu H, et al. Prenatal fluoride
exposure and cognitive outcomes in children at 4 and
6
–
12 years of age in Mexico.
Environ Health Perspect
.
2017;125(9):097017.
Green R, Lanphear B, Hornung R, et al. Association
between maternal fluoride exposure during pregnancy
and IQ scores in offspring in Canada.
JAMA Pediatr
.
2019;173(10):940
–
948.
Till C, Green R, Flora D, et al. Fluoride exposure from
infant formula and child IQ in a Canadian birth cohort.
Environ Int
. 2020;134:105315.
Grandjean P, Veneri D. Benchmark dose analysis for
maternal pregnancy urinary fluoride and IQ in children.
Environ Res
. 2023;215:114213.
Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ.
Neurotoxicity of sodium fluoride in rats.
Neurotoxicol
Teratol
. 1995;17(2):169
–
177.
National Toxicology Program.
Fluoride exposure and
neurodevelopmental effects
. Res Triangle Park (NC):
Natl Toxicol Program; 2024. Available from:
https://ntp.niehs.nih.gov/sites/default/files/2024-
08/fluoride_final_508.pdf
Grandjean P, Landrigan PJ. Neurobehavioural effects of
developmental
toxicity.
Lancet
Neurol
.
2014;13(3):330
–
338.
Peckham S, Lowery D, Spencer S. Are fluoride levels in
drinking water associated with hypothyroidism
prevalence in England? J
Epidemiol Community Health
.
2015;69(7):619
–
624.
Malin AJ, Riddell J, McCague H, Till C. Fluoride exposure
and thyroid function among children in Canada.
Environ
Int
. 2018;121(Pt 1):667
–
674.
Luke J. Fluoride deposition in the aged human pineal
gland.
Caries Res
. 2001;35(2):125
–
128.
Malin AJ, Till C. Exposure to fluoridated water and
attention deficit hyperactivity disorder prevalence
among children and adolescents in the United States:
an ecological association.
Environ Health
. 2015;14:17.
Riggs BL, Hodgson SF, O’Fallon WM, et al. Effect of
fluoride treatment on the fracture rate in
postmenopausal women with osteoporosis.
N Engl J
Med
. 1990;322(12):802
–
809.
Helte E, Alfthan G, Sorva A, et al. Fluoride exposure and
hip fractures: a cohort study in Swedish women.
Osteoporos Int
. 2022;33(1):123
–
130.
Slade GD, Spencer AJ, Roberts-Thomson KF. Water
fluoridation and child dental health: what the evidence
shows.
Aust Dent J
. 2021;66(2):152
–
158.
Wang J, Yang Y, Cheng X, et al. The association between
fluoride exposure and knee osteoarthritis in a Chinese
The American Journal of Medical Sciences and Pharmaceutical Research
13
https://www.theamericanjournals.com/index.php/tajmspr
The American Journal of Medical Sciences and Pharmaceutical Research
population.
Biol Trace Elem Res
. 2021;199(9):3315
–
3323.
Beltrán-Aguilar ED, Barker LK, Canto MT, et al.
Surveillance for dental caries, dental sealants, tooth
retention, edentulism, and enamel fluorosis
—
United
States, 1988
–
1994 and 1999
–
2002.
MMWR Surveill
Summ
. 2005;54(3):1
–
43.
